Management of common musculoskeletal disorders: physical therapy principles and methods

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Management of

Common Musculoskeletal Disorders Physical Therapy Principles and Methods THIRD EDITION

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Lippincott Philadelphia • New York

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Sponsoring Editor: Andrew Allen Development Editor: laura Dover Project Editor: Tom Gibbons Indexer: Victoria Boyle Design Coordinator: Doug Smock Interior DeSigner: Maria Karkucinski Cover Designer: Ilene Griff Production Manager: Helen Ewan Production Coordinator: Patricia McCloskey Compositor: Pine Tree Composition, Inc. Printer/Binder: Courier Book Company/ Kendallville Cover Printer: lehigh Third Edition Copyright © 1996 by Lippincott-Raven Publishers. Copyright © 1990, by J B. Lippincott Company. Copyright © 1983 by Harper & Row, Publishers, Inc. All rights reserved. No part of this book may be used or reproduced in any m,lnner whatsoever without written permission except for brief quotations embodied in critical articles and reviews. Printed in the United States of America. For information write Lippincott Williams & Wilkins, 227 East Washi.ngton Square, Philadelphia, PelUlsylvania 19106. Library of Congress Cataloging-in-Publication Data Hertling, Darlene. Management of common musculoskeletal disorders: physical therapy principles and methods / Darlene Hertling, Randolph M. Kessler; with 5 additional contributors: illustrations by Elizabeth Kessler. -3rd ed. p. cm. A Lippincott physical therapy title. Includes bibliographical references and index. ISB 0-397-55150--9 1. Physical therapy. 2. Musculoskeletal system-Diseases­ Patients-Rehabilitation. I. Kessler, Randolph M. U. Kessler, Randolph M. Ill. Title. [0 LM: 1. Bone Diseases-therapy. 2. Bone Diseases­ therapy. 3. Physical Therapy. 4. Muscular Diseases-ther­ apy. 5. Physical Therapy. WE 140 H574m 1996] RM700.H48 1996 616.7'062----- Il!mporomollldibulM joint: II. Developml'llt of th...• temporal components. J Dent Res 49.&>1- 75.1970

Christian F..L. Emb

ol~y ,lnd

evulutiull of movcment and function. In

lIy I{M. BilrnC'S

IR (cd,,): Phy, ""I The"'p)'. PI' 4$..02. Ph,l,hidphi". JB I.ipplllcoll. 1989 F'llkn\.f F: liu.mdl1 ·vclopmC'ut. Phil,ldclphiJ. WB S.ll1ders. llJ06 Rl:2scrald 1\·1JT Ilunhll\ Embryology. Rl.-giol1.,1 Approach. Ne\v York, Ililrp
A Fibril

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of Packing molecules

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brane into the interstitial pace, cleavage at terminal sites of the moleclll occurs, n the slightly short­ ened molecule is now call d tropocollagen. The tropocollagen molecule is the ba ie building block of coUagen, lntercellularly, five tropocollagen molecules rapidly aggregate in an overlapping array to form a collagen microfibril. The microfibril has been t med a "crystal­ lite" structure, owing to the consi tent spatial relation­ ship of its molecules,5l Groups of microfibrils orga­ nize into the subfibril, and subfibrils combine to form fibrils. It is at the lev 1 of the llagen fibril that the characteristic cros '-banding or periodicity observed in x-ray diffraction and lecrroll microscopic studies is demonstrated (Fig. 2-2). Thi cross-banding is th re­ sult of the specific ov rlapping and stacking of the tropocollagen molecul s within the larger units, em­ phasizing the highly structured mole ular organiza­ tion of collagen. The physical and med1anical proper­ ties of collagen, therefore, are directly governed by this hierarchy of organization. Bundles of collagen fibrils combine to form connec-

-'

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Collagen ,~~.--------'--- 3,000 A(44 D) - - - - - - ' - . . ,

molecule '

I 15 A Diameter

:~.---- - - - - 104

o

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0-.2

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0-.1

E Typical sequence in 0-.1 and 0-.2 chains

,­

/+----- 174 A - - - - -.....

Proline

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FIG. 2-1. Collagen fibril formation: (A) fibril with cross­ banding due to overlapping tropocollagen units, (B) extra­ cellular stacking of tropocollagen molecules, IC) one tropocollagen molecule of fixed 300-nm dimension, (D) the right-handed triple helix, and IE) the left-handed alpha helix illustrating the regularity of primary sequence. (illustra­ tion by Tagawa B. From Prockop OJ, Guzman NA: Collagen diseases and biosynthesis of collagen. Hosp Pract 12(12):61-68,1977)

FIG. 2-2. Electron micrograph of metal-shadowed replica

of collagen fibers from human skin, demonstrating cross­ banding periodicity. (de Ouve, C: A Guided Tour of the liv­ ing Cell, vol 1, P 38. New York, Scientific American Books, WH Freeman, 1984; and Jerome Gross, Harvard Medical School, Boston, MA 02114)

10

CHAPTER 2

•

Properties of Dense Connective Tissue and Wound Healing

tive tissue fascicles. Whenever subjected to stress dur­ ing formation, these fascicles form with distinct wave­ forms or crimps. The ang~e of crimping of collagen at this level of connective tissue development is both predictable and measurable. Collagen fascicles to­ gether make up the gross structure of tendon, liga­ ment, and joint capsule (Fig. 2-3). It is at the level of the DCT collagenous fascicle that a tendon or liga­ ment can first be mechanically tested. The compliance of OCT is primarily, therefore, a function of the re­ moval of the crimp. In other words, when working within physiological limits, collagen can become tem­ porarily elongated by straightening out the crimped fascicle. As a result of the dimensions set by the mole­ cular attachments, native collagen cannot shrink or be stretched with permanent elongation. linically speaking, any "permanent" longation signifies tear­ ing or denaturation of the collagen with irreversible damage. As yet, five classes and numerous subclasses of col­ ~agen have been identified. Of these classes, the larger structural, interstitial fibers of tendon and ligament contain mostly type I collagen, and in smaller quanti­ ties type II collagen. Articular cartilage is typically made up of type II collagen.

D

Ground Substance Composition

Groulld substallcc is the amorpholls, gel-like material occupying the interstitial space between the collagen fibers, and it is composed of a mixture of water and organic molecules, namely glycosalllil1og1YCilll5 (GAGs),

proteoglycalls, and glycoproteins. Ground substance has enormous water-binding properties, and acts as both a lubricant for movement of adjacent fibers over one another, as well as a source of nourishment for fibro­ blasts.1,3 GAGs (acid mucopolysaccharides), like tropocolla­ gen, are a product of fibroblast metabolism. GAGs in­ teract electrostatically with collagen fibers, binding them together, thus contributing to their aggregation and strength? The distinctive crimping in collagen fascicles is thought to be the result of the attachment of GAGs to the collagen fibers. 28 ,29,35 Examples of GAGs include hyaluronic acid, chondroitin sulfate, heparan sulfate, keratan sulfate, and derma tan sulfate. Hyaluronic acid is common in cartilage and is thought to be responsible for cohesion within the fibril, en­ abling the tissue to bear mechanical stresses without distortion. 9,40 Dermatan sulfate is found in dermis, tendons, ligaments, and fibrous cartilage-all struc­ tures containing mostly type I collagen. When GAGs covalently bind to protein chains in the extracellular matrix of DCT, they are called prateo­ glycans. Each type of connective tissue has characteris­ tic proteoglycans present in various proportions. Pro­ teog~ycans regulate collagen fibriUogenesis and accelerate polymerization of collagen monomers. 35 Structural glycoproteills are organic molecules contain­ ing a protein core to which carbohydrates attach. Un­ like proteoglycans, the protein core predominates. Glycoproteins, such as fibronectin, chondronectin, and laminin, play an important role in the interaction between DCT cells and their adhesion to collagen.

CLINICAL CONSIDERATION

E:vldence: x-ray

EM SEM

EM SEM OM

I

I

x-ray

SEMI

OM

Tendon

Ground substance viability depends on motion. GAGs have a half-life of 1.7 to 7 days, and motion is required for ground substance production.7° Early on, motion at the level of the DCT might imply gentle isometric contractions rather them gross osteokinematic move­ ments. The forces generated by gentle isometric con­ tractions are often sufficient to keep the DCT lubri­ cated during the phase of recovery in which pain-induced splinting occurs.

D -'-.......L_ _

15 A 35 A

Maturation Changes in Collagen

_ _ .-.l-..­

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100-200 A 500-5000 A

50-300p

100-500~l

Size scale

FIG. 2-3. Hierarchical organization of tendon. Note the cross-banding periodicity at the level of the collagen fibril, and the specific crimp formation in the collagen fiber fasci­ cle. (Kastelic J. Galeslburn bv human recombin.wt tumor nt:.·c.rosb factnr. Proc

. atl Acad Sci USA 82:S667-s
Hinter H, e~ al: pression of ment m~nlbrane Zone rlllal t;tability of c.oIlilgen.

Bi him Bioph)'s ta 79:~, 1964

52. Rigby Bj, Hirai N, Spikes )0: The mec:h,mica[ behavior of rat tendon. J Gen Physio[ 4]:265-~ 3, 1959

53, Rudolph R: Con~raction and tile centrol of contI7lction. World J Surg 4:279-287, 1980

54. Rudolph R, Vn.nde Berg J, Ellrlich UP: Wound contraction and scar contracture. In

Coheo el al (eds): Wound (-]calin~ pp 96-1l4. Philadelphia, WB Saunders Co, 1992

55. R)'on G, jn : Inflammation. Kalam zoo, MI, Upj hn Co, 1977

56. hlierner RP, Rutk.'dge BK: CultuTed human v,lscular cndothelinl cell surface ,K­ quires f'dh-llIU,19T Bollett AJ: Connt."\.1 v·' lissue polysoKcharide mct-465, 1978 6. Algom 0 : Psychophysical ana lysis of pain: A functional prospective. In GejssJer HC, Link SW, Townsend JT (f'ds): Cogniti on In formation Processin& and Psychop hys ics: Basic l,sues, pp 267- 291. Hilldal e, N), Law rence Erlbaum, 1992 7. Alma)' BC, Johansso n F, Von Knorring L, Te.rcnius L, Wa hlstrom A: Endorphi ns in chroni c pain: Differences in CSF e ndorphin levels bc'rwee-n organic and p syc hogrnic pain syndromes. Pol in 5 :153- 162, 1978 B. Anderson SD, Bausba um AI, Field s HL: Responses of medullary raph e:' n("urons to pe­ riph eral sti mulo. ti on and to systemi c o piates. Brain Rc·s 123:363- .168, t977 9. Balag ura 5, Ralph T: The anilJgesic effect of cJectrical stimulation of the' d i (~ nrephalon: and mesencepha lo n . Brain Res 60:369-381, 1973 10. Barnes IX, Fung 5J, Ad ams \'VL: in hibi tory effec ts of subs tantia nigra on impulse tran smission from nod ceptors. Pai n 6:207- 215, 1979 11. Basba um AI. Ma rley N, O ' Keefe J: Effects of s pinal co rd lesions 0 11 the a nalgesic prop­ er ties of electrical brain s timula tion. Presented at (l symposium he ld a t the Firs t \'Vorld Congress on Pajn. Ad vances in Pain Research. p 26.-'3, 1975 12, Basbemm AI, MClrley N, O'Keefe J, Clanton C: RevE',J's a l o f morphinC" ., nd sti mulus­ produced ana lgesia b )' s ubto ta l spina l cord lesions. Pai n 3:43-56, 1977 13. Black RG: Th e chronic pain syndrome. 5urg Clin N orlh Am 55:999-1 011, 1975 14. B<mic.-l JJ: Neurophysiologic and pathologic aspects eJmiq ues . P,in 4:299-359, 1978

88. Yeung IC, Y.1.ksh T L. Rub y TA ~ Concurren t mapping of brain sites for sensitivity to

th e direct application of morphine nnd foca l electrical stimulation in the production

of .:lntinlKiCl·plio ll in the rilt. Pain 4:23-40, 1977

RECOMMENDED READINGS Adler M : End orphin , enkephatins ,m d neurotr'-lilS mi tters. Med icill Times \10:32-37, 1 loss of extension> flexion Marked and equal limitation of sidebending and rotation; loss of extension> flexion Pain when joints are stressed

AAjoint Lower cervical spine (C3-T2) Sternoclavicul'a r Acromioclavicular Glenohumeral Humeroulnar Humeroradial Forearm Proximal radioulnar Distal radioulnar Wrist Midcarpal Trapeziometacarpal Carpometacarpals II-V Upper extremity digits

Limitation of all motions except flexion (sidebending = rotation > backward bending) Full elevation limited; pain at extreme range of motion Full elevation limited; pain at extreme range of motion Greater limitation of external rota­ tion, followed by abduction and internal rotation Loss of flexion> extension Loss of flexion> extension Equally restricted in pronation and supination in presence of elbow restriction Limitation; pronation = supination Limitation; pronation = supination Limitation; flexion = extension Limitation equal all directions Limitation abduction> extension Equally restricted all directions Limitation flexion> extension

C2A. occipitoatlantal joint; AA, atlantoaxial joint. (Adapted from references 14, 22, and 4 J)

extremes of movement (see following). Capsular restrictions typically accom­ pany arthritis or degenerative joint dis­ ease (fibrosis, inflammation, or effu­ sion), prolonged immobilization of a joint (fibrosis), or acute trauma to a joint (effusion). Only joints that are controlled by m uscles have a capsular pattern. Thus, joints such as the tibiofibular and sacroiliac do not exhibit a capsular pat­ tern. b. Noncapsular patterns of joint restric­ tions typically occur with intra-articu­ lar mechanical blockage or extra-articu­ lar lesions. Common causes include i. Isolated ligamentous or capsular adhesion. A common example of isolated ligamentous adhesion is that of adherence of the medial col­

Sacroiliac, sym­ physis pubis, sacrococcygeal Hip

Tibiofemoral' (knee) Tibiofibular Talocrural (ankle) Talocalcaneal (subtalar) Midtarsal First metatarsal­ phalangeal Metatarsophalan­ geal (II-V) Interphalangeal

Limited flexion/internal rotation; some limitation of abduction; no or little limitation of adduction and external rotation Flexion grossly limited; slight limitation of extension Pain when joint is stressed Loss of plantarflexion > dorsiflexion Increasing limitations of varus; joint fixed in valgus (inversion> eversion) Supination> pronation (limited dorsi­ flexion, plantar flexion, adduction, and medial rotation) Marked limitation of extension; slight limitation of flexion Variable; tend toward flexion restrictions Tend toward extension restrictions

(Adapted from references 14, 19, 37, 41 , and

Sal

lateral ligament at the knee to the medial femoral condyle during healing of a sprain. This results in restriction of knee flexion to about 90°, with extension being of full range. Isolated anterior capsular tightness at the shoulder often oc­ curs following an anterior disloca­ tion, resulting in a disproportion­ ate loss of external rotation. ii. Internal derangements, such as displacement of pieces of torn menisci and cartilaginous loose bodies. These typically produce a mechanical block to movement in a noncapsular pattern. The most common example is a "bucket han­ dle" medial meniscus tear, result­ ing in blockage of knee extension, with flexion remaining relatively free in the absence of significant ef­ fusion. iii. Extra-articular tissue tightness,

PART .,

such as reduced lengthening of muscles from contracture (fibrosis) or myositis ossificans. iv. Extra-articular inflammation or swellings, such as those accompa­ nying acute bursitis and neo­ plasms. 2. End feel at extremes of painful or restricted movements. This is the quality of the resis­ tance to movement that the examiner feels when coming to the end point of a particu­ lar movement. Some end feels may be nor­ mal or pathological, depending on the movement they accompany at a particular joint and the point in the range of move­ ment at which they are felt. Other end feels are strictly pathological. The testing of end feel can be performed on both classical (os­ teo kinematic) and accessory motions. a. End feels that may be normal or patho­ logic include: i. Capsular end feel. This is a firm, "leathery" feeling felt with a slight creep, for example, when forcing the normal shoulder into full exter­ na~ rotation. When felt in conjunc­ tion with a capsular pattern of re­ striction, and in the absence of significant inflammation or effu­ sion, it indicates capsular fibrosis. ii. Ligamentous end feel. This is a firm end feel with no give or creep. An example of normal ligamen­ tous end feel would be abduction of the extended knee. iii. Bony end feeL This feels abrupt, as w hen moving the normal elbow into full extension. When accompa­ nying a restriction of movement, it may suggest hypertrophic bony changes, such as those that occur with degenerative joint disease, or possible malunion of bony seg­ ments following healing of a frac­ ture. iv. Soft-tissue-approximation end feel. This is a soft end feel, as when fully flexing the normal elbow or knee. It may accompany joint re­ striction in the presence of signifi­ cant muscular hypertrophy. v. Muscular end feel. This more rub­ bery feel resembles what is felt at the extremes of straight-leg raising from tension on the hamstrings. It is less abrupt than a capsular end feel.

