Orthopedic Physical Assessment 4th Edition (with Companion DVD)

SAUNDERS ELSEVIER I 1830 Westline Indu ~trial Drive St. L()ui~, Missouri 63146 ORTHOPEDIC PHYSICAL ASSESSJ\'lENT EN...

Author: David J. Magee PhD BPT

333 downloads 3919 Views 94MB Size Report

This content was uploaded by our users and we assume good faith they have the permission to share this book. If you own the copyright to this book and it is wrongfully on our website, we offer a simple DMCA procedure to remove your content from our site. Start by pressing the button below!
Report copyright / DMCA form

DOWNLOAD PDF

SAUNDERS

ELSEVIER

I 1830 Westline Indu ~trial Drive St. L()ui~, Missouri 63146

ORTHOPEDIC PHYSICAL ASSESSJ\'lENT ENHANCED EDITION , 4 1 " EDITION Copyright 2006, Elsevier Sciences (USA). All rights reserved. ISBN 10: 1·4160-3I09-X ISBN 13: 978- 1-4160-3109-3 No part of tbis publication Illa\' be reproduced or transmitted in any fo rm or bv any means, el ec tronic

or mechanical , ineluding phorocop\', recording, or any inro rmatj on stor,lge and retrieval syste m, without

permissi on in writi.ng ti-om the publisher.

Permissio ns ma\' be sought din:ctlv fi'om Else,'itr's Health Sciences Ri ghts Department in Phil ad elphi a,

PA , USA: phone: (+ 1) 215 2387869, fax: (+ 1) 2152382239, c-mail: he .....~ /

!

:--..

".

Parietal bone --- __

Sphenoid bone Ethmoid bone Nasal septum

--------- Hard palate

A

- ----

~91~

~ -.:..~~~ ~~:-

-.

-

Frontal bone

--, Parietal bone

-~------------l---- O}J!~)-'-- ----- ----------bo", ~J. ~ ~~ .. ~~ '. ~~ M",",

Orbit

Nasal bone

Zygomatic - - - -- -- -- -.\-

Mandible --- -- -- -- -- -- -- -- --"

B

Squamous suture "

~-----,

"

/

L:;~::~bsOu~:re ----A------ -- -.""" , "' "

.

,,'- Sphenoid bone

r---- .'

-- -- ---Temporomandibular - -~.. t ~ - - -- --: - -JOin ,,--\. -Zygomatic arch,' / - -- -- -- /

Mastoid process '

c

.- -- -\--- -- ---- Frontal bone

~~ --;- -l.~~~: ,_ .- Nasal.bone --~ -- -.~~- ~ -- -- -- Ethmoid bone

Temporal bone:=' Occipital bone

Coronal suture

i,

( -- -. 1. -- -- -- - Zygomatic bone

~

_. _;

Maxilla

Exter~al auditory meatus

-:, - -- -- -- Mandible

Figure 2-1 Bones of the head and face. (A) Interior view. (B) Anterior view. (C) Lateral view. (From Jenkins, D.B.: Hollinshead's Functional Anatomy of the Limbs and Back. Philadelphia, W.B. Saunders Co., 1991, pp. 332-333.)

CHAPTER 2 • Head and Face

--=...--+--+--- Frontal sinus

+",~--f+-t-t---

Ethmoid sinus

Figure 2-2

The nasal sinuses. (Modified from Swartz, H.M.: Textbook o cal Diagnosis. Philadelphia, W.B. Saunders Co., 1989, p. 166

-1--....,..,.;--- Maxillary sinus

Table 2-1 Cranial Nerves and Methods of Testing Nerve I. Olfactory II. Optic

AJferent (Sensory)

Efferent (Motor)

Test

Smell: Nose

Identify familiar odors chocolate, coffee)

Sight: Eye

Test visual fields

III. Oculomotor

Voluntary motor: Levator of eyelid; superior, medial, and inferior recti; inferior oblique muscle of eyeball Autonomic: Smooth muscle of eyeball

Upward, downward, medial gaze Reaction to light

IV. TrocWear

Voluntary motor: Superior oblique muscle of eyeball

Downward and latera

Voluntary motor: Muscles of mastication

Corneal reflex Face sensation Clench teeth; push do chin to separate jaw

Voluntary motor: Lateral rectus muscle of eyeball

Lateral gaze

Voluntary motor: Facial muscles Autonomic: Lacrimal, submandibular, and sublingual glands

Close eyes tight Smile and show teeth Whistle and puff chee Identify familiar tastes sweet, sour)

V. Trigeminal

Touch, pain: Skin of face, mucous membranes of nose, sinuses, mouth, anterior tongue

VI. Abducens VII. Facial

VIII. VestibulococWear (acoustic nerve)

Taste: Anterior tongue

Hearing: Ear Balance: Ear

Hear watch ticking Hearing tests Balance and coordina test (continued on ne

70


Table 2-1 Cranial Nerves and Methods of Testing (Continued) Afferent (Sensory)

Efferent (Motor)

Touch, pain: Posterior tongue, pharynx Taste: Posterior tongue

Voluntary motor: Unimportant muscle of pharynx Autonomic: Parotid gland

Gag reflex Ability to swallow

Touch, pain: Pharynx, larynx, bronchi Taste: Tongue, epiglottis

Voluntary motor: Muscles of palate, pharynx, and larynx Autonomic: Thoracic and abdominal viscera

Gag reflex Ability to swallow Say "Ahhh"

Voluntary motor: Sternocleidomastoid and trapezius muscle

Resisted shoulder shmg

Voluntary motor: Muscles of tongue

Tongue protrusion (if injured, tongue deviate toward injured side)

Nerve IX. Glossopharyngeal

X. Vagus

XI. Accessory

XII. Hypoglossal

Test

Adapted from Hollinshead, W.H., and D.B. Jenkins: Flillctional Anatomy of the Limbs and Back. Philadelphia, W.B. Saunders Co., 1981, 358; and Reid, D.C.: Sports Injury Assessment and Rehabilitation. ew York, Churchill Livingstone, 1992, p. 860.

The lens is a crystalline structure located immediately behind the iris that permits images from varied distances to be focused on the retina. It is primarily the lens and its supporting ligaments that separate the eye into chambers-the anterior chamber (aqueous humor) and the posterior chamber (vitreous humor). Finally, the retina is the primary sensory structure of the eye that transforms light impulses into electrical impulses that are then transmitted by the optic nerve to the brain, which interprets the impulses as the objects seen. The external ear consists of cartilage covered with skin. Its primary purpose is to direct sound and to protect the external auditory meatus, through which sound is transmitted to the eardrum. The external ear, which is sometimes called the pinna, auricle, or trumpet, consists of the helix and lobule around the outside and the triangular fossa, antihelix, concha, tragus (car-

Sclera and conjunctiva

Eyebrow

Pupil

Eyelashes (cilia)

~upper eyelid

~=~-Lateral palpebral

Lacus----= lacrimalis

Medial palpebral commissure

Figure 2-3 External features of the eye.

commissure

Iris

Lower eyelid

Palpebral fissure

tilaginous projection anterior to external auditory m tus), and antitragus on the inside (Fig. 2-7). middle ear structures consist of the tympanic m brane, or eardrum, which vibrates when sound hit and sends vibrations through the ossicles-called malleus (hammer), incus (anvil), and stapes (stirru

Table 2-2 Muscles of the Eye: Their Actions and Nerve Supply Action

Muscles Acting

Nerve Supply

Moves pupil upward

Superior rectus

Oculomotor (CN

Moves pupil downward

Inferior rectus

Oculomotor (CN

Moves pupil medially

Medial rectus

Oculomotor (CN

Moves pupil laterally

Lateral rectus

Abducens (CN VI

Moves pupil downward and laterally

Superior oblique

TrocWear (CN IV

Moves pupil upward and laterally

Inferior oblique

Oculomotor (CN

Elevates upper eyelid

Levator palpebrae superioris

Oculomotor (CN

CN

=

cranial nerve.


-'I - perior oblique

c

- perior rectus

"

0

. '",'\\\\\\\-\.,

Lacrimal glan

c

Puncta

"

:;>

-

c:

edial rectus

-+--- Tear sac

~

~

....aleral rectus -;erior rectus -ferior oblique

>.

~

~ :'~ Canaliculi

Nasolacrimal

I

'

(~

Elevation

Intorsion

Figure 2-5

The lacrimal apparatus. (Modified from Swartz, H.M.: Textbook Physical Diagnosis. Philadelphia, W.B. Saunders Co., 1989, p. 1 Abduction

~

Gif(

B

Adduction

to the cochlea. The cocWea, which is part of the in ear, transmits the sound waves to the vestibulococW nerve (cranial nerve VIII), which transmits elect impulses to the brain for interpretation. The semic lar canals, the other part of the inner ear, playa sig cant role in maintaining balance. The external nose, like the external ear, con primarily of cartilage covered with skin. However proximal portion contains bone covered with skin.

Depression

Figure 2-4 ~luscles

(A) and movements (B) of the eye. (Modified from Swartz, H.M.: Textbook of Physical Diagnosis. Philadelphia, W.B. Saunders Co., 1989, pp. 125-126.)

~

Levator palpebrae musc

~

MOiler's muscle

~ ~

l c'\1S7'/.?'"/

Orbicularis oculi muscle

5 m

Confusion

Loss of consciousness

0

Tinnitus

No

Mild

Moderate

Severe

Often seve

Dizziness

No

Mild

Moderate

Severe

Usually sev

Headache

No

May be present (dull)

Often

Often

Often

Disorientation and unsteadiness

None or minimal

Some

Moderate

Severe (5-10 min)

Often seve (> 10 m

Blurred vision

No

No

No

Not usually

Possible

Postconcussion syndrome

No

Possible

Possible

Possible

Possible

Personality changes

No

No

No

Possible

Possible

Data from Vegso, J.J., and J.S. Torg: Field evaluation and management of intracranial injuries. In Torg, J.S. (ed.): Athletic Injuries Head, Neck and Face. St. Louis, Mosby-Year Book Inc., 1991, pp. 226-227.

to

th


ries) are the most common cause of loss of consciousness after trauma. They are defined as any alteration in cerebral function due to direct or indirect force to the head. Signs and symptoms of concussions are shown in Table 2-5. 2 - 4 Concussions can occur from a blow to the head or jaw or a fall on the buttocks from a height and can result in an inability to process information. Their effect is cumulative and the risk of having another concussion following an initial concussion is 4 to 6 times greater than someone who has not had a concussion. 3,5 Concussions can lead to continued and severe problems (e.g., post concussion syndrome, second impact syndrome).3,5-7 Kelly and Rosenberg 3,4 have developed a Standardized Assessment of Concussion SAC) (Fig. 2-11),8 which provides a concise evaluation method for concussion by including measures of orientation, immediate memory, concentration, delayed recall, and other parameters. To be maximally effective, athletes should have done baseline tests in their preparticipation evaluation (i.e., they should have done the SAC in the preparticipation evaluation).3,9 Lovell and Burke 10 have developed a similar form for ice hockey. There are many different grading systems for concussions, but the grades advocated by Torg l l are described here. With each grade of concussion, the igns and symptoms worsen, and sequelae are more evident. With a grade I concussion, the patient is slightly confused and may have a dazed look. The patient is completely lucid within 5 to 15 minutes; has no amneia, sequelae, or residual symptoms; and has had no loss of consciousness. Some people refer to the grade I concussion as the patient's having his or her "bell rung." With a grade II concussion, there is slight confuion, and posttraumatic amnesia becomes evident. Posttraumatic (anterograde) amnesia is the loss of memory for events occurring immediately after wakening or from the moment of injury. Posttraumatic amnesia is considered to be the length of time from injury until conscious memory returns. The patient who sustains a period of posttraumatic amnesia of less than 60 minutes is considered to have sustained a mild head injury. If the period of posttraumatic amnesia lasts from 1 to 24 hours, moderate head injury is considered to have occurred. If the posttraumatic amnesia lasts for more than 1 week, the patient is considered to have sustained a very serious head injury. If the duration of the posttraumatic amnesia is more than 7 days, full return to neurological function is highly unlikely. 12 With a grade II concussion, the patient may experience mild tinnitus (ringing in the ears), mild dizziness, and a dull headache with some disorientation. The patient who experienced a grade II concussion may also develop a postconcussion syndrome (i.e., have continual

Table 2-5 Signs and Symptoms of Concussions

Late (Delayed

Acute Lightheadedness Delayed motor and/or verbal responses Memory or cognitive dysfunction

Persistent low grade headache Easy fatiguability Sleep irregularities

Disorientation

Inability to perform activities

Amnesia

Depression/anxiety

Headache

Lethargy

Balance problems/ incoordination

Lightheadedness

Memory dysfunctio

Vertigo/dizziness

Personality changes

Concentration difficulties

Low frustration tole irritability

Loss of consciousness Blurred vision Vacant stare (befuddled facial expression)

Intolerance to brigh lights, loud sound

Photophobia Tinnints ausea Vomiting Increased emotionality Slurred or incoherent speech

neurological problems after the concussion), wh seen in about 10% of concussion cases. The sign symptoms of this syndrome include persistent aches, especially with exertion; inability to conce and irritability. The symptoms may last from weeks to several years.

Head Injury Severity Based on length of Posttraumatic Amnesia 1 week:

Serious (full return of neurological function unlikely)

SAC: Standardized Assessment of Concussion

NAME: AGE:

EXAMINER:

SEX:

_

3) CONCENTRATION:

_

Digits Backward: (if correct, go to next string length. If incorrect, read trial 2. Stop after incorrect on both trials.) 4-9-3 6-2-9 0 3-8-1-4 3-2-7-9 0 6-2-9-7-1 1-5-2-8-6 0 7-1-8-4-6-2 5-3-9-1-4-8 0

Nature of Injury:

_

Date of Exam:

Time:

No.

1) ORIENTATION: Month: Date: Day of Week: Year: Time (within 1 hour):

_ _

Months in Reverse Order: (entire reverse sequence correct for 1 point) DEC-NOV-OCT-SEP-AUG-JUL JUN-MAY-APR-MAR-FEB-JAN

o o o o o

0

/5

Concentration Total Score

/5

Orientation Total Score

EXERTIONAL MANEUVERS (when appropriate: 2) IMMEDIATE MEMORY: (all 3 trials are completed regardless of score on trials 1 & 2; score equals sum across all 3 trials) LIST Elbow Apple Carpet Saddle Bubble Total

TRIAL 1 o 1 o 1 o 1 o 1 o 1

Immediate Memory Score

TRIAL 2 o 1 o 1 o 1 o 1 o 1

5 jumping jacks 5 sit-ups

TRIAL 3 o 1 o 1 o 1 o 1 o 1

4) DELAYED RECALL

/15

Delayed Recall Score

5 push-ups 5 knee-bends

o o

Elbow Apple Carpet Saddle Bubble

o o

o

SUMMARY OF TOTAL SCORES: Orientation Immediate Memory Concentration Delayed Recall

/ 5 / 15 / 5 / 5

OVERALL TOTAL SCORE

/ 30

/5

Figure 2-11 Standardized Assessment of Concussion (SAC). (Redrawn from McCrea, M., J.P. Kelly, J. Kluge, B. Ackley, and C. Randolph: Standard assessment of concussion in football players. Neurology 48:586588, 1997.)

A patient with a grade III concussion has the same symptoms as someone with a grade II concussion and also experiences retrograde amnesia. Retrograde amnesia is loss of memory of events that occurred before the injury. It may take 5 to 10 minutes for retrograde amnesia to develop after the concussion, and amnesia may involve only a few minutes before the injury. For this reason, the patient should frequently be questioned about what happened before the injury oc-

curred and how it occurred, to see if there change in the patient's memory pattern. The ways some degree of permanent retrograde with these patients. With a grade IV concussion, the patient lo sciousness for 5 minutes or less. The level sciousness may vary; the patient may be comat porous, obtunded, lethargic, confused, or fu The patient goes through the following stage

78


Head Signs and Symptoms Requiring Specialist Care

Table 2-7 Location of Headache and Usual Causes Location

• Presence of amnesia

Usual Causes

Forehead

Sinusitis, eye or nose disorder, muscle s of occipital or suboccipital region

Side of head

Migraine, eye or ear disorder, auriculotemporal neuralgia

Occipital

Myofascial problems, herniated disc, eyestrain, hypertension, occipital neuralgia

• More than one first- or second-degree concussion

Parietal

• Prolonged disorientation, unsteadiness, or confusion (>2-3 min)

Hysteria (viselike), meningitis, constipat tumor

Face

Maxillary sinusitis, trigeminal neuralgia, dental problems, tumor

• Prolonged residual symptoms • Loss of consciousness • Prolonged headache • Postconcussion syndrome • Personality changes

• Blurred vision • Dizziness (>5 min) • Tinnitus (>5 min)

(cranial nerve VIII) normal? These questions give the examiner some idea of whether neurological structures have been injured and, if so, which ones. 7. What activities aggravate the particular problem? 8. What activities ease the particular problem? 9. Does the patient have a headache and if so where? (Tables 2-6 and 2-7) Is the headache' tolera~ ble? What type of headache is it? Is it a throbbing, pounding, boring, shocklike, dull, nagging, or constant-pressure type of headache? Is the pain of the

Table 2-6 Type of Headache Pain and Usual Causes Type of Pain

Usual Causes

Acute

Trauma, acute infection, impending cerebrovascular accident, subarachnoid hemorrhage

Chronic, recurrent

Migraine (definite pattern of irregular interval); eyestrain; noise; excessive eating, drinking, or smoking; inadequate ventilation

Continuous, recurrent

Trauma

Severe, intense

Meningitis, aneurysm (ruptured), migraine, brain tumor

Intense, transient, shocklike

Neuralgia

Throbbing, pulsating (vascular)

Migraine, fever, hypertension, aortic insufficiency, neuralgia

Constant, tight (bandlike), bilateral

Muscle contraction

headache aggravated by movement or by rest? Wh the exact location of the headache? Is the head affected by position or time of day? (Table 2-8) it cover the entire head, the sinus region, behind eyes, the hat band distribution, the neck, or the put area? It is important for the examiner to re the location, character, duration, and frequency o headache, as well as any factors that appear to e aggravate or relieve the pain, so that a diagnosis ca made and any changes can be noticed (Table 2-9) 10. Is the patient dizzy or unsteady or having p lems with balance? The examiner should also whether the dizziness is brought on by sudden st ing up, turning, or bending or whether it occurs w out movement. It must be remembered that "d ness" is a word sometimes used by patients to ind unsteadiness in walking. Dizziness is usually assoc with problems of the middle ear, vertebrobasilar i ficiency, or problems in the upper cervical spine. tigo implies a rotary component; the patient's env ment seems to whirl around the patient, or

Table 2-8 Effect of Position or Time of Day on Headache Position or Time of Day When Headache Is Worst

Usual Causes

Morning

Sinusitis, migraine, hypertensi alcoholism, sleeping positio

Afternoon

Eyestrain, muscle tension

ight

Intracranial disease, osteomyel nephritis

Bending

Sinusitis

Lying horizontal

Migraine


patient's body seems to rotate in relation to the environment. If the patient complains of dizziness or vertigo, the time of onset and duration of these attacks hould be noted. A description of the type of motion that occurs and any other associated symptoms should be included. Balance may be affected by problems within the brain or the semicircular canals in the inner ear. The examiner should also note whether the patient is talking about unsteadiness, loss of balance, or actual falling. 11. Is the patient unduly irritated or having trouble concentrating? The patient's state will give an indication of the severity of the injury. 12. Does the patient know where he or she is, who he or she is, the day, and the time of day? Does the patient have some idea of what was happening when the injury occurred? These types of questions give an indication of the severity of the injury. 13. Does the patient have any memory of past events or what occurred before or after the injury? This type of question tests for retrograde amnesia, posttraumatic amnesia, and injury severity, which can be determined by asking the patient straightforward questions about events in the patient's own past, such as birthdate or year of graduation from high school or university. Questions about the injury, preceding events, and posttraumatic events may also be asked. The examiner must ensure that the answer to such questions is known by the examiner or someone present at the time of the examination. Recent memory can be tested by giving the patient two to five common objects or names, such as the color "red," the number "5," the name "Mr. Smith," and the word "pride" to remember and then asking the patient to name them 5 or 10 minutes later. The patient may be asked to repeat the words two or three times when the examiner initially says them to test immediate recall or to ensure that the patient can say and recall the words. Immediate recall, another form of memory, is best tested by saying a series of single digits and asking the patient to repeat them. ormally, a person can repeat at least six digits, and many people can repeat eight or nine. The patient may also be asked to repeat the months of the year backward in a similar type of test. Memory is generally thought to be formed and stored in certain regions of the temporal lobes. The parietal lobe of the brain is thought to enable one to have an appreciation of the environment, to interpret visual stimuli, and to communicate. 14. Can the patient solve simple problems? Because concussions reduce the ability to process information, it is important to determine the patient's reasoning and processing ability. For example, does the patient know his or her home telephone number? Is the patient able to do the "minus 7" or "serial 7" test (i.e.,

count backward from 100 by sevens)? This test the examiner some idea of the patient's calcu ability and concentration skills. Mathematic abilit ability to add, subtract, multiply, and divide) ca be evaluated to test processing ability. In additio patient can be asked to name several important p from the present in reverse chronological order the last three presidents of the United States) give the names of some familiar capital cities. F the patient should be tested on whether abstrac tions can be comprehended. For example, one quote a common proverb such as "a bird in the is worth two in the bush" and then ask the pati explain what is meant. Patients with organic m impairment and certain patients with schizop may give a concrete answer, failing to recogniz abstract principle involved. 12 The ability to conce ize, abstract, plan ahead, and formulate rational ments of problems or events is largely a funct the frontal lobes. 15. Can the patient talk normally? Patients w sions of the parietal lobe have great difficulty in municating and understanding what is occ around them. Dysarthria indicates defects in ar tion, enunciation, or rhythm of speech. It usua sults from extraneural problems such as poordentures, malformation of the oral structures, o pairment of the musculature of the tongue, pharynx, or lips because of incoordination, wea or abnormal innervation. It is characterized by ring, slowness of speech, indistinct speech, and in normal speech rhythm. Dysphonia is a disor vocalization characterized by the abnormal prod of sounds from the larynx. Dysphonia is usually by various abnormalities of the larynx itself or innervation. The principal complaint of dyspho hoarseness, ranging from mild roughness of the to inability to produce sound. Dysphasia denot inability to use and understand written and s words as a result of disorders involving cortical c of speech or their interconnections in the dom cerebral hemisphere. With all of these condition peripheral mechanisms for speech remain intact. 16. Does the patient have any allergies, or patient receiving any medication? Allergies may the eyes and nose, as may medications. Medic themselves may mask some symptoms. 17. Is the patient having any problems wit eyes? Monocular diplopia (blurred vision when ing with one eye) may be due to hyphema, de lens, or other trauma to the globe of the eye. B lar diplopia (blurred vision when looking through eyes) occurs in 10% to 40% of patients with a z fracture. It may be caused by soft-tissue entrap neuromuscular injury (intraorbital or intramus

Table 2-9 Headaches: A Differential Diagnosis Disorder

Sex/Age Predominance

Nature of Pain

Frequency

Location

Duration

Prodromal Events

Precipita Facto

Migraine

Female/20 to 40 years

Builds to throbbing and intense

Usually not more than twice a week May be nocturnal

Usually unilateral

Several hours to days

Visual disturbances can occur contralateral to pain site

Unknown be phys emotion hormon dietary

Cluster (histamine) headache

Male/40 to 60 years

Excruciating, stabbing, burning, pulsating

1 to 4 episodes per 24 hours Nocturnal manifestation

Unilateral, eye, temple, forehead

Minutes to hours

Sleep disturbances or personaliry changes can occur

Unknown be sero histami hormon blood f

Hypertension headache

None

Dull, throbbing, nonlocalized

Variable

Entire

Variable

None

Activiry th increase blood pressure

Excruciating, spontaneous, lancinating, lightning Excruciating, spontaneous, lancinating, lightning Dull pain or pressure in head

Can occur many (12 or more) times per day Can occur many (12 or more) times per day

30 seconds to 1 minute

Disagreeable tingling

Touch (co to affec area

Generalized discomfort in or around the eyes Dull, persistent

Intensify with sustained visual effort

Trigeminal neuralgia (tic douloureux)

Female/40 to 60 years

Glossopharyngeal neuralgia

Male/40 to 60 years

Cervical neuralgia

None

Eye disorders

None

Sinus, ear, and nasal disorders

None

craniunl,

Variable

especially occipital region Unilateral along trigeminal nerve area Unilateral retrolingual area to ear

one

Movemen contact the phar

Bilateral, occipital, frontal, or facial Entire cranium

Variable

None

Posture o head movem

During and afrer visual effort

None

Impairme eye fun

Frontal, temporal,

Variable

None

Infection, allergy, chemica bending strainin

ear, nose,

occipital

Modified from Esposito,

30 seconds to 1 minute

C.T., G.A. Grim, and T.K. Binkley: Headaches: A differential diagnosis. J. Craniomand. Pract. 4:320-321, 1986


able 2-9 Headaches: A Differential Diagnosis (Continued)

Cause J.Somotor

Yes

asomotor

Minor

':=gh blood ressure;

diastolic > 120 mrn Hg

·

Familial Predisposition

urological

Nausea, vomiting, pallor, photophobia, mood disturbances, fluid retention Ipsilateral sweating of face, lacrimation, nasal congestion or discharge

Only as related to hypertension

None

· -eurological

None

• 'eurological, pressure on roots of spinal nerves

None

.ornea, iris, or

Other Possible Symptoms

Possible

mrraocuJar pain

Reddened conjunctiva, lacrimation

Dizziness, auditory disturbances Diminished vision,

sensitiviry to light, tearing .. ockage, inflammation, infection

8

hemorrhage, or edema. It disappears when one eye closed. Double vision, which occurs when the goo eye is closed, indicates that some structure of the eye injured. If it occurs with both eyes open, there something affecting the free movement of the eye (Tables 2-10 and 2-11). 18. Does the patient wear glasses or contact lenses If the patient wears glasses, are the lenses treate (hardened) or made of polycarbonate? If they ar hardened, how long ago were they treated? If conta lenses were worn, are they hard, soft, or extende wear? Were eye protectors worn? If so, what type wer

Table 2-10 Common Visual Eye Symptoms and Disease States Visual Symptom

Associated Causes

Loss of vision

Optic neuritis Detached retina Retinal hemorrhage Central retinal vascular occlusion

Spots

No pathological significance *

Flashes

Migraine Retinal detachment Posterior vitreous detachment

Loss of visual field or presence of shadows or curtains

Retinal detachment Retinal hemorrhage

Glare, photophobia

Iritis (inflammation of the iris) Meningitis (inflammation o the meninges)

Distortion of vision

Retinal detachment Macular edema

Difficulty seeing in dim light

Myopia Vitanlin A deficiency Retinal degeneration

Colored haloes around lights

Acute narrow angle glaucoma Opacities in lens or cornea

Colored vision changes

Cataracts Drugs (digitalis increases yellow vision)

Double vision

Extraocular muscle paresis or paralysis

one

* May precede a retinal detachment or be associated with fertility drugs. From Swartz, M.H.: Textbook of Physical Diagnosis. Philadelphia, W.B. Saunders Co., 1989, p. 132.

Table 2-11 Common Nonvisual Eye Symptoms and Disease States Nonvisual Symptom

Associated Causes

Itching

Dry eyes Eye fatigue Allergies

Tearing

Emotional states Hypersecretion of tears Blockage of drainage

Dryness

Sjogren's syndrome Decreased secretion as a result of aging

Sandiness, grittiness

Conjunctivitis

Fullness of eyes

Proptosis (bulging of the eyeball) Aging changes in the lids

Twitching

Fibrillation of orbicularis oculi

Eyelid heaviness

Fatigue Lid edema

Dizziness

Refractive error Cerebellar disease

Blinking

Local irritation Facial tic

Lids sticking together

Inflammatory disease of lids or conjunctivae

Foreign body sensation

Foreign body Corneal abrasion

Burning

Uncorrected refractive error Conjunctivitis Sjogren's syndrome

Throbbing, aching

Acute iritis (inflammation of the iris) Sinusitis (inflammation of the sinuses)

Tenderness

Lid inflammations Conjunctivitis Iritis

Headache

Refractive errors Migraine Sinusitis

Drawing sensation

Uncorrected refractive errors

From Swartz, M.H.: Textbook of Physical Diagnosis. Philadelphia, W.B. Saunders Co., 1989, p. 133.

they? Is there watering of the eyes? Is there any pain in the eyes? Small perforating injuries may be painless. If the patient complains of flashes of bright light, "a curtain falling in front of the eye," or floating black specks, these findings may be an indication of retinal detachment. These questions tell the examiner whether the eyewear or eyes need to be examined in greater detail.

19. Is the patient having any problem with Does the patient complain of an earache? If was the onset and what is the duration of the Does the patient complain of pain or a discha the ear? Is the earache associated with an up ratory tract infection, swimming, or trauma? tient should also be questioned on the m cleaning the ear. If there appears to be a hea the patient should be asked whether the he came on quickly or slowly, whether the pati best on the telephone (amplified sound) or i or noisy environment, and whether speech soft or loud. Does the patient use a hearing a 20. Is the patient having any problems nose? Has the patient used nose drops or spr how much? How often? How long have thes tions been used? Does the patient have any charge, and if so, what is its character-wat coid, purulent, crusty, or bloody? Does the have any odor (indicative of infection), and is eral or bilateral? Does the patient exhibit an ated nasal symptoms such as sneezing, nasa tion, itching, or mouth breathing? Does th complain of a nosebleed, and has the patient nosebleeds? If so, how frequent are the no what is the amount of the bleeding, and wha to be causing the bleeding? Positive respons of these questions indicate that the nose mu amined in greater detail. 21. If the examiner is concerned about th and teeth or the temporomandibular joints, related to these areas can be found in the c temporomandibular joints (see Chapter 4). It tant, however, to ensure that the patient's d clusion and biting alignment have not bee Are all the teeth present, and are they symm there any swelling or bleeding around the t the teeth mobile or is part of a tooth missin pulp exposed? Each of these questions helps d whether the teeth have been injured. Teeth been avulsed, if intact, should be reimp quickly as possible. If reimplanted after (dnsed in saline solution or water) within less minutes, the tooth has a 90% chance of being If it is not possible to reimplant the tooth, be kept moist in saline, or the patient shoul between the gum and cheek while dental sought. 22. Questions concerning the neck and spine can be found in Chapter 3.

... Observation

For proper observation 18 - 21 of the head and hat, helmet, mouth guard, or face guard sh


removed. If a neck injury is suspected or the patient resents an emergency situation, the examiner may rake the time to remove only those items that are lllterfering with immediate emergency care. If a neck ;njury is suspected, extreme caution should be obrved when removing the item. When assessing the ead and face, the examiner must also observe and ess the posture of the cervical spine and the tempoomandibular joints; see Chapters 3 and 4 for detailed escriptions of observation of these areas. When observing the head and face, it is essential · at the examiner look at the face to note the position d shape of the eyes, nose, mouth, teeth, and ears d look for deformity, asymmetry, facial imbalance, 'elling, lacerations, foreign bodies, or bleeding durg rest, with movement, or with different facial exressions. 22 One should also note, as much as possible, • e individual's normal facial expression. The facial ex_ression of the patient often reflects the patient's genral feeling and well-being. A dazed or vacant look ften indicates problems. While talking to the patient, • e examiner should watch for any asymmetry of facial otion or change in facial expression when the patient wers; some slight facial asymmetry is common. In ddition, small degrees of paralysis may not be obvious JIlless an exaggerated expression is attempted. If some -J. ial paralysis is suspected, the patient should be asked ·0 make exaggerated facial expressions that will demn trate the paralysis. If facial asymmetry is present, ne should note whether all of the features on one .de of the face are affected or only a portion of the :-J.ce is affected. For example, with facial nerve (cranial nerve VII) paralysis, the entire side of the face is af-ccted, although the most noticeable differences will ccur around the eye and one side of the mouth. If

only one side of the mouth is involved, then a pro lem with the trigeminal nerve (cranial nerve V) shou be suspected. Any changes in the shape of the face unusual features such as masses, edema, puffine coarseness, prominent eyes, amount of facial hair, e cessive perspiration, or skin color should be noted. E puffiness is often one of the earliest signs of edema the face. Skin color may include cyanosis, pallor, jau dice, or pigmentation, and each may be indicative different systemic problems. The examiner should view the patient from t front, side, behind, and above, noting the area behi the ears, at the hairline, and around the crown the head as well as on the face (Fig. 2-12 If one suspects a skull (cranial vault) injury, one shou look behind the ears, at the hairline, and around t crown of the head for any deformity, bruising, or la eration. Viewing from the front, the examiner should o serve the patient's hairline, noting any abnormalitie The soft tissues such as the eyelids, eyebrows, cheek lips, nose, and chin should be inspected for laceration bruising, or hematoma (Figs. 2-13 and 2-14). T eyes should be level. For example, a zygoma fractu causes the eye on the affected side to drop (F 2-15). The two eyes should be compared for prom nence or retraction (Fig. 2-16). If there appears to any bulging, especially unilaterally, the examin should tilt the patient's head forward or back an looking from above, compare each cornea with the below, noting whether one or both corneas bulge b yond the lid margins. If one or both eyes appear bulge, the examiner can rougWy measure the distan from the angle of the eye to the corneal apex \vith pocket ruler.

B Figure 2-12 Views of the head and face. (A) Anterior. (B) Side. (C) Posterior. (D) Altered facial features with smile.

Figure 2-13 Lacerations to the upper eyelid and eyebrow.

Figure 2-16

A severe glancing or direct blow to this right eye has resulted in ruptured globe. Note the depressed eye. (From Pashby, T.J., and R.C. Pashby: Treatment of sports eye injuries. In Schneider, R.C J.C. Kennedy, and M.L. Plant [eds.): Sports Injuries-Mechanism Prevention and Treatment. Baltimore, WillianlS & Wilkins, 1985 589.)

Figure 2-14 Contusion to the forehead caused by a racquetball ball.

Figure 2-15 Inferior displacement of the zygoma (1) results in depression of the lateral canthus and pupil (2) because of depression of the suspensory ligaments that attach to the lateral orbital (Whitnall's) tubercle. (Modified from Ellis, E.: Fractures of the zygomatic complex and arch. In Fonseca, R.J., and R.V. Walker [eds.]: Oral and Maxillofacial Trauma. Philadelphia, W.B. Saunders Co., 1991, p. 446.)

Immediate referral for further examination by a cialist is required for an embedded corneal fore body; haze or blood in the anterior chamber phema); decreased or partial vision; irregular, asymm ric, or poor pupil action; diplopia or double vis laceration of the eyelid or impaired lid function; pe ration or laceration of the globe; broken contact or shattered eyeglass in the eye; unexplained eye that is stabbing or deep and throbbing; blurred vi that does not clear with blinking; loss of all or par the visual field; protrusion of one eye relative to other; an injured eye that does not move as fully the uninjured eye; or abnormal pupil size or shape teardrop pupil usually indicates iris entrapment i corneal or scleral laceration. In addition, the should be observed from the lateral aspect. The n mal distance from the cornea to the angle of the ey 16 mm or less. The distances between the upper lower lids should be the same for both eyes. When eyes open, the superior eyelid should cover a por of the iris but not the pupil itself. If it covers mor the iris than the other upper eyelid does, or if it tends over the iris or pupil, ptosis or drooping of eyelid should be suspected. If the eyelid does cover part of the iris, retraction of the eyelid should suspected. Are the eyelids everted or inverted? N mally, they are neither. The examiner should also n whether the patient can close both eyes completely


Eye Signs and Symptoms Requiring Specialist Care • Foreign body that is not easily removed • Eye does not move properly • Altered pupil action • Abnormal pupil size or shape • Double vision • Blurred vision • Decreased or partial vision • Loss of part or all of visual field • Laceration of eye or eyelid • Blood between cornea and iris (hyphema) • Impaired eyelid function • Penetration of eye or eyelid • Eye pain • Sharp or throbbing eye pain • Protrusion or retraction of eye

eye injury is suspected, this action should be done ery carefully, because closing the eyes can increase amaocular pressure. The lids should be pressed to=ether only enough to bring the eyelashes together. _\ny inflammation or masses, especially on the lid mar;rn, should be noted. If present, a "black eye," or • riorbital contusion, should also be noted (Fig.

Figure 2-17 Black eye (periorbital ecchymosis).

2 -17). The lashes should be viewed to see if ther even distribution along the lid margins. "Racc eyes," which are purple discolorations of the eye and orbital regions, may indicate orbital fractures, b lar skull fractures, or a fracture of the base of anterior cranial fossa.1 8 This sign takes several hours develop. The conjunctiva should be inspected for hem rhage, laceration, and foreign bodies. 23 If the pat complains of "something in the eye," eversion of upper eyelid usually reveals a foreign body that often be easily brushed away. Displaced contact len are often found in this upper area of the eye. T conjunctival covering of the lower lid may be ex ined by having the patient look upward while the aminer draws the lower lid downward. The conjunc should be examined as being a continuous sheet epithelium from the globe to the lids. The color of sclera should also be noted. Posttraumatic conjunct hemorrhage (Fig. 2-18) and possible scleral lac tions (Fig. 2-19) should be noted, if present. In da skinned patients, pigmented areas may show up small dark spots or patches near the limbus. The sh and color of the cornea should be inspected. The an rior chambers of the eye should be inspected and co pared for clarity and depth. 23 If present, hyphema the form of haze or actual blood pooling (Fig. 2-2 in the anterior eye chamber should be noted. If th is any potential for or evidence of bleeding in anterior chamber of the eye, the patient's acti should be curtailed, because increased activity incre the chances of secondary hemorrhage during the week after injury. Examination of the cornea wit penlight shone obliquely on the eye should be car out to look for foreign bodies, abrasions, or lac tions. Corneal injuries can lead to lacrimation (t ing), photophobia (intolerance to light), or blepha spasm (spasm of the eyelid orbicular muscle) as wel extreme pain from exposure of sensory nerve endin Abrasions are readily outlined by a fluorescein s dipped into tears that have been exposed as the lo lid is pulled downward. The pupillary size (diameter range, 2 to 6 m mean, 3.5 mm), shape (round), and symmetry sho be compared with those of the other eye. Ellipt pupils often indicate a corneal laceration. The colo the irises of the eyes should be compared. When lo ing at the pupils, the examiner should note whe the pupils are equal. Are the pupils smaller or la than normal? Are they round or irregularly shap The pupils are normally slightly unequal in 5% of population, but inequality of pupil size should initi be viewed with suspicion. For example, unilateral d tion may be due to a sympathetic nerve response lowing a blow to the face. 2 Pupils tend to be sma

86


.I

Figure 2-18

(A) Posttraumatic conjunctival hemorrhage without other ocu orbital damage. (B) Posttraumatic conjunctival hemorrhage fr blunt injury, with a small hyphema (arrow). In this case, the was significant because of the presence of blood in the anteri chamber. (From Paton, D., and M.F. Goldberg: Managemen Ocular Injuries. Philadelphia, W.B. Saunders Co., 1976, p. 1 Subconjunctival ecchymosis with no lateral limit should sugge ous orbital fractures. (From Lew, D., and D.P. Sinn: Diagnos treatment of midface fractures. In Fonseca, R.J., and R. V. W [eds.]: Oral and Maxillofacial Trauma. Philadelphia, W.B. Sal Co., 1991, p. 250.)

in infants, the elderly, and persons with hyperopia (farsightedness), whereas they tend to be slightly dilated in persons with myopia (nearsightedness) or light-colored mses. The nose should be inspected for any deviations in shape, size, or color. 22 The skin should be smooth

Figure 2-19 Scleral rupture (arrow) at the limbus after blunt trauma. The iris and ciliary body have prolapsed into the subconjunctival space. (From

Paton, D., and M.F. Goldberg: Management of Ocular Injuries. Philadelphia, W.B. Saunders Co., 1976, p. 310.)

without swelling and should conform to the the face. The airways are usually oval and sy cally proportioned. If a discharge is present, its ter (i.e., color, smell, texture) should be no described. Bloody discharge occurs as a result staxis or trauma such as a nasal fracture, zygo ture, or skull fracture. Mucoid discharge is ty rhinitis. Bilateral purulent discharge can occur w per respiratory tract infection. Unilateral p thick, greenish, and often malodorous dischar ally indicates the presence of a foreign body. Depression of the nasal bridge can result fracture of the nasal bone. Nasal flaring is as with respiratory distress, whereas narrowing of ways on inspiration may be indicative of chron obstruction and be associated with mouth br The nasal mucosa should be deep pink and gl A film of clear discharge is often apparent on t septum. The nasal septum should be close to and fairly straight, appearing thicker anterior posteriorly. If present, a hematoma in the sep should be noted. Asymmetric posterior nasal may indicate a deviation of the nasal septum. With the patient's mouth closed, the lips sh observed for symmetry, color, edema, and surf normalities. Lipstick should be removed before


A

'gure 2-20 • -phema in the anterior chamber of the eye. (From Easterbrook, . and J. Cameron: Injuries in racquet sports. In Schneider, R.C., . Kennedy, and M.L. Plant [eds.]: Sports Injuries-Mechanisms, e\'ention and Treatment. Baltimore, Williams & Wilkins, 1985, p. :::6.

sment. The lips should be pink and have vertical d horizontal symmetry, both at rest and with moveent. Dry, cracked lips may be caused by dehydration - om wind or low humidity, whereas deep fissures at ~e corners of the mouth may indicate overclosure of - e mouth or riboflavin deficiency.

B Figure 2-22

A 9-year-old boy was hit in the mouth with a ball while he was playing baseball. The right maxillary central and lateral incisors we chipped. (A) Avulsed teeth rein1planted with finger pressure. (B) Radiograph of root canal with wide-open apex. Reimplanted quick these teeth may not require root canal treatment. (From Torg, J.S Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982, p. 247.)

Figure 2-21 Fracture of the neck of the condyle on the right (upper arrows) with fracture through the mandible on the san1e side (lolVer arrow). When one fracture is shown in the mandible, search carefully for the second. (From O'Donoghue, D.H.: Treatment of Injuries to Athletes. Philadelphia, W.B. Saunders Co., 1984, p. US.)

Drooping of the mouth on one side, sagging of lower eyelid, and flattening of the nasolabial fold s gest possible facial nerve (cranial nerve VII) invol ment. The patient is also unable to pucker the lips whistle. The shape and position of the jaw and teeth sho also be noted anteriorly and from the side. 22 Asymm try may indicate a fracture of the jaw (Fig. 2-2 whereas bleeding around the gums of the teeth m indicate fracture, avulsion, or loosening of the te (Fig. 2-22). If there are missing teeth, they must accounted for. If they are not accounted for, an xmay be required to ensure that the teeth have n entered the abdominal or chest cavity. If pain occ on percussion of the teeth, it often indicates dama to the periodontal ligament.

Figure 2-23 Auricle alignment. Normal position shown.

Figure 2-24 Hematoma auris seen in a wrestler.

From the side, the examlOer should look for any asymmetry or depression, which may indicate pathology. The examiner should inspect the auricles of the ears for size, shape, symmetry, landmarks, color, and position on the head. To determine the position of the auricle, the examiner can draw an imaginary line between the outer canthus of the eye and occipital protuberance (Fig. 2-23). The top of the auricle should touch or be above this line. I? The examiner can then draw another imaginary line perpendicular to the previous line and just anterior to the auricle. The auricle's position should be almost vertical. If the angle is more than 10° posterior or anterior, it is considered abnormal. An auricle that is set low or is at an unusual angle may indicate chromosomal aberrations or renal disorders. In addition, the lateral and medial surfaces and surrounding tissues should be examined, noting any deformities, lesions, or nodules. The auricles should be the same color as the facial skin without moles, cysts, or other lesions or deformities. Athletes, especially wrestlers, may exhibit a cauliflower ear (hematoma auris), which is a keloid scar forming in the auricle due to friction to or twisting of the ear (Fig. 2-24). Blueness may indicate some degree of cyanosis. Pallor or excessive redness may be the result of vasomotor instability or increased temperature. Frostbite can cause extreme pallor or blistering (Fig. 2 - 25). The examiner should look posteriorly for any asymmetry or depression. The positions of the ears (height, protrusion) can be compared by observing from behind. A low hairline may indicate conditions such as Klippel-Feil syndrome. The examiner should also look for the presence of Battle's sign. This sign, which takes as long as 24 hours to appear, is demonstrated by purple and blue discoloration of the skin in the

mastoid area and may indicate a temporal bo basilar skull fracture. The examiner then views the patient from ov (superior view) to note any asymmetry from (Fig. 2-26). This method is especially useful looking for a possible fracture of the zygoma 2-27). The deformity is easier to detect if the iner carefully places the index fingers below the

Figure 2-25

Auricular frostbite with development of massive vesicles that a ginning to resolve spontaneously. (From Schuller, D.E., and R Bruce: Ear, nose, throat and eye. In Strauss, R.H. [ed.]: Spor Medicine, 2nd ed. Philadelphia, W.B. Saunders Co., 1991, p.


Signs and Symptoms of Maxillary and Zygomatic Fractures • Facial asymmetry • Loss of cheek prominence • Palpable steps • Infraorbital rim (zygomaticomaxillary suture) • Lateral orbital rim (frontozygomatic suture) • Root of zygoma intraorally • Zygomatic arch between ear and eye (zygomaticotemporal suture) • Hypoesthesialanesthesia

• Cheek, side of nose, upper lip, and teeth on the injured side • Compression of infraorbital nerve as it courses along floor of the orbit to exit into the face via the foramen beneath the orbital rim

figure 2-26 lew of the patient from above to look for bilateral synmletry of the ceo

orbital margins along the zygomatic bodies and then gently pushes into the edema to reduce the effect of the edema (Fig. 2-28).

Figure 2-27 Typical fracture of zygomatic arch on the right (arrow). ate normal arch on the left. (From O'Donoghue, D.H.: Treatment of Injuries to Athletes. Philadelphia, W.B. Saunders Co., 1984, p. 114.)

90


Head Examination • Concussion • Headache • Memory tests • Neural watch (Glasgow Coma Scale) • Expanding intracranial lesion • Proprioception Figure 2-28

• Coordination

Method of assessing posterior displacement of the zygomatic complex from behind the patient. The examiner should firmly but carefully depress the fingers into the edematous soft tissues while palpating along the infraorbital areas. (Modified from Ellis, E.: Fractures of the zygomatic complex and arch. In Fonseca, R.J" and R.V. Walker [eds.]: Oral and Maxillofacial Trauma. Philadelphia, W.B. Sawlders Co., 1991, p. 443.)

• Head injury card

T

Examination

The examination of the head and face differs from the orthopedic assessment of other areas of the body because the assessment does not involve joints. The only joints that could be included in the assessment are the temporomandibular joints, and these joints are discussed in Chapter 4.

Examination of the Head Many problems in the head and face may be problems referred from the cervical spine, temporomandibular joint, or teeth. However, if one suspects a head injury, it is necessary to keep a close watch on the patient, noting any changes and when these changes occur. A neural watch should be implemented by the examiner so that any changes that occur over time can be determined easily (Table 2-12). The testing should occur at 15- or 30-minute intervals, depending on the severity of the injury and the changes recorded. As the examination for a head injury is performed, the examiner should attempt to determine the degree of head injury, for example, the level of concussion suffered (see Table 2-4). This determination of degree of injury is important because it has an effect on when the patient will be allowed to return to activity (Table 2-13).24,25 The issue of whether an athlete should be allowed to return to competition following a concussion, and how soon, is one that has not been completely settled, although clinicians are becoming more concerned about the consequences of concussions. 2,26-29 Research

has shown that the brain is vulnerable to reinjury to 5 days following concussions because of a blood flow and metabolic dysfunction. 2 If the iner is contemplating allowing the athlete to retu activity because all symptoms have disappeared, vocative stress tests should be considered before ing the athlete to return. These tests are comm related to the sport but may include jumping five sit-ups, five push-ups, five deep knee bends lying supine for 1 minute with feet elevated. activities should be viewed as activities that in intracranial pressure, which may lead to symptom Although the guidelines outlined in Table 2-13 appear excessively precautionary, they are design prevent second impact syndrome, which is poten catastrophic injury with a mortality rate clo 50%.6,31-35 The examiner should always be looking for the sibility of an expanding intracranial lesion res from a leaking or torn blood vessel. Normally brain has a fixed volume that is enclosed in a n pansile structure, namely, the skull and dura m These lesions may be caused by epidural hemor (usually tearing of one of the meningeal arterie result of high-speed impact), subarachnoid hemor (usually as a result of an aneurysm), or subdural orrhage (usually as a result of tearing of bridging between the brain and cavernous sinus). These in are emergency conditions that must be looked immediately because of their high mortality ra much as 50%). An expanding intracranial les indicated by an altered lucid state (state of cons ness), development of inequality of the pupils, un slowing of the heart rate that primarily occurs a lucid interval, irregular eye movements, and eye no longer track properly. There is also a tenden


able 2-12 Neural Watch Chart Time 1 Unit ~

Yital signs

IT Conscious and

II Speech

TWill awaken to

T~onverbal reaction to pain

(

)

Time 2 ( )

Time 3 (

)

Time 1 ( )

Unit

Blood pressure Pulse Respiration Temperamre

VI Pupils

Size on right Size on left Reacts on right Reacts on left

Oriented Disoriented Restless Combative

VII Ability to move

Right arm Left arm Right leg Left leg

Clear Rambling Garbled None

VII Sensation

Right side (normalj abnormal) Left side (normal/ abnormal) Dermatome affected (specify) Peripheral nerve affected (specify)

Name Shaking Light pain Strong pain Appropriate Inappropriate "Decerebrate" one

Time 2

T

(

(

)

lodified from American Academy of Orthopedic Surgeons: AtWetic Training and Sports Medicine. Park Ridge, IL, AAOS, 1984, p. 39

the patient to demonstrate increased body temperature and irregular respirations. Normal intracranial pressure measures from 4 to 15 mm Hg, and an intracranial ressure of more than 20 mrn Hg is considered abnormal. Intracranial pressure of 40 mm Hg causes neuro:ogical dysfunction and impairment. Although in the emergency care setting there is no way of determining the intracranial pressure, the signs and symptoms mentioned indicate that the pressure is increasing. Most patients who experience an increase in intracranial pressure complain of severe headache, and this symptom is often followed by vomiting (sometimes projectile vomiting). Finally, an expanding intracranial lesion causes increased weakness on one side of the body, the ide opposite that on which the lesion has occurred. Signs and symptoms that indicate a good possibility of recovery from a head injury, especially after the patient experiences unconsciousness, include response to noxious stimuli, eye opening, pupil activity, spontaneous eye movement, intact oculovestibular reflexes, and appropriate motor function responses. Neurological signs that indicate a poor prognosis after a head injury include nonreactive pupils, absence of oculovestibular reflexes, severe extension patterns or no motor function response at all, and increased intracranial pressure. 12

It is important when examining the unconsci conscious patient for a possible head injury to mine the level of consciousness of the indi

Signs and Symptoms of an Expanding Intracranial lesion • Altered state of consciousness • Nystagmus • Pupil inequality • Irregular eye movements • Abnormal slowing of heart • Irregular respiration • Severe headache • Intractable vomiting

• Positive expanding intracranial lesion tests (Iateralizing • Positive coordination tests • Decreasing muscle strength • Seizure

Table 2-13 Timetable for Return to Competition After Concussion Concussion Severity

First Concussion

Second Concussion

Third Concussion

Return to activity after 10- 30 minutes if asymptomatic *

Return in 1 week if asymptomatic

Return in 1 week if asymptomatic Must be cleared by speci

2° (Posttraumatic [anterograde] amnesia)

Return to activity in 1 week if asymptomatic Must be cleared by specialist if some posttraumatic amnesia remains for :s 1 hour

Return in 2 weeks if asymptomatic after 1 week Must be cleared by specialist

No contact, collision, or risk activity for 3-6 m Must be cleared by speci

3° (Retrograde amnesia)

Return to activity in 1 week if asymptomatic Must be cleared by specialist if some posttraumatic or retrograde amnesia remains for :s1 hour

Return in 1 month if asymptomatic for final week Must be cleared by specialist


4° (Unconscious < 5 min)

Return to activity in 1 month if asymptomatic for final week Must be cleared by specialist

No contact, collision, or high-risk activity for 3-6 months Must be cleared by specialist


5° (Unconscious >5 min)

Return to activity in 1-2 months if asymptomatic for final week Must be cleared by specialist

o contact, collision, or high-risk activity for 3-6 months Must be cleared by specialist


* Symptoms may include headache, dizziness, tinnitus, amnesia, disorientation, unsteadiness, blurred vision. Data from Cantu, R.C.: Guidelines for return to contact sports after cerebral concussion. Phys. Sportsmed. 14:75-83, 1986; and Robert Who plays? Who sits? Managing concussions on the sidelines. Phys. Sportsmed. 20:66-72, 1992.

which may be done with the Glasgow Coma Scale (Table 2-14). The first test relates to eye opening. Eye opening may occur spontaneously, in response to speech, or in response to pain, or there may be no response at all. Each of these responses is given a numerical value: spontaneous eye opening, 4; response to speech, 3; response to pain, 2; and no response, 1. Spontaneous opening of the eyes indicates functioning of the ascending reticular activating system. This finding does not necessarily mean that the patient is aware of the surroundings or of what is happening, but it does imply that the patient is in a state of arousal. A patient who opens his or her eyes in response to the examiner's voice is probably responding to the stimulus of sound, not necessarily to the command to open the eyes. If unsure, the examiner may try different sound-making objects (e.g., bell, horn) to elicit an appropriate response. The second test involves motor response; the patient is given a grade of 6 if there is a response to a verbal command. Otherwise, the patient is graded on a fivepoint scale depending on the motor response to a painful stimulus (see Table 2-14). When scoring mo-

tor responses, it is the ease with which the responses are elicited that constitutes the criteri the best response. Commands given to the p should be simple, such as, "Move your arm." patient should not be asked to squeeze the exam hand, nor should the examiner place something patient's hand and then ask the patient to gra This action may cause a reflex grasp, not a respo a command. 12 If the patient does not give a motor response verbal command, then the examiner should attem elicit a motor response to a painful stimulus. It type and quality of the patient's reaction to the p stimulus that constitute the scoring criteria. The lus should not be applied to the face, because p stimulus in the facial area may cause the eyes to tightly as a protective reaction. The painful sti may consist of applying a knuckle to the ste squeezing the trapezius muscle, or squeezing th tissue between the thumb and index finger 2-29). If the patient moves a limb when the p stimulus is applied to more than one point or tr remove the examiner's hand that is applying the


:Ul stimulus, the patient is localizing, and a value of 5 given. If the patient withdraws from the painful 'imulus rapidly, a normal reflex withdrawal is being own, and a value of 4 is given. However, if application of a painful stimulus creates decorticate or decerebrate posture (Fig. 2-30), an normal response is being demonstrated, and a alue of 3 is given for the decorticate posture (injury ove red nucleus) or a value of 2 is given for decererate posture (brain stem injury). Decorticate posturg results from lesions of the diencephalon area, hereas decerebrate posturing results from lesions of - e midbrain. With decorticate posturing, the arms, Tists, and fingers are flexed, the upper limbs are aducted, and the legs are extended, medially rotated, d plantar flexed. Decerebrate posturing, which a poorer prognosis, involves extension, adduction, d hyperpronation of the arms, whereas the lower bs are the same as for decorticate posturing. 36 De- rebrate rigidity is usually bilateral. If the patient exbits no reaction to the painful stimulus, a value .- 1 is given. It is important to be sure the "no" ponse is caused by a head injury and not a spinal :: rd injury leading to lack of feeling or sensation. Any ±fference in reaction between limbs should be care- y noted; this finding may be indicative of a specific - al injury. 12 In the third test, verbal response is graded on a fiveint scale to measure the patient's speech in response

to simple questions such as "Where are you?" or "A you winning the game?" For verbal responses, the tient who converses appropriately shows proper ori tation, being aware of oneself and the environm and is given a grade of 5. The patient who is confu is disoriented and unable to completely interact w the environment; this patient is able to converse us the appropriate words and is given a grade of 4. T patient exhibiting inappropriate speech is unable sustain a conversation with the examiner; this per would be given a grade of 3. A vocalizing patient o groans or makes incomprehensible sounds; this find leads to a grade of 2. Again, the examiner sho make note of any possible mechanical reason for inability to verbalize. If the patient makes no sou and thus has no verbal response, a grade of 1 is signed. It is vital that the initial score on the Glasgow Co Scale be obtained at the scene, as soon as possible a the onset of the injury. The scale can then be repea at 15- or 30-minute intervals, especially in the e stages, if changes are noted. If the score is betwee and 8, emergency care is required. With the Glasg Coma Scale, the initial score is used as a basis determining the severity of the patient's head inju Patients who maintain a score of 8 or less on Glasgow Coma Scale for 6 hours or longer are cons ered to have a serious head injury. A patient w scores between 9 and 11 is considered to be mod

Ie 2-14 lasgow Coma Scale

L,·es

Best motor response

Tim

---

--

Open

Spontaneously To verbal command To pain No response

4 3 2 1

To verbal command

Obeys

6

To painful stimulus·

Localizes pain Flexion-withdrawal Flexion-abnormal (decorticate rigidity) Extension (decerebrate rigidity) o response

5 4 3 2 1

---

--

Oriented and converses Disoriented and converses Inappropriate words Incomprehensible sounds No response

5 4 3 2 1

---

--

Best verbal responset

Total • Apply knuckles to sternum; observe arms. patient with painful stimulus if necessary.

t Arouse

Time 1 ( )

3-15

94


E Figure 2-29 Examples of painful stimuli applied by the examiner. (A) Knuckle to sternum. (B) Squeezing trapezius muscle. (C) Squeezing tissue between the thumb and index finger. (D) Squeezing a fingertip. (E) Squeezing an object between two fingers.

ately head injured, and one who scores 12 or higher i considered to have a mild head injury.12 The Rancho Los Amigos Scale of Cognitive Func tion may also be used to assess the patient's cognitiv abilities. This scale is an eight-level progression from level I, in which the patient is nonresponsive, to leve VIII, in which the patient's behavior is purposeful an appropriate (Table 2-15). The Rancho Los Amigo scale provides an assessment of cognitive function an behavior only, not of physical functioning. 12 If a person receives a head injury such as a mil concussion and is not referred to the hospital, th examiner should ensure that someone accompanies th person home and that someone at home knows wha has happened so he or she can monitor the patient i case the patient's condition worsens. Appropriate writ ten instructions should be sent home concerning th individual. The Head Injury Card is such an exampl (Fig. 2-31).


9

re 2-30 Decorticate rigidity. (B) Decerebrate rigidity.

Head Injury Card Please Read Carefully (Give one to an accompanying person and one to tfle player)

Head Injury Severity Based on Score Maintained on Glasgow Coma Scale (6 Hr+) or less:

Severe head injury

-11:

Moderate head injury

2+:

Mild head injury

NAME

AGE

_

SUSTAINED A HEAD INJURY AT

_ (time)

ON

_ (date)

';:'evin and colleagues 14 reported the use of the Galron Orientation and Amnesia Test (GOAT), which ey believe measures orientation to person, place, and e and the memory of events preceding and follow; head trauma (Fig. 2 - 32). As the patient improves, e rotal GOAT score should increase. The examiner may also wish to determine whether e patient has suffered an upper motor neuron lesion. e ting the deep tendon reflexes (see Table 1-24) or - e pathological reflexes (see Table 1-26) or having - e patient perform various balance and coordination

Important Warning: (S)He is to be taken to a hospital or a doctor immediately if (s)he: • • • • • •

ble 2-15 ancho Los Amigos Scale of Cognitive Function :"evel I

o response

VOMITS DEVELOPS A HEADACHE BECOMES RESTLESS OR IRRITABLE BECOMES DIZZY OR DROWSY OR CANNOT BE ROUSED HAS A FIT (CONVULSION) EXPERIENCES ANYTHING ELSE UNUSUAL

For the rest of today (s)he should: • • •

REST QUIETLY NOT CONSUME ALCOHOL NOT DRIVE A VEHICLE

:..evel II

Generalized response

Level III

Localized response

Level IV

Confused, agitated

Level V

Confused, inappropriate

(S)He should not train or play again without medical clearance by a doctor.

Level VI

Confused, appropriate

_ _ _ _ _ _ _ _ _ PHONE

Level VII

Automatic, appropriate

Level VIII

Purposeful, appropriate

AND

(Doctor) DATE

From Hagen, C., D. Malkmus, and P. Durham: Levels of cognitive functioning. In Rehabilitation of the Brain Injured AdultComprehensive Management. Professional Staff Association of Rancho Los Amigos, Downey, California, 1980.

_

Oueensland Health Department. Division of Heaith Promotion

Figure 2-31 Head injury card.

_


96

Galveston Orientation and Amnesia Test (GOAT) Name Age

Date of test _

Date of birth

Sex

M

Day of the week

F

_

M

T

Time

Diagnosis

W

Th

AM

Date of injury

_ When were you born? (4)

I. What is your name? (2)

Where do you live? (4)

S

_

_

2. Where are you now? (city) (5)

Location (e.g., hospital) (5) (unnecessary to state name of hospital)

3. On what date were you admitted to this hospital? (5)

How did you get here? (5)

_

_ _

4. What is the first event you can remember after the injury? (5) _ Can you describe in detail (e.g., date, time, companions) the first event you can recall after injury? (5)

_

before the accident? (5) _ Can you describe in detail (e.g, date, time, companions) the first event you can recall before injury?

5. Can you describe the last event you recall (5)

6. What time is it now? 7. What day of the week is it? 8. What day of the month is it?

_

(1 for each 1/2 hour removed from correct time, to maximum of 5) (1 for each day removed from correct one) (1 for each day removed from correct date, to maximum

of 5) 9. What is the month? 10. What is the year?

(5 for each month removed from correct one, to maximum of 5) (10 for each year removed from correct one, to maximum of 30) Total error points Total GOAT score (100 minus total error points)

Figure 2-32

Galveston Orientation and Amnesia Test. Examiner adds up only error points, not positive responses. For example, if patient remembe name but not last name, he or she would get 1 error point. (Modified from Levin, H.S., V.M. O'Donnell, and R.G. Grossman: The G orientation and amnesia test: A practical scale to assess cognition after head injury. J. Nerve Ment. Dis. 167:677,1979.)

tests may help to determine whether this type of lesion has occurred. However, the pathological reflexes may not be elicited owing to shock. Deep tendon reflexes are accentuated on the side of the body opposite that on which the brain injury has occurred. Balance can

play an important role in the assessment of injured patient. Balance involves the integration eral inputs (e.g., visual, proprioceptive, and ve systems), which are analyzed by the brain to proper action. For example, in standing, the

CHAPTER 2 • Head and Fac

tests, and others described under "Special T sess balance and coordination. Muscle tone and strength may also play assessing the patient for head injury. Increas eral muscle tone usually implies contralatera peduncle compression. Flaccid muscle ton brain stem infarction, spinal cord transaction, shock. Unilateral effects such as hemiparesi seen with a stroke.

Examination of the Face 19 - 23 ,37

B Figure 2-33 Performing coordination exercises. (A) Touching knee with opposite heel. (B) Touching nose with index finger with eyes closed.

inherently unstable, and only the integration of input from various sources enables the patient to stand and to make appropriate corrections to maintain proper standing posture. Balance and coordination can be tested in several ways. The patient can be asked to stand and walk a straight line with the eyes open and then with the eyes closed. The examiner should note any difference. The patient can be asked to bring the finger to the nose or the heel of the foot to the opposite knee with the eyes closed (Fig. 2-33). These

Figure 2-34 Testing for mandibular fracture. (A) Patient bites down on tongue depressor while examiner tries to pull it away. (B) Pressure at the angles of the mandible.

Once a head injury has been ruled out or i injury is suspected, the examiner can examin for injury. Major trauma and subsequent inju face should be assessed first. If major traum occurred, only those areas of the face that h affected by the trauma (e.g., eyes, nose, ears assessed. The patient may initially be tested tures with the use of a tongue depressor, if t can open the mouth. The patient is aske down as hard as possible on the tongue depre 2-34A). The examiner should note whethe tient is able to bite down strongly and hold traction and where any pain is elicited. To test for a maxillary fracture, the exami the anterior aspect of the maxilla with the one hand and places the fingers of the other the bridge of the patient's nose or forehead aminer then gently pulls the maxilla forw 2-35). If movement is felt by the fingers of hand at the nose or the examiner feels the moving forward, a Le Fort II or III fractur present (Fig. 2-36). If the maxilla moves movement at the nose, either the maxilla is tally fractured or a Le Fort I fracture is prese Le Fort I fracture, the palate is separated superior portion of the maxilla, and the upp bearing segment of the face moves alone.

98


Stabilize

f

Figure 2-35 Testing for maxillary fracture.

bones, midportion of the face, and maxilla move if a Le Fort II fracture is present. With a Le Fort III fracture, the middle third of the face separates from the upper third of the face; this is often called a craniofacial separation. The patient may complain of lip or cheek anesthesia and double vision (diplopia) with any of these fractures.

The examiner then asks the patient to open mouth slightly. The examiner carefully applies pres bilaterally at the angles of the mandible (Fig. 2-34 Localized pain, lower lip anesthesia, and intraoral eration may indicate a fracture of the mandible. occlusion of the teeth is often seen with fracture the mandible or maxilla (Fig. 2-37). Alteration smell (cranial nerve I) are often seen with frontob and nasoethmoid fractures. Skull fractures are o associated with clear nasal discharge (spinal fluid norrhea), clear ear discharge (otorrhea), or a taste. If the fluid is accompanied by blood, the e iner can use a gauze pad to collect the fluid. If brospinal fluid is mixed with the blood, a "halo" e may be seen as the fluid collects on the gauze (Fig. 2-38). If the eardrum has not been perfor blood may be seen behind it. Skull fractures may result in blurred or double vision, loss of smell (a mia), dizziness, tinnitus, and nausea and vomitin well as signs and symptoms of concussion. Or floor fractures or dislocations are often accompa by anesthesia of the skin in the midface or anest of the cheek, lip, maxillary teeth, and gingiva. 38 goma fractures are detected by observation (see 2-28). They may also cause unilateral epistaxis, do vision, and anesthesia and be associated with eye ries. Mouth opening may also be affected. After major trauma has been ruled out, the exam may test the muscles of the face (Table 2-16), cially if injury to these structures is suspected. muscles of the face are different from most muscl that they move the skin and soft tissues rather joints, if one excludes the temporomandibular j For example, the frontalis muscle may be weak i eyebrows do not raise symmetrically. The corrug muscle draws the eyebrows medially and down (frowning). The orbicularis oris muscle approxim and compresses the lips, whereas the zygomaticus cles raise the lateral angle of the mouth (smiling).

Facial Examination

Examination of the Eye 19- 22

• Bone and soft tissue contours

If the eyelids are swollen shut, the examiner sh initially assume that the globe has been rupture penetrating wound of the eyelid should be ass carefully, because it may be associated with a g injury. The examiner should not force the eyelid o because intraocular pressure can force extrusion o ocular contents if the globe has been ruptured. patient should also be instructed not to squeeze eyelids tight, because this action can increase the i ocular pressure from a normal value of 15 mm H to approximately 70 mm Hg.

• Fractures • Mandible • Maxilla • Zygoma • Skull • Cranial nerves • Facial muscles


1.....~~f1tI==-~

Uneven line of teeth

Figure 2-37

Malocclusion of teeth may be associated with fracture of ma maxilla.

Figure 2-36 I.e Fort fractures. (A) I.e Fort I. (B) Le Fort II. (C) Le Fort III.

To examine the normal functioning of the eye muscles and several of the cranial nerves (II, III, IV, and VI), the examiner asks the patient to move through the six cardinal positions of gaze (Fig. 2-39). The examiner holds the patient's chin steady with one hand and asks the patient to follow the examiner's other hand while the examiner traces a large "H" in the air. The examiner should hold the index finger or pencil approximately 25 cm (10 inches) from the patient's nose. From the midline, the finger or pencil is moved approximately 30 cm (12 inches) to the patient's right and held. It is then moved up approximately 20 cm (8 inches) and held, moved down 40 cm (16 inches) (20 cm relative to midline) and held, and moved slowly

back to midline. The same movement is repe the other side. The examiner should observe ment of both eyes, noting whether the eyes fol finger or pencil smoothly. The examiner shou observe any parallel movement of the eyes in a tions. If the eyes do not move in unison or o eye moves, there is something affecting the ac the muscles. One of the most common causes eye's not moving after trauma to the eye is a out" fracture of the orbital floor (Fig. 2-40). the inferior muscles become "caught" in the site, the affected eye demonstrates limited mo (Fig. 2-41), especially upward. The patient w

Blood

Orange halo o Gauze pad

Figure 2-38

An orange halo will form around the blood on a gauze pad cerebrospinal fluid is present.

100


Table 2-16 Muscles of the Face Action

Cranial Nerve

Muscles of the Mouth Orbicularis oris

Compresses lips against anterior teeth, closes mouth, protrudes lips

VII (Zygomatic, buccal, and mandibular branches)

Depressor anguli oris

Depresses angle of mouth

VII (Buccal and mandibular branches)

Levator anguli oris

Elevates angle of mouth

VII (Zygomatic and buccal branches)

Zygomaticus major

Draws angle of mouth upward and back


Risorius

Draws angle of mouth laterally


Elevates upper lip, flares nostril


Compresses cheeks against molar teeth; sucking and blowing

VII (Buccal branches)

Puckers skin of chin, protrudes lower lip

VII (Mandibular branches)

Compresses nostrils Dilates or flares nostrils


Closes eye forcefully Closes eye gently Squeezes lubricating tears against eyeball

VII (Temporal and zygomatic branches)

Procerus

Transverse wrinkling of bridge of nose

VII (Temporal and zygomatic branches)

Corrugator

Vertical wrinkling of bridge of nose

VII (Temporal branches)

Frontalis

Pulls scalp upward and back

VII (Temporal branches)

Muscle of the Lips Levator labii superioris

Muscle of the Cheek Buccinator

Muscle of the Chin Mentalis

Muscle of the Nose Nasalis

Muscle of the Eye Orbicularis oculi

Muscles of the Forehead

Adapted from Liebgott, B.: The Anatomical Basis of Dentistry. St. Louis, C.Y. Mosby, 1986, pp. 242-243.

Eye Examination Inferior oblique. CNIII

;

I

Inferior rectus. CNIII

I Inferior rectus. CNIII

• Six cardinal gaze positions • Pupils (size, equality, reactivity) • Nystagmus

lateral .... rectus. CNVI

lateral rectus..... CNVI Superior oblique, CNIV

Inferior oblique, CNIII

Superior rectus. CNIII

"

Superior oblique. CNIV

Figure 2-39 The six cardinal fields of gaze, showing eye muscles and cranial nerves (CN) involved in the movement.

• Visual field (peripheral vision) • Visual acuity • Symmetry of gaze • Foreign objects/corneal abrasion • Surrounding bone and soft tissue • Hyphema


Figure 2-40

Blow-out fracture of the orbital floor. The dashed line indicates normal position of the globe. The inferior oblique and inferior rectu muscles are "caught" in the fracture site, preventing the eye from returning to its normal position. (Modified from Paton, D., and M.F. Goldberg: Management of Ocular Injuries. Philadelphia, W.B. Saunders Co., 1976, p. 63.)

_'Pe of fracture may also demonstrate depression of the eye globe, blurred vision, double vision, and conunctival hemorrhage. Occasionally, when looking to the extreme side, the eyes will develop a rhythmic motion called end-point

nystagmus. Nystagmus is a rhythmic movemen eyes with an abnormal slow drifting away from and rapid return. With end-point nystagmus, th quick motion in the direction of the gaze follo a slow return. This test differentiates end-point

Figure 2-41 Fresh blow-out fracture of left orbit with limitation of upward (top) and downward (bottom) movements of the left eye. (From Paton, D., and M.F. Goldberg: Management of Ocular Injuries. Philadelphia, W.B. Saunders Co., 1976, p.65.)

102


mus from pathological nystagmus, in which there is a quick movement of the eyes in the same direction regardless of gaze. Pathological nystagmus exists in the region of full binocular vision, not just at the periphery. Cerebellar nystagmus is greater when the eyes are deviated toward the side of the lesion. While testing the cardinal positions, the examiner should also watch for lid lag. Normally, the upper lid covers the top of the iris, rising when the patient looks up and quickly lowering as the eye lowers. With lid lag, the upper lid delays lowering as the eye lowers. Peripheral vision or the visual field (peripheral limits of vision) can be tested \vith the confrontation test (Fig. 2-42). The patient is asked to cover the right eye while the examiner covers his or her own left eye, so that the open eyes of the examiner and of the patient are directly opposite each other. While the examiner and the patient look into each other's eye, the examiner fully extends his or her right arm to the side, midway between the patient and the examiner, and then moves it toward them with the fingers waving. The patient tells the examiner when the moving fingers are first seen. The examiner then compares the patient's response with the time or distance at which the examiner first noted the fingers. The test is then repeated to the other side. The nasal, temporal, superior, and inferior fields should all be tested in a similar fashion. The visual field should describe angles of 60° nasally, 90° temporally, 50° superiorly, and 70° inferiorly. Double simultaneous testing may also be performed. This method uses two stimuli (e.g., moving fingers) that are simultaneously presented in the right and left visual fields,

Figure 2-42 Confrontation eye test.

and the patient is asked which finger is moving. N mally, the patient should say "both" without hes tion. With any loss of vision field (i.e., if the patien unable to see in the same visual fields as before), patient must be referred for further examination. The eyelids should be everted to look at the und side of the eyelid and to give a clearer view of globe, especially if the patient complains of a fore body. The upper eyelid may be everted with the use a special lid retractor or a cotton swab (Fig. 2-4 The patient is asked to look down and to the ri and then down and to the left while the superior pect of the eye is examined. The examiner can ch the inferior aspect of the eye and its conjunctival lin by carefully pulling the lower eyelid downward gently holding it against the bony orbit. Next, patient is asked to look up and to the right and t up and to the left while the inferior aspect of the is examined. These two techniques may also be u to look for a contact lens that has migrated away fr the cornea. Both eyelids should be checked for laceration. L erations in the area of the lacrimal gland are especi important to detect because, if they are not loo after properly, the tearing function of the lacri gland may be lost (Fig. 2-44). The reaction of the pupils to light should then tested. First, the light in the room is dimmed. T pupils dilate in a dark environment or with a l focal distance and constrict in a light environment with a short focal distance. The examiner shines a light directly into one of the patient's eyes for appro mately 5 seconds (Fig. 2-45). Normally, constrict of the pupil occurs, followed by slight dilation. T pupillary reaction is classified as brisk (normal), sl gish, nonreactive, or fixed. An oval or slightly o pupil or one that is fixed and dilated indicates creased intracranial pressure. The fixation and dilat of both pupils is a terminal sign of anoxia and ische to the brain. If the dilation is significant, an injury the optic nerve may be suspected. If both pupils midsize, midposition, and nonreactive, midbrain da age is usually indicated. In a fully conscious, alert tient who has sustained a blow near the eye, a dilat fixed pupil usually implies injury to the ciliary nerves the eye rather than brain injury. The other eye tested similarly, and the results are compared. Normally, both pupils constrict when a light shined in one eye. The reaction of the eye being tes is called the direct light reflex; the reaction of other pupil is called the consensual light reflex. T reaction is brisker in the young and people with b eyes. 23 If the optic nerve is damaged, the affected pu constricts in response to light in the opposite eye (c


Figure 2-43

Eversion of the eyelid. (A) Grasping eyelash. (B) Putting mo cotton-tipped applicator over eyelid. (C) Everting eyelid ove cotton-tipped applicator.

c

Figure 2-44 A lower lid laceration (arrow). (From Pashby, T.J., and R.c. Pashby: Treatment of sports eye injuries. In Schneider, R.c., I.e. Kennedy, and M.L. Plant [eds.]: Sports Injuries-Mechanisms, Prevention, and Treatment. Baltimore, Williams & Wilkins, 1985, p. 576.)

Figure 2-45

Testing the pupils for reaction to (A) Light shining in eye. (B) Lig shining away from eye.

sensual) and dilates in response to light shined into it (direct). If the oculomotor nerve is affected, the affected pupil is fixed and dilated and does not respond to light, either directly or consensually. If the pupils do not react, it is an indication of injury to the oculomotor nerve and its connections or of injury to the head. The eye also appears laterally displaced owing to paresis of the medial rectus muscle. The pupil is then tested for "constriction to accommodation." The patient is asked to look at a distant object and then at a test object-a pencil or the examiner's finger held 10 cm (4 inches) from the bridge of the nose. The pupils dilate when the patient looks at a far object and constrict when the patient focuses on the near object. The eyes also adduct (go "crosseyed") when the patient looks at the close object. These actions are called the accommodation-convergence reflex. 23 When looking at distant objects, the eyes should be parallel. Deviation or lack of parallelism is called strabismus and indicates weakness of one of the extraocular muscles or Jack of neuraJ coordination. 39 When inspected under normaJ overhead light, the lens of the eye should be transparent. Shining a light on the lens may cause it to appear gray or yellow. The cornea should be smooth and clear. If the patient has extreme pain in the corneal area, a corneal abrasion should be suspected (Fig. 2-46). An appropriate specialist may test for corneal abrasion by using a fluorescein strip and a slit lamp. The cornea should be crystal clear when it is viewed, and the iris details should match those of the other eye. To check for depth of the anterior chamber of the eye or a narrow corneal angle, the examiner shines a light obliquely across each eye. Normally, it illuminates the entire iris. If the corneal angle is narrow because of a shallow anterior chamber, the examiner will be able to see a crescent-shaped shadow on the side of the iris away from the light (Fig. 2-47). This finding indicates an anatomic predisposition to narrow-angled glaucoma.

Figure 2-46

Corneal abrasion. (A) Without fluorescein. (B) With fluorescei (From Torg, ].5.: Athletic Injuries to the Head, Neck and Fac Philadelphia, Lea & Febiger, 1982, p. 262.)

To test for symmetry of gaze, the examiner a light source approximately 60 cm (24 inches) fro patient while standing directly in front of the p and holding the light distant enough to preven vergence of the patient's gaze. The patient is ask stare at the light. The dots of reflected light o two corneas should be in the same relative lo (Fig. 2-48). When one eye does not look direc the light, the reflected dot of light moves to th opposite the deviation. For example, if the eye de medially, the reflection appears more laterally p than in the other eye. The examiner can approx the angle of deviation by noting the position o


Cornea

Anterior chamber

=0-------- -

Lens

"gure 2-47 NORMAL ANGLE

- ,rmal and narrow corneal angle (depth of nterior chamber). (From Swartz, M.H.: :-extbook of Physical Diagnosis. Philadela, W.B. Saunders Co., 1989, p. 144.)

=0------ - -

.

.

NARROW ANGLE

Figure 2-48 -ymmetry of gaze. Note white "dots" of light on pupils.

Figure 2-49 Cover-uncover test for mild ocular de\iation. As patient gazes at a specific point (A), examiner covers one eye and looks for movement in uncovered eye (B).

B

106


reflection. Each millimeter of displacement in the reflection represents approximately 7° of ocular deviation. To bring out a mild deviation, a cover-uncover test may be used (Fig. 2-49). The patient looks at a specific point, such as the bridge of the examiner's nose. One of the patient's eyes is then covered \vith a card. Normally, the uncovered eye will not move. If it moves, it was not straight before the other eye was covered. The other eye is then tested in a similar fashion. Visual acuity is tested using a vision chart. Visual acuity is the ability of the eye to perceive fine detail, for example, when reading. If a standard eye wall chart is not available, a pocket visual acuity card may be used. This pocket card is usually viewed at a distance of 35 to 36 cm (14 inches). As with the wall chart, the patient is asked to examine the smallest line possible. If neither eye chart is available, any printed material may be used. If glasses or contact lenses are worn, the patient should be tested both without and with the corrective lenses. The test is done quickly so the patient cannot memorize the chart. Visual acuity is recorded as a fraction in which the numerator indicates the distance of the patient from the chart (e.g., 20 ft) and the denominator indicates the distance at which the normal eye can read the line. Thus, 20/100 means

Figure 2-50 "Saddle nose" deformity (arrow) that occurred as a result of loss of septal cartilage support secondary to septal hematoma and abscess. (From Handler, S.D.: Diagnosis and management of ma:illiofacial injuries. In Torg, I.S. [ed.]: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982, p. 232.)

the patient can read at 20 ft what the average p can read at 100 ft. The smaller the fraction, the the myopia (nearsightedness). Patients \vith corr vision of less than 20/40 should be referred t appropriate specialist. 23 Intraocular examination with an ophthalmosco available, may reveal lens, vitreous, or retinal dama

Examination of the Nose 19- 22

Patency of the nasal passages can be determine occluding one of the patient's nostrils by push finger against the side of it. The patient is then to breathe in and out of the opposite nostril wit mouth closed. The process is repeated on the side. Normally, no sound is heard, and the patien breathe easily through the open nostril. If available, a nasal speculum and light may be to inspect the nasal cavity. The nasal mucosa and binates can be inspected for color, foreign bodies abnormal masses (e.g., polyp). The nasal se should be in midline and straight and is nor thicker anteriorly than posteriorly. If the nasal ca are asymmetric, it may indicate a deviated septu the patient demonstrates a septal hematoma, it be treated fairly quickly, because the hematoma


Nasal Examination • Patency

ment or increased pain or numbness relative to o teeth. A tooth that has been avulsed may be clean with warm water and reinserted into the socket. patient is then referred to the appropriate specialist.

• Nasal cavities • Sinuses • Fracture • Nasal discharge (bloody, straw-colored, clear)

- use excessive pressure on the septum, making it avas:J1ar. This avascularity can result in a "saddle nose" eformity owing to necrosis and absorption of the unerlying cartilage (Fig. 2-50). Illumination of the frontal and maxillary sinuses may performed if sinus tenderness is present or infection uspected. The examination must be performed in a - mpletely darkened room. To illuminate the maxillary uses, the examiner places the light source lateral to - e patient's nose just beneath the medial aspect of the -e. The examiner then looks through the patient's n mouth for illumination of the hard palate. To uminate the frontal sinuses, the examiner places the gilt source against the medial aspect of each supraor-tal rim. The examiner looks for a dim red glow as gilt is transmitted just below the eyebrow. The sies usually show differing degrees of illumination. :be absence of a glow indicates either that the sinus is :; ed with secretions or that it has never developed.

amination of the Teeth 19 - 22 -:be examiner should observe the teeth to see if they .:re in normal position and whether any teeth are missg, chipped, or depressed (see Fig. 2-22). Using the _ oved index finger and thumb, the examiner can aply mild pressure to each tooth, pressing inward oward the tongue and outward toward the lips. Normally, a small amount of movement is seen. If a tooth loose, a positive test is indicated by excessive move-

Tooth Examination • Number of teeth • Position of teeth • Movement of teeth • Condition of teeth • Condition of gums

Examination of the Ear19 - 22

Examination of the ear deals primarily with whe the patient is able to hear. There are several tests may be used to test hearing.

Whispered Voice Test. The patient's response the examiner's whispered voice can be used to de mine hearing ability. The examiner masks the hea in one of the patient's ears by placing a finger ge in the patient's ear canal. Standing approximately to 60 cm (12 to 24 inches) away from the patient, examiner whispers one- or two-syllable words softly and asks the patient to repeat the words he If the patient has difficulty, the examiner gradu increases the loudness of the whisper until the pa responds appropriately. The procedure is repeate the other ear. The patient should be able to hear s whispered words in each ear at a distance of 30 to cm (12 to 24 inches) and respond correctly at 50% of the time. 18 ,19

Ticking Watch Test. The ticking watch test us nonelectric ticking watch to test high-frequency h ing. The examiner positions the watch approxima 15 cm (6 inches) from the ear to be tested, slo moving it toward the ear. The patient is asked to the examiner when the ticking is heard. The dist can be measured and will give some idea of the tient's ability to hear high-frequency sound. 18 ,19

Weber Test. The examiner places the base of a brating tuning fork on the midline vertex of the tient's head. The patient is asked if the sound is h equally well in both ears or is heard better in one (lateralization of sound). The patient should hear sound equally well in both ears (Figs. 2-51 and 2-5 If the sound is lateralized, the patient is asked to i tifY through which ear the sound is heard better. test the reliability of the patient's response, the ex iner repeats the procedure while occluding one ear a finger and asks the patient through which ear sound is heard better. It should be heard better in occluded ear. 18 ,19

Rinne Test. The Rinne test is performed by pla the base of the vibrating tuning fork against the tient's mastoid bone. The examiner counts or t the interval with a watch. The patient is asked to the examiner when the sound is no longer heard, the examiner notes the number of seconds. The ex iner then quickly positions a still-vibrating tine 1

108


A

c

B

Figure 2-51 The Weber test. When a vibrating tuning fork is placed on the center of the forehead (A), the sound is heard in the center \vithollt lateralization to either side (normal response). (B) In the presence of a conductive hearing loss, the sound is heard on the side of the conductive loss. (C) In the presence of sensorineural loss, the sound is better heard on the opposite (unaffected) side.

cm (0.5 to 0.8 inch) from the auditory canal, and the patient is asked to tell the examiner when the sound is no longer heard. The examiner then compares the number of seconds the sound was heard by bone conduction and by air conduction. The counting or timing of the interval between the two sounds determines the length of time that sound is heard by air conduction (see Fig. 2-52). Air-conducted sound should be heard twice as long as bone-conducted sound. For example, if bone conduction is heard for 15 seconds, the air conduction should be heard for 30 seconds. 18 - 20

culty in interpreting sounds. Sensorineural or pe tual hearing loss indicates that the patient has culty interpreting the sounds heard. Internal examination of the ear may be accomp with the use of an otoscope, if available. In this the examiner would observe the canal as well a eardrum (tympanic membrane), noting any bloc excessive wax, swelling, redness, transparency (u pearly gray), bulging, retraction, or perforation o eardrum.

Schwabach Test. This test is a comparison of the patient's and examiner's hearing by bone conduction. The examiner alternately places the vibrating tuning fork against the patient's mastoid process and against the examiner's mastoid bone until one of them no longer hears a sound. The examiner and patient should hear the sound for equal amounts of time. 18,19

Special Tests

Conductive hearing loss implies that the patient experiences reduction of all sounds rather than diffi-

Only those special tests that the examiner think have value are performed. For example, the tes expanding intracranial lesions would not be perfo with a facial injury unless an associated injury t brain or other neurological tissues is suspected.

Tests for Expanding Intracranial Lesions

For each of these tests, the patient must be ab stand normally when the eyes are open.

Ear Examination • Tenderness (exterior and interior) • Ear discharge (bloody, straw-colored, clear) • Hearing • Balance

Neurological Control Test-Upper Limb. patient is asked to stand with the arms forward 90° and the eyes closed. The patient is asked to this position for approximately 30 seconds. If th aminer notes that one arm tends to move or " outward and downward, the test is considered po for an expanding intracranial lesion on the side site the side with the drift.


Weber (away from the lesion)

considered positive for an expanding intracranial on the side opposite that with the drift.

Romberg Test. The patient is asked to stan the feet together and arms by the sides with th open. The examiner notes whether the patient h problem with balance. The patient is then ask close the eyes (for at least 20 seconds), and the iner notes any differences. A positive Romberg elicited if the patient sways or falls to one side the eyes are closed and is indicative of an exp intracranial lesion, possible disease of the spina posterior columns, or proprioceptive problems.

:"cm

tch tick ger twitching I

SENSORINEURAL LOSS Weber (to the left)

Walk or Stand in Tandem Test. Patients w panding intracranial lesions demonstrate increasi ficulty in walking in tandem ("walking the lin standing in tandem (one foot in front of Standing in tandem is more difficult to perform walking in tandem.

Tests for Coordination

tch tick : '1ger twitching I

CONDUCTIVE LOSS Tuning fork >512 cps

Weber (midline) Rinne (air » bone)

Finger-to-Nose Test. The patient stands with the eyes open and is asked to bring the finger to the nose. The test is repeated with th closed. Both arms are tested several times with in ing speed. Normally, the tests should be accomp easily, smoothly, and quickly with the eyes ope closed.

Finger-Thumb Test. The patient is asked to each finger with the thumb of the same hand normal or uninjured side is tested first, followed injured side. The examiner compares the two sid coordination and timing.

Hand "Flip" Test. The patient is asked to the back of the opposite, stationary hand wi anterior aspect of the fingers, "flip" the test hand and touch the opposite hand with the posterior of the fingers. The movement is repeated several with both sides being tested. The examiner com the two sides for coordination and speed.

cm

I

NORMAL

Figure 2-52 Bedside hearing tests and results with sensorineural or conductive oss in left ear and with normal hearing.

Neurological Control Test-Lower Limb. The patient is asked to sit on the edge of a table or in a chair with the legs extended in front and not touching the ground. The patient is then asked to close the eyes for approximately 20 to 30 seconds. If the examiner notes that one leg tends to move or drift, the test is

Finger Drumming Test. The patient is ask "drum" the index and middle finger of one ha and down as quickly as possible on the back other hand. The test is repeated with the op hand. The examiner compares the two sides for dination and speed.

Hand-Thigh Test. The patient is asked to p thigh with the hand as quickly as possible. The jured side is tested first. The patient may be as supinate and pronate the hand between each thigh contact to make the test more complex examiner watches for speed and coordinatio compares the two sides.

110


~ ~ I \

\

I I I I

I

1

I \

\ I

\

Patient

\

I \ \

I I

\ \ \ I \ \ I I I I

Tests for Proprioception

Proprioceptive Finger-Nose Test. The keeps the eyes closed. The examiner lightly one of the patient's fingers and asks the pa touch the patient's nose with that finger. Th iner then touches another finger on the othe and the patient again touches the nose. Patie proprioceptive loss have difficulty doing the te out visual input.

I

Proprioceptive Movement Test. The patie the eyes closed. The examiner moves the patie ger or toe up or down by grasping it on the lessen clues given by pressure. The patient th the examiner which way the digit moved.

Proprioceptive Space Test. The patient ke eyes closed. The examiner places one of the hands or feet in a selected position in space. tient is then asked to imitate that position w other limb or to find the hand or foot with th limb. True proprioceptive loss causes the patie unable to properly position or to find the norm with the limb that has proprioceptive loss. Figure 2-53 Past pointing. (Redrawn from Reilly, B.M.: Practical Strategies in Outpatient Medicine. Philadelphia, W.B. Saunders Co., 1991, p. 195.)

Past Pointing Test. The test is performed scribed under Tests for Coordination.

Past Pointing Test. The patient and examiner face each other. The examiner holds up both index fingers approximately 15 cm (6 inches) apart. The patient is asked to lift the arms over the head and then bring the arms down to touch the patient's index fingers to the examiner's index fingers (Fig. 2-53). The test is repeated with the patient's eyes closed. Normally, the test can be performed without difficulty. Patients with vestibular disease have problems with past pointing. The test may also be used to test proprioception. Heel-to-Knee Test. The patient, who is lying supine with the eyes open, is asked to take the heel of one foot and touch the opposite knee with the heel and then slide the heel down the shin. The test is repeated with the eyes closed, and both legs are tested. The test can be repeated several times with increasing speed, with the examiner noting any differences in coordination or the presence of tremor. Normally, the test should be accomplished easily, smootWy, and quickly with the eyes open and closed.

Figure 2-54 Test of corneal reflex.


Reflexes and Cutaneous Distribution With a head injury patient, deep tendon reflexes (see Table 1-24) should be performed. Accentuation of one or more of the reflexes may indicate trauma to the brain on the opposite side. Pathological reflexes (see Table 1-26) may also be altered with a head injury. The corneal reflex (trigeminal nerve, cranial nerve V) is used to test for damage or dysfunction to the pons. In some cases, the patient may look to one side o avoid involuntary blinking. The examiner touches the cornea (not the eyelashes or conjunctiva) with a mall, fine point of cotton (Fig. 2-54). The normal response is a bilateral blink, because the reflex arc con'lects both facial nerve nuclei. If the reflex is absent, the test is considered positive. The gag reflex may be tested using a tongue deressor that is inserted into the posterior pharynx and depressed toward the hypopharynx. The reflex tests -ranial nerves IX and X, and its absence in a trauma etting may indicate caudal brain stem dysfunction. Consensual light reflex may be tested by shining a ght into one eye. This action causes the "lighted" upi! to constrict. If there is normal communication etween the two oculomotor nerves, the "nonlighted" • upil also constricts. The jaw reflex is usually tested only if the temporomandibular joint or cervical spine is being examined. The examiner should check the sensation of the ead and face, keeping in mind the differences in dermatome and sensory nerve distributions (Fig. 2-55).

Lip anesthesia or paresthesia is often seen in p with mandibular fracture.

Nerve Injuries of the Head and Face

Bell's palsy involves paralysis of the facial nerve nerve VII) and usually occurs where the nerve e from the stylomastoid foramen. Pressure in th men caused by inflammation or trauma affe nerve and therefore the muscles of the face (oc frontalis, corrugator, orbicularis oculi, and th and mouth muscles) on one side. The inflam may result from a middle ear infection, viral inf chilling of the face, or tumor. The observable r smoothing of the face on the affected side ow loss of muscle action, the eye on the affecte remaining open, and the lower eyelid saggin patient is unable to wink, whistle, purse the wrinkle the forehead. Speech sounds, especially requiring pursing of the lips, are affected, resul slurred speech. The mouth droops, and it and th may deviate to the opposite side, especially in standing cases, of which there are remarkably few of patients having complete recovery within 2 weeks). Facial sensation on the affected side and taste sensation is sometimes lost as well.

Joint Play Movements

Because no articular joints are involved in the ment of the head and face, there are no joi movements to test.

Palpation

A

B

Figure 2-55 A) Sensory nerve distribution of the head, neck and face. (1) Ophthalmic nerve. (2) Maxillary nerve. (3) Mandibular nerve. (4) Trans-erse cutaneous nerve of neck (C2-C3). (5) Greater auricular nerve C2-C3). (6) Lesser auricular nerve (C2). (7) Greater occipital nerve C2-C3). (8) Cervical dorsal rami (C3-C5). (9) Suprascapular nerve C5-C6). (B) Dermatome pattern of the head, neck, and face. Note the overlap ofC3.

During palpation of the head and face, the ex should note any tenderness, deformity, crepi other signs and symptoms that may indicate the of pathology. The examiner should note the tex the skin and surrounding bony and soft tissues mally, the patient is palpated in the sitting or position, beginning with the skull and movin anterior to posterior, to the face, and finally lateral and posterior structures of the head. The skull is palpated by a gentle rotary movem the fingers, progressing systematically from fr back. ormally, the skin of the skull moves free has no tenderness, swelling, or depressions. The temporal area and temporalis muscle sho laterally palpated for tenderness and deformit external ear or auricle and the periauricular area also be palpated for tenderness or lacerations. The occiput should be palpated posteriorly f derness. The presence of Battle's sign sho

112


noted, if observed, because this sign is indicative of a basilar skull fracture. The face is palpated beginning superiorly and working inferiorly in a systematic manner. Like the skull, the forehead is palpated by gentle rotary movements of the fingers, feeling the movement of the skin and the occipitofrontalis muscle underneath. Normally, the skin of the forehead moves freely and is smooth and even with no tender areas. The examiner then palpates around the eye socket or orbital rim, moving over the eyebrow and supraorbital rims, around the lateral side of the eye, and along the zygomatic arch to the infraorbital rims, looking for deformity, crepitus, tenderness, and lacerations (Fig. 2-56A and B). The orbicularis oculi muscles surround the orbit, and the medial side of the orbital rim and nose are then palpated for tenderness, deformity, and fracture. The nasal bones, including the lateral and alar cartilage, are palpated for any crepitus or deviation (Fig. 2-56C). The septum should be inspected to see if it has widened, which may indicate a septal hematoma, which often occurs

with a fracture. It should also be determined w the patient can breathe through the nose or smel The frontal and maxillary sinuses should spected for swelling. To palpate the frontal sinus examiner uses the thumbs to press up under the brow on each side of the nose (Fig. 2-57A) examiner then presses under the zygomatic pro using either the thumbs or index and middle fing palpate the maxillary sinuses (Fig. 2-57B). No t ness or swelling over the soft tissue should be p The sinus areas may also be percussed to detec derness. A light tap directly over each sinus wi index finger can be used to detect tenderness. The examiner then moves inferiorly to palpa jaw. The examiner palpates the mandible along tire length, noting any tenderness, crepitus, or mity. The examiner, using a rubber glove, ma palpate along the mandible interiorly, noting an derness or pain (Fig. 2-57D). The "outside" may be used to stabilize the jaw during this proc The mandible may also be tapped with a finger

Figure 2-56

Palpation of the face. (A) Uppe rim. (B) Lower orbital rim. (C) (D) Mandible. (E) Maxilla.

c


Figure 2-57 (A) Palpation of frontal sinuses. (B) Palpation of maxillary sinuses.

the face, which may indicate a Le Fort fracture 2-58). The trachea should be palpated for midline pos The examiner places a thumb along each side o trachea, comparing the spaces between the trachea the sternocleidomastoid muscle, which should be metric. The hyoid bone and the thyroid and cr cartilages should be identified. Normally, they smooth and nontender and move when the pa swallows.

Diagnostic Imaging Plain Film Radiography

Anteroposterior View. The examiner should the normal bone contours, looking for fractures o various bones (Figs. 2-59 through 2-61).

gure 2-58 • alpation of maxillary fracture with anteroposterior "rocking" mon.

Lateral View. The examiner should again note contours, looking for the possibility of fractures ( 2-59 and 2-62).

Computed Tomography

length to see if signs of tenderness are elicited. The muscles of the cheek (buccinator) and mouth (orbicuaris oris) should be palpated at the same time. The maxilla may be palpated in a similar fashion, oth internally and externally, noting position of the eeth, tenderness, and any deformity (Fig. 2-56E). The examiner may grasp the teeth anteriorly to see if the teeth and mandible move in relation to the rest of

Computed tomography scans help to differentiate tween bone and soft tissue and give a more pr view of fractures (Figs. 2-63 and 2-64).

Magnetic Resonance Imaging

Magnetic resonance imaging is especially usefu demonstrating lesions of the soft tissues of the and face and for differentiating between bone and tissue (Figs. 2-65 and 2-66).

114


Figure 2-59

Incomplete fracture of angle o mandible on the left side (arro (A) Anteroposterior view. (B) eral view. (From O'Donoghue D.H.: Treatment of Injuries to Athletes. Philadelphia, W.B. S ders Co., 1984, p. 114.)

Figure 2-60 Anteroposterior skull radiograph showing a depressed parietal skull fracture (large arrow) with multiple bony fragments into the brain (small arrows). (From Albright, J.P., J. Van Gilder, G. EI Khoury, E. Crowley, and D. Foster: Head and neck injuries in sports. In Scott, W. ., B. Nisonson, and J.A. icholas [eds.): Principles of Sports Medicine. Baltimore, Williams & Wilkins, 1984, p. 53.)

Figure 2-61 Plain posteroanterior view showing blow-out fracture of the orbit (arrows). (From Paton, D., and M.F. Goldberg: Management of Ocular Injuries. Philadelphia, W.B. Saunders Co., 1976, p. 70.)

Figure 2-62 Lateral radiograph of the nasal bones demonstrating a nasal fracture (arrow). (From Torg, J,S.: Athletic Injuries to the Head, Neck and Face. Philadelphia, Lea & Febiger, 1982, p. 229.)


gure 2-63 al computed tomogram of orbital blow-out cture showing fracture of the orbit (1) with _ ital contents herniated into the maxillary si. (From Sinn, D.P., and N.D. Karas: Radio_ phic evaluation of facial injuries. In Fonseca, T., and R.V. Walker [eds.]: Oral and Maxillo-lal Trauma. Philadelphia, W.B. Saunders Co., 991.)

Figure 2-64

The computed tomographic scan is ideal for condyla tures as seen in the right condyle. (From Bruce, R., Fonseca: Mandibular fractures. In Fonseca, R.J., and Walker [eds.]: Oral and Maxillofacial Trauma. Philad W.B. Saunders Co., 1991, p. 389.)

Figure 2-65

Magnetic resonance images showing blow-out fractu ittal (A) and coronal (B) T1-weighted scans demonst blow-out fracture of the right orbit with depression orbital floor (JVhite arroJVs) into the superior maxillar The inferior rectus muscle (long arroJV) is clearly iden and is not entrapped by the floor fracture. (From Ha S.E.: The orbit. In Edelman, R.R., and J.R. Hesselin [eds.]: Clinical Magnetic Resonance Imaging. Philad W.B. Saunders Co., 1990, p. 619.)

116


Maxillary sinus Coronoid process of mandible

Temporalis muscle Masseter

Lateral pterygoid muscle Longus capitis muscle -

Adenoid tissue Pharyngobasilar fascia Mandibular condyle Internal jugular vein Hypoglossal nerve

Internal carotid artery Medulla Cerebellar tonsil

Nasolacrimal duct Orbital fat Maxillary sinus Temporalis muscle

Zygomatic arch Lateral pterygoid muscle

Clivus Medullary cistern Medulla

Cerebellar hemisphere

Pyramid iiiiiiiiiiiiiiiiiiiiiiiiiiii/"-Olive Mastoid sinus

!!!!!!!!!!!!!!!!!!~-

PICA, tonsillar segment

Figure 2-66

T1-weighted axial magnetic resonance images of the head and brain at two levels. PICA, posterior inferior cerebellar artery. (From Green JI, et aI: Brain: Indications, techniques, and atlas. In Edelman, R.R., and J.R. Hesselink [eds.]: Clinical Magnetic Resonance Imaging. Philadelphia, W.B. Saunders Co., 1990, p. 384.)


Precis of the Head and Face Assessment* History (sitting) Observation (sitting) Examination * (sitting) Head injury Neural watch Glasgow Coma Scale Concussion Memory tests Headache Expanding intracranial lesion Proprioception Coordination Head injury card Facial injury Bone and soft tissue contours Fractures Cranial nerves Facial muscles Eye injury Six cardinal gaze positions Pupils (size, equality, reactivity) Visual field (peripheral vision)

-When examining the head and face, if only one area has been injured (e.g., the nose), then only that area needs to be examined, provided the exanliner is certain that adjacent structures have not also been injured. After any examination, the patient should be warned of the possibiliry of exacerbation of symptoms as a result of the assessment.

Visual acuity Symmetry of gaze Hyphema Foreign objects, corneal abrasion Nystagmus Surrounding bone and soft tissue Nasal injury Patency Nasal cavities Sinuses Fracture Nose discharge (bloody, straw-colored, clear) Tooth injury Number of teeth Position of teeth Movement of teeth Condition of teeth Condition of gums Ear injury Tenderness or pain Ear discharge (bloody, straw-colored, clear) Hearing tests Balance Special tests Tests for expanding intracranial lesions Tests for coordination Tests for proprioception Reflexes and cutaneous distribution Palpation Diagnostic imagi1JtJ

Case Studies T When doing these case studies, the examiner should list the appropriate questions to be asked and why they are being asked, what to look for and why, and what things should be tested and why. Depending on the answers of the patient (and the examiner should consider different responses), several possible causes of the patient's problem may become evident (examples are given in parentheses). A differential diagnosis chart should be made up. (See Table 2-17 as an example.) The examiner can then decide how different diagnoses may affect the treatment plan. 1. A 27-year-old man was playing football. He received a "knee to the head," rendering him unconscious for approximately 3 minutes. How would you differentiate between a first-time, fourth-degree concussion and an expanding intracranial lesion? 2. A I3-year-old boy received "an elbow" in the nose and cheek while play-wrestling. The nose is crooked and painful and bled after the injury, and the cheek is sore. Describe your assessment plan for this patient (nasal fracture versus zygoma fracture). 3. A 23-year-old woman was in an automobile accident. She was a passenger in the front seat and was not wearing a seat belt. The car in which she was riding hit another car, which had run a red light. The woman's face hit the dashboard of the car, and she received a severe facial injury. Describe your assessment plan for this patient (Le Fort fracture versus mandibular fracture). 4. An 83-year-old man tripped in the bathroom and hit his chin against the bathtub, knocking himself uncon-

5.

6.

7.

8.

scious. Describe your assessment plan for this pa (cervical spine lesion versus mandibular fracture). An I8-year-old woman was playing squash. She not wearing eye protectors and was hit in the ey the ball. Describe your assessment plan for this p (ruptured globe versus "blow-out" fracture). A IS-year-old boy was playing field hockey. He not wearing a mouth guard and was hit in the m and jaw by the ball. There was a large amount o blood. Describe your assessment plan for this pa (tooth fracture versus mandible fracture). A I6-year-old male wrestler comes to you compl of ear pain. He has just finished a match, which lost. Describe your assessment plan for tllis patie (cauliflower ear versus external otitis). A I7-year-old female basketball player comes to complaining of eye pain. She says she received a in the eye" when she went up to get the ball. D your assessment plan for this patient (hyphema v corneal abrasion).

118


Table 2-17 Differential Diagnosis of 4° Concussion and Intracranial Lesion 0

Sign or Symptom

4 Concussion

Intracranial Lesion

Confusion

Yes, but should improve with time

Will have increased confusion

Amnesia

Posttraumatic, retrograde

Not usually

Loss of consciousness

Yes, but recovers

Lucid interval varies

Tinnitus

Severe

Not a factor

Dizziness

Severe, but improves

May get worse

Headache

Often

Severe

ystagmus or irregular eye movements

ot usually

Possible

Pupil inequality

Not usually

Possible early; present later

Irregular respiration

No


Slowing of heart

No


Intractable vomiting

ot usually

Possible

Lateralization

o

Yes

Yes, but improves

Yes, and gets worse

Seizure

Not usually

Possible early; probable late

Personality change

Possible

Possible

Coordination affected

REFERENCES Cited References 1. Albright, J.P., J. Van Gilder, G. El Khoury, E. Crowley, and D. Foster: Head and neck injuries in sports. In Scott, W.N., B. Nisonson, and J.A. Nicholas (eds.): Principles of Sports Medicine. Baltimore, Williams & Wilkins, 1984. 2. Wojtys, E.M., D. Hovda, G. Landry, A. Boland, M. Lovell, M. McCrea, and J. Minkoff: Concussion in sports. Am. J. Sports Med. 27:676-686, 1999. 3. Kelly, J.P., and J.H. Rosenberg: Diagnosis and management of concussion in sports. Neurology 48:575-580, 1997. 4. Kelly, J.P., and J.H. Rosenberg: Practice paran1eter: the management of concussions in sports: Report of the quality standards subcommittee. Neurology 48:581-585,1997. 5. Gronwell, D., and P. Wrightson: Cumulative effect of concussion. Lancet 2:995-997, 1975. 6. McCroty, P.R., and S.F. Berkovic: Second impact syndrome. Neurology 50:677-683, 1998. 7. Evans, R.W.: The post concussion syndrome: 130 years of controversy. Seminars in Neurology 14:32-39, 1994. 8. McCrea, M., J.P. Kelly, J. Kluge, B. Ackley, and C. Randolph: Standardized assessment of concussion in football players. Neurology 48:586-588,1997. 9. Lovell, M.R., and M.W. Collins: Neuropsychological assessment of the college football player. J. Head Trauma Rehabil. 13:926, 1998. 10. Lovell, M.R., and C.J. Burke: Concussions in ice hockey: The ational Hockey League progran1. In Cantu, R.C. (ed.): eurologic Athletic Head and Spine Injuries. Philadelphia, W.B. Saunders Co., 2000. 11. Torg, J.S.: Athletic Injuries to the Head, Neck and Face. St. Louis, Mosby-Year Book Inc., 1991. 12. Manzi, D.B., and P.A. Weaver: Head Injury: The Acute Care Phase. Thorofare, New Jersey, Slack Inc., 1987. 13. Lovell, M.R., G.L. Iverson, M.W. Collins, D. McKeag, and J.C. Maroon: Does the level of consciousness predict neurophysiological decrements after concussion? Clin. J. Sports Med. 9:193198,1999.

14. Levin, H.S., V.M. O'Donnell, and R.G. Grossman: Th ton orientation and anmesia test: A practical scale to as nition after head injury. J. Nerv. Ment. Dis. 167:6751979. 15. Brandt, J.: The Hopkins verbal learning test: Developm new memory test with six equivalent forms. Clin. Neur ogist 5:125-142,1991. 16. Maddocks, D., and M. Saling: europhysiological defi lowing concussion. Brain Inj. 10:99-103,1996. 17. Putukian, M., and R.J. Echemendia: Managing success head injuries-which tests guide return to play? Phys. med. 24(11):25-38, 1996. 18. Seidel, H.M., J.W. Ball, J.E. Dains, and G.W. Benedic Guide to Physical Examination. St. Louis, C.Y. Mosby 1987. 19. Swartz, M.H.: Textbook of Physical Diagnosis. Philade W.B. Saunders Co., 1989. 20. Reilly, B.M.: Practical Strategies in Outpatient Medicin delphia, W.B. Saw1ders Co., 1984. 21. Novey, D.W.: Rapid Access Guide to the Physical Exa Chicago, Year Book Medical Publishers, 1988. 22. Kelly, J.P.: Maxillofacial injuries. In Zachazewski, J.E., gee, W.S. Quillen (eds.): Athletic Injuries and Rehabili Philadelphia, W.B. Saunders Co., 1996. 23. Pashby, T.J., and R.C. Pashby: Treatment of sports ey In Fu, F.H., and D.A. Stone (eds.): Sports Injuries-M nisms, Prevention, and Treatment. Baltimore, Williams kins, 1994. 24. Cantu, R.C.: Guidelines for return to contact sports af bral concussion. Phys. Sporrsmed. 14:75-83, 1986. 25. Robert, W.O.: Who plays? Who sits? Managing concus the sidelines. Phys. Sportsmed. 20:66-72, 1992. 26. Leblanc, K.E.: Concussions in sports: Guidelines for re competition. Am. Fam. Phys. 50:801-808, 1994. 27. Macciocchi, S. ., J.T. Barth, W. Alves, R.W. Rimel, an Jane: europhysiological fi.mctioning and recovery afte head injury in collegiate athletes. eurosurg. 39:510-5 1996.


Macciocchi, S. ., J.T. Barth, and L.M. Littlefield: Outcome after sports concussion. In Cantu, R.C. (ed.): Neurologic Athletic Head and Spine Injuries. Philadelphia, W.B. Saunders Co., 2000. Cantu, RC.: Retmn to play guidelines after concussion. In Cantu, RC. (ed.): Neurologic Athletic Head and Spine Injuries. Philadelphia, W.B. Saunders Co., 2000. Kelly, J.P., J.S. Nichols, C.M. Filley, KO. Lillehei, D. Rubinstein, and B.K Kleinschmidt-DeMasters: Concussion in sportsguidelines for the prevention of catastrophic outcome. JAMA 266:2867-2869, 1991. Macciocchi, S. ., J.T. Barth, and L.M. Littlefield: Outcome after mild head injury. Clin. Sports Med. 17(1):27-36,1998. Polin, RS., W.M. Alves, and J.A. Jane: Sports and head injuries. In Evans, R W. (ed.): Nemology and Trauma. Philadelphia, W.B. Saunders Co., 1996. . - Cantu, RC.: Rermn to play guidelines after a head injury. Clin. ports Med. 17(1):45-60,1998. _ Pick, D.S.: Management of concussion in collision sportsguidelines for the sidelines. Postgrad. Med. 97:53-60, 1995. ~ Cantu, RC.: Second-impact syndrome. Cl.i..n. Sports Med. 17: 37-44, 1998. Topel, J.L.: Exan1ination of the comatose patient. In Weiner, W.J., and C.G. Goetz (eds.): Nemology for the on- eurologist. Philadelphia, J.B. Lippincott, 1989. Fonseca, RJ., and R V. Walker: Oral and Maxillofacial Trauma. Philadelphia, W.B. Saunders Co., 1991. Pollock, RA, and RO. Dingman: Management and reconstruction of athletic injmies of the face, anterior neck, and upper respiratory tract. In Schneider, RC., J.C. Kennedy, and M.L. Plant (eds.): Sports Injmies-Mechanisms, Treatment and Pre\·ention. Baltimore, Williams & Wilkins, 1985. Simpson, J.F., and KR Magee: Clinical Evaluation of the Ner\'Ous System. Boston, Little, Brown & Co., 1973.

General References - Hoc Committee on Classification of Headache: Classification of eadache. Arch. Nemol. 6:173-176, 1962. - erican Academy of Orthopedic Surgeons: Athletic Training and ports Medicine. Chicago, AAOS, 1991. er, N., G. Borim, and O. Sjaastad: Extracranial nerves in the posterior part of the head-anatomic variation and their possible cl.i..nical significant. Spine 23:1435-1441,1988. >oher, J.M., and G.A Thibodeau: Athletic Injury Assessment. St. Louis, C.V. Mosby Co., 1989. yd-Monk, H.: Examining the external eye. Nursing 80:58-63, 1980. ruce, R, and RJ. Fonseca: Mandibular fractures. In Fonseca, RJ., and R V. Walker (eds.): Oral and Maxillofacial Trauma. Philadelphia, W.B. Saunders Co., 1991. rucker, A.]., D.M. Kozart, C.W. ichols, and I.M. Raber: Diagnois and management of injuries to the eye and orbit. In Torg, J.S. ed.): Athletic Injuries to the Head, Neck and Face. St. Louis, ~10sby-Year Book Inc., 1991. 3runo, L.A, T.A Gennarelli, and J.S. Torg: Head injuries in athletics. In Welsh, RP., and R.J. Shephard (eds.): Current Therapy in Sports Medicine 1985-1986. St. Louis, CV. Mosby Co., 1985. Bruno, L.A., T.A Gennarelli, and J.S. Torg: Management guidelines for head injuries in athletics. Clin. Sports Med. 6:17-29, 1987. Burde, R.M.: Eye movements and vestibular system. In Pearlman, A.L., and RC. Collins (eds.): Neurological Pathophysiology. New York, Oxford University Press, 1984. Caillet, R.: Head and Face Pain Syndromes. Philadelphia, F.A. Davis Co., 1992. Canter, RC.: Guidelines for return to contact sports after a cerebral concussion. Phys. Sportsmed. 14:75-83, 1986. Cantu, RC. (ed.): Neurologic athletic head and neck injuries. Clin. Sports Med. 17(1):1-82, 1998. Cox, M.S., c.L. Schepens, and H.M. MacKenzie Freeman: Retinal detachment due to ocular contusion. Arch. Ophthal. 76:678-685, 1966.

Crovitz, H.P., and W.F. Daniel: Length of retrograde amnesia head injury: A revised formula. Cortex 23:695-698, 1987. Diamond, G.R, G.E. Quinn, T.J. Pashby, and M. Easterbrook Ophthalmologic injuries. Clin. Spotts Med. 1:469-482, 198 Easterbrook, M., and J. Cameron: Injuries in racquet sports. In Schneider, R.C., ].C. Kennedy, and M.L. Plant (eds.): Sports ries-Mechanisms, Treatment and Prevention. Baltimore, Wi & Wilkins, 1985. Edelman, RR, and J.R. Hessel.i..nk: Cl.i..nical Magnetic Resonanc Imaging. Philadelphia, W.B. Saunders Co., 1990. Ellis, E.: Fractures of the zygomatic complex and arch. In Fons RJ., and RV. Walker (eds.): Oral and Maxillofacial Trauma. delphia, W.B. Saunders Co., 1991. Fal1ey, T.D.: Athletic Training-Principles and Practice. Palo A California, Mayfield Pub. Co., 1986. Foreman, S.M., and A.C. Croft: Whiplash Injuries-The Cervic Acceleration/Deceleration Syndrome. Baltimore, Williams & kins, 1988. Frost, D.E., and B.D. Kendall: Applied surgical anatomy of the and neck. In Fonseca, RJ., and RV. Walker (eds.): Oral and Maxillofacial Trauma. Philadelphia, W.B. SalU1ders Co., 1991 Garrison, D.W.: Cranial Nerves-A Systems Approach. Springf Illinois, Charles C Thomas Pub., 1986. Gorman, B.D.: Ophthalmology and sports medicine. In Scott, B. Nisonson, and J.A. Nicholas (eds.): Principles of Sports M cine. Baltimore, Willian1s & Wilkins, 1984. Greenberg, M.S., and P.S. Springer: Diagnosis and managemen oral injuries. In Torg, J.S. (ed.): Athletic Injuries to the Hea eck, and Face. St. Louis, Mosby-Year Book Inc., 1991. Halling, AH.: The impottance of cl.i..nical signs and symptoms i evaluation of facial fractures. Athletic Training 17:102-1 03, Hancller, S.D.: Diagnosis and management of maxillofacial inju In Torg, J.S. (ed.): Athletic Injuries to the Head, Neck and Philadelphia, Lea & Febiger. 1982. Havener, W.H., and T.A Makley: Emergency management of injuries. Ohio State Med. J. 71:776-779, 1975. Hayward, R: Management of Acute Head Injuries. Oxford, Bl well Scientific Pub., 1980. Hildebrandt, J.R: Dental and maxillofacial injuries. Clin. Sport Med. 1:449-468,1982. Hollinshead, W.H., and D.B. Jenkins: Functional Anatomy of t Limbs and Back. Philadelphia, W.B. Saunders Co., 1981. Hugenholtz, H., and M.T. Richard: Return to athletic competi following concussion. CMA J. 127:827-829,1982. Jenkins, D.B.: Hollinshead's Functional Anatomy of the Limbs Back. Philadelphia, W.B. Saunders Co., 1991. Jordan, B.D.: Head injury in sports. In Jordan, B.D., P. Tsairis R.F. Warren (eds.): Sports Neurology. Rockville, Maryland. A Publishers Inc., 1989. Kinderknecht, ].J.: Head injuries. In Zachazewski, J.E., D.J. M W.S. Quillen (eds.): Athletic Injuries and Rehabilitation. Phil phia, W.B. Saunders Co., 1996. Kulund, D.N.: The Injured Athlete. Philadelphia, J.B. Lippinco Co., 1988. Kumamoto, D.P., M. Jacob, and D. Nickelsen: Oral trauma: O field assessment. Phys. Sportsmed. 23:53-62, 1995. Lampert, P.W., and J.M. Hardman: Morphological changes in of boxers. JAMA 251:2676-2679, 1984. Lew, D., and D.P. Sinn: Diagnosis and treatment of midface fr tures. In Fonseca, RJ., and RV. Walker (eds.): Oral and Ma facial Trauma. Philadelphia, W.B. Saunders Co., 1991. Liebgott, B.: The Anatomical Basis of Dentistry. St. Louis, CV Mosby, 1986. Mueller, F.D.: Catastrophic head and neck injuries. Phys. Sport 7:710-714,1979. Nasher, L.M.: A Systems Approach to Understanding and Asse Orientation and Balance Disorders. Clackamas, Oregon, NeuroCom International Inc., 1987. O'Donoghue, D.H.: Treatment of Injuries to Athletes. Philade W.B. Saunders Co., 1984. Pashby, RC., and T.J. Pashby: Ocular injuries in sports. In We RP., and RJ. Shephard (eds.): Current Therapy in Sports M cine 1985-1986. St. Louis, C.v. Mosby Co., 1985.

120


Paton, D., and M.F. Goldberg: Management of Ocular Injuries. Philadelphia, W.B. Saunders Co., 1976. Pavlov, H.: Radiographic evaluation of the skull and facial bones. In Torg, J.S. (ed.): Athletic Injuries to the Head, Neck, and Face. St. Louis, Mosby-Year Book Inc., 1991. Powers, M.P.: Diagnosis and management of dentoalveolar injuries. In Fonseca, RJ., and RV. Walker (eds.): Oral and Maxillofacial Trauma. Philadelphia, W.B. Saunders Co., 1991. Proctor, M.R, and RC. Cantu: Head and neck injuries in young athletes. Clin. Sports Med. 19(4):693-715,2000. Reid, D.C.: Sports Injury Assessment and Rehabilitation. New York, Churchill Livingstone, 1992. Rimel, RW., B. Giordani, J.T. Barth, T.J. Boll, and J.J. Jane: Disabiliry caused by minor head injury. Neurosurg. 9:221-228,1981. Root, J.D., B.D. Jordan, and RD. Zimmerman: Delayed presentation of subdural hematoma. Phys. Sportsmed. 21:61-68, 1993. Ross, RJ., 1.R Casson, O. Siegel, and M. Cole: Boxing injuries: Neurologic, radiologic and neuropsychologic evaluation. Clin. Sports Med. 6:41-51, 1987. Rousseau, AP.: Ocular trauma in sports. In MacKenzie Freeman, H.M. (ed.): Ocular Trauma in Sports. New York, Appleton-Century-Crofts, 1979. Roy, S., and R. Irvin: Sports Medicine-Prevention, Evaluation, Management and Rehabilitation. Englewood Cliffs, New Jersey, Prentice-Hall Inc., 1983. Sandusky, J.e.: Field evaluation of eye injuries. Athletic Training 16: 254-258, 1981. Schneider, RC.: Head and Neck Injuries in Football-Mechanisms, Treatment and Prevention. Baltimore, Williams & Wilkins, 1973. Schneider, RC., T.R Peterson, and RE. Anderson: Football. In Schneider, RC., J.e. Kennedy, and M.L. Plant (eds.): Sports Injuries-Mechanisms, Prevention and Treatment. Baltimore, Willianls & Wilkins, 1985. Schuller, D.E., and RA. Bmce: Ear, nose, throat, and eye. In

Strauss, RH. (ed.): Sports Medicine, 2nd ed. Philadelphia, Saunders Co., 1991. Schultz, RC., and D.L. de Camara: Athletic facial injuries. JA 252:3395-3398, 1984. Scott, W.N., B. isonson, and J.A icholas (eds.): Principle Sports Medicine. Baltimore, Williams & Wilkins, 1984. Shell, D., G.A. Carico, and RM. Patton: Can subdural hema result from repeated minor head injury? Phys. Sportsmed. 2 84,1993. Sinn, D.P., and N.D. Karas: Radiographic evaluation of facial ries. In Fonseca, R.J., and V. Walker (eds.): Oral and Maxi Trauma. Philadelphia, W.B. Saunders Co., 1991. Sitler, M.: Nasal septal injuries. Athletic Training 21:10-12, Solon, Re.: Maxillofacial trauma. In Scott, W.N., B. Nisons J.A. Nicholas (eds.): Principles of Sports Medicine. Baltimo liams & Wilkins, 1984. Starkey, C., and J. Ryan: Evaluation of Orthopedic and Athle Injuries. Philadelphia, F.A. Davis Co., 1996. Untevharnscheidt, F.: Boxing injuries. In Schneider, RC., J.C nedy, and M.L. Plant (eds.): Sports Injuries-Mechanisms vention and Treatment. Baltimore, Williams & Wilkins, 19 Vegso, J.J., and RC. Lehman: Field evaluation and managem head and neck injuries. Clin. Sports Med. 6:1-15, 1987. Vegso, J.J., and J.S. Torg: Field evaluation and management intracranial injuries. In Torg, J.S. (ed.): Athletic Injuries to Head, Neck and Face. Philadelphia, Lea & Febiger, 1982. Yinger, P.F.: How I manage corneal abrasions and lacerations Sportsmed. 14:170-179,1986. Wester, 1.: Bell's palsy: The present status of electrodiagnosis treatment. Physiother. Can. 23:218-221, 1971. Zagelbaum, B.M., and M.A Hochman: A close look at a 'red diagnosing vision-threatening causes. Phys. Sportsmed. 23: 1995.

£RVICAL SPIN£ Examination of the cervical spine involves determining -hether the injury or pathology occurs in the cervical ine or in a portion of the upper limb. Cyriax called dlls assessment the scanning examination. J In the inial assessment of a patient who complains of pain in - e neck and/or upper limb, this procedure is always -arried out unless the examiner is absolutely sure of - e location of the lesion. If the injury is in the neck, -- e scanning examination is definitely called for to rule ut neurological involvement. After the lesion site has een determined, a more detailed assessment of the - ~ected area is performed if it is outside the cervical EJine. Because many conditions affecting the cervical spine .:an be manifested in other parts of the body, the -ervical spine is a complicated area to assess properly, d adequate time must be allowed to ensure that as any causes or problems are examined as possible.

Applied Anatomy :be cervical spine consists of several ]0ll1ts. It is an -"Iea in which stability has been sacrificed for mobility, aking the cervical spine particularly vulnerable to in.ny. The atlanto-occipital joints (CO-C1) are the '0 uppermost joints. The principal motion of these '0 joints is flexion-extension (15° to 20°), or nodding _ the head. Side flexion is approximately 10°, whereas tation is negligible. The atlas (C1) has no vertebral dy as such. During development, the vertebral body : C1 evolves into the odontoid process, which is art of C2. The atlanto-occipital joints are ellipsoid .md act in unison. Along with the atlanto-axial joints, - ese joints are the most complex articulations of the rial skeleton. There are several ligaments that stabilize the atlantocipital joints. Anteriorly and posteriorly are the tlanto-occipital membranes. The anterior membrane is mengthened by the anterior longitudinal ligament. The posterior membrane replaces the ligamentum fla'Um between the atlas and occiput. The tectorial

membrane, which is a broad band covering th and its ligaments, is found within the vertebra and is a continuation of the posterior longitudina ment. The alar ligaments are two strong ro cords found on each side of the upper dens p upwards and laterally to attach on the medial s the occipital condyles. The alar ligaments limit and rotation. The atlanto-axial joints (C1- C2) constitu most mobile articulations of the spine. Flexion sion is approximately 10°, and side flexion is ap mately 5°. Rotation, which is approximately 50°, primary movement of these joints. With rotation is a decrease in height of the cervical spine at th as the vertebrae approximate because of the sh the facet joints. The odontoid process of C2 ac pivot point for the rotation. This middle, or m joint is classified as a pivot (trochoidal) join lateral atlanto-axial, or facet, joints are classi plane joints. Generally, if a person can talk and there is probably some motion occurring at C At the atlanto-axial joints, the main supportin ment is the transverse ligament of the atlas, holds the dens of the axis against the anterior a the atlas. It is this ligament that weakens or ru in rhematoid arthritis. As the ligament cross dens, there are two projections off the ligamen going superiorly to the occiput and one inferio the axis. The ligament and the projections form and the three parts taken together are called the form ligament of the atlas (Fig. 3 -1). It must be remembered that rotation past 50° cervical spine may lead to kinking of the contra vertebral artery; the ipsilateral vertebral artery ma at 45° of rotation (Fig. 3 - 2). This kinking may vertigo, nausea, tinnitus, "drop attacks" (falling out fainting), visual disturbances, or in rare stroke or death. There are 14 facet (apophyseal) joints in the cal spine. The upper four facet joints in the two thoracic vertebrae are often included in the ex

122

CHAPTER 3 • Cervical Spine

Tectorial membrane (reflected)

-----+--,

Atlanto-occipital joint --------~""

Atlanto-axial joint

-----+;,

Tectorial membrane (reflected)

Inferior crus

A

-------+

Figure 3-1

Articular capsule of left atlantooccipital joint -----,7,;-

Ligaments of the upper cenical spine. (A) Posterior deep'iew. (B) Posterior superficial view. (C) Superior view. (D) Lateral \iew.

~~--- P

a m Ligamentum f1avum ------rr'*'"+¥;1J!JI;1}

Articular cavities

of ax

B

Anterior arch

""'?!fjP:]§S;~~:::'OO

Superior

.rt'oo'"