Basic Concepts and Techniques

79

b. End feels that are strictly pathologic in­ clude: 1. Muscle-spasm end feel. Movement is stopped fairly abruptly, perhaps with some "rebound," owing to muscles contracting reflexively to prevent further movement. It usu­ ally accompanies pain felt at the point of restriction. When occur­ ring with a capsular restriction, it indicates some degree of synovial inflammation of the portion of the joint capsule being stretched dur­ ing the movement. ii. Capsular (abnormal) end feel. The range of motion is obviously re­ duced, in a movement pattern characteristic for each joint. Some authors divide abnormal capsular end feel into hard capsular end feel, when the feel has a tight resistance to creep or thick quality to it, and soft capsular end feel, when it is simi­ lar to normal but is painful w ith in­ duced muscle guarding. A hard end feel is seen in chronic inflam­ matory conditions. The soft capsu­ lar end feel is more often seen in acute inflammatory conditions, with stiffness occurring early in the range and increasing until the end range is reached. Maidand53 calls this "resistance through range." Many authors also describe a boggy end feel that typically ac­ companies joint effusion in the ab­ sence of significant synovial in­ flamma tion. n iii. Boggy end feel. This is a very soft, mushy end feel that typically ac­ companies joint effusion in the ab­ sence of significant synovial in­ flammation. It will usually occur together with a capsular pattern of restriction. iv. Internal derangement end feel. This is often a pronounced, springy rebound at the end point of movement. It typically accompa­ nies a noncapsular restriction from a mechanical block produced by a loose body or displaced meniscus. v. Empty end feel. The examiner feels no restriction to movement, but movement is stopped at the insis­ tence of the patient because of se­

80

CHAPTER 5

•

Assessment of Musculoskeletal Disorders and Concepts of Management

vere pain. This end feel is rela­ tively rare except with acute bursi­ tis at the shoulder or a few other painful extra-articular lesions such as neoplasms. The muscles do not contract to prevent movement since this would cause compres­ sion at the painful site and further pain. c. Additional abnormal end feels de­ scribed by Paris 67 include: i. Adhesions and scarring with a sudden sharp arrest in one direc­ tion, commonly seen at the knee ii. Bony block. This is a sudden hard stop short of normal range. Exam­ ples of abnormal bony blocks are callus formation, myositis ossifi­ cans, or fracture within a joint. iii. Bony grate. The end feel is rough and grating as occurs in the pres­ ence of advanced chondromalacia. IV. Pannus. This abnormal end feel is described as a soft, crunchy squelch. The exact nature is un­ known but may include synovial infold or trapped fat pad . v. Loose. Ligamentous laxity as seen in a ligamentous injury or rheuma­ toid arthritis. The importance of the end feel is that it gives some indication of what is likely to be the most effi­ cient treatment. 3. Another useful way to consider restricted motion is known as the barrier con­ cept. 6,31,37 Barriers exist at the end of nor­ mal active range of motion, when the soft tissues about the joint have reached a de­ gree of tension beyond which the person cannot voluntarily move. This is known as the physiologic barrier. Other barriers in­ clude: a. Within the total range of motion there is a range of passive movement avail­ able which the examiner can introduce (Fig. 5-2A). The limits to this barrier have been described by some as the elastic barrier. 31 At this point all the ten­ sion has been taken up within the joint and its surrounding tissues. b. Passively, the joint may be taken be­ yond its elastic barrier to the anatomic barrier. Here the soft tissues are on maximum stretch, and going farther will either cause failure of the soft tis­

sues or fracture. According to Sandoz 73 there is a small amount of potential space between the elastic barrier and anatomic barrier described as the para­ physiologic space (Fig. 5-2A). It is within this area that the high-velocity, low­ amplitude thrust appears to generate the popping which is sometimes elicited from this maneuver. 31 c. In a state of dysfunction, when motion is lost within the range, it can be de­ scribed as a major or minor loss of mo­ bility (see Fig. 5-2B). The barrier which prevents movement in the direction of motion lost is defined as the restrictive barrier. The barrier may be described according to the abnormal end feel pre­ viously discussed. d. The loose packed or resting position is often described as the point of ease (see Fig. 5_2A).31 Conversely, as one moves away from neutral or the point of maxi­ mum ease, in either direction, the soft tissue becomes more tense, where one begins to sense a certain amount of "bind" (see Fig. 5-2A). In the normal joint the point of ease is usually near the mid point of range. When there is a restrictive barrier, the point of ease will be found to have moved, usually to about the mid point of the remaining range (actual resting position). When there is a major restriction, the point of ease may be closer to the physiologic barrier at the normal end (see Fig. 5-2B) . 4. Pain on movement and the point in the range in which it is felt. a. Pain at the extremes of a movement in­ dicates i. A painful structure is being stretched. In this case, one should consider first, a lesion of the joint capsule or a ligament and second, a lesion of a muscle or tendon. For biarticular muscles, the constant­ length phenomenon can be used to differentiate the location. Other­ wise one must correlate this find­ ing with findings of resisted move­ ment tests (see III, following) in order to differentiate between cap­ suloligamentous and musculo­ tendinous lesions. If the lesion lies in a muscle or tendon, resistance to

PART I Anatomic Barrier

Basic Concepts and Techniques Neutral

81

Anatomic Barrier

\

Bind

Bind

".

I' Ease

.#

Ease

,

". ~

--'"

Passive ROM

~

Passive ROM

Elastic Barrier

Elastic Barrier

Paraphysio logical Barrier

t}

Paraphysiological Barner Range of Passive Movement

A

Passive Motion Available

Midline Neutral Pathological

Abnormal End Feel

Active Motion

a

In

FIG. 5-2. Soft tissue tension de­ velopment during examination procedures. IA) Normal mobility and associated barriers. IB) Dys­ function and associated restrictive barriers.

Motion Loss Total Passive ROM

B

the movement opposite the direc­ tion of the painful passive move­ ment will be painful, whereas with capsuloligamentous lesions re­ sisted movements are painless. ii. A painful structure is being squeezed. This usually occurs with extra-articular lesions such as ten­ dinitis and bursitis. An inflamed subdeltoid bursa is susceptible to impingement beneath the acromial arch; the trochanteric bursa is squeezed on abduction of the hip; the semimembranosus bursa, when swollen, is squeezed on full knee flexion. With supraspinatus tendinitis, pain will be felt on ele­ vation of the arm from squeezing of the involved part of the tendon between the greater tuberosity and the posterior rim of the glenoid cavity. b. A painful arc may occur with passive

movement tests. (See section on active movements for a discussion of its sig­ nificance.) 5. Joint sound on movement. When moving peripheral joints, the examiner will often feel or hear unusual joint sounds which mayor may not indicate pathology. a. Crepitus on movement. This is best de­ tected by active movement testing but may be noted on passive movement as well. (See section on active movements for discussion.) A creaking, leathery (snowball) crepitus (soft-tissue crepi­ tus) is sometimes perceived in patholo­ gies involving the tendons. 50 Soft tissue crepitus may be palpable in patients with degeneration of the rotator cuff and a bony crepitus will be evident in patients with osteoarthritis. b. Clicks, such as the normal vacuum dick, may be felt in the joint and are usually of no significance. In the nor­ mal knee, there is often a click on e ­

82

CHAPTER 5

•

Assessment of Musculoskeletal Disorders and Concepts of Management Glide

tension . They are particularly common in hypermobile joints in which the lax­ ity of ligaments enables a bone to click as it moves in relation to its fellow bone.13 Clicking is common in joints unsupported by muscles or when a loose body lies inside a jOillt. c. Snapping may be heard or felt around joints as ligaments or tendons catch and then slip over a bony prominence. Less common causes of a path ologic nature are i. A coarse clunking type of noise ac­ companying joint subluxation or instability (e.g., rotatory instability of the knee due to ligamentous damage or degenerative changes in the joint).1 3 ii. A semimembranosus bursa may snap as it jlilllpS from one side of the tendon to the other, as the knee extends. 14 iii. A trigger finger is often released into extens ion with a snap.14 d. Cracks may occur when traction is ap­ plied to a joint. Synovial fluid found in a joint cavity contains 15 percent gas, and the crack is thought to be caused by a bubble of gas coll apsing. 14,87

B. Passive joint-play movement tests (capsuloliga­ mentous stress tests) are designed to stress vari­ ous portions of the joint capsuJ e and major ligaments to detect the presence of painful le­ sions affecting these structures or loss of con­ tinuity of these structures. (For the meth od of performing the movements and the various movements performed at each joint, see the mobilization techniques included in the spe­ cific joint chapters in Part II.) Joint play is assessed by moving one of the articular surfaces of the joint in a direction that is either per­ pendicular or parallel to the joint (Fig. 5-3). The treat­ ment plane is at right angles to a line drawn from the axis of rotation to the center of the concave articulat­ ing surface and lies in the concave surface. Passively moving either bone in a direction perpendicular to the treatment plane constitutes a traction or distraction joint-play assessment, and moving either bone in a di­ rection parallel to the treatment plane constitutes a gliding or oscillation joint-play assessment. Tractjon joint-play assessments directed al"ong the axis of the long bone are called long axis extension or distractions to distinguish them from tractions administered per­ pendicular to the treatment plane. Joint-play mm(ement should be assessed in the

A

B

=-

=

c FIG. 5-3. Glides and traction. Traction is app/,ied perpen­ dicular, and glides are applied parallel to the treatment plane.

loose (resting) position in which laxity of capsule and ligaments is greatest and there is the least bone con­ tact (minimal congruency between the articular sur­ faces) .41 The greatest amount of joint play is available in the resting position that is usually considered in the mid range, or it may be just outside the range of pain and spasm (position of most comfort). If limitations in range of motion or pain prevent the examiner from placing the joint in the resting position, then the posi­ tion most closd y approximating the resting position should be used. This is called the actual resting posi­ tion .22 Examples of resting positions (loose-packed) are shown in Table 5-3. Joint-play assessment and treatment should not be performed or attempted in the maximal close~packed position (see Chapter 3, Arthrology). The close­ packed configuration usually occurs at a position that is the extreme of the most habitual position of the joint, whereas the mid range of a joint movement will be closer to the foose-packed or resting position.76 For

PART!

Basic Concepts and Techniques

83

TABLE 5-3 RESTING (LOOSE-PACKED) JOINT POS ITIONS

TABLE 5-4 CLOSE-PACKED POSITIONS OF THE JOINTS

JOINT(S)

POSITION

JOINT(SI

POSITION

Vertebral

Midway between flexion and extension Jaw slightly open (freeway space) Arm resting by side Arm resting by side 55-70° abd'uction; 30° horizontal adduction; neutral rotation

Vertebral Temporomandibular

Maximal extension Maximal retrusion (mouth closed with teeth clenched) or maximal anterior pOSition /mouth maximally opened) Maximum abduction and external rotation Arm maximally erevated Arm abducted 90°

Temporomandibular Sternoclavicular Acromioclavicular Glenohumeral

Elbow Humeroulnar Humeroradial Forearm Proximal radioulnar Distal radioulnar Radio/ulnocarpal Hand Midcarpal CarpometacarpaJ (2 through 5) Trapeziometacarpal

Metacarpophalangeal (MCP) Interphalangeal (IP) Hip Knee Ankle/Foot Talocrural Subtalar and

mid-tarsal

Tarsometatarsal

70° flexion and 10° supination Full extension and supination 70 ° flexion and 35 ° supination 10° supination Neutral with slight ulnar deviation Neutral with slight flexion and ulnar deviation Midway between flexion/exten­ sion, mid flexion, and mid ex­ tension Midway between flexion/ extension and between abduc­ tion/adduction First MCP joint: slight flexion MCP joints 2-5: Slight flexion with ulnar deviation Proximal IP joints : 10° flexion Distal IP joints: 30° flexion 30° flexion, 30° abduction, and slight lateral rotation 25° flexion Mid inversion/eversion and 10° plantar flexion Midway between extremes of range of motion with 10° plan­ tar flexion Midway between supination and pronation

Toes Metatarsophalangeal Neutral' (extension 10°) ,I nterphalangeal Slight flexion (Adapted from references 22, 41, and 49)

example, the close-packed position for the wrist joint ,i s full extension. The ot her extreme position of the joint that is less commonly assum ed i s also v ry con­ gruent and is called the potential close-packed posi­ tion. 3 ,49,89 E xamples of the close-packed positions of most synovial joints are shown in Table 5-4. If joint motion is to be avoided, the close-packed position can be used. or example, the spinal seg­ ments above and below a segment to be m obilized may be " locked" into a close-packed position in order to isolate the mobilizing force to a particular I vel.

Glenohumeral Sternoclavicular Acromioclavicular Elbow Humeroulnar

Humeroradial

Forearm Proximal radioulnar Distal radioulnar Radiocarpal Hand Midcarpal Carpometacarpal Trapeziometacarpal Metacarpo­ phalangeal (MCP) Interphalangeal Hip

Knee Ankle/Foot Talocrural Subtalar Mid'tarsal Tarsometatarsal

Full extension and supination 90° flexion, 5° supination

5° supination, full extension 5 ° supination Full extension with radial deviation Full extension Full opposition Full opposition First MCP: full extension Mep joints 2-5: Full flexion Full extension Ligamentous: Full extension, abduction, and internal

rotation

Bony: 90 ° flexion, slight abduction, and slight external rotation Full extension and external rotation Full Full Full Full

dorsiflexion inversion supination supination

Toes

Metatarsphalangeal Interphalangeal

Full extension Full extension

(Adapted from references 22, 41, 49)

Gen erally speaking, rotation will cause a close-packed p osition. Joint-p lay assessment entails determination of the type of r esistance felt at the end of range of motion (end feel), the type of pain, and the amount of excur­ sion p r esent in a particular direction. Excursion is de­ termined by comparing the joint with the same joint on the opposite side, assuming that it is not in dys­ function. Joint excursion is evaluated by performing either a glide or traction mobilization and by moving the bone up to and slightly through the first tissue stop. This corresponds to a grade 3 treatment glide or grade 2 to 3 treatment traction (see joint treatment techniques in Chapter 6, Introduction to Manual Ther­

84

CHAPTER 5

•

Assessment of Musculoskeletal Disorders and Concepts of Management

apy). The first tissue stop felt by the clin ician corre­ sponds with the end of the elastic phase and the be­ ginning of the plastic phase on the stress-strain curve. Following this scheme one can assess: 1. The degree of mobility (amplitude). The possibilities include: a. Hypermobility, suggesting a loss of continuity (partial tear or complete rupture) of the structure being tested b. Hypomobility, suggesting fibrosis, as from increased laying down of collagen in the presence of chronic stresses and low-grade inflammation, or suggesting adhesion to adjacent structures, as may occur during healing of a sprain. Hypo­ mobility may be d ue to protective mus­ cle spasm, in which case some degree of inflammation of the structure or syn­ oviallining is implied. c. Normal mobility, implying normal sta­ tus of the structure being tested 2. Presence of pain or muscle guarding (irri­ tability) at extremes of .m ovement. Pain on joint-play movement testing suggests the presence of a sprain or actual tear of the structure being stressed. 3. One must consider, then, six possible find­ ings on joint-play movement testing and their probable interpretations: a. Normal mobility-painless. There is no lesion of the structure tested. b. Normal mobility-painful. There is a minor sprain of the structure tested. c. Hypomobility-painless. A contracture or adhesion involves the tested struc­ ture. d. Hyp omobility-painful. A more acute sprain of the structure may be accom­ panied by guarding. If the hypomobil­ ity is due to muscle guarding, one can­ not, at this poi.'1t, know whether an actual tear or rupture exists. e. Hypermobility-painless. A complete rupture of the structure is suggested; there are no longer intact fibers from which pain can be elicited. f. H ypermobility-painful. A partial tear is present in which some fibers of the structure are still intact and being stressed. 4. Accessory movements are usually graded on a scale of 0 to 6, as listed in Table 5-5. 88 Such grading has the following treah)1ent irnplications: 22

TABLE 5·5 GRADING ACCESSORY JOINT MO VEMENT

GRADE

JOINT STATUS

o

Ankylosed Considerable hypomobility Slight hypomobility Normal Slight hypermobility Considerable hypermobility Unstable

1

2 3 4 5 6

a. Grades 0 and 6: Mobiliza tion is not in­ dicated. Surgery should be considered. b . Grade 1 and 2: Mobilization is indi­ ca ted . c. Grade 3: Mobilization is not indicated to increase joint extensibility. d. Grades 4 and 5: M ob iliza tion is not in­ dica ted to increase joint extensibility. Tapit, g, bracing, stabilization through exercises, and education regardin g pos­ ture an d positions to be avoided should be consid ered. III. Resisted Isom etric Tests These are tests designed to assess the status of musculotendinous tissue. Tradi tion al muscle test­ ing p rocedures th a t are included in the follow ing section on neurom uscular tests are u sed p rimarily to evaluate neurologic function, wh ereas the in­ tention of these tes ts is to determine whether there is some lesion, or loss of continu ity, of the musculoten dinous tissue itself. In or der to do so, ideally the clinician n eeds to stress the m uscle and tendon that is to be tested w ithou t stressing other joint tissu es. These tests are performed, then, as m aximal isom etric contractions, disallow ­ ing any m ovemen t of th e join t. Realistically, in most cases other tissues are going to be squeezed or compressed by the contracting m uscles, b ut this seldom p oses a p rob lem when the test is d one correctly. A particular m uscle and tendon are tested in th e position that best isola tes th em, and in a position in which they are at an optimal length for maximal contraction (usually a mid po­ si.tion). Maximal stabilization is requir ed to pre­ ven t substitution and to minimize joint move­ ment. When p erfom1ing resisted isometric tests, one must d etermine whether the contraction is strong or weak and whether it is painful or painless. Weakness may b e due to a n eurologic deficit or to actual loss of con tinui ty o f muscle or tendon tissue;

PART I Basic Concepts and Techniques appropriate neurologic testing may be performed to determine which is the case. few neurologic dis­ orders result in isolated weakness of a single mus­ cle. A painful contraction signifies the p resence of some painful lesion involving the muscle or ten­ don tissues being tested. In the majority of cases the problem will be in the tendon, since muscle strains are rare except in sports-related injuries. Very often the patient feels the most pain as the contraction is released rafher than during maxima~ contraction. \!\Then this occurs, it should be consid­ ered a positive test; the lengthening that occurs as a muscle relaxes apparently stresses the involved fibers sufficiently to cause more pain than does the shortening that occurs during contraction. Practi­ cally speaking, these resisted tests are often per­ formed in conjunction with standard neuromuscu­ lar strength tests. There are four possible findings on resisted move­ ment tests: A. Strong and painless-There is no lesion or neu­ rologic deficit involving the muscle or tendon tested. B. Strong and paillful-A minor lesion of the tested tendon or muscle exists; usually the tendon is at fault. Occasionally auxiliary re­ sisted tests must be performed to differentiate the involved structure from synergists. C. Weak and painless 1. There may be some interruption of the nerve supply to the muscle tested. The findings must be correlated with those of other muscle tests and neurologic tests. 2. There may be a complete rupture of ten­ don or muscle; there are no longer fibers intact from which pain can be elicited. D. Weak and painful 1. There may be a partial rupture of muscle or tendon in which there are still some in­ tact fibers that are being stressed. 2. This may be the result of painful inhibition in association with some serious patho­ logic conclition, such as a fracture or neo­ plasm or an acute inflammatory process.