Z/

!~--- Ar

Dens of atlas

~~~'V/'7 "T,,",~rn, ~

Transverse ligament of atlas

foramen

.~ Posterior arch

C Membrane tectoria

Posterior arch of atlas - - - -...... Transverse ligament of atlas - - - - Inferior longitudinal band of cruciform ligament

-------------z )

D

Ligamentum flavum II 'o~,) JI Spinal canal~_ Posterior longitudinal ligament - - - - - - - 1 1

Dens ;...:fi-~:-----

Body of axis

- * - - - Intervertebral disc

1 1 - - - - Anterior longitudinal ligament


Cervical Spine Resting position:

Slight extension

Close packed position:

Full extension

Capsular pattern:

Side flexion and rotation equa limited, extension

C1

C2 C3

C4 C5 'Jr...+~I------

Vertebral artery

~·~::::::--":C8

\ ure 3-2 e of vertebral artery in the cervical spine (anterior view). able turn at Cl as the artery wraps around the atlas.

ote

n of the cervical spine. The superior facets of the n'ical spine face upward, backward, and medially; the erior facets face downward, forward, and laterally Fig. 3-3). This plane facilitates flexion and extension, Jt it prevents simple rotation or side flexion without th occurring to some degree together. This is called oupled movement. These joints move Plimarily by _ ding and are classified as synovial (diarthrodial) ints. The capsules are lax to allow for sufficient o\'ement. At the same time, they provide support d a check-rein type of restriction. The greatest exion-extension of the facet joints occurs between C5 d C6; however, there is almost as much movement • C4-C5 and C6-C7. Because of this mobility, de.:-eneration is most likely to be seen at these levels. The eutral or resting position of the cervical spine is ghtly extended. The close packed position of the :.1 et joints is complete extension. The recurrent meningeal or sinuvertebral nerve innervates the anterior ura sac, the posterior annulus fibrosus, and the posterior longitudinal ligament. The facet joints are innerated by the medial branch of the dorsal primary rami. 2 or the remaining cervical vertebrae, the main ligaments are the anterior longitudinal ligament, the poserior longitudinal ligament, the ligamentum flavurn, .md the supraspinal and interspinal ligaments (Fig. ~ -4). There are also ligaments between the transverse

processes (intertransverse ligaments), but in the ce spine, they are rudimentary. Some anatomists 3- 6 refer to the costal or uncov bral processes as uncinate joints or joints of Lus (Fig. 3-5). These structures were described by Luschka in 1858. The uncus gives a "saddle" for the upper aspect of the cervical vertebra, which is pronounced posterolaterally; it has the effect of l ing side flexion. Extending from the uncus is a "j that appears to form because of a weakness in annulus fibrosus. The portion of the vertebra ab which "articulates" or conforms to the uncus, is c the echancrure, or notch. Notches are found from to Tl, but according to most authors,3-6 they are seen until age 6 to 9 years and are not fully devel until 18 years of age. There is some controversy whether tl1ey should be classified as real joints, be some authors believe they are the result of dege tion of the intervertebral disc; degeneration tend

B Figure 3-3

Cervical spine-plane of facet joints. (A) Lateral view. (B) Supe view.

124


Supraspinal Iigament--~

Interspinal ligament ----ffFi#f#fHhI

Figure 3-4

Median section of C4-C6 vertebrae to illustrate th vertebral disc and the ligaments of the cervical spin

occur faster in the cervical spine than in any other part of the spine. The intervertebral discs make up approximately 25% of the height of the cervical spine. No elisc is found between the atlas and the occiput (CO-Cl) or between the atlas and the axis (CI-C2). It is the eliscs rather than the vertebrae that give the cervical spine its lordotic shape (Fig. 3-6). The nucleus pulposus functions as a buffer to axial compression in elistributing compressive forces, whereas the annulus fibrosus acts to withstand tension within tl1e disc. The intervertebral elisc has some innervation on the periphery of the annulus fibrosus. 7 ,8 There are seven vertebrae in the cervical spine, with the body of each vertebra (except C 1) supporting the weight of those above it. The facet joints may bear some of the weight of the vertebrae above, but this weight is minimal. However, even this slight amOlmt of weight bearing can lead to spondylitic changes in these joints. The outer ring of the vertebral body is

(C3) (C4)

Cervical spine

(C5) (C6) (C7)

Figure 3-6 Lateral view of cervical spine and head.

Figure 3-5 Joints of Luschka.

made of cortical bone, and tl1e inner part is m cancellous bone covered with the cartilagino plate. The vertebral arch protects the spinal co spinous processes, most of which are bifid in th cal spine, provide for attachment of muscle transverse processes have basically the same fu In the cervical spine, the spinous processes are level of the facet joints of the same vertebra. Ge the spinous process is considered to be absen least rudimentary on Cl. This is why the first p vertebra descending from the external occiput berance is the spinous process of C2. Although there are seven cervical vertebrae, th eight cervical nerve roots. This difference occ


C1 C2 Disc C2 C3 Disc

C3

C4 Disc

C4

C5 Disc

C5

C6 Disc

C6 C7 C8

\ T1 ~

ure 3-7

- --erim view of cervical spine showing nerve roots. Note how each ical nerve root is numbered for the vertebra below it.

cause there is a nerve root exiting between the oc and C1 that is designated the C1 nerve root. I cervical spine, each nerve root is named for the bra below it. As an example, C5 nerve root between the C4 and C5 vertebrae (Fig. 3 -7). I rest of the spine, each nerve root is named fo vertebra above; the L4 nerve root, for example, between the L4 and L5 vertebrae. The switch in ing of the nerve roots from the one below to th above is made between the C7 and T1 vertebrae nerve root between these two vertebrae is called accounting for the fact that there are eight ce nerve roots and only seven cervical vertebrae.

T

Patient History

In addition to the questions listed under Patient

tory in Chapter 1, the examiner should obtai following information from the patient. 1. What is the patient's age? Spondylosis is seen in persons 25 years of age or older, and present in 60% of those older than 45 years and of those older than 65 years of age. Symptom osteoarthritis do not usually appear until a person years of age or older (Table 3 -1).

Ie 3-1 ifferential Diagnosis of Cervical Spondylosis, Spinal Stenosis, and Disc Herniation Cervical Disc Herniation *

Cervical Spinal Stenosis

Cervical Spondylosis ain

Unilateral

May be unilateral or bilateral

May be unilateral (mos conm1On) or bilateral

istribution of pain

Into affected dermatomes

Usually several dermatomes affected

Into affected derrnatorn

Increases

Increases

May increase (most com

Decreases

Decreases

May increase or decreas (most cornman)

Pain relieved by rest

No

Yes

No

Age group affected

60% of those >45 yr 85% of those >60 yr

11-70 yr Most common: 30-60 yr

17-60 yr No

:'ain on extension ain on flexion

Instability

Possible

No

Levels commonly affected

C5-6,C6-7

Varies

C5-C6

Onset

Slow

Slow (may be combined with spondylosis or disc herniation)

Sudden

Diagnostic imaging

Diagnostic

Diagnostic

Diagnostic (be sure clin signs support)

* Posterolateral protrusion.

126


2. How severe are the symptoms? Was the patient moving when d1e injury occurred? Watkins 9 provided a severity scale for neurological injury in football that can be used as a guideline for injury severity involving the cervical spine, especially if one is contemplating allowing the patient to return to activity (Fig. 3-8). A combined score (A+ B) of 4 is considered a mild episode, 4 to 7 is a moderate episode, and 8 to 10 is a severe episode. This scale can be combined with radiologic information on canal size (score C) to give a general determination of the possibility of symptoms returning if the patient returns to activity. In this case, a score of 6 (A+B+C) indicates minin1um risk, 6 to 10 is moderate risk, and 10 to 15 is severe risk. Watkins9 also points out that extenuating factors such as age of patient, level of activity, and risk versus benefit

also play a role and, although not include score, must be considered. 3. What was the mechanism of injury? Wa stretching, or overuse involved? These quest determine the type of injury. For example, tra cause a whiplash injury, stretching may lead ers," overuse or sustained postures may resu racic oudet symptoms, and a report of an onset in someone older than 55 years of indicate cervical spondylosis (Table 3-2). Wa tient hit from the side, front, or behind? Di tient see the accident coming? "Burners" or typically occur from a blow to part of the plexus or from stretching or compression of chial plexus (Fig. 3-9). The answers to th tions help the exan1iner determine how the

Watkins' Severity Scale for Neurological Deficit Neurological Deffcit

Grade I

Unilateral arm numbness or dysesthesia; loss of strength

2

Bilateral upper extremity loss of motor and sensory function

3

Ipsilateral arm, leg, and trunk loss of motor and sensory function

4

Transient quadriparesis (temporary sensory loss in all 4 limbs)

5

Transient quadriplegia (temporary motor loss in all 4 limbs) (A)

Score:

Grade

Time Symptoms Present

I

Less than 5 minutes

Figure 3-8

2

Less than I hour

3

less than 24 hours

Watkins' severity scale f logical deficit. (Data fro R.G.: eck injuries in f Watkins, R.G. [ed.]: Th Sports. St. Louis, Mosb Book Inc., 1996, p. 32

4

Less than I week

5

Greater than I week (B)

Score: Severity Score: A

+

B

=

(::;4: mild episode; 4-7: moderate episode; 8-10: severe episode)

Grade

Central Canal Diameter

1

>12 mm

2

Between 10-12

3

10 mm

4

8-10 mm

5 Score:

ermatome pattern eripheral nerve sensory distribution Resistance to stretch

Cramping, dull, ache

Dull

0

~

sharp

0

Neurogenic Tissue Burning, bright, lightning-like Yes

Intermittent

Intermittent

Longer symptom duration

No

No

Yes (ifnerve root pathological)

No

0

Muscle spasm

Boggy, hard capsular

Yes (if peripheral nerve or nerve root is affected) Soft tissue stretch

A

B

Figure 3-26

Brachial plexus tension test. (A) The patient abducts and then laterally rotates the arms Wltil symptoms are felt; patient then lowers th until symptoms disappear and the exanliner holds the patient's arms in the position. (B) While the shoulders are held in position, the flexes the elbows and places the hands behind the head. A positive test is indicated by return of symptoms.

Figure 3-27

Bikele's sign. (A) The ann ducted to 90° with the elbo flexed. (B) The aml and th elbow are extended.

A

as the test posmon is the mechanism of in these lesions, plexopathies, and radiculopathie brachial plexus lesions, more than one nerve commonly affected. The examiner side flexes tient's head to one side (for example, the righ applying a downward pressure on the opposit der (for example, the left) (Fig. 3-28). If the increased, it indicates irritation or compressio nerve roots or foraminal encroachments such a phytes in the area on the side being compre adhesions around the dural sleeves of the ne adjacent joint capsule or a hypomobile joint ca the side being stretched.

Figure 3-28 Shoulder depression test.

Shoulder Abduction (Relief) Test. This used to test for radicular symptoms especial involving the C4 or C5 nerve roots. The p sitting or lying down, and the examiner pas the patient actively elevates the arm through tion, so that the hand or forearm rests on to


151

ure 3-29 ulder abduction (Bakody's) test.

ad (Fig. 3_29).15,39 A decrease in or relief of symprn indicates a cervical extradural compression prob~ uch as a herniated disc, epidural vein compresn or nerve root compression, usually in the C4-C5 C5-C6 area. Differentiation is by the dermatome tribution of the symptom. This finding is also ed Bakody's sign.16 Abduction of the arm dee the length of the neurological pathway and reases the pressure on the lower nerve roots. 39 ,40 If e pain increases with the positioning of the arm, it plies that pressure is increasing in the interscalene angle. 16 Jackson's Compression Test. This test is a modifiation of the foraminal compression test. The patient tates the head to one side. The examiner then care';illy presses straight down on the head (Fig. 3-30).

-:be test is repeated with the head rotated to the other de. The test is positive if, on testing, pain radiates to the arm, indicating pressure on a nerve root. The all distribution (dermatome) can give some indicaon of which nerve root is affected. 15

Scalene Cramp Test. lO The patient sits and rotates ~ e head to the affected side and pulls the chin down nto the hollow above the clavicle by flexing the cervi-al spine. If pain increases, it is usually in the trigger oints of the scalenes toward which the head rotates. Radicular signs may indicate plexopathy or thoracic utlet symptoms. Valsalva Test. This test is used to determine the effect of increased pressure on the spinal cord. The examiner asks the patient to take a deep breath and hold it while bearing down, as if moving the bowels. A

Figure 3-30 Jackson's compression test.

positive test is indicated by increased pain, which may be caused by increased intrathecal pressure. This increa ed pressure \vithin the spinal cord usually results from a space-occupying lesion, such as a herniated disc, a tumor, or osteophytes. Test results are very subjective. The test should be done "vith care and caution, because the patient may become dizzy and pass out while performing the test or shortly afterward if the procedure blocks the blood supply to the brain. Tinel's Sign for Brachial Plexus Lesions. 41 The patient sits with the neck slightly side flexed. The examiner taps the area of the brachial plexus (Fig. 3 - 31) \vith a finger along the nerve trunks in such a way that the different nerve roots are tested. Pure local pain implies that there is an underlying cervical plexus lesion. A positive Tinel's sign (tingling sensation in the distribution of a nerve) mean the lesion is anatomically intact and some recovery is occurring. If pain is elicited in the distribution of a peripheral nerve, the ign is positive for a neuroma and indicates a disruption of the continuity of the nerve. Brachial Plexus Compression Test. 42 The examiner applies firm compression to the brachial ple>..'Us by squeezing the ple>..'Us under the thumb or fingers (Fig. 3 - 32). Pain at the site is not diagnostic; the test is positive only if pain radiates into the shoulder or upper

Figure 3-31 TineJ's sign for brachial plexus lesions. Dots indicate percussion points.

extremity. It is positive for mechanical cervical lesions having a mechanical component.

Tests for Upper Motor Neuron Lesions (Cervical Myelopathy) Romberg's Test. For Romberg's test, the patient is standing and is asked to close the eyes. The position is held for 20 to 30 seconds. If the body begins to sway excessively or the patient loses balance, the test is considered positive for an upper motor neuron lesion. Lhermitte's Sign. This is a test for the spinal cord itself and a possible upper motor neuron lesion. The patient is in the long leg sitting position on the examining table. The examiner passively flexes the patient's head and one hip simultaneously, with the leg kept straight (Fig. 3-33). A positive test occurs if there is a sharp pain down the spine and into the upper or lower limbs; it indicates dural or meningeal irritation in the spine or possible cervical myelopathy. 16 The test is similar to a combination of the Brodzinski test and the SLR test (see Chapter 9). If the patient can actively flex the head to the chest while in the supine lying position, the test is called the Soto- Hall test. If the hips are flexed to 135°, greater traction is placed on the spinal cord. IS

Figure 3-32 Maneuver

to

compress and squeeze the brachial plexus.

Tests for Vascular Signs

Vertebral artery testing is an important compon the cervical spine assessment in cases where end mobilization and manipulation treatment tech are contemplated especially if the techniques inv rotary component (greater than 45°) and the cervical spine (CO - C3).43-45 The vertebral artery pecially vulnerable to injury as it transitions fr protective area in the foramen wll1sversarium the cervical spine transverse processes, then l before it enters the cranial vault behind the first bra. Grant4 3 and Rivett et al 46 have reported th vertebral artery tests have not been conclusively to be effective in indicating stretching and occlu the vertebral artery but do say that the tests sho performed to decrease the risk of potentially strophic complications. If, when performing the bral artery tests, or if in the history, the patien plains of signs and symptoms that may be rela the vertebral artery, care should be taken when lizing the upper cervical spine. 44 •47 ,48

Vertebral Artery (Cervical Quadrant) Test the patient supine, the examiner passively tak patient's head and neck into extension and side (Fig. 3-34).49 After this movement is achieve examiner rotates the patient's neck to the sam


153

Figure 3-33 Lhermitte's sign. (A) Patient in long sitting. (B) Examiner flexes patient's head and hip sinmltaneously.

d holds it for approximately 30 seconds. A positive provokes referring symptoms if the opposite artery affected. This test must be done with care. If dizzior nystagmus occurs, it is an indication that the rtebral arteries are being compressed. The DeKleyn• -ieuwenhuyse testSO performs a similar function but

involves extension and rotation instead of extension and side flexion. Both tests may also be used to assess nerve root compression in the lower cervical spine. To test the upper cervical spine, the examiner "pokes" the patient's chin and follows with extension, side flexion, and rotation.

Signs and Symptoms Which May Indicate Possible Vertebral-Basilar Artery Problems43.46 • Malaise and nausea • Vomiting • DizzinessNertigo • Unsteadiness in walking, incoordination • Visual disturbances • Severe headaches • Weakness in extremities • Sensory changes in face or body • Dysarthria (difficulty with speech) • Unconsciousness, disorientation, light headed ness • Dysphagia (difficulty swallowing) • Hearing difficulties • Facial paralysis

Figure 3-34 Vertebral artery (cervical quadrant) test. Exanliner passively moves patient's head and neck into extension and side flexion (1), then rotation (2), holding for 30 seconds.

Static Vertebral Artery Tests. The examiner may test the following passive movements with the patient supine or sitting, as advocated by Grant,51 watching for eye nystagmus and complaints by the patient of dizziness, lightheadedness, or visual disturbances. Each of these tests is increasingly provocative; if symptoms occur with the first test, there is no need to progress to the next test.

In the sitting position: 1. Sustained full neck and head extension 2. Sustained full neck and head rotation, right and

3.

4. 5. 6. 7. 8.

left (if this movement causes symptoms, it is sometimes called a positive Barre-Lieon sign)16 Sustained full neck and head rotation with extension right and left (DeKleyn's test)16 Provocative movement position* Quick head movement into provocative position* Quick repeated head movement into provocative position * Head still, sustained trunk movement left and right (10 to 30 seconds) Head still, repeated trunk movement left and right

These tests are often more effective if done with patient sitting, because the blood must flow ag gravity and there is a restriction caused by the pas movement. However, tlle supine position al greater passive range of movement. 53 Movement the right tend to have more effect on the left verte artery, and movements to the left tend to have m effect on the right artery. Aspinall 54 advocated the use of a progressive s of clinical tests to evaluate the vertebral artery. W these tests, the examiner progressively moves from lower cervical spine and lower vertebral artery to upper cervical spine and upper vertebral artery whe is more vulnerable to pathology. Table 3-11 dem strates Aspinall's progressive clinical tests [or the ve bral arteries.

Hautant's Test. 16 ,55 This test has two parts an used to differentiate dizziness or vertigo caused articular problems from that caused by vascular p lems. The patient sits and forward flexes both arm 90° (Fig. 3-35). The eyes are then closed. The ex iner watches for any loss of arm position. If the a move, the cause is nonvascular. The patient is t

In supine position: 1. Sustained full neck and head extension 2. Sustained full neck and head rotation left and right 3. Sustained full neck and head rotation with extension left and right (if combined with side flexion, it is called the Hallpike maneuver 16 ). Extension combined with rotation has been found to be the position most likely to occlude the vertebral artery.43 4. Unilateral posteroanterior oscillation (Maitland's grade IV) of C1- C2 facet joints (prone lying) with head rotated left and right 5. Simulated mobilization and manipulation position Each position should be held for at least 10 to 30 seconds unless symptoms are evoked. Ten seconds should elapse between each test to ensure that there are no latent symptoms. Extension in isolation is more likely to test the patency of the intervertebral foramen, whereas rotation and side flexion or, especially, rotation and extension are more likely to test the vertebral artery (Table 3 _10).52 If symptoms are evoked, care should be taken concerning any treatment to follow.

*provocative position implies movement into the position that provokes symptoms

Table 3-10 Relationship of Head Position to Blood Flow to Head Neurological Function Head Position

Blood Flow

Neurologica Space

Neutral

Normal

ormal

Flexion

Normal

Normal

Extension

Usually normal

Decreased

Side flexion

Slight decrease in ipsilateral artery Normal in contralateral artery

Decrease on ipsilateral sid Increase on contralateral

Rotation

Slight decrease in ipsilateral artery Significant decrease in contralateral artery


Extension and rotation

Bilateral decrease, greater in contralateral artery

Bilateral decrea greater on ipsilateral sid

Flexion and rotation

Bilateral decrease



155

Ie 3-11 pinall's Progressive Clinical Tests for Vertebral Artery Pathology Position Vertebral Artery Area -.rea 1 (lower cervical spine) ea 2 (middle cervical spine)

Sitting Lying

x X X X X X

X X X

Active cervical rotation

X X

X X X X

X ~...rea

3 (upper cervical spine)

Test

X X

x

X X

x

X X

X X

X

X

x

Active cervical rotation Passive cervical rotation Active cervical extension Passive cervical extension Passive cervical extension with rotation Passive segmental extension with rotation Passive cervical flexion Cervical flexion with traction Accessory oscillatory anterior/posterior movement-transverse processes C2-C7 in combined extension and rotation Sustained manipulation position Active cervical rotation Passive cervical rotation Active cervical extension Passive cervical extension Passive cervical rotation with extension Cervical rotation with extension and traction Cervical rotation with flexion Accessory oscillatory anterior/posterior movement-transverse processes Cl-C2 in combined rotation and extension Sustained manipulation position

m Aspinall, W.: Clinical testing for the craniovertebral hypermobility syndrome. J. Orthop. Sports Phys. Ther. 12:180-181,1989.

~igure

3-35

Positioning for Hautant's test. (A) Forward flexion of both arms to 90°. (B) Rotation and extension of neck with arms forward flexed to 90°.

(Naffziger recommended 10 minutes!) and then the patient to cough. Pain may indicate a nerve problem or space-occupying lesion (e.g., tumor lightheadedness or similar symptoms occur with c pression of the jugular veins, the test should be te nated.

Tests for Vertigo and Dizziness

Temperature (Caloric) Test. The examiner a nately applies hot and cold test tubes several times behind the patient's ears on the side of the head; side is done in turn. A positive test is associated the inducement of vertigo, which indicates inner problems.

Figure 3-36 Naffziger's test (compression of jugular veins).

asked to rotate, or extend and rotate the neck and while holding this position, the eyes are again closed. If wavering of the arms occurs, the dysfunction is caused by vascular impairment to the brain. Each position should be held for 10 to 30 seconds. Barre's Test. 50 The patient stands with the shoulders forward flexed to 90°, elbows straight and forearms supinated, palms up ·and eyes closed, holding the position for 10 to 20 seconds. The test is considered positive if one arm slowly falls with simultaneous forearm pronation. The cause is thought to be diminished blood flow to the brain stem. This test is identical to the first part of Hautant's test. Underburg's Test.l 6 The patient stands with the shoulders forward flexed to 90°, elbows straight and forearms supinated. The patient then closes the eyes and marches in place while holding the extended and rotated head to one side. The test is repeated with head movement to the opposite side. The test is considered positive if there is dropping of the arms, loss of balance, or pronation of the hands; a positive result indicates decreased blood supply to the brain.

Naffziger's Test. 16,56 The patient is seated and the examiner stands behind the patient with his or her

-'-'-'

.-

Dizziness Test. The patient sits and the exam grasps the patient's head. The examiner actively ro the patient's head as far as possible to the right then to the left, holding the head at the extrem motion for a short time (10 to 30 seconds) while shoulders remain stationary. The patient's head is returned to neutral. Next, the patient's shoulders actively rotated as far to the right as possible, held 10 to 30 seconds, and then to the left as far as p ble, and held for 10 to 30 seconds while keeping head facing straight ahead. If the patient experie dizziness in both cases, the problem lies in the v bral arteries, because in both cases the vertebral a may be "kinked," decreasing the blood flow. If patient experiences dizziness only when the hea rotated, the problem lies within the semicircular ca of the inner ear. Fitz-Ritson 57 advocates a modi1ication of this For the first part of the test, he advocates that examiner hold the shoulders still while the patient idly rotates the head left and right with the closed. If vertigo results, the problem is in the vest lar nuclei or muscles and joints of the cervical spine addition, patients may lose their balance, veer to side, or possibly vomit. The second stage is the s as previously mentioned, except that the eyes closed. If vertigo is experienced this time, Fitz-Ri believes that the problem is in the cervical spine cause the vestibular apparatus is not being moved.

Tests for Cervical Instability

Sharp-Purser Test. This test should be perfor with extreme caution. It is a test to determine lm,:ation of the atlas on the axis (Fig. 3-37). If transverse ligament that maintains the position of odontoid process relative to Cl (Fig. 3-38) is to

.•

--_


157

Cervical Spine Clearing Tests* • Vertebral artery tests • Sharp-Purser test • Pettman's distraction test • Anterior shear test • Transverse ligament stress test • Lateral shear test • Lateral flexion alar ligament stress test • Rotational alar ligament stress test 'These tests should be performed if the examiner anticipates doing mobilization or manipulation techniques to the cervical spine

Normal relationship of C1 and C2

C1 slides forward on flexion

Figure 3-38 Forward translation of CIon C2 on flexion as a result of torn transverse ligament.

"I will translate forward (sublux) on C2 on flexion. -:nus, the examiner may find the patient reticent to do -orward flexion if the transverse ligament is damaged. ille examiner places one hand over the patient's foreead while the thumb of the other hand is placed over - e spinous process of the axis to stabilize it (Fig. 3:9). The patient is asked to slowly flex the head; while - 's is occurring, the examiner presses backward with - e palm. A positive test is indicated if the examiner -eels the head slide backward during the movement. -:ne slide backward indicates that the subluxation of - e atlas has been reduced, and the slide may be ac.:ompanied by a "clunk."

Figure 3-39 The Sharp-Purser test for subluxation of the atlas on the axis.

Figure 3-37 Subluxation of the atlas on neck flexion. Note the bulge in the posterior neck caused by the forward subluxation of the atlas, bringing the spinous process of the a.xis into prominence beneath the skin (arroJV). (Courtesy of Harold S. Robinson, M.D., Vancouver, British Columbia.)

Aspinall 58 advocates use of an additional test if the Sharp-Purser test is negative. The patient is placed in supine. The examiner stabilizes the occiput on the atlas in flexion and holds the occiput in this flexed position. The examiner then applies an anteriorly directed force to the posterior aspect of the atlas (Fig. 3-40). Normally, no movement or symptoms are perceived by the patient. For the test to be positive, the patient should feel a lump in the throat as the atlas moves toward the esophagus; this is indicative of hypermobility at the atlantoaxial articulation.

orly directed force through the posterior arch of C the spinous processes of C2 to T1 or bilate through the lan1ina of each vertebral body. In case, the normal end feel is tissue stretch with abrupt stop (Fig. 3-42). Positive signs especially w the upper cervical spine is tested include nystagm pupil changes, dizziness, soft end feel, nausea, facia lip paresthesia, and a lump sensation in the throat. i

Figure 3-40 Aspinall's transverse ligament test.

Pettman's Distraction Test. 59 This test is used to test the tectorial membrane. The patient lies supine with the head in neutral. The examiner applies gentle traction to the head. Provided no symptoms are produced, the patient's head is lifted forward, flexing the spine and traction is reapplied. If the patient complains of symptoms such as pain, or paresthesia in the second position, then the test is considered positive for a lax tectorial membrane (Fig. 3-41). Anterior Shear or Sagittal Stress Test. is ,59 This test is designed to test the integrity of the supporting ligamentous and capsular tissues of the cervical spine. It is similar to tl1e PACVP testing in the joint play section. The patient lies supine with the head in neutral resting on the bed. The examiner applies an antell-

Transverse Ligament Stress Test. 55 ,59 The pat lies supine with the exan1iner supporting the occ witl1 the palms and the third, fourth, and fifth fing The examiner places the index fingers in the s between the patient's occiput and C2 spinous pro so that the fingertips are overlying the neural arc Cl. The head and C1 are then carefully lifted an orly together, allowing no flexion or extension ( 3-43). This anterior shear is normally resisted by transverse ligament (Fig. 3-44). The position is for 10 to 20 seconds to see whether symptoms oc indicating a positive test. Positive symptoms inc soft end feel, muscle spasm, dizziness, nausea, pa thesia of the lip, face, or limb, nystagmus, or a l sensation in the throat. The test indicates hypermo ity at the atlantoaxial articulation.

Lateral Shear Test. 55 ,59 This test is used to de mine instability of the atlantoaxial articulation ca by odontoid dysplasia. The patient lies supine with head supported. The examiner places the radial sid the second metacarpophalangeal (MCP) joint of hand against the transverse process of the atlas and MCP joint of the other hand against the oppo transverse process of the axis. The examiner's ha are then carefully pushed together, causing a shea one bone on the other (Fig. 3-45). Normally, rn

B Figure 3-41 Pettman's distraction test. (A) First position. (B) Second (flexed) position.

CHAPTE R 3 • Cervical Spine

Figure TestIng . 3-43 the transverse ligament of Cl. Exanun . er's hands suppor head and Cl.

"11,"I"f'OOI~~ ~~ f dens Anterior arch Superior Foramen or

_

.

G"'o,",loe

-

Transverse I·Iga ment li(vr:rtebral artery) nsverse foramen ,.~ _ sverse process "--""'r Tran

@~ ~~7;cV::me, 10'

vertebral artery Posterior arch Posterior tubercle

~

spinal cord

Dens of atlas Superior articular facet Inferior articular process Lamina Spinous process

'~"

Spinal cord

"~Jc(r '\ \ (~)

t,'-'

0' 'ploo

Figure 3-44 Relations hi p 0 fCI to C2 and the position 0 f the transver e

"_,m

'--

~ '-B

Figure 3-45. lateral shear test. (B) Metacarpop halangeal J0111 (A) AtlantoaxIal .. ts agai transver e processes.

Figure 3-46 Alar ligament stress test. Examiner attempts ro side flex the patient's head while stabilizing the axis.

mal motion and no symptoms (cord or vascular) are produced. As this test is normally painful because of the compression of soft tissues against the bone, the patient should be warned beforehand that pain is a normal sensation to be expected. Lateral Flexion Alar Ligament Stress Test. 33 ,55,59 The patient lies supine with the head in the physiological neutral position while the examiner stabilizes the axis with a wide pinch grip around the spinous process and lamina (Fig. 3-46). The examiner then attempts to side flex the head and axis. Normally, if the ligament is intact, minimal side flexion occurs, with a strong capsular end feel. Rotational Alar Ligament Stress Test. 59 The patient is positioned in sitting. The examiner grips the lamina and spinous process of C2 between the finger and thumb. While stabilizing C2, the examiner passively rotates the patient's head left or right moving to the "no symptom" side first. If more than 20 0 to 30 0 rotation is possible without C2 moving, it is indicative of injury to the contralateral alar ligament especially if the lateral flexion alar stress test is positive in the same direction. If the excessive motion is in the opposite direction for both tests, the instability is due to an increase in the neutral zone in the joint (Fig. 3-47).

Tests for First Rib Mobility Although the first rib would normally be included with assessment of the thoracic spine, the examiner should always test for mobility of the first rib when examining the cervical spine, especially if side flexion is limited and there is pain or tenderness in the area of the first rib or Tl.

._.-

Figure 3-47

Rotational alar ligament stress test. While the examiner grips th lamina of C2, the patient's head is rotated left and right with t other hand.

For the first test, the patient lies supine while supported. The examiner palpates the first rib bi ally lateral to Tl and places his or her fingers the path of the patient's ribs just posterior to clavicles (Fig. 3-48). While palpating the ribs, th aminer notes the movement of both first ribs a patient takes a deep breath in and out, and any a metry is noted. The examiner then palpates one rib and side flexes the head to the opposite side the rib is felt to move up. The range of neck flexion is noted. The side flexion is then repeat the opposite side, and results from the two side compared. Asymmetry may be caused by hypomo of the first rib or tightness of the scalene muscle the same side. For the second test, the patien prone, and the examiner again palpates the firs (Fig. 3-49). Using the thumb, reinforced by the thumb, the examiner pushes the rib caudally, n the amount of movement, end feel, and presen pain. The other first rib is tested in a similar fas and the two sides are compared. Normally, a firm

---.


Figure 3-48 ~esting

mobility of the first rib (anterior aspect).

sue stretch is felt with no pain, except possibly where me examiner's thumbs are compressing soft tissue gainst the rib.

Tests for Thoracic Outlet Syndrome -ee Special Tests in Chapter 5.

eflexes and Cutaneous Distribution - the examiner suspects neurological involvement durrng the assessment, reflex testing and cutaneous sensa·on should be tested. For the cervical spine, the folowing reflexes should be checked for differences etween the two sides, as shown in Figure 3-50: bi-eps (C5-C6), the brachioradialis (C5-C6), the tri-eps (C7-C8), and the jaw jerk (cranial nerve V). The reflexes are tested with a reflex hammer. The examiner ests the biceps and jaw jerk reflexes by placing his or her thumb over the patient's biceps tendon or at midpoint of the chin and then tapping the thumbnail with the reflex hammer to elicit the reflex. The jaw reflex may also be tested with a tongue depressor (see Fig. 3-50B). The examiner holds the tongue depressor

,

Common Reflexes Checked in Cervical Spine Assessment • Biceps (C5, C6) • Triceps (C7, C8) • Hoffmann's sign (if upper motor neuron lesion suspected)

Figure 3-49 Testing mobility of the first rib (posterior aspect).

firmly against the lower teeth while the patien the jaw and then strikes the tongue depressor reflex hammer. The brachioradialis and t:1iceps are tested by directly tapping the tendon or mu If an upper motor neuron lesion is suspec pathological reflexes (for example, Babinski's should be checked (see Table 1-26). Hoff sign is the upper limb equivalent of the Babin To test for Hoffmann's sign, the examiner h patient's middlefinger and briskly flicks the dis lanx. A positive sign is noted if the interph joint of the thumb of the same hand flexes. and Meadows 60 advocated a dynamic Hoffman The patient is asked to repeatedly flex and ex head, and then the test is performed as descri viously. Denno and Meadows believed that namic test shows positive results earlier than t or normal Hoffmann's sign. Because an uppe neuron lesion affects both the upper and low initially unilaterally and at later stages bilatera binski's test may be performed if desired. Clonu easily seen by sudden dorsiflexion of the ankl ing in four or five reflex twitches of the plantar is also a sign of an upper motor neuron lesion. 6 The examiner then checks the dermatome of the various nerve roots as well as the sens tribution of the peripheral nerves (Figs. 3-51 52). Dermatomes vary from person to pers overlap a great deal, and the diagrams shown mations only. For example, C5 dermatome m

Figure 3-50

Testing of upper limb reflexes. (A Jaw. (B) Jaw (tongue depressor method). (C) Bracruoradialis. (D Biceps. (E) Triceps.

Figure 3-51

Sensory nerye distribution of the head, neck, and face. (1) Ophth mic nerve. (2) Maxillary nerve. (3) Mandibular nerve. (4) TraIlS\'e cutaneous nerve of neck (C2-C3). (5) Greater auricular nerve (C C3). (6) Lesser auricular nerve (C2). (7) Greater occipital nerve (C2-C3). (8) Cervical dorsal rami (C3-C5). (9) Suprascapular ne (C5-C6).


~'gure

3-52

ermatomes of the cervical spine.

C7

T1

distally on the radial side of the arm at the elbow, forearm, or wrist. Cervical radiculopathies may also show modified patterns. Levine et al 12 point out that about 45% of patients have modified patterns and do not follow strict dermatome patterns. Classically, these patients also have referred pain into the trapezius and periscapular area posteriorly and some will have pain into the breast area anteriorly. The examiner tests sensation by doing a sensory scanning examination. This is accomplished by running relaxed hands over the patient's head (sides and back); down over the shoulders, upper chest, and back; and down the arms, being

sure to cover all aspects of the arm. If any differe noted between the sides in this "sensation scan examiner may then use a pinwheel, pin, cotton b or brush, or a combination of these, to map o exact area of sensory difference. Because of the spinal cord and associated nerve and their relation to the other bony and soft tiss the cervical spine, referred pain is a relatively co experience in lesions of the cervical spine. With cervical spine, the intervertebral discs, facet joint other bony and soft tissues may refer pain to segments of the neck (dermatomes) or to the

the shoulder, the scapular area, and the whole of upper limb (Figs. 3-53 and 3-54).10,20 Table 3shows the muscles of the cervical spine and their re ral afpain.

Brachial Plexus Injuries of the Cervical Spine

Erb-Duchenne Paralysis. This paralysis is an up brachial plexus injury involving injury to the up nerve roots (C5, C6) as a result of compression stretching. The injmy frequently occurs at Erb's po With this injury, it is primarily the muscles of shoulder region and elbow that are affected; the m cles of the hand (especially the intrinsic muscles) not involved. However, sensation over the radial s faces of the forearm and hand and the deltoid area affected.

Figure 3-53 Referral of symptoms from the cervical spine to areas of the spine, head, shoulder girdle, and upper limb.

Klumpke (Dejerine-Klumpke) Paralysis. This jury involves the lower brachial pleA'US and results fr compression or stretching of the lower nerve ro (C8, T1). AU'ophy and weakness are evident in muscles of the forearm and hand as well as in triceps. The obvious changes are in the distal aspe of the upper limb. The resultant injury is a functionl hand. Sensory loss occurs prirn;uily on the ulnar s of the forearm and hand.

Brachial Plexus Birth Palsy.62 These injuries to brachial plexus occur in 0.1% to 0.4% of births w the majority showing full recovery "vithin 2 mont Those infants who have not recovered within months are at considerable risk to decreased stren and range of motion in the upper limb .

............... _._._._._~

------+

•

Semispinalis Levator scapulae Splenius muscles Trapezius

Figure 3-54

Muscles and their referred pain patterns. Diagram shows primarily one side.

-----

--

Sternocleidomastoid

Suboccipital


able 3-12 uscles of the Cervical Spine and Their Referral of Pain Muscle -:-rapezius

ernocleidomastoid

Referral Pattern

Back and top of head, front of ear over forehead to medial aspect of eye; cheek Behind ear, ear to forehead

• Posteroanterior unilateral vertebral pressure (specific)

lenius cervicis

Posterior neck and shoulder angle, side of head to eye

mispinalis cervicis

Back of head

mispinalis capitis

Band around head at level of forehead

boccipital -alenes

• Side glide of the cervical spine (general) • Anterior glide of the cervical spine (general)

Top of head

lultifidus

Joint Play Movements of the Cervical Spine

Right and left occiput, lateral aspect of head above ear to behind eye, tip of jaw SpinOLlS processes to medial border of scapula and along spine of scapula; may also refer to lateral aspect of Llpper arm

!enius capitis

Occiput to posterior neck and shoulder angle to base of spine of scapula Lateral aspect of head to eye Medial border of scapula and anterior chest down posterolateral aspect of arm to anterolateral and posterolateral aspect of hand

• Posterior glide of the cervical spine (general) • Traction glide of the cervical spine (general) • Rotation of the occiput on C1 (specific) • Posteroanterior central vertebral pressure (specific) • Transverse vertebral pressure (specific)

Anterior and Posterior Glide. The examiner holds the patient's head with one hand around the occiput and one hand around the chin, taking care to ensure that the patient is not choked. 28 The examiner then draws the head forward for anterior glide (Fig. 3-56) and posteriorly for posterior glide. While doing these movements, the exanliner must prevent flexion and extension of the head.

Traction Glide. The examiner places one hand around the patient's chin and the other hand on the occiput. 29 Traction is then applied in a straight longitudinal direction, with the majority of the pull being through the occiput (Fig. 3-57).

..

Burners and Stingers. 63,64 These are transient injues to the brachial plexus, which may be the result of auma (see Figure 3-9) combined with factors such stenosis or a degenerative disc (spondylosis). Recurrent burners are not associated with more severe neck njUlY but their effect on the nerve may be cumulative. 63

Joint Play Movements The joint play movements that are carried out in the -ervical spine may be general movements (called pasive intervertebral movements or PIVMs) that involve the entire cervical spine (first four below) or specific !11ovements isolated to one segment. As the joint play movements are performed, the exanuner should note any decreased ROM, pain, or difference in end feel. Side Glide. The exanliner holds the patient's head and moves it from side to side, keeping it in the same plane as the shoulder (Fig. 3-55).65

165

1

Figure 3-55 Side glide of the cervical spine. Glide

to

the right is illustrated.

Figure 3-56 Anterior glide of the cervical spine.

Rotation of the Occiput on Cl. The examiner holds the patient's head in position and palpates the transverse processes of Cl (Fig. 3-58). The examiner must first find the mastoid process on each side and then move the fingers inferiorly and anteriorly until a hard bump (i.e., the transverse process of Cl) is palpated on each side. Palpation in the area of the Cl transverse process is generally painful, so care must be taken. The examiner then rotates the patient's head while palpating the u·ansverse processes; the transverse process on the side to which the head is rotated will seem to disappear in the normal case. If this disappearance does not occur, there is restriction of movement between CO and CIon that side. Vertebral Pressures. For the last three joint play movements (Fig. 3-59), the patient lies prone with the forehead resting on the back of the hands. 49 These techniques are specific to each vertebra and are applied to each vertebra in turn or at least to the ones that the examination has indicated may be affected by pathology. They are sometimes called passive accessory intervertebral movements or PANMs.26 The examiner palpates the spinous processes of the cervical spine, starting at the C2 spinous process and working downward to the T2 spinous process. The positions of the

Figure 3-57 Traction glide of the cervical spine.

-

( ~

)

(l.»

Figure 3-58

Left rotation of the occiput on Cl. Note the index finger palpating the right transverse process of Cl.

examiner's hands, fingers, and thumbs in performin posteroanterior central vertebral pressures (PACVP are shown in Figure 3-59A. Pressure is then applie through the examiner's thumbs pushing carefully from the shoulders, and the vertebra is pushed forward. Th examiner must take care to apply pressure slowly, wit carefully controlled movements, so as to "feel" th movement, which in reality is minimal. This "springin test" may be repeated several times to determine th quality of the movement and the end feel. For posteroanterior unilateral vertebral pressur (PAUVP) , the examiner's fingers move laterally awa from the tip of d1e spinous process so that d1e thumb rest on the lamina or transverse process, about 2 to em (1 to 1.5 inches) lateral to the spinous process o the cervical or thoracic vertebra (see Fig. 3-59B). An terior springing pressure is applied as in the centra pressure technique. This pressure causes a minimal ro tation of the vertebral body. If one was to palpate th spinous process while doing the technique, the spinou process would be felt to move to the side the pressur is applied. Both sides should be done and compared. For transverse vertebral pressure (TVP), the exam iner's thumbs are placed along the side of the spinou process of the cervical or thoracic spine (see Fig. 3 59C). The examiner then applies a transverse springin pressure to the side of the spinous process, feeling fo the quality of movement. This pressure also cause rotation of the vertebral body.

~----.


1

Figure 3-59 Vertebral pressures ro the cervical pine. (A) Posteroanterior central \'ertebral pressure on tip of spinous process. (B) Posteroanterior unilateral vertebral pressure on posterior aspect of trans\'erse process. (C) Transver e \'ertebral pressure on side of spinous process.

Palpation .t: after completing the examination of the cervical pine, the examiner decides the problem is in another oint, palpation should be delayed until that joint is -ompletely examined. However, during palpation of the cervical spine, the examiner should note any tenderness, trigger points, mu cle spasm, or other signs and symptoms that may indicate the source of the athology. As with any palpation, the examiner should note the texture of the skin and surrounding bony and oft tissues on the posterior, lateral, and anterior a pects of the neck. Usually, palpation is performed with the patient supine so that maximum relaxation of the neck muscles is possible. However, the examiner may palpate with the patient sitting (patient resting the head on forearms that are resting on something at shoulder height) or lying prone (on a table with a face hole) if it is more comfortable for the patient.

To palpate the posterior structures, the examin stands at the patient's head behind the patient. Wi the patient in supine lying, the patient's head 'cupped" in the examiner' hand while the examin palpates with the finger of both hands. For the later and anterior structures, the examiner stands at the p tient's side. If the examiner suspects that the proble i in the cervical spine, palpation is done on the fo lowing structures (Fig. 3-60).

Posterior Aspect

External Occipital Protuberance. The protube ance may be found in the posterior midline. The e aminer palpates the posterior skull in midline an moves caudally until coming to a point where the fi gers "dip" inward. The part of the bone just befo the dip is the external occipital protuberance. The i

Mastoid Processes (Below and Behind Ear Lo If the examiner palpates the skull following the p rior aspect of the ear, there will be a point on the at which the finger again dips inward. The point before the dip is the mastoid process.

Mandible - - - - C1 transverse

Lateral Aspect >:--\,.---Spmous process

Figure 3-60 Palpation landmarks of the cervical spine.

ion, or "bump of knowledge," is the most obvious point on the external occipital protuberance and lies in the midline of the occiput. Spinous Processes and Facet Joints of Cervical Vertebrae. The spinous processes of C2, C6, and C7 are the most obvious. If the examiner palpates the occiput of the skull and descends in the midline, the C2 spinous process will be palpated as the first bump. The next spinous processes that are most obvious are C6 and C7, although C3, C4, and C5 can be differentiated with careful palpation. The examiner can differentiate between C6 and C7 by passively flexing and extending the patient's neck. With this movement, the C6 spinous process moves in and out and the C7 spinous process remains stationary. The movements between the spinous processes of C2 through C7 or Tl may be palpated by feeling between each set of spinous processes. While palpating between the spinous processes, the examiner can use the opposite hand or his/her chest to push the head into nodding flexion and releasing, causing the cervical spine to flex and extend and the palpating finger will feel the movement between the two spinous processes and tension (when flexing) in the interspinous and supraspinous ligaments. Relative movement between the cervical vertebrae can then be determined (i.e., hypomobility, normal movement, or hypermobility).28 The facet joint may be palpated 1.3 to 2.5 cm (0.5 to I inch) lateral to the spinous process. Usually the facet joints are not felt as distinct structures but rather as a hard bony mass under the fingers. The muscles in the adjacent area may be palpated for tenderness, swelling, and other signs of pathology. Careful palpation should also include the suboccipital structures.

Transverse Processes of Cervical Vertebrae. CI transverse process is the easiest to palpate. examiner first palpates the mastoid process and moves inferiorly and slightly anteriorly until a bump is felt. If the examiner applies slight pressu the bump, the patient should say it feels uncom able. These bumps are the transverse processes o If the examiner rotates the patient's head while pa ing the transverse processes of CI, the upper transverse process will protrude farther and the l one ,vill seem to disappear. The other transverse cesses may be palpated if the musculature is suffic relaxed. After the CI transverse process has bee cated, the examiner moves caudily, feeling for si bumps. Normally, the bumps are not directly in but rather follow the lordotic path of the cervical tebrae under the sternocleidomastoid muscle. T structures are situated more anteriorly than one m suspect (see Fig. 3-60). During flexion, the spac tween the mastoid and the transverse processe creases. On extension, it decreases. On side flexion mastoid and transverse processes approach one an on the side to which the head is side flexed and rate on the other side. 28

Lymph Nodes and Carotid Arteries. The ly nodes are palpable only if they are swollen. The n lie along the line of the sternocleidomastoid mu The carotid pulse may be palpated in the midpo of the neck, between the sternocleidomastoid m and the trachea. The examiner should determ whether the pulse is normal and equal on both sid

Temporomandibular Joints, Mandible, and rotid Glands. The temporomandibular joints ma palpated anterior to the external ear. The exam may either palpate directly over the joint or place little or index finger (pulp forward) in the externa to feel for movement in the joint. The examiner then move the fingers along the length of the ma ble, feeling for any abnormalities. The angle of mandible is at the level of the C2 vertebra. Norm the parotid gland is not palpable because it lies the angle of the mandible. If it is swollen, howev is palpable as a soft, boggy structure.


nterior Aspect Hyoid Bone, Thyroid Cartilage, and First Criid Ring. The hyoid bone may be palpated as part of uperior part of the trachea above the thyroid carage anterior to the C2-C3 vertebrae. The thyroid ~age lies anterior to the C4-CS vertebrae. With e neck in a neutral position, the thyroid cartilage can . y be moved. In extension, it is tight and crepitan may be felt. Adjacent to the cartilage is the thyId gland, which the examiner should palpate. If the _ .md is abnormal, it will be tender and enlarged. The ncoid ring is the first part of the trachea and lies ove the site for an emergency tracheostomy. The g moves when the patient swallows. Rough palpan of the ring may cause the patient to gag. While pating the hyoid bone, the examiner should ask the

patient to swallow; normally, the bone should and cause no pain. The cricoid ring and thyroi lage also move when palpated as the patient swa

Paranasal Sinuses. Returning to the face, the iner should palpate the paranasal sinuses (fron maxillary) for signs of tenderness and swellin 3-61).

First Three Ribs. The examiner palpates the brium sternum and, moving the fingers lateral lows the path of the first three ribs posteriorly whether one rib is protruded more than the The examiner should palpate the ribs individua with care, because it is difficult to palpate the they pass under the clavicle. The patient sho asked to breathe in and out deeply a few times the examiner can compare the movements of t during breathing. Normally, there is equal mob both sides. The first rib is more prone to pa than the second and third ribs and can refer the neck and/or shoulder.

Supraclavicular Fossa. The examiner can the supraclavicular fossa, which is superior to th cle. ormally, the fossa is a smooth indentatio examiner should palpate for swelling after traum sible fractured clavicle), abnormal soft tissue (p swollen glands), and abnormal bony tissue (p cervical rib). In addition, the examiner should the sternocleidomastoid muscle along its leng signs of pathology, especially in cases of torticoll

Diagnostic Imaging

Imaging techniques should primarily be perfor an adjunct to the clinical exam. The appeara many degenerative change or anatomical or con variations is relatively high in the cervical spi many of the changes have no relationship w patient's complaints. 66 ~P,r--

Frontal sinus

"'7'--t.::f--- Maxillary sinus

B Figure 3-61 Paranasal sinuses. Radiograph (A) and illustration (B) of frontal and ma.xillary sinuses.

Plain Film Radiography

Jormally, a standard et of x-rays for the cervica is made up of an anteroposterior view, a latera and an open or odontoid ("through-the-m view. Other views are included if other patholog suspected.

Anteroposterior View. The examiner shoul for or note the following (Figs. 3-62 and 3-63 shape of the vertebrae, the presence of any wedging or osteophytes, the disc space, and th ence of a cervical rib. Frontal alignmeat should ascertained.

Ce

Uncus

Figure 3-62 Anteroposterior films of the cervical spine. (A) Normal spine. (B) Cervical rib.

Lateral View. Lateral views of the cervical spine give the greatest amount of radiological information. The examiner should look for or note the following (Figs. 3-64, 3-65, and 3-66). 1. Normal or abnormal curvature. The curvature may be higWy variable, because 20% to 40% of

normal spines have a straight or slightl photic curve in neutral. 67 Are the "lines" o vertebrae normal? The line joining the an portion of the vertebral bodies (anterior bral line) should form a smooth, unbroke from C2 to C7 (see Fig. 3-65). Similar should be seen for tl1e posterior vertebral b

.--,~----

Condyle of mandible

Ir-----\-+--+~----Nasalseptum Atlanta-occipital joint

----~?tf3~~:1=~;~~i;e9rb.lf:~----------_-_ -~ Mastoid process Occipital condyle

Atlantoaxial joint ------w:"-':-~~-..... ~~F:SJ.2tt:....-.....---_Atlas

....-------Angle of mandible Odontoid

process-----~

Facet joint--------'--'-:"-ItUncinate

process-----~

A~~""""'"

::\.......-;~e~~=tt_:_~--------Uncovertebral joint

space

Spinous process-------~~~~~~kfifF~C:

::~i::]:::=\¥::;±~i::lP~7~------Laryngeal cartilage ~~p~~~~>-:-:-------Transverse process

Transverse process.

Dl-----~~t;;~~~H.,_h~~

~,------

Left first rib

'(:~~,J--"./I~~:...-g;~..,.~.__--- Trachea

Pedicle of vertebrai--~~b._f""C'~~~:""""T__=_1' arch

" - - - - - - Left second rib

Figure 3-63 Diagram of structures seen on anteroposterior cervical spine film.

----.


Figure 3-64 Lateral radiograph of the cervical spine. (A) Normal curve showing osteophytic lipping. (B) Cervical spine in flexion. (C) Cervical spine in extension.

B

(posterior vertebral line), which form the anterior aspect of the spinal canal, and the posterior aspect of the spinal canal (posterior canal line). Disruption of any of these lines would be an indication of instability possibly caused by ligamentous injury. 2. "Kinking" of the cervical spine. Kinking may be indicative of a subluxation or dislocation in the cervical spine. 3. General shape of the vertebrae. Is there any fusion, collapse, or wedging? The examiner should

4. 5.

6. 7.

count the vertebrae, because x-ray films do always show C7 or Tl, and it is essential they be visualized for a proper radiological amination. Displacement. Do the vertebrae sit in nor alignment with one another? Disc space. Is it normal? Narrow? Narrow may indicate cervical spondylosis. Lipping at the vertebral edges (see Fig. 3-64 Lipping indicates degeneration. Osteophytes (see Fig. 3-64A). Osteophytes

8.

9.

10. 11. 12. Figure 3-65 Normal cervical spine. Lateral projection. Note the alignment and appearance of the facet joints: A, anterior vertebral line; B, posterior vertebral line; C, posterior canal line. Retropharyngeal space (betJVeen top arrolVs) should not exceed 5 mm. Retrotracheal space (betlVeen bottom arrolVs) should not exceed 22 mm. (Modified from Forrester, D.M., and I.e. Brown: The Radiology of Joint Disease. Philadelphia: W.B. Saunders Co., 1987, p. 408.)

13.

dicate degeneration or abnormal movement stability). Normally, the ratio of the spinal canal diam to the vertebral body diameter (Torg ratio the cervical spine is 1. If this ratio is less 0.8, it is an indication of possible cervical st SiS. 13 ,68-71 This comparison is shown in Fi 3-65 (ratio AB:BC). Cantu69 points out this measurement is a static measurement may not apply to stenosis that occurs du movement of the cervical spine. Prevertebral soft-tissue width. Measured at level of the anteroinferior border of the C3 tebra, this width is normally 7 mm.7 2 Edem hemorrhage is suspected if the space is w than 7 mm. The retropharyngeal space, l between the anterior border of the verte body and the posterior border of the pharyn air shadow, should be from 2 to 5 mm in w at C3. From C4 to C7, the space is called retrotracheal space and should be 18 to 22 in width (see Fig. 3-65). Subluxation of the facets. Abnormal soft-tissue shadows. Forward shifting of CIon C2. This finding dicates instability between Cl and C2. N mally, the joint space between the odon process and the anterior arch of the atlas (so times called the atlas-dens index [ADI]) not exceed 2.5 to 3 mm in the adult. Instability. Instability is present when more 3.5 mm of horizontal displacement of one tebra occurs in relation to the adjacent verte

Odontoid process

Atlanto-occipital joint

Facet joint

-~~:'"'-7-~-~

V""'""-'I:""7.-''-7----,....---:-'-:"':-:-:-'--'-=__ Atlantoaxial joint

---p,:'---.,--y'S~~/

Articular process ---I-*-~"""':'-+'" Spinous process

Figure 3-66 Diagram of stmctmes seen on lateral film of the cervical spine.


L-

Occipital condyle

L-

Atlanta-occipital joint

173

' - - - - - Odontoid process

Joint space btwn C1-G2 ' - - - - - C2 superior articular proces

1----

gure 3-67 Jugh-the-mouth radiograph.

1----

Open or Odontoid ("Through-the-Mouth") "iew. This anteroposterior view enables the examiner determine the state of the odontoid process of C2 d its relation with Cl (Fig. 3-67). It may also show e atlanto-occipital and atlantoaxial joints. Oblique View. This view provides information on • e neural foramen and po tenor elements of the cervi-

Spinous process of C2

cal spine. The examiner should look for or note th follmving (Figs. 3-68 and 3-69):

1. Lipping of the joints of Luschka (osteophytes) 2. Overriding of the facet joints (subluxation, spon dylosis) 3. Facet joints and intervertebral foramen (see Fig 3-69)

Figure 3-68 Abnormal x-ray findings on oblique view. Note loss of normal curve; narrowing at C4, C5, and C6; osteophytes and lipping of C4, C5, and C6; and encroachment on intervertebral foramen at C4-C5, C5-C6, and C6-C7.

Figure 3-69

Oblique radiograph of the cervical spine showing intervertebral foramen and facet joints. Severe lipping in lower cervical spine and spondylosis are also evident.

ANTEROPOSTERIOR VIEW

PILLAR VIEW

\ ,,

J

\ \

Figure 3-70 Diagram of pillar view showing orientation of facet joints.

Pillar View. This special view is used to evaluate the lateral masses of the cervical spine and especially the facet joints (Fig. 3-70). It is usually reserved for patients with suspected facet fractures. 73

Figure 3-72

Postcontrast computed tomogram showing normally patent neur foramen at the C6-C7 level on the left side (open arrow). The n root sleeve fills with contrast medium and enters the neural foram On the right side (closed arrow), there is no evidence of filling o nerve root sleeve within the neural foramen secondary to lateral C7 disc herniation. (From Bell, G.R., and J.S. Ross: Diagnosis o

nen'e root compre ion: Myelography, compured tomography, a MRI. Orthop. Clin. North Am. 23:410, 1992.)

Computed Tomography Computed tomography (CT) helps to delineate the bone and soft-tissue anatomy of the cervical spine in cross section and can show, for example, a disc pro-

lapse. It also shows the true size and extent of os phytes better than do plain x-rays (Fig. 3-71). scans are especially useful for showing bone fragm in the spinal canal after a fracture and bony defect the vertebral bodies and neural arches. CT scans be combined with myelography to outline the sp cord and nerve roots inside the thecal sac (Fig. 3 -7 CT scans are used only after conventional radiogra have been taken and a need for them is shown.

Myelography

Figure 3-71 Foraminal tenosis caused by hypertrophic facet arthropathy and by spondylosis. Metrizamide-enhanced computed tomography scan through C5-C6 foramina details the markedly overgrown facet (white arrow) and the bony "bar," or spondylotic spurring (black an·oll's). The right foramen is almost occluded by abnormal bone. (From Dorwart, R.H., and D.L. LaMasters: Application of computed tomographic scanning of the cervical spine. Orthop. Clin. orth Am. 16:386, 1985.)

Myelograms are the modality of choice \vith brac ple).'Us avulsions, either Erb-Duchenne paralysis and C6) or Klumpke's paralysis (C7, C8, and They may also be used to demonstrate narrowin the intervertebral foramen and cervical spinal sten They may be used to outline the contour of the th sac, nerve roots, and spinal cord (Fig. 3-73).

Magnetic Resonance Imaging

This noninvasive technique can differentiate betw various soft tissues and bone (Fig. 3 -74). Becau shows differences based on water content, mag


Figure 3-74

ure 3-73

Magnetic resonance image of the cervical and upper thoracic spine. Sagittal view (left), with close-up of cervical spine (right). (From Foreman, S.M., and A.C. Crofi:: Whiplash Injuries: The Cervical AccelerationjDeceleration yndrome. Baltimore: William & Wilkins Co. 1988, p. 126.)

dogram of cervical pine.

onance imaging (MRI) can differentiate between e nucleus pulposus and the annulus fibrosus. MRI .ly be used to reveal disc protrusions, but it has been ported that patients showing these lesions are often .·mptomatic, highlighting the fact that diagnostic imging abnormalities should be considered only in relaon to the history and clinical exarnination.74 An MRI ows visualization of the nerve roots, spinal cord, and ecal sac as well as the bone and bone marrow. It is o used to identifY postoperative scarring and disc erniation. 75 Magnetic resonance angiography is also eful for determining the patency and tatu of the ertebral artery.76-78

eroradiography This technique also helps to delineate bone and soft ti sue by enhancing the interfaces between tissues (Fig. 3-75).

Figure 3-75 Xeroradiograph of cervical spine (lateral \iew). Arrow indicates calcified mass. (From Forrester, D.M., and I.C. Brown: The Radiology of Joint Disease. Philadelphia: W.B. Saunders Co., 1987, p. 420.)

1

176


Precis of the Cervical Spine Assessment* History Observation (standing or sitting) Examination (sitting) Active movements Flexion Extension Side flexion (right and left) Rotation (right and left) Combined movements (if necessary) Repetitive movements (if necessary) Sustained positions (if necessary) Resisted isometric movements (as in active movements) Peripheral joint scan Temporomandibular joints (open mouth and closed mouth) Shoulder girdle (elevation through abduction, elevation through forward flexion, elevation through plane of scapula, medial and lateral rotation with arm at side; medial and lateral rotation at 90° abduction) Elbow (flexion, e>.'tension, supination, pronation) Wrist (flexion, extension, radial and ulnar deviation) Fingers and thumb (flexion, extension, abduction, adduction) Myotomes Neck flexion (Cl,C2) eck side flexion (C3) Shoulder elevation (C4) Shoulder abduction (C5) Elbow flexion (C6) and/or extension (C7) Wrist flexion (C7) and/or extension (C6) Thumb extension (C8) and/or ulnar deviation (C8) Hand intrinsics (abduction or adduction) (Tl) Special tests Foraminal compression (Spurling's) test Distraction test Shoulder abduction test Vertebral artery tests Reflexes and cutaneous distribution Biceps (C5-C6) Triceps (C7-C8) Hoffmann's sign (or Babinski's Test) Sensory scan Examination, supine Passive movements

Flexion Extension Side flexion Rotation Special tests Upper limb tension test Vertebral artery tests

NOTE 1: The following tests should be performed if the examiner anticipates treating the patient by mob tion or manipuiatio'i. In this case, they are called clearing tests for treatment

Vertebral artery tests (supine or sitting) Sharp-Purser test (sitting) Pettrnan's distraction test (supine) Anterior shear test (supine) Transverse ligan1ent stress test (supine) Lateral shear test (supine) Lateral flexion alar ligament stress test (supin

OTE 2: If any of the above tests are positive, mobiliz or manipulation should only be performed with e treme care and the level exhibiting the positive si should be stabilized during the treatment

Joint play movements Side glide of cervical spine Anterior glide of cervical spine Posterior glide of cervical spine Traction glide of cervical spine Rotation of occiput on Cl Palpation Examination, prone Joint play movements Posteroanterior central vertebral pressure Posteroanterior unilateral vertebral pressure Transverse vertebral pressure Palpation Diagnostic imaging

After any exan1ination, the patient should be warned o the possibiliry of exacerbation of symptoms as a result the assessment.

-The precis is shown in an order that limits the amount of moving that the patient has to do but ensures that all necessa structures are tested.

Case Studies T When doing these case studies, the examiner should list the appropriate questions to be asked and why they are being asked, what to look for and Why, and what things should be tested and why. Depending on the answers of the patient (and the examiner should consider different responses), several possible causes of the patient's problems may become evident (examples are given in parentheses). A differential diagnosis chart should be made up (see Table 3-13 as an example). The examiner can then decide how different diagnoses may affect the treatment plan.


177

Ie 3-13 1ferential Diagnosis of Cervical Facet Syndrome, Cervical Nerve Root Lesion, and Thoracic Outlet Syndrome Facet Syndrome

igns and Symptoms

Cervical Nerve Root

Thoracic Outlet Syndrome

Possible

Yes

Possible

on hyperextension and rotation

Yes (often without increased referral of symptoms)

Yes with increased symptoms

No

ille stiffuess

Yes

Possible

Possible

No

Yes

Possible

referral

esthesia exes

Not affected

May be affected

May be affected

de spasm

Yes

Yes

Yes

Mayor may not be positive

Positive

May be positive

No

No

Possible

Possible

Not early (later small hand muscles)

ion tests or and coolness de weakness •.lSc1e fatigue and cramps

0

0

1. A 2-month-old baby is brought to you by a concerned parent. The child does not move the head properly, and the sternocleidomastoid muscle on the left side is prominent. Describe your assessment plan before beginning treatment (congenital torticollis versus Klippel- Feil syndrome). 2. A 54-year-old man comes to you complaining of neck stiffuess, especially on rising; sometimes he has numbness into his left arm. Describe your assessment plan (cervical spondylosis versus subacromial bursitis). 3. An 18-year-old male football player comes to you complaining of a "dead arm" after a tackle he made 2 days ago. Although he can now move the left arm, it still does not feel right. Describe your assessment plan (brachial plexus lesion versus acromioclavicular sprain). 4. A 23-year-old woman comes to you after a motor vehicle accident. Her car was hit from behind while stopped for a red light. She could tell the accident was going to occur because she could see in the rearview mirror that the car behind her was not going to be able to stop. The car that hit her was going 50 kph (30 mph), and skid marks were visible for only 5 m from the location of her car. Describe your assessment plan (cervical sprain versus cervical facet syndrome). 5. A woman comes to you complaining of persistent headaches that last for days at a time. She is 35 years old and has recently lost her job. She complains that she sometimes sees flashing lights and cannot stand having anyone around her when the pain is very bad. Describe your assessment plan for this patient (migraine versus tension headache). 6. A 26-year-old man comes to you complaining of pain

Possible

0

7.

8.

9.

10.

in his neck. The pain was evident yesterday when he got up and has not decreased significantly since then. He thinks that he may have "slept wrong." There is no previous history of trauma. Describe your assessment plan for this patient (acquired torticollis versus cervical disc lesion). A 75-year-old woman comes to you complaining primarily of neck pain but also of stiffuess. She exhibits a dowager's hump. There is no history of trauma. Describe your assessment plan for this patient (osteoporosis versus cervical spondylosis). A 47-year-old man comes to you complaining of elbow and neck pain. There is no recent history of trauma, but he remembers being in a motor vehicle accident 19 years ago. He now works at a desk all day. Describe your assessment for this patient (cervical spondylosis versus tennis elbow versus double-crush injury). A 16-year-old boy comes to you with a complaint of having hurt his neck. While "fooling" with some ftiends at the lake, he ran away from tllem and dove into the water to get away. The top of his head hit the bottom, and he felt a burning pain. The pain decreased as he came out of the water, but he still has a residual ache. Describe your plan for this patient (cervical fracture versus cervical sprain). A 14-year-old girl comes to you complaining of neck pain. She has long hair. She states that when she "whipped" her hair out of her eyes, which she has done many times before, she felt a sudden pain in her neck. Although the pain intensity has decreased, it is still there, and she cannot fully move her neck. Describe your assessment plan for this patient (cervical sprain versus acquired torticollis).

REFERENCES Cited References 1. Cyria.x, J,: Textbook of Orthopaedic Medicine, vol. 1: Diagnosis of Soft TisSlle Lesions. London, Bailliere Tindall, 1982.

2. Bogduk, N.: The innervation of the lumbar spine. Spine 8:286293, 1983.

r

3. Boreades, AG., and Gershon-Cohen: Luschka joints of the cervical spine. Radiology 66:181-187,1956. 4. Hall, M.C.: Luschka's Joint. Springfield, Illinois, Charles C Thomas, 1965. 5. Silberstein, C.E.: The evolution of degenerative changes in the cervical spine and an investigation into the "joint of Luschka." Clin. Orthop. 40:184-204, 1965. 6. Willis, T.A.: Luschka's joints. Clin. Orthop. 46:121-125, 1966. 7. Ferlic, D.: The nerve supply of the cervical intervertebral disc in man. Johns Hopkins Hosp. Bull. 113:347,1963. 8. Mednel, T., C.S. Wink, and M.L. Zimny: eural elements in human cervical intervertebral discs. Spine 17:132-135, 1992. 9. Watkins, R.G.: Neck injuries in football. In Watkins, R.G. (ed.): The Spine in Sports. St. Louis, Mosby-Year Book Inc., 1996. 10. Travell, T.G., and D.G. Simons: Myofascial Pain and Dysfunction: The Trigger Point Manual, vol. 1. Baltimore, Williams & Wilkins, 1983. 11. Malanga, GA.: The diagnosis and treatment of cen~cal radiculopathy. Med. Sci. Sports Exer. 29:S236-S245, 1997. 12. Levine, M.J., T.r Albert, and M.D. Smith: Cervical radiculopathy diagnosis and nonoperative management. r Am. Acad. Orthop. Surg. 4:305-316, 1996. 13. Tsairis, P., and B. Jordan: Neurological evaluation of cervical spinal disorders. In Camins, M.B., and P.F. O'Leary (eds.): Disorders of the Cervical Spine. Baltimore, Williams & Wilkins, 1992. 14. Petty, N.J., and A.P. Moore: Neuromusculoskeletal Examination and Assessment-A Handbook for Therapists. London, Churchill Livingstone, 1998. 15. Foreman, S.M., and A.C. Croft: Whiplash Injuries: The Cervical Acceleration/Deceleration Syndrome. Baltimore, Williams & Wilkins, 1988. 16. Evans, R.C.: Illustrated Essentials in Orthopedic Physical Assessment. St. Louis, Mosby-Year Book Inc., 1994. 17. Bradley, rp., rE. Tibone, and R.G. Watkins: History, physical examination, and diagnostic tests for neck and upper extremity problems. In Watkins, R.G. (ed.): The Spine in Sports. St. Louis, Mosby-Year Book Inc., 1996. 18. Meadows, J.T.: Orthopedic Differential Diagnosis in Physical Therapy-A Case SUidy Approach. New York, McGraw-Hill, 1999. 19. Janda, V.: Muscles and motor control in cervicogenic disorders: Assessment and management. In Grant, R. (ed.): Physical Therapy of the Cervical and Thoracic Spine. ew York, Churchill Livingstone, 1994. 20. Youdas, rW., T.R. Garrett, V.r Suman, C.L. Bogard, H.O. Hallman, and rR. Carey: Normal range of motion of the cervical spine: An initial goniometric sUidy. Phys. Ther. 72:770-780, 1992. rA Antinnes, M. Panjabi, D. Loustalot, and M. 21. Dvorak, Bonomo: Age and gender related normal motion of the cervical spine. Spine 17:S393-S398, 1992. 22. Toole, J., and S.H. Tucker: Influence of head position upon cervical circulation. Arch. Neurol. 2:616-623, 1960. 23. Reese, N.B.: Muscle and Sensory Testing. Philadelphia, W.B. Saunders Co., 1999. 24. Janda, Y: Muscles and cervicogenic pain syndrome. In Grant, R. (ed.): Physical Therapy of the Cervical and Thoracic Spine. New York, Churchill Livingstone, 1988. 25. Yi-Kai, L., Z. Yun-Kun, L. Cai-Mo, and Z. Shi-Zhen: Changes and implications of blood flow velocity of the vertebral artery during rotation and extension of the head. J. Manip. Physiol. Ther. 22:91-95, 1999. 26. Magarey, M.E.: Examination of the cervical and thoracic spine. In Grant, R. (ed.): Physical Therapy of the Cervical and Thoracic Spine. ew York, Churchill Livingstone, 1988. 27. Elvey, R.L.: The investigation of arm pain. In Boyling, J.D., and N. Palastanga (eds.): Grieve's Modern Manual Therapy: The Vertebral Column, 2nd ed. Edinburgh, Churchill Lhwgstone, 1994. 28. Magarey, M.E.: Exantination of the cervical spine. In Grieve, G.P. (ed.): Modern Manual Therapy of the Vertebral Column. Edinburgh, Churchill Livingstone, 1986.

r,

29. Schneider, R., H. Gosch, H. orrell, M. Jerva, L. Combs, R. Smith: Vascular insufficiency and differential distortion o brain and cord caused by cervicomedullary football injuries. Neurosurg. 33:363-375, 1970. 30. Vernon, H., and S. Mior: The neck disability index: A stud reliability and validiry. Manip. Physiol. Ther. 14:409-415 1991. 31. Stratford, PW., D.L. Riddle, rM. Binkley, G. Spadoni, M.D Westaway, and B. Padfield: Using the neck disability index make decisions concenting individual patients. Physiother. C 51:107-112,1999. 32. Cattrysse, E., R.A S\vinkels, R.A Oostendorp, and W. Duq Upper cervical instability: Are clinical tests reliable? Manual Therapy 2:91-97,1997. 33. Olson, KA., S.v. Paris, C. Spohr, and G. Gorniak: Radiogr assessment and reliability study of the craniovertebral sidebe ing test. J. Man. Manip. Therapy 6:87-96,1998. 34. Spurling, R.G., and W.B. Scoville: Lateral rupture of the cer intervertebral disc. Surg. Gynec. Obstet. 78:350-358, 1944 35. Kelly, Neurological problems in the athlete's shoulder. Pettrone, F.A. (ed.): Athletic Injuries of the Shoulder. New York, McGraw-Hill, 1995. 36. Wells, P.: Cervical dysfunction and shoulder problems. Phys therapy 68:66-73, 1982. 37. Butler, D.S.: Mobilisation of the Nervous System. Melbourn Churchill Livingstone, 1991. 38. Slater, H., D.S. Butler, and M.O. Shacklock: The dynamic c tral nervous system: Examination and assessment using tens tests. In Boyling, rD., and N. Palastanga (eds.): Grieve's M ern Manual Therapy: The Vertebral Column, 2nd ed. Edinburgh, Churchill Livingstone, 1994. 39. Davidson, R.I., E.J. Dunn, and rN. Metzmaker: The shoul abduction test in the diagnosis of radicular pain in cervical e tradural compressive monoradiculopathies. Spine 6:441-446 1981. 40. Farmer, rC., and R.r Wisneski: Cervical spine nerve root c pression: An analysis of neuroforantinal pressure with varyin head and arm positions. Spine 19:1850-1855, 1994. 41. Landi, A., and S. Copeland: Value of the Tinel sign in brach plexus lesions. Ann. R. Coli. Surg. Eng!. 61:470-471, 1979 42. Uchihara, T., T. Furukawa, and H. Tsukagoshi: Compressio brachial plexus as a diagnostic test of a cervical cord lesion. Spine 19:2170-2173, 1994. 43. Grant, R.: Vertebral artery testing-the Australian Physioth Association Protocol after 6 years. Manual Therapy 1:149-1 1996. 44. Kunnasmaa, K.T., and H.W. Thiel: Vertebral artery syndrom review of the literature. r Orthop. Med. 16:17- 20, 1994. 45. Bolton, P.S., P.E. Stick, and R.S. Lord: Failure of clinical te to predict cerebral ischemia before neck manipulation. Ma Physiol. Ther. 12:304-307, 1989. 46. Rivett, D.A., Kr Sharples, and P.D. Milburn: Effect of pre ipulative tests on vertebral artery and internal carotid artery blood flow: A pilot sUidy. J. Manip. Physiol. Ther. 22:3681999. 47. Rivett, D.A.: The premanipulative vertebral artery testing pr col. ew Zealand J. Physiother. 23:9-12, 1995. 48. Barker, S., M. Kesson, J. Ashmore, G. Turner, r Conway, a D. Stevens: Guidance for pre-manipulative testing of the cer spine. Manllal Therapy 5:37-40, 2000. 49. Maitland, G.D.: Vertebral Manipulation. London, Butterwo 1973. 50. Ombregt, L., P. Bisschop, H.J. ter Veer, and T. Van de Ve A System of Orthopedic Medicine. London, W.B. Saunders 1995. 51. Grant, R.: Vertebral artery insufficiency: A clinical protocol pre-manipulative testing of the cervical spine. In Boyling, rD and N. Palastanga (eds.): Grieve's Modern Manual Therapy Vertebral Column, 2nd ed. Edinburgh, Churchill Livingston 1994. 52. Haynes, M.J.: Doppler sUidies comparing the effects of cenr rotation and lateral flexion on vertebral artery blood flow. r Manip. Physiol. Ther. 19:378-384, 1996.

r

rr:

r


-3. Wadsworth, CT.: Manual Examination and Treatment of the Spine and Extremities. Baltimore, Williams & Wilkins, 1988. ;4. Aspinall, W.: Clinical testing for cervical mechanical disorders which produce ischemic vertigo. J. Orthop. Sports Phys. Ther. 11:176-182,1989. :I. Meadows, J.J., and D.J. Magee: An overview of dizziness and vertigo for the orthopedic manual therapist. In Boyling, J.D., and N. Palasta.nga (eds.): Grieve's Modern Manual Therapy: The Vertebral Column, 2nd ed. Ecti.nburgh, Churchill Livingstone, 1994. ;0. Gird, R.B., and H.C. Naffziger: Prolonged jugular compression: A new diagnostic test of neurological value. Trans. Am. Neuro!. Assoc. 66:45-49, 1940. - Fitz-Ritson, D.: Assessment of cervicogenic vertigo. J. Manip. Physio!. Ther. 14:193-198, 1991. :: Aspinall, W.: Clinical testing for the craniovertebral hypermobility syndrome. J. Orthop. Sports Phys. Ther. 12:47-54, 1990. :; Pettman, E.: Stress tests of the craruovertebral joints. In Bayling, J.D., and N. Palastanga (eds.): Grieve's Modern Manual Therapy: The Vertebral Column, 2nd ed. Ecti.nburgh, Churchill Livingstone, 1994. Denno, J.J., and G.R. Meadows: Early diagnosis of cervical pondylotic myelopathy: A useful clinical sign. Spine 16:13531355, 1991. Refshauge, K, and E. Gass: The neurological examination. In Refshauge, K, and E. Gass (eds.): Musculoskeletal Physiotherapy. Oxford, Butterworth-Heineman.n Ltd., 1995. _ Waters, P.M.: Obstetric brachial plexus injuries: Evaluation and management. J. Am. Acad. Orthop. Surg. 5:205-214, 1997. - Cantu, R.C.: Stingers, transient quadriplegia, and cervical spinal stenosis: Return to play criteria. Med. Sci. Sports Exer. 29:

233-S235,1997. •. Weinstein, S.M.: Assessment and rehabilitation of the athlete with a "stinger." A model for the management of noncatastrophic athletic cervical spine injury. Clin. Sports Med. 17:127135,1998. - Mennell, J.M.: Joint Pain. Boston, Little, Brown & Co., 1964. Johnson, M.J., and G.L. Lucas: Value of cervical spine radiographs as a screening too!. Clin. Orthop. Relat. Res. 340:102108,1997. - Helliwell, P.S., P.F. Evans, and V. Wright: The straight cervical spine'. Does it indicate muscle spasm? }. Bone Joint Surg. Br. 76: 103-106, 1994. Pavlov, H., J.S. Torg, B. Robie, and C. Jahre: Cervical spine tenosis: Determination with vertebral body method. Radiology 164:771-775,1987. 9. Cantu, R.C.: Functional cervical spinal stenosis: A contraindication to participation in contact sports. Med. Sci. Sports Exerc. 25:316-317, 1993. -0. Castro, F.P., J. Ricciardi, M.E. Brunet, M.T. Busch, and T.S. Whitecloud: Stinger, the Torg ratio, and the cervical spine. Am. J. Sports Med. 25:603-608, 1997. -1. Torg, J.S., H. Pavlov, S.E. Genuario, B. Sennett, R.J. Wisneski, B.H. Robie, and C. Jahre: eurapraxia of the cervical spinal cord with transient quadriplegia. J. Bone Joint Surg. 68A:13541370,1986. -1. Templeton, P.A., J.W. Young, S.E. Mirvis, et a1.: The value of retropharyngeal soft tissue measurements in tralUna of the adltlt cervical spine. Skeletal Radiol. 18:98-104,1987. -3. Harris, J.H.: Radiographic evaluation of spinal trauma. Orthop. Clin. North Am. 17:75-86,1986. -4. Reid, D.C.: Sports 1njmy Assessment and Rehabilitation. New York, Churchill Livingstone, 1992. -5. Bigg-Wither, G., and P. Kelly: Diagnostic imaging in musculoskeletal physiotherapy. In Refshauge, K., and E. Gass (eds.): Musculoskeletal Physiotherapy. Oxford, Butterworth-Heinemann Ltd., 1995. -6. Vaccaro, A.R., G.R. Klein, A.E. Flanders, T.J. Albert, R.A. Balderston, and J.M. Cotler: Long-term evaluation of vertebral artery injuries following cervical spine trauma using magnetic resonance angiography. Spine 23:789-795, 1998. -7. Furumoto, T., J. Nagase, K Takahashi, T. Itabashi, H. Iai, and

179

N. Ishige: Cervical myelopathy caused by the anomalies vertebral artery-A case report. Spine 21:2280-2283, 1996. 78. Combs, S.B., and J.J. Triano: Symptoms of neck artery compromise: Case presentations of risk estimate for treatment. J. Manip. Physio!. Ther. 20:274-278, 1997.

General References Aprill, C., A. Dwyer, and N. Bogduk: Cervical zygapophyseal joint pain patterns: A clinical evaluation. Spine 15:458-461, 1990. Bassett, L.W., R.H. Gold, and L.L. Seeger: MR! Atlas of the Musculoskeletal System. London, Martin Dunitz Ltd., 1989. Bateman, J.E.: The Shoulder and eck. Philadelphia, W.B. Saunders Co., 1972. Beatty, R.M., F.D. Fowler, and E.J. Hanson: The abducted arm as a sign of ruptured cervical disc. Neurosurgery 21:731-732,1987. Bell, G.R., and J.S. Ross: Diagnosis of nerve root compression: Myelography, computed tomography, and MR!. Orthop. Clin. North Am. 23:405-419, 1992. Beggs, 1.: Radiological assessment of degenerative diseases of the cervical spine. Semin. Orthop. 2:63-73, 1987. Bland, J.H.: Disorders of the Cervical Spine. Philadelphia, W.B. Saunders Co., 1994. Bogduk, N., and A. Marsland: The cervical zygapophyseal joints as a source of neck pain. Spine 13:610-617, 1988. Bonica, J.J.: The Management of Pain. Philadelphia, Lea & Febiger, 1953. Butler, D., and L. Gifford: The concept of adverse mechanical tension in the nervous system. Physiotherapy 75:622-636, 1989. Cailliet, R.: eck and Arm Pain. Philadelphia, FA Davis Co., 1964. Campbell, A.M., and D.G. Phillips: Cervical disc lesions with neurological disorder. Br. Med. J. 2:480-485, 1960. Cates, J.R., and M.M. Soriano: Cervical spondylotic myelopathy. J. Manip. Physio!. Ther. 18:471-475, 1995. Cervical Spine Research Society: The Cervical Spine. Philadelphia, J.B. Lippincott, 1989. Cibltlka, M.T.: Evaluation and treatment of cervical spine injuries. Coo. Sports Med. 8:691-701, 1989. Clark, c.R.: Examination of the neck. In Clark, C.R., and M. Bonfiglio (eds.): Orthopedics: Essentials of Diagnosis and Treatment. New York, Churchill Livingstone, 1994. Clark, C.R., C.M. Igram, G.Y. El-Khoury, and S. Ehara: Radiologic evaluation of cervical spine injuries. Spine 13:742-747, 1988. Collins, H.R.: An evaluation of cervical and lumbar discography. Clin. Orthop 107:133-138, 1975. Crouch, J.E.: Functional Human Anatomy. Philadelphia, Lea & Febiger, 1973. Darnell, M.W.: A proposed chronology of events for forward head posture. J. Craniomand. Pract. 1:50-54,1983. Dhirnitri, K, S. Brodeur, M. Croteau, S. Richard, and C.J. Seymour: Reliability of the cervical range of motion device in measuring upper cervical motion. J. Man. Manip. Ther. 6:31-36, 1998. Dorwart, R.H., and D.L. LaMasters: Application of computed tomographic scanning of the cervical spine. Orthop. Clin. North Anl. 16:381-393,1985. Dvorak, J., and V. Dvorak: Manual Medicine: Diagnostics. New York, Thieme-Stratton Inc., 1984. Edmeads, J.: Headaches and head pains associated with diseases of the cet"\~cal spine. Med. Clin. North Am. 62:533-544, 1978. Edwards, B.C.: Combined movements in the cervical spine (C2-7): Their value in examination and technique choice. Aust. J. Physiother. 26:165-171, 1980. Edwards, B.C.: Combined movements of the cervical spine in examination and treatment. In Grant, R. (ed.): Physical Therapy of the Cervical and Thoracic Spine. New York, Churchill Livingstone, 1988. Esposito, c.J., G.A. Crim, and T.K. Binkley: Headaches: A differential diagnosis. J. Craniomand. Pract. 4:318-322, 1986. Ferlic, D.: The range of motion of the "normal" cervical spine. Johns Hopkins Hosp. Bull. 110:59, 1962. Fielcti.ng, J.W.: Normal and selected abnormal motion of the cervical spine from the second cervical vertebra to the seventh cervical

Fielding, J.W., G.B. Cochran, J.F. Lawsing, and M. HoW: Tears of the transverse ligament of the atlas: A clinical and biomechanical study. J. Bone Joint Surg. Am. 56:1683-1691,1974. Forrester, D.M., and J.C. Brown: The Racliology of Joint Disease. Philadelphia: W.B. Saunders Co., 1987. Franco, J.L., and A. Herzog: A comparative assessment of neck muscle strength and vertebral stability. J. Orthop. Sports Phys. Ther. 8:351-356, 1987. Frykholm, R: Lower cervical vertebrae and intervertebral cliscs: Surgical anatomy and pathology. Acta Chit. Scand. 101-102:345359,1951-1952. Gould, G.A.: The Spine. In Gould, G.A. (ed.): Orthopeclic and Sports Physical Therapy. St. Louis, C.v. Mosby Co., 1990. Grant, R: Dizziness testing and manipulation of the cervical spine. In Grant, R (ed.): Physical Therapy of the Cervical and Thoracic Spine. ew York, Churchill Livingstone, 1988. Grieve, G.P.: Mobilisation of the Spine, 3rd ed. New York, Churchill Livingstone, 1979. Grieve, G.P.: Common Vertebral Joint Problems. ew York, Churchill Livingstone, 1981. Glmdry, C.R, and KB. Heithoff: Imaging evaluation of patients with spinal deformity. Orthop. Clin. North Am. 25:247-264, 1994. Harrelson, G.L.: Evaluation of brachial plexus injuries. Sportsmed. Update 4:3-9, 1989. Hensinger, RN.: Congenital anomalies of the cervical spine. Clin. Orthop. 264:16-38, 1991. Herrmann, D.B.: Valiclity smdy of head and neck flexion-extension motion comparing measurements of a pendulum goniometer and roentgenograms. J. Orthop. Sports Phys. Ther. 11:414-418, 1990. Hershman, E.B.: Injuries to the brachial plexus. In Torg, J.S. (ed.): Athletic Injuries to the Head, eck and Face. St. Louis, MosbyYear Book, 1991. HoW, M.: Normal motions in the upper portion of the cervical spine. J. Bone Joint Surg. Am. 46:1777-1779, 1964. HoW, M., and H.R Baker: The atlanto-a.ual joint: Roentgenographic and anatomic smdy of normal and abnormal motion. J. Bone Joint Surg. Am. 46:1739-1752, 1964. HoW, M.: Soft-tissue injuries of the neck. Clin. Orthop. 109:42-49, 1975. Hollinshead, W.H., and D.B. Jenkins: Functional Anatomy of the Limbs and Back. Philadelphia, W.B. Saunders Co., 1981. Hoppenfeld, S.: Physical Examination of the Spine and Extremities. New York, Appleton-Century-Crofts, 1976. Hu, R, R Burnham, D.C. Reid, M. Grace, and L. Saboe: Burners in contact sports. Clin. J. Sports Med. 1:236-242,1991. Jackson, R: The Cervical Syndrome. Springfield, Illinois, Charles C Thomas, 1976. Jordon, K: Assessment of published reliability smclies for cervical spine range of motion measurement tools. J. Manip. Physiol. Ther. 23:180-195,2000. Judge, RD., G.D. Zuidema, and F.T. Fitzgerald: Clinical Diagnosis: A Physiological Approach. Boston, Little, Brown & Co., 1982. Kapandji, LA.: The Physiology ofJoints, vol. 3: The Trunk and the Vertebral Colunm. New York, Churchill Livingstone, 1974. Kaye, J.J., and E.P. Nance: Cervical spine trauma. Orthop. Clin. North Am. 21:449-462, 1990. Kaye, S., and E. Mason: Clinical implications of the upper limb tension test. Physiotherapy 75:750-752,1989. Kenneally, M., H. Rubenach, and R Elvey: The upper limb tension test: The SLR rest of the arm. In Grant, R (ed.): Physical Therapy of the Cervical and Thoracic Spine. New York, Churchill Livingstone, 1988. Ketmer, N.W.: The racliology of cervical spine injury. J. Manip. Physiol. Ther. 14:518-526, 1991. Law, M.D., M. Bernhardt, and A.A. White: Evaluation and management of cervical spondylotic myelopathy. J. Bone Joint Surg. Am. 76:1420-1433,1994. Liebenson, C.S.: Thoracic outlet syndrome: Diagnosis and conservative management. J. Manip. Physiol. Ther. 11:493-499,1988.

Lysell, E.: Motion in the cervical spine. Acta Orthop. Scand. Supp 123:1-61,1969. Macnab,1.: Cervical spondylosis. Clin. Orthop. 109:69-77, 1975 Maigne, R: Orthopaeclic Meclicine: A New Approach to Vertebra Manipulation. Springfield, Illinois, Charles C Thomas, 1972. Maigne, R: Diagnosis and Treatment of Pain of Vertebral Origin: Manual Meclicine Approach. Baltimore, Williams & Wilkins, 19 Mathews, J.A., and J. Pemberton: Racliologic anatomy of the neck Physiotherapy 65:77-80, 1979. Matsunaga, S., T. Sakou, E. Taketomi, M. Yamaguchi, and T. Okano: The namral course of myelopathy caused by ossification the posterior longitudinal ligament in the cervical spine. Clin. O thop. 305:1668-1677,1994. McRae, R: Clinical Orthopaeclic Examination. New York, Church Livingstone, 1976. Meyer, S.A., KR Schulte, JI Callaghan, et al.: Cervical spinal ste nosis and stingers in collegiate football players. Am. J. Sports M 22:158-166, 1994. Miller, J.S., N.L. Polissar, and M. Haas: A racliographic compariso of neutral cervical posture with cervical flexion and extension ranges of motion. J. Manip. Physiol. Ther. 19:296-301, 1996. Nilsson, ], H.W. Christensen, and J. HartVigsen: The interexami reliability of measuring passive cervical range of motion, revisite J. Manip. Physiol. Ther. 19:302-305, 1996. Nilsson, N., J. Hartvigsen, and H.W. Christensen: Normal ranges passive cervical motion for women and men 20-60 years old. J. Manip. Physiol. Ther. 19:306-309,1996. Palmer, M.L., and M. Epler: Clinical Assessment Procedures in Ph ical Therapy. Philadelphia, J.B. Lippincott Co., 1990. Panjabi, M.M.: Cervical spine mechanics as a function of transecti of components. J. Biomech. 8:327-336, 1975. Patterson, R.H.: Cervical ribs and the scalenus muscle syndrome. Ann. Surg. 111:531-543,1940. Pavlov, H.: Radiographic evaluation of the cervical spine and relat structures. In Torg, J.S. (ed.): Athletic Injuries to the Head, Ne and Face. St. Louis, Mosby-Year Book Inc., 1991. Pavlov, H., J.S. Torg, B. Robie, and C. Jahre: Cervical spinal sten sis: Determination with vertebral body ratio method. Racliology 164:771-775,1987. Pedersen, H.E., C.F.J. Blunck, and E. Gardner: The anatomy of lumbosacral posterior rami and meningeal branches of spinal nerves (sinu-vertebral nerves). J. Bone Joint Surg. Am. 38:377391, 1956. Penning, L.: Functional pathology of the cervical spine. New York Excerpta Meclica Foundation, 1968. Penning, L.: Normal movements of the cervical spine. Am. J. Roe genol. 130:317-326,1978. Porterfield, JA., and C. DeRosa: Mechanical eck Pain. Philadelphia, W.B. SalU1ders Co., 1995. Post, M.: Physical Examination of the Musculoskeletal System. Ch cago, Year Book Meclical Publishers, 1987. Ratkovits, B.L.: Racliographic assessment. In Bland, J.H. (ed.): Di orders of the Lumbar Spine. Philadelphia, W.B. Sawlders Co., 1994. Refshauge, K: Testing adequacy of cerebral blood flow (vertebral artery testing). In Refshauge, K, and E. Gass (eds.): Musculosk etal Physiotherapy. Oxford, Butterworth-Heinemarm Ltd., 1995 Refshauge, KM.: Rotation: A valid premanipulative clizziness test? Does it preclict safe manipulation? J. Manip. Physiol. Ther. 17: 19,1994. Rheault, W., B. Albright, C. Byers, et al.: lntertester reliability of cervical range of motion device. J. Orthop. Sports Phys. Ther. 1 147-150,1992. Rockett, F.X.: Observations on the "burner": Traumatic cervical r cliculopathy. Clin. Orthop. 164:18-19, 1982. Rohim, KA., and J.L. Stanlbough: Racliographic evaluation of the degenerative cervical spine. Orthop. Clin. North Am. 23:395-4 1992. Rorabech, C.H., and W.R Harris: Factors affecting the prognosis brachial plexus injuries. J. Bone Joint Surg. Br. 63:404-407, 1981.

---------------------------.-~---------.


Rothman, RH.: The acute cervical disc. Clin. Orthop. 109:59-68, 1975. othman, R.H., and F.A. Simeone: The Spine. Philadelphia, W.B. aunders Co., 1982. -aunders, H.D., and R Salmders: Evaluation, Treatment and Pre"ention of Musculo keletal Disorders. Chaska, Minnesota, Educational Opportunities, 1995. h'aratllanl, P.J., T.A. Matyas, and E.F. Glasgow: Noninvasive discrimination of brachial plexus involvement in upper limb pain. pine 19:26-33, 1994. erk, H.H., W.C. Warters, and L. Zeiger: Evaluation and treatment of neck pain. Orthop. Clin. orth Am. 13:439-452, 1982. - uthwick, W.O., and K Keggi: The normal cervical spine. J. Bone Joint Surg. Am. 46:1767-1777, 1964. er, KP., and F.H. Bassett: The prolonged burner syndrome. Am. J. Sports Med. 18:591-594,1990. :.mwood, J.E., and G.H. Kraft: Diagnosis and assessment of brachial plexus injmies. Arch. Phys. Med. Rehabil. 52:52-60, 1971. tton, S.A., and J.M. Bryon: Dysfunction, evaluation and treatment of the cervical spine and thoracic inlet. 11/ Donatelli, R, and .\1.]. Wooden (eds.): Orthopedic Physical Therapy. ew York, Churchill Livingstone, 1989. derland, S.: Meningeal-neural relations in the intervertebral foramen. J. Neurosurg. 40:756-763, 1974. -ardiff, G.S.: Nerve injuries: Testing and treatment tactics. Phys. portsmed. 23:61-72,1995. -arlow, W.F.T., and H.G. Bammer: Syndrome of vertebral artety compression. eurology 7:331-340,1957. :-cmpleton, P.A., ].W. Young, S.E. Mirvis, and E.U. Buddemeyer: The value of retrophalangeal soft tissue measurements in trauma of the adult cervical spine. Skeletal Radio!. 16:98-104,1987. :- rg, J.S., H. Pavlov, and S.G. Glasgow: Radiographic evaluation of athletic injuries to the cervical spine. In Camins, M.B., and P.P. 'Leary (eds.): Disorders of the Cervical Spine. Baltimore, Wilams & Wilkins, 1992. rg, ].S., and I.A. Ramsey-Emrhein: Cervical spine and brachial l'leXlIS injuries-return to play recommendations. Phys. Sportsined. 25(7):61-88, 1997.

181

Troost, BT.: Dizziness and vertigo in vertebrobasilar disease. Stroke 11 :413-415, 1980. Vereschagin, KS., J.]' Wiens, G.S. Fanton, and M.F. Dillingham: Burners: Don't overlook or underestimate them. Phys. Sportsmed. 19:96-106,1991. Waldron, RL., and E.H. Wood: Cervical myelography. Clin. 01'thop. 97:74-89, 1973. Wasenko, ].J., and C.F. Lanzieri: Plain radiographic examination in cervical spine trauma. In Camins, M.B., and P.F. O'Leary (eds.): Disorders of the Cervical Spine. Baltimore, Williams & Wilkins, 1992. Weir, D.C.: Roentgenographic signs of cervical injury. Clin. Orthop. 109:9-17,1975. White, A.A., RM. Johnson, M.M. Panjabi, and W.O. Soutllwick: Biomechanical analysis of clinical stability in the cervical spine. Clin. Orthop. 109:85-96, 1975. White, A.A., and M.M. Panjabi: The clinical biomechanics of the occipito-atlantoaxial complex. Orthop. Clin. Torth Am. 9:867878,1978. White, A.A. and M.M. Panjabi: Clin.ical Biomechanics of the Spine. Philadelphia, J.B. Lippincott Co., 1978. Williams, P., and R Warwick (eds.): Gray's Anatomy, 36rll British ed. Edinburgh, Churchill Livingstone, 1980. Wong, A., and D.O. Nansel: Comparisons between active vs passive end-range assessments in subjects exhibiting cen,jcal range of motion asymmetries. J. Manip. Physio!. Ther. 15:159-163,1992. Worth, D.R: Movements of the head and neck. In Boyling, J.D., and N. Palastanga (eds.): Grieve's Modern Manual Therapy: The Vertebral Colunm, 2nd ed. Edinburgh, Churchill Livingstone, 1994. Wyke, B.: Neurology of the cen,jcal spine joints. Physiotherapy 65: 72-76,1979. Yu, Y.L., E. Woo, and c.y. Huang: Cen'ical spondylotic myelopathy and radicuJopathy. Acta 1 euro!. Scand. 75:367-373, 1987. Zatzkin, H.R, and F.W. Kveton: Evaluation of the cervical spine in whiplash injuries. Radiology 75:577-583,1960.

MPOROMANDIBULAR INT temporomandibular joints are two of the most uently used joints in the body, but they probably lye the least amount of attention. Without the e , we would be severely hindered when talking, g, yawning, kissing, or ucking. In any exarninaof the head and neck the temporomandibular should be included. Much of the work in thi ter has been developed from the teachings of Rodo.'

Applied Anatomy temporomandibular joint is a synovial, condylar, hinge-type joint with fibrocartilaginous surfaces er than hyaline cartilage and an articular disc; this - completely divides each joint into two cavities ~. 4-1). Both joints, one on each side of the jaw, t be considered together in any exanunation. ng with the teeth, these joints are considered to be rrijoint complex." Gliding, translation, or sliding movement occurs the upper cavity of the temporomandibular joint, reas rotation or hinge movement occurs in the er cavity. Rotation occurs from the beginning to midrange of movement. The upper head of the eral pterygoid muscle draws the disc, or meniscus, eriody and prepares for condylar rotation during \'ement. The rotation occurs through the two conar heads between the articular disc and the condyle. addition, the disc provides congruent contours and rication for the joint. Gliding, which occurs as a -ond movement, is a translatory movement of the ndyle and disc along the slope of the articular eminee. Both gliding and rotation are essential for full ening and closing of the mouth (Fig. 4-2). The psule of the temporomandibular joints is thin and e. In the resting position, the mouth is slightly

Superior compartment Inferior compartment

Neck of condyle

Figure 4-1 The temporomandibular joint.

open, the lips are together, and the teeth are not contact but slightly apart. In the close packed po iti the teeth are tightly clenched, and the heads of condyles are in the po terior aspect of the joint. Ce tric occlusion is the relation of the jaws and te when there is maximum contact of the teeth, and i the position assumed by the jaw in swallowing.

Temporomandibular Joints Resting position:

Mouth slightly open, lips together, teeth not in contact


Teeth tightly clenched

Capsular pattern:

Limitation of mouth opening

1

Figure 4-2

Normal fi.mctional movement of the condyle and dis ing the full range of opening and closing. ote that is rotated posteriorly on the condyle as the condyle i lated out of the fossa. The closing movement is the opposite of the opening movement.

The temporomanelibular joints actively elisplace only anteriorly and slightly laterally. When the mouth is opening, the condyles of the joint rest on the elise in the articular eminences, and any sudden movement, such as a yawn, may elisplace one or both condyles forward. As the mandible moves forward on opening, the disc moves medially and posteriorly until the collateral ligaments and lateral pterygoid stop its movement. The elise is then "seated" on the head of the manelible, and bOtll disc and mandible move forward to full opening. If this "seating" of the disc does not occur, full range of motion at the temporomandibular joint is limited. In the first phase, mainly rotation occurs, primarily in the infelior joint space. In the second phase, in which the mandible and disc move together, mainly translation occurs in the superior joint space. 2 The temporomandibular joints are innervated by branches of the auriculotemporal and masseteric branches of the manelibular nerve. The elise is innervated along its periphery but is aneural and avascular in its intermeeliate (force-bearing) zone. The temporomandibular, or lateral, ligament restrains movement of the lower jaw and prevents compression of the tissues behind tlle condyle. In reality, this collateral ligament is a thickening in the joint capsule. The sphenomandibular and stylomandibular ligaments act as "guieling" restraints to keep the condyle, elise, and temporal bone firmly opposed. The stylomanelibular ligament is a specialized band of deep cerebral fascia with thickening of the parotid fascia.

In the human, there are 20 deciduous, or tem ("baby"), teeth and 32 permanent teeth (Fig. The temporary teeth are shed between the age and 13 years. In the adult, the incisors are the teeth (four maxillary and four manelibular), wi maxillary incisors being larger than the manelibu

Central incisor (6-8)-------,

aJG>~\23l

Lateral incisor (7-12)

F!fJ

Canine (16-20)

Q£

~

First molar (12-16)---0 Second molar (20-30)-(fj)

A Central incisor (7-8)

~

Lateral incisor (7-10)

(9_13)i'fJ

Canine (9-14)--@C@ZV@a First premolar \J Second premolar (10-14) First molar (5-8) Second molar (10-14)

?

(@

@ ®

.I

0

(;? t1

m

Ill!>

rG

Third molar (wisdom tooth) (17-24)/-P

'B

Figure 4-3

Teeth in a child CA) and in an adult (E). Numbers indicate ag months for a child, in years for an adult) at which teeth erupt

Chapter 4 • Temporomandibular Joint

A

Mx

2 8

7

6

5

4

3

2

1

8

7

6

5

4

3

2

1

1

2

3

4

5

6

7

8

2

3

4

5

6

7

8

-.

Lt

4

3 Md

B Mx

5 5

4

3

6 2

1

1

2

3

4

5

Rt

Lt

5

4

3

2

1

1

8

2

3

4

5

7 Md

re 4-4 eric symbols for dentition in an adult (A) and in a child (B). Liebgott, B.: The Anatomical Basis of Dentistry. St. Louis, - Mosby Co., 1986.) ID

rs. The incisors are designed to cut food. The cae teeth (two maxillary and two mandibular) are the gest permanent teeth and are designed to cut and .If food. The premolars crush and break down the for digestion; usually they have two cusps. There e eight premolars in all, two on each side, top and ttom. The final set of teeth are the molars, which h and grind food for digestion. They have four or e cusps, and there are two or three on each side, top d bottom (total 8 to 12). The third molars are .illed wisdom teeth. Missing teeth, abnormal tooth ption, malocclusion, or dental caries (decay) may ad to problems of the temporomandibular joint. By ovention, the teeth are divided into four quadts-the upper left, the upper right, the lower left, nd the lower right quadrants (Fig. 4-4).

Patient History ..n addition to the questions listed under Patient His-ory in Chapter 1, the examiner should obtain the -allowing information from the patient. 1. Is there pain on opening or closing of the mouth? Pain in the fully opened position (e.g., pain sociated with opening to bite an apple, yawning) is probably caused by an extra-articular problem, whereas ain associated with biting firm objects (e.g., nuts, raw

185

fruit and vegetables) is probably caused by an intraarticular problem. 3 2. Is there pain on eating? Does the patient chew on the right? Left? Both sides equally? Loss of molars or worn dentures can lead to loss of vertical dimension, which can make chewing painful. Vertical dimension is the distance between any two arbitrary points on the face, one of these points being above and the other below the mouth, usually in midline. Often, chewing on one side is the result of malocclusion. 3 3. What movements of the jaw cause pain? The examiner should watch the patient's jaw movement while the patient is talking. A history of stiffness on waking with pain on function that disappears as the day goes on suggests osteoarthritis. 4 4. Do any of these actions cause pain or discomfott: Yawning? Biting? Chewing? Swallo\oving? Speaking? Shouting? If so, where? All of these actions cause movement, compression, and/or stretching of the soft tissues of the temporomandibular joints. 5. Does the patient breathe through the nose or the mouth? ormal breathing is through the nose with the lips closed and no "air gulping." If the patient is a "mouth breather," the tongue does not sit in the proper position against the palate. In the YOlmg, if the tongue does not push against the palate, developmental abnormalities may occur, because the tongue provides internal pressure to shape the mouth. The buccinator and orbicularis oris muscle complex provides external pressure to counterbalance the internal pressure of the tongue. Loss of normal neck balance often results in the individual's becoming a mouth breather and an upper respiratory breather, making greater use of the accessory muscles of respiration. Conditions such as adenoids, tonsils, and upper respiratory tract infections may cause the same problem. 6. Has the patient complained of any clicking? Normally, the condyles of the temporomandibular joint slide out of the concavity and onto the rim of the disc. Clicking is the result of abnormal motion of the disc and mandible. Clicking may occur when the condyle slides back off the rim into the center (Fig. 4-5).5 If the disc sticks or is bunched slightly, opening causes the condyle to abruptly move over the disc and into its normal position, resulting in a single click (see Fig. 4-5).6 There may be a partial anterior displacement (subluxation) or dislocation of the disc, which the condyle must override to reach its normal position when the mouth is fully open (Fig. 4-6). This override may also cause a click. Similarly, a click may occur if the disc is displaced anteriorly and/or medially causing the condyle to override the posterior rim of the disc later than normal during mouth opening. This is referred to as disc displacement with reduction. If clicking occurs in both directions, it is called reciprocal clicking (Fig.

Figure 4-5

Single click. Between positions 2 and 3, a click is felt as the condy moves across the posterior border into the intermediate zone of t disc. ormal condyle-disc function occurs during the remaining opening and closing movement. In the closed joint position (1), disc is again displaced forward (and medially) by activity of the superior lateral pterygoid muscle.

2

-----:lIE------3

Figure 4-6 Functional dislocation of the disc with reduction. During opening, the condyle passes over the posterior border of the disc into the intermediate area of the disc, thus reducing the dislocated disc.

4-7). The opening click occurs somewhere during the opening or protrusive path, and the click indicates the condyle is slipping over the thicker posterior border of the disc to its position in the thinner middle or intermediate zone. The closing (reciprocal) click occurs near the end of the closing or retrusive path as the pull of the superior lateral pterygoid muscle causes the disc to slip more anteriorly and the condyle to move over its posterior border. Clicks may also be caused by adhesions (Fig. 4-8), especially in people who clench their teeth (bruxism). These "adhesive" clicks occur only once, after the period of clenching. 7 If adhesions occur in the superior or inferior joint space, translation or rotation will be limited. This presents as a temporary closed lock, which then opens with a click.

5

If the articular eminence is abnormally develop (i.e., short, steep posterior slope or long, flat anter slope), the maximum anterior movement of the d may be reached before ma.--wnum translation of t condyle has occurred. As the condyle overrides t disc, a loud crack is heard, and the condyle-disc lea or jogs (subluxes) forward.? "Soft" or "popping" clicks that are sometimes hea in normal joints are caused by ligament moveme articular surface separation, or sucking of loose tiss behind the condyle as it moves forward. These cli usually result from muscle incoordination. "Hard" "cracking" clicks are more likely to indicate joint p thology or joint surface defects. Soft crepitus (like ru bing knuckles together) is a sound that sometimes o curs in symptomless joints and is not necessarily

Chapter 4 • Temporomandibular Joint

:: !lure 4-7 :Jprocal click. Benveen positions 2 and 3, a click is felr as the .'Ie moves across the posterior border of the disc. Normal yle-disc fimction occurs during the remaining opening and g movement until the closed joint position is approached. ond click is heard as the condyle once again moves from inrermediate zone to the posterior border of the disc be~en positions 8 and 1.

)r

'cation of pathology. Hard crepitus (like a footstep gravel) is indicative of arthritic changes in the -Ilts. The clicking may be caused by uncoordinated cle action of the lateral pterygoid muscles, a tear _ perforation in the disc, osteoarthrosis, or occlusal alance. Normally, the upper head of the lateral -erygoid muscle pulls the disc forward. If the disc s not move first, the condyle clicks over the disc as -' pulled forward by the lower head of the lateral -erygoid muscle. Iglarsh and Snyder-Mackler2 have ided disc displacement into four stages (Table -:-1 ). -. Has the mouth or jaw ever locked? Locking may ply that the mouth does not fully open or it does t fully close. Locking is usually preceded by reciproclicking. If the jaw has locked in the closed posin, the locking is probably caused by a disc, with the .:lOdyle being posterior or anteromedial to the disc.

rd

Even if translation is blocked (e.g., "locked" di mandible can still open 30 mm by rotation. If functional dislocation of the disc with reducti Fig. 4-6), the disc is usually positioned anter ally, and opening is limited. The patient compla the jaw "catches" sometimes, so the locking only occasionally and, at those times, opening ited. If there is functional anterior dislocation disc without reduction, a closed lock occurs. lock implies there has been anterior and/or

Table 4-1 Temporomandibular Disc Dysfunction Stage Stage 1

Disc slightly anterior and medial on mandibular condyle Inconsistent click (mayor may not be Mild or no pain

Stage 2

Disc anterior and medial Reciprocal click present (early on open on closing) Severe consistent pain

Stage 3

Reciprocal consistent click present (late opening, earlier on closing) Most paintll! stage

Stage 4

Click rare (disc no longer relocates) No pain

It.

Ie

or ab-

an

tgure 4-8 .-\0) Adhesion in the superior joint space. (B) The presence of the dhesion limits the joint to rotation only. (C) If the adhesion is ;reed, normal translation can occur.

Characteristics

2

8

,

-----*-----3

Figure 4-9 Closed lock. The condyle never assumes a normal relation to the disc but instead causes the disc to move forward ahead of it. This condition limits the distance the condyle can translate forward.

5

151

Figure 4-10 Open lock (disc incoordination). (1) The disc always stays in anterior position with the jaw closed. (1-4) Disc is displaced posterior to the condyle with one or two opening clicks. (5-6) The disc disturbs jaw closing after maximum opening. (6-1) The disc is again displaced to anterior position from the posterior with one or two clicks.

2 nd closing click

opening click

2

----~t_----:-_,_-- 3

2nd

Opening, click

6 5 Locking

displacement of the disc, so that the disc does not return to its normal position during the entire movement of the condyle. In this case, opening is limited to about 25 ffiffi, the mandible deviates to the affected side (Fig. 4-9), and lateral movement to the uninvolved side is reduced? If locking occurs in the open position, it is probably caused by subluxation of the joint or possibly by posterior disc displacement (see Fig. 4-9). With an open lock, there are two clicks on opening, when the condyle moves over the posterior rim of the disc and then when it moves over the anterior rim of the disc, and two clicks on closing. If, after the second click occurs on opening, the disc lies posterior to the condyle, it may not allow the condyle

to slide back (Fig. 4-10).8 If the condyle dislocates outside the fossa, it is a true dislocation with open lock; the patient cannot close the mouth, and the dislocation must be reduced. 8 8. Does the patient have any habits such as pipe smoking, using a cigarette holder, leaning on the chin che~ving gum, biting the nails, chewing hair, pursing and chewing lips, continually moving the mouth, o any other nervous habits? All these activities place additional stress on the temporomandibular joints. 9. Does the patient grind the teeth or hold them tightly? Bruxism is the forced clenching and grinding of the teeth, especially during sleep. This may lead to facial, jaw or tooth pain, or headaches in the morning

Chapter 4 • Temporomandibular ..Joint

1

19ure 4-11 .-\ Normal resting position of the tongue. Tongue ition cannot be seen because of teeth. Upper and wer teeth are not in contact. (B) Mouth opened to ow tongue against upper anterior palate. This would t be considered the normal resting position because - e mouth is open too much.

the front teeth are in contact and the back ones are facial and temporomandibular pain may develop a result of malocclusion. 10. Are any teeth missing? If so, which ones and ow many? The presence or absence of teeth and their iation to one another must be noted on a table mlllar to the one shown in Figure 4-4. Their pres~nce or absence can have an effect on the temporoandibular joints and their muscles. If some teeth are "TI.issing, others may deviate to fill in the space, altering -- e occlusion. 11. Are any teeth painful or sensitive? This finding may be indicative of dental caries or abscess. Tooth ,..,ain may lead to incorrect biting when chewing, which nuts abnormal stresses on the temporomandibular oints. 12. Does the patient have any difficulty swallowing? oes the patient swallow normally or gulp? What hapns to the tongue when the patient swallows? Does it move normally, anteriorly, or laterally? Is there any vidence of tongue thrust or thumb sucking? For exJ.illple, the facial nerve (cranial nerve VII) and the trigeminal nerve (cranial nerve V), which control facial expression and mastication and contribute to speech, also control anterior lip seal. If lip seal is weakened, the teeth may move anteriorly, an action that would e accentuated in "tongue thrusters." The normal restmg position of the tongue is against the anterior palate Fig. 4 -11). It is the position in which one would place the tongue to make a "clicking" sound. 13. Are there any ear problems such as hearing loss, ringing in the ears, blocking of the ears, earache, or dizziness? Symptoms such as these may be caused by inner ear, cervical spine, or temporomandibular joint problems. r-

~ot,

r

14. Does the patient have any habitual head po tures? For example, holding the telephone between t ear and the shoulder compacts the temporomandibul joint on that side. Reading or listening to someo while leaning one hand against the jaw has the sam effect. 15. Has the patient noticed any voice change Changes may be caused by muscle spasm. 16. Does the patient have headaches? If so, wher Temporomandibular joint problems can refer pain the head. Is there any history of infection or swoll glands? 17. Does the patient ever feel dizzy or faint? 18. Has the patient ever worn a dental splint? If s when? For how long? 19. Has the patient ever been seen by a dentist? periodontist (a dentist who specializes in the study tissues around the teeth and diseases of these tissues An orthodontist (a dentist who specializes in corre tion and prevention of irregularities of the teeth)? A endodontist (a dentist who specializes in the treatme of diseases of the tooth pulp, root canal, and peliapic areas)? If so, why did the patient see the specialist, an what was done?

T

Observation

When assessing the temporomandibular joints, the e aminer must also assess the posture of the cervic spine and head. For example, it is necessary that t head be "balanced" on the cervical spine and be proper postural alignment. 1. Is the face symmetrical horizontally and vertical and are facial proportions normal (Fig. 4-12)? T

Figure 4-12

Facial symmetry. Look fot symmetr both vertically and horizontally. Also note the changes in symmetry occurring with no smile (A) and smile (B).

A

8

examiner should check the eyebrows, eyes, nose, ears, and corners of the mouth for symmetry on both horizontal and vertical planes. Horizontally, the face of an adult is divided into thirds (Fig. 4-13); this demonstrates normal vertical dimension. Usually the upper and lower teeth are used to measure vertical dimension. The hOl;zontal bipupital, otic, and occlusive lines should be parallel to each other (Fig. 4-14). A quick way to measure the vertical dimension is to measure

Figure 4-15 Hair line

-----H-....",."--:"":::'O'-"~___:ilH!l_----

1

"3

Bipupitalline

A quick measurement of vertical dimension. Normally, the distance from lateral edge of eye to corner of mouth equals the distance from nose to point of chin.

-----I'!~~iI1:Ir':rt~~~t-----

1

"3 Nose line

------T-~:.....::::~-,I------

1

"3 Chin line - - - - - - 1 - - " ' " - " " ' - - - - ' 1 - - - - - -

Figure 4-13 Divisions of the face (vertical dimension).

---ft?;L-411:4-j-4;l1:>-~I_---

Bipupital line

---'50% humeral head diameter). Miniaci Test for Posterior Subluxation. 122 The atient lies supine with the shoulder off the edge of the examining table. The examiner uses one hand to flex (70° to 90°), adduct, and medially rotate the arm while pushing the humerus posteriorly. The patient

Jerk Test. 104 The patient sits with the arm medially rotated and forward flexed to 90°. The examiner grasps the patient's elbow and axially loads the humerus in a proximal direction. While maintaining the axial loading, the examiner moves the arm horizontally (cross-flexion/horizontal adduction) across the body (Fig. 5- 55). A positive test for recurrent posterior instability is the production of a sudden jerk or clunk as the humeral head slides off (subluxes) the back of the glenoid (Fig. 5-56). When the arm is returned to the original 90° abduction position, a second jerk may be felt as the head reduces. Circumduction Test. 123 The patient is in the standing position. The examiner stands behind the patient grasping the patient's forearm with the hand. The examiner begins circumduction by extending the patient's arm while maintaining slight abduction. As the circumduction continues into elevation, the arm is brought "over the top" and into the flexed and adducted position. As the arm moves into fonvard flexion and adduction from above, it is vulnerable to posterior subluxation if the patient is unstable posteriorly. If the examiner palpates the posterior aspect of the patient's shoulder as the arm moves downward in forward flexion and adduction, the humeral head will be felt to sublux posteriorly in a positive test and the patient will say "that's what it feels like when it bothers me" (Fig. 5-57).

Tests for Inferior and Multidirectional Shoulder Instability It is believed that if a patient demonstrates inferior instability, multidirectional instability is also present. Therefore, the patient with inferior instability will also demonstrate anterior and/or posterior instability. The primary complaint of these patients is pain rather than instability with symptoms most commonly in midrange. Transient neurological symptoms may also be present. 124 Test for Inferior Shoulder Instability (Sulcus Sign).104,112 The patient stands with the arm by the side and shoulder muscles relaxed. The examiner grasps the patient's forearm below the elbow and pulls the arm distally (Fig. 5-58). The presence of a sulcus sign (Fig. 5-59; see Fig. 5-8B) may be indicative of

258

CHAPTER 5 • Shoulder

Figure 5-53 Posterior drawer test of the shoulder. (A) and (B) The test. (C) and (D) Superimposed view of bones involved in test. (E) and (F) Radiographic images of test. (From Gerber, C., and Il Ganz: Clinical assessment of instability of the shoulder. J. Bone Joint Surg. Br. 66:554, 1984.)

Figure 5-55 ure 5-54

Jerk test.

aci test for posterior subhL'-abral crank test. (A) Crank test in rting with lateral humeral rotation. B) Crank test in sitting with medial umeral rotation.

catching sensation is felt when the humeral head is felt, the test is positive for a labral tear (Bankart or SLAP lesion).

Tests for Scapular Stability In order for the muscles of the glenohumeral joint to work in a normal coordinated fashion, the scapula must be stabilized by its muscles to act as a firm base for the glenohumeral muscles. Thus, when doing these

270


Figure 5-77 Pain provocation test. (A) Test with forearm pronated. (B) Test with forearm supinated.

tests, the examiner is watching for movement patterns of the scapula as well as winging of the scapula. Lateral Scapular Slide Test. 50 ,159 This test is used to determine the stability of the scapula during glenohumeral movements. The patient sits or stands with the arm resting at the side. The examiner measures the distance from the base of the spine of the scapula to the spinous process of T2 or T3 (most common), from the inferior angle of the scapula to the spinous process of T7 - T9, or from T2 to the superior angle of

Figure 5-78 Compression-rotation test.

the scapula. The patient is then tested holding two l5 (Fig. 5 -79) or four 50 other positions: 45° abductio (hands on waist, thumbs posteriorly),50,159 90° abduc tion with medial rotation,50,1 59 120° abduction,50 an 150° abduction. 50 Davies and Dickoff-Hoffman 50 an Kibler 159 state that in each position the distance mea sured should not vary more than 1 to 1.5 cm (0.5 t 0.75 inch) from the original measure. However, ther may be increased distances above 90° as the scapul rotates during scapulohumeral rhythm. Minimal pro traction of the scapula should occur, however, durin full elevation through abduction. It therefore is impor tant to look for asymmetry of movement between lef and right sides, as well as the amount of movemen when determining scapular stability. The test may also be performed by loading the arm (providing resistance) at 45° and greater abductio (scapular load test) to see how the scapula stabilize under dynamic load. This load may be applied anteri orly, posteriorly, inferiorly, or superiorly to the arm (Fig. 5-80). Again, the scapula should not move mor than 1.5 cm (0.75 inch). Odom and associates l6o hav stated that the test has poor reliability for differentiat ing normal and pathological shoulders. However, load ing the scapula, either by the weight of the arm or b applying a load to the arm, gives the clinician an indi cation of the stabilizing ability of the scapular contro muscles and whether abnormal winging or abnorma movement patterns occur.

A

B

c Figure 5-79 Lateral scapular slide test. Examiner measures from spinous process to scapula at level of base of spine of scapula (see arrows in A). (A) Arms at side. (B) Arms abducted, hands on waist, thumbs back. (C) Arms abducted to 90°, thumbs down.

272


In the different positions, the examiner may test scapular and humeral stability by performing an ecce tric movement at the shoulder by pushing the a forward (eccentric hold test). One arm is tested a time. As the arm is pushed forward eccentrically, t examiner should watch the relative movement at t scapulothoracic joint (protraction) and the glenoh meral joint (horizontal adduction). Normally, sligh more movement (relatively) will occur at the glenoh meral joint. If instability due to muscle weakness exi at either joint, excessive movement will be seen at th joint relative to the other joint. In addition, the exa iner should watch for winging of the scapula, whi indicates scapular instability.

Figure 5-80 Scapular load test in 45° abduction.

B

Figure 5-81 Wall (A) and floor (B) pushup test. (C) Closed kinetic chain upper extremity stability test touching opposite hand.

C

apart. Patients assume the pushup position with hand on each marker. When the examiner says "g the subject moves one hand to touch the other returns it to the original position and then does same with the other hand, repeating the motions 15 seconds. The number of touches or crossover the alloted time is counted. The test is repeated th times and the average is the test score. This tes designed primarily for young active patients.

ure 5-82 ular retraction test. Examiner uses hands to stabilize clavicle and ula.

Wall Pushup Test. 53 ,161 The patient is in a standing ition, arms length from a wall. The patient is then ed to do a "wall pushup" 15 to 20 times (Fig. 5: . Any weakness of the scapular muscles or winging ill usually show up with 5 to 10 pushups. For onger or younger people, a normal pushup on the oar will show similar scapular changes, usually with s repetitions. Goldbeck and Davies 162 have taken this - t further in what they describe as a closed kinetic - all upper extremity stability test. In this test, two

Figure 5-83 - apular isometric pinch test. (A) -tart position. (B) "Pinch" pasion.

Scapular Retraction Test. 53 ,161,163 The patient i the standing position. The examiner, standing beh the patient, places the fingers of one hand over clavicle with the heel of the hand over the spine of scapula to stabilize the clavicle and scapula and to h the scapula retracted. The examiner's other hand c presses the scapula against the chest wall (Fig. 5 Holding the scapula in this position provides a stable base for the rotator cuff muscles and often r tor cuff strength (if tested by a second examiner) improve. The test may also be positive in patients w a positive relocation test. If scapular retraction creases the pain, when the relocation test is perform it indicates that the weak scapular stabilizers must addressed in the treatment. 163

Scapular Isometric Pinch or Squeeze Test. 53 patient is in a standing position and is asked to acti "pinch" or retract the scapulae together as hard possible and to hold the position for as long as po ble (Fig. 5-83). Normally, an individual can hold

I

274


Figure 5-84

Figure 5-86

Scapular assistance test.

Acromioclavicular crossover, crossbody, or horizontal adduction te

contractions for 15 to 20 seconds with no burning pain or obvious muscle weakness. If burning pain occurs in less than 15 seconds, the scapular retractors are weak. When doing the test, the examiner must watch the patient carefully. Subconsciously, many patients will relax the contraction a slight amount which is barely noticeable but allows the patient to hold the contraction in a "comfort zone" for longer periods with no burning.

over the clavicle with the heel of the hand over spine of the scapula. This stabilizes the clavicle a scapula and holds the scapula retracted. The exa iner's other hand holds the inferior angle of the sc ula. As the patient actively abducts or forward fle the arm, the examiner stabilizes and pushes the infer medial border of the scapula up and laterally wh keeping the scapula retracted. Decreased pain wo

Scapular Assistance Test. 53 ,161,163 This test is used to evaluate scapular and acromial involvement in patients with impingement symptoms. The patient is in a standing position and the examiner stands behind the patient. The examiner places the fingers of one hand

t

Figure 5-85

Figure 5-87

Acromioclavicular shear test.

Ellman's compression-rotation test for glenohumeral arthritis.

Figure 5-88 Crank test used to test glenohumeral ligaments. (A) Arm by the side-superior glenohumeral ligament tested. (B) 45°-60° abduc· tion-middle glenohumeral ligament tested. (C) Over 90° abduction-inferior glenohumeral ligament tested.

Acromioclavicular Crossover, Crossbody, or Hor izontal Adduction Test. The patient stands an reaches the hand across to the opposite shoulder. Th test may also be performed passively by the examine With the patient in a sitting position, the examin passively forward flexes the arm to 90° and then hor zontally adducts the arm as far as possible (Fig. 5 86).25,133 If localized pain is felt over the acromiocla vicular joint, the test is positive.I64-166 Localized pai in the sternoclavicular joint would indicate that joint at fault. e a positive test and would indicate the scapular con01 muscles are weak as the assistance by the examiner lITlulates the activity of serratus anterior and lower ::rapezius during elevation (Fig. 5-84).

Other Shoulder Joint Tests Acromioclavicular Shear Test. 114 With the patient m the sitting position, the examiner cups his or her hands over the deltoid muscle, with one hand on the -Iavicle and one hand on the spine of the scapula. The examiner then squeezes the heels of the hands together (Fig. 5-85). A positive test is indicated by pain or abnormal movement at the acromioclavicular joint and is indicative of acromioclavicular joint pathology.

Ellman's Compression Rotation Test. 167 ,168 Th patient lies on the unaffected side. The examiner com presses the humeral head into the glenoid while th patient rotates the shoulder medially and laterally. the patient's symptoms are reproduced, glenohumer arthritis is suspected (Fig. 5 - 87).

Tests for Ligament Pathology

Crank Test. (Also see under "Tests for Anterio Instability.") The crank test may also be used as a te for the different glenohumeral ligaments (Fig. 5 88). For example, when the crank test is done with th arm by the side, primarily the superior glenohumer ligament and capsule are being tested. At 45° to 60

276


Figure 5-89

Posterior inferior ligament te Anterior view. (B) Posterior v

abduction, the middle glenohumeral ligament, the coracohumeral ligament, the inferior glenohumeral ligament (anterior band), and anterior capsule are being tested. Over 90° abduction, the inferior glenohumeral ligament and anterior capsule are being tested (see Table 5 -1) .1 69 ,170 Posterior Inferior Glenohumeral Ligament Test. lSl Just as the crank test may be used to test the superior glenohumeral ligament, middle glenohumeral ligament, and the anterior portion of the inferior glenohumeral ligament, the posterior inferior glenohumeral test may be used to test the posterior portion of the inferior glenohumeral ligament. The patient sits while the examiner forward flexes the arm to between 80° and 90° and then horizontally adducts the arm 40° with medial rotation (Fig. 5-89). While doing the movement, the examiner palpates the posteroinferior region of the glenoid. If the humerus protrudes or

pain is felt in the area, the test is considered po and indicates a lesion of the posterior portion o inferior glenohumeral ligament. If movement horizontal adduction) is restricted, it may also in a tight posterior capsule.

Coracoclavicular Ligament Test. The integr the conoid portion of the coracoclavicular lig may be tested by placing the patient in a side position on the unaffected side with the hand r against the lower back. The examiner stabilize clavicle while pulling the inferior angle of the sc away from the chest wall. The trapezoid portion ligament may be tested from the same position examiner stabilizes the clavicle and pulls the m border of the scapula away from the chest wall 5-90). Pain in either case in the area of the lig (anteriorly under the clavicle between the outer third and inner two-thirds) constitutes a positive t

Figure 5-90 Coracoclavicular ligament test. (A) Conoid portion. (B) Trapezoid portion.

• Speed's test (biceps) • Vergason's test (biceps) • Empty can test (supraspinatus) • Lift-off test (subscapularis) • Lag or "spring back" tests (subscapularis-medial rotation; infraspinatus-lateral rotation) • Trapezius weakness (3 positions) • Serratus anterior weakness • Pectoralis major and minor tightness

Figure 5-91 Speed's test (biceps or straight-arm test).

ests for Muscle or Tendon Pathology Speed's Test (Biceps or Straight-Ann Test). The aminer resists shoulder forward flexion by the patient hile the patient's forearm is first supinated, then proted, and the elbow is completely extended. The test ay also be performed by forward flexing the patient's ~ to 90° and then asking the patient to resist an - entric movement into extension first with the arm pinated, then pronated (Fig. 5-91). A positive test -its increased tenderness in the bicipital groove espeJ1ly with the arm supinated and is indicative of bicipiparatenonitis or tendinosis.'7 Speed's test is more ective than Yergason's test because the bone moves 'er more of the tendon during the Speed's test. It been reported 158 that this test may cause pain and ill therefore be positive if a SLAP lesion is present. If rofound weakness is found on resisted supination, a vere second- or third-degree (rupture) strain of the tal biceps should be suspected. l7I

only a small part of the tendon during the test because biceps tendon pain tends to occur with tion or palpation rather than with tension.

Ludington's Test. 173 The patient clasps both on top of or behind the head, allowing the inter ing fingers to support the weight of the upper (Fig. 5-93). This action allows maximum relaxati the biceps tendon in its resting position. The p then alternately contracts and relaxes the biceps cles. While the patient does the contractions and ations, the examiner palpates the biceps tendon, w will be felt on the uninvolved side but not on affected side if the test result is positive. A po

Yergason's Test. This test is primarily designed to - t the ability of the transverse humeral ligament to old the biceps tendon in the bicipital groove. With - e patient's elbow flexed to 90° and stabilized against - e thorax and with the forearm pronated, the examner resists supination while the patient also laterally tates the arm against resistance 172 (Fig. 5-92). If the xaminer palpates the biceps tendon in the bicipital ;roove during the supination and lateral rotation ovement, the tendon will be felt to "pop out" of the groove if the transverse humeral ligament is torn. Tenerness in the bicipital groove alone without the dislo-ation may be indicative of bicipital paratenonitis/tendinosis.1 7 This test is not as effective as Speed's test "hen testing the biceps tendon, because the bicipital groove moves only slightly over the tendon affecting

---

-----------------

---

278


Figure 5-93 Ludington's test.

result indicates rupture of the long head of biceps tendon. Gilchrest's Sign.1l4,174 While standing, the patient lifts a 2- to 3-kg (5- to 7-lb) weight over the head. The arm is laterally rotated fully and lowered to the side in the coronal plane. A positive test is indicated by discomfort or pain in the bicipital groove. A positive test indicates bicipital paratenonitis or tendinosis.1 7 In some cases, an audible snap or pain may be felt at between 90° and 100° abduction. Lippman's Test. 175 The patient sits or stands while the examiner holds the arm flexed to 90° with one hand. With the other hand, the examiner palpates the biceps tendon 7 to 8 cm (2.5 to 3 inches) below the glenohumeral joint and moves the biceps tendon from side to side in the bicipital groove. A sharp pain is a positive test and indicates bicipital paratenonitis or tendinosisY

Figure 5-94 Supraspinatus test.

Reuter's Sign.174 Normally, if elbow flexion sisted when the arm is pronated, some supinatio curs as the biceps attempts to help the brachialis cle flex the elbow. This supination movement is Reuter's sign. If it is absent, the distal biceps te has been disrupted.

Supraspinatus ("Empty Can" or Jobe) Te The patient's arm is abducted to 90° with neutral rotation, and resistance to abduction is provide

Figure 5-95 Drop-arm test. (A) The patient abducts the arm to 90°. (B) The patient tries to lower the arm slowly and is unable to do so; instead, the arm drops to his side. Examiner's hand illustrates the start position.

ure 5-96 . -off" sign. (A) Start position. (B) "Lift off" position. (C) Resistance to "lift off" provided by er. Examiner tests strength of subscapularis and watches positioning of scapula.

e examiner. The shoulder is then medially rotated d angled forward 30° (empty can position) so that e patient's thumbs point toward the floor (Fig. 5in the plane of the scapula. Others J77 have said at testing the arm with the thumb up ("full can") is t for maximum contraction of supraspinatus. Resisce to abduction is again given while the examiner ks for weakness or pain, reflecting a positive test - -ult. A positive test result indicates a tear of the praspinatus tendon or muscle, or neuropathy of the prascapular nerve. Drop-Arm (Codman's) Test. The examiner ab. cts the patient's shoulder to 90° and then asks the atient to slowly lower the arm to the side in the same - of movement (Fig. 5-95). A positive test is indi-ated if the patient is unable to return the arm to the de slowly or has severe pain when attempting to do . A positive result indicates a tear in the rotator cuff - mplex. J78 A complete tear (3° strain) of the rotator -uff is more common in older patients (50+ years). In ounger people, a partial tear (1° or 2° strain) is more -ely to occur when the patient is abducting the arm and a strong downward, eccentric load is applied to - e arm. Abrasion Sign.30 The patient sits and abducts the arm to 90° with the elbow flexed to 90°. The patient

then medially and laterally rotates the arm at shoulder. Normally, there are no signs and symptom If crepitus occurs, it is a sign that the rotator c tendons are frayed and are abrading against the un surfaces of the acromion process and the coracoac mial ligament.

Lift-off SignY7,179-18J The patient stands a places the dorsum of the hand on the back pocket against the mid lumbar spine. Great subscapularis tivity is seen with the second position (Fig. 5-96).1 The patient then lifts the hand away from the back. inability to do so indicates a lesion of the subscapul muscle. Abnormal motion in the scapula during test may indicate scapular instability. If the patien able to take the hand away from the back, the exa iner should apply a load pushing the hand toward back to test the strength of the subscapularis and test how the scapula acts under dynamic loading. W a torn subscapularis tendon, passive (and active) late rotation will increase. 180 If the patient's hand is passively medially rotated far as possible and the patient is asked to hold position, it will be found that the hand moves tow the back (subscapularis or medial rotation "spr back" or lag test) because subscapularis cannot h the position due to weakness or pain. This test is a

280


Figure 5-97 Subscapularis "spring back" or lag test. (A) Start position. (B) Patient is unable to hold the start position and hand "springs back" toward the lower back.

called the modified lift off test (Fig. 5-97).180,183 A small lag between maximum passive medial rotation and active medial rotation implies a partial tear (1°, 2°) of subscapularis. 179 This modified test is reported to be more accurate in diagnosing rotator cuff tear. 184 The test may also be used to test the rhomboids. Medial border winging of the scapula during the test may indicate that the rhomboids are affected. Stefko et aP85 reported that maximum isolation of the subscapularis was achieved by placing the hand against the posteroinferior border of the scapula (maximum medial rota-

Figure 5-98 Abdominal compression test.

tion test) and then attempting the lift off. In other positions for lift off, teres major, latissimus do posterior deltoid, or rhomboids may compensate f weak subscapularis.

Abdominal Compression (Belly-Press) Test. 17 This test is also used to test subscapularis muscle, e cially if the patient cannot medially rotate the shou enough to take it behind the back. The patient is standing position. The examiner places a hand on abdomen so that the examiner can feel how m pressure the patient is applying to the abdomen. patient places his or her hand of the shoulder b tested on the examiner's hand and pushes the han hard as he or she can into the stomach (medial sh der rotation). While pushing the hand into the ab men, the patient attempts to bring the elbow forw to the scapular plane causing greater medially shou rotation. If the patient is unable to maintain the p sure on the examiner's hand while moving the el forward or extends the shoulder, the test is positive a tear of the subscapularis muscle (Fig. 5-98).

Lateral Rotation Lag Sign (Infraspinatus "Spr Back" Test).85 The patient is seated or in stand position with the arm by the side and the elbow fle to 90°. The examiner passively abducts the arm to in the scapular plane, laterally rotates the shoulde end range (some authors say 45°)187 and asks the tient to hold it. For a positive test, the patient can hold the position and the hand "springs back" an orly towards midline indicating infraspinatus and t minor cannot hold the position due to weakness

rotation will have increased on the affected side (Fi 5-99). If the test is performed with the arm in 20° abdu tion or by the side in the scapular plane with th elbow at 90° and the shoulder laterally rotated, th examiner then takes the arm into maximum lateral ro tation and asks the patient to hold the position (Fi 5 -1 OOA). If the supraspinatus and infraspinatus a torn, the arm will medially rotate and "spring back anteriorly indicating a positive test (Fig. 5-100B This test has also been called the ERLS test (extern [sic. lateral] rotation lag sign). The anterior moveme of the arm has also been called the drop sign becau the arm "drops" back to 0° lateral rotation. 184 If th patient is able to hold the position, the strength infraspinatus can be graded as 3 or greater dependin on the resistance to the examiner's medially rotate force. 187

ure 5-99 -era! rotation lag test to test the teres minor and infraspinatus. is abducted 90°. Note how hand "springs forward" when red by examiner.

=

Hornblower's (Signe de Clairon) Sign.85,183,1 This test is designed to test the strength of teres m nor. The patient is in a standing position. The exam iner elevates the patient's arm to 90° in the scapul plane. The examiner then flexes the elbow to 90° an the patient is asked to laterally rotate the should against resistance. A positive test is indicated when th patient is unable to laterally rotate the arm. McCIusky85 offers a second way to do the test. Th patient is standing with the arms by the side and the is asked to bring the hands to the mouth (Fig. 5 lOlA). With a massive posterior rotator cuff tear, th

Figure 5-100 External rotation lag sign or drop test. (A) Start position. (B) Position in positive test.

282


A

B

Figure 5-101 Hornblower's (Signe de Clairon) sign. (A) Normal result. (B) Positive test. Patient must abduct tbe arm to bring tbe hand to tbe moutb.

Figure 5-103 Teres minor test.

Figure 5-102 Infraspinatus test.

patient is unable to do this without abducting the arm first (Fig. 5-101B). This abduction with hands to the mouth is called hornblower's sign. Infraspinatus Test. The patient stands with the arm at the side with the elbow at 90° and the humerus medially rotated to 45°. The examiner then applies a

medial rotation force that the patient resists. Pain o the inability to resist medial rotation indicates a pos tive test for an infraspinatus strain (Fig. 5 -102).

Teres Minor Test. The patient lies prone and plac the hand on the opposite posterior iliac crest. Th patient is then asked to extend and adduct the med ally rotated arm against resistance. Pain and/or weak ness indicates a positive test for teres minor strain (Fi 5-103).

Trapezius Weakness. 189 The patient is seated an places the hands together over the head. The examin

gure 5-104 ring for trapezius weakness. All portions of triceps. (B) ',per trapezius. (C) Middle trazius. (D) Lower trapezius.

ands behind the patient and pushes the elbows forard. Normally the three parts of the trapezius will asily be seen to contract to stabilize the scapula (Fig. - -104A). Upper trapezius can be separately tested by 1evating the shoulder with the arm slightly abducted r to resisted shoulder abduction and head side flexion Fig. 5_104B).190,191 If the shoulder is elevated with :he arm by the side, levator scapulae and rhomboids Me more likely to be involved as well. Middle trapezius -an be tested with the patient in a prone position with me arm abducted to 90° and laterally rotated. The test mvolves the examiner resisting horizontal extension of the arm watching for retraction of the scapula, which hould normally occur (Fig. 5 -1 04C). 190,191 If scapular protraction occurs, the middle fibers of trapezius are vealc. To test the lower trapezius, the patient is in prone lying with arm abducted to 120° and the shoulder laterally rotated. The examiner applies resistance to diagonal extension and watches for scapular retraction that should normally occur (Fig. 5-104D). If scapular protraction occurs, the lower trapezius is weak. 190 If the scapula is elevated more than normal it may indi-

cate a tight trapezius or the presence of cervical to collis. Serratus Anterior Weakness. 189 The patient is i

standing position and forward flexes the arm to 9 The examiner applies a backward force to the arm ( 5 -1 05). If serratus anterior is weak or paralyzed, medial border of the scapula will wing (classic wi ing). The patient will also have difficulty abducting forward flexing the arm above 90° with a weak serra anterior but it still may be possible with lower tra zius compensation. 34 A similar finding may be acco plished by doing a wall or floor pushup.

Rhomboid WeaknesS. 85 ,189 The patient is in a pr lying position or sitting with the test arm behind body so the hand is on the opposite side (oppo back pocket). The examiner places the index fin along and under the medial border of the scap while asking the patient to push the shoulder forw slightly against resistance to relax the trapezius (F 5-106A). The patient then is asked to raise the fo arm and hand away from the body. If the rhombo

284


normal. If the biceps is tight, full elbow flexion w not occur and the end feel will be a muscular tis stretch (Fig. 5-108).192

Triceps Tightness. The patient is in a sltUng po tion. The arm is fully elevated through forward flex and lateral rotation. While stabilizing the humerus, examiner flexes the elbow (see Fig. 6-11B).I92 N mally, the end feel would be soft tissue approximati If the triceps is tight, elbow flexion will be limited a the end feel will be muscular tissue stretch.

Figure 5-105 Testing for serratus anterior weakness. Punch out test: examiner applies a backward force.

are normal, the thumb is pushed away from under the scapula (Fig. 5-106B). Latissimus Dorsi Weakness. 123 The patient is in a standing position with the arms elevated in the plane of the scapula to 160°. Against resistance of the examiner, the patient is asked to medially rotate and extend the arm downward as if climbing a ladder (Fig. 5107). Biceps Tightness. The patient lies supine with the shoulder in extension over the edge of the examining table with the elbow flexed and the forearm supinated. The examiner then extends the elbow, which would normally have a bone-to-bone end feel if the biceps is

Figure 5-106 Testing for rhomboid weakness. (A) Start position. (B) Test position.

Pectoralis Major Contracture Test. The pati lies supine and clasps the hands together behind head. The arms are then lowered until the elbo touch the examining table (Fig. 5-109A). A posit test occurs if the elbows do not reach the table a indicates a tight pectoralis major muscle.

Pectoralis Minor Tightness. Pectoralis minor fu tions along with the rhomboids and levator scapulae stabilize the scapula during arm extension. Tightn of the pectoralis minor can lead to increased scapu protraction and tilting of the inferior angle of the sc ula posteriorly. Tightness of the pectoralis minor be tested by having the patient in a supine lying po tion. The examiner places the heel of the hand o the coracoid process and pushes it toward the exam ing table (Fig. 5-109B). Normally, the poster movement occurs with no discomfort to the pati and the scapula lies flat against the table. However there is tightness (muscle tissue stretch) over the p toralis minor muscle during the posterior moveme the test would be considered positive.

Tightness of Latissimus Dorsi, Pectoralis Ma and Pectoralis Minor. The patient is placed in a

Figure 5-108 Testing for biceps tightness.

ure 5-107 .ong for latissimus dorsi weakness.

gure 5-109 ting for tightness of (A) pectoralis major and (B) pectoralis miExaminer is testing end feel. Note position of examiner's hand A) humems and (B) coracoid process.

me lying posluon and is asked to fully elevate the arms through forward flexion. If the three muscles ave normal length, the arms will extend to rest gainst the examining table. If the scapula does not lie at against the table, it indicates pectoralis minor, pecoralis major and/or latissimus dorsi is tight (the scapula remains protracted) (Fig. 5-110).190

Figure 5-110 Testing for tightness of latissimus dorsi, pectoralis major, and pectoralis minor as a group.

286


Common Tests for Thoracic Outlet Syndrome • Upper limb tension tests

• Roos test • Wright test • Costoclavicular syndrome test

Tests for Neurological Function Upper Limb Tension (Brachial Plexus Tension) Test. 193 This test is the upper limb equivalent of the straight leg raising test of the lower limb. It is used when the patient has presented with upper limb radicular signs or peripheral nerve symptoms. The patient is positioned to stress the neurological tissue entering the arm. The patient lies supine. The test may be performed by placing the joints of the upper limb in different positions to stress each of the neurological tissues differently.194 There are, in effect, four upper limb tension tests (ULTI 1 to 4) (see Table 3-7 and Fig. 3-25).195 The key to performing the tests correctly is to ensure the shoulder is held in depression. If it is allowed to elevate, tension is taken off the neurological structures. Depending on the history, the examiner picks the ULTI that will stress the appropriate neurological tissue. Pain in the form of tingling or a stretch or ache in the cubital fossa indicates stretching of the dura mater in the cervical spine. The available range of passive movement at the elbow, when compared with the normal side, can give an indication of the restriction. Lateral or side flexion of the cervical spine to the opposite side can enhance the effect. If full ROM is not available in the shoulder, the test can still be performed by taking the shoulder to the point just short of pain in abduction and lateral rotation and performing the other maneuvers of the arm or by passively side flexing the cervical spine. The upper limb tension tests put tension on the upper limb neurological tissues even in normal individuals. Therefore, reproduction of the patient's symptoms, rather than stretching, constitutes a positive sign. This finding indicates the neurological tissue is being stressed but it does not tell the examiner where or why it is being stressed.

tion of venous flow may be seen individually. For reason, a diagnosis of thoracic outlet syndrome is u ally one of exclusion in which all other causes h been eliminated.196-198 In fact, neurogenic signs rare in thoracic outlet syndrome, and there is p correlation between the vascular signs of the condi and neurological involvement. Thoracic outlet t must not only decrease the pulse, they must also produce the patient's symptoms to be considered p tive. 199 The tests do not show high reliability. With thoracic outlet tests that involve taking pulse, the examiner must find the pulse before p tioning the patient's arm or cervical spine. Because pulse may be diminished even in a "normal" indiv ual, it is more important to look for the reproduct of symptoms than for diminution of the pulse. Un stated, the duration of these provocative tests sho be no more than one to two minutes. 197

Roos Test (EAST).200 The patient stands and ducts the arms to 90°, laterally rotates the shoul and flexes the elbows to 90° so that the elbows slightly behind the frontal plane. The patient t opens and closes the hands slowly for 3 minutes (F 5 -111). If the patient is unable to keep the arms the starting position for 3 minutes or suffers ische pain, heaviness or profound weakness of the arm,

Tinel's Sign (at the Shoulder). The area of the brachial plexus above the clavicle in the area of the scalene triangle is tapped. A positive sign is indicated by a tingling sensation in one or more of the nerve roots.

Tests for Thoracic Outlet Syndrome Thoracic outlet syndromes may combine neurological and vascular signs, or the signs and symptoms of neurological deficit, restriction of arterial flow, or restric-

Figure 5-111 Roos test.

Igure 5-112 'right test (A) and modified 'right test or maneuver (Allen UWleuver) (B).

urnbness and tingling of the hand during the 3 mintes, the test is considered positive for thoracic outlet ndrome on the affected side. Minor fatigue and disess are considered negative tests. The test is someillIles called the positive abduction and external rotation (AER) position test, the "hands-up" test, or - e elevated arm stress test (EAST).2oo-203 Wright Test or Maneuver. Wright 204 advocated -hyperabducting" the arm so that the hand is brought ver the head with the elbow and arm in the coronal lane with the shoulder laterally rotated (Fig. 51l2A). He advocated doing the test in the sitting and then the supine positions. Having the patient take a reath or rotating or extending the head and neck may ave an additional effect. The pulse is palpated for differences. This test is used to detect compression in the costoclavicular space and is similar to the costo-lavicular syndrome test described below. This test has been modified by examiners over time o that it has come to be described as follows. The examiner flexes the patient's elbow to 90° while the houlder is extended horizontally and rotated laterally Fig. 5 -1l2B). The patient then rotates the head away from the test side. The examiner palpates the radial pulse, which becomes absent (disappears) when the head is rotated away from the test side. The test done in this fashion has also been called the Allen maneuver. The pulse disappearance indicates a positive test result for thoracic outlet syndrome. Costoclavicular Syndrome (Military Brace) Test. The examiner palpates the radial pulse and then draws the patient's shoulder down and back (Fig. 5-113). A positive test is indicated by an absence of the pulse and

implies possible thoracic outlet syndrome (costoclavi cular syndrome). This test is particularly effective i patients who complain of symptoms while wearing backpack or heavy coat.

Provocative Elevation Test. 104 The patient elevate both arms above the horizontal and is asked to rapidl open and close the hands 15 times. If fatigue, cramp ing, or tingling occurs during the test, the test is posi tive for vascular insufficiency and thoracic outlet syn drome. This test is a modification of the Roos test.

Figure 5-113 Costoclavicular syndrome test.

288


Figure 5-114

Shoulder girdle passive elevation. (A) Start position. (B) Relief position.

A

Shoulder Girdle Passive Elevation. lOs This test is used on patients who already present with symptoms. The patient sits and the examiner grasps the patient's arms from behind and passively elevates the shoulder girdle up and forward into full elevation (a passive bilateral shoulder shrug), and the position is held for 30 or more seconds (Fig. 5 -114). Arterial relief is evidenced by stronger pulse, skin color change (more pink), and increased hand temperature. Venous relief is shown by decreased cyanosis and venous engorgement. Neurological signs go from numbness to pins and needles or tingling as well as some pain as the ischemia to

the nerve is released. This is referred to as a releas phenomenon.

Adson Maneuver. 2os This test is probably one o the most common methods of testing for thoracic out let syndrome reported in the literature. The examine locates the radial pulse. The patient's head is rotate to face the test shoulder (Fig. 5-115). The patien then extends the head while the examiner laterally ro tates and extends the patient's shoulder. The patient instructed to take a deep breath and hold it. A disap pearance of the pulse indicates a positive test.

terns of the nerve roots (Fig. 5 -118) as well as th cutaneous distribution of the peripheral nerves (Fig 5-119). Dermatomes vary from person to person, s the diagrams are estimations only. A scanning test fo altered sensation is performed by running the relaxe hands and fingers over the neck, shoulders, and ante rior and posterior chest area. Any difference in sensa tion between the two sides should be noted. Thes differences can be mapped more exactly using a pin wheel, a pin, a brush, and/or cotton batting. In thi way, the examiner can use sensation to help differenti ate between a peripheral nerve lesion and a nerve roo lesion referred from the cervical spine. True shoulder pain rarely extends below the elbow Pain in the acromioclavicular or sternoclavicular join tends to be localized to the affected joint and usuall does not spread or radiate. Pain can be referred to th shoulder and surrounding tissues from many struc tures,206 including the cervical spine, elbow, lungs

igure 5-117 .ositioning to test the reflexes around the shoulder. (A) Biceps. (B) :nceps. (C) Pectoralis major.

Halstead Maneuver. The examiner finds the radial pulse and applies a downward traction on the test extremity while the patient's neck is hyperextended and the head is rotated to the opposite side (Fig. 5-116). Absence or disappearance of a pulse indicates a positive test for thoracic outlet syndrome.

Reflexes and Cutaneous Distribution The reflexes in the shoulder region that are often assessed include the pectoralis major, clavicular portion C5 - C6), sternocostal portion (C7 - C8 and Tl), the biceps (C5-C6), and the triceps (C7-C8) (Fig. 5117).

Figure 5-118 Dermatome pattern of the shoulder. Dermatomes on one side only are illustrated.

290


- 4 - - Axillary nerve (partial loss) I\'.:::::jq-- Posterior brachial cutaneous nerve Lower lateral brachial cutaneous nerve

-+--+--+--Total sensory loss of axillary nerve

Figure 5-119 Cutaneous distribution of peripheral nerves around the shoulder.

heart, diaphragm, gallbladder, and spleen (Fig. 5 -120; Table 5-15).

Peripheral Nerve Injuries About the Shoulder Axillary (Circumflex) Nerve (C5-C6). The axillary nerve is the most commonly injured nerve in the shoulder, and the most common cause of injury is anterior dislocation of the shoulder or fracture of the neck of the humerus. 207 ,2o8 The nerve injury may occur during the dislocation itself or during the reduction. Other traumatic events (e.g., fracture, bullet, or stab wounds) or brachial plexus injuries, compression (e.g., crutches), or shoulder surgery also may affect the axillary nerve. Motor loss (see Tables 5-5 and 5-10) includes an inability to abduct the arm (deltoid), although the patient may attempt to laterally rotate the arm and use the long head of biceps to abduct the arm (trick movement). There is some weakness of lateral rotation owing to the loss of teres minor. The patient may attempt to use scapular movement (i.e., trapezius or serratus anterior) to compensate for the muscle loss (trick movement). Atrophy of the deltoid leads to loss of the lateral roundness (flattening) of the shoulder. Sensory loss is over the deltoid, with the main loss being a small, 2- to 3-cm (I-inch) circular area at the deltoid insertion (see Fig. 5 - 5).

Suprascapular Nerve (C5-C6). The suprascapu nerve may be injured by a fall on the posterior sho der, stretching, repeated microtrauma, or fracture the scapula. Commonly, the nerve is injured as passes through the suprascapular notch under transverse scapular (suprascapular) ligament or as winds around the spine of the scapula33 ,209-211 (Fig. 121). Often, it is hard to distinguish from rotator c syndrome, so the history and mechanism of injury come important for differential diagnosis. Most co monly, the condition is seen in people who work w their arms overhead or in activities involving cock and following through (e.g., pitching).31,212 Signs and symptoms include persistent rear shoul pain and paralysis of the supraspinatus (suprascapu notch) and infraspinatus (suprascapular notch a spine of scapula), leading to decreased strength of duction (supraspinatus) and lateral rotation (infraspi tus) of the shoulder. Wasting may also be evident the muscles over the scapula.

Musculocutaneous Nerve (C5-C6). This nerve not commonly injured, although it may be injured trauma (e.g., humeral dislocation or fracture) or conjunction with injury to the brachial plexus or ad cent axillary artery. Injury to this nerve (see Tables 5 and 5 -1 0) results primarily in loss of elbow flex (biceps and brachialis), shoulder forward flexion ( ceps and coracobrachialis), and decreased supinat strength (biceps). In addition, injury to its sens branch, the antebrachial cutaneous nerve, leads to tered sensation in the anterolateral aspect of the fo

~

m \j)

sPleen

Gallbladder

Figure 5-120 Structures referring pain to the shoulder.

I

houlder Muscles and Referral of Pain Muscle

Referral Pattern

_e\'ator capulae

Over muscle to posterior shoulder and along medial border of scapula

:A.tissimus dorsi

Interior angle of scapula up to posterior and anterior shoulder into posterior arm; may refer to area above iliac crest

omboids

Medial border of scapula

praspinatus

Over shoulder cap and above spine of scapula; sometimes down lateral aspect of arm to proximal forearm

:nfraspinatus

eres minor - bscapularis

~eres

major

eltoid - oracobrachialis

Anterolateral shoulder and medial border of scapula; may refer down lateral aspect of arm

Supraspinatus ----,'+:

li~~~~~\\\W~~~1H'J.M--

Biceps muscle Brachial artery

'==:"-~Wr~~~~~~~[~l--Radial

recurrent artery ..........--,:~~,..,!#.~f4---- Arcade

of Frohse

Figure 6-30 Canal or arcade of Frohse.

with this type of injury, and even it may show some weakness. The major branch of the radial nerve in the forearm is the posterior interosseous nerve, which is given of in front of the lateral epicondyle of the humerus. 25 ,38 This branch may be compressed as it passes between the two heads of the supinator in the arcade or cana of Frohse, a fibrous arch in the supinator muscle occurring in 30% of the population (Fig. 6-30). Compression leads to functional involvement of the forearm extensor muscles (see Table 6-2) and functional wris drop, so the patient has difficulty or is unable to stabilize the wrist for proper hand function. Diagnosis o this condition is often delayed because there is no sensory deficit. This compression zone is one of five sites in the tunnel through which the radial nerve passes. The nerve may also be compressed at the entrance to the tunnel anterior to the head of the radius near where the nerve supplies brachioradialis and extensor carpi radialis longus, between the ulnar half o the tendon of extensor carpi radialis brevis and its fascia, and at the distal border of supinator. 39 ,4o This condition, sometimes called radial tunnel syndrome, may mimic tennis elbOW. 19 ,39,41-44 If the patient has a persistent form of tennis elbow, a possible nerve lesion or cervical problem should be considered. A third area of pathology is compression of the superficial branch of the radial nerve as it passes under the tendon of the brachioradialis. This branch is sensory only, and the patient complains primarily of nocturnal pain along the dorsum of the wrist, thumb, and web space. The compression may be caused by trauma a tight cast, or any swelling in the area. The condition is referred to as cheiralgia paresthetica or Wartenberg's disease. 33

342

CHAPTER 6 • Elbow

Joint Play Movements of the Elbow Complex • Radial deviation of the ulna and radius on the humerus • Ulnar deviation of the ulna and radius on the humerus • Distraction of the olecranon from the humerus in 90° of flexion • Anteroposterior glide of the radius on the humerus

Joint Play Movements When examining the joint play movements (Fig. 631), the examiner must compare the injured side with the normal side. Radial and ulnar deviations of the ulna and radius on the humerus are performed in a fashion similar to those in the collateral ligament tests but with less elbow flexion. The examiner stabilizes the patient's el-

bow by holding the patient's humerus firmly an places the other hand above the patient's wrist, a ducting and adducting the forearm (see Fig. 6-31A The patient's elbow is almost straight (extended) du ing the movement, and the end feel should be bon to-bone. To distract the olecranon from the humerus, th examiner flexes the patient's elbow to 90°. Wrappin both hands around the patient's forearm close to th elbow, the examiner then applies a distractive force the elbow, ensuring that no torque is applied (see Fi 6-31B). If the patient has a sore shoulder, count force should be applied with one hand around th humerus. To test anteroposterior glide of the radius on th humerus, the examiner stabilizes the patient's forearm The patient's arm is held between the examiner's bod and arm. The examiner places the thumb of his or h hand over the anterior radial head while the flexe index finger is over the posterior radial head. The e aminer then pushes the radial head posteriorly with th

Figure 6-31

Joint play movements of the elbow complex. (A) Radial and ulnar deviation of the ulna on the humerus. (B) Distraction of the olecranon process from the humerus. (C) Anteroposterior movemen of the radius.

ure 6-32 t play of the head of the radius (method 2). Anteroposterior (A) and posteroanterior (B) glide of radius.

- umb and anteriorly with the index finger (see Fig. -31C). Commonly, posterior movement is easier to tain, with anterior movement, in normals, being the ~e ult of the radial head returning to its normal posion with a tissue stretch end feel. This movement ust be performed with care because it can be very c ainful as a result of pinching of the skin between the ~xaminer's digits and the bone. In addition, pain may e ult from the force being applied even in the normal .urn, so both sides must be compared. The anterior and posterior glide of the radius may e tested in a slightly different way as well. To do mteroposterior glide of the head of the radius, the ~atient is placed in supine with the arm by the side. The examiner stands beside the patient, facing the pa·ent's head, and holds the patient's arm slightly flexed y holding the hand between the examiner's thorax md elbow. The examiner places the thumbs over the ead of the radius and carefully applies an anteroposterior pressure to the head of the radius feeling the amount of movement and end feel. To do posteroanterior glide, the patient is in supine lying with the arm at the side and the hand resting on the stomach. The examiner places the thumbs over the posterior aspect of the radial head and carefully applies a posteroanterior pressure (Fig. 6 - 32).

Palpation

With the patient's arm relaxed, the examiner begin palpation on the anterior aspect of the elbow an moves to the medial aspect, the lateral aspect, an finally the posterior aspect (Fig. 6-33). The patien may sit or lie supine, whichever is more comfortable The examiner is looking for any tenderness, abnormal ity, change in temperature or in texture of the tissues or abnormal "bumps." As with all palpation, the in jured side must be compared with the normal or unin jured side.

Anterior Aspect

Cubital Fossa. The fossa is bound by the pronato teres muscle medially, the brachioradialis muscle later ally, and an imaginary line joining the two epicondyle superiorly. Within the fossa, the biceps tendon an brachial artery may be palpated. After crossing the el bow joint, the brachial artery divides into tw branches, the radial artery and the ulnar artery. Th examiner must be aware of the brachial artery becaus it has the potential for being injured as a result o severe trauma at the elbow (e.g., fracture, disloca tion). Trauma to this area may lead to compartmen

344

CHAPTER 6 • Elbow

syndromes such as Volkmann's ischemic contracture. The median and musculocutaneous nerves are also found in the fossa, but they are not palpable. Pressure on the median nerve may cause symptoms in its cutaneous distribution. Coronoid Process and Head of Radius. Within the cubital fossa, if the examiner palpates carefully so as not to hurt the patient, the coronoid process of the ulna, and the head of the radius may be palpated. Palpation of the radial head is facilitated by supination and pronation of the forearm. The examiner may palpate the head of the radius from the posterior aspect at the same time by placing the fingers over the head on

the posterior aspect and the thumb over it o anterior aspect. In addition to the muscles prev mentioned, the biceps and brachialis muscles m palpated for potential abnormality.

Medial Aspect

Medial Epicondyle. Originating from the m epicondyle are the wrist flexor-forearm pro groups of muscles. Both the muscle bellies and insertions into bone should be palpated. Tend over the epicondyle where the muscles insert is times called golfer's elbow or tennis elbow of th dial epicondyle.

Olecranon fossa

A

Medial supracond line

Olecranon fossa

Olecranon Groove for ulnar nerve -....>,,---,. Olecranon fossa----...... Olecranon

H---f--

Lateral supracondylar line

Medial epicondyle -----:;'+"rl--'15 mm

Adapted from Callahan, A.D.: Sensibility testing. In Hunter, J., L.H. Schneider, E. J. Mackin, and A.D. Callahan (eds.): Rehabilitation of the Hand: Surgery and Therapy. St. Louis, C.v. Mosby Co., 1990, p.605.

Allen Test. The patient is asked to open and c the hand several times as quickly as possible and t squeeze the hand tightly (Fig. 7-64).62,70 The ex iner's thumb and index finger are placed over the dial and ulnar arteries, compressing them. As an al nate technique, the examiner may use both ha

A B

C

Figure 7-64

\ D

acing one thumb over each artery to compress the ery and placing the fingers on the posterior aspect ; the arm for stability. The patient then opens the and while pressure is maintained over the arteries. ne artery is tested by releasing the pressure over that .m:ery to see if the hand flushes. The other artery is - en tested in a similar fashion. Both hands should be -e ted for comparison. This test determines the pa-ency of the radial and ulnar arteries and determines

Allen test. (A) The patient opens and closes the hand. (B) While the patient holds the hand closed, the examiner compresses the radial and ulnar arteries. (C) One artery (in this case, the radial artery) is then released and the examiner notes the filling pattern of the hand until the circulation is normal. (D) The process is then repeated wit the other artery. (E) Alternate hand hold.

which artery provides the major blood supply to the hand.

Digit Blood Flow. To test distal blood flow, the examiner compresses the nail bed and notes the time taken for color to return to the nail. Normally, when the pressure is released, color should return to the nail bed within 3 seconds. If return takes longer, arterial insufficiency to the fingers should be suspected. Com-

402

CHAPTER 7 • Forearm, Wrist, and Hand

Measurement for Swelling. Swelling may measured with a tape measure, as long as the e is consistent with the measuring points. When ing swelling, the examiner commonly measures the proximal interphalangeal joints individually, the metacarpophalangeal joints as a group, and the palm and wrist. The values for both sides a pared.

Reflexes and Cutaneous Distribution

Figure 7-65 Volumeter used to measure hand volume.

parison with the normal side gives some indication of restricted flow. Hand Volume Test. If the examiner is concerned about changes in hand size, a volumeter (Fig. 7 - 65) may be used. This device can be used to assess change in hand size resulting from localized swelling, generalized edema, or atrophy.36 Comparisons with the normal limb give the examiner an idea of changes occurring in the affected hand. Care must be taken when doing this test to ensure accurate readings. There is often a 10-mL difference between right and left hands and between dominant and nondominant hands. If swelling is the problem, differences of 30 to 50 mL can be noted. 20 ,71

Although it is possible to obtain reflexes from t dons crossing the wrist, this is not commonly d fact, no deep tendon reflexes are routinely te the forearm, wrist, and hand. The only reflex th be tested in the hand is Hoffman's reflex, wh pathological reflex. This reflex may be tested if per motor neuron lesion is suspected. To test flex, the examiner "flicks" the terminal phalanx index, middle, or ring finger. A positive test cated by reflex flexion of the distal phalanx thumb or a finger that was not "flicked." The examiner must be aware of the sensory d tion of the ulnar, median, and radial nerves hand (Fig. 7-66) and must be prepared to c peripheral nerve sensory distribution with ner sensory (dermatome) distributions. As previous tioned, there is variability in both distributions been reported, however, that each peripheral n the upper limb has a "constant" area in the ha is always affected if the nerve is injured. For th nerve, it is on the dorsum of the thumb near t of the anatomical snuff box; for the median ner the tip of the index finger; and for the ulnar n is the tip of the little finger. 72 The median nerve gives off a sensory branch the wrist before it passes through the carpal This sensory branch supplies the skin of the pal 7 -67). Thus, most commonly, carpal tunnel sy

- \ - - - - Radial nerve --.l,-\,---

Median nerve

-+--"'~:-=+-~---=t-- UI nar

nerve

Figure 7-66 Peripheral nerve distribution in the hand.

Dorsal surface

Palmar surface

/\ I 1\\"\\ I

II

Dorsal su rface

Palmar surface

ure 7-67 " ory distribution of branches of the ulnar and median nerves _ en off above the wrist.

s not affect the median sensory distribution in the .llm but results in altered sensation in the fingers. everal sensation tests may be carried out in the md. Table 7 -11 illustrates the tests used and the ~nsation and nerve fibers tested. Pinprick is used to t for pain. Constant light touch, which is a compont of fine discrimination, may be tested in the hand mg a Semmes-Weinstein pressure esthesiometer (Von - ey test). This kit has 20 probes, each with different ~ cknesses of nylon monofilament (Fig. 7-68). The tient is blindfolded or otherwise unable to see the d, and each filament is applied perpendicularly to

.mn/cold - ,non wool

Fiber/Receptor Type

Esthesiometer Probe No.

Calculated Pressure (g/mm 2 )

Pain

Free nerve endings

2.44-2.83

3.25-4.86

Normal light touch

Temperature

Free nerve endings

3.22-4.56

11.1-47.3

Diminished light touch point localization * intact

4.74-6.10

68.0-243.0

Minimal light touch, area localizationt intact

6.10-6.65

243.0-439.0

Sensation

Moving touch

Quick adapting

ger stroking

Moving touch

Quick adapting

lion's test

Moving touch

Quick adapting

_aning fork

Vibration

Quick adapting

- n Frey

Constant touch

Slow adapting

-eber's test

Constant touch

Slow adapting

ok-up test

Constant touch

Slow adapting

Constant touch

Slow adapting

Constant touch

Slow adapting

_ ecision sensory grip ross grip

the finger, with the smallest filament being used firs The filament is pushed against the finger until th filament bends. The next filament is then used, and s on until the patient feels one before or just as bends. 21 ,41 The test is repeated three times to ensure positive result. 68 Normal values vary between probe 2.44 and 2.83 (Table 7-12). When doing th

Table 7-12 Light Touch Testing Using Semmes-Weinstein Pressure Esthesiometer

Ie 7-11 ests for Cutaneous Sensibility Test

Figure 7-68

The Semmes-Weinstein monofilament is applied perpendicular to th skin for 1 to 1.5 seconds, held in place for 1 to 1.5 seconds, and lifted for 1 to 1.5 seconds. (From Waylett-Rendall, J.: Sensibility evaluation and rehabilitation. Orthop. Clin. North Am. 19:51, 1988.)

odified from Dellon, A.L.: The paper clip: Light hardware to aluate sensibility in the hand. Contemp. Orthop. 1:40, 1979.

Interpretation

Sensation but no localization sensibility

* Point localization: the dowel is in contact with the skin point stimulated. t Area localization: the dowel is in contact with any point inside the zone of the area being tested (in the hand or foot). From Omer, G.E.: Report of the Committee for Evaluation of the Clinical Result in Peripheral Nerve Injury. J. Hand Surg. Am. 8:755 1983.

404


-,""

- ...

I~:

I

Nt ~! I

,'l ,

,

I I I

~

I I I

~

I', I : I

..I __ __ I ~

I I I

L_ : I

I I I

I

: I

I I I

_ L __ I~_

Palmar aspect

Figure 7-69 Grid pattern used for recording results of light touch sensation testing.

Semmes-Weinstein test, the hand and fingers are monly divided into a grid (Fig. 7-69), and onl point (usually in the center) is tested in each squ is primarily the palmar aspect of the hand t tested. Stereognosis or tactile gnosis, which is the abi identifY common objects by touch, should al tested. Objects are placed in the patient's hand the patient is blindfolded or otherwise unable the object. The time taken to recognize the ob noted. Normal subjects can usually name the within 3 seconds of contact. 67 Vibratory sense is tested using a 256-cps frequency) or 30-cps (low-frequency) tuning fork patient, who cannot see the test site, indicates vibration is felt as the examiner touches the skin the vibrating tuning fork and whether the vib feels the same. The score is the number of c responses divided by the total number ofpresentati

Table 7-13 Forearm, Wrist, and Hand Muscles and Referral of Muscles

Figure 7-70 Symptoms can be referred to the wrist and hand from the elbow, shoulder, and cervical spine.

Referral Pattern

Brachioradialis

Lateral epicondyle, lateral forearm, and web space between thumb and inde finger

Extensor carpi ulnaris

Medial side of dorsum of w

Extensor carpi radialis brevis

Middle of dorsum of wrist

Extensor carpi radialis longus

Lateral epicondyle, forearm lateral dorsum of hand

Extensor digitorum

Forearm, wrist to appropri digit

Extensor indices

Dorsum of wrist to index f

Palmaris longus

Anterior aspect of forearm palm

Flexor carpi ulnaris

Anteromedial wrist into lat palm

Flexor carpi radialis

Forearm to anterolateral w

Flexor digitorum superficialis

Palm into appropriate digi

Flexor pollicis longus

Thumb

Adductor pollicis

Anterolateral and posterola palm into thumb

Opponens pollicis

Anterolateral wrist into ant thumb

Abductor digiti minimi

Dorsomedial surface of han little finger

Interossei

Into adjacent digit, and for interossei, dorsum of han

king was felt and what it felt like. t must be remembered that pain may be referred to wrist and hand from the cervical or upper thoracic e, shoulder, and elbow. Seldom is wrist or hand referred up the limb (Fig. 7-70). Table 7-13 \\'s the muscles acting on the forearm, wrist, and nd and their pain referral patterns when injured. The examiner can attempt a differential diagnosis of resthesia in the hand if altered sensation is present. -omparison with a normal dermatome chart should made, and the examiner should remember that re is a fair amount of variability and overlap with rmatomes (Fig. 7-71). In addition, there are areas the hand where sensation is more important (Fig. - - -2). Abnormal sensation may mean the following: 1. Numbness in the thumb only may be caused by pressure on the digital nerve on the outer aspect of the thumb. 2. A "pins and needles" feeling in the thumb may be caused by a contusion of the thenar branch of the median nerve. 3. Paresthesia in the thumb and index finger may be caused by a C5 disc lesion or C6 nerve root palsy. 4. Paresthesia in the thumb, index finger, and middle finger may be caused by a C5 disc lesion, C6 nerve root palsy, or thoracic outlet syndrome.

C7

igure 7-71 ermatomes of the hand. Note overlap at dermatomes. Both views e palmar.

Figure 7-72 Importance of hand sensation. Darker areas indicate where sensation is most important; lighter areas, where sensation is a little less important; and white areas, where sensation is least important. (Redrawn from Tubiana, R.: The Hand. Philadelphia, W.B. Sawlders Co., 1981, p. 74.)

5. Paresthesia of the thumb, index finger, middle finger, and half of the ring finger on the palmar aspect may be caused by an injury to the median nerve, possibly through the carpal tunnel; on the dorsal aspect, it could be caused by injury to the radial nerve. 6. umbness of the thumb and middle finger may be caused by a tumor of the humerus. 7. Paresthesia on all five digits in one or both hands may be caused by a thoracic outlet syndrome. If it is in both hands, it may be caused by a central cervical disc protrusion. The level of protrusion would be indicated by the distribution of the paresthesia. 8. Paresthesia of the index and middle fingers may be caused by a trigger finger or "stick" palsy, if it is on the palmar aspect, or by a C6 disc lesion or C7 nerve root palsy. On the dorsal aspect of the hand, it may be caused by a carpal exostosis or subluxation. Stick palsy is the result of an inordinant amount of pressure from a cane or crutches on the ulnar nerve as it passes through the palm. 9. Paresthesia of the index, middle, and ring fingers may be caused by a C6 disc lesion, C7 nerve root injury, or carpal tunnel syndrome. 10. Paresthesia of all four fingers may be caused by a C6 disc lesion or injury to the C7 nerve root. 11. Paresthesia of the middle finger only may be caused by a C6 disc lesion or C7 nerve root lesion. 12. Paresthesia of the middle and ring fingers may be caused by a C6 disc lesion, C7 nerve root lesion, or stick palsy. 13. Paresthesia of the middle, ring, and little fingers may be caused by a C7 disc lesion or C8 nerve root palsy. The same would be true if there were paralysis of the ring and little fingers. This

406


paresthesia may also be the result of a thoracic outlet syndrome. 14. Paresthesia on the ulnar side of the ring finger and the entire little finger may be caused by pressure of the ulnar nerve at the elbow or in the palm.

Peripheral Nerve Injuries of the Forearm, Wrist, and Hand Carpal Tunnel Syndrome. The most common "tunnel" syndrome in the body is the carpal tunnel syndrome, in which the median nerve is compressed under the flexor retinaculum at the wrist (see Fig. 729). This compression may follow trauma (for example, a Colles fracture or lunate dislocation), flexor tendon paratenonitis, a ganglion, arthritis (osteoarthritis or rheumatoid arthritis), or collagen disease. As many as 20% of pregnant women may experience median nerve symptoms, because compression of the nerve as a result of fluid retention causes swelling in the carpal tunnel. With carpal tunnel syndrome, the symptoms, which are primarily distal to the wrist, are usually worse at night and include burning, tingling, pins and needles, and numbness into the median nerve sensory distribution (Table 7-14). In severe cases, pain may be referred to the forearm. Symptoms are often aggravated by wrist movements, and long-standing cases show atrophy and weakness of the thenar muscles (flexor and abductor pollicis brevis, opponents pollicis) and the lateral two lumbricals. The condition is most common in women between 40 and 60 years of age, and although it may occur bilaterally, it is seen most commonly in the dominant hand. It is also commonly seen in younger patients who use their wrists a great deal in repetitive manual labor or are exposed to vibra-

tion. 74 Because of the apparent connection betw carpal tunnel syndrome and cervical lesions resultin double crush syndromes, the examiner should care to include cervical assessment if the history pears to warrant such inclusion.7 5 - 77