D

Neuromuscular Tests

If, at this point in the examination, one suspects that there may be a lesion interfering with neural conduc­ tion, the appropriate clinical tests should be per­ formed in an attempt to detect loss of neurologic func­ tion. The common nerve lesions are extrinsic. Loss of conduction usually results from pressure on a nerve

85

from some adjacent structure or structures. In the common nerve disorders, the pressure is usually minor or intermittent, or both, and usually involves a single nerve or segment. For this reason, the manifes­ tations of the disorder are often quite subtle; findings on evaluation are largely subjective, and some objec­ tive signs may be detected only with more sophisti­ cated electrotesting procedures. \!\Then neurologic function is assessed clinically and a deficit is detected, the approximate site of the lesion can be estimated by correlating the extent of the deficit with peripheral nerve and segmental distributions. More central or serious lesions must be suspected when the extent of the deficit exceeds the distribution of a single segment or a single peripheral nerve. Pe­ ripheral nerve and segmental innervations are indi­ cated in Table 5-6 and Figure 5-4. Key segmental distri­ butions, both myotomal and dermatomal, are listed in Table 5-7. These are the muscles and skin areas that are most likely to be affected by involvement of a particu­ lar segment. These are important to know, since seg­ mental deficits, such as those that occur with disk pro­ trusions, are very common neural disorders seen clinically. Because of the overlapping of dermatomes and myotomes in the extremities, lesions involving a single segment, even when conduction is completely interrupted, result in only subtle deficits. The tests described below may be used when per­ forming clinical neurologic assessment.

STRENGTH TESTS Traditional muscle testing procedures should be em­ ployed . It is often necessary to repeat a test, compar­ ing the strength carefully to the normal side if possi­ ble, since weaknesses resulting from common nerve lesions are usually subtle. Weaknesses and asymme­ tries in strength are noted.

SENSORY TESTS A pin, wisp of cotton, and tuning fork may be u sed to assess conduction along sensory pathways. Pressure on a nerve will usually result in loss of conduction along the large myelinated fibers first and the small unmyelinated fibers last. Therefore, minor deficits will often be manifested first by loss of vibration sense, with sensation to touch and noxious stimula­ tion being reduced with more severe or long-lasting pressure. When performing sensory tests, a particular area on the normal side is tested and the patient is asked if the sensation is perceived. Then the involved side (text co ntinues on page 88)

86

CHAPTER 5

TABLE 5-6

•

Assessment of Musculoskeletal Disorders and Concepts of Management

PERIPHERAL NERVES AND SEGMENTAL INNERVATION

CORD SEGMENT

NERVES

PLEXUS

Deep neck muscles (sternomastoid and trapezius also participate)

Cl-C4

Cervical

Cervical

Scaleni Diaphragm

C3-C5 C3-C5

Phrenic

Adduction of arm from behind to front

Pectoralis major and minor

C5-C8 TI

Forward thrust of shoulder Elevation of scapula Medial adduction and elevation of scapula Abduction of arm Lateral rotation of arm Medial rotation of arm Adduction of arm front to back

Serratus anterior Levator scapulae Rhomboids

C5-G C5 (C3- C4) C4-C5

Medial and lateral pectoral (from medial and lateral' cords of plexus) Long thoracic Dorsal scapular

Supraspinatus Infraspinatus Latissimus dorsi, teres major, and subscapularis

C4-C6 C4-C6 C5-C8

Suprascapular

Adbuction of arm Lateral rotation of arm Flexion of forearm Supination of forearm Adduction of arm Flexion of forearm

Deltoid Teres minor Biceps brachii

C5-C6 C4-C5 C5-C6

Axil/ary (from posterior cord of plexus) Musculocutaneous (from lateral cord of plexus)

Coracobrachialis

C5-G

Flexion of forearm Ulnar flexion of hand Flexion of terminal phalanx of ring finger and little fin­ ger Flexion of hand

Brachialis Flexor carpi ulnaris Flexor digitorum profundus (ulnar portion)

G-TJ G-TI

Ulnar (from medial cord of plexus)

Adduction of metacarpal of thumb Abduction of little finger Opposition of little finger Flexion of little finger Flexion of proximal phalanx; extension of two distal phalanges; adduction and' abduction of fingers

Adductor pol/icis

C8- TI

Ulnar

Brachial

Abductor digiti quinti Opponens digiti quinti Flexor digiti quinti brevis Interossei

C8-TI G-TI G-TI C8-TI

Pronation of forearm Radial flexion of hand FI'e xion of hand Flexion of middle phalanx of index, middle, ring, little fingers Flexion of hand Flexion of terminal phalanx of thumb

Pronator teres Flexor carpi radialis Palmaris longus Flexor digitorum sublimis

C6-G C6-G G-TI G-TJ

Median (C6,G from lateral cord of plexus; C8, TJ from medial cord of plexus)

Brachial

Flexor pol/icis longus

G-TJ

Median

Brachial

Flexion of terminal phalanx of index finger, and middle finger Flexion of hand

Flexor digitorum profundus (radial portion)

G-T I

ACTION TO BE TESTED

MUSCLES

Shoulder Girdle and Upper Extremity Flexion of neck Extension of neck Rotation of neck Lateral bending of neck Elevation of upper thorax Inspiration

Brachial

Subscapular (from posterior cord of plexus) Brachial

Brachial

C5 ~C6

(continued)

(

\

\

PART I TABLE 5-6

Basic Concepts and Techniques

87

Continued

ACTION TO BE TESTED

MUSCLES

CORD SEGMENT

NERVES

PLEXUS

Median

Brachial

Shoulder Girdle and Upper Extremity Abduction of metacarpal of thumb Flexion of proximal phalanx of thumb Opposition of metacarpal of thumb

Abductor polilcis brevis

Cl-TI

Flexor pollieis brevis

Cl-TI

Opponens pollicis

C8-TI

Flexion of proximal' phalanx and extension of 2 distal phalanges of all fingers

Lumbricales (the two lateral) Lumbricales (the two medial)

C8-TI

Median Ulnar

Brachial

Extension of forearm

Triceps brachii and anconeus

C6-C8

Radial (from posterior cord of plexus)

Brachial

Flexion of forearm Radial extension of hand Extension of phalanges of fingers Extension of hand Extension of phalanges of little finger Extension of hand

Brach/oradialis Extensor carpi radiali.s Extensor digitorum communis

C5-C6 C6-C8 C6-C8

Extensor digiti quinti proprius

C6-C8

Ulnar extension of hand Supination of forearm Abduction of metacarpal of thumb Radial extension of hand Extension of thumb

Extensor carpi ulnaris Supinator Abductor pollicis longus

C6-C8 C5-Cl C7-C8

Radial

Brachial

Extensor pollicis brevis and longus Extensor indicis proprius

C6-C8

Radial extension of hand Extension of index finger Extension of hand

C6-C8

Trunk and Thorax Elevation of ribs Depression of ribs Contraction of abdomen Anteroflexion of trunk Lateral flexion of trunk

Thoracic, abdominal, and back

Thoracic and posterior lumbosacral branches

Hip Girdle and Lower Extremity Flexion of hip Flexion of hip and eversion of thigh Extension of leg Adduction of thigh

Adduction of thigh Lateral rotation of thigh Abduction of thigh Medial rotation of thigh Flexion of thigh Lateral rotation of thigh Abduction of thigh

Iliopsoas Sartorius

Ll-L3 L2-L3

Quadriceps femoris Pectineus Adductor longus Adductor brevis Adductor mag nus Gracilis Obturator extern us

L2-L4 L2-U L2-L3 L2-L4 L3-L4 L2-L4 L3-L4

Gluteus medius and minimus Tensor fasciae latae Piriformis Gluteus maxim us

Femoral

Lumbar

Obturator

Lumbar

L4-S1

Superior gluteal

Sacral

L4-L5 L5-SI L4-S2

Inferior gluteal (continued,

88

CHAPTER 5

TABLE 5-6

•

Assessment of Musculoskeletal Disorders and Concepts of Management

CONTINUED

ACTION TO BE TESTED

MUSCLES

CORD SEGMENT

NERVES

PLEXUS

Hip Girdle and Lower Extremity

Lateral rotation of thigh

Obturator internus Gemelli Ouadratus femoris

LS-Sl L4-S1 L4-S1

Muscular ,branches from sacral plexus

Flexion of leg (assist in extension of thigh)

Biceps femoris

L4-S2

Sciatic (trunk)

Sacral

Semitendinosus Semimembranosus

L4-S1 L4-S1

Dorsiflexion of foot Supination of foot Extension of toes II-V Dorsiflexion of foot Extension of great toe Dorsiflexion of foot Extension of great toe and the three medial toes

Tibialis anterior

L4-LS

Deep peroneal

Sacral

Extensor digitorum longus

L4-S1

Extensor hallucis longus

L4-S1

Extensor digitorum brevis

L4-S1

Plantar flexion of foot in pronation

Peronei

LS-SI

Superficial peroneal

Sacral

Plantar flexion of foot in supination Plantar flexion of foot in supination Flexion of terminal phalanx of toes II-V Plantar flexion of foot in supination Fi'exion of terminal phalanx of great toe FI'exion of middle phalanx of toes II-V Flexion of proximal phalanx of great toe Spreading and closing of toes Flexion of proximal phalanx of toes

Tibialis posterior and triceps surae Flexor digitorum longus

LS-S2

Tibial

Sacral

Flexor hallucis longus

LS-S2

Flexor digitorum brevis

LS-Sl

Flexor hallucis brevis

LS-S2

Small muscles of foot

SI-S2

Perineal and sphincters

S2-S4

Pudendal

Sacral

Voluntary control of pelvic floor

LS-S2

(Chusid JG: Correlative Neuroanatomy and Functional Neurology. Los Altos, CA, Lange Medical Publications, 1970)

is retested and the patient again asked if the sensa­ tion is felt If sensation is intact on both sides, the pa­ tient is asked if it felt the same on both sides, This procedure is followed when testing each key seg­ mental sensory area and each peripheral nerve distri­ bution, Sensory deficits and asymmetries in percep­ tion are noted.

DEEP TENDON REFLEXES Lower motor neuron lesions, such as segmental or pe­ ripheral nerve disorders, may result in d iminution of

certain deep-tendon reflexes, while more central, upper motor neuron lesions may cause hyperreflexia. The important assessments to make when testing deep tendon reflexes are whether the responses at ho­ mologous tendons are symmetrical and whether any responses are clonic. The presence of hyporeflexia is difficult to judge, since some persons normally have reflexes that are difficult to elicit In general, if it is equally difficult to elicit responses at corresponding tendons, no significance can be attributed , However, if upper extremity responses are difficult to elicit but lower extremity responses are strong, a myelopathy

PART I

89

!

PoSlculan.

Radial

Dorsal cutan.

C7 Median

Median

Ant. culan.

)

Saphenous

Lat. culan.

FemQral Femoral saphenous

)

Sup. peroneal

Common peroneal

Sural~

Tibial

Deep peroneal

A

FIG. 5-4.

or some other more serious pathologic process should be considered. COORDINATION, TONE, AND PATHOLOGIC REFLEXES

Coordination, tone, and pathologic reflexes should be assessed if myelopathy or other upper motor neuron disturbances are suspected. For example, myelopathy resulting from cervical spondylosis may result in a mildly spastic gait, increased lower extremity tone, lower extremity hyperreflexia, and perhaps a positive Babinski response (dorsiflexion of big toe in response to noxious stimulation along the sole of the foot).

OJ

SClatlc{

pero[neal Sural--\-..... Tibial

Planlars!

B

Segmental and peripheral nerve distribution.

ltral,

exia. ;ting t hoany ia is have it is ding ever, t but .athy

Basic Concepts and Techniques

Palpation

Palpation tests are usually conveniently performed at the same time as the inspection tests discussed previ­ ously. As in inspection, palpation tests should be or­ ganized according to layers, assessing the status of the skin, subcutaneous soft tissues, and bony structures (including tendon and ligament attadunents). Signifi­ cant findings are documented. Palpation of all tissues associated with the area of

symptoms discloses both physiologic and structural changes. The uninvolved side should be palpated first so that the patient has some idea of what to expect. The palpatory examination includes, but is not neces­ sarily limited to, palpation of the myofascial struc­ tures in the form of layer palpation and palpation of the bony structures. The tissues that can be palpated rnclude the skin, subcutaneous fascia, blood vessels, nerves, muscle sheaths, muscle bellies, musculotendi­ nous junctions, tendons, deep fascia, ligaments, bones, and joint spaces. For practical purposes, layer palpation may be cate­ gorized into superficial and deep palpation. Superfi­ cia[ palpatory examination includes assessment of tis­ sue temperature and moisture as well as light touch to determine the extensibility and integrity of the super­ ficial connective tissue.

SK.IN

The examiner uses the back of the hand to initially discern variations in skin temperature and sweating between symptomatic and nonsymptomatic areas. The movement of the skin over the underlying but superficial structures is checked next. Depending on

90

CHy\PTER 5

•

I\ssessment of Musculoskeletal Disorders and Concepts of Management

TABLE 5 · 7

KEY SEGMENTAL DISTRI'BUTIONS (MYOTOMAL AND DERMATOMALj

SEGMEN'TS

KEY MOVEMENTS TO TEST

C4

Shoulder shrug, diaphragmatic function Shoulder abduction, external rotation Elbow flexion, wrist extension Elbow extension, wrist flexion Ulnar deviation, thumb abduction, small finger abduction Approximation of fingers Hip flexion Knee extension, hip flexion Knee extension, ankle dorsiflexion Ankle/large toe dorsiflexion, eversion of ankle Plantar flexion, eversion, knee flexion Knee flexion, ankle plantar flexion

C5 C6 Cl C8

TI L2 L3 L4 L5

51 52 Cranial nerve V C5, C6 (Cl) ,C8 (L3-L4) L5

51-52

C6

Cl C8 L2 L3 L4 L5

51 52 53-54

REFLEXES TO TEST Jaw jerk 29 ,66 Biceps, brachioradialis Triceps Patellar tendon (quadriceps) Great toe jerk32,83 Achilles tendon KEY SEGMENTAL SENSORY AREAS TO TEST (distal part of segment)

Thumb and index finger, radial border of

hand Middle three fingers Ring and small finger, ulnar border of hand Medial thigh Anteromedial, distal thigh Medial aspect of large toe Web space between large and second toes Below lateral malleolus Back of heel Saddle, anal region

Note: Others (e.g., upper cervical, thoracic, and lumbar) are less definite due to overlapping .

(Chusid JG : Correlative Neuroanatomy and Functional Neurology.

Los Altos, CA Lange Medical Publications, 1970)

because of minor mechanical causes involving one or two apophyseal joints, the overlying skin is tender to pinching and rolling while the muscles are painful to palpation and feel cordlike. 44 This is felt to be initiated by nociceptive activity in the posterior primary der­ matome and myotome. In general, the following should be noted: Tenderness. Minor pressure on a nerve supplying a particular area of skin may result in d ysesthesia that may be perceived as a painful burning sensation to normally non-noxious stimulation, such as light touch. A similar phenomenon may also occur in the presence of lesions involving other tissues innervated by the same segment. This is believed to be the result of summation of otherwise subthreshold afferent input to a segment of the spinal cord. Moisture and Texture. Moisture and texture may be altered with changes in vascularity or changes in sym­ pathetic activity to the part. In the presence of in­ creased sympathetic activity, such as that which commonly occurs in the chronic stages of reflex sympathetic dystrophy, the skin will be abnormally moist and very smooth. With reduced sympathetic ac­ tivity, sometimes preceding a reflex sympathetic dys­ trophy, the skin may be dry and scaly. Sudomotor studies have utilized an electrical skin resistance method for measuring sweat gland activity.46,47,48 Temperature. Skin temperature will be elevated in the presence of an underlying inflammatory process or with reduced sympathetic activity.1,l8,35 A reduc­ tion in skin temperature may accompany vascular de­ ficiency, increased sympathetic activity, or fibro-fatty infiltration. 39 Thermocouples and infrared thermogra­ phy are sometimes used for differential diagnosis of certain conditions.64 Mobili-ty. The skin should be moved relative to the underlying tissues to examine for the presence of skin adhesions. This is especially important following heal­ ing of surgical and other traumatic wounds. SU8CUTy\NEOUS SOFT TISSUES

the body part being tested, either the palm or the fin­ gertips are used to detect restrictions. On broad body surfaces, the palm is firmly but lightly placed on the skin and then displaced in all directions to identify tension and resistance to gentle displacement. More vigorous displacement in the form of skin rolling (if tolerated and indicated) is often an impor­ tant part of layer pa}pation; it gives additional infor­ mation about the extensibility of the subcutaneous tis­ sues and possible infiltration of the skin and subcutaneous tissue by cellulitis. 51,52 According to the minor in tervertebral derangement theory of !\1aigne,

The soft tissues are palpated deep to the skin-fat, fas­ cia, muscles, tendons, joint capsules and ligaments, nerves, and blood vessels. No more pressure than what is necessary is used. A common mistake is to press harder and harder in an attempt to distinguish deep structures. This only serves to desensitize the palpating fingertips and does not aJ;sist in d etermin­ ing the nature of the tissues being palpated. The deep palpatory examination includes compres­ sion, which is palpation through layers of tissue per­ pendicular to the tissue, and shear. Shear is movement of the myofascial tissues between layers, moving par­

PART I

allel to the tissue. 8 Translational muscle play is an ef­ fective assessment tool for assessing the mobility of a muscle or muscle group within the fascial sheath. Pal­ pation may progress to probing, to grasping, or dis­ placing muscle bellies and tendons. Resistance to dis­ placement or stretch and crepitus or "catching" should be noted. It is most revealing to palpate the en­ tire extent of a tendon sheath during contraction of its respective muscle. A characteristic vibration, as if the tendon needs lubrication, represents tenosynovitis. 88 Soft tissue palpation may offer information concern­ ing the following: Tenderness. Tenderness to deep palpation is a very unreliable finding. In itself it is never indicative of the site of a pathologic process because of the prevalence of referred tenderness with lesions of deep somatic tissues. The phenomenon is similar in all respects to that of referred pain. In many common lesions, the area of primary tenderness does not correspond well to the site of the lesion. Patients with low back disor­ ders are often most tender in the buttock, those with supraspinatus tendinitis are most tender over the lat­ eral brachial region, and persons with trochanteric bursitis are most tender over the lateral aspect of the thigh. These "trigger points," or referred areas of ten­ derness, are found in some area of the segment corre­ sponding to the segment in which the lesion exists. Generally, tenderness associated with more superfi­ cial lesions, such as medial ligament sprains at the knee, corresponds more closely with the site of the le­ sion than does tenderness occurring with more deeply situated pathologic processes. Edema and Swelling. The size and location of local­ ized soft-tissue swellings are noted. Abnormal fluid accumulations should be differentiated as intra- or extra-articular. Articular effusion will be restricted to the confines of the joint capsule; pressure applied over one side of the joint may, therefore, cause increased distention observed over the opposite side. This type of ballottement test can be used with more superficial joints. Often articular effusion is distinguished by its characteristic distribution at a particular joint; these distributions are discussed in the chapters on specific regions. Extra-articular swelling may accompany acute inflammatory processes, such as abscesses and those following acute trauma, because of protein and plasma leaking from capillary walls. Generalized tis­ sue edema may accompany vascular disorders, lym­ phatic obstructions, and electrolyte imbalances. Consistency, Continuity, and Mobility. Normal soft tissue is supple and easily moved against underlying tissue. Palpation for abnormalities such as indurated areas, loss of mobility, stringiness, doughiness, nod­ ules, and gaps is done and results noted.

Basic Concepts and Techniques

91

Pulse. Palpating for the pulse of various major arter­ ies can assist in assessing the status of blood supply to the part. Heart rate may also be determined. BONY STRUCTURES

Bony structures also include ligaments and tendon at­ tachments. When palpating bony structures, the fol­ lowing should be noted: Tenderness. As with deep, soft-tissue tenderness, tenderness at various bony sites may be referred and is therefore often misleading. Lesions involving both ligaments and tendons commonly occur at the site where these structures join the periosteum. Typically, these are highly innervated regions and may be ten­ der to palpation in the presence of tenoperiosteal or periosteoligamentous strains and sprains. Periosteal tenderness will also accompany specific bony lesions, such as stress fractures or other fractures. Enlargements. Bony hypertrophy often accompanies healing of a fracture and degenerative joint disease. In the latter, the bony changes will be noted at the joint margins in more superficial joints. Bony Relationships. Structural malalignrnents, as discussed in the section on inspection, may be de­ tected clinically by assessing the relationships, in the various planes of reference, of one bony structure to another. This is especially important following heal­ ing of fractures and in cases of vague, subtle, insidious disorders that may have a pathomechanical basis.

D

Provocation Tests

Provocation tests (auxiliary tests) are employed only when no symptoms have been produced by full active movements and other selective tissue tension tests. Additional strategies may be required to reproduce symptoms. Initial provocation tests may be undertaken in which gentle passive overpressure is applied at the end range of active or passive movement. Sometimes the symptoms are only at the end range, which the pa­ tient tends to avoid by moving just short of this point. Additional tests may include repeated active motions and repeated motions at various speeds and sustained pressures. Should gentle overpressure, sustained pressure, or repeated motions fail to reproduce the pain, greater stress on the structures can be achieved by combined motions or by coupling movements in two or three di­ rections, for example, quadrant tests (see Chapter 20, The Lumbar Spine). These tests have a considerable capacity to reproduce the patient's pain.

92

D

CHAPTER 5

•

Assessment of Muscul'oskeletal Disorders and Concepts of Management

Special Tests

The administration of certain special tests, which per­ tain to the anatomy and pathologic condition of each peripheral joint or spina1 region being examined, may be considered. These tests are structured to uncover a specific type of pathology, condition, or injury and are most helpful when previous portions of the examina­ tron have led the examiner to suspect the nature of the pathology or condition. There are usually three types of special tests: joint and ligamentous tests, neuromus­ cul ar tests, and neurologic tests. These might include tests for joint instability and muscle/tendon pathology and dysfunction. If the examiner suspects a problem with movement of the spinal cord, nerve root, or nerve, any of the tests that stretch the cord may be performed. These include the straight-leg raising test and well leg test, the slump test (see Chapter 20, The Lumbar Spine), the first thoracic nerve root test (see Chapter 19, The Cervical Spine), and upper limb tension tests (see Chapter 9, The Shoulder and Shou1der Girdle). Other considerations may include tests for intermit­ tent claudication and tests for malingering or non-or­ ganic pain.

D

Examination of Related Areas

It is often necessary to test other related joints to de­ termine if pain arises from these joints. For example, when assessing the lumbar spine, one may need to consider the sacroiliac or rup joint instead of, or in ad­ dition to, the spine. When examining the shoulder, one should consider lesion areas known to refer pain to it, including problems of the neck; for example, a herniated cervical disk may radiate pain to the shoul­ der or scapula, an elbow or distal humeral pathologies can radiate pain proximally (uncommon), and a my­ ocardial infarction may radiate pain to the left shoul­ der. Shoulder symptoms may also be related to irrita­ tion of the diaphragm, which shares the same root innervation as the dermatome covering the shoulder's summit. A general physical examination including the chest may be necessary.

D

Functional Assessment

Some aspects of functional assessment should be in­ cluded during the examination of the joint. This pro­ cedure may be as simple as observation of certain pa­ tient activities involving the joint or region being examined, or be more complex, such as a more de­ tailed examination involving objective measurement of function.al task performance.

After any examination, the patient should always be warned of the possibilities of exacerbation of symp­ toms as a result of the assessment.

D

Other Investigations

Plain film radiography is the most common first-order diagnostic screening procedure in the evaluation of musculoskeletal diseases and dysfunction. X-ray films need not be taken routinely in all patients, and a par­ ticular radiological lesion does not necessarily prove that it is the source of the patient's pain. They are often of most value in demonstrating that no abnor­ mality is present in the bone or joints. At times, find­ ings simply support a moderately firm clinical diag­ nosis; in others cases, however, the films may provide the only due to a clinically obscure situation. If radi­ ographs are available, they should be reviewed. If they are not available but the examiner believes they are needed, he may request them before proceeding with treatment. The manual therapist must recognize the presence of skeletal conditions that contraindjcate manual examination and treatment. It is generally felt that procedural tests such as com­ puted tomography (CT) should be kept in reserve for chronic disorders, especially mechanical disorders, that remain undiagnosed and for situations in wruch surgical intervention is planned. 44 Depending on availability and merit, such tests may include: Computed tomography (CT) Magnetic resonance imaging (MRI) Myelography or radiculography Discography Bone scanning RADIOGRAPHIC EXAMINATION

X-rays are the very short wavelength representatives on the spectrwn of electromagnetic radiation. X-ray film, like photograpruc film , has a clear celluloid or plastic base coated with a silver bromide emulsion which undergoes alterations in response to radiant en­ ergy. Chemical development then renders this visible as differential blackening, and the resultant shadows or negatives are available for interpretation. As the primary x-ray beam traverses a body part it will be absorbed to varying degrees depending on the density and volume of the tissue elements it encoun­ ters. High density bone will absorb more x-rays than the adjacent soft tissues, leaving fewer photons avail­ able to expose the film, and the resultant image will have a wrute area of radiopacity. Fat and gas have lower x-r ay absorption, permitting more film blacken­ ing or radiolucency.

PART I I'ays mp-

rder n of ~ lms

par­

rove are Inor~d-

liag­ ~;ide

radi-

In conventional x-ray films, the absorption densities of many musculoskeletal tissues-cartilage, tendon, and muscle-are identical. Fortunately, fat is often present along tissue p lanes and between m uscle lay­ ers, providi ng v isibility by virtue of its lower absorp­ tion density (Fig. 5-5). With experience, the examiner becomes able to detect on x-ray examination many important soft-tissue changes such as effusi n in joints, tendinous calcifications, ectopic bone in mus­ cle, and tissu displaced by a tumor. Further, the stud­ ies enable the examiner to see fractures, disloca tions, foreign bodies, and indication of bone loss (Fig. 5-6). For osteoporosis to be evident on film, approximately 30 to 35 percent of the bone m ust be lost, Basic proficiency in film interpretation is generally considered a clinical skill beyond the scope of manual therapy. H owever, a working knowledge of radiologi­ cal fundamentals and t rminology will greatly faciH-

Basic Concepts and Techniques

93

A

~: If E ey

F:

:om­ for drs, 'hich , on B

FIG. 5-6. (AJ Roentgenogram of a fracture of the proximal humerus, and (Sl axillary view of an anterior dislocation of the snoulder. A large defect (compression fracture) is pre­ sent in the posterior position of the humeral head (Hill-Sack lesion) . In both situations, the humeral head lies anterior to the glenoid cavity. (D'Ambrosia RD: Musculoskeletal Disor­ ders: Regional Examination and Differential Diagnosis, 2nd ed. Philadelphia, JB Lippincott, 1986)

tives -ray id or J ion It en­ . ible 10ws

art it n the 'oun­ than Ivail­ ' will have :ken-

FIG. 5-5. Normal calcareous density, muscle density, and fat density. Fat pads help to outline tendons and articular cartilage at the kn ee. ( D'Ambrosia RD : Musculoskeletal Dis­ orders: Regional Exam ination and Differential Diagnosis, 2nd ed . Philadelphia, JB Lippincott, 1986)

tate the study of the musculoskeletal system and give access to pertinent information from the radiologist's report to form a more thorough history and physical evaluation of the patient. The first step is to become familiar with the appea r­ ance of normal bones and tissues. They are charac­ terized by darity, contrast, and transparency of the structures as opposed to the hazin ess, indistinctness, and translucency associated with diseased tissue. 24 Healthy bone and tissue are further characterized by evenness and regularity of outline, structure, and den­ sity, Observation of bone films should include: I. External observations of bone A. Bone shape: Each bone has its own character­ istic shape and surface features (Fig. 5-7). The

94

CHAPTER 5

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Assessment of Musculoskeletal Disorders and Concepts of Management

5·7. (A) Radiograph shows normal shape of

the bones of the wrist and hand. (8) Radiograph of a

hand with senile osteoporosis shows a uniform loss of

bone density with a thin. sharply defined cortex. A

fracture of the distal radius is .present. (A from D'Am­

brosia RD: Musculoskeletal Disorders: Regional Exami­

nation and Differential Diagnosis. 2nd ed. Philadel­

B phia. JB Lippincott. 1986; 8 from Greenfield GB: Radiology of Bone Disease. 4th ed. Philadelphia. JB Lippincott, 1986)

most frequently encountered example of a de­ viation from normal shape is a displa ced fr ac­ ture. 86 B. Bony surfaces: Cortical bone should be smooth, white, and intact, except for cortical roughening normally seen at the site of ten­ don attachments. Abnormalities of bone sur­ faces may include p eriosteal bone fo rmation due to an underlying bone infection and focal erosions in rheumatoid arthritis. II. Internal structure of bone A. Diffuse changes: Less bone density than nor­ mal can be appreciated by comparin g normal x-ray films w ith those wruch reflect disu se demineralization (see Fig. 5-7). B. Foca'i abnormalities: Slowly growing destruc­ tive bone lesions will modily the shape of sur­ rounding bones and will often evoke a sclerotic reaction at the margin, ,·vrueh is evident by an increase in density (see Fig. 5-7). More ra diaJly growing lesions are characterized by a poorly defined, permeative pattern of destruction.

Spinal radiographs are nearly always included to rule out fracture, dislocation, anomaly, or bone pathology. The radiographs are also used in biome­ chanical analysis to establish an initial course of treat­ ment for patients. Radiographs of extremity skeletal structures may be incl uded to rule out primary ex­ tremity pathologic p rocesses. Study of any skeletal region requires at least hovo views, preferably at right angles to each other (such as an anterop osterior [AP] and a lateral view). The pa­ tient's his tory and clinieal evaluation are guides that he lp determine the differen t views that should be used. At times, modifications and supplementary techniq ues are required to provide precise diagnosis for effective therap y. For example, in the anteroposte­ rior or fro ntal projection of the knee, it cannot be de­ termined whether the pa tella is in front of, behind, or even within the femur (Fig. 5-SA,B). A lateral view wil l obviously localize the patella and give useful in­ formation about its configuration (Fig. 5-SC,D) . How­ ever, if there are really concerns about structural in­ tegrity of the patella itself, in order to rule out a

_ ~I ~

acture, a tangential or axial view of it would be nec­ _ ry (Fig. 5-8E,F) .86

m. Special examination Other supplementary techniques and modifica­ tions that may be required to provide precise di­ agnosis for effective therapy and often of particu­ lar interest to the manual therapist include: A. Stress view: Although clinical tests for insta­ bility usually subjectively document that lax­ ity is present, standard radiographs should be taken. They will indicate if the laxity is caused by an avulsion of the ligament with its bony attachment or by an epiphyseal separation. In order to determine whether the ligaments are intact after a joint injury, the joint may be x­ rayed in a position that would normally tighten or stress the ligament in question; for example, by applying the appropriate varus-valgus or anteroposterior stress to a joint as a standard radiograph is taken. They have proved particularly useful for docu­ menting instabilities at the ankle and epiphy­ seal injuries of the knee (Fig. 5-9).43 B. Dynamic studies: X-ray examinations in both still and cinematic format can be used to as­ sess ftmctional mobility as weB as integrity of structure. Examples include cervical spine subluxations (Fig. 5·10) and upper limb mo­ tion at the wrist joint.