Guyon's (Pisohamate) Canal. The ulnar nerv sometimes compressed as it passes through the piso mate, or Guyon's canal (Fig. 7-73). The nerve be compressed from trauma (e.g., fractured hook hamate), use of crutches, or chronic pressure, as people who cycle long distances while leaning on handlebars or who use pneumatic jackhammers. ulnar nerve gives off two sensory branches above wrist. These branches supply the palmar and do aspects of the hand, as illustrated in Figure 7-67, do not pass through Guyon's canal. Therefore, if ulnar nerve is compressed in the canal, only the fin show an altered sensation (see Table 7-14). Mo loss includes the muscles of the hypothenar ernine (flexor digiti minirni, abductor digiti minimi, oppon digiti minirni) , adductor pollicis, the interossei, me two lumbricals, and palmaris brevis.

Joint Play Movements

When assessing joint play movements, the exam should remember that if the patient complains of ability or pain on wrist flexion, the lesion is proba in the midcarpal joints. If the patient complains inability or pain on wrist extension, the lesion is pr ably in the radiocarpal joints, because it is in th joints that most of the movement occurs during th actions. If the patient complains of pain or inability supination and pronation, the lesion is probably in ulnameniscocarpal joint or inferior radioulnar joint.

Table 7-14 Nerve Injuries (Neuropathy) About the Wrist and Hand Nerve

Motor Loss

Sensory Loss

Median nerve (C6-C8, Tl; carpal tunnel)

Flexor pollicis brevis Abductor pollicis brevis Opponens pollicis Lateral two lumbricals

Palmar and dorsal thumb, index, middle and lateral half of ring finger If lesion above carpal tunnel, palmar sensation also affected

Thumb opposition Thumb flexion Weak or no pinch Weak grip

Ulnar nerve (C7, C8, Tl; pisohamate canal)

Flexor digiti minimi Abductor digiti minimi Opponens digiti minimi Adductor pollicis Interossei Medial two lumbricals Palmaris brevis

Little finger, half of ring finger Palm often not affected

Thumb adduction Inability to extend PIP and joints of fourth and fifth fingers Finger abduction Finger adduction Flexion of little finger

DIP

=

distal interphalangeal; PIP

=

proximal interphalangeal.

Functional Loss

of nerve relative to pisohamate liganlent and flexor retinaculum.

::

-amate

-';----Hamate

----/---f-// Pisohamate ligament

B

The amount of movement obtained by the joint play uld be compared with that of the normal side and !1 idered significant only if there is a difference beeen the two sides. Reproduction of the patient's :nptoms would also give an indication of the joints - fault.

Joint Play Movements of the Hand Vrist • Long-axis extension (traction or distraction)

Intermetacarpal Joints

Fingers

• Anteroposterior glide

• Long-axis extension (traction or distraction)



• Side glide

• Rotation

• Side tilt

• Side glide

Anteroposterior glide is applied at the wrist in two positions. The examiner first places the stabilizing hand around the distal end of the radius and ulna just proximal to the radiocarpal joint and then places the other hand around the proximal row of carpal bones. If the examiner's hands are positioned properly, they should touch each other (Fig. 7 -74). The examiner applies an anteroposterior gliding movement of the proximal row of carpal bones on the radius and ulna testing the amount of movement and end feel. Then, the stabilizing hand is moved slightly distally «1 cm) so that it is around the proximal row of carpal bones. The exam-

fist o perform long-axis extension at the wrist, the exlIIliner stabilizes the radius and ulna with one hand the patient's elbow may be flexed to 90°, and stabilization may be applied at the elbow if there is no athology at the elbow) and places the other hand just Jistal to the wrist. The examiner then applies a longimdinal traction movement with the distal hand.

Figure 7-74 Position for testing joint play movements of the wrist.

408


iner places the mobilizing hand around the distal row of carpal bones. An anteroposterior gliding movement is applied to the distal row of carpal bones on the proximal row to test the amount of movement and end feel. These movements are sometimes called the anteroposterior drawer tests of the wrist. 3 If the examiner then moves the stabilizing hand slightly distally (< 1 cm) again, the hand will be around the distal carpal bones. The mobilizing hand is then placed around the metacarpals, and an anteroposterior gliding movement is applied to the base of the metacarpals to test the amount of joint play and end feel. Side glide is performed in a similar fashion, except that a side-to-side movement is performed instead of an anteroposterior movement. To perform side tilting of the carpals on the radius and ulna, the examiner stabilizes the radius and ulna by placing the stabilizing hand around the distal radius and ulna just proximal to the radiocarpal joint and the mobilizing hand around the patient's hand and then radially and ulnarly deviating the hand on the radius and ulna. The above joint play movements are general ones involving different "rows" of carpal bones. To check the joint play movements of the individual carpal bones, a technique such as Kaltenborn's technique should be used. Kaltenborn 78 suggested 10 tests to determine the mobility of each of the carpal bones. The movement of each of the bones is determined in a sequential manner, and both sides are tested for comparison. These tests are sometimes referred to as ballottement tests or shear tests. 3 The examiner may use Kaltenborn's order or any other order as long as each bone and its relationship to adjacent bones is tested individually. For example, some people start by testing the movement of the lunate relative to the radius, then move to the capitate (relative to the lunate), followed by scaphoid-radius, scaphoid-trapezoid/trapezium,

triquetrum-radius, and triquetrum-hamate. Pisifo may be tested individually.

Intermetacarpal Joints

To accomplish anteroposterior glide at the interme carpal joints, the examiner stabilizes one metacar bone and moves the adjacent metacarpal anteriorly a posteriorly in relation to the fixed bone to determ the amount of joint play and the end feel. The proc is repeated for each joint.

Fingers

The joint play movements for the fingers are the sa for the metacarpophalangeal, proximal interphalange and distal interphalangeal joints; the hand position the examiner simply moves farther distally. To perform long-axis extension, the examiner s bilizes the proximal segment or bone using one ha while placing the second hand around the distal s ment or bone of the particular joint to be tested. W the mobilizing hand, the examiner applies a longitu nal traction to the joint.

Anteroposterior glide is accomplished by stabilizi the proximal bone with one hand. The mobilizi hand is placed around the distal segment of the jo and the examiner applies an anterior and/or poster movement to the distal segment, being sure to ma tain the joint surfaces parallel to one another wh determining the amount of movement and end (Fig. 7-75). A minimal amount of traction may applied to bring about slight separation of the jo surfaces. Rotation of the joints of the fingers is accomplish by stabilizing the proximal segment with one ha

Kaltenborn's Carpal Mobilization • Fixate the capitate and move the trapezoid • Fixate the capitate and move the scaphoid • Fixate the capitate and move the lunate • Fixate the capitate and move the hamate • Fixate the scaphoid and move the trapezoid and trapezium • Fixate the radius and move the scaphoid • Fixate the radius and move the lunate • Fixate the ulna and move the triquetrum • Fixate the triquetrum and move the hamate • Fixate the triquetrum and move the pisiform

Figure 7-75 Position for testing joint play movements of the fingers.

ulnar styloid is palpated on the medial aspect. T radial styloid extends farther distally than the ul styloid. By palpating over the dorsum of the w crossing the radius and ulna, the examiner should tempt to palpate the six extensor tendon tunnels (n ing any crepitus or restriction to movement), mov lateral to medial (see Fig. 7-33): ~

ure 7-76 _arion of the wrist llSing both hands.

-th the other hand, the examiner applies slight tracn to the joint to distract the joint surfaces and then ates the distal segment on the proximal segment to ermine the end feel and joint play. To perform side glide joint play to the joints of the - gers, the proximal segment is stabilized with one d, while the examiner applies slight traction to the mt with the mobilizing hand to distract the joint aces and then moves the distal segment sideways, >eping the joint surfaces parallel to one another to termine joint play and end feel.

alpalion palpate the forearm, wrist, and hand, the examiner proximally and works distally, first on the dorsal ace and then on the anterior surface (Fig. 7 -76). e muscles of the forearm are palpated first for any gns of tenderness or pathology.

orsal Surface n the dorsal aspect, the examiner begins on the umb side of the hand and palpates the "snuff box," e carpal bones, and the metacarpal bones and phages. Anatomic Snuff Box. The snuff box is located be'een the tendons of extensor pollicis longus and exnsor pollicis brevis and can best be seen by having - e patient actively extend the thumb. The scaphoid ne may be palpated inside the snuff box. Tenderness !- the scaphoid bone is often treated as a fracture until roven otherwise because of the possibility of avascular ecrosis of the bone. With the wrist in anatomic pasion, proximal palpation is used to find the radial styid on the lateral aspect. Moving medially over the .ldius, the examiner comes to the radial (Lister's) tuercle. The extensor pollicis longus tendon moves around the tubercle to enter the thumb, which gives it

Tunnel 1: abductor pollicis longus and extensor p Iicis brevis Tunnel 2: extensor carpi radialis longus and brevis Tunnel 3: extensor pollicis longus Tunnel 4: extensor digitorum and extensor indice Tunnel 5: extensor digiti minimi Tunnel 6: extensor carpi ulnaris

Carpal Bones. In the anatomic snuff box, the ex iner can begin palpating the proximal row of ca bones, starting with the scaphoid bone. When palp ing the carpal bones, the examiner usually palp them on the anterior and dorsal surfaces at the sa time by applying anteroposterior joint play-like mo ments. The proximal row of carpal bones from lat to medial (in the anatomic position) are the scaph lunate, triquetrum (just below the ulnar styloid), pisiform. On the anterior aspect, the examiner should t care to ensure proper positioning of the lunate bo If it dislocates or subluxes, it tends to move anterio into the carpal tunnel, which may lead to symptom carpal tunnel syndrome. The pisiform is often easie palpate if the patient's wrist is flexed. The exam may then palpate the pisiform where the flexor c ulnaris tendon inserts into it. Returning to the anatomic snuff box and mov distally, the examiner palpates the trapezium bone. this is done, the radial pulse is often palpated in anatomic snuff box. The distal row of carpal bo from lateral to medial (in the anatomic position) palpated individually: trapezium, trapezoid, capi (distal to lunate and a slight indentation before metacarpal), and hamate (distal to triquetrum; hook of the hamate on the anterior surface is easiest part to palpate). On the dorsal aspect, the examiner could begin pation at the distal row of carpals. If the exam places a finger over the middle metacarpal and sl along it until the finger drops into a "hole" or dep sion, this depression is the capitate bone. Moving m dially (hamate) and laterally (trapezoid, trapezium), other bones of the distal row may be palpated again doing anteroposterior joint play-like movements. If examiner then moves proximally from the capitate, finger will rest on the lunate. Moving medially (triq

410


lies over the tendons of the flexor digitorum supe alis, which lie over the tendons of the flexor digito profundus. The palmaris longus tendon may s times be used for tendon repairs or transfers.

Palmar Fascia and Intrinsic Muscles. The e iner should then move distally to palpate the pa fascia and intrinsic muscles of the thenar and hypo nar eminences for indications of pathology.

Figure 7-77 Palpation of the proximal interphalangeal joint of the left second finger.

trum) and laterally (scaphoid), these carpals may be palpated. Metacarpal Bones and Phalanges. The examiner returns to the trapezium bone and moves farther distally to palpate the first metacarpal joint and the first metacarpal bone. Moving medially, the examiner palpates each metacarpal bone on the anterior and dorsal surface in turn. A similar procedure is carried out for the metacarpophalangeal and interphalangeal joints and the phalanges. These structures are also palpated on their medial and lateral aspects for tenderness, swelling, altered temperature, or other signs of pathology (Fig. 7 -77).

Anterior Surface Pulses. Proximally, the radial and ulnar pulses are palpated first. The radial pulse on the anterolateral aspect of the wrist on top of the radius is easiest to palpate and is the one most frequently used when taking a pulse. It runs between the tendons of flexor carpi radialis and abductor pollicis longus. The ulnar pulse may be palpated lateral to the tendon of flexor carpi ulnaris. It is more difficult to palpate because it runs deeper and lies under the pisiform and the palmar fascia. Tendons. Moving across the anterior aspect, the examiner may be able to palpate the long flexor tendons (see Fig. 7- 33) in a lateral-to-medial direction: flexor carpi radialis, flexor pollicis longus, flexor digitorum superficialis, flexor digitorum profundus, palmaris longus, and flexor carpi ulnaris (inserts into pisiform). The examiner should also palpate the hollow between the flexor carpi ulnaris, the pisiform, and the ulnar styloid. In this hollow lies the triangular cartilaginous disc or complex (TFCC).52 The palmaris longus (if present)

Skin Flexion Creases. From an anatomic poi view, the examiner should note the various skin fle creases of the wrist, hand, and fingers (Fig. 7 The flexion creases indicate lines of adherence bet the skin and fascia with no intervening adipose ti The following creases should be noted:

1. The proximal skin crease of the wrist indi the upper limit of the synovial sheaths o flexor tendons. 2. The middle skin crease of the wrist indicate wrist (radiocarpal) joint. 3. The distal skin crease of the wrist indicate upper margin of the flexor retinaculum. 4. The radial longitudinal skin crease of the encircles the thenar eminence. (Palm reader fer to this line as the "life line.") 5. The proximal transverse line of the palm across the shafts of the metacarpal bones, cating the superficial palmar arterial arch. ( readers refer to this line as the "head line.") 6. The distal transverse line of the palm lies the heads of the second to fourth metacar (Palm readers refer to this line as the " line. ") 7. The proximal skin crease of the fingers is 2 (0.8 inch) distal to the metacarpophalan joints. 8. The middle skin crease of the fingers is mad of two lines and lies over the proximal i phalangeal joints. 9. The distal skin crease of the fingers lies ove distal interphalangeal joints. 10. On the flexor and extensor aspects, the creases over the proximal and distal interpha geal joints lie proximal to the joint. On extensor aspect, the metacarpophalangeal cre lie proximal to the joint; on the flexor as they lie distal to the joint.

Arches. In addition, the examiner should ensure viability of the arches of the hand (see Fig. 7 The carpal transverse arch is the result of the s of the carpal bones, which in part forms the c tunnel. The flexor retinaculum forms the roof for tunnel. The metacarpal transverse arch is forme

Distal phalanx------+'T

+ - - - - - - - Distal finger

Middle phalanx-------+±

crease

+ - - - - - - - Middle finger crease

Proximal phalanx ------+-+

+ - - - - - - - Proximal finger crease ~=±--+--~E=;4~-

Capitate-----';~+-+_++

Trapezoid -------''>'-

Distal transverse crease A-o'1'-+-+-7-f-f--="'7."':7--h.!.---- Proximal transverse crease .---::.f-f----- Radial longitudinal crease

Trapezium - - - - Scaphoid - - - - -

- - - - - - Distal wrist crease

,...=;-+--------- Middle wrist crease \........,< N

~

c

0

.0

. ~ OJ .
:2

OJ

u

.0

.0 OJ

~

~

>

0.

0.

4

6

6

E ~ '5 1 l' ~ ffi « en ~ 6

OJ

6

n

L5 nerve Cauda equina ----'----'

gure 9-10 ... coronal schematic view of the exiting lumbar spinal nerve roots. 'ote that the exiting root takes the name of tile vertebral body der which it travels into the neural foramen. Because of the way -e nerve roots exit, U- L5 elise pathology usually affects the L5 t rather than the U root. (Redrawn from Borenstein, D.G., S.W. lesel, and S.D. Boden: Low Back Pain: Medical Diagnosis and mprehensive Management, Philadelphia, W.B. Saunders, 1995,

- .)

Patient History oblems of the lumbar spine are very difficult to diagose. Most of the examination commonly revolves ound differentiating symptoms of a herniated disc

symptoms into the leg from other conditions (e. inflammatory reaction, sprains, strains, facet syndrom more likely to cause localized pain. IS If there are n radicular symptoms below the knee, it often becom very difficult for the examiner to determine where the spine the problem is, or for that matter, wheth the problem is truly in the lumbar spine or comin from problems in the pelvic joints, primarily the acr iliac joints, or the hips. WaddelP points out that only about 15% of cases can a definitive diagnosis as the pathology of back pain be made. Hall 19 broke lo back pain into four categories-two of which are ba pain dominant and two of which are leg pain dom nant (Table 9-2). Pattern one suggests disc involv ment whereas pattern two suggests facet joint involv ment. Pattern three suggests nerve root involveme (primarily by a disc or some other space occupyi lesion or an injury accompanied by inflammatory swe ing) and pattern four suggests neurogenic intermitte claudication (pressure on the cauda equina). Thu only by taking a careful history, followed by a detail examination is the examiner able to determine t cause of the problem. 20 - 22 Even then, some doubt m remam. In addition to the questions listed under Patie History in Chapter 1, the examiner should obtain t following information from the patient:

Ie 9-2 atterns of Back Pain Pattern ck Dominant Pain/

Aggravating Movement

Relieving Movement

Onset

Duration

Probable Cause

Disc in,·oh·em (minor herruation, pondylosis) prain, strain

1

Back/buttocks (>90% back pain) Myotomes seldom affected Dermatomes not affected

Flexion StifF in morning

Extension

Hours to days

Days to months sudden or low

2

Back/buttocks Myotomes seldom affected Dermatomes not affected

Extension/ rotation

Flexion

,\1inute to hours

Da~

Facet joint involvement strain

3

Leg (usually below knee) Myotomes commonly affected (especially in chronic cases) Pain in dermatomes

Flexion

Extension

Hours day

\\'eeks to months

Nerve root irritation (most likely cause-elise hernation)

4

Leg (usually below knee) (May be bilateral) Myotomes commonly affected (especially in chronic cases) Pain in dermatomes

Walking (extension)

Rest (sitting) and/or postural change

\Vith walking

~1echanical

Cause

..eg Pain Dominant/ • on Mechanical Cause

Where Pain Worst

.10dified from Hall, H.: A simple approach to back pain management. Patient Care 15:77-91, 1992.

to

to weeks ( udden)

?

Neurogenic intermittant claudication (stenosis)

474

CHAPTER 9 • Lumbar Spine

1. What is the patient's age?23 Different conditions affect patients at different ages. For example, disc problems usually occur between the ages of 15 and 40 years, and ankylosing spondylitis is evident between 18 and 45 years. Osteoarthritis and spondylosis are more evident in people older than 45 years of age, and malignancy of the spine is most common in people older than 50 years of age.

2. What is the patient's occupation?3,24 Back pai tends to be more prevalent in people with strenuou occupations 25 although it has been reported that famil ial influences have an effect as well as occupation. 26.2 For example, truck drivers (vibration) and warehous workers have a very high incidence of back injury.2 Patients who have chronic low back pain develop deconditioning syndrome, which compounds th

Table 9-3 Some Implications of Painful Reactions Activity

Reaction of Pain

Lying sleeping

Possible Structural and Pathological Implications Decreased compressive forces-low intradiscal pressures Absence of forces produced by muscle activity

i

Change of position-noxious mechanical stress Decreased mechanoreceptor input Motor segment "relaxed" into a position compromising affected structure Poor external support (bed) onmusculoskeletal cause

First rising (stiffues)

i

Nocturnal imbibition of fluid, disc volume greatest Mechanical inflammatory component (apophyseal joints) Prolonged stiffuess, active inflammatory disease (e.g., ankylosing spondylitis)

Sitting

i

Compressive forces High intradiscal pressure Intradiscal pressure reduced Decreased paraspinal muscle activity

With extension

i

Greater compromise of structures of lateral and central canals Compressive forces on lower apophyseal joints Little compressive load on lower apophyseal joints Greater volume lateral and central canals Reduced disc bulge posteriorly

With flexion

i

Very high intradiscal pressures Increased compressive loads upper and mid apophyseal joints Mechanical deformation of spine

Sitting to standing

i i

Walking

i

Shock loads greater than body weight Compressive loads (vertical creep) Leg pain Neurological claudication Vascular claudication

Drrmg

i

Sitting: compressive forces Vibration: vibro creep repetitive loading, decreased hysteresis loading, decreas hysteresis Increased dural tension sitting with legs extended Short hamstrings: pull lumbar spine into greater flexion

Coughing, neezing straining

i

Increased pressure subarachnoid space (increased blood flow, Batson's plexus, compromises space in lateral and central canal) Increased intradiscal pressure Mechanical "jarring" of sudden uncontrolled movement

Prolonged sitting

Gradual creep of tissues Creep, time for reversal, difficulty in straightening up Extension of spine, increase disc bulge posteriorly

From ]lill, G.A.: Examination of the lumbar spine. In Grieve, G.P. (ed.): Modern Manual Therapy of the Vertebral Column. Edinburgh, Churchill Livingstone, 1986. p. 553.

Some Mechanisms of Musculoskeletal Pain Behavior of Pain Constant ache ain on movement "ain accumulates with activity

ain increases with sustained posmres

tent nerve root pain

Possible Mechanisms Inflammatory process, venous hypertension Noxious mechanical stimulus (stretch, pressure, crush) Repeated mechanical stress Inflammatory process Degenerative disc- hysteresis decreased, less protection from repetitive loading Fatigue of supporting muscles Gradual creep of tissues may stress affected part of motor unit Movement has produced an acute and temporary neurapraxia

- m Jull, G.A.: Examination of the lumbar spine. In Grieve, G.P. .): Modern Manual Therapy of the Vertebral Column. Edinburgh, :lUrchill Livingstone, 1986, p. 553.

lower back tends to be 15% to 20% higher in m than in women because men are taller and their wei is distributed higher in the body. 5. How long has the problem bothered the patie Acute back pain lasts 3 to 4 weeks. Subacute back p lasts up to 12 weeks. Chronic pain is anything lon than 3 months. WaddeiP has outlined predictors (y low flags) of chronicity with back pain patients.

Predictors of Chronicity Within the First 6 to 8 Weeks ("Yellow Flags")3 • Nerve root pain or specific spinal pathology • Reported severity of pain at the acute stage • Beliefs about pain being work-related • Psychologic distress • Psychosocial aspects of work • Compensation • Time off work The longer someone is off work with back pain, the lower the probability that they will return to work

roblem as it leads to decreased muscle strength, imaired motor control, and decreased coordination and rural controJ.29 How active is the patient at work ual job, light duties, full time, frequent days off cause of back pain, unemployed because of back, - tired)? 3. What is the patient's sex? Lower back pain has a gher incidence in women. Female patients should be ed about any changes that occur with menstruation, h as altered pain patterns, irregular menses, and -elling of the abdomen or breasts_ Knowledge of the , te of the most recent pelvic examination is also use':..:1. Ankylosing spondylitis is more common in men. 4. What was the mechanism of injury? Lifting comonly causes low back pain (Tables 9-3 and 9-4). -:b.is is not surprising when one considers the forces : -erted on the lumbar spine and disc. For example, a ---kg (170-lb) man lifting a 91-kg (200-lb) weight proximately 36 cm (14 inches) from the interverteral disc exerts a force of 940 kg (2072 lb) on that ~ c. The force exerted on the disc can be calculated as ~oughly 10 times the weight being lifted. Pressure on - e intervertebral discs varies depending on the posion of the spine. Nachemson and colleagues l6 ,17 owed that pressure on the disc can be decreased by creasing the supported inclination of the back rest e.g., an angle of 130° decreases the pressure on the c by 50%). Using the arms for support can also ecrease the pressure on the disc. When one is stand:ng, the disc pressure is approximately 35% of the pres;ure that occurs in the relaxed sitting position. The

6. Where are the sites and boundaries of pain? H the patient point to the location or locations. N whether the patient indicates a specific joint whether the pain is more general. The more spec the pain, the easier it is to localize the area of path ogy. Unilateral pain with no referral below the k may be caused by injury to muscles (strain) or li ments (sprain), the facet joint, or in some cases, sacroiliac joints. This is called mechanical low b

"Mechanical" low Back Pain 3 • Pain is usually cyclic

• Low back pain is often referred to the buttocks and thigh • Morning stiffness or pain is common • Start pain (Le., when starting movement) is common • There is pain on forward flexion and often also on returning to the erect position

• Pain is often produced or aggravated by extension, side flexion, rotation, standing, walking, sitting, and exercise in general • Pain usually becomes worse over the course of the day • Pain is relieved by a change of position • Pain is relieved by lying down, especially in the fetal position

476


Figure 9-11

Centralization of pain is the progre sive retreat of the most distal exten of referred or radicular pain toward the lumbar midline. Peripheralization of pain moves in the opposite direction.

Centralization

--------------~ Peripheralization

pain or in older books, "lumbago." With each of the e injuries, there is seldom if ever peripheralization of the symptoms. The symptoms tend to stay centralized in the back. If the muscles and ligaments are affected, movement will decrease and pain will increase with repeated movements. If the pain extends to the hip, the hip must be cleared by examination. With facet joint problems, the range of motion remains the same (it may be restricted from the beginning) as does the pain with repeated movements. The sacroiliac joints will show pain when pain provoking (stress) tests are used. A minor disc injury (protrusion) may show the same symptoms but the pain is more likely to be bilateral if it is a central protrusion. 30 7. Is there any radiation of pain? Is the pain centralizing or peripheralizing (Fig. 9-11 )?31,32 Centralization implies the pain is moving towards or is centered in the lumbar spine. Peripheralization implies the pain is being referred or is moving into the limb. If so, it is helpful for the examiner to remember and correlate this information with dermatome findings when evaluating sensation. The examiner must be careful when looking at the lumbar spine that he or she does not consider every back problem a disc problem. It has been reported that disc problems account for only about 5% of low back pain cases. 33 Some authors 19 feel the only definitive clinical diagnosis of a disc problem i neurological pain extending below the knee. This mean that although there may be pain in the back and in the leg, the leg pain is dominant. 3 Pain on the anterolateral aspect of the leg is higWy suggestive of L4 disc problems whereas pain radiating to the posterior aspect of the foot is suggestive of L5 disc problems if the history indicates a disc may be injured. 34 Pain radiating into the leg below the knee is highly suggestive of a di c Ie ion but isolated back or buttock pain does not rule out the disc. Minor injuries such as

protrusion of the disc may result only in back or b tock pain. 34 Such an injury makes diagnoses more di cult because such pain may also be the result of mus or ligament injury, or injury or degeneration to t adjacent facet joints. Lumbar and sacroiliac pain tend to be referred the buttock and posterior leg (and sometimes to t lateral aspect of the leg). Hip pain tends to be in t groin and anterior thigh although it may be referred the knee (usually medial side). The hip can be rul out later in the examination by the absence of a h capsular pattern and a negative sign of the buttock The examiner must also determine whether the musc loskeletal system is involved or whether the pain being referred from another structure or system (e. abdominal organs). Abnormal signs and symptoms "red flags" (see Table 1-1) would lead the examin to consider causes other than the musculoskele system. 8. Is the pain deep? Superficial? Shooting? Burnin Aching? Questions related to the depth and type pain often help to locate the structure injured and t source of pain. 9. Is the pain improving? Worsening? Staying t same? These questions give an indication of wheth the condition is settling down and improving or it m indicate that the condition is in the inflammati phase (acute) or in the healing phase. Does the patie complain of more pain than the injury would sugg should occur? If so, psychosocial testing may be appr priate. 10. Is there any increase in pain with coughin Sneezing? Deep breathing? Laughing? All of these tions increase the intrathecal pressure (the pressu inside the covering of the spinal cord) and would in cate the problem is in the lumbar spine and affecti the neurological tissue.

-ally increase or decrease the pain or cause diffi:.llty?31,36 For example, if sitting increases the pain and ther symptoms, the examiner may suspect that sused flexion is causing mechanical deformation of the _me or increasing the intradiscal pressureY Classi'.illy, disc pathology causes increased pain on sitting, :ting, twisting, and bending. 38 It is the most common _ace occupying lesion in the lumbar spine and therere is the most common cause of radiating pain below - e knee. If standing increases the pain and other mptoms, the examiner may suspect that extension, pecially relaxed standing, is the cause. If walking ineases the pain and other symptoms, extension is obably causing the mechanical deformation, because alking accentuates extension. If lying (especially one lying) increases the pain and other symptoms, tension may be the cause. Persistent pain or progrese increase in pain while the patient is in the supine ition may lead the examiner to suspect neurogenic pace-occupying lesions, such as an infection, swellg, or tumor. It must be remembered that pain may diate to the lumbar spine from pathological condins in other areas as well as from direct mechanical oblems. For example, tumors of the pancreas refer ain to the low back. Stiffuess and/or pain afrer rest ay be indicative of ankylosing spondylitis or Scheuerann's disease. Pain from mechanical breakdown tends increase with activity and decrease with rest. Disco= nic pain increases if the patient maintains a single

o -

,~#

\\\\t1~;:::.;---~

Hamstrings

Figure 9-13

Muscles "balancing" the pelvis. (Modified fro,n Dyrek, D.A., L.]. Micheli, and D.J. Magee: Injuries to the thoracolumbar spine and pelvis. In Zachazewski, J.E., D.]. Magee, and W.S. Quillen [eds.): Athletic Injuries and Rehabilitation. Philadelphia, W.B. Sawlders Co., 1996, p. 470.)

posture (especially flexion) for a long period. Pain arising from the spine almost always is influenced by posture and movement. The normal lumbosacral angle in the standing position is 140°, the normal lumbar lordotic curve is about 50°, the normal sacral angle is 30° (Fig. 9-12), and the normal pelvic angle is 30°. In this position, the pelvis would be said to be in neutral (neutral pelvis). The pelvis is the key to proper back posture. For the pelvis to "sit" properly on the femora, the abdominal, hip flexor, hip extensor, and back extensor muscles must be strong, supple, and balanced (Fig. 9-13). Any deviation in the normal alignment should be noted and recorded. What types of shoes does the patient wear? Heel heights can modify the pelvic angle and lumbar curve, altering the stress on the spine. 39 gure 9-12 mOlal angles of the spine and sacrum. a = Lumbosacral angle 40°); b = Lumbar lordotic curve (50°); c = sacral angle (30°); . ;. = pelvic angle (30°).

12. Is the pain worse in the morning or evening? Does the pain get better or worse as the day progresses? For example, osteoarthritis of the facet joints leads to morning stiffness, which in turn is relieved by activity.

478


Table 9-5 Differential Diagnosis of Mechanical Low Back Pain

Muscle Strain

Herniated Nucleus Pulposus

Osteoarthritis

Spinal Stenosis

Spondylolisthesis

Scolios

Age (yr)

20-40

30-50

>50

>60

20

30

Pain pattern Location

Back (unilateral)

Back, leg (lUlilateral) Acute (prior episodes) ~

Back (unilateral)

Leg (bilateral)

Back

Back

Insidious

Insidious

Insidious

Insidiou

Onset

Acute

Standing Sitting Bending

i i

i i

Straight leg raise

-

Plain x-ray

-

~

i

+

~ ~ -

-

+

i

i

i

i

+ (stress)

-

-

+

+

+

i

~ ~

~

~

From Borenstein, D.G., S.W. Wiesel, and S.D. Boden: Low Back Pain: Medical Diagnosis and Comprehensive Management. Philadelphia, W Saunders Co., 1995, p. 189.

13. Which movements hurt? Which movements are stim Table 9-5 demonstrates some of the causes of mechanical low back pain and their symptoms. The examiner must help the patient differentiate between true pain and discomfort that is caused by stretching. Postural, or static, muscles (e.g., iliopsoas) tend to respond to pathology with tightness in the form of spasm or adaptive shortening; dynamic, or phasic, muscles (e.g., abdominals) tend to respond with atrophy. Pathology affecting both types of muscles can lead to a "pelvic crossed syndrome" (discussed later). Does the patient describe a painful arc of movement on forward or side flexion? If so, it may indicate a disc protrusion with a nerve root riding over the bulge or instability in part of the range of motion. 36 Patients with lumbar instability or lumbar muscle spasm have trouble moving to the seated position, whereas patients with discogenic pain usually have pain in flexion e.g. sitting) and the pain may increase the longer they are seated. 14. I paresthesia (a "pins and needles" feeling) or e the ia present? A sensation or a lack of sensation ma: e experienced if there is pressure on a nerve roor. Par the ia occurs if pressure is relieved from a nerve trunk· whereas if the pressure is on the nerve trunk a numb ensation is felt. Does the patient experience any pare thesia or tingling and numbness in the extremitie perineal (saddle) area, or pelvic area? Abnormal sensation in the perineal area often have associated micturition (urination) problems. These symptoms may indicate a myelopathy and are considered by many to be an emergency surgical situation because of

potential long-term bowel and bladder problems if t pressure on the spinal cord is not relieved as soon possible. 4 o,4! The examiner must remember that t adult spinal cord ends at the bottom of the Ll vert bra and becomes the cauda equina within the spin column. The nerve roots extend in such a way that is rare for the disc to pinch on the nerve root of t same level. For example, the L5 nerve root is mo likely to be compressed by the L4 intervertebral d than by the L5 intervertebral disc (Fig. 9-14). Seldo is the nerve root compressed by the disc at the sam level, except when the protrusion is more lateral. 15. Has the patient noticed any weakness or d crease in strength? This may be due to an injury to t muscles themselves, their nerve supply, or reflex inhib tion caused by pain. 22 ,42 16. What is the patient's usual activity or pastim Before the injury, did the patient modifY or perfor any unusual repetitive or high-stress activity? Su questions help the examiner determine whether t cause of injury was macrotrauma, microtrauma, or combination of both. 17. Which activities aggravate the pain? Is the anything in the patient's lifestyle that increases t pain? Many common positions assumed by patients a similar to those in some of the provocative spec tests. For example, getting into and sitting in a car similar to the slump test and straight leg raise te Long sitting in bed is a form of straight leg rais Reaching up into a cupboard can be similar to upper limb tension test. A word of caution is advise There can be a 10 0 to 20 0 difference in straight l

o o

L4

L5

Fifth lumbar root ---2'i!lP"1 L5

81

igure 9-14 .ossible effects of disc herniation. (A) Herniation of the disc between L4 and LS compresses the fifth umbar root. (B) Large herniation of the LS-S1 disc compromises not only the nerve root crossing it 5rst sacral nerve root) but also the nerve root emerging through the same foramen (fifth lumbar nerve :"OOt). (C) Massive central sequestration of the disc at the L4-LSlevel involves all of the nerve roots in - e cauda equina and may result in bowel and bladder paralysis. (Redrawn from MacNab, 1.: Backache. Baltimore, Williams & Wilkins, 1977, pp. 96-97.)

~a.ise

in lying and slttmg because of the change in ordosis and position of the pelvis. 3 18. Which activities ease the pain? If there are posions that relieve the pain, the examiner should use an understanding of anatomy to determine which tissues 'ould have stress taken off them in the pain-relieving DOstures, and these postures may later be used as resting postures during the treatment. 19. What is the patient's sleeping position? Is there any problem sleeping? What type of mattress is used hard, soft)? The best sleeping position is in side lying ith the legs bent in a semifetal position. If the patient lies prone, the lumbar spine often falls into extension mcreasing the stress on the posterior elements of the '·ertebrae. In supine lying, the spine tends to flatten out, decreasing the stress on the posterior elements. 20. Does the patient have any difficulty with micturition? If so, the examiner should proceed with caution, because the condition may involve more than the lumbar spine (e.g., a myelopathy, cauda equina syndrome, tabes dorsalis, tumor, multiple sclerosis). Con\'ersely, these symptoms may result from a disc protruion or spinal stenosis with minimal or no back pain or ciatica. A disc derangement can cause total urinary retention; chronic, longstanding partial retention; ve-

sicular irritability; or the loss of desire or awareness of the necessity to void. 21. Is the patient receiving any medication? For example, long-term use of steroid therapy can lead to osteoporosis. Also, if the patient has taken medication just before the assessment, the examiner may not get a true reading of the pain. 22. Is the patient able to cope during daily activities? Does the patient have trouble with work, leisure activities, washing or dressing? How far can the patient walk before the pain begins?43 What is the patient's level of disability? Disability implies the effect of the pathology on activity not pain. Thus, disability testing commonly revolves around activities of daily living and functional activities. Thus, this question may be tied in with the use of the questions in the functional assessment seen later. Finally, the examiner must be aware that, although in most cases, people who have low back pain have simple mechanical back problems, or have nerve root problems involving the disc, there is always the possibility of serious spinal pathology. Wadde1l 3 outlines signs and symptoms that would lead the examiner to conclude more serious pathology is present in the lumbar spine (Table 9-6).

480


Table 9-6 Indications of Serious Spinal Pathology

Red Flags Presentation age 55 years Violent trauma, such as a faU from a height, car accident Constant, progressive, nonmechanical pain Thoracic pain Previous history carcinoma systemic steroids drug abuse, HIV Systematically unwell weight loss Persisting severe restriction of lumbar flexion Widespread neurology Structural deformity Investigations when required sedimentation rate (ESR) >25 plain x-ray: vertebral collapse or bone destruction

Cauda Eguina Syndrome/ Widespread Neurologic Disorder Difficulty with micturition Loss of anal sphincter tone or fecal incontinence Saddle anesthesia about the anus, perineum or genitals Widespread (> one nerve root) or progressive motor weakness in the legs or gait disturbance Sensory level

Inflammatory Disorders (Ankylosing Spondylitis and Related Disorders)

Gradual onset before age 40 years Marked morning stiffness Persisting limitation of spinal movements in all directions Peripheral joint involvement Iritis, skin rashes (psoriasis), colitis, urethral discharge Family history

From Waddell, G.: The Back Pain Revolution. New York, Churchill Livingstone, 1998, p. 12 .

... Observation The patient must be suitably undressed. Males must wear only shorts, and females must wear only a bra and shorts. When doing the observation, the examiner should note the willingness of the patient to move and the pattern of movement. The patient should be observed for the following traits, first in standing and then sitting position.

Body Type There are three general body types (see Fig. 15-19): ectomorphic-thin body build, characterized by retan 'e prominence of structures developed from the em.'onic ectoderm; mesomorphic-muscular or sturdy y build, characterized by relative prominence of trucrure developed from the embryonic mesoderm; an endomorphic-heavy (fat) body build, characterized b. r latiye prominence of structures developed from the embryonic endoderm.

Gait Does the gait appear to be normal when the patient walks into the examination area, or is it altered in

some way? If it is altered, the examiner must take tim to find out whether the problem is in the limb 0 whether the gait is altered to relieve symptoms els where.

Attitude

What is the appearance of the patient? Is the patien tense, bored, lethargic, healthy looking, emaciate overweight?

Total Spinal Posture

The patient should be examined in the habitual relaxe posture (see Chapter 15) that he or she would usual adopt. With acute back pain, the patient presents wi some degree of antalgic (painful) posturing. Usually, loss of lumbar lordosis is present and there may be lateral shift or scoliosis. This posturing is involunt and often cannot be reduced because of the musc spasm. 44 ,45 The patient should be observed anteriorly, laterall and posteriorly (Fig. 9-15). During the observatio the examiner should pay particular attention whether the patient holds the pelvis "in neutral" natu rally, or if not, is he or she able to achieve the neutr

I

A ~'gure

B

o

C

9-15

-:ews of the patient in the standing position. (A) Anterior view. (B) Posterior view. (C) Lateral Lateral view with excessive lordosis.

elvis posmon (normal lordotic curve with ASISs beg slightly lower than PSISs). Many people with back ain are unable to maintain a neutral pelvis position. ~\nteriorly, the head should be straight on the shoulers, and the nose should be in line with the manurium, sternum, and xiphisternum or umbilicus. The :houlders and clavicle should be level and equal, although the dominant side may be slightly lower. The ~'aist angles should be equal. Does the patient show a ateral shift or list (Fig. 9-16)? Such a shift may be ~traight lateral movement or it may be a scoliosis (roation involved). The straight shift is more likely to be -aused by mechanical dysfunction and muscle spasm and is likely to disappear on lying down or hanging. 3 ,46 True scoliosis commonly has compensating curves and does not change with hanging or lying down. The arbitrary "high" points on both iliac crests should be the same height. If they are not, the possibility of unequal leg length should be considered. The difference in height would indicate a functional limb length discrepancy. This discrepancy could be caused by altered bone length, altered mechanics (e.g., pronated

\~ew.

Main curve Compensatory curve

\I ')

Sciatic "list" or lateral shift

Figure 9-16 Lateral shift or list.

Scoliosis

482


Table 9-7 Functional Limb Length Difference Joint Foot

Functional Lengthening

Functional Shortening

Supination

Pronation

Knee

Extension

Flexion

Hip

Lowering Extension Lateral rotation

Lifting Flexion Medial rotation

Sacroiliac

Anterior rotation

Posterior rotation

Erector spinae (tight)

ASIS low

From Wallace, L.A.: Lower quarter pain: Mechanical evaluation and treatment. In Grieve, G.P. (ed.): Modern Manual Therapy of the Vertebral Column. Edinburgh, Churchill Livingstone, 1986, p. 467. Iliopsoas (tight)

foot on one side), or JOint dysfunction (Table 9-7). The anterior superior iliac spines (ASISs) should be level. The patellae should point straight ahead. The lower limbs should be straight and not in genu varum or genu valgum. The heads of the fibulae should be level. The medial malleoli should be level, as should be the lateral malleoli. The medial longitudinal arches of the feet should be evident, and the feet should angle out equally. The arms should be an equal distance from the trunk and equally medially or laterally ro-

Figure 9-17 Congenital scoliosis and a diastematomyelia in a 9-year-old girl. This type of hairy patch strongly indicates a congenital maldevelopment of the neural axis. (From Rothman, R.H., and F.A. Simeone: The Spine. Philadelphia, W.B. Saunders Co., 1982, p. 371.)

Figure 9-18 The pelvic crossed syndrome as described by Janda and J ulI.

tated. Any protrusion or depression of the sternum ribs, or costocartilage, as well as any bowing of bon should be noted. The bony or soft-tissue contot should be equal on both sides. From the side, the examiner should look at the hea to ensure that the ear lobe is in line with the tip of th shoulder (acromion process) and the arbitrary high point of the iliac crest. Each segment of the spin should have a normal curve. Are any of the curv exaggerated or decreased? Is lordosis present? Kypho sis? Do the shoulders droop forward? Normally with neutral pelvis, the ASISs are slightly lower than th posterior superior iliac spines (PSISs). Are the kne straight, flexed, or in recurvatum (hyperextended)? From behind, the examiner should note the level the shoulders, spines and inferior angles of the scapul and any deformities (e.g., a Sprengel's deformity). An lateral spinal curve (scoliosis) should be noted (Fi 9-17). If the scoliotic curve is due to a disc herni tion, the herniation usually occurs on the convex sid of the curve. 47 The waist angles should be equal fro the posterior aspect, as they were from the anteri aspect. The PSISs should be level. The examin should note whether the PSISs are higher or low than the ASISs and the patient's ability to maintain

e level. The Achilles tendons and heels should appear be straight. The examiner should note whether ere is any protrusion of the ribs or bowing of bones. Any deviation in the normal spinal postural alignment ould be noted and recorded. The various possible urces of pathology related to posture are discussed in hapter 15. Janda and Jull 48 described a lumbar or pelvic crossed syndrome (Fig. 9 -18) to show the effect of uscle imbalance on the ability of a patient to hold d maintain a neutral pelvis. With this syndrome, they ypothesized that there was a combination of weak, ng muscles and short, strong muscles, which resulted an imbalance pattern leading to low back pain. 49 They felt that only by treating the different groups propriately, could the back pain be relieved. The -eak, long inhibited muscles were the abdorninals and _ uteus maximus whereas the strong tight (shortened) uscles were the hip flexors (primarily iliopsoas) and . e back extensors. The imbalance pattern promotes creased lumbar lordosis because of the forward pelvic t and hip flexion contracture and overactivity of the :lp flexors compensating for the weak abdominals. The -eak gluteals result in increased activity in the hammngs and erector spinae as compensation to assist hip xtension. Interestingly, although the long spinal ex-ensors show increased activity, the short lumbar mus- es (e.g., multifidus, rotatores) show weakness. Also, - e hamstrings show tightness as they attempt to pull - e pelvis backward to compensate for the anterior ·0

Igure 9-19 _-eurofibromatosis with scoliosis. Note the .:.lie au lait spots on the right side of the :runlc (From Tachdjian, M.O.: Pediatric Or- opedics. Philadelphia, W.B. Salmders Co., .990, p. 1290.)

gluteus medius results in increased activity of quadratus lumborum and tensor fasciae latae on same side. This syndrome is often seen in conjunct with upper crossed syndrome (see Chapter 3, "Ce cal Spine"). The two syndromes together are called layer syndrome. 48

Markings

A "faun's beard" (tuft of hair) may indicate a sp bifida occulta or diastematomyelia (see Fig. 9-17) Cafe au lait spots may indicate neurofibromatosis collagen disease (Fig. 9 -19). Unusual skin marki or the presence of skin lesions in the midline may l the examiner to consider the possibility of underly neural and mesodermal anomalies. Musculoskel anomalies tend to form at the same time embryolo cally. Thus, if the examiner finds one anomaly, possibility of other anomalies must be considered.

Step Deformity

A step deformity in the lumbar spine may indicat spondylolisthesis. The "step" occurs because the nous process of one vertebra becomes prominent w either the vertebra above (for example, spondy spondylolisthesis) or the affected vertebra (for exam spondylolytic spondylolisthesis) slips forward on one below (Fig. 9-20).

484


Figure 9-20

__ Bump

Step deformity in the lumbar spine. (A) Caused by spondylosis. (B) Caused by spondylolisthesis. (C) Spinous process protrusion caused by step deformity.

A

in the lumbar spine. Unless there is a history of defini tive trauma to a peripheral joint, a screening or scan ning examination must accompany assessment of tha joint to rule out problems within the lumbar spin referring symptoms to that joint. It is often helpful a this stage to ask the patient to demonstrate the move ments that produce or have produced the pain. If the patient is asked to do this, time must be allowed fo symptoms to disappear before the remainder of th examination is carried out.

Active Movements

Examination The examiner must remember that when assessing the lumbar pine referral of symptoms or the presence of neurological .TIlptoms often makes it necessary to "clear" or rule the lower limb pathology. Many of the symptoms that occur in the lower limb may originate

Active movements are performed with the patien standing (Fig. 9-21). The examiner is looking for dif ferences in range of motion (ROM) and the patient willingness to do the movement. The ROM taking place during the active movement is normally the sum mation of the movements of the entire lumbar spine not just movement at one level, along with hip move ment. The most painful movements are done last. 1 the problem is mechanical, at least one or more of the movements will be painful. 21 While the patient is doing the active movements, the examiner looks for limitation of movement and its po sible causes, such as pain, spasm, stiffness, or blocking As the patient reaches the full range of active move ment, passive overpressure may be applied, but only i the active movements appear to be full and pain free The overpressure must be applied with extreme care because the upper body weight is already being applied to the lumbar joints by virtue of their position and gravity. If the patient reports that a sustained position increases the symptoms, then the examiner should consider having the patient maintain the position (e.g. flexion) at the end of the ROM for 10 to 20 second to see whether symptoms increase. Likewise, if repeti tive motion or combined movements have been

c

o

E

F

Figure 9-21 Active movements of the lumbar spine. (A and B) Measuring forward flexion using tape measure. (C) Extension. (D) Side flexion (anterior view). (E) Side flexion (posterior view). (F) Rotation (standing). (G) Rotation (sitting).

G

486


reported in the history as causing symptoms, these movements should be performed as well, but only after the patient has completed the basic movements.

Active Movements of the lumbar Spine • Forward flexion (40° to 60°) • Extension (20° to 35°) • Side (lateral) flexion, left and right (15° to 20°) • Rotation, left and right (3° to 18°) • Sustained postures (if necessary) • Repetitive motion (if necessary) • Combined movements (if necessary)

The greatest motion in the lumbar spine occurs between the L4 and LS vertebrae and between L5 and S1. There is considerable individual variability in the ROM of the lumbar spine (Fig. 9-22).51-55 In reality, little obvious movement occurs in the lumbar spine especially in the individual segments because of the shape of the facet joints, tightness of the ligaments, presence of the intervertebral discs, and size of the vertebral bodies. For flexion (forward bending), the maximum ROM in the lumbar spine is normally 40° to 60°. The examiner must be sure to differentiate the movement occurring in the lumbar spine from that occurring in the hips or thoracic spine. It must be remembered that ome patients can touch their toes by flexing the hips, even if no movement occurs in the spine. On forward flexion, the lumbar spine should move from its normal lordotic curvature to at least a straight or slightly flexed curve (Fig. 9-23).56 If this change in the spine does not occur, there is probably some hypomobility in the lumbar spine due either to tight structures or mu de spasm. The degree of injury also has an effect.

ROTATION Lor R

T10-11 T11-12 T12-L1 L1-2 L2-3 L3-4 L4-5 L5-S1

For example, the more severely a disc is injured (fo example, if sequestration has occurred rather than protrusion), the greater will be the limitation of move ment. 57 With disc degeneration, intersegmental motio may increase as disc degeneration increases up to certain point and follows Kirkaldy-Willis'58 descriptio of degenerative changes in the dise. He divided th changes into three stages-dysfunctional, unstable and stable. During the first two phases, intersegmenta motion increases in flexion, rotation, and side flexionS and then decreases in the final stabilization phase During the unstable phase, it is often possible to se an instability jog during one or more movements especially flexion, returning to neutral from flexion, o side flexion. 6o ,61 An instability "jog" is a sudden move ment shift or "rippling" of the muscles during actiy movement. It is an indication of an unstable seg ment. 56 Similarly, muscle twitching during movemen or complaints of something "slipping out" during lum bar spine movement may indicate instability.62 If th patient bends one or both knees on forward flexion the examiner should watch for nerve root symptoms o tight hamstrings, especially if spinal flexion is decrease when the knees are straight. If tight hamstrings 0 nerve root symptoms are suspected, the examine would perform suitable tests (see "Special Tests" sec tion) to determine if the hamstrings or nerve roo restriction (see discussion of knee flexion test) are th cause of the problem. When returning to the uprigh posture from forward flexion, the patient with no bac pain first rotates the hips and pelvis to about 45° 0 flexion; during the last 45° of extension, the low bac resumes its lordosis. In patients with back pain, com monly, most movement occurs in the hips, accompa nied by knee flexion, and sometimes with hand sup port working up the thighs. 63 As with the thoraci spine, the examiner may use a tape measure to deter mine the increase in spacing of the spinous processe on forward flexion. ormally, the measurement shoul increase 7 to 8 cm (2.8 to 3.1 inches) if it is taken between the T12 spinous process and SI (see Fig

T10-11

SIDE FLEXION Lor R

T11-12 T12-L1 L1-2 L2-3 L3-4 L4-5 L5-S1

Figure 9-22 Average range of motion in the lumbar spine. (Adapted from Grieve, G.P.: Common Vertebral Joint Problems. Edinburgh, Churchill Livingstone, 1981.)

EXTENSION

gure 9-23 n forward flexion, the lumbar curve should normally flatten or go o slight flexion, as shown.

-21A and B). The examiner should note how far . lward the patient is able to bend (i.e., to midthigh, ees, midtibia, or floor) and compare this finding ith the results of straight leg raising tests (see "Speal Tests" section). Straight leg raising, especially if ilateral, is essentially the same movement done pas'-ely, except that it is a movement occurring from dow upward instead of from above downward. During the active movements, especially during flexn and/or extension, the examiner should watch for a ainfu1 arc. The pain seen in a lumbar painful arc - nds to be neurologically based (i.e., it is lancinating r lightening-like), but may also be due to instability. - - it does occur on movement in the lumbar spine, it is ely a space occupying lesion (most likely, a small erniation of the disc) is pinching the nerve root in art of the range as the nerve root moves with the -notion. 46 Maigne 44 describes an active movement flexion maeuver to help confirm lumbar movement and control. In this "happy round maneuver," the patient bends 'orward and places the hands on a bed or on the back f a chair. The patient then attempts to arch or hunch

Figure 9-24 The sphinx position.

unable to sustain the hunched position. Extension (backward bending) is normally limited 20° to 35° in the lumbar spine. While performing t movement, the patient is asked to place the hands the small of the back to help stabilize the back. Bo dillon and DayM advocate doing this movement in t prone lying position to hyperextend the spine. Th called the resulting position the sphinx position. T patient hyperextends the spine by resting on the bows with the hands holding the chin (Fig. 9-24) a allows the abdominal wall to relax. The position held for 10 to 20 seconds to see if symptoms occur, if present, become worse. Side (lateral) flexion or side bending is appro mately 15° to 20° in the lumbar spine. The patient asked to run the hand down the side of the leg a not to bend forward or backward while performing t movement. The examiner can then "eyeball" t movement and compare it with that of the other si The distance from the fingertips to the floor on bo sides may also be measured, noting any difference. the spine, the movement of side flexion is a coupl movement with rotation. Because of the position the facet joints, both side flexion and rotation occ together although the amount of movement and dir tion of movement may not be the same. Table 9 shows how different authors interpret the coup movement in the spine. As the patient side flexes, t examiner should watch the lumbar curve. Normal the lumbar curve forms a smooth curve on side fl ion, and there should be no obvious sharp angulati at only one level. If angulation does occur, it m indicate hypomobility below the level or hypermobil above the level in the lumbar spine (Fig. 9-25). M vein and Ju1l 65 advocate having the patient do a late shift (Fig. 9-26) in addition to side flexion. They f lateral shift in the lumbar spine focuses the movem more in the lower spine (L4-Sl) and helps elimin the compensating movements in the rest of the spine Rotation in the lumbar spine is normally 3° to 1 to the left or right, and it is accomplished by a she ing movement of the lumbar vertebrae on each oth Although the patient is usually in the standing po tion, rotation may be performed while sitting to elim nate pelvic and hip movement. If the patient stan the examiner must take care to watch for this accesso movement and try to eliminate it by stabilizing t pelvis. If a movement such as side flexion toward the pa ful side increases the symptoms, the lesion is probab intra-articular, because the muscles and ligaments that side are relaxed. If a disc protrusion is present a lateral to the nerve root, side flexion to the pain side increases the pain and radicular symptoms on th

488


Table 9-8 Coupled Movements (Side Flexion and Rotation) Believed to Occur in the Spine in Different Positions (note the differences) Author MacConnaill Farfan Kaltenborn Grieve Fryette Pearcy

In Neutral

Contralateral

Oxland

In Flexion

Ipsilateral Contralateral Ipsilateral Ipsilateral Ipsilateral Ipsilateral (L5-S1) Contralateral (IA, 5) Ipsilateral (L5-S1)* Contralateral

In Extension

Contralateral Contralateral Ipsilateral Contralateral Ipsilateral

(L5-S1)** Ipsilateral implies both movements occur in the same direction, contralateral implies they occur in opposite directions

* If side flexion induced first * * If rotation induced first

Figure 9-25

side. If a movement such as side flexion away from the painful side alters the symptoms, the lesion may be articular or muscular in origin, or it may be a disc protrusion medial to the nerve root (Fig. 9-27). McKenzie 31 advocates repeating the active movements, especially flexion and extension, 10 times to see whether the movement increases or decreases the symptoms. He also advocates, like Mulvein and Jull,65 a side gliding movement in which the head and feet remain in position and the patient shifts the pelvis to the left and to the right. If the examiner finds that side flexion and rotation have been equally limited, and extension has been limited to a lesser extent, a capsular pattern may be suspected. A capsular pattern in one lumbar segment, however, is difficult to detect. Because back injuries rarely occur during a "pure" movement such as flexion, extension, side flexion, or ro tion it has been advocated that combined moveof the spine should be included in the exarnina- The examiner may want to test the following mor babitual combined movements: lateral flexion in flexion: lateral flexion in extension; flexion and rotation: an extension and rotation. These combined movemen Fig. 9-28) may cause signs and symptom different from those produced by single plane mo emen and are definitely indicated if the patient has sho"'n that a combined movement is what causes the symptom . For example, if the patient is suffering from a facet ndrome combined extension and rotation is the movement most likely to exacerbate symp-

Lateral (side) flexion. Note that lower lumbar spine stays straight and upper lumbar and lower thoracic spine side flexes. This finding would indicate h~' pomobility in the lower lumbar spine.

Figure 9-26 Lumbar lateral shift.

A

B

ure 9-27 ents with herniated disc problems may sometimes list to one side. This is a voluntary or involuntary hanism to alleviate nerve root irritation. The list in some patients is toward the side of the sciatica; ,thers, it is toward the opposite side. A reasonable hypothesis suggests that when the herniation is -era! to the nerve root (A), the list is to the side opposite the sciatica because a list to the same side uld elicit pain. Conversely, when the herniation is medial to the nerve root (B), the list is toward the . of the sciatica because tilting away would irritate the root and cause pain. (Fom White, AA., and _1. Panjabi: Clinical Biomechanics of the Spine, 2nd ed. Philadelphia, J.B. Lippincott, 1990, p. 415.)

B - gure 9-28 ,mbined active movements. (A) Lateral flexion in flexion. (B) Lateral flexion in extension. Rotation and flexion. (D) Rotation and extension.

o

490


Figure 9-29

toms. 68 Other symptoms that would indicate facet in volvement include absence of radicular signs 0 neurological deficit, hip and buttock pain, and some times leg pain above the knee, no paresthesia, and 10 back stiffness. 69 ,70 While the patient is standing, a "quick test" of th lower peripheral joints may be performed (Fig. 9-29 provided the examiner feels the patient has the abili to do the test. The patient squats down as far possible, bounces two or three times, and returns t the standing position. This action quickly tests the an kles, knees, and hips as well as the sacrum for an pathological condition. If the patient can fully squa and bounce without any signs and symptoms, the joints are probably free of pathology related to th complaint. However, this test should be used on. with caution and should not be done with patien suspected of having arthritis or pathology in the lowe limb joints, pregnant patients, or older patients wh exhibit weakness and hypomobility. If this test is nega tive, there is no need to test the peripheral join(peripheral joint scan) with the patient in the lyin;: position.

Quick test.

Figure 9-30

Trendelenburg and SI nerve root test. (A) Anterior view, negative test. (B) Side view, negative test. (C) Posterior view, positive test for a weak right gluteus medius.

up and down on the toes four or five times. This is, . effect, a modified Trendelenberg test. While the paent does this, the examiner should watch for Trendeburg's sign (Fig. 9-30). A positive Trendelenburg go is shown by the nonstance side ilium dropping own instead of elevating as it normally would when QIlding on the leg. A positive sign may be caused by a eak gluteus medius muscle or a coxa vara (abnormal aft-neck angle of the femur) on the stance leg side. If · e patient is unable to complete the movement by gog up and down on the toes, the examiner should pect an S1 nerve root lesion. Both legs are tested. McKenzie advocates doing flexion movements with - e patient in the supine lying position as welPl In - e standing position, flexion in the spine takes place om above downward, so pain at the end of the ROM dicates that L5-S1 is affected. When the patient is in · e supine lying position, with the knees being lifted · the chest, flexion takes place from below upward so - at pain at the beginning of movement indicates that

=-

greater stretch is placed on L5-S1 when the patient is in the lying position. During the observation stage of the assessment, the examiner will have noted any changes in functional limb length (see Table 9-7). Wallace 7' developed a method for measuring functional leg length. The patient is first assessed in a relaxed stance. In this position, the examiner palpates the ASISs and the PSISs, noting any asymmetry. The examiner then places the patient in a symmetric stance, ensuring that the subtalar joint is in the neutral position (see Chapter 13), the toes are straight ahead, and the knees are extended. The ASISs and PSISs are again assessed for asymmetry. If differences are still noted, the examiner should check for structural leg length differences (see Chapters 10 and 11), sacroiliac joint dysfunction, or weak gluteus medius or quadratus lumborum (Fig. 9-31). The pelvis may also be leveled with the use of calibrated blocks or cards so that the functional length difference can be recorded.

'/

1

~

---"T-

\

\

i~ 7-

--/,,1

1\

-\

It

-,f-"

I\,

~-/

~

AI I --"?-::

\...~

~

(

A

B

c

Igure 9-31 =:tfect of different leg lengths and posture. Note presence of scoliosis on the side with the "short" limb. •\) Normal. (B) Short left femur. (C) Short left tibia. (D) Pronation of left foot.

D

J

"-

492


Passive Movements In the lumbar spine, passive movements are very difficult to perform because of the weight of the body. If active movements are full and pain free, overpressure can be attempted with care. However, it is safer to check the end feel of the individual vertebrae in the lumbar spine during the assessment of joint play movements. The end feel is the same, but the examiner has better control of the patient and is less likely to overstress the joints.

Passive Movements of the Lumbar Spine and Normal End Feel

movement of the lumbar spine. The lumbar sp should be in a neutral position, and the painful mo ments should be done last. The examiner should k in mind that strong abdominal muscles help to red the load on the lumbar spine by approximately 3 and on the thoracic spine by approximately 50%, a result of the increased intrathoracic and intra-abdo nal pressures caused by the contraction of these m cles. Table 9-9 lists the muscles acting on the lum vertebrae.

Resisted Isometric Movements of the Lumbar Spine • Forward flexion

• Flexion (tissue stretch)

• Extension

• Extension (tissue stretch)

• Side flexion (left and right)

• Side flexion (tissue stretch)

• Rotation (left and right)

• Rotation (tissue stretch)

• Dynamic abdominal endurance • Double straight leg lowering • Dynamic extensor endurance

Resisted Isometric Movements Resisted isometric muscle strength of the lumbar spine is first tested in the neutral position. The patient is seated. The contraction must be resisted and isometric so that no movement occurs (Fig. 9-32). Because of the strength of the trunk muscles, the examiner should say, "Don't let me move you," so that minimal movement occurs. The examiner tests flexion, extension, side flexion, and rotation. Fig. 9-33 shows the axes of

• Isotonic horizontal side support • Internal/external abdominal oblique test

Provided neutral isometric testing is normal or o causes a small amount of pain, the examiner can go to other tests, which will place greater stress on muscles. These tests are often dynamic and prov both concentric and eccentric work for the musc

Figure 9-32

Positioning for resisted isometric move ments of the lumbar spine. (A) Flexion extension, and side flexion. (B) Rotatio to right.

~---------------

Linea alba

- - - - - - - - - Rectus abdominus

~---

External oblique

-++-+---- Internal oblique

+-+-+++---- Transverse abdominus - - Psoas

SIDE FLEXION - -

~-----H+mf-:

/ r H + , ' H : - - - - Quadratus lumborum

/ /I-~--- Latissimus dorsi ) V~='-"""=""'S...-5~~-h'----- Transversalis

-++-=='7-77'------- Longissimus Spinalis

-----..."",~...,...--'lorth Am. 14:475-489, 1983. ctly, N.J., and A.P. Moore: Neuromusculoskeletal examination and assessment. New York, Churchill Livingstone, 1987. Phillips, D.R., and L.T. Twomey: A comparison of manual diagnosis \\~th a diagnosis established by a uni-levellumbar spinal block procedure. Man. Ther. 2:82-87, 1996. olly, D.W., F.X. Kilkelly, KA. McHale, L.M. Asplund, M. Mulligan, and A.S. Chang: Measurement of lumbar lordosis-evaluation of intraobserver, interobserver and technique variability. Spine 21:1530-1536,1996. orter, R.W., and e.G. Miller: Back pain and trunk list. Spine 11: 596-600,1986. orter, R.W., and I.F. TraiJescu: Diurnal changes in straight leg raising. Spine 15:103-106, 1990. orterfield, J.A., and C. DeRosa: Mechanical Low Back Pain: Perspectives in Functional Anatomy. Philadelphia, W.B. Saunders Co., 1991. uick Reference Guide for Physicians: Acute Low Back Problems in Adults. Assessment and Treatment. Rockville, Maryland, D .S. Department of Health and Human Services, 1994. Ramsey, R.H.: The anatomy of the ligamentum flava. Clin. Orthop. 44:129-140,1966. Rankine, ].J., D.G. Fortune, e.E. Hutchinson, D.G. Hughes, and C.J. Main: Pain drawings in the assessment of nerve root compression: a comparative study \~th lumbar spine magnetic resonance imaging. Spine 23:1668-1676, 1998. Rauschnig, W., KB. Heithoff, D.W. Stoller, et al.: Radiology. In Weinstein, J.N., and S.W. Weisel (eds.): The Lumbar Spine. Philadelphia, W.B. Saunders Co., 1990.

Richardson, J.K, and Z.A. Iglarsh: Clinical Orthopedic Physic Therapy. Philadelphia, W.B. Salmders Co., 1994. Riddle, D.L.: Classification and low back pain: A re\iew of th literature and critical analysis of selected systems. Phy . Ther 708-737,1998. Robinson, L.R.: Role of neurophysiologic evaluation in diagn Am. Acad. Orthop. Surg. 8:190-199,2000. Rose, K, and P. Balasubramaniam: Nerve root canals in the lu spine. Spine 9:16-18, 1984. Rothman, R.H., and F.A. Simeone: The Spine. Philadelplua. W Saunders Co., 1982. Rydevik, B., M.D. Brown, and G. Lundberg: Pathoanatomya pathophysiology of nerve root compression. Spine 9:7-15,1 Saal, J.S.: The role of inflammation in lumbar pain. Spine 20: 1827,1995. Saunders, H.D., and R. Saunders: Evaluation, Treatment and vention of Musculoskeletal Disorders. Chaska, Mirmesota, S ders Group, 1993. Schenk, R.: A combined approach to lumbar examination. ]. M Manip. Ther. 4:77-80, 1996. Seimen, L.P.: Low Back Pain: Clinical Diagnosis and Manage Norwalk, Connecticut, Appleton-Century-Crofts, 1983. Selby, D.K: When to operate and what to operate on. Orthop North Am. 14:577-588,1983. Selim, A.J., G. Fincke, X.S. Ren, R.A. Deyo, A. Lee, K Skinn L. Kazis: Patient characteristics and patterns of use for lumb spine radiographs-results from the veterans health study. S 25:2440-2444,2000. Shacldock, M.O., D.S. Butler, and H. Slater: The dynamic cen nervous system: Structure and clinical neurobiomechanics. I ing, J.D., and N. Palastanga (eds.): Grieve's Modern Manua apy. Edinburgh, Churchill Li~ngstone, 1994. Shiqing, X., Z. Quanzhi, and F. Dehao: Significance of the st leg raise test in the diagnosis and clinical evaluation of lowe lumbar intervertebral disc protrusion. J. Bone Joint Surg. A 517-522, 1987. Simmons, E.D., R.D. Guyer, A. Graham-Smith, and R. Herzo Radiographic assessments for patients with low back pain. S 20:1839-1841,1995. Smith, S.A., J.B. Massie, R. Chesnut, and S.R. Garfin: Straigh raising: Anatomical effects on the spinal nerve root with and out filsion. Spine 18:992-999, 1993. Snook, S.H.: Low back pain in industry. American Academy o thopaedic Surgeons Symposium on Idiopathic Low Back Pa Louis, C.Y. Mosby Co., 1982, pp. 23-38. Sorensen, F.B.: Physical measurements as risk indicators for lo trouble over a one year period. Spine 9:106-119,1984. Spivak, J.M.: Degenerative lumbar spine stenosis. J. Bone Join Anl. 80:1053-1066, 1998. Sullivan, M.S., L.D. Schoaf, and D.L. Riddle: The relationship lumbar flexion to disability in patients with low back pain. P Ther. 80:240-250,2000. Supik, L.F., and M.]. Broom: Sciatic tension signs and lumba herniation. Spine 19:1066-1069, 1994. Tachdjian, M.O.: Pediatric Orthopedics. Philadelphia, W.B. S Co., 1972. Tenhula, J.A., S.J. Rose, and A. Delitto: Association between tion of lateral lumbar shift, movement tests and side of sym in patients \~th low back pain syndrome. Phys. Ther. 70:48 486,1990. Thelander, D., M. Fagerlwld, S. Friberg, and S. Larsson: Stra raising test versus radiologic size, shape, and position of lum disc hernias. Spine 17:395-399, 1992. Troyanovich, S.J., D.D. Harrison, and D.E. Harrison: Low ba and the lumbar intervertebral disc: Clinical considerations fo doctor of chiropractic. J. Manip. Physiol. Ther. 22:96-104 Van Wijmen, P.M.: The use of repeated movements in the M method of spinal examination. In Boyling, J.D., and N. Pal (eds.): Grieve's Modern Manual Therapy: The Vertebral Co 2nd ed. Edinburgh, Churchill Livingstone, 1994. Vanharanta, H., B.L. Sachs, M. Spivey, et al.: A comparison o

566


discography, pain response and radiographic disc height. Spine 13: 321-324,1988. Waddell, G.: Clinical assessment of lumbar impairment. Clin. Orthop. 221:110-120, 1987. Waddell, G., and C.l. Main: Assessment of severity in low back disorders. Spine 9:204-208,1984. Watkins, RG.: History, physical examination, and diagnostic tests for back and lower extremity problems. In Watkins, RG. (ed.): The Spine in Sports. St. Louis, C.v. Mosby Co., 1996. Weise, M.D., S.R Gartin, RH. Gelberman, M.M. Katz, and RP. Thorne: Lower extremity sensibility testing in patients with herniated lumbar intervertebral discs. J. Bone Joint Surg. Am. 67: 1219-1224,1985. Weissman, B.N.W., and C.B. Sledge: Orthopedic Radiology. Philadelphia, W.B. Saunders Co., 1986. White, A.A., and M.M. Panjabi: Clinical Biomechanics of the Spine. Philadelphia, J.B. Lippincott Co., 1978. Wiesel, S.W., P. Bernini, and RH. Rothman: The Aging Lumbar Spine. Philadelphia, W.B. Saunders Co., 1982.

Williams, M., M. Solomonov, B.H. Zhou, R V. Baralta, and M. Harris: Multifidus spasms elicited by prolonged lumbar flexion. Spine 25:2916-2924, 2000. Williams, P.L., and Warwick, R (eds.): Gray's Anatomy, 36th Bri ed. Edinburgh, Churchill Livingstone, 1980. Williams, RM., C.H. Goldsmith, and T. Minuk: Validity of the double inclinometer method for measuring lumbar flexion. Physiother. Can. 50:147-152,1998. Wittink, H., T.H. Michel, R Kulich, A. Wagner, A. Sukiennik, R Maciewicz, and W. Rogers: Aerobic fitness testing in patients wrchronic low back pain-which test is best? Spine 25:1704-171 2000. Yingling, V.R., and S.M. McGill: Anterior shear of spinal motion segments- kinematics, kinetics and resultant injuries observed in porcine model. Spine 24:1882-1889, 1999. Yong-Hing, K., and W.H. Kirkaldy-Willis: The pathophysiology or degenerative disease of the lumbar spine. Orthop. Clin. North • 14:491-504,1983.

£LVIS e sacroiliac joints form the "key" of the arch be·een the two pelvic bones; with the symphysis pubis, · ey help to transfer the weight from the spine to the ver limbs and provide elasticity to the pelvic ring. ·s triad of joints also acts as a buffer to decrease the · rce of jars and bumps to the spine and upper body · used by contact of the lower limbs with the ground. ecause of this shock-absorbing function, the structure .- the sacroiliac and symphysis pubis joints is different · om that of most joints that are assessed. Assessment .- the sacroiliac joints and symphysis pubis should be -luded in the examination of the lumbar spine and/ hips if there is no direct trauma to either one of ese joints. l Normally, a comprehensive examination .- the sacroiliac joints is not made until examination of e lumbar spine and/or hip has been completed. If th of these joints are examined and the problem still pears to be present and remains undiagnosed, an amination of the pelvis should be initiated.

Applied Anatomy e sacroiliac joints are part synovial joint and part l1desmosis. A syndesmosis is a type of fibrous joint in hich the intervening fibrous connective tissue forms interosseous membrane or ligament. The synovial rtion of the joint is C-shaped, with the convex iliac dace of the C facing anteriorly and inferiorly. Kaandji 2 states that the greater or the more acute the gle of the C, the more stable the joint and the less • e likelihood of a lesion to the joint. The sacral sur.- -e is slightly concave. The size, shape, and roughness of the articular sur· ces vary greatly among individuals. In the child, these urfaces are smooth. In the adult, they become irreguM depressions and elevations that fit into one another; y so doing, they restrict movement at the joint and dd strength to the joint for transferring weight from ~e lower limb to the spine. The articular surface of ~e ilium is covered with fibrocartilage; the articular urface of the sacrum is covered with hyaline cartilage that is three times thicker than that of the ilium. In

older persons, parts of the joint surfaces may be obliterated by adhesions.

Sacroiliac Joint Resting position:

Neutral

Capsular pattern:

Pain when joints are stressed

Close pack:

Nutation

loose pack:

Counternutation

Although the sacroiliac joints are relatively mobile in young people, they become progressively stiffer with age. In some cases, ankylosis results. The movements that occur in the sacroiliac and symphysis pubis joints are slight compared with the movements occurring in the spinal joints. The sacroiliac joints are supported by several strong ligaments (Fig. 10 -1) - the long posterior sacroiliac ligaments that limit anterior pelvic rotation 3 or sacral counternutation, the short posterior sacroiliac ligament that limits all p.elvic and sacral movement, the posterior interosseous ligament that forms part of the sacroiliac articulation (the syndesmosis), and the anterior sacroiliac ligaments. 4 The sacrotuberous ligament and sacrospinous ligament limit nutation and posterior innominate rotation. 4 The iliolumbar ligament stabilizes LS on the ilium. 4 The sacroiliac joints and symphysis pubis have no muscles that control their movements directly although the muscles do provide pelvic stability. However, they are influenced by the action of the muscles moving the lumbar spine and hip, because many of these muscles attach to the sacrum and pelvis. The muscles that support the pelvic girdle as well as the lumbar spine and hips can be divided into groups.5-7 The inner group consists of deep musclestransverse abdominus, diaphragm, multifidus, and pelvic floor muscles. The outer group consists of four

567

568

CHAPTER 10 • Pelvis

Anterior longitudinal ligament

----~-+i-I,.l.j.

Iliolumbar ligament ~~~?: Level of gluteal folds.

y forced anterior diagonal patternY The sacrum is wer on the side of the pelvis that has rotated back·ard. The most common rotation of the innominate nes is left posterior torsion or rotation (pathological -ounternutation). The posterior rotational dysfunctions Me usually the result of falling on an ischeal tuberosity, Jfting when forward flexed with the knees straight, ~epeated standing on one leg, vertical thrusting onto ill extended leg, or sustaining hyperflexion and abducon of hips. 3. Are both pubic bones level at the symphysis puis? The examiner tests for level equality by placing one finger or thumb on the superior aspect of each ubic bone and comparing the heights (Fig. 10-12). If the ASIS on one side is higher, the pubic bone on that side is suspected to be higher, and this can be

confirmed by this procedure, indicating a backward torsion problem of the ilium on that side. This procedure is usually done with the patient lying supine. 4. Does the patient, when standing, have equal weight on both feet, favor one leg, or have a lateral pelvic tilt? This finding may indicate pathology in the sacroiliac joints, the leg, the spine, or a short leg. 5. Are the ASISs equidistant from the center line of the body? 6. What type of pelvis does the patient have?20 Gynecoid and android types are the most common (as described in Fig. 10-13 and Table 10-1). 7. Is the sacrovertebral or lumbosacral angle normal (140°)? 8. Is the pelvic angle or inclination normal (30°)? 9. Is the sacral angle normal (30°) (Fig. 10-14)?

- - - - - - - - - - - - - - - - - - -

-----

574


10. Are the iliac crests level? Altered leg length rna alter their height. 11. Are the PSISs level? 12. Are the buttock contours or gluteal folds n mal? The painful side is often flatter if there is loss tone in the gluteus maximus muscle. 13. Is there any unilateral or bilateral spasm of erector spinae muscles? 14. Are the ischial tuberosities level? If one tuber ity is higher, it may indicate an upslip of the ilium the sacrum on that side. 16 15. Is there excessive lumbar lordosis? Forward backward sacral torsion may increase or decrease lordosis. 16. Are the PSISs equidistant from the center ill of the body? 17. Are the sacral sulci equal? If one is deeper. may indicate a sacral torsion. 18. Do the feet face forward to the same degre Often, the affected limb is medially rotated. Wi spasm of the piriformis muscle, the limb is later rotated on the affected side. Figure 10-12

T

Determining level of pubic bones.

Examination

Before assessing the pelvic joints, the examiner sho first assess the lumbar spine and hip, unless the hist definitely indicates that one of the pelvic joints i fault. The lumbar spine and hip can, and frequen do, refer pain to the sacroiliac joint area. Because

A Pelvic inlet

Figure 10-13

B

Sacrosciatic ------l;f-notch Ischial spine

Gynecoid (predominantly female) and androl-' (primarily male) pelvises. (A) Anterior view. (B) Lateral view. (C) Anterior view of the pu and ischium.

,1")\

~,.~\ '\-.

C Subpubic arch --'r--"h"-7"

GYNECOID

ANDROID

able 10-1 Comparison of the Two Most Common Types of Pelvis Feature

Gynecoid

Android

:nIet

Round

Triangular

-acrosciatic notch

Average size

Narrow

acrum ~ ubpubic

arch

Average

Forward

Inclination curved

Inclination straight

croiliac joints are in part a syndesmosis, movements these joints are minimal compared with those of the ther peripheral joints. It should also be remembered - at any condition that alters the position of the sa.:rum relative to the ilium causes a corresponding - ange in the position of the symphysis pubis. Although many tests and test movements have been 'escribed to help determine if there is sacroiliac dys- ction, many of them are imprecise and their reliility has been questioned. 21 - 27 At the present time, - ey are the best tests available. It is important for the ~xaminer to consider all aspects of the assessment in- uding the history and the patient's symptoms along ith the various tests and movements before diagnosg sacroiliac joint problems. 4 ,S,21,28-30

ctive Movements - -nlike other peripheral joints, the sacroiliac joints do ot have muscles that directly control their movement, However, because contraction of the muscles of the ther joints may stress these joints or the symphysis =,ubis, the examiner must be careful during the active r resisted isometric movements of other joints and be ure to ask the patient about the exact location of the _all on each movement. For example, resisted abducon of the hip can cause pain in the sacroiliac joint on ~e same side if the joint is injured, because the glu-eus medius muscle pulls the ilium away from the sa.:rum when it contracts strongly. In addition, side flexon to the same side increases the shearing stress to the croiliac joint on that side. The examiner is attemptillg to reproduce the patient's symptoms rather than list looking for pain. The sacroiliac joints move in a "nodding" fashion of anteroposterior rotation. Normally, the PSISs approximate when the patient stands and separate when the atient lies prone. When he or she stands on one leg, me pubic bone on the supported side moves forward ill relation to the pubic bone on the opposite side as a result of rotation at the sacroiliac joint. The stability at the sacroiliac joint is determined by tWO factors-form closure and force closure. Form

Figure 10-14 Normal angles of the pelvic joints. a = Lumbosacral angle (140°). b = Lumbar lordotic curve (50°). c = Sacral angle (30°). d = Pelvic angle (30°).

closure refers to the close packed position of the joint where no outside forces are necessary to hold the joint stable. Thus, intrinsic factors such as joint shape, coefficient of friction of the joint surfaces, and integrity of the ligaments contribute to form closure. s Force closure would be similar to the loose packed position in that extrinsic factors, primarily the muscles and their neurological control, along with the capsule are needed to maintain stability of the joint as well as the forces applied to the joint. S These two forms of closure enable the sacroiliac joints to self lock as they go into close pack and slightly release, when the joint unlocks. During the active movements of the pelvic joints, the examiner looks for unequal movement, loss of or increase in movement (hypomobility or hypermobility), tissue contracture, tenderness, or inflammation. The movements of the spine put a stress on the sacroiliac joints as well as on the lumbar and lumbosacral joints. During forward flexion of the trunk, the innominate bones and pelvic girdle as a whole rotate anteriorly as a unit on the femoral heads bilaterally. The same thing occurs when one rises from supine lying to sitting. If one leg is actively extended at the hip, the innominate on that side will unilaterally rotate anteriorly.s During the anterior rotation of the innominate bones (counternutation), the innominate slides posteriorly along its long arm and inferiorly down its

576


Active Movements That Stress the Sacroiliac Joints • Forward flexion of the spine (40° to 60°) • Extension of the spine (20° to 35°) • Rotation of the spine, left and right

W to 18°)

• Side flexion of the spine, left and right (15° to 20°) • Flexion of the hip (100° to 120°) • Abduction of the hip (30° to 50°) • Adduction of the hip (30°) • Extension of the hip (0° to 15°) • Medial rotation of the hip (30° to 40°) • Lateral rotation of the hip (40° to 60°)

short arm (Fig. 10-15).5 Initially, the sacrum nutates up to about 60° of forward flexion, but once the deep posterior structures (deep and posterior oblique muscle sysems, thoracolumbar fascia, and the sacrotuberous ligament) become tight, the innominates continue to rotate anteriorly on the femoral heads, but the sacrum begins to counternutate. 5 This counternutation causes the sacroiliac joint to be vulnerable to instability as greater muscle action (force closure) is required to maintain stability with counternutation.7 Thus, the earlier counternutation occurs during forward flexion, the more vulnerable is the sacroiliac joint to instability problems. Excessive counternutation is more likely to occur in patients who have tight hamstrings. 5

Ant. Rotation Innominate

Figure 10-15 When the innominate anteriorly rotates, its articular surface glides inferoposteriorly relative to the sacrum. (From Lee, D.: The Pelvic Girdle, 2nd ed. Edinburgh, Churchill Livingstone, 1999, p. 51.)

Figure 10-16 Examiner palpating PSIS prior to forward flexion.

To test forward flexion, the patient stands \\1 weight equally distributed on both legs. The exam in sits behind the patient and palpates both PSIS (Fi::10-16). The patient is asked to bend forward and symmetry of movement of the PSIS superiorly noted. At the same time, the examiner should note th~ amount of flexion that has occurred when sacral nut.:tion begins. This can be done by having the patier.repeat the forward bending motion while the examine palpates the PSIS (inferior aspect) on one side wi one thumb while the other thumb palpates the sacr base so the thumbs are parallel. In the first 45° forward flexion, the sacrum will move forward (nutate (Fig. 10-17A), but near 60° (normally), the sacrUlh will begin to counternutate or move backwards (Fi~ 10-17B).5 During the sacral counternutation, the n\"-< ----.,'J'----- Posterior inferior iliac spine t;f--7"~-+-,f------

Coccyx

"-=,.......'------- Ischial tuberosity

The examiner then places the thumbs over the pubic tubercles and moves the fingers laterally until the bony greater trochanter of the femur is felt. The trochanters are usually level. The trochanteric bursa lies over the greater trochanter and is palpable only if it is swollen. Returning to the ASIS, the examiner can move on to palpate the femoral triangle, which has as its boundaries the inguinal ligament superiorly, the adductor longus muscle medially, and the sartorius muscle laterally. It is in the superior aspect of the triangle that the examiner palpates for swollen lymph nodes. The femoral pulse can be palpated deeper in the triangle. Although almost impossible to palpate, the femoral nerve lies lateral to the artery, whereas the femoral vein lies medial to it. The psoas bursa may also be palpated within the femoral triangle, but only if it is swollen. Before moving on to the posterior structures, the examiner should determine whether the adjacent musculature-the abductor, flexor, and adductor muscles-shows any indication of pathology (e.g., muscle spasm, pain).

Posterior Aspect To complete the posterior palpation, the patient lie the prone position, and the following structures a:_ palpated. Iliac Crest and Posterior Superior Iliac Spine Again, the examiner places the fingers on the iliac cr and moves posteriorly until they rest on the PSI which is at the level of the S2 spinous process. many patients, dimples indicate the position of th PSIS. Ischial Tuberosity. If the examiner then moves ill tally from the PSIS and down to the level of gluteal folds, the ischial tuberosities may be palpate It is important that they be palpated, because the harr: string muscles attach here, and the bony prominenc are what one "sits on." Sacral Sulcus and Sacroiliac Joints. Returning t the PSIS as a starting point, the examiner should pa..-

19ure 10-63 • alpation of the right sacroiliac joint.

_ate slightly below it on the sacrum adjacent to the ·um. (This area is sometimes referred to as the sacral sulcus.) The depth on the right side should be com_ared with that on the left side. If one side is deeper Lhan the other, sacral torsion or rotation on the ilium Hound the horizontal plane may be indicated. If the examiner then moves slightly medially and iistal to the PSIS, the fingers will rest adjacent to the ;;;acroiliac joints. To palpate these joints, the patient's mee is flexed to 90° or greater and the hip is passively :nedially rotated while the examiner palpates the sacro'ac joint on the same side (Fig. 10-63). This proceure is identical to the prone gapping test previously escribed under Passive Movements. The procedure is repeated on the other side, and the two results are .:ompared. Sacrum, Lumbosacral Joint, Coccyx, Sacral HiaSacral Cornua, and Sacrotuberous and Sacro-

tus,

..0..;-.,,------:7'"""'--\- Sacral articular facet

0~(i~-:::..t.:::"'----,4- Sacral canal -h.,...,..,H-..,-f---!+-- Sacral spinous process

-'1----'+---- Sacral foramen A'I7-t~-f---~-4"::"-----

spinous Ligaments. The examiner again returns the PSIS and moves to the midline of the sacrum where the S2 spinous process can be palpated. Moving superiorly over two spinous processes, th fingers now rest on the spinous process of L5. As check, the examiner may look to see if the fingers re just below a horizontal line drawn from the high poi of the iliac crests. This horizontal line normally pass through the interspace between L4 and L5. Havin found the L5 spinous process, the examiner then pa pates between the spinous processes of L5 and S feeling for signs of pathology at the lumbosacral join Moving laterally approximately 2 to 3 cm (0.8 to 1 inches), the fingers lie over the lumbosacral fac joints, which are not palpable. However, the overlyin structures may be palpated for tenderness or spasm which may indicate pathology of these joints or relat structures. In a similar fashion, the spinous process and facet joints of the other lumbar spines and inte vening structures can be palpated. The examiner then returns to the S2 spinous proce or tubercle. Carefully palpating farther distally, just b fore the coccyx, the examiner may be able to palpa the sacral hiatus lying in the midline. If the fingers a moved slightly laterally, the sacral cornua, which co stitute the distal aspect of the sacrum, may be palpat (Fig. 10-64). To palpate the coccyx properly, the examiner pe forms a rectal examination (Fig. 10 - 65). A rubb glove is put on, and the index finger is lubricated. Th index finger is then carefully pushed into the rectum the patient relaxes the sphincter muscles. The inde finger then palpates the anterior surface of the coccy while the thumb of the same hand palpates its post rior aspect. While holding the coccyx between the fi ger and thumb, the examiner is able to move it bac and forth, rocking it at the sacrococcygeal joint. No mally, this action should not cause pain. The examiner then returns to the PSIS. Movin straight down or distally from the PSIS, the finge follow the path of the sacrotuberous ligament, whic should be palpated for tenderness. Slightly more tha halfway between the PSIS and ischial tuberosity an slightly medially, the fingers pass over the sacrosp nous ligament, which is deep to the sacrotuberou ligament. Tenderness in this area may indicate patho ogy of this ligament.

Sacral hiatus Sacral cornu

--==-=f------ Coccyx

Diagnostic Imaging 51 Plain Film Radiography

Figure 10-64 Posterior view of the sacrum and coccyx.

On plain film radiography, anteroposterior view (Fig 10-66 and 10-67), the examiner should look for o note the following:

600


-----------r:::::::=~=::::::::::::==::::::::::::~

Ilium Greater trochanter ------f-----..,;-----::::--

Ischial tuberosity

--:7"'----j'-----r---..::....q-----',~=---------lIiac

crest

Iliac tubercle------f i r - - -.....- - - - - - - - A n t e r i o r superior iliac spine

Greater trochanter ----'7'1""~ Head of femur -----1-+----'

'\'r----">,,--------Acetabulum

Figure 11-55

Landmarks of the hip (anterior view)

t------Symphysis pubis

Lesser trochanter -----\~r---.I ' - - - - - - - - - I s c h i a l tuberosity

ment is felt. As slight resistance is maintained, the patient's hip is taken into abduction while maintaining flexion in an arc of movement. As the movement is performed, the examiner should look for any irregularity in the movement (e.g., "bumps"), pain, or patient apprehension, which may give an indication of where the pathology is occurring in the hip (see Fig. 1154D).64 This motion also causes impingement of the femoral neck against the acetabular rim so it should be performed with care. 16 - J8

Palpation

During palpation of the hip and associated mu the examiner should note any tenderness, temper muscle spasm, or other signs and symptoms tha indicate the source of pathology.

Anterior Aspect

The following structures should be palpated anter as shown in Figure 11- 55.

644

CHAPTER 11 • Hip

~---Inguinalligament ~--

Iliacus muscle

Femoral nerve Femoral artery

--j'---+:Tl~.!~~

Femoral vein Psoas muscle --+---H+--\1hI'H> . f/,~O'r+- Pectineus muscle

Sartorius muscle -+---\f\-\ \ VI f 11,1 +''-I++-- Adductor longus muscle

Figure 11-56 Femoral triangle containing the femoral artery, vein, and nerve. Note the inguinal ligament above, iliacus and psoas laterally, and adductors medially. The sartorius attaches to the anterosuperior spine, whereas the adductor muscles attach along the pubic ramus. (Modified from Anson, B.J.: Atlas of Human Anatomy. Philadelphia, W.B. Saunders Co., 1963, p. 583.)

Iliac Crest, Greater Trochanter, and Anterior Superior Iliac Spine. The iliac crests are easily palpated and should be level. The crest should be palpated for any tenderness, because several muscles insert into this structure. In athletes, a condition called a "hip pointer" may be located on the iliac crest. This occurs from a strain or contusion of the muscles that insert into the crest. The iliac tubercle is felt during palpation along the lateral aspect of the crest. The examiner

then moves anteriorly to the ASIS. The greater trochanter, located approximately 10 cm (4 inches) dist10 blocks 5-10 blocks B or A = B; with lateral overpull the quadriceps, B > A. (Redrawn from Kolowich, P.A., L.E. Paulo.. T.D. Rosenberg, and S. Farnsworth. Lateral release of the patella: Indications and contraindications. Am. J. Sports Med. 18:361, 1990.)

Zohler's Sign. 50 The patient lies supine with th knees extended. The examiner pulls the patella distill and holds it in this position. The patient is asked t contract the quadriceps (Fig. 12-113). Pain is indicative of a positive test for chondromalacia patellae However, the test may be positive (false positive) in large proportion of the normal population.

Figure 12-111 Passive patellar tilt test. (From Kolowich, P.A., L.E. Paulos, T.D. Rosenberg, and S. Farnsworth: Lateral release of the patella: Indications and contraindications. Am. J. Sports Med. 18:361,1990.)

Figure 12-113 Zohler's sign for chondromalacia patellae.

Vf-+-----

Frund's Sign. The patient is in the sitting posit The examiner percusses the patella in various positi of knee flexion. Pain is indicative of a positive test may signify chondromalacia patellae.

Anterior superior iliac spine

Other Tests

++----i~----

Q-Angle or Patellofemoral Angle. The Q-an (quadriceps angle) is defined as the angle between quadriceps muscles (primarily the rectus femoris) the patellar tendon and represents the angle of qua ceps muscle force (Fig. 12-114).168 The angle is tained by first ensuring that the lower limbs are right angle to the line joining the two anterior su rior iliac spines (ASISs). A line is then drawn from ASIS to the midpoint of the patella on the same and from the tibial tubercle to the midpoint of patella. The angle formed by the crossing of these lines is called the Q-angle. The foot should be pla in a neutral position in regard to supination and p nation and the hip in a neutral position in regard medial and lateral rotation, because it has been fo that different foot and hip positions alter the angle. 169 ormally, the Q-angle is 13° for males and 18° females when the knee is straight (Fig. 12-115). angle less than 13° may be associated with chondro

a-Angle

1++-+------- Midpoint of patella I H+-+-------- Tibial tubercle

Figure 12-114 Quadriceps angle (Q-angle).

Femoral neck anteversion

MedM-Lat

A

Increased a-angle (>20°)

Femoral neck retroversion

CJ'

Med.:

La\.

B

Decreased a-angle «15°)

Figure 12-115

(A) Femoral neck anteversion a lateral tibial torsion increase the angle and lead to lateral trackin the patella on the femoral sulcu (B) Femoral neck retroversion a medial tibial torsion decrease th Q-angle and tend to centralize tracking of the patella. (Redraw from Tria, A.]., and R.c. Palum Conservative treatment of patel femoral pain. Semin. Orthop. 5 116-117,1990.)

730

CHAPTER 12 • Knee

Figure 12-116

Q-angle in flexed position. Exaggerated Q-angle in the patient's right knee is seen as residual positive Q-angle with the knee flexed. Normally, the Q-angle in flexion should be 0°. (From Hughston, I.C., W.M. Walsh, and G. Puddu: Pate lar Subluxation and Dislocation. Philadelphia, W.B. Saunders Co., 1984, p. 24

lacia patellae or patella alta. An angle greater than 18° is often associated with chondromalacia patellae, subluxing patella, increased femoral anteversion, genu valgum, lateral displacement of tibial tubercle, or increased lateral tibial torsion. During the test, whic may be done either with radiographs or physically or. the patient, the quadriceps should be relaxed. If measured with the patient in the sitting position, the Qangle should be 0° (Fig. 12-116). While the patient i in a sitting position, the presence of the "bayonet sign," which indicates an abnormal alignment of the quadriceps musculature, patellar tendon, or tibial shaft_ should be noted (Fig. 12-117). Hughston advocates doing the test with the quadnceps contracted. l l l If measured with the quadricep contracted and the knee fully extended, the Q-angl should be 8° to 10°. Any angle greater than 10° 1

A

B

Figure 12-117 Increased Q-angle. (A) Bayonet sign. Tibia vara of proximal third causes a markedly increased Q-angle. Alignment of the quadriceps, patellar tendon, and tibial shaft resembles a French bayonet. (B) Q-angle with the knee in full extension is only slightly increased over normal. (C) However, with the knee flexed at 30°, there is failure of the tibia to derotate normally and failure of the patellar tendon to line up with the anterior crest of the tibia. This is not an infrequent finding in patients with patellofemoral arthralgia. (A, From Hughston, J.C., W.M. Walsh, and G. Puddu: Patellar Subluxation and Dislocation. Philadelphia, W.B. Saunders Co., 1984, p. 26; B and C, From Ficat, R.P., and D.S. Hungerford: Disorders of the Patello-Femoral Joint. Baltimore, Williams & Wilkins, 1977, p. 117.)

c

Axis of patellar tendon

Transepicondylar line - - - - i t - .-f-. f-

fill I

II i I I

'

~;)III i hI), \c J;I P.'I""'""'" to

transepicondylar line

/1

Figure 12-118 Tubercle sulcus angle of 90°. With the knee flexed to 90°, the transepicondylar line is assessed. The axis of the patellar tendon is compared with a perpendicular to the transepicondylar line. (Modified from Kolowich, P.A., L.E. Paulos, T.D. Rosenberg, and S. Farnsworth: Lateral release of the patella: Indications and contraindications. Am. J. Sports Med. 18:361,1990.)

Daniel's Quadriceps Neutral Angle Test. 174 T patient lies supine, and the unaffected leg is test first. The patient's hip is flexed to 450, and the knee flexed to 90° with the foot flat on the examining tab The patient is asked to extend the knee isometrica while the examiner holds down the foot. If tibial d placement is noted, knee flexion is decreased (posteri tibial displacement) or increased (anterior tibial d placement). The process is repeated until the angle which there is no tibial displacement is reached (F 12 -120). This angle, the quadriceps neutral angle, a erages 70° (range, 60° to 90°). The injured knee placed in the same neutral angle position, and t patient is asked to contract the quadriceps. Any ant rior displacement is indicative of posterior cruciate lig ment insufficiency. The quadriceps neutral angle is p marily used for machine testing of laxity (e.g., K 1000 arthrometer, Stryker knee laxity test apparatus).

Wilson Test. This is a test for osteochondritis di secans. The patient sits with the knee flexed over t examining table. The knee is then actively extend with the tibia medially rotated. At approximately 3 of flexion (0° being straight leg), the pain in the kn increases, and the patient is asked to stop the flexi movement. The patient is then asked to rotate t tibia laterally, and the pain disappears. This findi indicates a positive test, which is indicative of oste chondritis dissecans of the femoral condyle. The test positive only if the lesion is at the classic site for oste

considered abnormal. The examiner must ensure that a standardized measurement procedure is used to ensure consistent values. 170 Tubercle Sulcus Angle (Q-Angle at 90°).22,165 This measurement is also used to measure the angle of quadriceps pull. A vertical line is drawn from the center of the patella to the center of the tibial tubercle. A second horizontal line is drawn through the femoral epicondyle (Fig. 12-118). Normally the lines are perpendicular. Angles greater than lO° from the perpendicular are considered abnormal. Lateral patellar subluxation may affect the results. Another measurement, which is similar to the Qangle, is the A-angle, which measures the relation of the patella to the tibial tubercle. This measurement, which is not as commonly used as the Q-angle, consists of a vertical line that divides the patella into two halves and a line drawn from the tibial tubercle to the apex of the inferior pole of the patella. The resulting angle is the A-angle (Fig. 12-119).171,172 Some have questioned the reliability of this measurement because of the difficulty in consistently finding appropriate landmarks. 173

Inferior patellar pole _-'-'-_

A angle

tuberosity width

Figure 12-119

Location of landmarks of the A-angle. (Redrawn from Ehrat, M., J Edwards, D. Hastings, and T. Worrell: Reliability of assessing patel alignment. The A-angle. J. Orthop. Sports Phys. Ther. 19:23, 1994

732

CHAPTER 12 • Knee

J

4~1 /.'~

/.2

Quadriceps neutral angle 60-75°

A

B

c

Figure 12-120 During open chain knee extension, tibial translation is a function of the shear force produced by the patellar tendon, (A) Quadriceps neutral position, The patellar tendon force is perpendicular to the tibial plateaus and results in compression of the joint surfaces without shear force, (B) At flexion angles less than the angle of the quadriceps neutral position, orientation of the patellar tendon produces anterior shear of the tibia, (C) At angles greater than the angle of the quadriceps neutral position, patellar tendon force causes a posterior shear of the tibia, (From Daniel, D,M" M,L Stone, P, Barnett, and K Sachs: Use of the quadriceps active test to diagnose posterior cruciate ligament disruption and measure posterior laxity of the knee, I. Bone Joint Surg, Am, 70:386-391, 1988,)

\

! \,"

Figure 12-121 Classic site of osteochondritis dissecans,

~ I

knee to 90°, accompanied by hip flexion (Fig. 12123). Pressure is then applied to the lateral femora. epicondyle, or 1 to 2 cm (0.4 to 0.8 inch) proximal t it, with the thumb. While the pressure is maintained the patient's knee is passively extended. At approximately 30° of flexion (0° being straight leg), the patient complains of severe pain over the lateral femora. condyle. Pain indicates a positive test. The patienstates that it is the same pain that occurs with activity.

chondritis dissecans of the knee, namely, the medial femoral condyle near the intercondylar notch (Fig, 12-121). Fairbank's Apprehension Test. This is a test for dislocation of the patella. I II , 175 The patient lies in the supine position with the quadriceps muscles relaxed and the knee flexed to 30° while the examiner carefully and slowly pushes the patella laterally (Fig. 12-122). If the patient feels the patella is going to dislocate, the patient will contract the quadriceps muscles to bring the patella back "into line." This action indicates a positive test. The patient will also have an apprehensive look. Noble Compression Test. This is a test for iliotibial band friction syndrome. 176 The patient lies in the supine position, and the examiner flexes the patient's

Figure 12-122 Apprehension test. (Redrawn from Hughston, I.e., W.M. Walsh, and G. Puddu: Patellar Subluxation and Dislocation. Philadelphia, W.B. Saunders Co., 1984, p. 29.)

intermedius are tight. Testing for a tight rectus femor is described in the hip chapter (Chapter 11).

Test for Knee Extension Contracture (Hee Height Difference).177 The patient lies prone with th thighs supported and the legs relaxed. The examine measures the difference in heel height (Fig. 12 -124) One centimeter of difference approximates 1°, depend ing on leg length. The test, along with the accompa nying end feel, would be used to test for joint contrac ture (tissue stretch) and possibly tight hamstring (muscle stretch). Swelling may also cause a positiv test.

Figure 12-123

Tests for Hamstrings Tightness. These tests ar described in Chapter 11.

Noble compression test.

Measurement of Leg Length. The patient lies i the supine position with the legs at a right angle to line joining the two ASISs. With a tape measure, th examiner obtains the distance from one ASIS to th lateral or medial malleolus on that side, placing th metal end of the tape measure immediately distal t and up against the ASIS (Fig. 12-125). The tape i stretched so that the other hand pushes the tap against the distal aspect of the medial (or lateral) mal leolus, and the reading on the tape measure is noted The other side is tested similarly. A difference betwee the two sides of as much as 1.0 to 1.5 cm is consid ered normal. However, the examiner must remembe

Functional Test for Quadriceps Contusion. The patient lies in the prone position while the examiner passively flexes the knee as much as possible. If passive knee flexion is 90° or more, it is only a mild contusion. If passive knee flexion is less than 90°, the contusion is moderate to severe, and the patient should not be allowed to bear weight. Normally, the heel-tobuttock distance should not exceed 10 cm (4 inches) in men and 5 cm (2 inches) in women. This test may also be used to test tightness of the quadriceps (vasti) muscles. If the range is limited and the end feel is

HEEL HEIGHT DIFFERENCE (centimeters)

~HHD LLSL HHD = Tan LLSL

Figure 12-124 Heel height difference. The patient lies prone on the examining table with the lower limbs supported by the thighs. The difference in heel height is measured. The conversion of heel height difference to de· grees of extension loss depends on the leg length. The tangent of angle IJ is the heel height difference (HHD) divided by the lower· leg segment length (LLSL). The LLSL is proportional to patient height. (From Daniel, D., W. Akeson, and J. Q'COImer [eds.]: Knee Ligaments: Structure, Injury and Repair. New York, Raven Press, 1990,

p.32.)

e

734

CHAPTER 12 • Knee

knee, ankle, or foot problems-primarily, ankle or foot problems. Measurement of Muscle Bulk (Anthropometric Measurements for Effusion and Atrophy). The examiner selects areas where muscle bulk or swelling i greatest and measures the circumference of the leg. It is important to note on the patient's chart how far above or below the apex or base of the patella one i measuring and whether the tape measure is placed above or below that mark. The following are common measurement points: Figure 12-125 Measuring leg length (to the lateral malleolus).

that even this difference may result in pathological symptoms. If there is a difference, the examiner can determine its site of occurrence by measuring from the high point on the iliac crest to the greater trochanter (for coxa vara) , from the greater trochanter to the lateral knee joint line (for femoral shaft length), and from the medial knee joint line to the medial malleolus (for tibial length). The two legs are then compared. The examiner must also remember that torsion deformities to the femur or tibia can alter leg length. Functional Leg Length. The patient stands in the normal relaxed stance. The examiner palpates the ASISs and then the posterior superior iliac spines (PSISs) and notes any differences. The examiner then positions the patient so that the patient's subtalar joints are in neutral while bearing weight (see Chapter 13). While the patient holds this position with the toes straight ahead and the knee straight, the examiner repalpates the ASISs and the PSISs. If the previously noted differences remain, the pelvis and sacroiliac joints should be evaluated further. If the previously noted differences disappear, the examiner should suspect a functional leg length difference caused by hip,

1. 2. 3. 4. 5. 6.

15 cm (6 inches) below the apex of the patella Apex of the patella or joint line 5 cm (2 inches) above the base of the patella 10 cm (4 inches) above the base of the patella 15 cm (6 inches) above the base of the patella 23 cm (9 inches) above the base of the patella.

Hughston 35 advocated using the lateral joint line rather than the patella for the beginning point 0 measurement; he believed that the joint line was more constant. The examiner must also note, if possible. whether swelling or muscle bulk is being measured an remember that there is no correlation between muscl bulk and strength.

Reflexes and Cutaneous Distribution Having completed the ligamentous and other tests o' the knee, if a scanning examination has not been carried out, the examiner next determines whether the reflexes around the knee joint are normal especially I; neurological involvement is suspected (Fig. 12-126 The patellar (L3-L4) and medial hamstring (L5-S1 reflexes should be checked for differences between the two sides.

Figure 12-126 Reflexes of the knee. (A) Patellar (L3). (B) Medial hamstrings (L5).

Iliohypogastric nerve (L1)

----'l.-------- Subcostal nerve (T12) ---"...,....---- Genitofemoral nerve (L1,2)

+---

Ilioinguinal nerve (L1) Dorsal rami (S1,2,3) - - - - - - ' r -

-t-+----

Medial and intermediate cutaneous nerve of thigh (femoral) (L2,3)

-+---- Obturator nerve (L2,3,4)

-+---+---

Lateral cutaneous nerve of thigh (L2,3)

------+--t--_+_

Medial cutaneous nerve of thigh (femoral) (L2,3)

Figure 12-127 Peripheral nerve sensory distribution about the knee.

----+

-----r

Posterior cutaneous nerve of thigh (S1,2,3) Saphenous nerve (femoral) (L3,4) - - - - - - - - f -

- + - - + - - - - Lateral cutaneous nerve of calf (peroneal) (L5,S1,2) ----+-+_

-+-1:---- Superficial peroneal nerve (L4,5,S1)

The examiner must keep in mind the dermatome patterns of the various nerve roots (Fig. 12-127) as well as the cutaneous distribution of the peripheral nerves (Fig. 12-128). To test for altered sensation, a sensation scanning examination should be performed using relaxed hands and fingers to cover all aspects of the thigh, knee, and leg. Any differences in sensation should be noted and can be mapped out further with the use of a pinwheel, pin, cotton batten, or soft brush. True knee pain tends to be localized to the knee, but it may also be referred to the hip or ankle (Fig. 12-129). In a similar fashion, pain may be referred to the knee from the lumbar spine, hip (e.g., slipped capital femoral epiphysis in children), and ankle. Sometimes a lesion of the medial meniscus leads to irritation of the infrapatellar branch of the saphenous nerve. The result is a hyperaesthetic area the size of a quarter on the medial side of the knee. This finding is called

Turner's sign. 50 Muscles about the knee and their pain referral pattern are shown in Table 12-10.

Peripheral Nerve Injuries About the Knee Common Peroneal Nerve (L4 through 82). This nerve is vulnerable to injury in the posterolateral knee and as it winds around the head of the fibula. It has also been reported that the nerve may be stretched as a result of pulling on the peroneus longus muscle in a lateral ankle sprain,177-179 direct trauma, or a varus stress to the knee. 22 The result is weakness or paralysis of muscles supplied by the deep and superficial peroneal nerves, the two branches of the common peroneal nerve (Table 12-11). This causes an inability to dorsiflex the foot (drop foot), resulting in a steppage gait and an inability to evert the foot. Sensory loss is as shown in Figure 12-130.

736

CHAPTER 12 • Knee

Figure 12-128 Dermatomes abour the knee.

Table 12-10 Knee Muscles and Referral of Pain Muscle

Figure 12-129 Patterns of referred pain to and from the knee.

Referral Pattern

Tensor fasciae latae

Lateral aspect of thigh

Sartorius

Over course of muscle (anterior thigh)

Quadriceps

Anterior thigh, patella, lateral thigh and knee (vastus lateralis)

Adductor longus and brevis

Superior anterolateral thigh, anterior thigh, proximal to patella and sometimes down anteromedialleg

Adductor magnus

Medial thigh from groin to adductor tubercle

Gracilis

Medial thigh (primarily the midportion)

Semimembranosus and s'emitendinosus

Ischial tuberosity, posterior and posteromedial calf

Biceps femoris

Posterior knee up posterior thigh

Popliteus

Posterior knee

Gastrocnemius

Posterior knee, posterolateral cali and posteromedial calf to foot instep

Plantaris

Posterior knee and calf

thi~

Table 12-11 Peripheral Nerve Injuries (Neuropathy) About the Knee Nerve

Muscle Weakness

Sensory Alteration

Reflexes Affected

Common peroneal nerve

Tibialis anterior (DP) Extensor digitomm brevis (DP) Extensor digitomm longus (DP) Extensor hallucis longus (DP) Peroneus tertius (DP) Peroneus longus (SP) Peroneus brevis (SP)

Area around head of fibula Web space between first and second toes (DP) Lateral aspect of leg and dorsum of foot (SP)

No common reflexes affected

Saphenous nerve

None

Medial side of knee, may extend down medial side of leg to medial malleolus

None

DP = deep peroneal branch; SP = superficial peroneal branch.

Lateral sural cutaneous Lateral sural cutaneous and sural

Deep peroneal

Semitendinosus Semimembranosus

Biceps short head

Deep peroneal nerve '-tf--+--Tibialis anterior Peroneus longus I/A'I\-/--

Peroneus brevis

III'." f - f - - Superficial

peroneal nerve If IIJIf'f--- Extensor digitorum longus

Adductor magnus, posterior part

--~+l11I

Common Tibial nerve peroneal nerve -T7'JIfI!1--;:"r-\-- Plantaris f9"~--';;;H::::-

Deep peroneal nerve

Popliteus

Peroneus longus -----+\t\\ Peroneus brevis

Soleus

Iff-+--+- Flexor

Superficial peroneal nerve

hallucis longus

Extensor hallucis longus

Flexor digitorum longus

- - - Peroneus tertius

Tibialis posterior

i!\fi'tn:---=- Extensor hallucis and digitorum brevis

Anterior view

Figure 12-130 Common peroneal nerve.

Gastrocnemius

Posterior view

738

CHAPTER 12 • Knee

Figure 12-131 Joint play movements of the knee. (A) Posterior movement of the tibia on the femur. (B) Anterior movemenr of the tibia on the femur. (C) Patellar movement, distally. (D) Patellar movement, laterally. (E) Anteroposterior movement of the superior tibiofibular joint.

Joint Play Movements For joint play movements on the knee, the patient i placed in the supine position (Fig. 12-131). The movement on the affected side is compared with that on the normal side.

Joint Play Movements of the Knee Complex Saphenous Nerve (L2 through IA). The saphenous nerve is a sensory branch of the femoral nerve that arises near the inguinal ligament and passes down the leg to supply the skin on the medial side of the knee and calf. The nerve is sometimes injured during surgery or trauma, or it may be entrapped as it passes between the vastus medialis and adductor magnus muscles. Entrapment may lead to medial knee pain (burning) that is aggravated by walking, standing, and quadriceps exercises.18o-182 Sensory loss after surgery or trauma is shown in Figure 12-127.

• Backward glide of tibia on femur • Forward glide of tibia on femur • Medial translation of tibia on femur • Lateral translation of tibia on femur • Medial displacement of patella • Lateral displacement of patella • Depression of patella • Anteroposterior movement of fibula on tibia

Figure 12-132 Medial and lateral shift of tibia on femur. (A) Medial translation for anterior cruciate pathology. (B) Lateral translation for posterior cruciate pathology.

Backward and Forward Movements of Tibia on Femur

Medial and Lateral Displacements of Patella

The patient is asked to lie in the supine position with the test knee flexed to 90° and the hip flexed to 45°. The examiner then places the heel of the hand over the tibial tuberosity while stabilizing the patient's limb with the other hand and pushing backward with the heel of the hand. The end feel of the movement is normally tissue stretch. To perform the forward movement, the examiner places both hands around the posterior aspect of the tibia. Before performing the joint play movement, the examiner must ensure that the hamstrings and gastrocnemius muscles are relaxed. The tibia is then drawn forward on the femur. The examiner feels the quality of the movement, which normally is tissue stretch. These joint play movements are similar to those used in the anterior and posterior drawer tests for ligamentous stability.

The patient is in the supine position with the slightly flexed on a pillow or over the examiner's (30° flexion). The examiner's thumbs are p against the medial or lateral edge of the patella, force is applied to the side of the patella, wit fingers used for stabilization. The process is the peated, with pressure applied to the other side o patella. The other knee is tested as a comparison. This joint play is similar to the passive moveme the patella; as in the passive test, the patella c displaced by approximately half of its width me and laterally. The examiner must do the move slowly and carefully to ensure that the patella i prone to dislocation.

Medial and Lateral Translation of Tibia on Femur

The patient is in a supine position with the slightly flexed. The examiner then places one over the patient's patella so that the pisiform rests over the base of the patella. The other ha placed so that the finger and thumb can gras medial and lateral edges of the patella to dire movement. The examiner then rests the first hand the second hand and applies a caudal force to the of the patella, directing the caudal movement wit second hand so that the patella does not grind a the femoral condyles.

The patient lies supine, and the patient's leg is held between the examiner's trunk and arm. To test medial translation, the examiner puts one hand on the lateral side of the tibia and one hand on the medial side of the femur. The tibia is then pushed or translated medially on the femur. Excessive movement may indicate a torn anterior cruciate ligament (Fig. 12-132). To test lateral translation, the examiner puts one hand on the medial side of the tibia and one hand on the lateral side of the femur. The tibia is then pushed or translated laterally on the femur. Excessive movement may indicate a torn posterior cruciate ligament. The normal end feel of each movement is tissue stretch. 50 Liorzou20 reports that Galway did a similar test with the knee flexed to 90° and the foot on the examining table. If the tibial plateau bulges laterally, the Wrisberg ligament or lateral meniscus may be injured.

Depression (Distal Movement) of Patella

Anteroposterior Movement of Fibula on Tibia

The patient is supine with the knee flexed to 90 the hip to 45°. The examiner then sits on the pat foot and places one hand around the patient's kn stabilize the knee and leg. The mobilizing ha placed around the head of the fibula. The fibu

740

CHAPTER 12 • Knee

7.' 1
:ation and Dislocation. Philadelphia, W.B. Saunders Co., 1984. 112. Noyes, F.R, D.L. Butler, E.S. Grood, et al: Clinical paradoxe of anterior cmciate instability and a new test to detect its instability. Orthop. Trans. 2:36, 1978. 113. Hanks, G.A, D.M. Joyner, and A. Kalenak: Anterolateral instability of the knee. Am. J. Sports Med. 9:225-231, 1981. 114. Hughston, J,C., and L.A. Norwood: The posterolateral drawer test and external rotational recurvatum test for posterolateral rotary instability of the knee. Clin. Orthop. 147:82-87, 1980 115. LaPrade, R.F., and G.C. Terry: Injuries to the posterolateral aspect of the knee-association of anatomic injury patterns with clinical instability. Am. J. Sports Med. 25:433-438, 199116. Owens, T.e.: Posteromedial pivot shift of the knee: A new tes for rupture of the posterior cruciate ligament. J, Bone Joint Surg. Am. 76:532-539, 1994. 117. Chen, F.S., A.S. Rokito, and M.l. Pitman: Acute and chronic posterolateral rotary instability of the knee. J, Am. Acad. Orthop. Surg. 8:97-110,2000. 118. Ferrari, J.D., and B.R Bach: Posterolateral instability of the knee: Diagnosis and treatment of acute and chronic instability Sports Med. Arthro. Rev. 7:273-288, 1999. 119. Covey, D.e.: Injuries of the posterolateral corner of the knee. J, Bone Joint Surg. Anl. 83:106-117,2001. 120. Jakob, RP., H. Hassler, and H.U. Staeubli: Observations on rotary instability of the lateral compartment of the knee. Acta Orthop. Scand. (Suppl. 191)52:1-32, 1981. 121. Swain, RA, and F.D. Wilson: Diagnosing posterolateral rot~ knee instability: Two clinical tests hold key. Phys. Sportsmed. 21:95-102,1993. 122. Loomer, RL.: A test for knee posterolateral rotary instability. Clin. Orthop. 264:235-238, 1991. 123. Veltri, D.M., and RF. Warren: Posterolateral instability of the knee. J, Bone Joint Surg. Am. 76:460-472, 1994. 124. Veltri, D.M., and R.F. Warren: Anatomy, biomechanics and physical findings in posterolateral knee instability. Clin. Sports Med. 13:599-614, 1994. 125. Veltri, D.M., X.-H. Deng, P.A Torzelli, RF. Warren, and M.l Maynard: The role of the cruciate and posterolateral ligaments instability of the knee-a biomechanical study. Am. J. Sports Med. 23:436-443, 1995. 126. LaPrade, RF., and F. Wentorf: Acute knee injuries-on the field and sideline evaluation. Phys. Sportsmed. 27(10):55-61, 1999. 127. Shelbourne, KD., F. Benedict, J.R McCarroll, and AC. Rettig: Dynamic posterior shift test: An adjuvant in evaluation of

128.

129. 130.

131.

132.

133.

134.

135. 136.

137.

138.

139.

140.

141.

142.

143.

144. 145.

146. 147.

148.

posterior tibial subluxation. Am. J. Sports Med. 17:275-277, 1989. Shino, K, S. Horibe, and K Ono: The voluntary evoked posterolateral drawer sign in the knee with posterolateral instability. Clin. Orthop. 215:179-186, 1987. Ferrari, D.A, J.D. Ferrari, and J. Coumas: Posterolateral instability of the knee. J. Bone Joint Surg. Am. 76:187-192, 1994. Daniel, D.M., and M.L. Stone: Instrumented measurement of knee motion. In Daniel, D., W. Akeson, and J. O'Conner (eds.): Knee Ligaments: Structure, Function, Injnry and Repair. New York, Raven Press, 1990. Harter, R.A, L.R. Osternig, and KM. Singer: Instmmented Lachman tests for the evaluation of anterior laxity after reconstruction of the anterior cmciate ligament. J. Bone Joint Surg. Am. 71:975-983, 1989. Daniel, D.M., L.L. Malcolm, G. Losse, M.L. Stone, R. Sachs, and R. Burks: Instrumented measurement of anterior laxity of the knee. J. Bone Joint Surg. Am. 67:720-726, 1985. Tyler, T.F., M.P. McHugh, G.W. Gleim, and S.J. Nicholas: Association of KT-l 000 measurements with clinical tests of the knee stability 1 year following anterior cmciate ligament reconstruction. J. Orthop. Sports Phys. Ther. 29:540-545, 1999. Edixhoven, P., R. Huiskes, R. De Graff, T.J. van Reno, and T.J. Slooff: Accuracy and reproducibility of instmmented knee drawer tests. J. Orthop. Res. 5:378-387, 1987. Andersson, C., and J. Gillquist: Instrumented testing for evaluation of sagittal knee laxity. Clin. Orthop. 256:178-184, 1990. Markolf, KL., and H.C. Amstutz: The clinical relevance of instrumented testing for ACL insufficiency: Experience with the UCLA clinical knee testing apparatus. Clin. Orthop. 223:198207, 1987. Anderson, AF., R.B. Snyder, C.F. Federspiel, and A.B. Lipscomb: Instrumented evaluation of knee laxity: A comparison of five arthrometers. An1. J. Sports Med. 20:135-140, 1992. Daniel, D.M., and M.L. Stone: Diagnosis of knee ligament injury: Tests and measurements of joint laxity. In Feagin, J.A (ed.): The Crucial Ligaments. Edinburgh, Churchill Livingstone, 1988. Bach, B.R., and J.e. Johnson: Ligament testing devices. In Scott, W.N. (ed.): Ligament and Extensor Mechanism Injuries of the Knee: Diagnosis and Treatment. St. Louis, Mosby-Year Book Inc., 1991. Daniel, D.M., and M.L. Stone: KT-I000 anterior-posterior displacement measurements. In Daniel, D., W. Akeson, and J. O'Conner (eds.): Knee Ligaments: Stmcture, Function, Injury and Repair. New York, Raven Press, 1990. Wright, R.W., and S.J. Luhmann: The effect of knee effusions on KT-I000 arthrometry-a cadaver study. Am. J. Sports Med. 26:571-574, 1998. Stratford, P.W., D. Miseferi, R. Ogilvie, J. Binkley, and J. Wuori: Assessing the responsiveness of five KT 1000 knee arthrometer measures used to evaluate anterior laxity at the knee joint. Clin. J. Sport Med. 1:225-228, 1991. Wroble, R.R., E.S. Grood, F.R. Noyes, and D,J. Schmitt: Reproducibility of genucom knee analysis system testing. An1. J. Sports Med. 18:387-395,1990. Wroble, R.R., L.A. Van Ginkel, E.S. Grood, F.R. Noyes, and B.L. Shaffer: Repeatability of the KT-I000 arthrometer in a normal population. Am. J. Sports Med. 18:396-399, 1990. Highgenboten, e.L., A Jackson, N.B. Meske: Genucom, KT1000 and Stryker knee laxity measuring device comparisons: Device reproducibility and interdevice comparison in asymptomatic subjects. An1. J. Sports Med. 17:743-746,1989. McQuade, K]., J.A. Sidles, and KV. Larson: Reliability of the genucom knee analysis system. Clin. Orthop. 245:216-219, 1989. Highgenboten, C.L., AW. Jackson, KA Jansson, and N.B. Meske: KT-I000 arthrometer: Conscious and unconscious test results using 15, 20 and 30 pounds of force. Am. J. Sports Med. 20:450-454, 1992. Kowalk, D.L., E.M. Wojtys, J. Disher, and P. Loubert: Quantitative analysis of the measuring capabilities of the KT-1000 knee ligament arthrometer. Am. J. Sports Med. 21:744-747, 1993.

149. Forster, I.W., C.D. Warren-Smith, and M. Tew: Is the KT1000 knee ligament arthrometer reliable? J. Bone Joint Surg. Br. 71:843-847, 1989. 150. Huber, F.E., J.J. Irgang, C. Harner, and S. Lephart: Intrates and intertester reliability of the KT-I000 arthrometer in the assessment of posterior laxity of the knee. Am. J. Sports Med 25:479-485, 1997. 151. Stratford, P.W., and J. Binkley: A review of the McMurray te Definition, interpretation and clinical usefulness. J. Orthop. Sports Phys. Ther. 22:116-120, 1995. 152. Bernstein, J.: Meniscal tears of the knee-diagnosis and individualized treatment. Phys. Sportsmed. 28(3):83-90,2000. 153. Shelbourne, KD., D,J. Martini, J.R. McCarrell, and C.D. Va Meter: Correlation of joint line tenderness and meniscallesio in patients with acute anterior cruciate ligament tears. Am. J. Sports Med. 23:166-169, 1995. 154. McMurray, T.P.: The semilunar cartilages. Br. J. Surg. 29:40 414,1942. 155. Evans, P,J., G.D. Bell, and C. Frank: Prospective evaluation o the McMurray test. Am. J. Sports Med. 21:604-608, 1993. 156. Kim, S,J., B.H. Min, and D.Y. Han: Paradoxical phenomena the McMurray test: An arthroscopic examination. Am. J. Spo Med. 24:83-87, 1996. 157. Apley, AG.: The diagnosis of meniscus injuries: Some new clinical methods. J. Bone Joint Surg. Br. 29:78-84, 1947. 158. Oni, 0.0.: The knee jerk test for diagnosis oftorn meniscus. Clin. Orthop. 193:309, 1985. 159. Helfet, A.: Disorders of the Knee. Philadelphia, J.B. Lippinco Co., 1974. 160. Anderson, AF., and AB. Lipscomb: Clinical diagnosis of me niscal tears: Description of a new manipulative test. Am. J. Sports Med. 14:291-293,1988. 161. Mital, M.A., and J. Hayden: Pain in the knee in children: Th medial plica shelf syndrome. Orthop. Clin. North An1. 10:71 722,1979. 162. Mann, G., A. Finsterbush, U. Frankel, and Y. Maton: A method of diagnosing small amounts of fluid in the knee. J. Bone Joint Surg. Br. 73:346-347, 1991. 163. Sibley, M.B., and F.H. Fu: Knee injuries. In Fu, F.H., and D.A Stone (eds.): Sports Injuries: Mechanisms, Prevention, Treatment. Baltimore, Williams & Wilkins, 1994. 164. Muller, K, and L. Snyder-Mackler: Diagnosis of patellofemor pain after arthroscopic meniscectomy. J. Orthop. Sports Phys Ther. 30:138-142,2000. 165. McConnell, J.: The management of chondromalacia patellae: long term solution. Aust. J. Physiother. 32:215-223, 1986. 166. Kolowich, P.A., L.E. Paulos, T.D. Rosenberg, and S. Farnsworth: Lateral release of the patella: Indications and contraind cations. Am. J. Sports Med. 18:359-365, 1990. 167. Watson, e.J., H.M. Leddy, T.D. Dynjan, and J.L. Parham: Reliability of the laternal pull test and tilt test to assess patella alignment in subjects with symptomatic knees: Student raters. J. Orthop. Sports Phys. Ther. 3:368-374,2001. 168. Schulthies, S.S., R.S. Francis, AG. Fisher, and KM. Van de Graaff: Does the Q-angle reflect the force on the patella in th frontal plane. Phys. Ther. 75:24-30, 1995. 169. Olerud, C., and P. Berg: The variation of the Q angle with different positions of the foot. Clin. Orthop. 191 :162-165, 1984. 170. Guerra, J.P., M,J. Arnold, and R.L. Gajdosik: Q-angle: Effect of isometric quadriceps contraction and body position. J. Orthop. Sports Phys. Ther. 19:200-204, 1994. 171. Arno, S.: The A-angle: A quantitative measurement of patella alignment and realignment. J. Orthop. Sports Phys. Ther. 12 237-242,1990. 172. DiVeta, J.A., and W.D. Vogelbach: The clinical efficacy of th A-angle in measuring patellar alignment. J. Orthop. Sports Phys. Ther. 16:136-139, 1992. 173. Ehrat, M., J. Edwards, D. Hastings, and T. Worrell: Reliabili of assessing patellar alignment: The A-angle. J. Orthop. Sport Phys. Ther. 19:22-27, 1994. 174. Daniel, D.M., M.L. Stone, P. Barnett, and R. Sachs: Use of the quadriceps active test to diagnose posterior cruciate liga-

760

175. 176. 177. 178. 179. 180. 181. 182. 183. 184.

185.

186. 187. 188.

189. 190. 191. 192.

193. 194.

195.

196. 197.

198. 199.

CHAPTER 12 • Knee

ment disruption and measure posterior laxity of the knee. J. Bone Joint Surg. Am. 70:386-391, 1988. Fairbank, H.AT.: Internal derangement of the knee in children and adolescents. Proc. Roy. Soc. Med. 30:427-432, 1937. Noble, H.B., M.R Hajek, and M. Porter: Diagnosis and treatment of iliotibial band tighmess in runners. Phys. Sportsmed. 10:67-74,1982. Daniel, D.M., and M.L. Stone: Case studies. In Daniel, D., W. Akeson, and J. O'Conner (eds.): Knee Ligaments: Structure, Injuty and Repair. New York, Raven Press, 1990. Hyslop, G.H.: Injuries of the deep and superficial peroneal nerves complicating ankle sprain. Am. J. Surg. 51:436-438, 1941. Sidey, J.D.: Weak ankles: A study of common peroneal entrapment neuropathy. Br. Med. J. 56:623-626,1969. Pecina, M.M., J. Krmpotic-Nemanic, and A.D. Markiewitz: Tunnel Syndromes. Boca Raton, Florida, CRC Press, 1991. Worth, R.M., D.B. Kettlekamp, RJ. Defalque, and KU. Duane: Saphenous nerve entrapment: A cause of medial nerve pain. Am. J. Sports Med. 12:80-81, 1984. Cox, J.S., and J.B. Blanda: Periarticular pathologies. In DeLee, J.C., and D. Drez (eds.): Orthopedic Sports Medicine. Philadelphia, W.B. Saunders Co., 1994. Lin, J., and C. Chang: A medial soft tissue mass of the knee. Phys. Sportsmed. 27(10):87-90, 1999. O'Shea, KJ., KP. Murphy, D. Heekin, and P.J. Herzwurm: The diagnostic accuracy of histOly, physical exanlination and radiographs in the evaluation of traumatic knee disorders. Am. J. Sports Med. 24:164-167, 1996. Gelb, H.J., S.G. Glasgow, AA Sapega, and J.S. Torg: Magnetic resonance imaging of knee disorders: Clinical value and cost-effectiveness in a sports medicine practice. Am. J. Sports Med. 24:99-103, 1996. Stiell, LG., G.A. Wells, and R.H. Hoag: Implementation of the Ottawa knee rules for the use of radiography in acute knee injuries. JAMA 278:2075-2079, 1997. Carson, W.G. Jr., S.L. James, R.L. Larson, et al.: Patellofemoral disorders: Physical and radiographic evaluation: I: Physical examination. Clin. Orthop. 185:178-186,1984. Merchant, A.C.: Extensor mechanism injuries: Classification and diagnosis. In Scott, W.N. (ed.): Ligament and Extensor Mechanism Injuries of the Knee: Diagnosis and Treatment. St. Louis, Mosby-Year Book Inc., 1991. Davies, AP., D.A Calder, T. Marshall, and M.M. Glasgow: Plain radiography in the degenerate knee. J. Bone Joint Surg. Br. 81:632-635, 1999. Tatum, R: Osteochondritis dissecans of the knee: a radiology case report. J. Manip. Physiol. Ther. 23:347-351,2000. Schenck, R.C., and J.M. Goodnight: Osteochondritis dissecans-current concepts review. J. Bone Joint Surg. Am. 78: 439-456,1996. Woods, G.W., R.F. Stanley, and H.S. Tullos: Lateral capsular sign: X-ray clue to a significant knee instability. Am. J. Sports Med. 7:27-33, 1979. Altchek, D.W.: Diagnosing acute knee injuries: The office exam. Phys. Sportsmed. 21:85-96, 1993. Schils, J.P., D. Resnick, and D.J. Sartoris: Diagnostic imaging of ligamentous injuries of the knee. In Daniel, D., W. Akeson, and J. O'CorUler (eds.): Knee Ligaments: Structure, Injuty and Repair. New York, Raven Press, 1990. Beaconsfield, T., E. Pintore, N. Maffulli, and G.J. Petri: Radiographic measurements in patellofemoral disorders. Clin. Orthop. 308:18-28, 1994. Grana, W.A: Diagnostic evaluation. In Larson, RL., and W.A Grana (eds.): The Knee: Form, Function, Pathology and Treatment. Philadelphia, W.B. Saunders Co., 1993. Grelsamer, RP., and S. Meadows: The modified Insall-Salvati ratio for assessment of patellar height. Clin. Orthop. 282:170176, 1992. Haas, S.B., and G.R Scuderi: Examination and radiographic assessment of the patellofemoral joint. Semin. Orthop. 5:108114,1990. Grelsamer, R.P., C.S. Proctor, and AN. Brazos: Evaluation of

200. 201.

202.

203. 204. 205.

206.

207. 208. 209. 210.

211. 212.

213. 214.

215.

216. 217. 218.

patellar shape in the sagittal plane: A clinical analysis. Am. J. Sports Med. 22:61-66, 1994. Berg, E.E., S.L. Mason, and M.J. Zucas: Patellar height ratios: A comparison of four measurement methods. Am. J. Sports Med. 24:218-221, 1996. Hewett, T.E., F.R Noyes, and M.D. Lee: Diagnosis of complete and partial posterior cruciate ligament ruptures-stress radiography compared with KT-I000 and posterior drawer testing. Am. J. Sports Med. 25:648-655, 1997. Shelbourne, KD., T.J. Davis, and T.E. Klootwyk: The relationship between intercondylar notch width of the femur and the incidence of anterior cruciate ligament tears-a prospective study. Am. J. Sports Med. 26:402-408, 1998. Speakman, H.B., and J. Weisberg: The vastus medialis controversy. Physiotherapy 63:249-254, 1977. Murray, T.F., J.-Y. Dupont, and J.P. Fulkerson: Axial and lateral radiographs in evaluating patellofemoral malalignment. Am J. Sports Med. 27:580-584, 1999. Davies, AP., M.L. Costa, S.T. Donnell, M.M. Glasgow, and L Shepstone: The sulcus angle and malalignment of the extensor mechanisms of the knee. J. Bone Joint Surg. Br. 82:11621166,2000. Ghelman, B., and S. Schraft: Arthrography of the knee. In Scott, W.N. (ed.): Ligament and Extensor Mechanism Injuries of the Knee: Diagnosis and Treatment. St. Louis, Mosby-Year Book Inc., 1991. Mital, M.A, and L.L Karlin: Diagnostic arthroscopy in sports injuries. Orthop. Clin. North Am. 11:771-785,1980. McClelland, C.J.: Arthroscopy and arthroscopic surgety of the knee. Physiotherapy 70:154-156, 1984. Noyes, F.R, R W. Bassett, E.S. Grood, and D.L. Butler: Arthroscopy in acute traumatic hemarmrosis of the knee. J. Bone Joint Surg. Am. 62:687-695,757, 1980. LaPrade, RF., T.J. Gilbert, T.S. Bollom, F. Wentorf, and G. Chaljub: The magnetic resonance imaging appearance of individual structures of the posterolateral knee-a prospective study of normal knees and knees wim surgically verified grade III injuries. Am. J. Sports Med. 28:191-199,2000. Potter, H.G.: Imaging of the multiple-ligament-injured knee. Clin. Sports Med. 19:425-441,2000. Glashow, J.L., and M.J. Friedman: Diagnosis of knee ligamenr injuries: Magnetic resonance imaging. In Scott, W.N. (ed.): Ligament and Extensor Mechanism Injuries of me Knee: Diagnosis and Treatment. St. Louis, Mosby-Year Book Inc., 1991 Arendt, E.A: Assessment of the athlete wim an acutely injured knee. In Griffin, L.Y. (ed.): Rehabilitation of the Injured Knee St. Louis, C.V. Mosby Co., 1995. Gelb, H.J., S.G. Glasgow, AA. Sapega, and J.S. Torg: Magnetic resonance imaging of knee disorders: Clinical value and cost effectiveness in a sports medicine practice. Am. J. Sports Med. 24:99-103, 1996. Adalberth, T., H. Roos, M. Lauren, P. Akeson, M. Sloth, K Jonsson, A Lindstrand, and L.S. Lohmander: Magnetic resonance imaging, scintigraphy and armroscopic evaluation of traumatic hemarthrosis of me knee. Am. J. Sports Med. 25: 231-237,1997. Munshi, M., M. Davidson, P.B. MacDonald, W. Froese, and 1:Sutherland: The efficacy of magnetic resonance imaging in acute knee injuries. Clin. J. Sports Med. 10:34-39,2000. Potter, H.G., J.M. Linklater, A.A Allen, J.A Hannafin, and S.B. Haas: Magnetic resonance imaging of articular cartilage of me knee. J. Bone Joint Surg. Am. 80:1276-1284, 1998. Ross, G., AW. Chapman, AR Newberg, and AD. Scheller: Magnetic resonance imaging for me evaluation of acute posterolateral complex injuries of the knee. Am. J. Sports Med. 2:444-448, 1997.

General References Adams, J.C.: Outline of Ormopedics. London, E & S Livingstone, Ltd., 1968. Ahstrom, J.P.: Reliability of history and physical examination in diagnosis of meniscus pathology. Curro Pract. Orthop. Surg., vol. 7. St Louis, C.V. Mosby Co., 1977.

function assessment chart. J. Bone Joint Surg. Br. 60:308-309, 1978. Amis, A.A.: Anatomy and biomechanics of the posterior cruciate ligament. Sports Med. Arthro. Rev. 7:225-234, 1999. Ando, T., H. Hirose, M. Inoue, K Shino, and T. Doi: A new method using computed tomographic scan to measure the rectus femoris-patellar tendon Q-angle comparison with conventional method. Clin. Orthop. 289:213-219, 1993. Andriacchi, T.P., and D. Birac: Functional testing in the anterior cruciate ligament-deficient knee. Clin. Orthop. 288:40-47, 1993. Aprin, H., J. Shapiro, and M. Gershwind: Arthrography (plica views): A noninvasive method for diagnosis and prognosis of plica syndronK Clin. Orthop. 183:90-95, 1984. Arnold, J.A., T.P. Coker, L.M. Heaton, et al.: Natural history of anterior cruciate tears. Anl. J. Sports Med. 7:305-313, 1979. Back, B.R., and R.F. Warren: Radiographic indicators of the anterior cruciate ligament injury. In Feagin, J.A (ed.): The Crucial Ligaments. Edinburgh, Churchill Livingstone, 1988. Bassett, L.W., and R.H. Gold: Magnetic resonance imaging of the musculoskeletal system: An overview. Clin. Orthop. 244:17-28, 1989. Bassett, L.W., R.H. Gold, and L.L. Seeger: MRl Atlas of the Musculoskeletal System. London, Martin Dunitz, 1989. Beetham, W.P., H.P. Polley, C.H. Slocumb, and W.F. Weaver: Physical Extremities of the Joint. Philadelphia, W.B. Salmders Co., 1965. Bigg-Wither, G., and P. Kelly: Diagnostic imaging in musculoskeletal physiotherapy. In Refshauge, K, and E. Gass (eds.): Musculoskeletal Physiotherapy: Clinical Science and Practice. Oxford, Butterworth-Heinemarm Ltd., 1995. Booker, J.M., and G.A Thibodeau: Athletic Injury Assessment. St. Louis, C.V. Mosby Co., 1989. Brantigan, O.C., and AF. Voshell: The mechanics of the ligaments and menisci of the knee joint. J. Bone Joint Surg. 23:44-66, 1941. Bryant, J.T., and T.D. Cooke: A biomechanical function of the ACL: Prevention of medial translation of the tibia. In Feagin, J.A. (ed.): The Crucial Ligaments. Edinburgh, Churchill Livingstone, 1988. Bull, A.M., H.N. Andersen, O. Basso, J. Targett, and A.A Amis: Incidence and mechanism of the pivot shift-an in vitro study. Ciin. Orthop. Relat. Res. 363:219-231,1999. Burk, D.L., M.K Dalirtka, E. Kinal, et al.: Meniscal and ganglion cysts of the knee: MRevaluation. Am. J. Roentgenol. 150:331336, 1988. Cabaud, H.E., and D.B. Slocum: The diagnosis of chronic anterolateral rotary instability of the knee. Am. J. Sports Med. 5:99-104, 1977. Cailliet, R.: Knee Pain and Disability. Philadelphia, F.A Davis Co., 1973. Clancy, W.G.: Evaluation of acute knee injuries. Anlerican Association of Orthopaedic Surgeons, Symposium on Sports Medicine: The Knee. St. Louis, C.v. Mosby Co., 1985. Clarkson, H.M., and G.B. Gilewich: Musculoskeletal Assessment: Joint Range of Motion and Manual Muscle Strength. Baltimore, Williams & Wilkins, 1989. Cole, B.]., and C.D. Harner: Degenerative arthritis of the knee in active patients: evaluation and management. J. Am. Acad. Orthop. Surg. 7:389-402, 1999. Collins, H.R.: Anterolateral rotary instability. American Association of Orthopaedic Surgeons, Symposium on the Athlete's Knee. St. Louis, C.v. Mosby Co., 1980. Conlan, T., W.P. Garth, and J.E. Lemons: Evaluation of the medial soft tissue restraints of the extensor mechanism of the knee. J. Bone Joint Surg. Am. 75:682-693, 1993. Cooper, D.E.: Tests for posterolateral instability of the knee in normal subjects: Results of exanunation lmder anaesthesia. J. Bone Joint Surg. Am. 73:30-36, 1991. Crues, J.V., R. Ryu, and F.W. Morgan: Meniscal pathology: The expanding role of magnetic resonance imaging. Clin. Orthop. 252: 80-87, 1990. Cyriax, J.: Textbook of Orthopaedic Medicine, vol. 1: Diagnosis of Soft Tissue Lesions. London, Bailliere Tindall, 1975.

marks of the normal knee. Clin. Orthop. 156:201-206, 1981. Davies, G.J.: Examining the knee. Phys. Sportsmed. 6:48-67, 197 De Haven, KE., and H.R. Collins: Diagnosis of internal derangement of the knee: The role of arthroscopy. J. Bone Joint Surg. Am. 57:802-810, 1975. Deutsch, AL., F.G. Shellock, and J.H. Mink: Imaging of the patel lofemoral joint: Emphasis on advanced techniques. In Fu, F.H., and D.A. Stone (eds.): Sports Injuries: Mechanisms, Prevention, Treatment. Baltimore, Williams & Wilkins, 1994. Donaldson, W.F., R.F. Warren, and T. Wickiewicz: A comparison o acute anterior cruciate liganlent exanlinations: Initial vs exanlination under anesthesia. Am. J. Sports Med. 13:5-9, 1985. Dontigny, R.L.: Terminal extension exercises for the knee. Phys. Ther. 52:45-46, 1972. Doppman, J.L.: Baker's cyst and the normal gastrocnemiosenlimem branosus bursa. Am. J. Roentgenol. 94:646-652, 1965. Dowd, G.S., and G. Bentley: Radiographic assessment of patellar instability and chondromalacia patellae. J. Bone Joint Surg. Br. 6 297-300,1986. Ehrlich, M.G., and R.E. Strain: Epiphyseal injuries about the knee. Orthop. Clin. North Anl. 10:91-103,1979. Ellison, AE.: The pathogenesis and treatment of anterolateral rotar instability. Clin. Orthop. 147:51-55, 1980. Engle, R.P.: Examination of the knee. In Engle, R.P. (ed.): Knee Ligament Rehabilitation. New York, Churchill Livingstone, 1991 Evans, R.C.: Illustrated Essentials in Orthopedic Physical Assessme St. Louis, C.v. Mosby Co., 1994. Ewald, F.e.: The knee society total knee arthroplasty roentgenographic evaluation and scoring system. Clin. Orthop. 248:9-12, 1989. Feagin, J.A.: Introduction: principles of diagnosis and treatment. In Feagin, J.A (ed.): The Crucial Ligaments. Edinburgh, Churchill Livingstone, 1988. Feagin, J.A., H.E. Cabaud, and W.W. Curl: The anterior cruciate ligament: Radiographic and clinical signs of successful and unsuccessful repairs. Clin. Orthop. 164:54-58, 1982. Fetto, J.F., and J.L. Marshall: The natural history and diagnosis of anterior cruciate ligament insufficiency. Clin. Orthop. 147:29-38 1980. Fleming, B.C., B.D. Beynnon, and R.J. Johnson: The use of knee laxity testers for the determination of anterior-posterior stability o the knee: Pitfalls in practice. In Jackson, D.W. (ed.): The Anterio Cmciate Liganlent: Current and Future Concepts. New York, Raven Press, 1993. Fowler, P.J.: The classification and early diagnosis of knee joint inst bility. Clin. Orthop. 147:15-21, 1980. Francis, R.S., and D.E. Scott: Hypertrophy of the vastus medialis in knee extension. Phys. Ther. 54:1066-1070, 1974. Frankel, V.H., A.H. Burstein, and D.B. Brooks: BiomechaIucs of internal derangement of the knee. J. Bone Joint Surg. Am. 53: 945-962,1971. Franklin, J.L., T.D. Rosenberg, L.E. Paulos, and E.P. France: Radi graphic assessment of instability of the knee due to rupture of th anterior cruciate ligament: A quadriceps contraction tecluuque. J. Bone Joint Surg. Am. 73:365-372, 1991. Fu, F.H., M.J. Seel, and R.A. Berger: Patellofemoral biomechanics. In Fox, J.M., and W. Del Pizzo (eds.): The Patellofemoral Joint. New York, McGraw-Hill Inc., 1993. Fulkerson, J.P.: Evaluation of the peripatellar soft tissues and retina ulum in patients with patellofemoral pain. Clin. Sports Med. 8: 197-202,1989. Fulkerson, J.P.: Awareness of the retinaculum in evaluating patellofemoral pain. Am. J. Sports Med. 10:147-149,1982. Fulkerson, J.P.: Patellofemoral pain disorders: Evaluation and management. J. Am. Acad. OrtilOp. Surg. 2:124-132, 1994. GartiaIld, J.J.: Fundamentals of Orthopedics. Philadelphia, W.B. Saunders Co., 1979. Gersoff, W.K, and W.G. Clancy: Diagnosis of acute and chronic anterior cruciate ligament tears. Clin. Sports Med. 7:727-738, 1988. Gillquist, J.: Diagnosis and classification of the instability of the kne joint. Sem. Orthop. 2:18-22, 1987.

762

CHAPTER 12 • Knee

Ginsburg, ].H., and J.C. Ellsasser: Problem areas in the diagnosis and treatment of ligament injuries of the knee. Clin. Orthop. 132: 201-205, 1978. Goodfellow,]., D.S. Hungerford, and C. Woods: Patellofemoral joint mechanics and pathology: Chondromalacia patellae. ]. Bone Joint Surg. Br. 58:291-299,1976. Gough, ].V., and G. Laclley: An investigation into the effectiveness of various forms of quadriceps exercises. Physiotherapy 57:356361, 1971. Greenmill, B.J.: The importance of the medial quadriceps expansion in medial ligament injury. Can. J. Surg. 10:312-317,1967. Griffin, L.Y., J. Agel, M.J. Albohm, E.A. Arendt, RW. Dick, W.E. Garrett, ].G. Garrick, T.E. Hewett, L. Huston, M.L. Ireland, R.J. Johnson, W.B. Kibler, S. Lephart, J.L. Lewis, T.N. Lindenfeld, B.R Mandelbaum, P. Marchak, C.T. Tietz, and E.M. Wojtys: Noncontact anterior cruciate ligament injuries: risk factors and prevention strategies.]. Am. Acad. Orthop. Surg. 8:141-150,2000. Grood, E.S., S.F. Stowers, and F.R Noyes: Limits of movement in the human knee: Effect of sectioning the posterior cruciate ligament and posterolateral structures. ]. Bone Joint Surg. Am. 70: 88-97,1988. Gurtler, R.A., R Stine, and J.S. Torg: Lachman test evaluated: Quantification of a clinical observation. Clin. Orthop. 216:141150, 1987. Guzzanti, V., A. Gigante, A. DiLazzaro, and C. Fabbriciani: Patellofemoral malalignment in adolescents: Computerized tomographic assessment with and without quadriceps contraction. Am. J. Sports Med. 22:55-60, 1994. Hardaker, W.G., T.L. Shipple, and F.H. Bassett: Diagnosis and treatment of the plica syndrome of the knee. ]. Bone Joint Surg. Am. 62:221-225,1980. Heyerman, W.B., and W.A. Hoyt: Anterolateral rotary instability associated with chronic anterior cruciate insufficiency. Clin. Orthop. Relat. Res. 134:144-148, 1978. Hilyard, A: Recent developments in the management of patellofemoral pain: The McConnell programme. Physiotherapy 76:559565, 1990. Hollinshead, W.H., and D.B. Jenkins: Functional Anatomy of the Limbs and Back. Philadelphia, W.B. Saunders Co., 1981. Hoppenfeld, S.: Physical Examination of the Spine and Extremities. New York, Appleton-Century-Crofts, 1976. Hoppenfeld, S.: Physical examination of the knee joint by complaint. Orthop. Clin. North Am. 10:3-20,1979. Hughston, ].C., ].R Andrews, M.]. Cross, and A Moschi: Classification of knee liganlent instabilities: Part 1. The medial compartment and cruciate ligaments. ]. Bone Joint Surg. Am. 58:159-172, 1976. Hughston, J.C.,].A Bowden,].R Andrews, and L.A. Norwood: Acute tears of the posterior cruciate ligament. J. Bone Joint Surg. Am. 62:438-450, 1980. Insall, J., K.A Falvo, and D.W. Wise: Chondromalacia patellae: A prospective study. J. Bone Joint Surg. Am. 58:1-8,1976. Iobst, C.A, and C.L. Stanitsk:i: Acute knee injuries. Clin. Sports Med. 19:621-635,2000. Jackson, J.P.: Internal derangement of the knee joint. Physiotherapy 52:229-232, 1966. Jakob, RP.: Pathomechanical and clinical components of the pivot shift sign. Sem. Orthop. 2:9-17, 1987. Jakob, RP., H.U. Staubli, and JT. Deland: Grading the pivot shift: Objective tests with implications for treatment. ]. Bone Joint Surg. Br. 69:294-299, 1987. Jensen, K.: Manual laxity tests for anterior cruciate ligament injuries. J. Orthop. Sports Phys. Ther. 11:474-481,1990. Kapandji, L.A.: The Physiology of the Joints, vol. 2: Lower Limb. New York, Churchill Livingstone, 1970. Kennedy, J.C., R. Stewart, and D.M. Walker: Anterolateral rotary instability of the knee joint: An early analysis of the Ellison repair. J. Bone Joint Surg. Anl. 60:1031-1032, 1978. Kranler, J.F., D. Nusca, P. Fowler, and S. Webster-Bogaert: Testretest reliability of the one-leg hop test following ACL reconstruction. Clin. ]. Sport Med. 2:240-243, 1992. Kursunoglu-Brailme, S., and D. Resnick: Magnetic resonance imaging of the knee. Orthop. Clin. North Am. 21:561-572, 1990.

Larson, RL.: Clinical evaluation. In Larson, RL., and W.A Grana (eds.): The Knee: Form, FlIDction, Pathology and Treatment. Philadelphia, W.B. Saunders Co., 1993. Leib, F.J., and J. Perry: Quadriceps function. ]. Bone Joint Surg. Am. 50:1535-1548, 1968. Liu, S.H., L. Osti, F. Dorey, and L. Yao: Anterior cruciare ligament rear: A new diagnostic index on magnetic resonance imaging. Clin. Orthop. Relat. Res. 302:147-150, 1994. Logan, AL.: The Knee: Clinical Applications. Gaithersburg, Maryland, Aspen Publishers, 1994. Losee, RE.: The pivor shift. In Feagin, J.A (ed.): The Crucial Ligaments. Edinburgh, Churchill Livingsrone, 1988. Losee, RE.: Concepts of the pivot shift. Clin. Orthop. 172:45-51, 1983. Lucie, RS., ].D. Wiedel, and D.G. Messner: The acute pivot shift: Clinical correlation. Am. J. Sports Med. 12:189-191,1984. Macnicol, M.F.: The Problem Knee: Diagnosis and Managemenr in the Younger Patient. London, Wm. Heinemarm Med. Books, 1986. Malek, M.M., and RE. Manjini: Patellofemoral pain syndrome: A comprehensive and conservative approach. ]. Orthop. Sports Phys. Ther. 2:108-116, 1981. Malone, T., and ST. Kegerreis: Evaluation process. In Mangine, RE. (ed.): Physical Therapy of the Knee. Edinburgh, Churchill Livingsrone, 1988. Mandelbaum, B.R., J.E. Browne, F. Fu, L. Micheli, J.B. Moselly, C Erggelet, T. Minas, and L. Peterson: Articular cartilage lesions of the knee. Am. J. Sports Med. 26:853-861, 1998. Mandelbaum, B.R., G.A Finerman, M.A. Reicher, er al.: Magnetic resonance imaging as a rool for evaluation of traumatic knee injuries. Am. ]. Sports Med. 14:361-370,1986. Mayor, D.: Anaromical and functional aspects of the knee joinr. Physiotherapy 52:224-228, 1966. McLean, S.G., R]. Neal, PT. Myers, and M.R Walters: Knee joinr kinematics during the sidesrep curting manoeuver: porential for injury in women. Med. Sci. Sports. Exerc. 31:959-968, 1999. McRae, R: Clinical Orthopaedic Examination. New York, Churchill Livingstone, 1976. Meislin, RJ.: Managing collareralligament tears of the knee. Phys. Sportsmed. 24:67-80, 1996. Meister, B.R., S.P. Michael, R.A Moyer, ].D. Kelly, and C.D. Schneck: Anatomy and kinematics of the lateral collateral ligament of the knee. Am. J. Sporrs Med. 28:869-878,2000. Merchant, A.C.: The lateral patellar compression syndrome. In Fu, F.H., and D.A. Stone (eds.): Sports Injuries: Mechanisms, Prevention, Treatment. Baltimore, Williams & Wilkins, 1994. Meszler, D., T.]. Manal, and L. Snyder-Mackler: Disorders of the tibiofemoral joint-evaluation, diagnosis and inrervention. Orthop Phys. Ther. Clin. North Am. 7:347-366, 1998. Moller, B.N., and S. Kadin: Entrapment of the common peroneal nerve. Am. ]. Sports Med. 15:90-91, 1987. Moran, D.]., and RT. Floyd: The Lachman tesr: Alternative techluques and applications for anterior cruciare ligament evaluation. Sports Med. Update 5:3-5, 1990. Muller, W., R. Biedert, F. Hefti, R.P. Jakob, U. Munzinger, and H.U. Staubli: OAK knee evaluation: A new way ro assess knee ligament injuries. Clin. Orthop. 232:37-50, 1988. Myrer, J.W., S.S. Schulthies, and C.W. Fellingham: Relative and absolute reliability of the KT -1000 arthromerer for injured knees. Am. J. Sports Med. 24:104-108, 1992. Nelson, E.W., and RF. LaPrade: The anrerior intermeniscalligamenof the knee-an anaromic study. Am. J. Sport Med. 28:74-76, 2000. Norwood, L.A, and M.]. Cross: Anterior cruciate ligamenr: Functional anaromy of irs bunclles in rorary insrabilities. Am. J. Spons Med. 7:23-26, 1979. Norwood, L.A, and ].C. Hughston: Combined anrerolareral-anteromedial rorary instability of the knee. Clin. Orthop. 147:62-67, 1980. Noyes, F.R, and E.S. Grood: Diagnosis of knee ligament injuries: Clinical concepts. In Feagin,].A (ed.): The Crucial Ligamenrs. Edinburgh, Churchill Livingstone, 1988. Noyes, F.R, E.S. Grood, and D.L. Butler: Clinical laxity tests and

thop. 146:84-89, 1980. Nunn, K.D., and l.L. Mayhew: Comparison of three methods of assessing strength imbalances at the knee. l. Orthop. Sports Phys. Thee. 10:134-137,1988. Oberlander, M.A, R.M. Shalvoy, and J.C. Hughston: The accuracy of the clinical knee examination documented by arthroscopy: A prospective study. Am. J. Sports Med. 21:773-778, 1993. O'Donoghue, D.H.: Treatment of Injuries to Athletes, 4th ed. Philadelphia, W.B. Saunders Co., 1984. Ogata, K., l.A McCarthy, J. Dunlap, and P.R. Manske: Pathomechanisms of posterior sag of the tibia in posterior cruciate deficient knees. Am. l. Sports Med. 16:630-636, 1988. Ombregt, L., P. Bisschop, H.J. ter Veer, and T. Van de Velde: A System of Orthopedic Medicine. London, W.B. Saunders Co., 1995. Palmer, M.L., and M. Epler: Clinical Assessment Procedures in Physical Therapy. Philadelphia, J.B. Lippincott Co., 1990. Patel, D.: Superior lateral-medial approach to arthroscopic meniscectomy. Orthop. Clin. North Am. 13:299-305, 1982. Percy, E.C., and R.T. Strother: Patellalgia. Phys. Sports Med. 13:4359, 1985. Perty, J.: Function of quadriceps. l. Can. Physiother. Assoc. 24:130132, 1972. Pickett, J.C., and E.L. Radin: Chondromalacia of the Patella. Baltimore, Williams & Wilkins, 1983. Pipkin, G.: Knee injuries: The role of the suprapatellar plica and suprapatellar bursa in simulating internal derangements. Clin. Orthop. 74:161-176,1971. Powers, C.M., S. Mortenson, D. Nishimoto, and D. Simon: Criterion-related validity of a clinical measurement to determine the medial/lateral component of patellar orientation. J. Orthop. Sports Phys. Thee. 29:372-377, 1999. Pynsent, P., l. Fairbank, and A Carr: Outcome Measures in Orthopedics. Oxford, Butterworth-Heinemann Ltd., 1993. Reid, D.C.: Functional Anatomy and Joint Mobilization. Edmonton, University of Alberta Bookstore, 1980. Reid, D.C.: Sports Injuty Assessment and Rehabilitation. New York, Churchill Livingstone, 1992. Reid, D.C.: The myth, mystic and frustration of anterior knee pain. Clin. J. Sport Med. 3:139-143, 1993. Reider, B., and S.D. D'Agata: Factors predisposing to knee injury. In DeLee, J.C., and D. Drez (eds.): Orthopedic Sports Medicine. Philadelphia, W.B. Saunders Co., 1994. Reider, B., J.L. Marshall, B. Koslin, B. Ring, and F.G. Girgis: The anterior aspect of the knee joint. l. Bone Joint Surg. Am. 63:351356, 1981. Reilly, B.M.: Practical Strategies in Outpatient Medicine. Philadelphia, W.B. Saunders Co., 1984. Renstrom, P., and R.J. Johnson: Anatomy and biomechanics of the menisci. Clin. Sports Med. 9:523-538, 1990. Rovere, G.D., and D.M. Adair: Anterior cruciate-deficient knees: A review of the literature. Am. J. Sports Med. 11:412-419,1983. Rubinstein, R.A, D. Shelbourne, J.R. McCarroll, C.D. Van Meter, and A.C. Rettig: The accuracy of the clinical examination in the setting of posterior cruciate ligament injuries. Am. J. Sports Med. 22:550-557, 1994. Rusche, K., and R.E. Mangine: Pathomechanics of injury to the patellofemoral and tibiofemoral joint. In Mangine, R.E. (ed.): Physical Therapy of the Knee. Edinburgh, Churchill Livingstone, 1988.

Orthop. Relat. Res. 370:201-207,2000. Smillie, 1.S.: Diseases of the knee joint. Physiotherapy 70:144-15 1984. Stanitski, C.L.: Patellofemoral mechanism. In Stanitski, C.L., l.C DeLee, and D. Drez (eds.): Pediatric and Adolescent Sports M cine. Philadelphia, W.B. Sawlders Co., 1994. Starkey, C., and J. Ryan: Evaluation of Orthopedic and Athletic Injuries. Philadelphia, F.A Davis Co., 1996. Swenson, T.M.: Physical diagnosis of the multiple-ligament-injur knee. Clin. Sports Med. 19:415-423,2000. Tachdjian, M.O.: Pediatric Orthopedics. Philadelphia, W.B. Saun Co., 1972. Tegner, Y., and l. Lysholm: Rating systems in the evaluation of k ligament injuries. Clin. Orthop. 198:43-49, 1985. Teitge, R.A, W. Faerber, P. Des Madryl, and T.M. Matelic: Stres radiographs of the patellofemoral joint. J. Bone Joint Surg. Am 78:193-203,1996. Travell, l.G., and D.G. Simons: Myofascial Pain and Dysfunction The Trigger Point Manual. Baltimore, Williams & Wilkins, 198 Tria, Al., and R.C. Palumbo: Conservative treatment of patellofe oral pain. Semin. Orthop. 5:115-121, 1990. Trickey, E.L.: Injuries to the posterior cruciate ligament: Diagnos and treatment of early injuries and reconstruction of late instab ity. Clin. Orthop. 147:76-81, 1980. Turner, l.S., and 1.S. Smillie: The effect of tibial torsion on the pathology of the knee. l. Bone Joint Surg. Br. 63:396-398, 1 Wallace, L.A., R.E. Mangine, and T.R. Malone: The knee. In Go J.A (ed.): Orthopedic and Sports Physical Therapy. St. Louis, C.v. Mosby Co., 1990. Walsh, W.M.: Patellofemoral joint. In DeLee, l.C., and D. Drez (eds.): Orthopedic Sports Medicine. Philadelphia, W.B. Saunde Co., 1994. Warren, L.F., l. Marshall, and F. Girgis: The prime static stabilize the medial side of the knee. J. Bone Joint Surg. Am. 56:665-6 1974. Warren, L.F., and l. Marshall: The supporting structures and laye on the medial side of the knee. J. Bone Joint Surg. Am. 61:56 62, 1979. Warson, C.l., M. Prepps, W. Galt, A Redding, and D. Dobbs: Reliability of McConnell's classification of patellar orientation i symptomatic and asymptomatic subjects. J. Orthop. Sports Phy Thee. 29:378-385, 1999. Wechsler, L.R., and N.A Busis: Sports neurology. In Fu, F.H., a D.A. Stone (eds.): Sports Injuries: Mechanisms, Prevention, Tr ment. Baltimore, Williams & Wilkins, 1994. Weiss, J.R., J.J. Irrgang, R. Sawhney, S. Dearwater, and F.H. Fu: fi.mctional assessment of anterior cruciate ligament deficiency in acute and clinical setting. J. Orthop. Sports Phys. Ther. 11 :372 373, 1990. Weissman, B.N.W., and C.B. Sledge: Orthopedic Radiology. Phil delphia, W.B. Saunders Co., 1986. Welsh, R.P.: Knee joint structure and function. Clin. Orthop. 14 14, 1980. Wiles, P., and R. Sweetnam: Essentials of Orthopedics. London, A Churchill, Ltd., 1965. Wojtys, E.M. (ed.): The ACL Deficient Knee. Rosemont, Illinois, American Academy of Orthopedic Surgeons, 1994. Woo, S. L.-Y., R.E. Debski, J.D. Withrow, and M.A. Janaushek: Biomechanics of knee ligaments. Am. J. Sports Med. 27:533-5 1999.

At least 80% of the general population has foot problems, but these problems can often be corrected by proper assessment, treatment, and, above all, care of the feet. Lesions of the ankle and foot can alter the mechanics of gait and, as a result, cause stress on other lower limb joints, which in turn may lead to pathology in these joints. The foot and ankle combine flexibility with stability because of the many bones, their shapes, and their attachments. The lower leg, ankle, and foot have two principal functions: propulsion and support. For propulsion, they act like a flexible lever; for support, they act like a rigid structure that holds up the entire body.

Functions of the Foot • Acts as a support base that provides the necessary stability for upright posture with minimal muscle effort • Provides a mechanism for rotation of the tibia and fibula during the stance phase of gait • Provides flexibility to adapt to uneven terrain • Provides flexibility for absorption of shock

vided into three sections- hindfoot (rearfoot), mid foot, and forefoot.

T

Applied Anatomy

Hindfoot (Rearfoot)

Tibiofibular Joint. The inferior (distal) tibiofibula joint is a fibrous or syndesmosis type of joint. It supported by the anterior tibiofibular, posterior tibiof bular, and inferior transverse ligaments as well as th interosseous ligaments (Fig. 13-1). The movements this joint are minimal but allow a small amount o "spread" (1 to 2 mm) at the ankle joint during dors flexion. This same action allows the fibula to move u and down during dorsiflexion and plantar flexion. Dor siflexion at the ankle joint will cause the fibula t move superiorly, putting stress on both the inferio tibiofibular joint at the ankle and the superior tibiofib ular joint at the knee. The fibula carries more of th axial load when it is dorsiflexed. On average, the fibul carries about 17% of the axial loading. 2 The joint supplied by the deep peroneal and tibial nerves.

• Acts as a lever during push-off

Although the joints of the lower leg, ankle, and foot are discussed separately, they act as functional groups, not as isolated joints. As the terminal part of the lower kinetic chain, the lower leg, ankle, and foot have the ability to distribute and dissipate the different forces (e.g., compressive, shearing, rotary, tensile) acting on the body through contact with the ground. l This is especially evident during gait. In the foot, the movement occurring at each individual joint is minimal. However, when combined, there normally is sufficient range of motion (ROM) in all of the joints to allow functional mobility as well as functional stability. For ease of understanding, the joints of the foot are di-

Talocrural (Ankle) Joint. The talocrural joint is uniaxial, modified hinge, synovial joint located be tween the talus, the medial malleolus of the tibia and the lateral malleolus of the fibula. The talus shaped so that in dorsiflexion it is wedged between th malleoli, allowing little or no inversion or eversion a the ankle joint. The talus is approximately 2.4 mm (0.1 inch) wider anteriorly than posteriorly. The me dial malleolus is shorter, extending halfway down th talus, whereas the lateral malleolus extends almost t the level of the subtalar joint. The joint is supplied b branches of the tibial and deep peroneal nerves. The talocrural joint is designed for stability, espe cially in dorsiflexion. In plantar flexion, it is muc more mobile. This joint is responsible for the anterior

76

766

CHAPTER 13 • Lower Leg, Ankle, and Foot

Tibia

Talonavicular ligament Navicular

Deltoid ligament

t

nterior tibiotalar Posterior tibiotalar

Intermediate cuneiform

Tibiocalcanean

Medial cuneiform

Dorsal cuneonavicular ligaments

Tibionavicular Talus

Dorsal]- Ligaments . . of first Plantar tarsometatarsal joint

---+---+

First metatarsal Sustentaculum tali --+--f---~

Calcaneus - - - - - \ - +

Plantar calcaneonavicular ligament Tuberosity of navicular bone

A Tibia Anterior tibiofibular ligament Anterior talofibular ligament Talus

Posterior tibiofibular ligament

Talonavicular ligament Navicular

Posterior talofibular ligament

Dorsal cuneonavicular ligaments Dorsal cuneocuboid ligament Dorsal tarsometatarsal ligaments

Calcaneofibular ligament

Calcaneus

Cervical ligament Dorsal metatarsal ligaments Fifth metatarsal Dorsal tarsometatarsal ligaments

Long plantar nerve Bifurcated ligament Cuboid

B Figure 13-1 Ligaments of the hindfoot and midfoot. (A) Medial view. (B) Lateral view.

posterior (dorsiflexion-plantar flexion) movement that occurs in the ankle-foot complex. Its close packed position is maximum dorsiflexion, and its capsular pattern is more limitation of plantar flexion than of dorsiflexion. This joint is most stable in the dorsiflexed posi-

tion. The resting posltlon is 10° of plantar flexion. midway between maximum inversion and maximurr: eversion. The talocrural joint has one degree of freedom, and the movements possible at this joint are dorsiflexion and plantar flexion.

Tibial slip of posterior talofibular ligament Posterior tibiofibular ligament Medial malleolus

Inferior transverse ligament

Talus

Lateral malleolus

y

Posterior tibiotala Tlblocalcanean

Posterior talofibular ligament Posterior talocalcaneal ligament _-+4--'t\iT---;

"':';;L--+_ _

Calcaneofibular ligament

Deltoid ligament

Sustentaculum tali

Groove for flexor hallucis longus muscle

-r+---+-- Calcaneus

c Interosseous ligament of tibiofibular syndesmosis

Anterior talofibular ligament

Fibula Medial malleolus

Medial malleolus

Lateral malleolus

Talus Lateral malleolus Deltoid ligament Posterior talofibular ligament

Sustentaculum tali

Posterior talofibular ligament

E

Interosseous talocalcanean ligament

Calcaneus

Deep anterior talotibial ligame

Medial malleolu

D

Figure 13-1 (Continued) (C) Posterior view. (D) Coronal section through the left talocrural and talocalcanean joints. (E) Superior view of ligaments on the lateral aspect. (F) Superior view of deep deltoid ligament on the medial aspect.

On the medial side of the joint, the major ligament is the deltoid or medial collateral ligament, which consists of four separate ligaments: the tibionavicular, tibiocalcanean, and posterior tibiotalar ligaments superficially, all of which resist talar abduction, and the anterior tibiotalar ligament, which lies deep to the other three ligaments and resists lateral translation and lateral rotation of the talus. On the lateral aspect, the talocrural joint is supported by the anterior talofibular ligament, which provides stability against excessive inversion of the talus; the posterior talofibular ligament,

Deep posterior talotibial ligame

F

which resists ankle dorsiflexion, adduction ("tilt"), m dial rotation, and medial translation of the talus; an the calcaneofibular ligament, which provides stabili against maximum inversion at the ankle and subtal joints. The anterior talofibular ligament is the ligame most commonly injured by a lateral ankle sprain, fo lowed by the calcaneofibular ligament.

Subtalar (Talocalcanean) Joint. The subtalar joi is a synovial joint having three degrees of freedom an a close packed position of supination. Supporting th

768


subtalar joint are the lateral talocalcanean and medial talocalcanean ligaments. In addition, the interosseous talocalcanean and cervical ligaments limit eversion. The movements possible at the subtalar joint are gliding and rotation. With injury to the area (e.g., sprain, fracture), this joint and the talocrural joint often become hypomobile, partially because the talus has no muscles attaching to it. Medial rotation of the leg causes a valgus (outward) movement of the calcaneus, whereas lateral rotation of the leg produces a varus (inward) movement of the calcaneus. The axis of the joint is at an angle of 40° to 45° inclined vertically and 15° to 18° to the sagittal plane.

Plantar tarsometatarsal ligament Cuneiforms

Metatarsal

Plantar cuneonavicular ligaments

Plantar metatarsal ligaments

Tuberosity of navicular bone

Groove for peroneus longus muscle

Plantar calcaneonavicular (spring) ligament

Joints of the Hindfoot Tibiofibular joint

Talocrural (ankle) joint

Subtalar joint

Deltoid ligament

Resting position: Close packed position: Capsular pattern:

Plantar flexion Maximum dorsiflexion

Resting position:

10° plantar flexion, midway between inversion and eversion Maximum dorsiflexion

Close packed position: Capsular pattern: Resting position:

Close packed position: Capsular pattern:

Cuboid Calcaneofibular ligament

Pain on stress

~

Long plantar ligament Short plantar ligament

Groove for flexor hallucis longus muscle

Figure 13-2

Plantar flexion, dorsiflexion Midway between extremes of range of motion Supination Varus, valgus

Midfoot (Midtarsal Joints) In isolation, the midtarsal joints allow only a minimal amount of movement. Taken together, however, they allow significant movement to enable the foot to adapt to many different positions without putting undue stress on the joints. Chopart's joint refers collectively to the midtarsal joints between the talus-calcaneus and the navicular-cuboid. Talocalcaneonavicular Joint. The talocalcaneonavicular joint is a ball-and-socket synovial joint with three degrees of freedom. Its close packed position is supination, and the dorsal talonavicular ligament, bifurcated ligament, and plantar calcaneonavicular (spring) ligament support the joint (see Fig. 13 -1; Fig. 13-2). Movements possible at this joint are gliding and rotation.

Ligaments on plantar aspect of foot.

Cuneonavicular Joint. The cuneonavicular joint is a plane synovial joint with a close packed position o' supination. The movements possible at this joint are slight gliding and rotation. Cuboideonavicular Joint. The cuboideonavicular joint is fibrous, its close packed position being supination. The movements possible at this joint are slighgliding and rotation. Intercuneifonn Joints. The intercuneiform join are plane synovial joints with a close packed positio of supination. The movements possible at these join are slight gliding and rotation. Cuneocuboid Joint. The cuneocuboid joint is plane synovial joint with a close packed position 0 supination. The movements of slight gliding and rotation are possible at this joint.

Joints of the Midfoot (Midtarsal Joints) Resting position:

Midway between extremes of range of motion


Supination

Capsular pattern:

Dorsiflexion, plantar flexion, adduction, medial rotation

Calcaneocuboid Joint. The calcaneocuboid joint is saddle shaped with a close packed position of supination. Supporting this joint are the bifurcated ligament, the calcaneocuboid ligament, and the long plantar ligaments. The movement possible at this joint is gliding with conjunct rotation.

Forefoot Tarsometatarsal Joints. The tarsometatarsal joints are plane synovial joints with a close packed position of supination. The movement possible at these joints is gliding. Taken together, these joints are referred to as Lisfranc's joint. 3 Intermetatarsal Joints. The four intermetatarsal joints are plane synovial joints with a close packed position of supination. The movement possible at these joints is gliding. Metatarsophalangeal Joints. The five metatarsophalangeal joints are condyloid synovial joints with two degrees of freedom. Their close packed position is full extension. Their capsular pattern is variable for the lateral four joints and more limitation of extension than flexion for the hallux (big toe); their resting position is 10° of extension. The movements possible at these joints are flexion, extension, abduction, and adduction.

Joints of the Forefoot Tarsometatarsal joints


Metatarsophalangeal joints

Resting position:

Close packed position: Capsular pattern:

Interphalangeal joints


Midway between extremes of range of motion Supination None Midway between extremes of range of motion (10° extension) Full extension Big toe: extension, flexion 2nd-5th toe: variable Slight flexion Full extension Flexion, extension

Interphalangeal Joints. The interphalangeal joints are synovial hinge joints with one degree of freedom. The close packed position is full extension, and the capsular pattern is more limitation of flexion than of extension. The restirig position of the distal and proximal interphalangeal joints is slight flexion. The movements possible at these joints are flexion and extension.

T

Patient History

It is important to take a detailed and complete history when assessing the lower leg, ankle, and foot. In addition to the questions listed under "Patient History" in Chapter 1, the examiner should obtain the following information from the patient: 1. What is the patient's occupation? Whether the patient stands a great deal and the types of surfaces on which the patient usually stands may have bearing on what is causing the problem. 2. What was the mechanism of injury? What was the position of the foot at the time of the injury? Ankle sprains occur most often when the foot is plantar flexed, inverted, and addllcted, with injury to the anterior talofibular ligament, anterolateral capsule, and possibly the distal tibiofibular ligament. 4 ,5 This same mechanism can lead to a malleolar or talar dome fracture and sinus tarsi syndrome. 6 With injury to the lateral ligaments, the structures (articular surfaces) may be damaged on the medial side owing to compression leading to medial as well as lateral pain.? In fact, if the lateral ligaments are completely torn and the capsule disrupted, medial pain may predominate. Achilles tendinosis or paratenonitis often arises as the result of overuse, increased activity, or change in a high-stress training program. A dorsiflexion injury, accompanied by a snapping and pain on the lateral aspect that rapidly diminishes, may indicate a tear of the peroneal retinaculum. s Table 13 -1 gives some causes of overuse injuries in the lower limb. 9 3. Did the patient notice a transient or fixed deformity of the foot or ankle at the time of injury? Was there any transitory locking (e.g., loose body, muscle spasm)? An affirmative answer may indicate a fracture causing immediate swelling that decreased as it spread into the surrounding tissue. 4. Was the patient able to continue the activity after the injury? If so, the injury is probably not too severe, provided there is no loss of stability. Inability to bear weight, severe pain, and rapid swelling indicate a severe injury.s Walking is compatible with a seconddegree sprain; pain with running usually indicates a first-degree injury.lo

770


Table 13-1 Causes of Overuse Injuries to the Lower Limb Prolonged training season Impact force of activity Training or competing on hard surfaces Change of training surface Downhill running Lack of flexibility Individual muscle weakness or poor reciprocal muscle strength Overstriding Poor posture High mileage or sudden change in mileage Too much, too soon Overtraining Anatomic factors (e.g., malalignment) Wrong type of footwear Road and/or sidewalk camber From Taunton, J., c. Smith, and D.l. Magee: Leg, foot and ankle injuries. In Zachazewski, J.E., D.l. Magee, and W.S. Quillen: Athletic Injuries and Rehabilitation. Philadelphia, W.B. Saunders Co., 1996, p. 730.

5. Was there any swelling or bruising (ecchymosis)? How quickly and where did it develop? This question can elicit some idea of the type of swelling (e.g., blood, synovial, purulent) and whether it is intracapsular or extracapsular. 6. Are symptoms improving, becoming worse, or staying the same? It is important to know the type of onset (macrotrauma, microtrauma) and the duration and intensity of symptoms (acute, subacute, chronic). 7. What are the sites and boundaries of pain or abnormal sensation? The examiner should note whether the pattern is one of a dermatome, a peripheral nerve, or another painful structure. 8. What is the patient's usual activity or pastime? Answers to this question should give some idea of the stresses placed on the lower leg, ankle, and foot, how frequently they are applied, and whether the patient is suffering from a repetitive stress injury. 9. Does activity make a difference? Pain after activity suggests overuse. For example, with overuse injuries, pain initially comes on after the activity. As the injury progresses, pain or soreness is present at the beginning of the activity, then goes away during the activity, only to return afterward. In later stages of the problem, the pain is constantly present. Pain during the activity suggests stress on the injured structure. 10. Where is the pain? Does the patient indicate a specific location or area? For example, with shin splints

or a compartment syndrome, the patient usually indicates a diffuse area. With a stress fracture, the area of pain tends to be more specific. Anterolateral ankle impingement will demonstrate anterolateral ankle joint tenderness, anterolateral ankle joint swelling (extracapsular), pain with force dorsiflexion and eversion, pain with single leg squat, pain with activities and possible absence of ankle instability. I I Peroneal tendon problems show posterolateral pain and may be associated with lateral ankle instability.12 11. Does walking on various terrains make a difference in regard to the foot problem? If so, which terrains cause the most obvious problem? For example. walking on grass (an uneven surface) may bother the patient more than walking on a sidewalk (a relatively even surface), or the patient may find walking on a relatively soft surface (e.g., grass) easier than walking on a hard surface (e.g., cement). Prepared surfaces such as sidewalks, roads, and playing fields often have a camber to allow water runoff. This camber can cause problems in some cases of overuse. 12. What types of shoes does the patient wear? What kind of heel do the shoes have? Are the shoes in good condition? Does the patient make use of orthoses? If so, are they still functional? When an appointment is being made for an assessment, the patient should be told not to wear new shoes, so the examiner can use the shoes to determine the patient's usual shoe wear pattern. The examiner should also note whether the shoes offer proper support. Any orthoses used by the patient should also be brought to the assessment. 13. Is there any history of previous injury or affliction? For example, poliomyelitis may lead to a pe cavus. Systemic conditions such as diabetes, gout, psoriasis, and collagen diseases may manifest themselve first in the foot. 14. For active people, especially runners or jogger. the following questions should also be considered l3 : a. How long has the patient been running or jogging? b. On what type of terrain and surface does the patient train? c. In what types of workouts does the patient participate? Have the workouts changed lately? Ho,,many workouts are done per week? How far doe the patient run per week? (Joggers run approximately 2 to 30 km [1.2 to 18.6 miles] per week at a pace of 5 to 10 minutes/km, and sports runners run 30 to 65 km [18.6 to 40 miles] per week at a pace of 5 to 6 minutes/km. Longdistance runners run 60 to 180 km [37 to 112 miles] per week at a pace of 4 to 5 minutes/krn. Elite runners run 100 to 270 km [62 to 168 miles] per week at a pace of 3.3 to 4 minutes/krn.

d. What types of warm-up, stretching, and postexercise routines does the patient do? The answers give the examiner some idea of whether the warm-up and stretching activities are static or ballistic and whether these activities could be detrimental. e. What types and styles of athletic shoes does the patient wear? (The patient should have the shoes at the examination.) Are they "control" or "cushioning" shoes? People with a cavus foot are more likely to need a cushioning shoe, whereas those with a planus foot are more likely to need a control shoe. The examiner should be able to tell if the shoes fit properly. f. Does the patient wear socks while training? If so, what kind (e.g., cotton, wool, nylon) and how many pairs? g. When was the patient's last race? How long was it? When is the patient's next race? The answers give the examiner some idea of how long the problem has been present and how long it will be until maximum stress is again placed on the joints.

A

B Figure 13-4

(A) Open-chain (non-weight-bearing) supination of the subtalar jo (right foot). When the non-weight-bearing foot is moved at the subtalar joint in the direction of supination, the talus is stable, and the calcaneus and foot move around the talus. The calcaneus and foot invert, plantar flex, and adduct. These positional changes, asso ated with subtalar joint supination, are readily visible when compa with the pronated position of the subtalar joint. (B) Open-chain (non-weight-bearing) pronation of the subtalar joint (right foot). When the subtalar joint is moved into a pronated position in the non-weight-bearing foot, the foot abducts, everts, and dorsiflexes around the stable talus. The positional variances can best be apprec ated by comparing this illustration with the supinated position of t subtalar joint. (From Root, M.L., W.P. Orien, and J.H. Weed: No mal and Abnormal Function of the Foot. Los Angeles, Clinical Bio mechanics Corp., 1977, p. 29.)

T B Figure 13-3 (A) Closed-chain (weight-bearing) supination of the subtalar joint (right foot). Supination of the subtalar joint in the weight-bearing foot results in motion of both the calcaneus and the talus. The calcaneus moves in the frontal plane, and the talus moves in the transverse and sagittal planes. The calcaneus inverts, and the talus simultaneously abducts and dorsiflexes relative to the calcaneus. The leg follows the motion of the talus in the transverse plane and laterally rotates. The leg also follows the sagittal plane motion of the talus to some degree. The dorsiflexion motion of the talus on the calcaneus, therefore, tends to impart a slight extension motion to the knee. (B) Closed-chain (weight-bearing) pronation of the subtalar joint (right foot). Pronation of the subtalar joint in the weightbearing foot results in eversion of the calcaneus; the talus adducts and plantar flexes relative to the calcaneus. The leg follows the talus in a transverse plane and medially rotates. In a sagittal plane, the leg also moves to some extent with the talus. As the talus plantar flexes, the proximal aspect of the tibia moves forward to flex the knee slightly. (From Root, M.L., W.P. Orien, and J.H. Weed: Normal and Abnormal Ftillction of the Foot. Los Angeles, Clinical Biomechanics Corp., 1977, p. 30.)

Observation

Observation of the foot is extensive. Because of t stresses the foot is subjected to and because it, like t hand, can project signs of systemic problems and d ease, the examiner should carry out a careful and m ticulous inspection of the foot. When performing the observation, one should member to compare the weight-bearing (closed-cha with the non-weight-bearing (open-chain) posture the foot. 14 During open-chain motion, the talus considered fixed; during closed-chain motion, the tal moves to help the foot and leg adapt to the terra and to the stresses that are applied to the foot. Ev though the calcaneus is touching a surface in close chain movement, for descriptive purposes, it is s considered to be moving. The weight-bearing stan of the foot shows how the body compensates f structural abnormalities (Fig. 13-3). The non-weigh bearing posture shows functional and structural abi ties without compensation (Fig. 13-4). The observ tion includes looking at the patient from the fro from the side, and from behind in the weight-beari

772


A

c

B