ARTHROGRAMS rthrography is the study of structures in an encapsu­ lated joint using radiographic contrast media. Contrast medium is injected directly into the joint space, dis­ tending the capsule and outlining internal structures. When the clinical question is one of a torn meniscus (Fig. 5-11), focal erosion of articular cartilage or a non­ opaque intramuscular fragment, arthrography is most informative. Arthrography has been commonly used in evaluating the knee and shoulder joint. Evaluation of the shoulder joint can determine the presence of rotator cuff tears (Fig. 5-12), bicipital tend'initis or tears, and the presence of adhesive capsulitis.

MYELOGRAPHY Myelography is the study of spinal cord, nerve roots, and dura mater using radiographic contrast media. Myelography is now performed almost exclusively with water-soluble dyes through a spinal puncture. This technique is used to detect nerve root entrap­ ment, spinal stenosis, and tumors of the spinal canal. Extradural techniques can yield supp~ementary infor­ mation regarding the state of the disk. Indentation of the dural sac or fWing defects indicate abnormality

_ __

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_ '-I II

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"-~

that needs explanation (see Fig. 20-4). In spite of the decreased incidence of spinal headache and discom­ fort during this procedure, it is still significantly inva­ sive and is usually reserved for chronic disorders that remain undiagnosed and unabated and in situations wh en surgical intervention is planned. 13 ,56 Plain films or CT may also be used to visualize more anatomic detail. When CT scanning is used in conjunction with myelography, the image is referred to as a CT myelo­ gram.

DISCOGRAPHY Discography involves the injection under x-ray con­ trol of a contrast medium (a water-soluble radiopaque dye) into the nucleus puIposus. Although rarely indi­ cated, the technique can provide some useful infor­ mation with respect to disk disease and the level of impingement (see Figs. 20-2A, 20-3A). The test inter­ pretation depends on radiographic abnormalities of degeneration, identification of annular tears, epidural flow, or vertebral flow through vessels transiting the vertebral end-plate. 56 Other contrast studies include angiography and ar­ teriography (Fig. 5-13), used in evaluating hypervas­ cular tumors and determining vascular anatomy,7-81 and venography.

COMPUTED TOMOGRAPHY Computed tomography uses a computerized display to recreate a three-dimensional image. Cuts of film are taken at specific levels of the body. Tomograms may be plain or computer-enhanced. In the latter case, they are referred to as CT scans (computed tomography scans) or CAT scans (computer-assisted or enhanced tomography).50 Computed tomography has rapidly become the diagnostic procedure of choice for many conditions. Its diagnostic capabilities are based on tis­ sue attenuation of an x-ray beam. Two features render it most useful for musculoskeletal radiology: greater tissue contrast resolution than conventional radiogra­ phy, and the inherent ability to display cross-sectional anatomy.30 The CT scan can also be contrast-enhanced (dye injected around the structure) to indicate tumor, bone, or soft-tissue involvement. They are then re­ ferred to as CTAs (computed tomoarthrograms).50 A CA T spinal scan is used to outline structural spinal problems involving both bone and soft tissues. These include spinal stenosis, vertebral diseases, disk pro­ lapse, and abnormalities in the facet joint. The process begins when an x-ray source rotates around the supine patient and x~rays penetrate the body from numerous angles. Detectors in the sur­ rounding scanner measure tissue x-ray attenuation and transmit this information to the computer. The com puter then reconstructs the body image using

96

CHAPTER 5

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Assessment of Musculoskeletal Disorders and Concepts of Management

c

A

B

FIG. 5·8. Positioning and resulting x-ray appearance in standard projection for radiography of the knee. (A-B) Anterioposterior (AP.) projection. (e, D ) Lateral projection. (E,F) Tangential patel/'ar (sunrise) view. (D'Ambrosia RD: Musculoskeletal Disorders: Regional Examination and Differential Diagnosis, 2nd ed . Philadelphia, JB Lippincott, J 986) (continued)

these measurements taken at the periphery of the axial slice of the body being scanned (Fig. 5-14). NUCLEAR MAGNETIC RESONANCE AND MAGNETIC RESONANCE I'M AGING The nuclear magnetic resonance (NMR) scanner is one of the newest tools primarily devised to evaluate ver­ tebral lesions. The development of surface coil tech­ nology in the mid-1980s 21 established magnetic reso­ nance imaging (MRl) as a reasonable alternative to myelography and CT in the study of intervertebral disk disease.2 This technique uses no ionizing radia­ tion to visua Fize the structures being evaluated and can be used to obtain an image of bone and soft tissue (spinal cord and paravertebral masses). Recently, in orthopedic eva ~uation, the capabilities of MRI have expanded its role in examination of joints (Fig. 5-15). Excellent soft tissue and bone marrow contrast has led to the early detection of soft tissue and bone tumors.

BONE SCANS Radioactive isotopes hav e been developed that will preferentially go to bone, showing increased uptake in portions of the skeleton which are hypervascu}ar or which have an increased rate of bone mineral turnover (Fig. 5-16). Its major role is in identifying pathologic changes, especiall y infections, tumors, in­ flammatory diseases, or metabolic bone disease.1 0,28,60 It is not specific in differential diagnosis of disease. It is, however, useful in locating a lesion that is sympto­ matic but not yet visible on roentgenograms. This pro­ cedure reveals metastases in 95% of cases?5

THERMOGRAPHY Thermography is a noninvasive procedure that im­ ages the temperature distribution of the body sur­ faces. In contrast to radiography, computed tomogra­ (text continues 011 page 98)

(

PART I Basic Concepts and Techniques

97

E

F

FIG. 5·9. Sagittal stress roentgenogram of the knee. (AJ W hen a posterior drawer is done, the tibia has a normal re­ lationship to the femoral condyles . ,(B) With an anterior drawer, the tibia sub /uxes forward, suggesting anteriome­ dial rotary instability. (D'Ambrosia RD: Musculoskeletal Dis­ orders : Regional Examination and Differential Diagnosis, 2nd ed . Philadelphia, JB Lippincott, 1986)

FIG. 5·8. {Continued)

A

B FIG. 5·10. Dynamic study of the cervical spine. (A) Flexion view shows marked anterior atlanto-axial subluxati.on. (B) Extension view shows normal atlanto-axial relationships. (Greenfield GB: Radi o logy of Bone Disease, 4th ed, p 856. Philadelphia, JB Lippincott, 1986)

98

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Assessment of Musculoskeletal Disord ers and Concepts of Management

'O ST

~ FIG. 5-1 1. Arthrogram shows a vertical tear (arrow) in the medial meniscus. (D'Ambrosia RD: Musculoskeletal Disor­ ders: Regional Examination and Differential Diagnosis, 2nd ed. Philadelphia, JB Lippincott, 1986)

phy, or myelography, which show only anatomic changes, thermography demonstrates functional changes in circulation consequent to da mage to nerves, ligaments, muscles, or jOints. 68,69,84,94 The pro­ cedure allows one to determine the degree of involve­ men t of, for example, a 11mb in reflex sympathetic dy­ strophy or peripheral vascular disease. It also permits one to note the activity in stress fractures and diseases such as rheumatoid arthritis and to detect soft tissue tumors such as breast cancer. 12,96

ULTRASON OGRAPHY

O ther technologies such as ultrasound have been sug­ gested as h aving p o ten tial for noninvasive measure-

FIG. 5-13. Angiogram shows anterior displacement of the popliteal artery, and a large soft tissue mass showing tumor vessels . (GreenfieldGB : Radiology of Bone Disease, 5th ed . Philadelphia, JB Lippincott, 1990)

men t of spinal mobility57 High frequency sOllnd waves are reflected differently depen ding on the den­ sity of the reflecting tissues. TILey are received and used to form images of portions of the body. Ultra­ sonography is also ideally used for evalua tin g soft tis­ sue masses in the extrem ities. It has been used in the knee and popli teal space to search for possib le p opliteal cysts or vascular aneurysms (see Fig. 5-1 5B ).30

ELECTRODIAGNOSTIC TESTING

FIG. 5-12. Arthrogram of the shoulder in a patient with a rotator cuff tear. The dye can be seen to leak into the sub­ deltoid bursa through the tear. (D 'Ambrosia RD: Muscu­ loskeletal Disorders: Regional Examination and Differential Diagnosis, 2nd' ed . Philadelphia, JB Lippincott, 1986)

The electromyogram (EMG ) is the most com monly done of these tests and is extremely useful in evaluat­ ing nerve root denervation , m llscular d isease, and p e­ ripheral neuropathies, It is a helpful tool in the evalu­ ation of herniated disk syndrome. Radicular pain with motor weakness (motor n erve involvement) is well evaluated by EMG.33 It m ust be remembered, how­

PART I

Basic Concepts and Techniques

99

FIG. 5-14. Computed to­ mography scans show a large soft-tissue mass posterior to the left knee. (Greenfield GB: Radiology of Bone Disease, Stll ed. Philadelphia, JB Lip­ pincott, 1990)

FIG. 5-15. Soft tissue mass in the popliteal regi on. (A ) Lateral roentgenogram, (8 ) ultra­ sound scan, and (C) magnetic resonance imag ing scan throu gh th e popliteal region show extent of th e mass. (D'Ambrosia RD: Musculoskeletal Disorders: Regional Examination and Differential Diagnosis, 2nd ed. Philadelphia, JB Lippincott, 1986)

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Assessment of Musculoskeletal Disorders and Concepts of Management

Nerve conduction studies, measuring the velocity of an artificially induced signal through a peripheral nerve, may help to identify the existence and site of peripheral nerve root compression. 82 A current re­ search interest is utilizing somatosensory evoked po­ tentials (SSEP) to assess the afferent system in order to identify lesions of nerves that fail to provoke motor involvement. L

RI • L

R LABORATORY INVESTIGATIONS

A

Data derived from studies of blood and other material in the laboratory are peculiarly disappointing as diag­ nostic aids in the search for the common causes of musculoskeletal pain.96 In the differential diagnosis of more serious pathologic conditions some studies may be invaluable. Bone-marrow examination may be in­ dicated for the diagnosis of generalized disorders, es­ pecially myeloma and tuberculosis?9

B

CLINICAL DECISION-MAKING AND DATA COLLECTION

.0 L

c

R

L

R

o

FIG. 5-16. Whole body bone scan . rAJ Normal adolescent scan. rB) Abnormal bone scan showing foci of reactive bone formation consistent with metastatic disease of bone. (C) Abnormal bone scan showing patient with metastatic disease of bone. (0) Abnormal bone scan showing reactive bone formation secondary to bone tumor. (Turek SL: Or­ thopaedics: Principles and Their Application, 4th ed. Philadelphia, J8 Lippincott, J 984)

ever, that it takes 21 days for the EMG to record de­ nervation potentials. Electromyography has been used for some time to analyze normal function and pathologic conditions in the spinal musculature. Two distinct patterns of EMG activity have clearly been identified in trunk move­ ments: (1) trunk stabilization and (2) initiation of mo­ tion. 4,63 Different movements recruit muscles in dif­ ferent patterns of activity, but most spinal intrinsic musculature is involved in the initiation of most movement and maintenance of posture 56

Treatment Planning

Having completed all parts of the assessment, the ex­ aminer is now prepared to look at the pertinent sub­ jective and objective facts, note the significant signs and symptoms to determine what is causing the pa­ tient's problems, and design a treatment regimen based on the findings. The reevaluation process should be built into each treatment regimen. Quanti­ fied data obtained within the reevaluation phase help to guide future decisions and to promote cost-effec­ tive treatment. Clinical decision-making involves a series of inter­ related steps that enable the physical therapist to plan an effective treatment compatible with the needs and goals of the patient and members of the health care team. Various systems and labels for describing the intellectual processes involved in clinical decision­ making have been suggested: clinical reasoning,40 clinical problem solving,85 and clinical judgment. 17 The intellectual processes involved in clinical deci­ sion-making are not addressed in this chapter; rather, the purpose of this presentation is to offer a series of considerations to facilitate effective clinical problem solving. A varied spectrum of models to aid clini­ cians in their daily decisions has been devel­ oped.9,19,20,34,40,65,71,74,90,91 ,93,95 Having several mod­ els may allow clinicians to identify which model works best with different types of patients. Often, patients present with a mixture of signs and symptoms that indicates overlapping problems. The novice may recognize the typical feature of an injury

PART I

yet fail to exclude other potentially coexisting disor­ ders that may share or p red ispose to the clinical pre­ sentation. 40 Only the exam iner's knowledg , clinical experi nce, and diagnosis followed by trial treatment can conclu ively delineate the problem. Diagnosis is one of the main decisional acts in clinical rea oning. 23

D

Guides to Correlation an d Interpretation

Correlation and interpreta tion of the examination find ings is one of the mos t critical step in clinical de­ cision-making. This requires th t the clinician give meaning and relevance to the data obtained d uring the examina tion . The diagnostician must often make use of abstract relationships such as proximal-distal, deep- superfi­ cial, and gradual-sudden and not be centered p urely on disjointed lists of signs and symp toms.40 At tim es, when faced with an atypical p roblem, th e deci ion may b an duca ted guess, ince ery fe~ problems are textbook p erfect. The p recise dia gnos i of patients with low back pain, for example, is unknown 'n 80 to 90 p ercent of patien ts.78 Terms such as "disk disease" and "facet jOint syndrome" in most instan es are am­ biguous because it is difficult to measure th ese phe­ nomena or to dearly define their contribu tion to p ain in a gi en patient. 15 Instead, t rms such as "10w back pain with referral into the leg," "low back pain with­ out radiation," and "chronic p ain syndrome" are more well-defined and unambiguous. The Quebec Task Force on Spinal Disorders Classi­ fica tion System (QTFSD) clearly recognized this dilemma of diagnosis. TIley recommended only 11 classifica tions of activity-related spinal disorders. 77 DeRosa an d P orterfield15 have proposed a modified version of the QTFSD classifica tion scheme most rele­ vant to physical therapy diagnosis (see Table 20-1). Judgments relating to the nature and extent of the disorder and the resultant degree of d isability can b e made by correlating the information ob tained d uring a comp rehensive initial p atien t examina tion. With re­ spect to the n ature of the p roblem, it is impor tant to judge whether the disease tate is a "medical" disor­ der or if perhaps operant behav ior patterns have de­ veloped tha t m ay accolU1t for a significant part of the disability. The linician hould con ider wheth r the degree of disability is con istent w ith th e apparent na­ ture and extent of the physical lesi n or whether th e patient is exhib iting disability beha iors that are out of proportion to clinical findings. If th latter is the case, the possibility that the disease state is bein g maintained by external consequ nces tha t have a rein­ forcing effect should be considered. It is essential that such determinations be m ade, since trea bnent di-

Basic Co ncepts and Techniqu es

101

reeted at some physical p athologic process in the pres­ ence of an operant disease state will be futile and can further reinforce "learned" dic:;ability behaviors.

D

The Nature of the Lesion

If it appear that some physical pa thologic process is primarily responsib l for the patien t's disorder, the na ture of the lesion should be estimated as precisely as p ossible. To do so, the informa tion obtained on ex­ amina tion mll t b e correlated w ith knowledge of anatomy, ph ysiology, kinesiology, and pathology in order to identify the involved tissue or tissu s. Some estimate should also be made concerning the ex tent to w hich these tissues are involved . A few common le­ sion m ake up the m ajority of dis rd ers affecting each musculoskeletal tissue. For each of these lesions, there are also consistent key cl in ical findings. In develop ing judgments concerning th natur of common clinical disorders, it is helpful to be aware of the lesions com­ mon to each tissue and how they are manifested clini­ cally. Th e followin g description s are meant t guide the clinician in this respect but are not meant to be all­ inclu sive.

BONE

Fractures are best iden tified in the physician's exami­ nation thro ugh the use of roentgenograms. When ex­ amining a p atient follow ing healing of a fracture, it is im por tant to determine any malunion of bone on in­ spection of bone structure and alignmen t, as this m ay affect eventual fun ctioning of the part. Di loca tions are also best detected through the physician's inter­ pretation of roen tgenogra ms, although dislocations are often obvious on insp ection. ARTICULAR CARTILAGE

Degeneration from wearing due to fa tigue is the most common lesion affecting this tissue. It causes rough­ ening of the norm ally smooth surface layers of carti­ lage. Clinically this is manifested as crepitus on move­ men ts in which opposition of joint surfaces is m aintained by w eight-bearing or other compressive f rces. However, considerable degeneration m ust usually take place before crepitus is detected clini­ cally. A loose bod y is a fragment of articular cartjlage that has broken away and lies free in the joint. This m ay occur in the late stages of cartilage d egeneration or as a result of avascular necr sis of an area f subchon­ dral bone (osteochonruosi ). A loose body becomes symp toma tic when it alters the m echanical function­

102

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Assessment of Musculoskeletal Disorders and Concepts of Management

ing of the joint, usually causing a restriction of move­ ment in a noncapsular pattern (joint block) .

INTRA-ARTICULAR FIBROCARTILAGE The common disorder affecting intra-articular fibro­ cartilaginous disks and menisci is tearing, usually from traumatic injury. Forces sufficient to tear a meniscus or disk in the extremities will usually also cause some strain on the joint capsule to which these structures attach. This causes synovia! inflammation in the acute stage. Thus, movement is likely to be re­ stricted in a capsular pattern. Minor displacement of a tom fragment of fibrocarti­ lage may simply result in "clicking" of the joint on specific movements. Lower extremity joints, namely the knee, may give way when a tag of a tom meniscus is caught between the articular surfaces, suddenly in­ terfering with the normal mechanics of the joint. A major displacement of a tom fragment may grossly interfere with normal mechanics and block joint movement in a noncapsular pattern. The classic example is a "bucket-handle" tear of a medial menis­ cus. When the annular ring of a vertebral disk is tom, secondary neurologic symptoms or signs may result from bulging of the nucleus against adjacent nerve tis­ sue.

JOI NT CAPSULE Fibrosis (see section on capsular tightness) typically occurs with prolonged immobilization of a joint, in as­ sociation with a chronic, low-grade inflammatory process such as occurs with degenerative joint dis­ ease, and with resolution of acute inflammation of the synovium. Joint motion is limited in a capsular pat­ tern, and there is a capsular end feel at the extremes of movement. Synovial inflammation is commonly caused by rheumatoid arthritis, acute trauma to the joint, joint infection, and arthrotomy. Joint motion is limited in a capsular pattern. There is a painful muscle spasm end feel at the points of restriction of movements. Inflammation of the synovium results in an in­ creased production of synovial fluid, causing capsular distention and loss of the capsular laxity necessary for full movement. In the more superficial joints, the artic­ ular sweUing can be observed and palpated. If the ef­ fusion persists after resolution of the synovial inflam­ mation, motion will continue to be limited in a capsular fashion, with a boggy end feel to movement. Patients with capsular pathology typically have some combination of fibrosis, synovial inflammation,

and effusion. Therefore, end feels are not always dis­ tinct. Forces sufficient to sprain a ligament usually cause some capsular disruption as well. Occasionally in traumatic injuries, a particular portion of a joint cap­ sule is ruptured, such as the anterior capsule of the shoulder when the humerus dislocates anteriorly. Synovial inflammation and joint effusion usually fol­ low capsular sprains. In the case of a sprain, the joint-play movement that stresses the involved portion of the capsule will be of normal amplitude. In more severe sprains, the joint may be slightly hypermobile, with a painful muscle­ guarding end feel.

LIGAMENTS The history of a sprain invariably includes a traumatic onset. In the case of a mild sprain, the joint-play movement that stresses the ligament is of norma] am­ plitude and is painful. More severe sprains (partial ruptures) will present as somewhat hypermobile and painful on the associated joint-play test. The synovial lining of the adjacent aspect of the joint capsule will often become inflamed, resulting in capsular effusion in the acute stage. There is usually tenderness over the site of the lesion. The onset of a rupture is also usually traumatic. The associated joint-play movement test will be hypermo­ bile and painless in the chronic stages. Even in the acute stage it is usually painless, since there are no fibers intact from which to elicit pain. If adjacent cap­ sular tissue is also sprained, there may be some pain on stress testing in the acute stage. Capsular effusion often does not occur because fluid leaks through the defect. In the chronic stages the patient may give a history of instability. The joint gives way during activ­ ities that stress it in the direction that the ruptured lig­ ament is supposed to check.

BURSAE The common disorder of bursae is inflammation, sec­ ondary to chronic irritation, infection, gout, or, rarely, acute trauma. Movement of the nearby joint will cause pain or restriction of motion, or both, in a noncapsular pattern. There may be a painful arc of movement as well. In acute bursitis, such as at the shoulder, the end feel to movement is often empty and painful; protec­ tive muscle spasm would only serve to squeeze the in­ flamed structure, increasing the pain. There is usually tenderness over the site of the lesion.

PART I

TENDONS Tendinitis is a minor lesion of tendon tissue involving microscopic tearing and a chronic, low-grade inflam­ matory process. In most cases it is degenerative; the lesion results from tissue fatigue rather than from acute injury. Since progression of the pathologic process will result in a partial tear (macroscopic) or rupture of the tendon, tendinitis should be considered on a continuum with more serious lesions. The key clinical sign associated with tendinitis is a strong but painful resisted test of the involved muscu­ lotendinous structure. There may be pain at the ex­ tremes of the passive movement or movements that stretch the tendon. Seldom is there limitation of move­ ment. There may be palpable tenderness at the site of the lesion or referred tenderness into the related seg­ ment, or both. When the involved part of a tendon is that which passes through a sheath, two other terms are often used: tenosynovitis and tenovaginitis. Tenosynovitis is an inflammation of the synovial lining of a sheath re­ s~lt~g from friction of a roughened tendon gliding withm the sheath. This will present similarly to ten­ dinitis, but there is often pain on activity that pro­ duces movement of the tendon within the sheath. Thus, active movement in the direction or opposite the direction of pull of the tendon may be painful. In tenovaginitis, a tendon gliding within a swollen, thick­ ened sheath causes pain. The clas ic example occurs with rheumatoid arthritis. The clinical signs are essen­ tially the same as those for tenosynovitis. There may be palpable and visible swelling of the tendon sheath . In the case of a partial tendon tear, actual loss of continuity of tendon tissue will cause weak and painful responses to the resisted test for the musculo­ tendinous complex. The passive movement that stretches the tendon may be painful. When the tendon has tom completely, the findings of the related resisted test will be weak and painless. In some cases, for example, rupture of the Achilles tendon, there may be a palpable gap at the site of the rupture.

MUSCLES Muscle strains and ruptures are relatively rare. When they do occur they are invariably the result of acute trauma and are therefore most prevalent in sports· medicine settings. Muscles, being well vascularized and resilient, do not commonly undergo fatigue de­ generation as do tendons. In the case of a strain, a minor tear of muscle fibers ,:,ill result in a strong and painful finding on the re­ sIsted test that stresses the involved muscle. There

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may be pain on full passive stretch of the muscle, as well as palpable tenderness. In the case of a rupture, the associated resisted test results will be weak and painless. A gap may be palpable, or occasionally visi­ ble, at the site of the defect.

NERVES The common conditions affecting nerves are those in which some extrinsic source of pressure results in al­ tered cond uction along some or all of the nerve fibers-the so-called entrapment syndromes. The most common sites of pressure are the points of exit of the lower cervical and lower lumbar spinal nerves from the intervertebral foramina. Here pressure is usually from a protruding disk or projecting osteophyte. There are other common sites of pressure farther out in the periphery that affect the nerves to the extremi­ ties. As indicated in Chapter 4, Pain, pressure tends to alter conduction first along the largest fibers and last along the smallest. Altered nerve conduction is usu­ ally m~nifested subjectively before any objective clini­ cal eVIdence of neurologic dysfunction can be de­ tected. In fact, in the case of the common entrapment syndromes, objective clinical findings are rare, and when present they are usually quite subtle. Often more sophisticated electrodiagnostic tests are re­ quired to objectively detect changes in nerve conduc­ tion. The subjective complaints associated with common entrapment disorders can generally be classified as paresthesia (pins-and-needles), dysesthesia (altered sensation in response to some external stimulus), and p.ain. Although some patients may describe paresthe­ SIa and dysesthesia as painful, pain is usually not a primary comp laint when there is pressure on a nerve farther o ut in the periphery rather than at the nerve­ root level. Thus, patients with thoracic outlet syn­ drome, ulnar nerve palsy, and carpal tunnel syn­ drome, as well as those who have sat too long with the legs crossed, do not complain of pain but of a pins-and-needles sensation. Pain is a common com­ plaint, however, in cases in which there is pressure on a nerve at nerve-root level. With initial pressure, w~en the larger, myelinated, "fast pain" fibers are shmulated, patients describe a sharp, shooting der­ matomic quality of pain. With prolonged or increased pressure, when the larger fibers cease to conduct and the small, unmyelinated C fibers are stimulated, a dull, aching sclerotomic type of pain wiH be per­ ceived. Paresthesia, the primary subjective complaint with pressure farther out 'n the periphery, may occur wi th the onset of pressure or when the pressure is released, or both. For example, a person usually feels little or

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nothing when sitting with legs crossed, with pressure applied to the tibial or peroneal nerve. It is not w1til the person uncrosses the legs, releasing the pressure, that the pins-and-needles sensation of the foot being " asleep" is felt. A similar situation holds true for pres­ sure on the lower cord of the brachial plexus from de­ pression of the shoulder girdle; the patient invariably describes the onset of pins-and-needles in the early morning hours (lor 2 AM) some time after the pres­ sure is released. It seems that the interval between the rel ease of pressure and the onset of paresthesia is in some way proportional to the length of time during which the pressure was appbed. In other common nerve problems, the onset of symptoms occurs when the pressure is applied. For example, many patients with carpal tunnel syndrome describe paresthesia felt primarily during fine finger movements; the tension on the finger flexor tendons produces pressure on the median nerve sufficient to cause symptoms. Similarly, when a person sits or lies with pressure over the ulnar groove, pins-and-needles are usually felt in the ulnar side of the hand while the pressure is applied, and cease to be felt after the pressure is released. As mentioned, more objective findi'ngs associated with common nerve-pressure disorders are usually very subtle when present. They are more common with nerve-root pressure from a disk protrusion than with more peripheral entrapment syndromes. The earliest evidence of decreased conduction will be re­ lated to those functions mediated by the largest myeIi­ nated fibers, since these fibers are most sensitive to pressure. Therefore, reduced vibration sense is often the earliest deficit detected by clinical testing. With in­ creased or prolonged pressure, diminished deep-ten­ don reflexes may be noted, followed by reduced mus­ cle strength. Finally, there is reduced sensation, first to light touch, then to noxious stimulation. Because of overlapping derma tomes and myotomes, and because each muscle and skin area typically receives innerva­ tion from more than one segment, even completely severing a nerve root will usually cause only a minor deficit.

D

Extent of the Lesion

"When clinicians speak of acute and chronic lesions, it is often unclear whether they are referring to the length of time that the pathologic process has existed, the severity of the disorder, or the nature of the in­ flammatory process. There are relatively few consis­ tent clinical findings related to either the duration or the severity of common musculoskeletal problems. However, there are certain symptoms and signs that are consistently present with acute inflammatory processes and others that are pathognomonic of le­

sions in which a more chronic inflammatory state ex­ ists. Acute inflammation is that stage or type of inflam­ matory process in which hyperemia, increased capil­ lary permeability with protein and plasma leakage, and an influx of granulocytes and other defense cells take place. Chronic inflammation is characterized by an attempt at repair, with increased numbers of fibro­ cytes and other "tissue-building" cells, and the pres­ ence of granula tion tissue. An acute lesion is charac­ terized by the following clinical findings: 1. Pain is relatively constant. 2. On passive range of motion of the related joint, there is a musd e spasm end feel or an empty end feel to movement. 3. Pain is likely to be referred over a relatively diffuse area of the related segment. 4. There may be a measurable increase in skin tem­ perature over the site of the lesion. S. There is often difficulty in falling asleep or diffi­ culty in remaining asleep, or both.

In the presence of cmonic lesions, the patient is likely to present with the following symptoms or signs: 1. Pain is increased by specific activities and relieved by rest. 2. On passive movement of the related joint, there is no muscle spasm or empty end feel. 3. Pain is likely to be felt over a relatively localized area, close to the site of the lesion, although often not directly over the site of the lesion. 4. There is little or no temperature elevation over the involved part. S. Unless the lesion involves the shoulder or hip, there is little or no difficulty in sleeping.

D

Setting Goals and Priorities

Following the diagnosis, the clinician establishes short-term and long-term goals of treatment. Deter­ mining appropriate treatment goals assists the thera­ pist in planning, prioritizing, and measuring the effec­ tiveness of treatment. The goals are deriv ed from the patient's symptom(s), signs, and diagnosis and from the patient's personal, vocational, and social goals. In­ volvement of the patient is critical in achieving patient compliance.1 6 Information obtained from the patient should be integrated with the subjective and objective assessment data. A goal statement should be gener­ ated with the patient's full cooperation and under­ standing. Long-term goals id.entify the functional behaviors to be attained by the patient by the end of the treat­ ment program. Once long-term goals have been estab­

PART I lished, the next step is to determine the component skills that will be needed to attain these goals. Short­ term goals identify the progressive functional levels to be attained by the patient at specific intervals within the projected period of treatment. 9 The clinician should determine the appropriate sequence of sub­ skills and prioritize them accordingly. The patient ad­ vances through the sequence of short-term goals lmti] he achieves the final end point of long-term goals. The goals and diagnosis direct treatment.

CONCEPTS OF MANAGEMENT Only those procedures that may not be well under­ stood or are new to most professional training pro­ grams are discussed in this section. It is assumed that the reader is familiar with many basic therapeutic procedures and modalities, such as therapeutic exer­ cise, use of assistive devices, and electrotherapy. The application of these forms of treatment, in conjunction with traditional therapies, to specific pathologic proc­ esses affecting the various extremity regions is dis­ cussed in Parts Two and Three.

o

Rehabilitation

The correlation and interpretation of findings from a comprehensive initial patient examination is the basis for developing a treatment plan. During the initial ex­ amination clinicians seek to elicit information that re­ lates to the nature and extent of the pathologic process as weU as to the degree of disability. The choice of therapeutic procedures depends on this information. The primary considerations are the site of the lesion and the type of tissue involved. Once the nature of the lesion has been determined, there is often a tendency to direct treatment primarily at the site of the lesion with the expectation that resolving the pathologic process will alleviate any resultant physical dysfunc­ tion, and will in turn restore the patient to a normal health state. There are many potential fallacies to this approach that make it unsuitable as a reliable treatment model. First, such an approach ignores the secondary effects that a lesion involving a particular structure may have on the normal functioning of other related structures. It calls for treatment of "anatomic structures" rather than "physiologic units." By considering the synovial joints as the basic physiologic-rather than ana­ tomic-unit of the musculoskeletal system, one is bet­ ter prepared to respect the interactions of the various components of this system under normal and abnor­ mal conditions. This is essential, since an alteration in one component of a functional unit often leads to dys­

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function of other components of the same or neigh­ boring units, which may act to maintain the primary pathologic condition, predispose to recurrence, or re­ sult in secondary disease. Thus, even in the case of rel­ atively localized lesions, clinicians must respect such interactions and be prepared to deal with them thera­ peutically. For example, a painful lesion of the supraspinatus tendon tends to result in reflex inhibition of the supraspinatus and other rotator cuff muscles. This will predispose to subacromial impingement from ab­ normal movement of the head of the humerus during elevation activities, which may further traumatize the supraspinatus tendon as well as the subdeltoid bursa. Also, muscles such as the deltoid and the trapezius may reflexively contract abnormally during move­ ment of the arm, secondary to abnormal afferent input from the site of the lesion to the lower cervical seg­ ments . This may further interfere with normal joint mechanics at the shoulder as well as at the neck, to which the trapezius attaches. It should be clear that ef­ fective treatment of this problem involves more than resolution of the pathologic process affecting the ten­ don. The rotator cuff muscles must, at some time, be strengthened; excessive elevation of the arm must be temporarily avoided; and relaxation of abnormally contracting muscles should be promoted. If one were to treat only the lesion of the tendon, it is likely that treatment would be ineffective or take much longer than necessary to be effective. Continued subacromial impingement would enhance the chance of recur­ rence. The patient would also be predisposed to the development of a coexistent cervical lesion from in­ creased stresses to the neck due to abnormal muscle activity. Second, an approach in which treatment is aimed exclusively at some discrete pathologic process tends to ignore etiologic considerations. Temporary amelio­ ration may ensue without true resolution of the prob­ lem. Unless underlying causes, such as biomechanical abnormalities, are recognized and dealt with, chronic recurrent problems can be expected. Thus, a patient with chondromalacia patellae resulting from abnor­ mal foot pronation may temporarily do very well on a program of reduced activity and strengthening of the vastus medialis muscle. However, the patient is likely to experience similar problems with the resumption of normal activity levels unless the alignment of the foot and leg is corrected. Similarly, the patient with trochanteric bursitis caused by a tight iliotibial band usually responds well to ultrasound over the site of the lesion, but if extensibility of the iliotibial band is not incr'e ased, relief will be shorHived. The clinician should implement the concept that prevention is the ultimate cure by attempting to identify etiologic fac­ tors and by employing appropriate measures to deal

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with them. This should be a m ajor consideration in fa­ tigue disorders that are chronic, since they tend to be seU-resolving once the cause of the abnormal stresses is corrected. (See the outlined treatment of chronic disorders that follows.) Third, and most important, when treatment is di­ rected only at a physical disorder, the psychosocial implications of the problem are not given due respect. Comprehensive rehabilitation requires restoration of an optimal level of function. Although a physical dis­ order may have been the original cause of physical dysfunction or other "disease behaviors" such as com­ plaints of pain, there are often other factors that may serve to maintain or inhibit the disability behaviors. Such "motivational factors" m ay eventually assume a greater influence on the disability state than the origi­ naf pathology (see Fig. 5-1). These factors must be rec­ ognized since they often determine whether treatment is successful, whether an optimal level of fWlCtion is restored, and whether disability behaviors (pain com­ plaints, physical dysfunction, and functional depen­ dence) are resolved. If being d isabled carries exces­ sively negative consequences for the patient, such as often occurs in sports-medicine settings, these conse­ quences will strongly inhibit the disab ility state. As a result, the patient often attempts to d o more than is appropriate and imposes deleterious effects on the le­ sion. This may counteract any beneficial effects of other treatment procedures. On the other hand, if the patient stands to gain in some way from being dis­ abled, such as time away from work, financial com­ pensation, or \·v ekomed dependence, the potential for gain may have a significant reinforcing effect on the disability state. The patient is not likely to improve in spite of otherwise effective treatment of the p athologic condition. In both of these situations, the psychosocial motivational influences are likely to have a greater ef­ fect on the disease state than the physical process it­ self. Unless these inBuences are d ealt with, the patient cannot be truly rehabilitated. To estimate the relative influence of such factors, the clinician must determine whether the degree of disability is consistent with the symptoms and signs manif ested by the disease. If there are inconsistencies, significant psychosocial in­ fluences affecting the nature of the disability state should be suspected.