Figure 13-5 (A) During static stance, grOlmd reaction forces (arrolVs) directed upward against the plantar aspects of both feet maintain the transverse plane equilibrium and stability of the lower extremities and pelvis. Equal ground reaction forces are exerted on the lateral and medial plantar surfaces of both feet. (B) When the trunk is rotated to the right, the right foot supinates and the left pronates. The right forefoot inverts from the ground; vertical grow1d reaction forces are greater against the lateral side of the forefoot (large arrolV) and less against the medial side of the forefoot (small arrolV). The left forefoot remains flat on the ground, and vertical ground reaction forces are distributed evenly against the forefoot (equal arrolVs). (C) When the trw1k is rotated to the left, ground reaction exerts unequal forces against the left forefoot and equal forces against the right forefoot. (From Root, M.L., W.P. Orien, and J.H. Weed: Normal and Abnormal Function of the Foot. Los Angeles, Clinical Biomechanics Corp., 1977, p. 102.)

(standing) posllJ.on and from the front, from the side, and from behind in the sitting position with the legs and feet not bearing weight. The examiner should note the patient's willingness and ability to use the feet. The bony and soft-tissue contours of the foot should be normal, and any deviation should be noted. Often, painful callosities may be found over abnormal bony prominences. Any scars or sinuses should also be noted.

Weight-Bearing Position, Anterior View

With the patient in a standing position, the examiner should observe whether the patient's hips and trunk. are in normal position. Excessive lateral rotation of the hip or rotation of the trunk: away from the opposite hip elevates the medial longitudinal arch of the foor. whereas medial rotation of the hip or trunk. rotation toward the opposite hip tends to flatten the arch (Fig

Figure 13-6 Swelling within the talocrural and subtalar joint capsule.

Table 13-2 Causes of Toeing-In and Toeing-Out in Children Level of Affection

Toe-In

Toe-Out

Feet-ankles

Pronated feet (protective toeing-in) Metatarsus varus Talipes varus and equinovarus

Pes valgus due to contracture of triceps surae muscle Talipes calcaneovalgus Congenital convex pes planovalgus

Leg-knee

Tibia vara (Blount's disease) and developmental genu varum Abnormal medial tibial torsion Genu valgum-developmental (protective toeing-in to shift body center of gravity medially)

Lateral tibial torsion Congenital absence of hypoplasia of the fibula

Femur-hip

Abnormal femoral antetorsion Spasticity of medial rotators of hip (cerebral palsy)

Abnormal femoral retroversion Flaccid paralysis of medial rotators of hip

Acetabulum

Maldirected-facing anteriorly

Maldirected-facing posteriorly

From Tachdjian, M.O.: Pediatric Orthopedics. Philadelphia, W.B. Saunders Co., 1990, p. 2817.

13-5). Medial rotation of the hip can also cause pigeon toes, a condition more commonly associated with medial tibial torsion or rotation. If the iliotibial band is tight, the tightness may cause eversion and lateral rotation of the foot. The examiner should also look at the tibia to note any local or general bone swelling (Fig. 13-6). Does the tibia have a normal shape, or is it bowed? Is there any torsional deformity? The medial malleolus usually lies anterior to the lateral malleolus. Pigeon toes, or toe-in deformity, is the result of a medial tibial torsion deformity; it does not constitute a foot deformity (Table 13-2). Figure 13 -7 shows the anterosuperior view of the feet in the weight-bearing stance. The examiner should note whether there is any asymmetry, any malalignment (Table 13-3), or any excessive supination or

Figure 13-7 Anterosuperior view of the feet (weight-bearing position).

pronation of the foot. Supination of the foot involves inversion of the heel, adduction of the forefoot, and plantar flexion at the subtalar joint and midtarsal joints so that the medial longitudinal arch is accentuated (Fig. 13-8A). In addition, there is lateral rotation of the leg in relation to the foot. Supination of the foot causes the proximal aspect of the tibia to move posteriorly. It is required during propulsion to give rigidity to the foot and requires less muscle work than pronation. Pronation of the foot involves eversion of the heel, abduction of the forefoot, medial rotation of the leg in relation to the foot, and dorsiflexion of the subtalar and midtarsal joints (Fig. 13-8B), resulting in a decrease in the medial longitudinal arch. This movement causes the proximal aspect of the tibia to move anteriorly. The pronated foot has greater subtalar motion than the supinated foot and requires more muscle work to maintain stance stability than the supinated foot. The foot is much more mobile in this position. The definitions used in this chapter are the ones preferred by orthopedists and podiatrists. Anatomists and kinesiologists such as Kapandji lS refer to inversion as a combination of adduction and supination and to eversion as a combination of abduction and pronation. Lipscomb and Ibrahim l6 as well as Williams and Warwick l ? define supination and pronation as opposite the terms just mentioned. Because of the confusion in terminology concerning the terms supination and pronation, readers of books and articles on the foot must be careful to discern exactly what each author means. In the infant, the foot is normally pronated. As the child matures, the foot begins to supinate, accompanied by development of the medial longitudinal arch. The foot also appears to be more pronated in the infant because of the fat pad in the medial longitudinal arch.

774


Table 13-3 Malalignment About the Foot and Ankle Possible Correlated Motions or Postures

Malalignment

Possible Compensatory Motions or Postures Hypermobile first ray Subtalar or midtarsal excessive pronation Hip or knee flexion Genu recurvation

Ankle equinus

Rearfoot varus Excessive subtalar supination (calcaneal varus)

Tibial; tibial and femoral; or tibial femoral, and pelvic lateral rotation

Excessive medial rotation along the lower quarter chain Hallux valgus Plantar flexed first ray Functional forefoot valgus Excessive or prolonged midtarsal pronation

Rearfoot valgus Excessive subtalar pronation (calcaneal valgus)

Tibial; tibial and femoral; or tibial, femoral, and pelvic medial rotation Hallux valgus

Excessive lateral rotation along the lower quarter chain Functional forefoot varus

Forefoot varus

Subtalar supination and related rotation along the lower quarter

Plantar flexed first ray Hallux valgus Excessive midtarsal or subtalar pronation or prolonged pronation Excessive tibial; tibial and femoral; or tibial, femoral, and pelvic medial rotation, or all with contralateral lumbar spine rotation

Forefoot valgus

Hallux valgus Subtalar pronation and related rotation along the lower quarter

Excessive midtarsal or subtalar supination Excessive tibial; tibial and femoral; or tibial, femoral, and pelvic lateral rotation, or all with ipsilateral lumbar spine rotation

Metatarsus adductus

Hallux valgus Medial tibial torsion Flatfoot Toeing-in

Hallux valgus

Forefoot valgus Subtalar pronation and related rotation along the lower quarter

Excessive tibial; tibial and femoral; or tibial, femoral, and pelvic lateral rotation, or all with ipsilateral lumbar spine rotation

From Riegger-Krugh, C. and J.J. Keysor: Skeletal malalignment of the lower quarter: Correlated and compensatory motions and postures. J. Orthop. Sports Phys. Ther. 23:166, 1996.

The examiner should note how the patient stands and walks. ormally, in standing, 50% to 60% of the weight is taken on the heel and 40% to 50% is taken by the metatarsal heads. The foot assumes a slight toeout position. This angle (the Fick angle) is approximately 12° to 18° from the sagittal axis of the body. developing from 5° in children (Fig. 13-9).18 Durin~ movement, the foot is subjected to high loading, an pathology may cause the gait to be altered. The cumu· lative force to which each foot is subjected during the day is the equivalent of 639 metric tons in a person who weighs approximately 90 kg, or the equivalent of walking 13 km per day.

\

Figure 13-8

A

B

Supination (A) and pronation (B) of the foot (non-weight-bearing .

5-18°

Index plus

Index minus

Index plus-minu

Figure 13-10 Metatarsal classifications.

Figure 13-9 Fick angle.

Foot loading During Gait Walking:

1.2 times the body weight

Running:

2 times the body weight

Jumping (from height of 60 em [2 feet]):

5 times the body weight

When weight bearing, if the relation of the foot to the ankle is normal, all of the metatarsal bones bear weight, and all of the metatarsal heads lie in the same transverse plane. The forefoot and hindfoot should be parallel to each other and to the floor. The midtarsal joints are in maximum pronation, and the subtalar joint is in neutral position. The subtalar and talocrural joints should be parallel to the floor. Finally, the posterior bisection of the calcaneus and distal one third of the leg should form two vertical, parallel lines. 19 If the examiner has noted any asymmetry in standing, the examiner should place the talus (or foot) in neutral (see Special Tests) to see if the asymmetry disappears. If the asymmetry is present in normal standing, it is a functional asymmetry. If it is still present when the foot is in neutral, it is also an anatomic or structural asymmetry, in which case a structural deformity is probably causing the asymmetry. Leg-heel and forefoot-heel alignment (see Special Tests) may also be checked, especially if asymmetry is present.

The examiner should note whether the patient us a cane or other walking aid. Use of a cane in t opposite hand diminishes the stress on the ankle joi and foot by approximately one third. Any prominent bumps or exostoses should be note as should any splaying (widening) of the forefoo Splaying of the forefoot and metatarsus primus varus more evident in weight bearing. There are three typ of forefoot,20 based on the length of the metatars bones (Fig. 13 -1 0):

1. Index plus type. The first metatarsal (1) is long than the second (2), with the others (3, 4, a 5) of progressively decreasing lengths, so th 1 > 2 > 3 > 4 > 5. This can result in Egyptian type foot (Fig. 13 -11 ). 2. Index plus-minus type. The first metatarsal equal in length to the second metatarsal, with t others progressively diminishing in length, so th 1 = 2 > 3 > 4 > 5. This results in a squar type foot (see Fig. 13 -11). 3. Index minus type. The second metatarsal longer than the first and third metatarsals. T fourth and fifth metatarsals are progressive shorter than the third, so that 1 < 2 > 3 > 4 5. This results in a Morton's or Greek type fo (see Fig. 13-11).

The examiner should note whether the toenails a pear normal. Older individuals will show more brit

776


Squared foot 9%

Mortons or Greek foot 22%

Any swelling or pitting edema within the ankle and foot should be noted (Fig. 13-12). If there is any swelling, it should be noted whether it is intracapsular or extracapsular. Swelling above the lateral malleolus may be related to a fibular fracture or disruption of the syndesmosis. Peroneal retinacular injury may be indicated by swelling posterior to the lateral malleolus. Lateral ankle sprains initially swell distal to the lateral malleolus, but swelling may spread into the foot if the capsule has been torn (Table 13-4).8 The examiner should also check the patient's gait for the position of the foot at heel strike, at foot flat, and at toe off. The gait cycle is described in greater detail in Chapter 14. Any vasomotor changes should be recorded, including loss of hair on the foot, toenail changes, osteoporosis as seen on radiographs, and possible differences in temperature between the limbs. Systemic diseases such as diabetes can also lead to foot problems as a result of altered sensation, which facilitates injury. The examiner should look for any circulatory impairment or presence of varicose veins. Brick-red color or cyanosis when the limb is dependent is an indication of impairment. Does this condition change to rapid blanching, or does it stay normal on elevation of the limbs? Change indicates circulatory impairment.

Egyptian foot 69%

Figure 13-11 Types of feet seen in the general population.

nails. The examiner should look for warts, calluses, and corns. Warts are especially tender to the pinch (but not to direct pressure), but calluses are not. Plantar warts also tend to separate from the surrounding tissues, but calluses do not. Corns are similar to calluses, but have a central nidus. They may be hard (on outside or upper aspect of toes) or soft (between toes) because of moisture.

.... "

,

..

~..

..

..........

. ..

..'O .. '. " ..

.. "

:

"

From behind, the examiner compares the bulk of the calf muscles and notes any differences. Variation may be caused by peripheral nerve lesions, nerve root problems, or atrophy resulting from disuse after injury. The Achilles tendons on each side should be compared. If a tendon appears to curve out (Fig. 13-13), it may

".

' "'

A

Weight-Bearing Position, Posterior View

~

.. .

B

Figure 13-12 Ankle sprain. (A) Note pattern of pitting edema on top of the right foot. (B) The swelling is intracapsular, as indicated by swelling on both sides of the right Achilles tendon.

Table 13-4 Classification of Ankle Sprains Severity

Pathology

Signs and Symptoms

Disability

Grade I (mild) stable

Mild stretch o instability Single ligament involved (usually anterior talofibular ligament)

No hemorrhage Minimal swelling Point tenderness o anterior drawer sign o varus laxity

No or little limp Minimal functional loss Difficulty hopping Recovery 8 days (range, 2-10)

Grade II (moderate) stable

Large spectrum of injury Mild to moderate instability Complete tearing of anterior talofibular ligament, or partial tearing of anterior talofibular plus calcaneofibular ligaments

Some hemorrhage Localized swelling (margins of Achilles tendon less defined) Anterior drawer sign may be present No varus laxity

Limp with walking Unable to toe raiase Unable to hop Unable to run Recovery 20 days (range, 10-30)

Grade III (severe) n'lo-ligament, unstable

Significant instability Complete tear of anterior capsule, anterior talofibular and calcaneofibular ligaments

Diffuse swelling on both sides of Achilles tendon, early hemorrhage Possible tenderness medially and laterally Positive anterior drawer sign Positive varus laxity

Unable to bear weight fully Significant pain inhibition Initially almost complete loss of range of motion Recovery 40 days (range, 30-90)

From Reid, D.C.: Sports Injury Assessment and Rehabilitation. New York, Churchill Livingstone, 1992, p. 226.

indicate a fallen medial longitudinal arch, resulting in a pes planus (flatfoot) condition (Helbing's sign).2! The examiner observes the calcaneus for normality of shape and position. Runners often build up bone and a callus on the heel, producing a "pump bump" (Haglund's deformity) as a result of pressure on the heel (Fig. 13-14).

Figure 13-14 I I

II II II I I

"

I I I I I

Ll NORMAL

DEVIATION

(Foot pronated)

Figure 13-13 Normal and deviated Achilles tendon. The deviation is often seen with pes planus (flatfoot) and when the medial longitudinal arch is lower or has "dropped."

Posterior view of the leg and foot. Note "pump bumps."

The malleoli are compared for POSltlOning. Normally, the lateral malleolus extends farther distally than the medial malleolus; however, the medial malleolus extends farther anteriorly.

Weight-Bearing Position, Lateral View With the side view, the the longitudinal arches examiner should note higher than the lateral

examiner is primarily observing of the foot (Fig. 13 -15). The whether the medial arch is arch (as would be expected).

778


Hindfoot

,Midfoot \, \ ,,

Forefoot

Longitudinal arch

Tarsal arch

Posterior metarsal arch Anterior metatarsal arch

Figure 13-15 Lateral and medial views of the feet showing longitudinal arches.

Figure 13-17 Divisions and arches of the foot (medial view).

Differences in the arches may often be determined by looking at the footprint patterns (Fig. 13 -16). The footprint pattern can be established by putting a light film of baby oil and then powder on the patient's foot and asking the patient to step down on a piece of colored paper. The arches of the feet (Fig. 13 -17) are maintained by three mechanisms 22 : (1) wedging of the interlocking tarsal and metatarsal bones; (2) tightening of the ligaments on the plantar aspect of the foot; and (3) the intrinsic and extrinsic muscles of the foot and their tendons, which help to support the arches. The longitudinal arches form a cone as a result of the angle of

First metatarsal

Second metatarsal

Third metatarsal

Fourth metatarsal

0

0 °0

o

°0oo

o

o NORMAL

Figure 13-16 Footprint patterns.

PES PLANUS

PES CAVUS

Fifth metatarsal

Figure 13-18

Q

~

Angle formed by each metatarsal with the floor. (Modified from Jahss, M.H.: Disorders of the Foot. Philadelphia, W.B. Saunders Co.. 1991, p. 1231.)

Tibialis posterior tendon Flexor digitorum longus tendon Flexor hallucis longus tendon

Plantar calcaneonavicular ligament Medial cuneiform

Figure 13-19 Supports of the medial longitudinal arch of the foot.

Tibialis anterior tendon Calcaneus

Represents plantar aponeurosis, abductor hallucis, and flexor digitorum brevis muscles

Sesamoid bone

the metatarsal bones in relation to the floor. With the medial longitudinal arch being more evident, this angle is greater on the medial side. The angle formed by each of the metatarsals with the floor is shown in Figure 13-18. The medial longitudinal arch consists of the calcaneal tuberosity, the talus, the navicular, three cuneiforms, and the first, second, and third metatarsal bones (Figs. 13-19 and 13-20). This arch is maintained by the tibialis anterior, tibialis posterior, flexor digitorum longus, flexor hallucis longus, abductor hallucis, and flexor digitorum brevis muscles; the plantar fascia; and the plantar calcaneonavicular ligament. The calcaneus, cuboid, and fourth and fifth metatarsal bones make up the lateral longitudinal arch (Fig. 13 - 21). This arch is more stable and less adjustable

Metatarsal arch

Figure 13-20 Arches of the foot (medial view).

Figure 13-21 Supports of the lateral longitudinal arch of the foot: plantar aponeurosis (including the abductor digiti minimi and the flexor digitorum brevis IV and V); long plantar ligament; short plantar ligament.

Calcaneus --!--,L-

Plantar aponeurosis

Proximal fifth phalanx

780


Lateral ) cuneiform

Intermediate cuneiform

...----..... FALLEN ARCH

NORMAL

Figure 13-23 Fallen metatarsal arch.

Figure 13-22 Supports of the transverse arch of the foot.

metatarsal bones. The arch is sometimes divided into three parts: tarsal, posterior metatarsal, and anterior metatarsal. A loss of the anterior metatarsal arch results in callus formation under the heads of the metatarsal bones (especially the second and third metatarsal heads). The metatarsophalangeal joints are slightly extended when the patient is in the normal standin~ position because the longitudinal arches of the foo curve down toward the toes. 22

than the medial longitudinal arch. The arch is maintained by the peroneus longus, peroneus brevis, peroneus tertius, abductor digiti minimi, and flexor digitorum brevis muscles; the plantar fascia; the long plantar ligament; and the short plantar ligament. 22 The transverse arch is maintained by the tibialis posterior, tibialis anterior, and peroneus longus muscles and the plantar fascia (Fig. 13-22). This arch consists of the navicular, cuneiforms, cuboid, and

Figure 13-24 Talipes equinovarus (clubfoot) in a child aged 4 months. (A) Anterior view. (B) Posterior view. (From Klenerman, L.: The Foot and Its Disorders. Boston, Blackwell Scientific Publications, 1982, p.64.)

A

B

Injuries

Equinus Deformity (Talipes Equinus). This def mity is characterized by limited dorsiflexion (less th 10°) at the talocrural joint, usually as a result of co tracture of the gastrocnemius or soleus muscles Achilles tendon. It may also be caused by structu bone deformity (primarily in the talus), trauma, or flammatory disease. The deformity causes increas stress to the forefoot, which may lead to a rock bottom foot and excessive pronation at the subta joint. This deviation can contribute to conditions su as plantar fasciitis, metatarsalgia, heel spurs, and ta navicular pain. 13

Equinus

JI

:\

Clubfoot. This congenital deformity is relativ common and can take many forms, the most comm of which is talipes equinovarus. Its cause is unknow but there are probably multifactorial genetic cau modified by environmental factors. 23 It sometimes exists with other congenital deformities, such as sp bifida and cleft palate. The flexible form is eas treated, but the resistant type often requires surge On assessment, the ROM is limited and the foot h abnormal form (see Fig. 13-25).

Claw toes

Figure 13-25

... Heel in

Components of talipes equinovarus.

varus

Non-weight-Searing Position With the patient in a supine, non-weight-bearing position, the examiner should look for abnormalities such as callosities, plantar warts, scars, and sinuses or pressure sores on the soles of the feet. In addition, by looking at the foot from anterior to posterior, as shown in Figure 13-23, the examiner can observe whether the patient has a "fallen" metatarsal arch. Normally, in the nonweight-bearing position, the arch can be seen. If it falls, callosities are often found over the metatarsal heads. The arch may be reversed, or it may fall because of an equinus forefoot, pes cavus, rheumatoid arthritis, short heel cord, or hammer toes. Abnormal width of one ankle in relation to the other (Keen's sign) may be caused by swelling, loss of integrity of the syndesmosis, or a malleolar fracture. Young children should be assessed for clubfoot deformities, the most common of which is talipes equinovarus (Figs. 13-24 and 13-25). These types of deformities are often associated with other anomalies, such as spina bifida.

Hindfoot Varus (Subtalar or Rearfoot Varu This structural deviation involves inversion of the c caneus when the subtalar joint is in the neutral po tion. The hindfoot is mildly rigid with calcaneal ev sion; therefore, pronation is limited. It may contribu to the appearance of a pes cavus foot, making t medial longitudinal arch appear accentuated. It may the result of tibia varus (genu varum), and, because the extra subtalar pronation necessary at the beginni of stance, normal supination during early propulsi may be prevented. This deviation can contribute conditions such as retrocalcaneal exostosis (pum bumps), shin splints, plantar fasciitis, hamstring strai and knee and ankle pathology (Fig. 13-26).13

Figure 13-26 Hindfoot deformities (right foot). (A) Hindfoot varus. (B) Hindfoot valgus.

A

B

782


Hindfoot (Rearfoot) Valgus. This structural deformity involves eversion of the calcaneus when the subtalar joint is in the neutral position. The hindfoot is mobile, which may lead to excessive pronation and limited supination. It may result from genu valgum (knock knees) and may contribute to the appearance of a pes planus foot, with the medial longitudinal arch appearing flattened. Because of the increased mobility, it is less likely to cause problems than hindfoot varus. It is often associated with tibia valgus (see Fig. 13-26) and has been associated with posterior tibial tendon insufficiency.24

the head and neck of the talus to its trochlea has not been achieved.1 3,25,26 Clinically, it contributes to decreasing the medial longitudinal arch and therefore resembles pes planus. With this deformity, during the weight-bearing phase of gait, the midtarsal joint is completely pronated in an attempt to bring the first metatarsal head in contact with the ground. The prolonged rotation that results can contribute to conditions such as tibialis posterior paratenonitis, patellofemoral syndrome, toe deformities, ligamentous stress (medially), shin splints, plantar fasciitis, postural fatigue, and Morton's neuroma (see Fig. 13-27).

Forefoot Valgus. This structural midtarsal deviation involves eversion of the forefoot on the hindfoot when the subtalar joint is in the neutral position because the normal valgus tilt (35° to 45°) of the head and neck of the talus to its trochlea has been exceeded. With this deformity, during the weight-bearing phase of gait, the midtarsal joint is supinated so that the lateral aspect of the foot is brought into contact with the ground. Like hindfoot valgus, it contributes to decreasing the medial longitudinal arch and therefore clinically resembles a planus foot. The prolonged supination can contribute to conditions such as lateral ankle sprains, iliotibial band syndrome, plantar fasciitis, anterior tarsal tunnel syndrome, toe deformities, sesamoiditis, and leg and thigh pain (Fig. 13-27).13,25

Metatarsus Adductus (Hooked Forefoot). Thi deformity is the most common foot deviation in children. It may be seen at birth but often is not noticed until the child begins to stand. The foot appears to be adducted and supinated, and the hindfoot mayor may not be in valgus. It may be associated with hip dysplasia. Eighty-five to 90% of cases resolve spontaneously.~:::

Forefoot Varus. This structural midtarsal joint deviation involves inversion of the forefoot on the hindfoot when the subtalar joint is in the neutral position. It occurs because the normal valgus tilt (35° to 45°) of

A

B

Figure 13-27 Forefoot deformities (right foot). (A) Forefoot varus. (B) Forefoot valgus.

Pes Cavus ("Hollow Foot" or Rigid Foot). Ape cavus may be caused by a congenital problem; a neurological problem such as spina bifida, poliomyelitis, or Charcot-Marie-Tooth disease; talipes equinovarus; or muscle imbalance. There may also be a genetic factor. because it tends to run in families. The longitudinal arches are accentuated (Fig. 1328), and the metatarsal heads are lower in relation t the hindfoot so that there is a "dropping" of the forefoot on the hindfoot at the tarsometatarsal joints. The soft tissues of the sole of the foot are abnormall short, which gives tl).e foot a shortened appearance. 1:the deformity persists, the bones eventually alter their shape, perpetuating the deformity. The heel is normal. at least initially. Claw toes are often associated with the condition because of the dropping of the forefoo combined with the pull of the extensor tendons. The examiner often finds painful callosities beneath th metatarsal heads that are caused by the loss of th metatarsal arch and tenderness along the deforme toes. There is pain in the tarsal region after time because of osteoarthritic changes in these joints. The longitudinal arches are high on both the media. and lateral aspects, so that a lateral longitudinal arc can in some severe cases be seen, and the forefoot thickened and splayed (Table 13-5). The metatar heads are prominent on the sole of the foot, and the toes do not touch the ground, even on active or passive movement. This type of deformity leads to a rigi foot with very little ability to absorb shock and adapto stress. People with this deformity have difficul doing repetitive stress activity (e.g., long distance running, ballet) and require a cushioning shoe. In sever cases, the cavus foot is often associated with neurolOgIcal disorders. 23

Figure 13-28 Pes cavus (Uhollow foot"). ote the high medial longitudinal arch, early clawing of the big toe, and the heel in varus. (From Klenerman, L.: The Foot and Its Disorders. Boston, Blackwell Scientific Publications, 1982, p. 72.)

Pes Planus (Flatfoot or Mobile Foot). Flatfoot may be congenital, or it may result from trauma, muscle weakness, ligament laxity, "dropping" of the talar head, paralysis, or a pronated foot. For example, a traumatic flatfoot may follow fracture of the calcaneus. It may also be caused by a postural deformity, such as medial rotation of the hips or medial tibial torsion. It is a relatively common foot deformity that often causes little or no problem. Therefore, the examiner should

Table 13-5 Pes Cavus Classification Classification

Features

1. Mild

Longitudinal arch appears high N.W.B. Longitudinal arch almost normal W.B. Toes clawed N.W.B. Toes may be normal W.B. May have hindfoot varus

2. Moderate

Longitudinal arch high NW.B. and W.B. Claw toes evident .W.B. and W.B. Calluses under prominent metatarsal heads Dorsiflexion may be limited Forefoot plantar flexed on hindfoot

3. Severe

Calcaneus cannot pronate past 5° varus Heel in varus, foot in valgus Decreased R.O.M. in foot

N.W.B. = non-weight-bearing; W.B. range of motion.

=

weight bearing; R.O.M.

not necessarily assume that a flat, mobile foot needs to be treated. Because the foot is mobile, patients with flatfoot function very well without treatment and often need only a control shoe to avoid problems in prolonged stress situations. It must be remembered that all infants have flatfeet up to approximately 2 years of age. This appearance in part results from the fat pad in the longitudinal arch and in part from the incomplete formation of the arches. With pes planus, the medial longitudinal arch is reduced, so that on standing its borders are close to or in contact with the ground. If the condition persists into adulthood, it may become a permanent structural deformity, leading to a defect or alteration of the tarsal bones and the talonavicular joints. There are two types of flatfoot deformities. The first type (rigid or congenital flatfoot) is relatively rare. The calcaneus is found in a valgus position, whereas the midtarsal region is in pronation. The talus faces medially and downward, and the navicular is displaced dorsally and laterally on the talus. There are accompanying soft-tissue contractures and bony changes. The second type is acquired or flexible flatfoot (Fig. 1329). In this case, the deformity is similar to the rigid flatfoot, but the foot is mobile (Table 13-6) and there are few, if any, soft-tissue contractures and bony changes. It is usually caused by hereditary factors and is sometimes called a hypermobile flatfoot. Flexible flatfoot may result from tibial or femoral torsion, coxa vara, or a defect in the subtalar joint. If the patient is asked to stand on tiptoes and the arch appears, it is an

784


Table 13-6 Pes Planus Classification Classification

Features 0

0

1. Mild

4 to 6 hindfoot valgus 4 0 to 6 0 forefoot valgus

2. Moderate

6 0 to 10 0 hindfoot valgus 6 0 to 10 0 forefoot varus Poor shock absorption at heel strike

3. Severe

10 to 15 0 hindfoot valgus 8 0 to 10 0 forefoot varus Equinus deformity may be present

Figure 13-29

0

Pes planus (flatfoot).

indication that the patient has a mobile flatfoot. This type of flatfoot seldom needs treatment. Rocker-Bottom Foot. In the rocker-bottom foot deformity, the forefoot is dorsiflexed on the hindfoot. This results in a "broken midfoot," so that the medial and longitudinal arches are absent and the foot appears to be "bent" the wrong way (i.e., convex to the floor instead of the normal concave).

to overuse, trauma, or excessive pressure. The common areas of occurrence in the foot are on the dorsa;, aspect of the tarsometatarsal joint, the head of the fifth metatarsal bone, the calcaneus (where it is often calle a pump bump or runner's bump), the insertion of the plantar fascia, and the superior aspect of the navicular bone. Most often these exostoses are the result 0': poorly fitting footwear that leads to undue pressure on the bone.

Splay Foot. This deformity, which is broadening of the forefoot, is often caused by weakness of the intrinsic muscles and associated weakness of the intermetatarsal ligament and dropping of the anterior metatarsal arch. Morton's Metatarsalgia (Interdigital Neuroma). Morton's metatarsalgia refers to the formation of an interdigital neuroma as a result of injury to one of the digital nerves (Fig. 13-30). Usually, it is the digital nerve between the third and fourth toes, so the examiner must take care to differentially diagnose the condition from a stress fracture of one of the metatarsals in the same area (march fracture). (A stress fracture will be more painful when the bone is palpated and a bone scan would be positive.) While walking or running, the patient is suddenly seized with an agonizing pain on the outer border of the forefoot. The pain is often intermittent, like a cramp, shooting up the side and to the tip of the affected toe or the adjacent two toes. If the metatarsal bones are squeezed together, pain is elicited because of the pressure on the digital nerve. On palpation, pain is more likely to be between the bones rather than on the bone. The condition tends to occur more frequently in women than in men. Exostosis (Bony Spur). Exostosis is an abnormal bony outgrowth extending from the surface of the bone (Fig. 13 - 31). It is actually an increase in the bone mass at the site of an irritative lesion in response

Figure 13-30

The applied anatomy of Morron's metatarsalgia. The interdigital nerve to the space between the third and fourth digits has been divided 2 cm above the neuroma and is reflected downward. The plantar digital vessels are seen entering the neuroma. The end of the flat dissector is on the upper margin of the transverse ligament. The end of the probe points to the intermetatarsophalangeal bursa. (From Klenerman, L.: The Foot and Its Disorders. Boston, BlackweJ: Scientific Publications, 1982, p. 143.)

Figure 13-31 Common areas of exostosis formation in the foot.

Hallux Valgus. Hallux valgus is a relatively common condition in which there is medial deviation of the head of the first metatarsal bone in relation to the center of the body and lateral deviation of the head in relation to the center of the foot (Fig. 13-32). The cause of hallux valgus is varied. It may result from a hereditary factor and is often familial. Women tend to be affected more than men. Trying to keep up with fashion may be a contributing factor if the patient wears tight or pointed shoes, tight stockings, or highheeled shoes. 27 As the metatarsal bones move medially, the base of the proximal phalanx is carried with it, and the phalanx

into it, causing the distal end as well as the dista phalanx to deviate laterally in relation to the center o the body. The long flexor and extensor muscles then have a "bowstring" effect as they are displaced to the lateral side of the joint. A callus develops over the medial side of the head o the metatarsal bone, and the bursa becomes thickened and inflamed; excessive bone (exostosis) forms, resulting in a bunion (Fig. 13-33).9,28 These three changes-callus, thickened bursa, and exostosismake up the bunion, a condition separate from hallux valgus, although it is the result of hallux valgus. In normal persons, the metatarsophalangeal angle (the angle between the longitudinal axis of the metatarsal bone and the proximal phalanx) is 8° to 20° (Fig. 13 - 34). This angle is increased to varying degrees in hallux valgus. The first type (congruous hallux valgus) is a simple exaggeration of the normal relation of the metatarsa to the phalanx of the big toe. The deformity does no progress, and the valgus deformity is between 20° and 30°. The opposing joint surfaces are congruent. It requires little treatment, and often the biggest problem is cosmetic. The second type (pathological hallux valgus) is a potentially progressive deformity, increasing from 20° to 60°. The joint surfaces are no longer congruent and some may even go to subluxation. This type may occur in deviated (early) and subluxed (later) stages. When looking at the foot, the examiner may find that there is a widening gap between the first and

Figure 13-32 (A) An example of congruous hallux valgus. (B) Pathological hallux valgus with bilateral bunions and overlapped toes. ote how the deviating big toe (hallux) rotates and pushes under the second toe. (B from Gartland, JI: Fundamentals of Orthopedics. Philadelphia, W.B. Sawlders Co., 1987, p. 401.)

786


Callus

Bursa

Figure 13-33 (A) Bunions apparent on both feet. (B) Schematic line drawing of a bunion.

B ated with hallux valgus, it results in a splayed foot. It is often associated with a pronated foot.

A

second metatarsal bones (increased intermetatarsal angle) and a lateral deflection of the phalanx at the metatarsophalangeal joint. The joint capsule lengthens on the medial aspect and is contracted on the lateral aspect. The toes rotate on the long axis so that the toenail faces medially because of the pull of the adductor hallucis muscle. Sometimes, the big toe deviates so far that it lies over or under the second toe. Of all hallux valgus cases, 80% are caused by metatarsus primus varus, in which the intermetatarsal or metatarsal angle is increased to more than 15° (Fig. 13-35).29,30 Metatarsus primus varus is an abduction deformity of the first metatarsal bone in relation to the tarsal and other metatarsal bones so that the medial border of the forefoot is curved. Normally, this angle is between 0° and 15°.

Hallux Rigidus. Hallux rigidus is a condition in which dorsiflexion or extension of the big toe is limited because of osteoarthritis of the first metatarsophalangeal joint. 32 Hallux rigidus may also be caused by an anatomic abnormality of the foot, an abnormally long first metatarsal bone (index plus type forefoot; see Fig. 13-10), pronation of the forefoot, or trauma. There are two types: acute and chronic. The acute, or adolescent, type is seen primarily in young people with long, narrow, pronated feet an occurs more frequently in boys than in girls. Pain an stiffness in the big toe come on quickly; the pain is described as constant, burning, throbbing, or aching. Tenderness may be palpated over the metatarsophalan-

Bunionette (Tailor's Bunion). This deformity is characterized by prominence of the lateral aspect of the fifth toe metatarsal head (Fig. 13-36).3l If associ-

20-60°

NORMAL NORMAL

CONGRUOUS

Figure 13-34 Metatarsophalangeal (hallux valgus) angle.

PATHOLOGIC

METATARSUS PRIMUS VARUS

Figure 13-35 Normal foot and metatarsus primus varus. (Note increased intermetatarsal angle.)

geal joint, and the toe is initially held stiff because of muscle spasm. The first metatarsal head may be elevated, large, and tender. The weight distribution pattern in the gait is shown in Figure 13-37. The second (chronic) type of hallux rigidus is much more common and is seen primarily in adults-again, in men more frequently than in women. It is frequently bilateral and is usually the result of repeated minor trauma resulting in osteoarthritic changes to the metatarsophalangeal joint of the big toe. The toe stiffens gradually, and the pain, once established, persists. The patient complains primarily of pain at the base of the big toe on walking. Plantar Flexed First Ray. This structural deformity occurs when the first ray (big toe) lies lower than the other four metatarsal bones, so that the forefoot is everted when the metatarsal bones are aligned. If present congenitally, it is indicative of a cavus foot. In its acquired form, it is seen as compensation for tibia varum (genu varum) with limited calcaneal eversion. This deformity can contribute to the same conditions seen with forefoot valgus. 13 The neutral position of the

Figure 13-36 A bunionette or tailor's bunion.

Callus

first ray is the posltlon in which the first metatarsa head lies in the same transverse plane as the second through fourth metatarsal heads when they are maximally dorsiflexed. 33

Turf Toe. Turf toe is a hyperextension injury (sprain) combined with compressive loading to the metatarsophalangeal joint of the hallux. It can cause a significant functional disability, especially in sports where the hallux is put under high loads. It is often related to the use of flexible footwear and artificial turf. 34,35

Morton's (Atavistic or Grecian) Foot. With a Morton's foot, the second toe is longer than the first. The length difference may be due to different lengths of the metatarsals (see Fig. 13 -1 0). Increased stress is put on this longer toe, and the big toe tends to be hypomobile. There is often hypertrophy of the second metatarsal bone because more stress is put through the second toe. In fact, the second metatarsal can become as large as the first metatarsal. People with this deformity often have difficulty putting on tight-fitting footwear (e.g., skates, ski boots) or dancing (e.g., en pointe in ballet). The different types of feet and their proportional representations in the population are shown in Figure 13 -ll.

Claw Toes. A claw-toe deformity results in hyperextension of the metatarsophalangeal joints and flexion of the proximal and distal interphalangeal joints (Fig. 13-38A). Claw toes usually result from the defective actions of lumbrical and interosseus muscles that cause the toes to become functionless. This condition may be unilateral or bilateral and may be associated with pes cavus, fallen metatarsal arch, spina bifida, or other neurological problems.

Hammer Toes. A hammer-toe deformity consists o an extension contracture at the metatarsophalangeal joint and flexion contracture at the proximal interphalangeal joint; the distal interphalangeal joint may be flexed, straight, or hyperextended (Fig. 13-38B).28,36

Figure 13-37 Weight-bearing patterns in hallux rigid us. (A) Hallux rigid us gait pattern. (B) Normal gait pattern. (C) Shoe develops oblique creases with hallux rigidus. (C, Redrawn from Jahss, M.H.: Disorders of the Foot. Philadelphia, W.B. Saunders Co., 1991, p. 60.)

A

B

c

788


Head of talus ---------::....-+\

Figure 13-39 Pes planus (flatfoot) or calcaneus in valgus can lead to misshapen shoes. Note the prominence of the talar head.

B Callus

Callus

Figure 13-38 Toe deformities. (A) Claw toe. ote that the proximal and distal interphalangeal joints are hyperflexed and the metatarsophalangeal joint is dorsally subluxated. (B) Hanlmer toe. Note the flexion deformity of the proximal interphalangeal joints. The distal interphalangeal joint is in neutral position or slight flexion. (C) Mallet toe. There is flexion contracture of the distal interphalangeal joint. The proximal interphalangeal and metatarsophalangeal joints are in neutral position.

The interosseus muscles are unable to hold the proximal phalanx in the neutral position and therefore lose their flexion effect. This results in clawing of the toe by the long flexors and extensors leading to and accentuating the deformity. The causes of hammer toe include an imbalance of the synergic muscles, hereditary factors, and mechanical factors such as poorly fitting shoes or hallux valgus. It is usually seen only in one toe-the second toe. Often, there is a callus or corn over the dorsum of the flexed joint. The condition is

often asymptomatic, especially if the hammer toe i flexible or serniflexible. The rigid type of hammer toe is likely to cause the greatest problems. Mallet Toe. Mallet toe is associated with a flexion deformity of the distal interphalangeal joint (Fig. 1338C).28,36 It can occur on any of the four lateral toe Often, a corn or callus is present over the dorsum of the affected joint. The condition is usually asymptomatic. It is commonly seen with ill-fitting or poorl~ designed footwear. 31 Polydactyly. This developmental anomaly is characterized by the presence of an extra digit or toe. It may be seen in isolation or with other anomalies such as polydactyly of the hands and syndactyly (webbing) 0 the toes. The primary concern with this anomaly i cosmesis. 37

Shoes The examiner looks at the patient's shoes, both inside and outside, for weight-bearing and wear patterns (Figs. 13-39 and 13-40). With the normal foot, the greatest wear on the shoe is beneath the ball of the

Figure 13-40 Misshapen shoes caused by severely pronated feet. (From Gartland, J.J.: Fundamentals of Orthopedics. Philadelphia, W.B. Saunders Co., 1987, p. 398.)

eral aspect of the heel. If shoes are too small or too narrow, they may pinch the feet, causing deformities and affecting normal growth. If shoes are worn out, they offer little support. If shoes are stiff, they limit proper movement of the foot. Platform-type or high-heeled shoes often cause painful knees because the patient wearing these shoes usually walks with the knees flexed, which may increase the stress on the patella. Continuous wearing of highheeled shoes may also lead to contracture of the calf muscles as well as sore knees and a painful back, because the lumbar spine goes into increased lordotic posture to maintain the center of gravity in its normal position. In addition, these shoes increase the potential for ankle sprains and fractures because a raised center of gravity puts the wearer off balance. High-heeled and pointed shoes often contribute to hallux valgus, bunions, march fractures, and Morton's metatarsalgia as a result of the toes' being pushed together. Shoes with a negative heel may lead to hyperextension of the knees and patellofemoral syndrome. High-cut or high-top shoes that cover the medial and lateral malleoli offer more support than low-cut shoes or those that do not cover the malleoli. Excessive bulging on the medial side of the shoe suggests a valgus or everted foot, whereas excessive bulging on the lateral side suggests an inverted foot. Drop foot resulting from musculature weakness scuffs the toe of the shoe. Oblique forefoot creases in the shoe indicate possible hallux rigidus; absence of forefoot creases indicates no toe-off action during gait.

Weight-Bearing Active Movements of the lower leg, Ankle, and Foot • Plantar flexion (flexion), standing on the toes • Dorsiflexion (extension), standing on the heels • Supination, standing on the lateral edge of the foot • Pronation, standing on the medial edge of the foot • Toe extension • Toe flexion • Combined movements (if necessary) • Sustained positions (if necessary) • Repetitive movements (if necessary)

Non-Weight-Bearing Active Movements of the lower leg, Ankle, and Foot • Plantar flexion (flexion), 50° • Dorsiflexion (extension), 20° • Supination, 45° to 60° • Pronation, 15° to 30° • Toe extension, lateral four toes (MTP, 40°; PIP, 0°; DIP, 30°) and great toe (MTP, 70°; IP, 0°) • Toe flexion, lateral four toes (MTP, 40°; PIP, 35°; DIP, 60°) and great toe (MTP, 45°; IP, 90°) • Toe abduction • Toe adduction

... Examination As with any assessment, the examiner must compare one side with the other and note any asymmetry. This comparison is necessary because of individual differences among normal people.

• Combined movements (if necessary) • Sustained positions (if necessary) • Repetitive movements (if necessary) DIP = distal interphalangeal joint; MTP = metatarsophalangeal joint; PIP = proximal interphalangeal joint.

Active Movements The first movements tested during the examination are active, with painful movements being done last. These movements should be done in both weight-bearing (Figs. 13-41 and 13-42) and non-weight-bearing (long leg sitting or supine lying; Fig. 13 -43) positions, and any differences should be noted because foot deformities and deviations in addition to decreased ROM can lead to injury.38 Lindsjo and colleagues 39 advocated testing weight-bearing ROM by putting the test foot on a 30-cm (12-inch) stool for ease of measurement and flexing the knee. Plantar Flexion. Plantar flexion of the ankle is approximately 50° (see Fig. 13-43A), and the patient's

heel normally inverts when the movement is performe in weight bearing (Fig. 13-44). If heel inversion doe not occur, the foot is unstable, or there is tibialis pos terior dysfunction or tightness. 4o

Dorsiflexion. Dorsiflexion of the ankle is usually 20 past the anatomic position (plantigrade), which is wit the foot at 90° to the bones of the leg (see Fig. 13 43B). For normal locomotion, 10° of dorsiflexion an 20° to 25° of plantar flexion at the ankle are required.

Supination and Pronation. Supination is 45° t 60° and pronation is 15° to 30°, although there variability among individuals (see Fig. 13-43C an D). It is more important to compare the movemen

790


c

A

F

E Figure 13-41

Active movements (weight-bearing posture). (A) Plantar flexion. (B) Dorsiflexion. (C) Supination. (D) Pronation. (E) Toe extension. (F) Toe flexion.

DORSI FLEXORS

Inverters

d'-

Everters

~

PLANTAR FLEXORS

Figure 13-42 Motion diagram of the ankle. 1 = tibialis anterior; 2 = extensor hallucis longus; 3 = extensor digitorum longus; 4 = peroneus tertius; 5 = peroneus brevis; 6 = peroneus longus; 7 = Achilles tendon (soleus and gastrocnemius); 8 = flexor hallucis longus; 9 = flexor digitorum longus; 10 = tibialis posterior.

with that of the patient's normal side (Figs. 13-4and 13-46). Supination combines the movements 0 inversion, adduction, and plantar flexion; pronation combines the movements of eversion, abduction, an dorsiflexion of the foot and ankle. As the patient doe the movement, the examiner should watch for the po sibility of subluxation of various tendons. The peronea. tendons are especially prone to subluxation, and their subluxation is evident on eversion (Fig. 13-47). If tibialis anterior is weak, supination will be affected. If the peronei are weak or the tendons sublux, pronation will be affected. Toe Extension and Flexion. Movement of the toe occurs at the metatarsophalangeal and proximal and distal interphalangeal joints (see Fig. 13-43E and F . Extension of the great toe occurs primarily at the metatarsophalangeal joint (70°); there is minimal or no extension at the interphalangeal joint. For the great toe, 45° flexion occurs at the metatarsophalangeal joint, and 90° occurs at the interphalangeal joint.

A

c

o

Figure 13-43 Active movements (non-weight-bearing posture). (A) Plantar flexion. (B) Dorsiflexion. (C) Supination. (D) Pronation. (E) Toe extension. (F) Toe flexion. (G) Toe abduction. (H) Toe adduction.

Figure 13-44 Inversion of heel while standing on toes (plantar flexion of ankle).

792


SUPINATION (Non-weight-bearing)

PRONATION (Non-weight-bearing) Foot in pronation

Foot in supination

Figure 13-46 Anterior view of the foot in pronation and supination (weight-bearing stance).

PRONATION (Weight-bearing)

SUPINATION (Weight-bearing)

Figure 13-45 Supination and pronation of the foot in weight-bearing and nonweight-bearing postures (posterior views of the right limb).

on the inner or outer borders of the feet, pain and difficulty are experienced in the presence of a subtalar lesion. The examiner should also check the efficiency of the toes. Are the toes straight and parallel? Is the patient able to flex, extend, adduct, and abduct the toes? The toes have a primarily ambulatory function, although. with training, they can develop a prehensile function. The toes extend the weight-bearing area forward and.

For the lateral four toes, extension occurs primarily at the metatarsophalangeal (40 and distal interphalangeal joints (30 Extension at the proximal interphalangeal joints is negligible. For the lateral four toes, 40 flexion occurs at the metatarsophalangeal joints, 35 occurs at the proximal interphalangeal joints, and 60 occurs at the distal interphalangeal joints. 0

)

0

).

0 0 0

Toe Abduction and Adduction. Abduction and adduction of the toes are measured with the second toe as midline. Although the range of motion of abduction can be measured, this is not usually done. The common practice is to ask the patient to spread the toes and then bring them back together (see Fig. 13-43G and H). The amount and quality of movement are compared with those of the unaffected side. If the history has indicated that weight-bearing or non-weight-bearing combined or repetitive movements or sustained postures result in symptoms, these movements should also be tested. The patient should be asked to walk on the toes, heels, and outer and inner borders of the feet. These actions give an indication of the patient's muscle power and control and the functional ROM. With a third-degree strain (rupture) of the Achilles tendon, the patient is not able to walk on the toes. Lack of dorsiflexion makes it difficult for the patient to walk on the heels. When the patient walks

Figure 13-47 Habitual subluxation of the peroneal tendons. The peroneal tendons pass anterior to the retrofibular sulcus but not anterior to the distal fibula, in contradistinction to traumatic subluxation. (From Kelikian. H., and A.S. Kelikian: Disorders of the Ankle. Philadelphia, W.B. Saunders Co., 1985, p. 765.)

by so doing, reduce the load on the metatarsal heads. The great toe also has a primary function of "pushing off" during gait. When assessing the active movements, the examiner must remember that peripheral nerve injuries may alter the pattern of movement. For example, the common peroneal nerve may be injured as it winds around the head of the fibula, resulting in altered nerve conduction to the peroneus longus and brevis muscles (superficial peroneal nerve) and/or the tibialis anterior, extensor digitorum longus, and extensor hallucis longus (deep peroneal nerve).41 In such cases, the movements controlled by these muscles are altered. In addition, there are sensory changes that must be noted.

Passive Movements of the Lower Leg, Ankle, and Foot and Normal End Feel • Plantar flexion at the talocrural joint (tissue stretch) • Dorsiflexion at the talocrural joint (tissue stretch) • Inversion at the subtalar joint (tissue stretCh) • Eversion of the subtalar joint (tissue stretch) • Adduction at the midtarsal joints (tissue stretch) • Abduction at the midtarsal joints (tissue stretCh) • Flexion of the toes (tissue stretch) • Extension of the toes (tissue stretch) • Adduction of the toes (tissue stretch)

Passive Movements The passive movements of the lower leg, ankle, and foot are performed with the patient in a non-weightbearing position (Fig. 13-48). As with other joints, if the active ROM is full, overpressure can be applied to test end feel during the active, non-weight-bearing movements to negate the need to do passive movements. Each movement should be carefully checked, especially if deformities or asymmetries have been noticed during the observation. These deformities or asymmetries may cause problems in other areas of the lower kinetic chain. For example, limited dorsiflexion or tight heel cords may lead to anterior knee pain or ankle injuries. 42 Because the gastrocnemius is a twojoint muscle, dorsiflexion should be tested with the knee straight. In a baby or young child, there is greater mobility and flexibility than in an adult. For example, in the newborn, the foot can readily be dorsiflexed passively, so that the toes and dorsum of the foot touch the skin over the tibia. In the adult, however, dorsiflexion is limited to 20° more than plantigrade. If the patient can only attain plantigrade (90°), then the gastrocnemius or soleus is tight. If gastrocnemius is tight, the ankle ROM is limited with the knee extended. If soleus is tight, the ankle ROM is limited with the knee flexed. If tibialis posterior is tight, supination of the foot will be limited. Some movements may be tested in combination to more closely approximate what occurs functionally. For example, instead of testing plantar flexion, adduction, and inversion separately, supination, as a combined movement, may be tested. Similarly, pronation may be tested as a combined movement, instead of dorsiflexion, abduction, and eversion. During passive movements of the ankle and foot, any capsular patterns should be noted. The capsular pattern of the talocrural joint is more limitation of plantar flexion than of dorsiflexion; the subtalar joint capsular pattern shows more limitation of varus range than of valgus ROM. The midtarsal joint capsular pat-

• Abduction of the toes (tissue stretch)

tern is dorsiflexion most limited, followed by plantar flexion, adduction, and medial rotation. The first metatarsophalangeal joint has a capsular pattern in which extension is most limited, followed by flexion. The pattern for the second through fifth metatarsophalangeal joints is variable. The capsular pattern of the interphalangeal joints is flexion most limited, followed by extension.

Resisted Isometric Movements The resisted isometric movements are performed to test the contractile tissue around the foot, ankle, and lower leg. The patient is in the sitting or supine lying position, and the patient's foot is placed in the anatomic position (plantigrade or 90°; Fig. 13-49). Table 13 -7 shows the muscles acting over the foot and article.

Resisted Isometric Movements of the Lower Leg, Ankle, and Foot • Knee flexion • Plantar flexion • Dorsiflexion • Supination • Pronation • Toe extension • Toe flexion

Dorsiflexion is sometimes tested with the patient's hip flexed to 45° and the knee flexed to 90°, as illustrated in Figure 13-49B. Testing with the patient in

794


A

c

E

G Figure 13-48 Passive movements of the ankle. (A) Plantar flexion. (B) Dorsiflexion. (C) Inversion. (D) Eversion. (E) Abduction and adduction. (F) Toe flexion. (G) Toe abduction.

this posmon enables the examiner to exert a greater isometric force. Resisted isometric knee flexion mu t be performed, because the triceps surae (gastrocnemius and soleus muscles together) act on the knee as well as on the ankle and foot. If the history has indicated that eccentric, concentric, or econcentric muscle action has caused symptoms, these movements should also be tested, but only after the isometric tests have been completed.

Functional Assessment If the patient is able to do the movements already described with little difficulty, functional tests may be performed to see whether these sequential activitie

Figure 13-49 Resisted isometric movements of the lower leg, ankle, and foot. (A) Knee flexion. (B) Dorsiflexion. (C) Plantar flexion. (D) Supination. (E) Pronation. (F) Toe extension.

Table 13-7 Muscles of the Lower Limb, Ankle, and Foot: Their Actions, Nerve Supply, and Nerve Root Derivation (Peripheral Nerves) Action

Nerve Supply

Muscles Acting

Plantar flexion (flexion) of ankle

1. 2. 3. 4. 5. 6. 7. 8.

Gastocnemius* 50leus* Plantaris Flexor digitomm longus Peroneus longus Peroneus brevis Flexor hallucis longus Tibialis posterior

Tibial Tibial Tibial Tibial 5uperficial peroneal 5uperficial peroneal Tibial Tibial

Dorsiflexion (extension) of ankle

1. 2. 3. 4.

Tibialis anterior Extensor digitomm longus Extensor hallucis longus Peroneus tertius

Deep Deep Deep Deep

peroneal peroneal peroneal peroneal

Nerve Roo Derivation

51-52 51-52 51-52 52-53 L5,51-52 L5,51-52 52-53 L4-L5

L4-L5 L5,51 L5,51 L5,51 (continued on next page

796


Table 13-7 (continued) Action

Muscles Acting

Nerve Supply

Nerve Root Derivation

1. 2. 3. 4. 5.

Tibialis posterior Flexor digitorum longus Flexor hallucis longus Tibialis anterior Extensor hallucis longus

Tibial Tibial Tibial Deep peroneal Deep peroneal

Eversion

1. 2. 3. 4.

Peroneus longus Peroneus brevis Peroneus tertius Extensor digitomm longus

Superficial peroneal Superficial peroneal Deep peroneal Deep peroneal

L5,S1-S2 L5,S1-52 L5,Sl L5,Sl

Flexion of toes

1. 2. 3. 4. 5.

Tibial Tibial Tibial (medial plantar branch) Tibial (medial plantar branch) Tibial (lateral plantar branch)

S2-S3 S2-S3 S2-S3 S2-53 S2-S3

Tibial (lateral plantar branch) Tibial (lateral plantar branch) Tibial (1st by medial plantar branch; 2nd through 4th by lateral plantar branch)

S2-S3 S2-S3 S2-S3

Deep peroneal Deep peroneal Deep peroneal (lateral terminal branch) Tibial (1st by medial plantar branch; 2nd through 4th by lateral plantar branch)

L5,51 L5,Sl

Inversion

Extension of toes

Flexor digitorum longus Flexor hallucis longus Flexor digitorum brevis Flexor hallucis brevis Flexor accessorius (Quadratus plantae) 6. Interossei 7. Flexor digiti minirni brevis 8. Lumbricals (metatarsophalangeal joints)

1. 2. 3. 4.

Extensor digitorum longus Extensor hallucis longus Extensor digitorum brevis Lumbricals (interphalangeal joints)

Abduction of toes

1. Abductor hallucis 2. Abductor digiti minimi 3. Dorsal interossei

Tibial (medial plantar branch) Tibial (lateral plantar branch) Tibial (lateral plantar branch)

Adduction of toes

1. Adductor hallucis 2. Plantar interossei

Tibial (lateral plantar branch) Tibial (lateral plantar branch)

L4-L5

S2-S3 S2-S3 L4-L5 L5,Sl

Sl-S2 S2-S3

S2-S3 52-S3 52-S3 S2-S3 S2-S3

* The gastrocnemius and soleus muscles are sometimes grouped together as the triceps surae muscles.

Functional Activities of the Lower Leg, Ankle, and Foot (in Sequential Order) • Squatting (both ankles should dorsiflex symmetrically) • Standing on toes (both ankles should plantar flex symmetrically) • Squatting and bouncing at the end of a squat • Standing on one foot at a time • Standing on the toes, one foot at a time • Going up and down stairs • Walking on the toes • Running straight ahead • Running, twisting, and cutting • Jumping • Jumping and going into a full squat

produce pain or other symptoms. Full ROM is often not necessary for the patient to lead a functional life. These activities, which are examples only, must be geared to the individual patient. Older patients shoul not be expected to do some of the activities unle they have been doing these or similar ones in the recent past (Table 13-8). Because the functional tests place a stress on the other lower limb joints (e.g.. knee, hip, sacroiliac, lumbar joints), the examiner must ensure that these joints exhibit no pathology before all of the tests are completed. On the other hand, functional tests for other joints in the lower limb (e.g., hop test for the knee) may not be sensitive enough to test ankle function. 43 As the patient completes the activities, the examiner must assess whether any symptom (e.g., intermittent claudication or anterior compartment syndrome) occur within a specific time frame. 44 ,45 Balance and proprioception are tested by asking the patient to stand on the unaffected leg and then on the affected leg, first with the eyes open, and then with

Table 13-8 Functional Testing of the Foot and Ankle Starting Potision

Action

Functional Test

Standing on one leg*

Lift toes and forefeet off ground (dorsiflexion)

10 to 15 Repetitions: Functional 5 to 9 Repetitions: Functionally fair 1 to 4 Repetitions: Functionally poor o Repetitions: Nonfunctional


Lift heels off ground (plantar flexion)



Lift lateral aspect of foot off ground (ankle eversion)



Lift medial aspect of foot off ground (ankle inversion)


Seated

Pull small towel up under toes or pick up and release small object (i.e., pencil, marble, cottonball) (toe flexion)


Seated

Lift toes off ground (toe extension)


*Hand may hold something for balance only. Data from Palmer, M.L., and M. Epler: Clinical Assessment Procedures in Physical Therapy. Philadelphia, J.B. Lippincott Co., 1990, pp. 308310.

Range of Motion Necessary at the Foot and Ankle for Selected locomotion Activities Descending stairs:

Full dorsiflexion (20°)

Walking:

Dorsiflexion (10°); plantar flexion (20° to 25°)

the eyes closed. Any differences in balance time or difficulty in balancing give an idea of proprioceptive ability, especially differences that occurred when the patient's eyes were closed (Fig. 13-50).46 Kaikkonen and colleagues47 developed a numerical scoring system to evaluate functional outcome after ankle injury (Table 13-9). Other scales have been developed for specific pathologies (e.g., fractures) about the ankle. 48 - 51

T

Special Tests

When assessing the lower leg, ankle, and foot, it is important to always assess the neutral position of the

B Figure 13-50 Balance and proprioception. (A) One leg, with eyes open. (B) One leg, with eyes closed.

798


Table 13-9 Scoring Scale for Subjective and Functional Follow-up Evaluation After Ankle Injury* I

II

III

IV

V

Subjective assessment of the injured anklet No symptoms of any kind Mild symptoms Moderate symptoms Severe symptoms

15 10 5 0

Can you walk normally? Yes No

15 0

Can you run normally? Yes Jo

10 0

Climbing down stairs:j: Less than 18 seconds 18 to 20 seconds Longer than 20 seconds

10 5 0

Rising on heels with injured leg More than 40 times 30 to 39 times Fewer than 30 times

10 5 0

VI

VII

VIII

IX

Rising on toes with injured leg More than 40 times 30 to 39 times Fewer than 30 times

10 5 0

Single-limbed stance with injured leg§ Longer than 55 seconds 50 to 55 seconds Less than 50 seconds

10 5 0

Laxity of the ankle joints (ADS) Stable (~5 rom) Moderate instability (6-10 mm) Severe instability (> 10 mm)

10 5 0

Dorsiflexion range of motion, injured leg ;;::10 0 50_9 0 30° = Op none + stable = 5p, rigid = 2p, laxid = Op

Ankle (max. 15 points) 74-75. Deformity (rigid, laxid): none = 15p, mild lOp, moderate = 5p, severe = Op

=

Feet (max. 15 points) 76-77. Deformity (rigid, laxid): None = 15p, mild lOp, moderate = 5p, severe = Op

=

SUM: right: _ OBJECTIVE SCORE: _

left: _

Both (R/2

+

U2):_

0

SUBJ. + OBJ. SCORE: (lower extremities)

TOTAL LOCOMOTION SCORE: (a

+

(b)

b) - -

Figure 14-13

T

Abnormal Gait

Discussed next are some of the more common gait abnormalities; this list is by no means inclusive.

Antalgic (Painful) Gait The antalgic or painful gait is self-protective and is the result of injury to the pelvis, hip, knee, ankle, or foot. The stance phase on the affect~d leg is shorter than that on the nonaffected leg, because the patient attempts to remove weight from the affected leg as quickly as possible; therefore, the amount of time on each leg should be noted. The swing phase of the uninvolved leg is decreased. The result is a shorter step length on the uninvolved side, decreased walking velocity, and decreased cadence. 28 In addition, the painful region is often supported by one hand, if it is within reach, and the other arm, acting as a counterbalance, is outstretched. If a painful hip is causing the

problem, the patient also shifts the body weight over the painful hip. This shift decreases the pull of the abductor muscles, which decreases the pressure on the femoral head, from more than two times the body weight to approximately body weight, owing to vertical instead of angular placement of the load over the hip. Flynn and Widmann 47 have outlined some of the causes ofa painful limp in children (Table 14-5).

Arthrogenic (Stiff Hip or Knee) Gait The arthrogenic gait results from stiffness, laxity, or deformity, and it may be painful or pain free. If the knee or hip is fused or the knee has recently been removed from a cylinder cast, the pelvis must be elevated by exaggerated plantar flexion of the opposite ankle and circumduction of the stiff leg (circumducted gait) to provide toe clearance. The patient with this gait lifts the entire leg higher than normal to clear the ground because of a stiff hip or knee (Fig.

Differential Diagnosis of Antalgic Gait 10 Years

Toddler's fracture (tibia or foot) Osteomyelitis, septic arthritis, discitis Arthritis (juvenile rheumatoid arthritis, Lyme disease) Discoid lateral meniscus Foreign body in the foot Benign or malignant Ulmor

Fracture (especially physeal) Osteomyelitis, septic arthritis, discitis Legg-Calve-Perthes disease Transient synovitis Osteochondritis dissecans (knee or ankle) Discoid lateral meniscus Sever's apophysitis (calcaneus) Accessory tarsal navicular Foreign body in the foot Arthritis (junveile rheumatoid arthritis, Lyme disease) Benign or malignant tumor

Stress fracture (femur, tibia, foot, pars interarticularis) Osteomyelitis, septic arthritis, discitis Slipped capital femoral epiphysis Osgood-Schlatter disease or Sinding-Larsen-Johanssen syndrome Osteochondritis dissecans (knee or ankle) Chondromalacia patellae Arthritis (Lyme disease, gonococcal) Accessory tarsal navicular Tarsal coalition Benign or malignant tumor

© 2001 American Academy of Orthopaedic Surgeons. Reprinted from the Jouma! of the American Academy of Orthopaedic Surgeons, Volume 9(2), pp. 89-98.

14-14). The arc of movement helps to decrease the elevation needed to "clear" the affected leg. Because of the loss of flexibility in the hip, knee, or both, the gait lengths are different for the two legs. When the stiff limb is bearing weight, the gait length is usually smaller.

Figure 14-14 Arthrogenic (stiff knee or hip) gait. (A) Excessive plantar flexion. (B) Circumduction.

Ataxic Gait If the patient has poor sensation or lacks muscle coordination, there is a tendency toward poor balance and a broad base (Fig. 14-15). The gait of a person with cerebellar ataxia includes a lurch or stagger, and all movements are exaggerated. The feet of an individual

866

CHAPTER 14 • Assessment of Gait

contracture often results in increased lumbar lordosis and extension of the trunk combined with knee flexion to get the foot on the ground. With a knee flexion contracture, the patient demonstrates excessive ankle dorsiflexion from late swing phase to early stance phase on the uninvolved leg and early heel rise on the involved side in terminal stance. Plantar flexion contracture at the ankle results in knee hyperextension (midstance of affected leg) and forward bending of the trunk with hip flexion (midstance to terminal stance of affected leg). Heel rise on the affected leg also occurs earlier. 28

Equinus Gait

Figure 14-15

This childhood gait is seen with talipes equinovarus (club foot) (Table 14-6). Weight bearing is primarily on the dorsolateral or lateral edge of the foot, depending on the degree of deformity. The weight-bearing phase on the affected limb is decreased, and a limp is present. The pelvis and femur are laterally rotated to partially compensate for tibial and foot medial rotation. I

I

Gluteus Maximus Gait

Ataxic gait. (From Judge, R-D., G.D. Zuidema, and F.T. Fitzgerald: Clinical Diagnosis: A Physiological Approach. Boston, Little, Brown & Co., 1982, p. 438.)

with sensory ataxia slap the ground because they cannot be felt. The patient also watches the feet while walking. The resulting gait is irregular, jerky, and weaving.

Contracture Gaits Joints of the lower limb may exhibit contracture if immobilization has been prolonged or pathology to the joint has not been properly cared for. Hip flexion

If the gluteus maximus muscle, which is a primary hip extensor, is weak, the patient thrusts the thorax posteriorly at initial contact (heel strike) to maintain hip extension of the stance leg. The resulting gait involves a characteristic backward lurch of the trunk (Fig. 14-16).

Gluteus Medius (Trendelenburg's) Gait

If the hip abductor muscles (gluteus medius and minimus) are weak, the stabilizing effect of these muscles during stance phase is lost, and the patient exhibits an excessive lateral list in which the thorax is thrust later-

Table 14-6 Differential Diagnosis of a Nonantalgic Limp Equinus Gait (Toe-Walking) Idiopathic tight Achilles tendon Clubfoot (residual or untreated) Cerebral palsy Limb-length discrepancy

Trendelenburg Gait Legg-Calve-Perthes disease Developmental dysplasia of the hip Slipped capital femoral epiphysis Muscular dystrophy Hemiplegic cerebral palsy Weak gluteus medius

Circumduction Gait/ Vaulting Gait Limb-length discrepancy Cerebral palsy Any cause of ankle or knee stiffness

Steppage Gait Cerebral palsy Myelodysplasia Charcot-Marie-Tooth disease Friedreich's ataxia Tibial nerve palsy

© 2001 American Academy of Orthopaedic Surgeons. Reprinted from the Journal of the American Academy of Orthopaedic Surgeons, Volume 9(2), pp. 89-98.

Figure 14-17

Figure 14-16

Gluteus medius (Trendelenburg's)

Gluteus maximus gait.

ally to keep the center of gravity over the stance leg (Fig. 14-17). A positive Trendelenburg's sign is also exhibited (i.e., the contralateral side droops because the ipsilateral hip abductors do not stabilize or prevent the droop). If there is bilateral weakness of the gluteus medius muscles, the gait shows accentuated side-toside movement, resulting in a "wobbling" gait or "chorus girl swing." This gait may also be seen in patients with congenital dislocation of the hip and coxa vara (see Table 14-6).

Hemiplegic or Hemiparetic Gait The patient with hemiplegic or herniparetic gait swings the paraplegic leg outward and ahead in a circle (circumduction) or pushes it ahead (Fig. 14-18). In addition, the affected upper limb is carried across the trunk for balance. This is sometimes referred to as a neurogenic or flaccid gait.

Parkinsonian Gait The neck, trunk, and knees of a patient with parkinsonian gait are flexed. The gait is characterized by shuffling or short rapid steps (marche a petits pas) at times. The arms are held stiffly and do not have their normal associative movement (Fig. 14-19). During the gait, the patient may lean forward and walk progressively faster as though unable to stop (festination).

Figure 14-18 Hemiplegic (hemiparetic) gait. (From Judge, R.D., G.D. Zuidema, and FT. Fitzgerald: Clinical Diagnosis: A Physiological Approach. Boston, Little, Brown & Co., 1982, p.438.)

Figure 14-19

Parkinsonian gait. (From Judge, R.D., G.D. Zuidem and F.T. Fitzgerald: Clinica Diagnosis: A Physiological proach. Boston, Little, Bro & Co., 1982, p. 496.)

868


Plantar Flexor Gait If the plantar flexor muscles are unable to perform their function, ankle and knee stability are greatly affected. Loss of the plantar flexors results in decrease or absence of push-off. The stance phase is less, and there is a shorter step length on the unaffected side. 28

Psoatic Limp The psoatic limp is seen in patients with conditions affecting the hip, such as Legg-Calve- Perthes disease. The patient demonstrates a difficulty in swing-through, and the limp may be accompanied by exaggerated trunk and pelvic movement. 28 The limp may be caused by weakness or reflex inhibition of the psoas major muscle. Classic manifestations of this limp are lateral rotation, flexion, and adduction of the hip (Fig. 1420). The patient exaggerates movement of the pelvis and trunk to help move the thigh into flexion.

Quadriceps Gait If the quadriceps muscles have been injured (e.g., femoral nerve neuropathy, reflex inhibition, trauma), the patient compensates in the trunk and lower leg. For-

ward flexion of the trunk combined with strong ankle plantar flexion causes the knee to extend (hyperextend). If the trunk, hip flexors, and ankle muscles cannot perform this movement, the patient may use a hand to extend the knee. 28

Scissors Gait This gait is the result of spastic paralysis of the hip adductor muscles, which causes the knees to be drawn together so that the legs can be swung forward only with great effort (Fig. 14-21). This is seen in spastic paraplegics and may be referred to as a neurogenic or spastic gait.

Short leg Gait If one leg is shorter than the other or there is a deformity in one of the bones of the leg, the p'!tient demonstrates a lateral shift to the affected side, and the pelvis tilts down on the affected side, creating a limp (Fig. 14-22). The patient may also supinate the foot on the affected side to try to "lengthen" the limb. The joints of the unaffected limb may demonstrate exaggerated flexion, or hip hiking may occur during the swing phase to allow the foot to clear the ground. 28 The weight-bearing period may be the same for the two legs. With proper footwear, the gait may appear normal. This gait may also be termed painless osteogenic gait.

Figure 14-21 Scissors gait. (From Judge, R.D., G.D. Zuidema, and F.T. Fitzgerald: Clinical Diagnosis: A Physiological Approach. Boston, Little, Brown & Co., 1982, p. 439.)

Figure 14-20 Psoatic limp. Note lateral rotation, flexion, and abduction of affected hip.

Figure 14-23 Steppage or drop foot gait. (From Judge, R.D., G.D. Zuidema, and FT. Fitzgerald: Clinical Diagnosis: A Physiological Approach. Boston, Little, Brown & Co., 1982, p.438.)

Figure 14-22 Short leg gait.

pensate and avoid dragging the toes against the ground, the patient lifts the knee higher than normal (Fig. 14-23). At initial contact, the foot slaps on the ground because of loss of control of the dorsiflexor muscles due to injury to the muscles, their peripheral nerve supply, or the nerve roots supplying the muscles (see Table 14-6).48

Steppage or Drop Foot Gait The patient with a steppage gait has weak or paralyzed dorsiflexor muscles, resulting in a drop foot. To com-

Table 14-7 lists common gait pathologies that can modifY gait and the phase in which the deviation occurs. 30

Table 14-7 Common Gait Pathologies Deviation

Phase

Cause

Excessive foot pronation

Midstance through toe off

Compensated forefoot or rearfoot varus deformity; uncompensated forefoot valgus deformity; pes planus; decreased ankle dorsiflexion; increased tibial varum; long limb; uncompensated medial rotation of tibia or femur; weak tibialis posterior

Excessive foot supination

Heel strike through midstance

Compensated forefoot valgus deformity; pes cavus; short limb; uncompensated lateral rotation of tibia or femur

BOlillCing or exaggerated plantar flexion


Heel cord contracture; increased tone of gastrocnemius and soleus

Insufficient push-off


Gastrocnemius and soleus weakness; Achilles tendon rupture; metatarsalgia; hallux rigidus

Foot slap

Heel strike to foot flat

Dorsiflexor weakness

Steppage gait (hip and knee flex to clear foot)

Acceleration through deceleration

Dorsiflexor weakness (continued on next page)

870


Table 14-7 (continued) Deviation

Phase

Cause

Excessive knee flexion

Heel strike through toe off

Hamstring contracture; decreased range of motion in ankle dorsiflexion; plantar flexor muscle weakness; lengthened limb; hip flexion contracture

Genu recurvatum (knee hyperextension)


Quadriceps femoris weak or short; compensated hamstring weakness; Achilles tendon contracture; habit

Excessive medial or lateral femur rotation (femoral torsion)


Medial or lateral hamstrings tight, respectively; opposite muscle group weakness; anteversion or retroversion, respectively

Increased base of support (>4 inches)


Abductor muscle contracture; instability; genu valgum; leg length discrepancy

Decreased base of support «2 inches)


Adductor muscle contracture; genu varum

Circumduction


Increased limb length; abductor muscle shortening or overuse

Hip hiking


Increased limb length; hamstring weakness; quadratus lumborum shortening

Inadequate hip flexion

Acceleration through heel strike

Hip flexor muscle weakness; hip extensor muscle shortening; increased limb length

Inadequate hip extension


Hip flexion contracture; hip extensor muscle weakness

Excessive trunk back bending


Hip extensor of flexor muscle weakness; hip pain; decreased range of motion of knee

Excessive trunk forward bending

Deceleration through midstance

Quadriceps femoris and gluteus maximus weakness

Excessive trunk lateral flexion (compensated Trendelenburg's gait)

Foot flat through heel off

Gluteus medius weakness

Pelvic drop

Foot flat through heel off

Contralateral gluteus medius weakness

Modified from Giallonardo, L.M.: Gait. In Myers, RS. (ed.): Saunders Manual of Physical Therapy Practice. Philadelphia, W.B. Saunders Co., 1995, p. 1112.

REFERENCES Cited References 1. Sutherland, D.H., and F. Valencia: Pediatric gait: Normal and abnormal development. In Drennan, I.C. (ed.): The Child's Foot and Ankle. New York, Raven Press, 1992. 2. Eastlack, M.E., I. Arvidson, L. Snyder-Mackler, JV. Danoff, and C.L. McGarvey: Interrater reliability of videotaped observational gait-analysis assessments. Phys. Ther. 71:465-472, 1991. 3. Martin, P.E., G.D. Heise, and D.W. Morgan: Interrelationships between mechanical power, energy transfers, and walking and running economy. Med. Sci. Sports Exerc. 25:508-515, 1993. 4. Wall, J .C., and C. Kirtley: Strategies for clinical gait assessment. Orthop. Phys. Ther. Clin. North Am. 10:35-37,2001. 5. Bowker, rH., and C.B. Hall: Normal human gait. In Atlas of Orthotics: Biomechanical Principles and Applications. St. Louis, C.V. Mosby Co., 1975. 6. Inman, V.T., H.J. Ralston, and F. Todd: Human locomotion. In Rose, J., and J.G. Gamble (eds.): Human Locomotion. Baltimore, Williams & Wilkins, 1994.

7. Sutherland, D.H., KR Kaufman, and J.R Moitoza: Kinematics of normal human walking. Itt Rose, J., and J.G. Gamble (eds. : Human Locomotion. Baltimore, Williams & Wilkins, 1994. 8. Adams, J.M., and J. Perty: Gait analysis: Clinical applications. In Rose, I., and J.G. Gamble (eds.): Human Locomotion. Baltimore, Williams & Wilkins, 1994. 9. Koerner, LB.: Normal Human Locomotion and the Gait of the Amputee. Edmonton, University of Alberta Bookstore, 1979. 10. Koerner, 1.: Observation of Human Gait [videotapes]. Health Sciences Audiovisual Education, University of Alberta, 1984. 11. Perry,].: Gait Analysis: Normal and Pathological Function. Thorofare, New Jersey, Slack Inc., 1994. 12. Olsson, E.C.: Methods of studying gait. In Smidt, G.L. (ed.): Gait in Rehabilitation. New York, Churchill Livingstone, 1990. 13. Shiavi, R.: Electromyographic patterns in normal adult locomotion. In Smidt, G.L. (ed.): Gait in Rehabilitation. New York, Churchill Livingstone, 1990.

Sports Med. 14:497-500,1986. 15. Barry-Greb, T.L., and A.L. Harrison: Posture, gait and fi.mctional abilities of the adolescent, pregnant, and elderly female. Orthop. Phys. Ther. Clin. North Am. 5:1-21, 1996. 16. Mann, R.A., GT. Moran, and S.E. Dougherty: Comparative electromyography of the lower extremity in jogging, running, and sprinting. Am. J, Sports Med. 14:501-510,1986. 17. Biden, E., J. O'Conner, and J,J. Collins: Gait analysis. In Daniel, D., W. Akeson, and J, O'Conner (eds.): Knee Ligaments: Structure, Function, Injury and Repair. New York, Raven Press, 1990. 18. Hoppenfeld, S.: Physical Examination of the Spine and Extremities. New York, Appleton-Century-Crofts, 1976. 19. Barry-Greb, T.L., and A.L. Harrison: Posture, gait, and functional abilities of the adolescent, pregnant and elderly female. Orthop. Phys. Ther. Clin. North Am. 5:1-21, 1996. 20. Sutherland, D.H., R. Olshen, L. Cooper, and S.L. Woo: The development of mature gait. J, Bone Joint Surg. Am. 62:336353, 1980. 21. Subotnick, S.L: Variations in angles of gait in running. Phys. Sportsmed. 7:110-114, 1979. 22. Sekiya, N., H. Nagasaki, H. Ito, and T. Furuna. Optimal walking in terms of variability in step length. J, Orthop. Sports Phys. Ther. 26:266-272, 1997. 23. Ostrosky, KM., J.M. Van Swearingen, R.G. Burdett, and Z. Gee: A comparison of gait characteristics in young and old subjects. Phys. Ther. 74:637-646, 1994. 24. Waters, R.L., H.J. Hislop, J. Perry, L. Thomas, and J. Campbell: Comparative cost of walking in young and old adults. J. Orthop. Res. 1:73-76,1983. 25. Nuber, G.W.: Biomechanics of the foot and ankle during gait. Clin. Sports Med. 7:1-13, 1988. 26. Rodgers, M.M.: Dynamic foot mechanics. J, Orthop. Sports Phys. Ther. 21:306-316, 1995. 27. Perry, J" and H.J, Hislop: The mechanics of walking: A clinical interpretation. In Perry, J" and H.J. Hislop (eds.): Principles of Lower-Extremity Bracing. ew York, American Physical Therapy Association, 1970. 28. Epler, M.: Gait. In Richardson, J.K, and Z.A. Iglarsh (eds.): Clinical Orthopedic Physical Therapy. Philadelphia, W.B. Saunders Co., 1994. 29. Krebs, D.E., D. Wong, D. Jevsevar, P.O. Riley, and W.A. Hodge: Trunk kinematics during locomotor activities. Phys. Ther. 72:505-514, 1992. 30. Giallonardo, L.M.: Gait. In Myers, R.S. (ed.): Saunders Manual of Physical Therapy Practice. Philadelphia, W.B. Saunders Co., 1995. 31. Lyu, S.R., K Ogata, and 1. Hoshiko: Effects of a cane on floor reaction force and centre of force during gait. Clin. Orthop. Relat. Res. 375:313-319,2000. 32. Rab, GT.: Muscle. In Rose, J., and J.G. Gamble (eds.): Human Locomotion. Baltimore, Williams & Wilkins, 1994. 33. Dillon, P.Z., W.F. Updyke, and W.C. Allen: Gait analysis with reference to chondromalacia patella. J. Orthop. Sports Phys. Ther. 5:127-131, 1983. 34. Sutherland, D.H., L. Cooper, and D. Daniel: The role of the ankle plantar flexors in normal walking. J. Bone Joint Surg. Am. 62:354-363, 1980. 35. Arnadottir, S.A., and V.S. Mereer: Effects of footwear on measurements of balance and gait in women between the ages of 65 and 93 years. Phys. Ther. 80:17-27,2000. 36. Mann, R.A., J,L. Hagy, V. White, and D. Liddell: The initiation of gait. J, Bone Joint Surg. Am. 61:232-239, 1979. 37. The Pathokinesiology Service and The Physical Therapy Department, Rancho Los Amigos Medical Center: Observational Gait Analysis. Downey, California, Los Amigos Research and Educational Institute, Inc., 1996. 38. Ebbeling, C.J., J. Hamill, and J.A. Crussemeyer: Lower extremity mechanics and energy cost of walking on high-heeled shoes. J, Orthop. Sports Phys. Ther. 19:190-196, 1994. 39. Coutts, F.: Gait analysis in the therapeutic environment. Manual Therapy 4:2-10, 1999.

41. 42. 43. 44.

45. 46. 47. 48.

of step widths and step lengths: a comparison of measurements made directly from a grid with those made from a video recording. J. Orthop. Sports Phys. Ther. 30:410-417,2000. Song, KM., S.E. Halliday, and D.G. Little: The effect of limblength discrepancy on gait. J, Bone Joint Surg. Am. 79:16901698, 1997. Larsson, S.E., and B. Jonsson: Locomotion score in rheumatoid arthritis. Acta Orthop. Scand. 60:271-277, 1989. Wolf, S.L.: A method of quantifYing ambulatory activities. Phys. Ther. 59:767-768, 1979. Wolf, S.L., P.A. Catlin, K Gage, K Curucharri, R. Robertson, and K Stephen: Establishing the reliability arid validity of measurements of walking time using the Emory fi.mctional ambulation profile. Phys. Ther. 79:1122-1133, 1999. Gleim, G.W., N.S. Stachenfeld, and J.A. Nicholas: The influence of flexibility on the economy of walking and jogging. J. Orthop Res. 8:814-823, 1990. Murray, M.P., L.A. Mollinger, G.M. Gardner, and S.B. Sepic: Kinematic and EMG patterns during slow, free, and fast walking J, Orthop. Res. 2:272-280, 1984. FIYlill, J,M., and R.F. Widmann: The limping child: evaluation and diagnosis. J. Am. Acad. Orthop. Surg. 9:89-98,2001. Morag, E., D.E. Hurwitz, T.P. Andriacchi, M. Hichey, and G.B Andersson: Abnormalities in muscle function during gait in relation to the level of lumbar disc herniation. Spine 25:829-833, 2000.

General References

Andriacchi, T.P., G.B. Andersson, R.W. Fermier, D. Stern, and J,O. Galante: A study of lower-l.i.mb mechanics during stair cJ.i.mbing. J. Bone Joint Surg. Am. 62:749-757, 1980. Brown, L.P., and P. Yavorsky: Locomotor biomechanics and pathomechanics: A review. J, Orthop. Sports Phys. Ther. 9:3-10, 1987 Burdett, R.G., G.S. Skrinar, and S.R. Simon: Comparison of mechanical work and metabolic energy consumption during normal gait. J. Orthop. Res. 1:63-72, 1983. Chondera, J,D.: Analysis of gait from footprints. Physiotherapy 60: 179-181,1974. Cook, T.M., KP. Farrell, LA. Carey, J,M. Gibbs, and G.E. Wiger: Effects of restricted knee flexion and walking speed on the vertical ground reaction force during gait. J, Orthop. Sports Phys. Ther. 25:236-244, 1997. Crowinschield, R.D., R.A. Brand, and R.C. Johnson: The effects of walking velocity and age on hip kinematics and kinetics. Clin. Orthop. 132:140-144,1978. Eberhart, H.D., VT. Inman, and B. Bresler: Principal elements in human locomotion. In Klopsteg, P.E., and P.D. Wilson (eds.): Human Limbs and Their Substitutes. New York, McGraw-Hill, 1954. Engel, G.M., and LT. Staheli: The natural history of torsion and other factors influencing gait in childhood. Clin. Orthop. 99:1217,1974. Finley, F.R., KA. Cody, and R.V. Finizie: Locomotion patterns in elderly women. Arch. Phys. Med. Rehabil. 50:140-146, 1969. Gage, J.R., and S. Ounpuu: Gait analysis in clinical practice. Semin. Orthop. 4:72-87, 1989. Garbalosa, J,C., R. Donatelli, and M.J, Wooden: Dysfi.mction, evaluation and treatment of the foot and ankle. In Donatelli, R., and M.J. Wooden (eds.): Orthopedic Physical Therapy. Edinburgh, Churchill Livingstone, 1989. Gaudet, G., R. Goodman, M. Landry, G. Russell, and J.C. Wall: Measurement of step length and step \vidth: A comparison of videotape and direct measurements. Physiother. Can. 42:12-15, 1990. Gilbert, J.A., G.M. Maxwell, J,H. McElhaney, and F.W. Clippinger: A system to measure the forces and moments at the knee and hip during level walking. J. Orthop. Res. 2:281-288, 1984. Gray, G.W.: Chain Reaction Successful Strategies for Closed Chain Testing and Rehabilitation. Adrian, Michigan, Wynn Marketing, 1989.

872


Grieve, D.W.: The assessment of gait. Physiotherapy 55:452-460, 1969. Grieve, D.W.: Timing and placement of the feet. Semin. Orthop. 4: 130-134,1989. Gruebel-Lee, D.M.: Disorders of Hip. Philadelphia, I.B. Lippincott Co., 1983. Herzog, W., and P.J. Conway: Gait analysis of sacroiliac joint patients. J. Manip. Physiol. Ther. 17:124-127, 1994. Hreljac, A.: Preferred and energetically optimal gait transition speeds in human locomotion. Med. Sci. Sports Exerc. 25:1158-1162, 1993. Inman, V.T.: The Joints of the Ankle. Baltimore, Williams & Wilkins, 1976. Inman, VT.: Functional aspects of the abductor muscles of the hip. J. Bone Joint Surg. 29:607-619, 1947. Inman, VT.: Human locomotion: The classic. Clin. Orthop. 288:39, 1993. Judge, R.D., G.D. Zuidema, and FT. Fitzgerald: Clinical Diagnosis: A Physiological Approach. Boston, Little, Brown & Co., 1982. Kadaba, M.P., H.K. Ramakrishnan, and M.E. Wootten: Measurement of lower extremity kinematics during level walking. I. Orthop. Res. 8:383-392, 1990. Kadaba, M.P., H.K. Ramarkrishnan, M.E. Wootten, J. Gainey, G. Gordon, and G.Y Cochran: Repeatability of kinematic, kinetic, and electromyographic data in normal adult gait. I. Orthop. Res. 7:849-860, 1989. Katoh, Y., E.Y. Chao, R.K. Laughman, E. Schneider, and B.F. Morrey: Biomechanical analysis of foot function during gait and clinical applications. Clin. Orthop. 177:23-33, 1983. Kay, R.M., S. Dennis, S. Rothlefson, R.A Reynolds, D.L. Skaggs, and VT. Tolo: The effect of preoperative gait analysis on orthopedic decision making. Clin. Orthop. Relat. Res. 372:217-222, 2000. Krebs, D.E., C.E. Robbins, L. Lavine, and R.W. Mann: Hip biomechanics during gait. I. Orthop. Sports Phys. Ther. 28:51-59, 1998. Law, H.T.: Introduction: Techniques for the measurement of parameters related to human locomotion and their clinical applications. Semin. Orthop. 4:65-71, 1989. Lee, D.: Instability of the sacroiliac joint and the consequences to gait. J. Man. Manip. Ther. 4:22-29, 1996. Lehmann, I.F.: Push off and propulsion of the body in normal and abnormal gait. Clin. Orthop. 288:97-108, 1993. Macleod, J.: Clinical Examination. New York, Churchill Livingstone, 1976. Mann, R.A., and J.L. Hagy: The function of the toes in walking, jogging, and running. [correction: 155:293]. Clin. Orthop. 142: 24-29,1979. McCulloch, M.D., D. Brunt, and D. Van der Linden: The effect of foot orthotics and gait velocity on lower limb kinematics and temporal events of stance. I. Orthop. Sports Phys. Ther. 17:2-10, 1993. McPoil, T.G., and M.W. Cornwall: Applied sports biomechanics in rehabilitation: Running. In Zachazewski, I.E., D.I. Magee, and W.S. Quillen (eds.): Athletic Injuries and Rehabilitation. Philadelphia, W.B. Saunders Co., 1996. Minerti, AE., C. Capelli, P. Zamparo, P.E. di Prampero, and F. Saibene: Effects of stride frequency on mechanical power and energy expenditure of walking. Med. Sci. Sports Exerc. 27:11941202,1995. Murray, M.P., AB. Drought, and R.C. Kory: Walking patterns of normal men. I. Bone Joint Surg. An1. 46:335-360, 1964.

Murray, M.P.: Gait as a total pattern of movement. An1. I. Phys. Med. 46:290-333, 1967. Murray, M.P., D.R. Gore, and B.H. Clarkson: Walking patterns of patients with unilateral pain due to osteoarthritis and avascular necrosis. I. Bone Joint Surg. Am. 53:259-274, 1971. Olsson, E.: Gait analysis in orthopedics. Semin. Orthop. 4:111-119, 1989. Perry, I.: Anatomy and biomechanics of the hindfoot. Clin. Orthop. 177:9-15, 1983. Perry, J.: Pathological gait. In Atlas of Orthotics: Biomechanical Prinicples and Applications. St. Louis, C.V. Mosby Co., 1975. Perry, J., and H. Hislop: Principles of Lower Extremity Bracing. Washington, American Physical Therapy Association, 1967. Root, M.L., W.P. Orien, and I.H. Weed: Normal and Abnormal Function of the Foot. Los Angeles, Clinical Biomechanics Corp., 1977. Saunders, J.B.M., V.T. Inman, and H.O. Eberhart: The major determinants in normal and pathological gait. I. Bone Joint Surg. Am. 35:543-558, 1953. Schwab, G.H., D.R. Moynes, F.W. Jobe, and J. Perry: Lower extremity electromyographic analysis of running gait. Clin. Orthop. 176:166-170,1983. Simon, S.R., R.A. Mann, J.L. Hagy, and L.T. Larsen: Role of tI1e posterior calf muscles in a normal gait. I. Bone Joint Surg. Am. 60:465-472, 1978. Skinner, S.: Development of gait. In Rose, J., and J.G. Gamble (eds.): Human Locomotion. Baltimore, Williams & Wilkins, 1994. Smidt, G.L.: Gait assessment and training in clinical practice. In Smidt, G.L. (ed.): Gait in Rehabilitation. New York, Churchill Livingstone, 1990. Thurston, A.I., and J.D. Harris: Normal kinematics of tI1e lumbar spine and pelvis. Spine 8:199-205, 1983. Tiberio, D., and G.W. Gray: Kinematics and kinetics during gait. In Donatelli, R., and M.J. Wooden (eds.): Orthopedic Physical Therapy. Edinburgh, Churchill Livingstone, 1989. Todd, F.N., L.W. Lamoreux, S.R. Ski.tmer, et aI.: Variations in the gait of normal children. J. Bone Joint Surg. Am. 71:196-204, 1989. Tomaro, I., and R.G. Burdett: The effects of foot orthotics on the EMG activity of selected leg muscles during gait. I. Orthop. Sports Phys. Ther. 17:532-536,1993. Tomberlin, J.P., and H.D. Saunders: Evaluation, Treatment and Prevention of Musculoskeletal Disorders. Chaska, Mitmesota, The Saunders Group, 1994. Veicsteinas, A, P. Aghemo, R. Mrgaria, P. Cova, and M. Pozzolini: Energy cost of walking with lesions of the foot. J. Bone Joint Surg. Am. 61:1073-1076, 1979. Wadsworth, CT.: Manual Examination and Treatment of the Spine and Extremities. Baltimore, Williams & Wilkins, 1988. Winter, D.A: Energy assessment in pathological gait. Physiother. Can. 30:183-191, 1978. Wooten, M.E., M.P. Kadaba, and G.V. Cochran: Dynamic electromyography: 1. Numerical representation using principal component analysis. J. Orthop. Res. 8:247-258, 1990. Wooten, M.E., M.P. Kadaba, and G.Y. Cochran: Dynamic electromyography: II. Normal patterns during gait. J. Orthop. Res. 8: 259-265, 1990. Wright, D.G., S.M. Desai, and W.H. Henderson: Action of the subtalar and ankle joint complex during the stance phase of walking. J. Bone Joint Surg. Am. 46:361-382,464,1964. Wyatt, M.P.: Gait in children. In Smidt, G.L. (ed.): Gait in Rehabilitation. New York, Churchill Livingstone, 1990.