D Treatment of Patients with Physical Disorders Although the principle of "treating the patient, not the disease" has become somewhat of a cliche, its applica­ tion to patients with common musculoskeletal disor­ ders is too often overlooked. The first and foremost

consideration when devising a therapeutic program should always be how the patient's ability to function normally has been compromised. One must ask, what conditions are responsible for the dysfunction and are these conditions reversible? If they are reversible, what would be the most appropriate means of inter­ vening therapeutically so as to affect these conditions? If the conditions at fault appear irreversible, what can be done to optimize residual function? And finally, what can be done to prevent recurrences, secondary problems, and progression of the existing disorder? With such an approach, therapy is disability-oriented rather than pathology-oriented. The primary goal of management becomes restoration of an optimal level of functioning rather than simply resolution of some pathologic process. Resolution of a physical disorder does not necessarily lead to restoration of function, re­ duction in pain behavior, or other necessary signs of improvement. In the case of many common musculoskeletal disor­ ders, in which the degree of disability appears to be consistent with the nature and extent of the lesion, physical treatment will constitute a major component of the therapeutic program. When this is the case, clin­ icians must choose, among the various forms of inter­ vention at their disposa l, the procedures and modali­ ties most appropriate for the management of the specific disorder. Treatment must be individualized for each patient and according to the nature and ex­ tent of the pathologic process. The tendency to incor­ porate "standardized" programs of exercises and other treatments, usually for the sake of efficiency, should be avoided. The controversies over and mis­ conceptions about so many forms of treatment (e.g., massage, manipulation, traction, and certain exer­ cises) stem largely from their having been advocated or misconstrued as panaceas for disorders affecting certain regions. CLASSIFYING PATHOLOGIES: ACUTE VERSUS CHRONIC

As a preface to discussing specific types of treatments and their respective applications, some general con­ cepts that are related to the overall approach to physi­ cal treatment are considered. As mentioned previ­ ously, approaches to treating a physical disorder should depend on its nature and extent. The two com­ mon terms used clinically to classify pathologic processes according to their nature and extent are acute and chronic. These terms should not be used to refer to the severity or duration of a disorder, since when used in these contexts they have little relation­ ship to symptoms and signs. A patient with a rela­ tively severe lesion such as a ligamentous rupture, for

PART I example, may present with much iess pain and dys­ function than one who has sustained a minor sprain. It is well known, even to those outside the health care professions, that a sprained ankle may be more painful and disabling shortly after injury than a frac­ tured ankle. With respect to duration, disorders of fairly recent onset often present with subtle symptoms and signs when compared with certain long-standing problems. If a clinician has two patients, one with re­ cent onset of aching in the shoulder but no gross loss of function and the other with long-standing severe pain and dysfunction, which condition is acute and which is chronic? The terms acute and chronic do have some signifi­ cance when used to refer to the nature of the symp­ toms and signs with which a patient presents, as dif­ ferentiated earlier in this chapter. This is because symptoms and signs reflect the nature of various dis­ orders and, more specifically, they tend to reflect the nature of the inflammation or repair process that ac­ companies any physical lesion. Because these symp­ tom-sign complexes do relate to the nature of patho­ logic processes, they are used here as a basis for a discussion of general approaches to management. The following scheme is based on the definitions of acute and chronic.

TREATMENT OF ACUTE AND CHRONIC DISORDERS I. General concepts

A. Consider the nature and extent of the disorder, whether acute or chronic. 1. The terms are sometimes used to refer to duration of the problem and not to symp­ toms and signs. 2. They should be used to refer to the nature of the inflammatory process. a. Acute hyperemic phase i. Pain is felt at rest and aggravated by activity. ii. Pain is felt over a relatively diffuse area and may be referred into any or all of the related segments (scle­ rotome). . iii. Passive movement of related joints when limited is restricted by pain, muscle guarding, or both. iv. The skin temperature over the site of the lesion is often elevated. b. Chronic/ repara tive phase i. There is no pain at rest and pain is felt only with specific activities. ii. Pain is felt over a fairly localized

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area, close to the site of the lesion (often not directly over the site of the lesion, however). iii. Movement of related joints, when limited, is restricted by soft-tissue tightness; pain is felt only at the ex­ tremes of movement or through a small arc of movement 3. The terms are not useful in describing the severity of the lesion. For example, a pa­ tient with a complete rupture of a ligament may present with less pain and disability and with fewer cardinal inflammatory signs than a person with only a partial tear of a ligament. B. Assess, control, and monitor the patient's func­

tional status. 1. Assess the degree of disability from find­ ings of the history and physical examina­ tion. Compare disease (injury) status with health (normal) status, and compare with other symptoms and signs. a. Is the degree of disability consistent with the apparent nature and extent of the disorder? This yields important in­ formation relating to the patient's moti­ vational status and is a major consider­ ation in treatment planning. i. The "well-motivated" patient is one for whom the consequences of injury (disability) are punishing. For example, they imply time away from desirable situations or possibility of financial loss. It can be presumed that resolution of the disease will lead to resolution of the disability state. A medical ap­ proach to treatment is appropriate. ii. The "poorly motivated" patient is one for whom the consequences of disability are reinforcing. For exam­ ple, they offer time away from un­ desirable situations or the possibil­ ity of financial gain. It cannot be presumed that treatment of the disease will result in resolution of the disability state. Rehabilitation must include attempts to alter the consequences to disability. An op­ erant approach must be incorpo­ rated into the treatment program. b. Record and use information as a base­ line by which to judge progress. 2. Control functional status (see below under techniques of management).

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a. In appropriate activities must be re­ stricted to p reven t prolongation or re­ currence of the d isord er . b. Appropriate activities m ust be resumed as the p athologic process resolves. This is the ultimate goal ofmanagement. 3. Monitor functional status to judge im­

provement. The patient is not rehabilitated until an optimal level of functi on is re­ stored, regardless of the sta te of the lesion. II. Treatment of acute inflammatory disorders (traumatic) The p rimary goal is to promote progression to a chronic s tate w hile minimizing dysfunction. A. Physiologic intervention to control the acute in­

flammatory response 1. Ice--to red uce blood fl ow 2. Com pression-to p revent and reduce swelling 3. Elevation-to p reven t and reduce swelling and hyperemia 4. Relaxa tion-to reduce pain and muscle spasm

B. Avoidance and prevention of continued trauma and irritation by reducing loading of the pari' 1. Braces, slings, splints, assistive devices,

strapping a. Lower extremity--Crutches or canes to red uce forces of w eight-bea ring; sp lints, braces, or strapping to reduce fo rces of movement b. Upper extremity-Slings to reduce forces o f gravity and , therefore, p os­ tural muscle tone; splints, braces, or trapping to red uce the forces imposed by movement c. Spine- Passive support with collar or corset if ind icated 2. Control of activities causing undesirable loading of the p art. This requires careful, well-understood instructions to the patient. C. Maintaining optimal levels of junction and pre­

venting unnecessanj dysfunction 1. Isometric resistive exercises to maintain m uscle function, while avoiding undesir­ able m ovement of the p art 2. In acute nuclear prolapse, isom etric activi­ ties (e.g., pelvic tilt exercises, straining, and Val salva maneuvers) mu st be avoided. 3. With respect to the spi ne: a. Rest is interspersed with periods of controUed activity. b. Posi tions that increase intradiskal p res­ sure should be avoided (e.g., acute disk protrusions). 4. Gentle active or passive m ovement (when

approp riate according to the nature of the d isorder) to avoid pain and muscle guard­ ing III. Treatment of chronic disorders A. Ca usative factors. The majority of disorders seen in m ost clinical settings have two pri­ ma ry causes: 1. Abnormal modeling of tissue d uring reso­ lution of an acu te d isorder . The following are examp les: a. Malmuon of fractures resulting in a challge in the direction or magnitude of forces acting on the part during use (in­ creased s tress) b. Abnormalities in collagen matu ration or p roduction (scarring, fib rosis, adhe­ sions). An excess amount of collagen may be p roduced, and that which is p roduced may n ot be oriented along the normal lines of s tress. Abnormal collagen cross-links are formed, and the tissue may adhere to adjacen t struc­ tures. The net result is reduced extensi­ bility, and therefore reduced capacity to a ttenuate energy by deforming when sh:essed. 2. Fatigue response of tiss ues. The two types of response are a. Tissue breakd own-the rate of attrition exceeds the rate of repair (e.g., stress fractures, cartilage degeneration). The tissue becomes "weaker" and begins to yield under loading conditions. It oc­ curs with ntild to mod era tely increased stress levels in tissues with low regen­ era tive capacity (e.g., articular carti­ lage); with higher stress levels in other tissues (e.g., tendon, bone); under con­ d itions of altered tissue metabolism (e.g. , h ypovascularity). b. Tissue hypertrophy (e. g., fibrosis and sclerosis) occurs w ith m ild to m oder­ ately increased stress levels in tissues w ith good regenerative/ repair capac­ ity, acting over a prolonged p eriod of time. Tissue becomes stiffer, with re­ duced energy attenuation capacity. In­ di vidual fi bers or b'abeculae begin to yield under loading conditions, result­ ing in low-grade inflammation, pain, increased tiss ue p rod uction, and so on. B. Treatment planning 1. Red uce stresses to involved tissue over

time. a. Reduce magnitude of loading (control of activities).

PARi I Basic Concepts and Techniques b. Reduce magnitude of stresses by alter­ ing direction or magnitude of forces acting on the part through control of activities, use of protective/assistive devices, and use of orthotic devices to control position of the part. c. Increase surface area of loading (e.g., foot orthosis). d. Provide for external energy attenuation (e.g., pads, helmets, cushioned heels). 2. Increase energy-attenuating capacity of the part. a. Increase compensatory muscle strength / activity with strengthening exercises; increase neuromuscular facil­ itative (afferent) input (e.g., taping, co­ ordination training). b. Increase tissue extensibility (ability to deform without loss of structural in­ tegrity): i. Active stretching ii. Passive stretching, using passive range-of~motion stretching for musculotendinous tightness and specific joint mobilization for cap­ suloligamentous tightness iii. Use of ultrasound in conjunction with stretch iv. Use of transverse friction massage to increase interfiber mobility and to prevent or reduce fibrous adhe­ sion without longitudinally stress­ ing the tissue v. Soft tissue manipulations directed at muscle, ligaments, and fascial layers to restore mobility and ex­ tensibility c. Promote increase in structural integrity of the part (increased "strength"). This requires tissue hypertrophy, without loss of extensibility from overproduc­ tion of immature collagenous tissue, and so on, and maturation of collagen fiber orientation along normal lines of stress and development of appropriate cross-links. The necessary stimulus is stress to the part. This means gradual, con­ trolled return to participation in high­ stress-level activities (training). 3. Resumption of optimal activity levels and prevention of recurrence. Judgments are based on: a. Clinical evidence of having accom­ plished above objectives b. Awareness of the nature of stresses im-

109

posed by various activities and an esti­ mate of the capacity of th p art to with­ stand those stresses. This requires bio­ mechanical assessment and analysis and familiarity with research related to biomechanical properties of muscu­ loskeletal tissues under various condi­ tions of loading and healing. c. Extrinsic "motivational " factors-the consequences of disability for the pa­ tient Patients with true chronic pain syndrome should not be treated with the emphasis on pain modulation. Whereas acute pain bears a relatively straightforward relationship to peripheral stimulus, nocic p tion, and tissue damage, chronic pain disability becomes in­ creasingly dissociated from the or'ginal physical basis and there may be little if any evidence of any remain­ ing nociceptive stimulus. Emphasis should focus on functional restoration which utilizes sp orts medicine principles. This approach emphasizes the recognition, through objective quantitative assessment of physical function, of the loss of physical capacity that accom­ panies disuse (termed the deconditioning syndrome).57 The focus should be on augmenting function and on increasing physical activity, mobility, strength, en­ durance, and cardiovascular improvement.

o

Evaluation of Treatment Program

The last step is ongoing and involves continuous reevaluation of the patient and efficacy of treatment. Recognition of the original problems that have been solved and those that need further attention must be made. New short-term goals should be established and appropriate procedures selected. In determining and implementing revised goa[s and related treatment and criteria, the clinician is again at the probJem-solv­ ing stages of determining and administering treat­ ment. When long-term goals are reached or are close to being reached, discharge planning and plan for fol­ low-up care (when indicated) can b initiated. The overall success of the treatment plan is dependent on the therapist's clinical decision-making skills and on engaging the patient's cooperation and motivation. 65

REFERENCES 1. Ag.u,,,a l A I Lloyd KN, Dovey P: n1e dermography of th e spine and sJcroiliac joints in spond ylitis. Rheu m Phys Med 10:349-355. 1970 2. Ap riU C: Radiolgic im' ging tCCh.liqu 01 the spin e. fn Hochseh uler SH. Cotler HB. Gu yer RD (ed5): Rehabilitation 01 the pine. pp 79-111. St Louis . V Mosby. 1993 3. B-240. Philadelphi., Lea & l'eb iger, 1988 58. McKenz ie RA: The Lumbar Spine: Mechanicil l DiagnOSis and Therapy. Waikana e, New Lea limd , Sp inal Pub lica tions/ 198'1 59. McKenz.ie RA: The Cervica l and Thoracic Sp ine: Mech(lnica l DiagnOSiS J nd Thc rnpy. \'Va ikanae, New ZeaJMd, Spi !1.11 Publications, 1990 60. McNeil BJ: Va llie o f bone scannin g in neoplastic d i..coca!'C. Semin N ucl Med 4:277, 1984 61. Menne ll JM; Back Pain: Diagno5;is nnd Tre..l tment Using M1:u upu lativ e Techniques. Boston. l.itlle, Bro"",, & Co, 1960 62. M itchel l n. Jr, Moran PS, Pru'ZZ.o NA : An EVol lllan on Jn d Tr~() tme.n t ~1mlu a l of Os­ teopathi. Muscle En.rgy Proced ures. Valley Park, MO, Mitchell, Moran, and Pruzz o Associates, 1979 63. Morris J, Benne r G, Lucas D: An electromyogra phi c s tudy of the intrill5ic muscles of the back in man . ) An" t 196:509-520, 1962 64. N yberg R: Cl i.n irnl i.lSSessm (![1 t of th e l o~..t b ack: Active movemen t and p al pation tes t­ ing. 1n l3asmajian JV, Nyberg R (cds): Ra tiona l Man lk'l.l Ther,lpies, pp 97- 140. Balti­ more, Williams & Wil kins, 1993 65. O'Su lli Vilo 56: Cl in iC'llt d ecbion maki ng: PI (tn ning e ffecti ve treatm ents. In O'Sulli vPY. t Louis, C V Mo by, 1990

H o p penfeld 5: Phys ical Exam ination o f the Spine a nd Extrem ities . New York . App le ton­

Cenlu rv-Crof'ts, 1976

KJ Jtet'lbom FM : Ihe Spine: Basic Evalua tion a nd Mobili za ti on Techruq ucs , 2nd t;:d. Os lo~

Olaf 'o rl is Bokha nd I, 1993

CLIN ICAL DECISION-MAKING AN D DATA CO LLECTION Boiss onall[t we (cd): Exam ination in Ph ysical ThcrJPy Practice: Screen ing for Medica l

Disease. New York, Ch u ~ hil1 Livingstone, 1991

Feinstein A: Scientific methodology in cljnical med icine, Pdf t T: Introduc ti on, principles

and concepts. Ann Intern 1ed 6 1:564-579, J964

Feinstein A: Scienti IC meth odo l og~ in clinical medicine, Part IV: Acqui sition of d in icil l

data. 11 Jntem Mc've

(c'd): Modern Manual TIle rapy of the Ve rtebral Column, pp 640-655. Edinburg h,

Churchill Livingstone, 1986

129. Lt'>"$ter M ~ : Spina l tab ili za tion atld com pl ia nce u tilizing th e the.rapeutic ball. In:

Proceed ings, 5th In te rna tional Conference of the ln tc mJtional Federntio n of Or­

th opaedic Manipulative TherapiSts, p 159. Vail, CO, 1992

130. Lewit K: Manuelle fherapie (i.m Rahmen de r artli chen Rt?hnbiJitation) . Leipzig, l A

Barth, 1973

131. Lewi t K: Manipulative Thera py in Rehd pain ::;yndromes responsive to simp le therercises ior [he A uto nomic Nervolls System. Sp ringfield, Charles C

Thomas, 1981

182. Polen-no F, P;)njabi ~.f~.1: Ro le of trunk ro tdtion endu rance exercise in Cu Bed back

treatment. Arch Phy. Med R"h.,b 67:620, 1986

183. Pope. M, Punjabi M: l3iomechan ic"d Rchabil

67(6):375-379, 198"

~kG ui ghan FJ, _Un. W ,McDona ld 'A~ (cds): n-ess an d Tensi on Control. 2nd ed . i CW

Yo rk, Plenum Press, 1984

Muse M; Stress-related post traumatic chronic pain synd rome: Behav ior, 1984

r,

r.