ASS£SSM£NT OF POSTUR£ TPostural Development Through evolution, human beings have assumed an upright erect or bipedal posture. The advantage of an erect posture is that it enables the hands to be free and the eyes to be farther from the ground so that the individual can see farther ahead. The disadvantages include an increased strain on the spine and lower limbs and comparative difficulties in respiration and transport of the blood to the brain. Posture, which is the relative disposition of the body at anyone moment, is a composite of the positions of the different joints of the body at that time. The position of each joint has an effect on the position of the other joints. Classically, ideal postural alignment (viewed from the side) is defined as a straight line (line of gravity) that passes through the ear lobe, the bodies of the cervical vertebrae, the tip of the shoulder, midway through the thorax, through the bodies of the lumbar vertebrae, slightly posterior to the hip joint, slightly anterior to the axis of the knee joint, and just anterior to the lateral malleolus. 1 Correct posture is the position in which minimum stress is applied to each joint. Upright posture is the normal standing posture for humans. If the upright posture is correct, minimal muscle activity is needed to maintain the position. Any position that increases the stress to the joints may be called faulty posture. If a person has strong, flexible muscles, faulty postures may not affect the joints because he or she has the ability to change position readily so that the stresses do not become excessive. If the joints are stiff (hypomobile) or too mobile (hypermobile), or the muscles are weak, shortened or lengthened, however, the posture cannot be easily altered to the correct alignment, and the result can be some form of pathology. The pathology may be the result of the cumulative effect of repeated small stresses (microtrauma) over a long period of time or of constant abnormal stresses (macrotrauma) over a short pe-

riod of time. These chronic stresses can result in the same problems that are seen when a sudden (acute) severe stress is applied to the body. The abnormal stresses cause excessive wearing of the articular surfaces of joints and produce osteophytes and traction spurs, which represent the body's attempt to alter its structure to accommodate these repeated stresses. The soft tissue (e.g., muscles, ligaments) may become weakened, stretched, or traumatized by the increased stress. The application of an acute stress on the chronic stress may exacerbate the problem and produce the signs and symptoms that initially prompt the patient to seek aid. At birth, the entire spine is concave forward, or flexed (Fig. 15 -1). Curves of the spine found at birth are called primary curves. The curves that retain this position, those of the thoracic spine and sacrum, are therefore classified as primary curves of the spine. As the child grows (Fig. 15-2), secondary curves appear and are convex forward, or extended. At about the age of 3 months, when the child begins to lift the head, the cervical spine becomes convex forward, producing the cervical lordosis. In the lumbar spine, the secondary curve develops slightly later (6 to 8 months), when the child begins to sit up and walk. In old age, the secondary curves again begin to disappear as the spine starts to return to a flexed position as the result of disc degeneration, ligamentous calcification, osteoporosis, and vertebral wedging. In the child, the center of gravity is at the level of the twelfth thoracic vertebra. As the child grows older, the center of gravity drops, eventually reaching the level of the second sacral vertebra in adults (slightly higher in males). The child stands with a wide base to maintain balance, and the knees are flexed. The knees are slightly bowed (genu varum) until about 18 months of age. The child then becomes slightly knockkneed (genu valgum) until the age of 3 years. By the age of 6 years, the legs should naturally straighten (Fig. 15-3). The lumbar spine in the child has an exaggerated lumbar curve, or excessive lordosis. This

873

874

CHAPTER 15 • Assessment of Posture

Figure 15-1 Postural development. (A) Flexed posture in a newborn. (B) Development of secondary cervical curve. (C) Development of secondary lumbar curve.

accentuated curve is caused by the presence of large abdominal contents, weakness of the abdominal musculature, and the small pelvis characteristic of children at this age. Initially, a child is flatfooted, or appears to be, as the result of the minimal development of the medial longitudinal arch and the fat pad that is found in the arch. As the child grows, the fat pad slowly decreases in size, making the medial arch more evident. In addition, as the foot develops and the muscles strengthen, the

NO.1

No.2

No.3

NO.4

arches of the feet develop normally and become more evident. During adolescence, posture changes because of hormonal influence with the onset of puberty and musculoskeletal growth. Human beings go through two growth spurts, one when they are very young and a more obvious one when they are in adolescence. This second growth spurt lasts 2.5 to 4 years. 2 During this period, growth is accompanied by sexual maturation. Females develop quicker and sooner than males.

NOo;6

Figure 15-2 Postural changes with age. Apparent kyphosis at 6 and 8 years is caused by scapular winging. (From McMorris, R.O.: Faulry postures. Pediatr. Clin. North Am. 8:214, 1961.)

, 2 yrs.

4 Yrs.

6 yrs.

I

8 yrs.

10 yrs.

18 yrs.

Figure 15-3

Newbornmoderate genu varum

6 monthsminimal genu varum

2 years, 6 monthsphysiological genu valgum

Protective toeing-in

1 year, 7 monthslegs straight

Physiological evolution of lower limb alignment at various ages in infancy and childhood. (Redrawn from Tachdjian, M.O.: Pediatric Orthopedics. Philadelphia, W.B. Saunders Co., 1972, p. 1463.)

4 to 6 yearslegs straight with normal toeing-out

Females enter puberty between 8 and 14 years of age, and puberty lasts about 3 years. Males enter puberty between 9.5 and 16 years of age, and it lasts up to 5 years. 2 It is during this period that body differences arise between males and females, with males tending toward longer leg and arm length, wider shoulders, smaller hip width, and greater overall skeletal size and height than females. Because of the rapid growth spurt, individuals, especially males, may appear ungainly, and poor postural habits and changes are more likely to occur at this age.

Anatomic Factors Affecting Correct Posture

Factors Affecting Posture

• Neurogenic outflow and inflow

Several anatomic features may affect correct posture. These factors may be enhanced or cause additional problems when combined with pathological or congenital states, such as Klippel-Feil syndrome, Scheuermann's disease (juvenile kyphosis), scoliosis, or disc disease.

• Bony contours (e.g., hemivertebra) • Laxity of ligamentous structures • Fascial and musculotendinous tightness (e.g., tensor fasciae latae, pectorals, hip flexors) • Muscle tonus (e.g., gluteus maximus, abdominals, erector spinae) • Pelvic angle (normal is 30°) • Joint position and mobility

Causes of Poor Posture There are many examples of poor posture (Fig. 15-4). Some of the causes are postural (positional), and some are structural.

876


TYPES

A

OF FAULTY

B

c

POSTURE

o

E

Figure 15-4 Examples of faulty posture. (From McMorris, R.O.: Faulty postures. Pediatr. Clin. North Am. 8:217, 1961.)

I

I

GOOD

Relaxed Faulty Posture

I

I

Kyphosis Lordosis

I

I

Sway Back

I I

Flat Back

Postural (Positional) Factors The most common postural problem is poor postural habit; that is, for whatever reason, the patient does not maintain a correct posture. This type of posture is often seen in the person who stands or sits for long periods and begins to slouch. Maintenance of correct posture requires muscles that are strong, flexible, and easily adaptable to environmental change. These muscles must continually work against gravity and in harmony with one another to maintain an upright posture. Another cause of poor postural habits, especially in children, is not wanting to appear taller than one's peers. If a child has an early, rapid growth spurt there may be a tendency to slouch so as not to "stand out" and appear different. Such a spurt may also result in the unequal growth of the various structures, and this may lead to altered posture; for example, the growth of muscle may not keep up with the growth of bone. This process is sometimes evident in adolescents with tight hamstrings. Another cause of poor posture is muscle imbalance or muscle contracture. For example, a tight iliopsoas muscle increases the lumbar lordosis in the lumbar spine. Pain may also cause poor posture. Pressure on a nerve root in the lumbar spine can lead to pain in the back and result in a scoliosis as the body unconsciously adopts a posture that decreases the pain. Respiratory conditions (e.g., emphysema), general weakness, excess weight, loss of proprioception, or muscle spasm (as seen in cerebral palsy or with trauma, as examples) may also lead to poor posture.

I

Round Back

The majority of postural nonstructural faults are relatively easy to correct after the problem has been identified. The treatment involves strengthening weak muscles, stretching tight structures, and teaching the patient that it is his or her responsibility to maintain a correct upright posture in standing, sitting, and other activities of daily living.

Structural Factors Structural deformities, which are the result of congenital anomalies, developmental problems, trauma, or disease, may cause an alteration of posture. For example a significant difference in leg length or an anomaly of the spine such as a hemivertebra may alter the posture. Structural deformities involve mainly changes in bone and therefore are not easily correctable without surgery. However, patients often can be relieved of symptoms by proper postural care instruction.

T

Common Spinal Deformities

Lordosis Lordosis is an excessive anterior curvature of the spine (Fig. 15-5).3-7 Pathologically, it is an exaggeration of the normal curves found in the cervical and lumbar spines. Causes of increased lordosis include (1) postural deformity; (2) lax muscles, especially the abdominal muscles in combination with tight muscles, especially hip flexors or lumbar extensors; (3) a heavy abdomen, resulting from excess weight or pregnancy'

deformity, such as kyphosis (Fig. 15-6); (5) hip flexion contracture; (6) spondylolisthesis; (7) congenital problems, such as bilateral congenital dislocation of the hip; (8) failure of segmentation of the neural arch of a facet joint segment; or (9) fashion (e.g., wearing high-heeled shoes). There are two types of exaggerated lordosis, pathological lordosis and swayback deformity. Pathological Lordosis. In the patient with pathological lordosis, one may often observe sagging shoulders (scapulae are protracted and arms are medially rotated), medial rotation of the legs, and poking forward of the head so that it is in front of the center of gravity. This posture is adopted in an attempt to keep the center of gravity where it should be. Deviation in one part of the body often leads to deviation in another part of the body in an attempt to maintain the correct center of gravity and the correct visual plane. This type of exaggerated lordosis is the most common postural deviation seen. The pelvic angle, normally approximately 30°, is increased with lordosis. With excessive or pathological lordosis, there is an increase in the pelvic angle to approximately 40°, accompanied by a mobile spine and an anterior pelvic tilt. Exaggerated lumbar lordosis is usually accompanied by weakness of the deep lumbar extensors, and tightness of the hip flexors and tensor fasciae latae combined with weak abdominals. 8

Figure 15-6 Faulty posture illustrating exaggerated lordosis and kyphosis. (From Kendall, F.P., and E.K. McCreary: Muscles: Testing and Function. Baltimore, Williams & Wilkins, 1983, p. 281.)

Figure 15-5 Examples of lordosis.

Swayback Deformity. With a swayback deformity, there is increased pelvic inclination to approximately 40°, and the thoracolumbar spine exhibits a kyphosis (Fig. 15 -7). A swayback deformity results in the spine's bending back rather sharply at the lumbosacral angle. With this postural deformity, the entire pelvis shifts anteriorly, causing the hips to move into extension. To maintain the center of gravity in its normal position, the thoracic spine flexes on the lumbar spine. The result is an increase in the lumbar and thoracic curves. Such a deformity may be associated with tightness of the hip extensors, lower lumbar extensors, and upper abdominals, along with weakness of the hip flexors, lower abdominals, and lower thoracic extensors. l

Kyphosis Exaggerated lordosis

Swayback

Kyphosis is excessive posterior curvature of the spine (Figs. 15-8 and 15_9).5,7,9-13 Pathologically, it is an

878


Figure 15-9 Faulty posture illustrating thoracic kyphosis. (From Moe, J.H., D.S. Bradford, RB. Winter, and J.E. Lonstein: Scoliosis and Other Spinal Deformities. Philadelphia, W.B. Saunders Co., 1978, p. 152.)

Figure 15-7 Faulty posture illustrating a swayback. (From Kendall, F.P., and E.K. McCreary: Muscles: Testing and Function. Baltimore, Williams & Wilkins, 1983, p. 284.)

exaggeration of the normal curve found in the thoracic spine. There are several causes of kyphosis, including tuberculosis, vertebral compression fractures, Scheuermann's disease, ankylosing spondylitis, senile osteoporosis, tumors, compensation in conjunction with lordosis, and congenital anomalies. 9 The congenital anomalies include a partial segmental defect, as seen in osseous metaplasia, or centrum hypoplasia and aplasia.12.14.15 In addition, paralysis may lead to a kyphosis because of the loss of muscle action needed to maintain the correct posture combined with the forces of gravity. Pathological conditions such as Scheuermann's vertebral osteochondritis may also result in a structural kyphosis (Fig. 15-10). In this condition, inflammation of the bone and cartilage occurs around the ring epiphysis of the vertebral body. The condition often leads to an anterior wedging of the vertebra. It is a growth disorder that affects approximately 10% of the population, and in most cases several vertebrae are affected. The most common area for the disease to occur is between T10 and L2. There are four types of kyphosis. Round Back. The patient with a round back has a long, rounded curve with decreased pelvic inclination «30°) and thoracolumbar kyphosis. The patient often presents with the trunk flexed forward and a decreased lumbar curve. On examination, there are tight hip extensors and trunk flexors with weak hip flexors and lumbar extensors.

Flat back

Figure 15-8 Examples of kyphosis.

Hump back

Round back

A classic x-ray appearance of the spine in a patient with Scheuermann's disease. Note the wedged vertebra (1), Schmorl's nodules (2), and marked irregularity of the vertebral end plates (3). (From Moe, J,H., D.S. Bradford, RB. Winter, and J,E. Lonstein: Scoliosis and Other Spinal Deformities. Philadelphia, W.B. Saunders Co., 1978, p. 332.)

-0

Figure 15-11 Humpback or gibbus deformity.

Figure 15-12 Faulty posture illustrating flat back. (From Kendall, F.P., and E.K. McCreary: Muscles: Testing and Function. Baltimore, Willianls & Wilkins, 1983, p. 285.)

caused by osteoporosis, in which the thoracic vertebral bodies begin to degenerate and wedge in an anterior direction, resulting in a kyphosis (Fig. 15 -13). Humpback or Gibbus. With humpback, there is a localized, sharp posterior angulation in the thoracic spine (Fig. 15-11). Flat Back. A patient with flat back has decreased pelvic inclination to 20° and a mobile lumbar spine (Fig. 15-12). Dowager's Hump This is often seen in older patients, especially women. The deformity commonly is

Scoliosis Scoliosis is a lateral curvature of the spine. 9 ,1l,16-22 This type of deformity is often the most visible spinal deformity, especially in its severe forms. The most famous example of scoliosis is the "hunchback of Notre Dame." In the cervical spine, a scoliosis is called a torticollis. There are several types of scoliosis, some of

880


AGE 75 20 ............................................................ _

. 7-9 em

Figure 15-13 Loss of height resulting from osteoporosis leading to dowager's hump. Note the flexed head and protruding abdomen, which occur partially to maintain the center of gravity in its normal position.

which are nonstructural (Fig. 15 -14) and some which are structural. Nonstructural scoliosis may be caused by postural problems, hysteria, nerve root irritation, inflammation, or compensation caused by leg length discrepancy or contracture (in the lumbar spine).2! Structural scoliosis primarily involves bony deformity, which may be congenital or acquired or excessive muscle weakness as seen in a long term quadriplegic. This type of scoliosis may be caused by wedge vertebra, hernivertebra (Fig. 15-15), or failure of segmentation. It may be idiopathic (genetic) (Fig. 15 -16); neuromuscular, resulting from an upper or lower motor neuron lesion; or myopathic, resulting from muscular disease. Or, it may be caused by arthrogryposis, resulting from persistent joint contracture,15 or by conditions such as neurofibromatosis, mesenchymal disorders, or trauma. It may accompany infection, tumors, and inflammatory conditions that result in bone destruction. Torticollis may occur because of neuromuscular problems, congenital problems (abnormal

sternocleidomastoid muscle), in conjunction with malocclusion of the temporomandibular joints or with ear problems (referred to the cervical spine). With structural scoliosis, the patient lacks normal flexibility, and side bending becomes asymmetric. This type of scoliosis may be progressive, and the curve does not disappear on forward flexion. With nonstructural scoliosis, there is no bony deformity; this type of scoliosis is not progressive. The spine shows segmental limitation, and side bending is usually symmetric. The nonstructural scoliotic curve disappears on forward flexion. This type of scoliosis is usually found in the cervical, lumbar, or thoracolumbar area. Idiopathic scoliosis accounts for 75% to 85% of all cases of structural scoliosis. The vertebral bodies rotate into the convexity of the curve, with the spinous processes going toward the concavity of the curve. There is a fixed rotational prominence on the convex side which is best seen on forward flexion from the skyline view. This prominence is sometimes called a "razorback spine." The disc spaces are narrowed on the concave side and widened on the convex side. There i distortion of the vertebral body, and vital capacity i considerably lowered if the lateral curvature exceed 60°; compression and malposition of the organs within the rib cage also occur. Examples of scoliotic curve are shown in Figure 15 -17. Table 15-1 provides a summary of postural deviations and associated muscle dysfunction. 23

T

Patient History

As with any history, the examiner must ensure that the information obtained is as complete as possible. By listening to the patient, the examiner can often comprehend the problem. The information should include a history of the problem, the patient's general condition and health, and family history. If a child is being examined, the examiner must also obtain prenatal and postnatal histories, including the health of or injurie suffered by the mother during pregnancy, any complications during pregnancy or delivery, and drugs taken by the mother during that period, especially during the first trimester, which is the period in which most of the congenital anomalies develop. It should be remembered that it is unusual for a patient to present with just a postural problem. It is the symptoms produced by the pathology that are causing the postural abnormality that initiate the consultation. The examiner therefore must be cognizant 0·various underlying pathological conditions when assessing posture. The following questions should be asked: 1. Was there any history of injury? If so, what was the mechanism of injury? For example, lifting often

Figure 15-14 Congenital muscular torticollis on the right in a lOyear-old boy (A through D). Note the contracted sternocleidomastoid muscle. (From Tachdjian, M.O.: Pediatric Orthopedics. Philadelphia, W.B. Saunders Co., 1972, p. 74.)

Figure 15-15 Scoliosis caused by hemivertebra. (From Moe, I.H., D.S. Bradford, R.B. Winter, and I.E. Lonstein: Scoliosis and Other Spinal Deformities. Philadelphia, W.B. Saunders Co., 1978, p. 134.)

causes lower spine problems, which may lead to altered posture. 2. If there is a history of injury, had the patient experienced any back injury or pain previously? If so, what caused that injury or pain? Was it a specific posture, sustained posture, or caused by repetitive movements? If so, what were the postures and/or movements? 3. Are there any postures (e.g., standing with one foot on low stool, sitting \vith legs crossed) that give the patient relief or increase the patient's symptoms?24 The examiner can later test these postures to help determine the problem. 4. Does the family have any history of back prob-

882


Figure 15-16 Idiopathic strucrural right thoracic scoliosis. (From Tachdjian, M.O.: Pediatric Orthopedics. Philadelphia, W.B. Saunders Co., 1972, p. 1200).

Right thoracic curve

~I ~ ALeft lumbar curve

Figure 15-17 Examples of scoliosis curve patterns.

Right thoracic-lumbar curve

-},::"a:i,

left lumbar curve (double major curve)

lems or other special problems? Conditions such as hemivertebra, scoliosis, and Klippel-Feil syndrome may be congenital. 5. Has the patient had any previous illnesses, surgery, or severe injuries? 6. Is there a history of any other conditions, such as connective tissue diseases, that have a high incidence of associated spinal problems? 7. Does footwear make a difference to the patient' posture or symptoms? For example, high-heeled shoe often lead to excessive lordosis. 25 8. How old is the patient? Many spinal problem begin in childhood or are the result of degeneration in the aged. 9. In the child, has there been a growth spurt? If so, when did it begin? Growth spurts often lead te tight muscles and altered posture. 10. For females, when did menarche begin? Doe back pain appear to be associated with menses? Men -che indicates the point at which approximately tV thirds of the female adolescent growth spurt has been completed. 11. For males, has there been a voice change? If so.

Postural Defect

Joints Commonly Affected

Muscles Commonly Shortened

Muscles Commonly Weakened

Forward head posmre

Atlanto-occipital joint Cervical spine Temporomandibular joint Scapulothoracic joint Glenohumeral joint

Levator scapulae Sternocleidomastoid Scalenes Suboccipital muscles Upper trapezius Pectoralis major and minor

Hyoid muscles Lower cervical and thoracic erector spinae Middle and lower trapezius Rhomboids

Swayback posture

Thoracolumbar spine Pelvic joints Hip joint

Upper abdominals Internal intercostals Hip extensors Lower lumbar extensors

Lower abdominal muscles Lower thoracic extensors Hip flexor muscles

Lordotic posture

Thoracolumbar spine Pelvic joints Hip joint

Lumbar extensors Tight hip flexors

Abdominal muscles

Kyphotic posture

Thoracic spine

Intercostales Pectoralis major Serrams anterior Levator scapulae Upper trapezius

Thoracic erector spinae Rhomboids Middle and lower trapezius

Flat back posture

Lumbar spine Pelvic joints

Abdominals Hip extensors

Lumbar extensor muscles Hip flexor muscles

Flat upper back posture

Cervicothoracic spine Scapulothoracic joint

Thoracic erector spinae Scapula retractors

Scapular protractor muscles Anterior intercostal muscles

Scoliosis

Cervicothoracolumbar spine Pelvic joints Hip joint Foot joints

Muscles on the concave side Hip adductors Foot supinators on the short side

Muscles on the convex side Hip abductor muscles Foot pronator muscles on the long side

From Giallonardo, L.M.: Posture. In Myers, R..S. (ed.): Saunders Manual of Physical Therapy Practice. Philadelphia, W.B. Salmders Co., 1995, p. 1092.

when? This question also gives an indication of maturity or onset of puberty. 12. If a deformity is present, is it progressive or stationary? 13. Does the patient experience any neurological symptoms (e.g., a "pins and needles" feeling or numbness)? 14. What is the nature, extent, type, and duration of the pain? 15. What positions or activities increase the pain or discomfort? 16. What positions or activities decrease the pain or discomfort? 17. For children, is there difficulty in fitting clothes? For example, with scoliosis, the hem of a dress is usually uneven because of the spinal curvature. 18. Does the patient have any difficulty breathing? Structural deformities such as idiopathic scoliosis can lead to breathing problems in severe cases.

19. Which hand is the dominant one? Often, the dominant side shows a lower shoulder, with the hip slightly deviated to that side (Fig. 15-18). The spine may deviate slightly to the opposite side, and the opposite foot is slightly more pronated. s The gluteus medius on the dominant side may also be weaker. 20. Has there been any previous treatment? If so, what was it? Was it successful?

T

Observation

To assess posture correctly, the patient must be adequately undressed. Male patients should be in shorts, and female patients should be in a bra and shorts. Ideally, the patient should not wear shoes or stockings. However, if the patient uses walking aids, braces, collars, or orthoses, they should be noted and may be

/

r

884


Figure 15-18 Effect of handedness on posture. (A) Right hand dominant. (B) Left hand dominant. (From Kendall, F.P., and E.K McCreary: Muscles: Testing and Function. Baltimore, Williams & Wilkins, 1983, p. 294.)

used after the patient has been assessed in the "natural" state to determine the effect of the appliances. The patient should be examined in the habitual, relaxed posture that is usually adopted. Often, it takes some time for the patient to adopt the usual posture because of tenseness, uneasiness, or uncertainty. In the standing and sitting positions, the assessment is the same as the observation for the upper and lower limb scanning examinations of the cervical and lumbar spines. Assessment of posture should be carried out with the patient in the standing, sitting, and lying (supine and prone) positions. After the patient has been examined in these positions, the examiner may decide to include other habitual, sustained, or repetitive postures assumed by the patient to see whether these postures increase or alter symptoms. The patient may also be assessed wearing different footwear to determine their effects on the posture and symptoms. When observing a patient for abnormalities in posture, the examiner looks for asymmetry as a possible indication of what may be causing the postural fault.

Some asymmetry between left and right sides is normal. The examiner must be able to differentiate normal deviations from asymmetry caused by pathology. Postural deviations may not always cause symptom . but they may do so with time. 26 As the examiner is watching for asymmetry, he or she should also note potential causes of asymmetry. For example, the examiner should always watch for the presence of muscle wasting, soft tissue or bony swelling or enlargement, scars, and skin changes that may indicate present or past pathology.

Standing The examiner should first determine the patient's body type (Fig. 15-19).24 There are three body types: ectomorphic, mesomorphic, and endomorphic. The ectomorph is a person who has a thin body build characterized by a relative prominence of structures developed from the embryonic ectoderm. The mesomorph has a muscular or sturdy body build character-

ized by relative prominence of structures developed by the embryonic mesoderm. The endomorph has a heavy or fat body build characterized by relative prominence of structures developed from the embryonic endoderm.

Body Types • Ectomorph • Mesomorph • Endomorph

In addition to body type, the examiner should note the emotional attitude of the patient. Is the patient tense, bored, or lethargic? Does the patient appear to be healthy, emaciated, or overweight? Answers to these questions can help the examiner determine how much must be done to correct any problems. For example, if the patient is lethargic, it may take longer to correct the problem than if he or she appears truly interested in correcting the problem. The examiner must remem-

ber that posture is in many ways an expression of one's personality, sense of well-being, and self-esteem.

Anterior View When observing the patient from the front (Fig. 1520), the examiner should note whether the following conditions hold true: 1. The head is straight on the shoulders (in midline). The examiner should note whether the head is habitually tilted to one side or rotated (e.g., torticollis) (Fig. 15-21). The cause of altered head position must be established. For example, it may be the result of weak muscles, trauma, a hearing loss, temporomandibular joint problems, or the wearing of bifocal glasses. 2. The posture of the jaw is normal. In the resting position, normal jaw posture is when the lips are gently pressed together, the teeth are slightly apart (freeway space), and the tip of the tongue is behind the upper teeth in the roof of the mouth. This position maintains the mandible in a good posture (i.e., slight negative pressure in the mouth reduces the work of the muscles). It also enables respiration through the nose and diaphragmatic breathing.

Athletic

Figure 15-19

Asthenic

Pyknic

Male and female body types. (From Debrunner, H.D.: Orthopedic Diagnosis. London, E & S Livingstone, 1970, p. 86.)

Athletic (mesomorphic)

Asthenic (ectomorphic)

Pyknic (endomorphic)

886


Figure 15-20 Posmre in the standing position (anterior view).

Figure 15-21 Congenital torticollis in 18-year-old girl. ote the asymmetry of the face. (From Tachdjian, M.O.: Pediatric Orthopedics. Philadelphia, W.B. SalU1ders Co., 1972, p. 68.)

3. The tip of the nose is in line with the manubrium sternum, xiphisternum, and umbilicus. This line is the anterior line of reference used to divide the body into right and left halves. If the umbilicus is used as a reference point, the examiner should remember that the umbilicus is almost always slightly off center. 4. The upper trapezius neck line is equal on both sides. The muscle bulk of the trapezius muscles should be equal, and the slope of the muscles should be approximately equal. Because the dominant arm usually shows greater laxity by being slightly lower, the slope on the dominant side may be slightly greater. 5. The shoulders are level. In most cases, the dominant side is slightly lower. 6. The clavicles and acromioclavicular joints are level and equal. They should be symmetric; any deviation should be noted. Deviations may be caused by subluxations or dislocations of the acromioclavicular or sternoclavicular joints, fractures, or clavicular rotation. 7. There is no protrusion, depression, or lateralization of the sternum, ribs, or costocartilage. If there are changes, they should be noted. 8. The waist angles are equal, and the arms are equidistant from the waist. If a scoliosis is present, one arm hangs closer to the body than the other arm. The examiner should also note whether the arms are equally rotated medially or laterally. 9. The carrying angles at each elbow are equal. Any deviation should be noted. The normal carrying angle varies from 5° to 15°. 10. The palms of both hands face the body in the relaxed standing position. Any differences should be noted and may give an indication of rotation in the upper limb. 11. The "high points" of the iliac crest are the same height on each side (Fig. 15-22). With a scoliosis, the patient may feel that one hip is "higher" than the other. This apparent high pelvis results from the lateral shift of the trunk; the pelvis is usually level. The same condition can cause the patient to feel that one leg is shorter than the other. 12. The anterior superior iliac spines (ASISs) are level. If one ASIS is higher than the other, there is a possibility that one leg is shorter than the other or that the pelvis is rotated more or shifted up or down more on one side. 13. The pubic bones are level at the symphysis pubis. Any deviation should be noted. 14. The patellae of the knees point straight ahead. Sometimes the patellae face outward ("frog eyes" patellae) or inward ("squinting" patellae). The position of the patella may also be altered by torsion of the femoral neck (anteversion-retroversion), femoral shaft, or tibial shaft. 15. The knees are straight. The knees may be in genu varum or genu valgum. If the ankles are together

Figure 15-22 Viewing height equality. (A) Iliac crests. (B) Anterior superior iliac spines.

Figure 15-23 and the knees are more than two finger-widths apart, the patient has some genu varum. If the knees are touching and the feet are apart, the patient has some genu valgum. Genu valgum is more likely to be seen in females. The examiner should note whether the deformity results from the femur, tibia, or both. In children, the knees go through a progression of being straight, going into genu varum (Fig. 15-23), being straight, going into genu valgum (Fig. 15-24), and finally being straight again during the first 6 years of life (see Fig. 15-3).11 16. The heads of the fibulae are level. 17. The medial and lateral malleoli of the ankles are level. Normally, the medial malleoli are slightly anterior to the lateral malleoli, but the lateral malleoli extend farther distally. 18. Two arches are present in the feet and equal on the two sides. In this position, only the medial longitudinal arch is visible. The examiner should note any pes planus (flatfoot) or pronated foot, pes cavus ("hollow" foot) or supinated foot, or other deformities. 19. The feet angle out equally (this Fick angle is usually 5° to 18° [see Fig. 14-12]; Fig. 15-25). This finding means that the tibias are normally slightly laterally rotated (lateral tibial torsion). The presence of pigeon toes usually indicates medial rotation of the tibias (medial tibial torsion), especially if the patella face straight ahead. If the patella face inward (squinting patella) in the presence of "pigeon toes" or outward, the

Bilateral genu varum in mother and son. Note the associated medial tibial torsion. (From Tachdjian, M.O.: Pediatric Orthopedics. Philadelphia, W.B. Saunders Co., 1972, p. 1462.)

problem may be in the femur (abnormal femoral torsion or hip retroversion/anteversion problems). 20. There is no bowing of bone. Any bowing may indicate diseases such as osteomalacia or osteoporosis. 21. The bony and soft-tissue contours are equally symmetric on the two halves of the body. Any indication of muscle wasting, muscle hypertrophy on one side, or bony asymmetry should be noted. Such a finding may indicate muscle or nerve pathology, or it may simply be related to the patient's job or recreational pursuits. For example, a rodeo bull rider will show hypertrophy of the muscles and bones on one side (the arm that he uses to hang on!). In addition, the patient's skin is observed for abnormalities such as hairy patches (e.g., diastematomyelia), pigmented lesions (e.g., cafe au lait spots, neurofibromatosis), subcutaneous tumors, and scars (e.g., EhlersDanlos syndrome), all of which may lead to or contribute to postural problems (Fig. 15-26).

Lateral View From the side, the examiner should note whether the following conditions hold true: 1. The ear lobe is in line with the tip of the shoul-

888


Figure 15-24 Bilateral genu valgum in an adolescent. (From Tachdjian, M.O.: Pediatric Orthopedics. Philadelphia, W.B. Salmders Co., 1972, p. 1467.)

Figure 15-25 Exaggerated lateral tibial torsion. In stance, with the patellae facing straight forward, the feet point outward. (From Tachdjian, M.O.: Pediatric Orthopedics. Philadelphia, W.B. Salmders Co., 1972, p. 1461.)

Figure 15-26 Abnormal skin markings. (A) Cafe au lait areas of pigmentation seen in neurofibromatosis. (B) Lumbar hair patch seen in diastematomyelia. (From Moe, J.H., D.S. Bradford, R.B. Winter, and J.E. Lonstein: Scoliosis and Other Spinal Deformities. Philadelphia, W.B. Saunders Co., 1978, p. 20.)

Figure 15-27 Posture in the standing position (side view).

iliac crest. This line is the lateral line of reference dividing the body into front and back halves (Fig. 1527). If the chin pokes forward, an excessive lumbar lordosis may also be present. This compensatory change is caused by the body's attempt to maintain the center of gravity in the normal position. 2. Each spinal segment has a normal curve (Fig. 15-28). Large gluteus maximus muscles or excessive fat may give the appearance of an exaggerated lordosis. The examiner should look at the spine in relation to the sacrum, not the gluteal muscles. Likewise, the scapulae may give the illusion of an increased kyphosis in the thoracic spine, especially if they are flat and the patient has rounded shoulders. 3. The shoulders are in proper alignment. If the shoulders droop forward (i.e., the scapulae protract), "rounded shoulders" are indicated. This improper alignment may be caused by habit or by tight pectoral muscles or weak scapular stabilizers.

o

Figure 15-29 Normal pelvic angle.

4. The chest, abdominal, and back muscles have proper tone. Weakness or spasm of any of these muscles can lead to postural alterations. 5. There are no chest deformities, such as pectus carinatum (undue prominence of the sternum) or pectus excavatum (undue depression of the sternum). 6. The pelvic angle is normal (30°; Fig. 15-29). The posterior superior iliac spine should be slightly higher than the anterior superior iliac spine. 7. The knees are straight, flexed, or in recurvatum (hyperextended). Usually, in the normal standing position, the knees are slightly flexed (0° to 5°). Hyperextension of the knees may cause an increase in lordosis in the lumbar spine. Tight hamstrings or gastrocnemius muscles can also cause knee flexion. Figure 15-30 illustrates normal posture and some of the abnormal deviations seen when viewing the patient from the side.

Posterior View

Figure 15-28 Correct postural alignment. (From Kendall, F.P., and E.K. McCreary: Muscles: Testing and Function. Baltimore, Williams & Wilkins, 1983, p. 280.)

When viewing from behind (Fig. 15-31), the examiner should note whether the following conditions hold true: 1. The shoulders are level, and the head is in midline. These findings should be compared with those from the anterior view. 2. The spines and inferior angles of the scapulae are level (Fig. 15-32), and the medial borders of the scapulae are equidistant from the spine. If not, is there a rotational or winging deformity of one of the scapulae? Defects such as Sprengel's deformity should be noted (Fig. 15-33).

890


NECK erect; -- chin and head in balance directly above shoulders

NECK slightly forward; chin slightly out

NECK markedly forward; chin markedly out

UPPER BACK normally rounded

UPPER BACK slightly more rounded

UPPER BACK markedly rounded

TRUNK erect

TRUNK inclined to rear slightly

TRUNK inclined to rear markedly

Figure 15-30 Postural deviations obvious from the side view. (Redrawn from Reedco Research, Auburn, New York.)

ABDOMEN flat

ABDOMEN protruding

LOWER BACK normally curved

LOWER BACK slightly hollow

ABDOMEN protruding and sagging

LOWER BACK markedly hollow

3. The spine is straight or curved laterally, indicating scoliosis. A plumbline may be dropped from the spinous process of the seventh cervical vertebra (Fig. 15-34).27 Normally, the line passes through the gluteal cleft. This line is the posterior line of reference used to divide the body into right and left halves po teriorly. The distance from the vertical string to the gluteal cleft can be measured. This distance is sometimes used as a measurement of spinal imbalance, an it is noted whether the deviation is to the left or right If a torticollis or cervico-thoracic scoliosis is present. the plumbline should be dropped from the occipita; protuberance. 9 4. The ribs protrude or are symmetric on both sides. 5. The waist angles are level. 6. The arms are equidistant from the body and equally rotated.

Figure 15-31 Posture in the standing position (posterior view).

Figure 15-32 Correct postural alignment. (From Kendall, F.P., and E.K. McCreary: Muscles: Testing and Function. Baltimore, Williams & Wilkins, 1983, p. 290.)

Figure 15-33

Sprengel's deformiry. Note the small, high scapula on the right. (From Tachdjian, M.O.: Pediatric Orthopedics. Philadelphia, W.B. Saunders Co., 1972, p. 82.)

Figure 15-34

The patient is viewed from the back to evaluate the spine defor mity. (A) A typical right thoraci curve is shown. The left shoulde is lower and the right scapula more prominent. Note the decreased distance between the rig arm and the thorax, with the sh of the thorax to the right. The iliac crest appears higher, but th is caused by the shift of the tho rax, with fullness on the right a elimination of the waistline. The high hip is thus only apparent, real. (B) Plumbline dropped fro the prominent vertebra of C7 (vertebra prominens) measures decompensation of the upper th rax over the pelvis. The distance from the vertical plumbline to t gluteal cleft is measured in cent meters and is recorded, noting direction of fall from the occipi protuberance (inion). (From Mo J.H., D.S. Bradford, R.B. Winte and I.E. Lonstein: Scoliosis and Other Spinal Deformities. Philadelphia, W.B. Saunders Co., 1978, p. 14.)

892


Figure 15-35 Viewing height equality. (A) Posterior superior iliac spines. (B) Gluteal folds.

B

7. The posterior superior iliac spines (PSISs) are level (Fig. 15-35). If one is higher than the other, one leg may be shorter or rotation of the pelvis may be present. The examiner should note how the PSISs relate to the ASISs. If the ASIS on one side and the PSIS on the other side are higher, there is a torsion deformity (anterior or posterior) at the sacroiliac joint.

Figure 15-36 (A and B) Functional scoliosis resulting from short leg. (C and D) The spinal position with short leg is corrected. (From Tachdjian, M.O.: Pediatric Orthopedics. Philadelphia, W.B. Saunders Co., 1972, p. un.)

If the ASIS and PSIS on one side are higher than the ASIS and PSIS on the other side, there may be an upslip at the sacroiliac joint on the high side. 8. The gluteal folds are level. Muscle weaknes. nerve root problems, or nerve palsy may lead to asymmetry. 9. The knee joints are level. If they are not, it may

/ HEAD erect; gravity line passes directly through center

\ J \

I

SHOULDERS level horizontally

1 ) \

j

HEAD twisted or turned to one side slightly

\

/

\

One SHOULDER slightly higher than other

1 / \.

I

HEAD twisted or turned to one side markedly

\

\.

I

One SHOULDER markedly higher than other

\

Figure 15-37

\

Postural deviations obvious from the posterior view. (Redrawn from Reedco Research, Auburn, New York.)

SPINE straight

SPINE slightly curved laterally

SPINE markedly curved laterally

HIPS level horizontally

One HIP slightly higher

One HIP markedly higher

~

)J ~

j)~

FEET pointed straight ahead

indicate that one leg is shorter than the other (Fig. 15-36). 10. Both of the Achilles tendons descend straight to the calcanei. If the tendons angle out, it may indicate a flatfoot deformity (pes planus). 11. The heels are straight or are angled in (rearfoot varus) or out (rearfoot valgus). 12. Bowing of femur or tibia is present or absent. Figure 15 - 37 illustrates the normal posture and some of the abnormal deviations seen when viewing from behind. When viewing posture, the examiner should remember that the pelvis is usually the key to proper back

FEET painted out

FEET painted out markedly; ankles sag in pronation

posture. The normal pelvic angle is 30°, and the pelvis is held or balanced in this position by muscles. For the pelvis to "sit properly" on the femur, the following muscles must be strong, supple (mobile), and balanced: abdominals, hip flexors, hip extensors, superficial and deep back extensors, hip rotators, and hip abductors and adductors. If the height of the patient is measured, especially in a child, the focal height of the child may be estimated by the use of a chart such as the one shown in Table 15-2. 28 After the standing posture has been assessed, the examiner may decide to assess some additional pos-

894


Table 15-2 Percentage of Mature Height AUained at Different Ages Percentage of Eventual Height Chronologie Age (Years)

Boys

Girls

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18

42.2 49.5 53.8 58.0 61.8 65.2 69.0 72.0 75.0 78.0 81.1 84.2 87.3 91.5 96.1 98.3 99.3 99.8

44.7 52.8 57.0 61.8 66.2 70.3 74.0 77.5 80.7 84.4 88.4 92.9 96.5 98.3 99.1 99.6 100.0 100.0

Forward Flexion Having completed the assessment of normal standing, the examiner asks the patient to flex forward at the hips with the fingertips of both hands together so that the arms drop vertically (Fig. 15-38). The feet should be together, and both knees should be straight. Any alteration from this posture will cause the spine to rotate, giving a false view. From this position, using the anterior and posterior skyline views, the examiner can note the following: 1. Whether there is any asymmetry of the rib cage (e.g., rib hump). If a hump is.present, a level and tape measure may be used to obtain the perpendicular distance between the hump and hollow (Fig. 15-39).9 2. Whether there is any asymmetry in the spinal musculature. 3. Whether a pathological kyphosis is present. 4. Whether lumbar spine straightens or flexes as it normally should. 5. Whether there is any restriction to forward bending such as spondylolisthesis or tight hamstrings (Figs. 15-40 and 15-41).

From Bayley, N.: The accurate prediction of growth and adult height. Mod. Probl. Pediatr. 7:234-255, 1954.

tures (e.g., positional, sustained, or repetitive), especially if the patient has complained in the history that these different positions have caused problems or symptoms.

A

If, in the history, the patient complained that sustained forward flexion caused symptoms, the examiner should ask the patient to assume the symptom-causing posture and maintain it for 15 to 30 seconds to determine whether symptoms arise or increase. Flexion has been found to decrease the stress on the facet joints, but it can increase the pressure in the nucleus pulpoSUS. 29 ,30 Likewise, if repetitive forward flexion or com-

B

Figure 15-38 Posture in forward flexion. (A) Normal range of motion. Note reversal of lumbar curve. (B) Excessive range of motion due to excessive hip mobility.

Hump - - - - - -

--,.

Hollow - - - - - - - - - _ - - , .

A

Figure 15-39 Rib hump in forward bending test. (A) Posterior view. (B) Anterior view. The two sides are compared. ote the presence of a right thoracic prominence. (C) Measurement of the prominence. The spirit level is positioned with the zero mark over the palpable spinous process in the area of maximal prominence. The level is made horizontal and the distance to the apex of the deformity (5 to 6 em) noted. The perpendicular distance from the level to the hollow is measured at the sanle distance from the midline. A 2.4-cm right thoracic prominence is shown. (From Moe, I.H., D.S. Bradford, R.B. Winter, and I.E. Lonstein: Scoliosis and Other Spinal Deformities. Philadelphia, W.B. Saunders Co., 1978, p. 17.)

bined movements (e.g., extension and rotation) have caused symptoms, the patient should be asked to do the repetitive or combined movements. Loading the spine by lifting an object may also cause symptoms and may be investigated if symptoms are not too great.

Sitting With the patient seated on a stool so that the feet are on the ground and the back is unsupported, the examiner looks at the patient's posture (Fig. 15 -42). Sitting without a back support causes the patient to support his or her own posture and increases the amount of muscle activity needed to maintain the posture. 29

Figure 15-40 Abnormal forward bending resulting from tight hamstrings, in a patient with spondylolisthesis. (From Moe, I.H., D.S. Bradford, R.B. Winter, and I.E. Lonstein: Scoliosis and Other Spinal Deformities. Philadelphia, W.B. Saunders Co., 1978, p. 19.)

896


This observation is carried out, as in the standing position, from the front, back, and side. If any anteroposterior or lateral deviations of the spine are observed, the examiner should recall whether they were present when the patient was examined while standing. It should be noted whether the spinal curves increase or decrease when the patient is in the sitting position and how the curves change with different sitting postures,3l From the front, it can be noted whether the knees are the same distance from the floor. If they are not, this may indicate a shortened tibia. From the side, it can be noted whether one knee protrudes farther than the other. If it does, this may indicate a shortened femur on the other ide. If the patient has complained in the history that going from standing to sitting or sitting to standing resulted in symptoms, the patient should be asked to repeat these maneuvers, provided the movements do not exacerbate the symptoms too much. Figure 15-41 Forward bending position for viewing kyphosis (lateral view). (A) Normal thoracic roundness is demonstrated with a gentle curve to the whole spine. (B) An area of increased bending is seen in the thoracic spine, indicating structural changes, in a patient with Scheuermann's disease. (From Moe, J,H., D.S. Bradford, R.B. Winter, and J.E. Lonstein: Scoliosis and Other Spinal Deformities. Philadelphia, W.B. Saunders Co., 1978, p. 18.)

I

Figure 15-42 Posture in sitting position. (A) Anterior view. (B) Side view.

A

B

Figure 15-43 Structural kyphosis does not disappear on extension. (From Moe, rH., D.S. Bradford, R.B. Winter, and J.E. Lonstein: Scoliosis and Other Spinal Deformities. Philadelphia, W.B. Saunders Co., 1978, p. 339.)

Supine Lying With the patient in the supine lying position, the examiner notes the position of the head and cervical spine as well as the shoulder girdle. The chest area is observed for any protrusion (e.g., pectus carinatum) or sunken areas (e.g., pectus excavatum). The abdominal musculature should be observed to see whether it is strong or flabby, and the waist angles should be noted to see whether they are equal. As in the standing position, the ASISs should be viewed to see if they are level. Any extension in the lumbar spine should be noted. In addition, it should be noted whether bending the knees helps to decrease the lumbar curve; if it does, it may indicate tight hip flexors. The lower limbs should descend parallel from the pelvis. If they do not, or if they cannot be aligned parallel and at right angles to a line joining the ASISs, it may indicate an abduction or adduction contracture at the hip. If, in the history, the patient has complained of symptoms on arising from supine lying or from going into the supine position, the examiner should ask the patient to repeat these movements, provided they do not exacerbate the symptoms.

Prone Lying With the patient lying prone, the examiner notes the position of the head, neck, and shoulder girdle, as previously described. The head should be positioned so that it is not rotated, side flexed, or extended. Any condition such as Sprengel's deformity or rib hump should be noted, as should any spinal deviations. The

examiner should determine whether the PSISs are level and should ensure that the musculature of the buttocks, posterior thighs, and calves is normal (Fig. 15-43). As with supine lying, if assuming the position or recovering from the position causes symptoms, the patient should be asked to repeat these movements, as long as symptoms are not made worse.

T

Examination

Assessment of posture primarily involves history and observation. If, on completing the history and observation, the examiner believes that a direct examination is necessary, the procedures outlined in this text for tlle various areas of the body should be followed. In addition' there are postural alignment measures such as the flexicurve ruler and other measures that may be used to record postural alignments and changes. 32 With every postural assessment, however, the examiner should perform two tests: the leg length measurement 33 - 36 and the slump test.

Leg Length Measurement. The patient lies supine with the pelvis set square or "balanced" on the legs (i.e., the legs at an angle of 90° to a line joining the ASISs). The legs should be 15 to 20 cm (6 to 8 inches) apart and parallel to each other (Fig. 15-44). The examiner then places one end of the tape measure against the distal aspect of the ASIS, holding it firmly against the bone. The index finger of the other hand is placed immediately distal to the medial or lateral mal-

898


Figure 15-44 Measuring leg length (A) to medial malleolus; (B) to lateral malleolus.

leolus and pushed against it. The thumbnail is brought down against the tip of the index fingers so that the tape measure is pinched between them. A reading is taken where the thumb and finger pinch together. A slight difference, up to 1.0 to 1.5 cm (0.4 to 0.6 inch), is considered normal but can still be relevant if pathology is present. Further information on measurement of true leg length may be found in Chapter 11. Slump Test. The patient is seated on the edge of the examining table with the legs supported, the hips in neutral position (i.e., no rotation or abductionadduction), and the hands behind the back (Fig. 1545). The examination is performed in several steps. First, the patient is asked to "slump" the back into thoracic and lumbar flexion. The examiner maintains the patient's chin in the neutral position to prevent neck and head flexion. The examiner then uses one arm to apply overpressure across the shoulders to maintain flexion of the thoracic and lumbar spines. While this position is held, the patient is asked to actively flex the cervical spine and head as far as possible (i.e., chin to chest). The examiner then applies overpressure to maintain flexion of all three parts of

the spine (cervical, thoracic, and lumbar), using the hand of the same arm to maintain overpressure in the cervical spine. With the other hand, the examiner then holds the patient's foot in maximum dorsiflexion. While the examiner holds these positions, the patient is asked to actively straighten the knee as much as possible. The test is repeated with the other leg and then with both legs at the same time. If the patient is unable to fully extend the knee because of pain, the examiner releases the overpressure to the cervical spine and the patient actively extends the neck. If the knee extends farther, the symptoms decrease with neck extension, or the positioning of the patient increases the patient's symptoms, then the test is considered positive for increased tension in the neuromeningeal tracty-39 Further information on the slump test may be found in Chapter 9. Additional Tests. Other tests may also be performed based on what the examiner has observed. For example, if the hip flexors appear tight, the Thomas test should be performed (see Chapter 11). Refer to Table 15 - 3 for a detailed presentation of good and faulty posture.

Figure 15-45

Sequence of subject posrures in the slump test. (A) Patient sits erect. (B) Patient slumps lumbar and thoracic spine while examiner holds head in neutral. (C) Exam iner pushes down on shoulders while patient holds head in neutral. (D) Patient flexes head. (E) Examiner carefully applies overpressure to cervical spine. (F) Examiner extends patient's knee and dorsiflexes foot. (G) Patient extends head. If symptoms are reproduced at any stage, further sequential movements are not attempted.

900


Table 15-3 Good and Faulty Posture: Summary Chart Good Posture

Part

Faulty Posture

Head is held erect in a position of good balance.

Head

Chin up too high. Head protruding forward. Head tilted or rotated to one side.

Arms hang relaxed at the sides with palms of the hands facing toward the body. Elbows are slightly bent, so forearms hang slightly forward. Shoulders are level, and neither one is more forward or backward than the other when seen from the side. Scapulae lie flat against the rib cage. They are neither too close together nor too wide apart. In adults, a separation of approximately 10 cm (4 inches) is average.

Arms and shoulders

Holding the arms stiffly in any position forward, backward, or out from the body. Arms turned so that palms of hands face backward. One shoulder higher than the other. Both shoulders hiked up. One or both shoulders drooping forward or sloping. Shoulders rotated either clockwise or counterclockwise. Scapulae pulled back too hard. Scapulae too far apart. Scapulae too prominent, standing out from the rib cage ("winged scapulae").

A good position of the chest is one in which it is slightly up and slightly forward (while the back remains in good alignment). The chest appears to be in a position about halfway between that of a full inspiration and a forced expiration.

Chest

Depressed, or "hollow-chest" position. Lifred and held up too high, brought about by arching the back. Ribs more prominent on one side than on the other. Lower ribs flaring out or protruding.

In young children up to about the age of 10, the abdomen normally protrudes somewhat. In older children and adults, it should be flat.

Abdomen

Entire abdomen protrudes. Lower part of the abdomen protrudes while the upper part is pulled in.

The front of the pelvis and the thighs are in a straight line. The buttocks are not prominent in back but instead slope slightly downward. The spine has four natural curves. In the neck and lower back, the curve is forward, and in the upper back and lowest part of the spine (sacral region), it is backward. The sacral curve is a fixed curve, whereas the other three are flexible.

Spine and pelvis (side view)

The low back arches forward too much (lordosis). The pelvis tilts forward too much. The front of the thigh forms an angle with the pelvis when this tilt is present. The normal forward curve in the low back has straightened out. The pelvis tips backward and there is a slightly backward slant to the line of the pelvis in relation to the front of the hips (flat back). Increased backward curve in the upper back (kyphosis or round upper back). Increased forward curve in the neck. Almost always accompanied by round upper back and seen as a forward head. Lateral curve of the spine (scoliosis); toward one side (C-curve), toward both sides (5curve).

Good and Faulty Posture: Summary Chart (continued) Good Posture

Part

Faulty Posture

Ideally, the body weight is borne evenly on both feet, and the hips are level. One side is not more prominent than the other as seen from front or back, nor is one hip more forward or backward than the other as seen from the side. The spine does not curve to the left or the right side. (A slight deviation to the left in right-handed individuals and to the right in left-handed individuals should not be considered abnormal. Also, because a tendency toward a slightly low right shoulder and slightly high right hip is frequently found in right-handed people, and vice versa for left-handed, such deviations should not be considered abnormal.)

Hips, pelvis, and spine (back view)

One hip is higher than the other (lateral pelvic tilt). Sometimes it is not really much higher but appears so because a sideways sway of the body has made it more prominent. (Tailors and dressmakers ofren notice a lateral tilt because the hemline of skirts or length of trousers must be adjusted to the difference.) The hips are rotated so that one is farther forward than the other (clockwise or counterclockwise rotation).

Legs are straight up and down. Patellae face straight ahead when feet are in good position. Looking at the knees from the side, the knees are straight (i.e., neither bent forward nor "locked" backward).

Knees and legs

Knees touch when feet are apart (genu valgum). Knees are apart when feet touch (genu varum). Knee curves slightly backward (hyperextended knee) (genu recurvatum). Knee bends slightly forward, that is, it is not as straight as it should be (flexed knee). Patellae face slightly toward each other (medially rotated femurs). Patellae face slightly outward (laterally rotated femurs).

In standing, the longitudinal arch has the shape of a half dome. Barefoot or in shoes without heels, the feet toe-out slightly. In shoes with heels, the feet are parallel. In walking with or without heels, the feet are parallel, and the weight is transferred from the heel along the outer border to the ball of the foot. In running, the feet are parallel or toe-in slightly. The weight is on the balls of the feet and toes because the heels do not come in contact with the ground.

Foot

Low longitudinal arch or flatfoot. Low metatarsal arch, usually indicated by calluses under the ball of the foot. Weight borne on the inner side of the foot (pronation). "Ankle rolls in." Weight borne on the outer border of the foot (supination). "Ankle rolls out." Toeing-out while walking or while standing in shoes with heels ("outflared" or "sluefooted"). Toeing-in while walking or standing ("pigeon-toed").

Toes should be straight, tllat is, neither curled downward nor bent upward. They should extend forward in line with the foot and not be squeezed together or overlap.

Toes

Toes bend up at the first joint and down at middle and end joints so that the weight rests on the tips of the toes (han1l11er toes). This fault is often associated with wearing shoes that are too short. Big toe slants inward toward the midline of the foot (hallus valgus). This fault is often associated with wearing shoes that are too narrow and pointed at the toes.

Modified from Kendall, F.P., and E.K. McCreary: Muscles: Testing and Function. Baltimore, Williams & Wilkins, 1983.

902


Precis of the Postural Assessment History Observation Standing (front, side, and behind) Forward flexion (front, side, and behind) Sitting (front, side, and behind) Supine lying Prone lying Examination Leg length measurement Slump test Examination of specific joints (see appropriate chapter)

As with any assessment, the patient must be warned that there may be some discomfort after the examination and that this discomfort is normal. Discomfort after any assessment should decrease within 24 hours. The examiner must keep in mind that several joints may be affected at the same time, either as the result of or as the cause of faulty posture. Therefore, the examination of posture may be an extensive one, with observation both of the posture in general and of several specific joints in detail.

REFERENCES Cited References 1. Kisner, C., and L.A Colby: Therapeutic Exercise: Foundations and Techniques. Philadelphia, F.A Davis Co., 1985. 2. Barry-Greb, T.L., and AL. Harrison: Posture, gait, and functional abilities of the adolescent, pregnant, and elderly female. Orthop. Phys. Ther. Clin. North Am. 5:1-21,1996. 3. Fahrni, W.H.: Backache: Assessment and Treatment. Vancouver, Canada, Musquean Publishers Ltd., 1976. 4. Finneson, B.E.: Low Back Pain. Philadelphia, J.B. Lippincott Co., 1981. 5. Kendall, F.P., and E.K McCreary: Muscles: Testing and Function. Baltimore, Willianls & Wilkins, 1983. 6. McKenzie, R.A: The Lumbar Spine: Mechanical Diagnosis and Therapy. Waikanae, New Zealand, Spinal Publications, 1981. 7. Wiles, P., and R. Sweetnam: Essentials of Orthopaedics. London, J & A Churchill Co., 1965. 8. Porterfield, J.A., and C. DeRosa: Mechanical Low Back Pain: Prospectives in Functional Anatomy. Philadelphia, W.B. Saunders Co., 1991. 9. Moe, J.H., D.S. Bradford, R.B. Winter, and I.E. Lonstein: Scoliosis and Other Spinal Deformities. Philadelphia, W.B. Saunders Co., 1978. 10. McMorris, R.O.: Faulty postures. Pediatr. Clin. North Am. 8: 213-224, 1961. 11. Tachdjian, M.O.: Pediatric Orthopedics. Philadelphia, W.B. Saunders Co., 1972. 12. Tsou, P.M.: Embryology and congenital kyphosis. Clin. Orthop. 128:18-25, 1977. 13. White, AA, M.M. Panjabi, and C.C. Thomas: The clinical biomechanics of kyphotic deformities. Clin. Orthop. 128:8-17, 1977. 14. Hensinger, R.N.: Kyphosis secondary to skeletal dysplasias and metabolic disease. Clin. Orthop. 128:113-128, 1977. 15. Tsou, P.M., A Yau, and AR. Hodgson: Embryogenesis and prenatal development of congenital vertebral anomalies and their classification. Clin. Orthop. 152:211-231,1980. 16. Cailliet, R.: Scoliosis: Diagnosis and Management. Philadelphia, F.A. Davis Co., 1975. 17. Figueiredo, U.M., and I.1.P. Mames: Juvenile idiopathic scoliosis. I. Bone Joint Surg. Br. 63:61-66, 1981. 18. Goldstein, L.A, and T.R. Waugh: Classification and terminology of scoliosis. Clin. Orthop. 93:10-22, 1973. 19. James, I.1.P.: The etiology of scoliosis. I. Bone Joint Surg. Br. 52:410-419, 1970. 20. White, AA: Kinematics of the normal spine as related to scoliosis. I. Biomech. 4:405-411, 1971. 21. Papaioannou, T., 1. Stokes, and I. Kenwright: Scoliosis associated with limb length inequality. I. Bone Joint Surg. Am. 64: 59-62, 1982.

22. Debrunner, H.U.: Orthopaedic Diagnosis. London, E & S Livingstone, 1970. 23. Giallonardo, L. M.: Posture. In Myers, R.S. (ed.): Saunders Manual of Physical Therapy Practice. Philadelphia, W.B. Saunders Co., 1995. 24. Dolan, P., M.A Adams, and W.e. Hutton: Commonly adopted postures and their affect on the lumbar spine. Spine 13: 197201, 1988. 25. Opila, KA, S.S. Wagner, S. Schiowitz, and J. Chen: Postural alignment in barefoot and high-heeled stance. Spine 13:542547,1988. 26. Griegel-Morris, P., K Larson, K Mueller-Klaus, and C.A Oatis: Incidence of common postural abnormalities in the cervical, shoulder, and thoracic regions and their association with pain in two age groups of health subjects. Phys. Ther. 72:425-430, 1992. 27. McLean, 1.P., M.G. Gillan, J.e. Ross, R.M. Aspden, and R.W. Porter: A comparison of methods for measuring trunk list-a simple plumbline is best. Spine 21:1667-1670, 1996. 28. Bayley, N.: The accurate prediction of growth and adult height. Mod. Probl. Pediatr. 7:234-255, 1954. 29. Adams, M.A, and W.C. Hutton: The effect of posture on the lumbar spine. J. Bone Joint Surg. Br. 67:625-629, 1985. 30. Adams, M.A, and W.C. Hutton: The effect of posture on the role of the apophyseal joints in resulting intervertebral compressive forces. J. Bone Joint Surg. Br. 62:358-362, 1980. 31. Black, KM., P. McClure, and M. Polansky: The influence of different sitting positions on cervical and lumbar posture. Spine 21:65-70,1996. 32. Arnold, C.M., B. Beatty, E.L. Harrison, and W. Olszynski: The reliability of five clinical postural alignment measures for women with osteoporosis. Physiother. Can. 52:286-294,2000. 33. Clarke, G.R.: Unequal leg length: An accurate method of detection and some clinical results. Rheumat. Phys. Med. 11:385390,1972. 34. Fisk, J.W., and M.L. Baigent: Clinical and radiological assessment of leg length. N.Z. Med. J. 81:477-480, 1975. 35. Nichols, P.J.R., and N.T.I. Bailey: The accuracy of measuring leg-length differences. Br. Med. I. 2:1247-1248, 1955. 36. Woerman, AL., and S.A Binder-Macleod: Leg-length discrepancy assessment: Accuracy and precision in five clinical methods of evaluation. J. Orthop. Sports Phys. Ther. 5:230-239, 1984. 37. Maitland, G.D.: The slump test: Examination and treatment. Aust. I. Physiother. 31:215-219, 1985. 38. Philip, K, P. Lew, and T.A Matyas: The inter-therapist reliability of the slump test. Aust. I. Physiother. 35:89-94, 1989. 39. Butler, D.S.: Mobilisation of the Nervous System. Melbourne, Churchill Livingstone, 1991.

General References Anderson, B.J.G., R. Ortengon, AI. Nachemson, et al.: The sitting posture: An electromyographic and discometric study. Orthop. Clin. North Am. 6:105-120,1975. Cailliet, R.: Nerve and Arm Pain. Philadelphia, F.A Davis Co., 1964. Cartas, 0., M. Nordin, V.H. Frankel, R. Malgady, and A Scheikhzadeh: Quantification of tnmk muscle performance in standing, semistanding, and sitting postures in healthy men. Spine 18:603609,1993. Cyriax, J.: Textbook of Orthopaedic Medicine, Vol. 1: Diagnosis of Soft Tissue Lesions. London, Bailliere Tindall, 1982. Dieck, G.S., J.L. Kelsey, V.K Goel, M.M. Panjabi, S.D. Walter, and M.H. Laprade: An epidemiological study of the relationship between postural asymmetry in the teen years and subsequent back and neck pain. Spine 10:872-877, 1985. During, J., H. Goudfrooij, W. Keessen, T.W. Beeker, and A Crowe: Towards standards for posture-postural characteristics of the lower back system in normal and pathological conditions. Spine 10:8387, 1985. Fischer, P.: Clinical measurement and significance of leg length and iliac crest height discrepancies. J. Man. Manip. Ther. 5:57-60, 1997. Itoi, E.: Roentgenographic analysis of posture in spinal osteoporotics. Spine 16:750-756, 1991. Kapandji, LA: The Physiology of the Joints, Vol. 2: The Trunk and Vertebral Column. New York, Churchill Livingstone, 1974. Kappler, R.: Postural balance and motion patterns. J. Anl. Osteopath. Assoc. 81:598-606, 1982. Littler, W.A.: Cardiorespiratory failure and scoliosis. Physiotherapy 60:69-70,1974. MacDougall, J.D., H.A. Wenger, and H.J. Green: Physiological Testing of the Elite Athlete. Ottawa, Canadian Association of Sports Sciences, 1982. Matthews, D.K: Measurement in Physical Education. Philadelphia, W.B. Saunders Co., 1973. McKinnis, D.L.: The posture-movement dynamic. In Richardson, J.K, and Z.A Iglarsh (eds.): Clinical Orthopedic Physical Therapy. Philadelphia, W.B. Saunders Co., 1994. Mellin, G., and M. Poussa: Spinal mobility and posture in 8- to 16year-old children. J. Orthop. Res. 10:211-216,1992. Mennell, J.: Back Pain: Diagnosis and Treatment Using Manipulative Techniques. Boston, Little, Brown & Co., 1960.

of pressure and supportive forces during human activities. J. Appl. Physiol. 23:831-838, 1967. Nashner, L.M.: Sensory, neuromuscular and biomechanical contributions to human balance. In Duncan, P.W. (ed.): Balance: Proceedings of the American Physical Therapy Association Forum. Alexandria, American Physical Therapy Association, 1990. Opila, KA: Gender and somatotype differences in postural alignment: Response to high-heeled shoes and simulated weight gain. Clin. Biomech. 3:145-152, 1988. Pacelli, L.C.: Straight talk on posture. Phys. Sportsmed. 19:124127, 1991. Portnoy, H., and F. Morin: Electromyographic study of postural muscles in various positions and movements. Am. J. Physiol. 186: 122-126,1956. Riemann, B.L., N.A Caggiano, and S.M. Lephart: Examination of a clinical method of assessing postural control during a functional performance task. J. Sports Rehab. 8:171-183, 1999. Rothman, R.H., and F.A Simeone: The Spine. Philadelphia, W.B. Saunders Co., 1982. Torell, G., A Nordwall, and A Nachemson: The changing pattern of scoliosis treatment due to effective screening. J. Bone Joint Surg. Am. 63:337-341, 1981. Tsai, L., and T. Wredmark: Spinal posture, sagittal mobility and subjective rating of back problems in former female elite gymnasts. Spine 18:872-875, 1993. Vallos, J.P., A.J. Nitz, AJ. Threlkeld, R. Shapiro, and T. Horn: Electromyographic activity of selected trunk and hip muscles during a squat lift. Spine 19:687-695, 1994. Walker, M.L., J.M. Rothstein, S.D. Finucane, and R.L. Lamb: Relationships between lumbar lordosis, pelvic tilt, and abdominal muscle performance. Phys. Ther. 67:512-516, 1987. Williams, M.M., J.A Hawley, R.A McKenzie, and P.M. van Wijmen: A comparison of the effects of two sitting postures on back and referred pain. Spine 16:1185-1191, 1991. Wolfson, L.I., R. Whipple, P. Amerman, and A Kleinberg: Stressing the postural response: A quantitative method for testing balance. J. Am. Geriatr. Soc. 34:845-850, 1986. Woollacott, M.: Postural control mechanisms in the young and old. In Duncan, P.W. (ed.): Balance: Proceedings of the American Physical Therapy Association Forum. Alexandria, American Physical Therapy Association, 1990.

ASS~SSM~NT OF T"~ AMPUT~~ An amputation is defined as the removal of part or all of a limb or some other outgrowth of the body. If fingers and partial nonmutilating hand injuries are excluded, lower-limb amputations are much more frequent than upper-limb amputations.! However, upperlimb amputations cause greater functional loss because the upper limbs are used more functionally and in many more diverse ways. There is also a greater functional sensory loss when an upper limb is involved. In addition, the upper-limb amputation causes a more obvious disfigurement and alteration of body image, which affects the actions and reactions of both the amputee and those he or she interacts with. I ,2 Amputations are considered to be a treatment of last resort when other methods such as revascularization or reattachment have failed or are not considered suitable treatment options. 2- S Assessment of the amputee patient may involve assessing a patient before the amputation or after the amputation has taken place. In the first instance, the assessment is primarily carried out by one or more physicians deciding whether there is a need for such a procedure and then deciding the level at which the amputation should occur. In some cases, indexes or scores 6 - 19 may be used although some 20 have questioned their usefulness in the final outcome, especially in the case of trauma. There are several indications for amputations. 21 The most common are trauma due to compound fractures, blood vessel rupture, stab or gunshot injuries, compression injuries, severe burns or cold injuries,22 and vascular disease as the result of systemic problems such as diabetes, arteriosclerosis, embolism, venous insufficiency, or peripheral vascular disease often aggravated by cigarette smoking. 23 About 75% of amputations in older patients fall within this second category.24 The presence of suspected vascular disease may include more than the physical examination when considering whether to amputate. These other tests include blood

tests, chest x-rays, electrocardiography, Doppler studies, arteriography, venograms, thermography, and transcutaneous P0 2 readings. 22 When trauma is the cause, the aim of the amputation is to restore maximum length with good soft tissue covering. 22 In addition, amputations may be performed because of infections, tumors (both benign and more commonly, malignant types), neurological disorders (such as an anaesthetic limb from, for example, a complete plexus avulsion 2S ), congenital deformity (e.g., partial or total absence of a limb), and amputations for cosmetic reasons (e.g., extra digit).2s-28 Younger people tend to experience more congenital, malignancy, and trauma related amputations whereas older people experience multiple pathophysiological mechanisms as previously mentioned.

Causes of Amputation • Trauma • Vascular disease • Infection • Tumors • Neurological disorders • Congenital deformity

If the examiner has the opportunity to do a preoperative physical assessment of the patient who has been scheduled for an amputation, then the examiner should take the time to determine the patient's available muscle strength, range of motion (ROM) and functional mobility bilaterally to provide a base line for future comparison if necessary. The size and position of any abnormal tissue degeneration or potential

905

906

CHAPTER 16 • Assessment of the Amputee

pressure areas should be recorded accurately and functional levels should be assessed and recorded. If at all possible in this preoperative period, the patient should be given some instruction in bed mobility, as well as climbing in and out of bed with or without support. In addition, the examiner should ensure that the patient knows how to provide suitable care for pressure areas and preserve joint mobility to prevent any contractures from forming. If a lower-limb amputation is anticipated, the patient should be taught to use ambulatory aids such as crutches or wheelchair so that he or she can maintain as much mobility as possible after the amputation.

T

Levels of Amputation

Amputation surgery, whether performed to the upper limb or the lower limb, can occur at various levels (Figs. 16-1 and 16-2).29 For the most part, this chapter deals with assessment of the lower-limb amputee primarily because these amputations are more common. However, functional loss is usually greater for upper-limb amputees. Thus, upper-limb amputee assessment deals much more with different functional demands than lower-limb assessment. Figure 16-3 shows the percentage impairment caused by an upperlimb amputation. 30

Fore quarter amputation (Implies removal of part of scapula, clavicle and all of upper limb) Shoulder disarticulation (Amputation through glenohumeral joint)

Above elbow (AE)

Figure 16-1 Common levels of amputation-upper limb. Elbow disarticulation a) Short BE

Below elbow (BE)

b) Medium BE

c) Long BE

Wrist disarticulation Metacarpophalangeal disarticu lation

Phalangeal amputation

Interphalangeal disarticulation

1

Hemipelvecotomy (Hindquarter amputation or complete hip amputation)

~'=======~

Hip disarticulation (Complete thigh amputation) (Implies amputation through trochanters, femoral neck or hip disarticulation)

a) Short AK (Upper thigh amputation) 3-4 inches below ischial tuberosity

Above knee (AK) amputation (Partial thigh amputation)

b) Middle AK (Middle thigh amputation) 10-12 inches below ischial tuberosity

:=======*~;;~===

c) Supracondylar amputation (Lower thigh amputation) Knee disarticulation (Compete leg amputation)

a) Very short B K - - - - - - - - - i less than 2 inches below knee joint line !=======~M:~~==== b) Short BK - - - - - - - - - - i

~======*****====

(Upper leg amputation) 2-4 inches below knee joint Below Knee (BK) amputation (Partial leg amputation)

c) Medium BK-:;::;:~-----1=======~~!==== (Middle leg amputation) 5-8 inches below knee joint

I

d) Long B K - - - - - - - - - - I (Lower leg amputation) 8+ inches below knee joint

~

Syme amputation (Amputation just above ankle)

Chopart disarticulation (Partial tarsal amputation) through midtarsal joints

Ankle disarticulation (Complete tarsal amputation)

Lisfranc's amputation (Complete metatarsal amputation) through tarsometatarsal joints Transmetatarsal amputation (Partial metatarsal amputation) through metatarsal bones

Toe amputation (Compete phalangeal amputation)

Figure 16-2 Common levels of amputation-lower limb.

908


100% of extremity or 60% of whole man

MP 100% loss of thumb IP50%

MP 100% loss of finger

Amputation surgery may be one of two typesopen or closed. Open or primary amputation is used in cases of infection in which the wound is left open after the amputated part is removed to allow clearance of infection. It requires a second procedure to close the wound. More commonly, a closed amputation is performed. This procedure is used when tissue viability is as normal as possible. At the time of the amputation, the skin flaps are closed as is the wound. Commonly, the skin flaps are closed on the posterior and distal aspect of the stump as adhesions are less likely and an incision line is further from the bone, but other methods are also sometimes used. 31 The goal of amputation surgery is to create a dynamically balanced residual limb with good motor control and sensation. 32 The patient will need a well-healed, well-shaped residual stump with the greatest functional length possible in the limb. 32 The higher the level of the amputation, the greater the handicap.25 In the lower-limb, immediate prosthetic fitting helps facilitate early mobilization \vith more normal gait patterns. 26 Amputation should be

100% loss of hand

Figure 16-3 Amputation impairment. Percentage of impairments related to whole body, extremity, hand, or digit. MP = Metacarpophalangeal; IP = Interphalangeal; PIP = Proximal interphalangeal; DIP = Distal interphalangeal. (Redrawn from Swanson, A.B., G. de Groot Swanson, and C. Goran-Hagert: Evaluation of hand nmction. In Hlmter, J.M., L.H. Schneider, E.J. Macklin, and A.D. Callahan (eds.): Rehabilitation of the Hand. St. Louis, C.V. Mosby Co., 1990, p. 119.)

considered to be a reconstructive procedure leaving the patient with the best of possible alternatives. 33 The second opportunity where the amputee patient may be assessed is following the surgery. This is more likely to be done by the physician or other health care professionals. In this case, the aim of the assessment i primarily to determine what functional deficits the patient has, assessing the fitting of the prosthesis, and watching for complications. A good assessment enable the clinician to assist the patient in understanding and dealing with the specific physical and social limitation that the amputation has brought to his or her pattern of life. 34 It is this second scenario that will be described in the remainder of this chapter.

T Patient History34 As with any assessment, the initial part of the examina-

tion will include the patient's history as it relates to the amputation, its cause, and any related factor,

When doing the assessment of the amputee, it is important to determine the patient's past medical, surgical, preoperative ambulatory and functional status for both upper and lower limbs, and preoperative symptoms. As part of this "past history," the examiner must develop some understanding of the patient's recreational activities, past psychiatric history (which may include information of alcohol or drug abuse), current

Pertinent Information in Patient AssessmenF4 Relevant Patient Information • educational level • occupational history • avocational activities • psychiatric history, alcohol and drug use, problems with the law (it is important to have family objective corroboration) • current stressors including recent losses • is the patient pain sensitive or tolerant • previous associations with patients having disabilities • compliance with medical treatment; obstacles to compliance

Family Structure • marital adjustment • sexual history • family roles; strengths and problem areas • health of others

The Patient's Perspective • current mood • anxieties and ideas associated with them • what the patient imagines his/her future to be, that is, how the disability will change lifestyle, social relations, vocational future; self concept • the degree to which self esteem is related to physique and physical skills • comfort in meeting a psychiatrisUpsychologist • how the patient thinks the adjustment is going • the most pressing immediate concern • the patient's understanding of the cause and probable course of disability • how much the patient wants to know about the treatment as it progresses. How the patient prefers having a medical update

stressors (including recent losses), pain tolerance, previous association with patients who have disabilities, and compliance with medical treatments. 24 In addition, information on family structure and possible support groups including family and friends must be discussed. Issues such as marital status, sexual history, family roles including familial support, strengths, and problems should be ascertained as they can impact gready on the outcome and how the patient ultimately functions as an amputee. 35 ,36 The examiner must determine and develop an understanding for any patient anxieties, why they are present, whether these anxieties can be dealt with by the examiner or will other health care specialists need to be involved, what the patient imagines his or her future to be, and how the disability will change his or her lifestyle, social relations, vocational future, and self concept (Table 16-1). All of these factors must be considered if the examiner hopes to have a successful outcome to treatment. For the present medical history, the following questions should be asked: 1. What is the patient's occupation? Does the patient have any concerns about returning to his or her job? If so, what are the patient's future occupational plans? Is any vocational guidance or training required? 2. What is the patient's present medical status? For example, what was the reason for the amputation? The presence of any systemic disease such as diabetes, cardiovascular or respiratory problems, arthritic joints, and lifestyle factors all have a bearing on successful treatment outcomes. Systemic disease or trauma may prolong the healing process and the speed of recovery may be delayed. 3. How long ago did the amputation occur? In recent amputations, the initial concern is the healing of the stump and the prevention of complications. If the amputation surgery was a revision procedure, why was the revision necessary? Was the problem one of poor tissue viability or was the procedure performed to enable the patient to obtain better functional results? 4. If the amputation occurred some time ago (3 to 6 months or longer), has the patient experienced any complications over that period such as tissue breakdown, ulcer formation, or blisters? 5. If the patient has a prosthesis, what does the patient think about the prosthesis, its fit, and function? How long has the prosthesis been worn (years? months?)? How long is the prosthesis worn each day? Is it worn every day? Is the suspension adequate? Are there any skin abrasions? Inadequacies in these areas will lead to patient frustration, disappointment, and, ultimately, to the patient becoming discouraged about using the prosthesis and, in fact, may come to the state where the patient does not want to wear the prosthesis. If the prosthesis is uncomfortable or excessively

910


Table 16-1 Patient Motivational and General Problems Problem

Cause

Findings

Solution

Discouraged patient

Performance does not equal expectations

Does not wear prosthesis Complaints not related to physical findings

Sympathetic explanation of reasonable realistic goals Training

Failure to maintain good prosthetic habits

Lack of training New situations Poor motivation

Hip or knee flexion contracture Pressure sores Poor socket fit Abnormal gait patterns

Retraining Sympathetic encouragement

Poor hygiene

Poor motivation

Dermatitis Abscess formation Hidradenitis (inflammation of sweat glands)

Wash limb Clean socks Clean socket Antibiotics Surgical drainage

Rest pain

Phantom pain/sensation

Pain in missing segment of limb

Provide clistracting sensation (a) wrapping (b) temperature changes (c) activity with prosthesis (d) transcutaneous nerve stimulation

Neuroma

Positive Tinel's sign

Excise neuroma

Ischemia

Crampy pain aggravated by activity

Unweight limb Stop smoking Revise amputation

Modified from Smith, A.G.: Common problems of lower extremity amputees. Orthop. Clin.

noisy, it is unlikely the patient will use it or if it is used, it is unlikely the patient will use it properly. In the case of a lower-limb prosthesis, the patient may refuse to bear weight on the prosthesis. Cosmesis is another problem that is often of concern for the amputee, especially for women, and when the amputation is in the upper limb as in both instances the extremity is sometimes not covered with clothing. The examiner must differentiate between the discomfort of using something new and the discomfort caused by a specific prosthetic fault. In some cases, a Prosthesis Evaluation Questionnaire 37 may be useful (Fig. 16-4). 6. Has the patient been looking after the stump properly, ensuring proper limb and sock hygiene? Failure to do so easily leads to complications such as skin breakdown, infection, and ulcers (see Table 16-1).32 The remaining stump should be washed with care using mild soap. The stump sock should be changed and cleaned regularly and the prosthesis socket should also be cleaned regularly with mild soap and water. 32 7. Does the patient have any pain or abnormal sensation? Where is the pain or abnormal sensation? Is the pain intermittent or constant? What is the intensity of the pain (a visual analog scale may be used-see Fig. 1-3)? Where is the pain? What type of pain or abnor-

orth Am. 13:576, 1982.

mal sensation is it? Phantom sensation is an abnormal feeling the patient has for the limb but the patient feels the sensation as being in the amputated part o the limb even though that part of the limb is not there. 22 ,38-40 This sensation is an almost universal consequence of limb amputation. 41 ,42 It may take numerous forms including the feeling that someone is touching the amputated limb, pressure being applied to the missing body part, cold, wetness, itching, tickle, pain. or fatigue. The intensity of these sensations may vary and may change over time. The sensations commonly have different meaning to different people. Phantom sensations are more commonly felt in the distal part o the excised extremity because the distal part of an extremity tends to be more ricWy innervated. 38 Phantom pain is described as a painful sensation perceived in the missing body part in the case of an amputation, in the paralyzed part of a spinal cord injury patient, or following a nerve root avulsion in the case of a neurological injury.22,38-41 Eighty percent o amputees experience some phantom pain sometime during the injury healing process. Phantom pain is relatively common, but is unpredictable in terms of predisposing factors, severity, frequency, duration or character, aggravation by internal or external stimuli, or Text continued on page 914

Sample Items in the 10 Prosthesis Evaluation Questionnaire (respondents are asked to rate the item over the past 4 weeks) Item Prosthesis Function Usefulness

1. The fit of your prosthesis

Rating

I

I

terrible

2. The comfort of your prosthesis while standing still when using your prosthesis Residual limb health

3. How much of the time your residual limb was swollen to the point of changing the fit of your prosthesis

4. How much you have sweat in your prosthesis Appearance

5. The appearance of your prosthesis (how it has looked)

excellent

.I

I

terrible

excellent

I

I all the time

never

I

I

extreme amount

not at all l.

I terrible

6. How limited your choice of clothing was because of your prosthesis Sounds

7. How often your prosthesis has made sounds (belching, squeaking, clicking, etc.) 8. How bothersome these sounds were to you

I worst possible

I excellent

I not at all

I

I

always

never

I

extremely bothersome

I not at all

(continued on next page Figure 16-4

Orthopedic Physical Assessment 4th Edition (with Companion DVD)

Illustrated Orthopedic Physical Assessment

Illustrated Orthopedic Physical Assessment

Orthopedic Imaging: A Practical Approach 4th Edition

Orthopedic Rehabilitation, Assessment, and Enablement

Introduction to Physical Polymer Science, 4th Edition

Assessment of Childhood Disorders, 4th Edition

Assessment Made Incredibly Easy, 4th Edition

Assessment Made Incredibly Easy, 4th Edition

Handbook Of Geriatric Assessment, 4th Edition

Handbook Of Geriatric Assessment, 4th Edition

Physical Assessment for Nurses

Differential Diagnosis for the Orthopedic Physical Therapist

The Practice of English Language Teaching with DVD (4th Edition) (Longman Handbooks for Language Teachers)

Agile Web Development with Rails, 4th Edition

Discrete Mathematics with Applications, 4th Edition

Discrete Mathematics with Applications, 4th Edition

Physical Therapist's Clinical Companion, 2000

Textbook of Physical Diagnosis with DVD: History and Examination With STUDENT CONSULT Online Access

Health Assessment Through The Life Span 4th Edition

Orthopedic Surgery in Patients with Hemophilia

DVD Authoring with Adobe Encore DVD: A Professional Guide to Creative DVD Production and Adobe Integration

The Inventor's Notebook: A Patent It Yourself Companion 4th Edition

DVD и многое другое (+DVD)

Fundamental Orthopedic Management: For the Physical Therapist Assistant

Colposcopy: Principles and Practice, Text with DVD

American Sign Language Demystified with DVD

Real Analysis (4th Edition)

Orthopedic Physical Assessment 4th Edition (with Companion DVD)

Illustrated Orthopedic Physical Assessment

Illustrated Orthopedic Physical Assessment

Orthopedic Imaging: A Practical Approach 4th Edition

Orthopedic Rehabilitation, Assessment, and Enablement

Introduction to Physical Polymer Science, 4th Edition

Assessment of Childhood Disorders, 4th Edition

Assessment Made Incredibly Easy, 4th Edition

Assessment Made Incredibly Easy, 4th Edition

Handbook Of Geriatric Assessment, 4th Edition

Handbook Of Geriatric Assessment, 4th Edition

Physical Assessment for Nurses

Differential Diagnosis for the Orthopedic Physical Therapist

The Practice of English Language Teaching with DVD (4th Edition) (Longman Handbooks for Language Teachers)

Agile Web Development with Rails, 4th Edition

Discrete Mathematics with Applications, 4th Edition

Discrete Mathematics with Applications, 4th Edition

Physical Therapist's Clinical Companion, 2000

Textbook of Physical Diagnosis with DVD: History and Examination With STUDENT CONSULT Online Access

Health Assessment Through The Life Span 4th Edition

Orthopedic Surgery in Patients with Hemophilia

DVD Authoring with Adobe Encore DVD: A Professional Guide to Creative DVD Production and Adobe Integration

The Inventor's Notebook: A Patent It Yourself Companion 4th Edition

DVD и многое другое (+DVD)

Fundamental Orthopedic Management: For the Physical Therapist Assistant

Colposcopy: Principles and Practice, Text with DVD

American Sign Language Demystified with DVD

Real Analysis (4th Edition)

Recommend Documents