MANAGEMENT OF STRESS

BIOFEEDBACK Asfour 55, Khali l TM, Waly SM, et al: Bio feed ba k in ba ck mu scle s tren gthe ning. Spine

15:510-513, 1990

Biedermann H), Ing lis J, Monga TN, Shanks GL Diffe.re.ntial treatment res ponses on so­

matic pain ind icd tors i;l fter EMG bio reed a k tra inin g in back pain piltien ts. lJ1t J P"y­

chosom 36:5}-57, 1989

Blanch" rd EB, Ahles TA: Bioieedback therapy. tn Bonica Loese r JD, Cha p man R, e l al

(eds): Th e t" nagem en l o f I\ l in, 2nd ed, pp 1722- 1732. Phllad elphia, Lea & Fcbiger,

1990

Blancha rd ES, Appleba um KA, Guam ieri p. et 01: A control led evaluation of th~ rma l

biofeedback combin ed w ith cognitive therapy in the treatmen t of v(:I scular heada ches. I

Consult O in Psychol 58'216-224, 1990

BI.mchard EB, [ ichobon NL, RadnH. Ct , et al: The role of home practice of thermal

biofeed back. J Co n. u lt Chn PgychoI 59:507-5 12, 1991

Blanchr :e ~s

Jr

of the digit, semiflexed, in his remaining fin­ gers. This must be performed with caution. M- A pronation or supination of the distal end of the bone is produced by the operator's more distal hand. Supination is a joint-play movement (conjunct ro­ tation) necessary for flexion, especially at the in­ terphalangeal joints. Pronation occurs during ex­ tension. Note: The same techniques may be used at the carpometacarpal joint of the thumb. As for their specific uses in this case, consider the con­ vex-concave rule and how it applies to this sellar joint.

,d

J­

a­ ~d

>y is to

In

ar ~al

at

In

lat .so

lC­

ne ~nt

REFERENCES 1. American Academy of Orthopedic Surgeons: Symposium on Tendon Surgery in the Hand. Philadelphia. CV Mosby. 1975 2. American Society for Surgery of the Hand: The Hand: Examination and diagnosis. Aurora, CO: The Society, 1978 3. American Society for Surgery of the Hand: The Hand: Examination and diagnosis. New '{ark, Churchill Livingstone, 1983 4. Bajelis 0: Myofascial release, IV: Management of sports injuries. Presented at a

course on physical therapy, management of the extremities, Seattle, July 1986

5. Barcroft H, Edholm OG: The effect of temperature on blood flow and deep tempera­ ture in the human forearm. J Physiol102:5-20, 1943 6. Baxter PL, Ballard MS: Evaluation of the hand by functional tests. In Hunter ]M, Schneider LH, Mackin EJ, Bell JA (cds): Rehabilitation of the Hand. St. Louis, CV Mosby, 1984 7. Becker AH: Traction for knee-flexion contractures. Phys Ther 59: I114, 1979 8. Boyes jH (ed): Bunnell's Surgery olthe Hand. Philadelphia, jB Lippincott. 1970 9. Brand PW: Clinical Mechanics of the Hand. St. Louis, CV Mosby, 1985 10. Brand PW: Hand rehabilitation management by objectives. In Hunter JM, Schneider LH. Mackin Ej, Bell jA (eds): Rehabilitation of the Hand. St. Louis. CV Mosby. 1978 11. Brown CP, McGrouther DA: The excursion of the tendon of the flexor pollicis longus and its relation to dynamic splintage. J Hand Surg 9A:787-791, 1984 12. Bunnell S: Ischaemic contracture, local, in the hand. J Bone Joint Surg 35A:88-101, 1953 13. Cailliet R: Hand Pain and Impairment, 4th ed. Philadelphia, FA Davis, 1994 14. Cailliet R: Reflex sympathetic referred pain. In Shoulder Pain, 2nd cd. Philadelphia, FA Davis. 1991:108-124 15. Cain HD, Liebgold HB: Compressive centripetal wrapping technique for reduction of edema. Arch Phys Med 48:420-423. 1967 16. Campbell-Reid DA, McGrouther DA: Surgery of the Thumb. Boston, Butterworths, 1986 17. Carter PR: Common Hand Injuries and Infections: A Practical Approach to Early Treatment. Philadelphia, WB Saunders, 1983

Clinical Applications-Peripheral Joints

283

18. Cornacchia M: Considerazioni sulla meccanica articolare del pollice. Chir Organi Mov 33:137-153.1949 19. Corrigan B, Maitland GD: Practical Orthopaedic Medicine. Boston, Butterworths, 1985 20. Cyriax J: Textbook of Orthopaedic Medicine, vol 1, 11th ed. Baltimore, Williams & Wilkins. 1984:136-137 21. Cyriax J: Textbook of Orthopaedic Medicine, vol 2, 5th ed. Baltimore, Williams & Wilkins. 1969:333-338 22. De Palma F: The M,magement of Fractures and Dislocations: An Atlas, 2nd ed. Philadelphia. WB Sounders. 1970 23. Dell PC, Brushart TM, Smith RT: Treatment of trapeziometacarpal arthritis. Results of resection arthroplasty. J Hand Surg 5:243-249, 1978 24. Dellon AL: Evaluation of Sensibility and Re--Education of Sensation in the Hand Baltimore, Williams & Wilkins, 1981 25. deTakas G: Nature of painful vasodilatation in causalgic states. Arch Neur Psychiat 50:318-326. 1943 26. Eaton RG: Joint Injuries of the Hand. Springfield, m., Charles C. Thomas, 1971 27. Eaton RG: Replacement of the trapezium for arthritis of the basal articulation. A new technique with stabilization by tenodesis. J Bone Joint Surg 61A:76-83, 1979 28. Ebner M: Connective Tissue Manipulation, Therapy and Therapeutic Application. Malabar, FL, Robert Knieger, 1985 29. Evjenth 0, Hamberg J: Muscle Stretching in Manual Therapy: A Clinical Manual~ The Extremities, vol 1. AUta, Sweden, Alfta Rehab FDrleg, 1984 30. Ferlic DC, Busbee GA, Clayton ML: Degenerative arthritis of the carpometacarpal joint of the thumb. A clinical follow-up of 11 Niebauer prostheses. J Hand Surg 2:212-215. 1977 31. Fess EE, Harmon KS, Strockland JW, et al: Evaluation of the hand by objective mea­ surement. Tn Hunter JM, Schneider LH, Markin EJ, Bell JA (eds): Rehabilitation of the Hand. St. Louis. CV Mosby. 1978 32. Fess EE, Moran CA: Clinical Assessment Recommendations. Aurora, CO, American Society of Hand Therapists, 1981 33. Flatt AE, Fischer GW: Stability during tlexion and extension at the MCP joints. In La Main Rheumatoide, Monographie du GEM. Paris, L'Expansion Scientifique Franitaise,1967:51---tJ1 34. Flalt AE: The Pathomechanics of Ulnar Drift. Final Report. Washington DC, Depart­ ment of Health, Education, and Welfare, 1971 35. Flax H], Miller RV, Horvath SM: Alterations in peripheral circuJalion and tissue temperature fotlowing local application of short-wave diathermy. Arch Phys Med Rehabil 3:630-u37. 1949 36. Gersten JW, Wakin KG, Herrick JF, Krusen FH: The effect of microwave diathermy on the peripheral circulation and on tissue temperature in man. Arch Phys Med Re­ habiI30:7-25. 1949 37. Gen'is WH: A review of excision of the trapezium for osteoarthritis of the tri.1peziometacarpal joint after 25 years. J Bone Joint Surg 55B:56~57, 1973 38. Glazer RM: Rehabilitation. In Happenstall RB (ed): Fracture Treatment and Healing. Philadelphia. WB Saunders. 1980 39. Grant JCB, Basmajian JV: Grant's Method of Anatomy, 9th ed. Baltimore, Williams & Wilkins. 1991 40. Hakstian RW, Tubiana R: Ulnar deviation of the fingers. The role of joint structure and function. J Bone Joint Surg 49A:299-316, 1967 41. Haugen P, Stern-Knudsen 0: The effect of a small stretch on latency relaxation and the short-range elastic stiffness in isoltlted frog muscle fibres. Acta Physiol Scand 112:121-128.1981 42. Hazelton Ff, Smidt GL, Flatt AE: The influence of wrist position on the force pro­ duced by the finger flexors. J Biomech 8:301-306,1975 43. Hollinshead WH: Anatomy for Surgeons, vol 3: The Back and Limbs, 4th ed. New York. Harper Medical, 1985 44. Hoppenfeld S: Physical Examination of the Spine and Extremities. New York, Ap­ pleton-Century-Crofts, 1976 45. Hunter JM, Schneider LH, Mackin EJ, et a1 (eds): Rehabilitation of the Hand. St. Louis, CV Mosby, 1984 46. Jackman RV: Device to stretch the Achilles tendon. J Am Phys Ther Assoc 43:729, 1963 47. Jebson RH, Tilylor N, Trieschman RB, et at: An objective and standardized test of hand function. Arch Phys Med RehabiI5:311-319. 1969 48. Jenkins RB, Little RW: A constitutive equation for parallel-fibered clastic tissue. J Biomech 7:397-402. 1974 49. Johnson G: Functional orthopedics IT: Advanced techniques of soft-tissue mobiliza­ tion for evaluation and treatment of the extremities and trunk. Presented at a course at the Institute of Physical Arts, San Francisco, 1985 50. Johnson RK, Shrewsbury MM: The pronator quadratus in motions and in stabiliza­ tion of the radius and ulna at the distal radioulnar joint. J Hand Surg 1:205-209, 1976 51. Kaltenborn FM: Mobilization of the Extremity Joints, 3rd ed. Oslo, Olaf Norlis Bokhandel. 1980 52. Kapandji IA: Biomechanics of the interphalangeal joint of the thumb. [n Tubiana R (ed): The Hand. vol I. Philadelphia. WB Saunders. 1981 53. Kapandji IA: The Physiology of the Joints, vol 1: Upper Limb. 5th ed. New York, Churchill Livingstone, 1982 54. Kapandji IA: Biomechanics of the thumb. In Tubiana R (ed): The Hand, volT. Philadelphia. WB Saunders. 1981 55. Kaplan EB: The participation of the Mer joint of the thumb in the act of opposition. Bull Hosp joint Dis 27:39-45,1966 56. Kauer JMG. Functional anatomy of the carpometacarpal joint of the thumb. Clin Or­ thop 220:7-13, 1987 57. Kiloh LG, Nevin S: Isolated neuritis of the anterior interosseous ncrvc. Br Med J 1:850-851.1952 58. Kisner C, Colby LA: Therapeutic Exercise: Foundations and Techniques, 2nd ed. Philadelphia. FA Davis, 1990 59. Knott M. Voss DE: Proprioceptive Neuromuscular Facilitation, Patterns and Tech­ niques. New York, Hoeber & Harper, 1956 60. Knutsson E: Proprioceptive neuromuscular facilitation. Scand J Rehab Med rSuppl 7J:106-112.1980 61. Kottke Ff, Pauley DL, Ptak KA: The rationale for prolonged stretching for correction of shortening of connective tissue. Arch Phys Med RehabiI47:345-352, 1966 62. Kuckynski K: The thumb and saddle. Hand 7:120-195. 1975

284

CHAPTER 11

•

The Wrist and Hand Complex

63. Landsmeer ]MF: Power grip and precision handling. Ann Rheum Dis 22:164--197, 1962 64. Landsmeer IMF: The anatomy of the dorsal aponeurosis of the human finger and its functional significance. Anat Rec 104:31-453, ]949 65. Lankford LL: Reflex sympathetic dystrophy. In Green LL (ed): Operative Hand Surgery, vol L New York, Churchill Livingstone, 1982 66. Lehmann JF, DeLateur BI, Silverman DRT: Selective heating effects of ultrasound in human beings. Arch Phys Med Rehabil 47:331-339,1966 67. Lewis OJ, Hamshere RJ, Bucknill TM: The anatomy of the wrist joint. J Anat 106:539-552, 1970 68. Lister GO, Kleinert HE, Kutz IE, et aL Arthritis of the trapezial articulations treated by prosthetic replacement. Hand 9:117-129, 1977 69. Lister GD: The Hand. Diagnosis and Indications, 2nd cd. New York, Churchill Liv­ ingstone, 1984 70. Little KE; Toward more effective manipulative management of chronic myofascial strain and stress syndromes. I AOA 68:675-685, 1969 71. Littler JW: Principles of reconstructive surgery of the hand. In JM Converse (ed): Re­ constructive Plastic Surgery. Philadelphia, JB Lippincott, 1977 72. Long e, Conrad OW, Hall EA: Intrinsic-extrinsic muscle control of the hand in power grip and precision handling. J Bone loint Surg 52A:853-867, 1970 73. MacConaill MA: Mechanical anatomy of the carpus and its bearing on surgical problems. I Anat 75:166-175, 1941 74. Madden JW, de Vore G, Arem AJ: A rational postoperative management program for MCP joint implant arthroplasty. I Hand Surg 2:358-366,1977 75. Marie P, Meige H, Patrikious; Paralysie radiale dissoci, 1983 30. Ja nd a V: Muscles. cen tral n en~ ou s m o tor regulation a.nd bJ ck probhmts. tn Knurr 1 (ed ): Th e Neu robiologic Mcch.3 nisms in M ll lli pulnti ve ' l,e rapy. Lo nJon, P knunl Press, 1978 31. Je.ns e n K, Di Fa bio RP: Evalua tio n of L'Ccc ntric exerci se in tre(ltrnen t of pa h.:'U " r tendini ­ !'i• . Phys Ther 69;211 - 216, t989 32. Jo nh iJgc n 5, Nem eth C, Eriksso n E: H amstrin.g in juries in sp ri nters; Th e role of con­ centric t n cnj,lrged ilio pSOd­

PART 1/

tensor mechanism disorders can accentuate the symp­ toms of patellar tendinitis (inflexibility of hamstrings or triceps surae) , Traditionally, extensor mechanism rehabilitation has been used with patellar tendinitis, but more re­ cently work on the eccentric function of the quadri­ ceps has been emphasized, The basis of this program is to use activities that place maximal stress on the tendon to increase its tensile stress by performing variations of quick mini-squats. 53 Biomechanicallink­ age with ankle mechanics has demonstrated that most patients present with weakness of the ankle dorsiflex~ ors. Again, good results have been obtained with a program of eccentric work 124,283 Flexibility training is important: it increases the elasticity of the muscle-tendon unit and may increase the tensile strength of the tendon. Ice massage to the inflamed area and friction massage to the tendon are also helpful.

o ,Popliteal and Semimembranosus Tendinitis

,

.

r

of :10' 1t

n

is

Tendinitis of the popliteal or semimembranosus ten­ dons follows overuse injuries, usually from long-dis­ tance running. Hyperpronation of the foot may result in either popliteal or bicipital tendinitis at the knee secondary to overuse. In popliteal tendinitis the patient complains of lo­ calized pain over the lateral aspect of the knee. With the knee in the "figure-four" position, the LCL and popliteal tendon are stretched and can be palpated. When the popliteal tendon is inflamed, joint tender­ ness is noticed at its insertion on the lateral surface of the femoral condyle. 124 Tendinitis of the semimembranosus can mimic a meniscal injury because of its proximity to the joint line. The semimembranosus functions synergistically with the popliteus to prevent excessive external rota­ tion of the tibia. Therefore, hyperpronating problems of the foot can stress the insertion of the semimembra­ nosus. Treatment consists of rest, ice for the first 72 hours, ultrasound, and flexibility and strengthening exer­ cises. Proper training techniques and appropriate shoes should also be addressed.

o Osgood-Schlatter Disease Osgood-Schlatter disease used to be considered a form of osteochondritis associated with a partial avul­ sion of the patellar tendon at its insertion into the tib­ ial tubercle before this apophysis unites. More re-

Clinical Applications-Peripheral Joints

3 63

cently the process has been viewed as one part of the spectrum of mechanical problems related to the exten­ sor mechanism.282 Almost all patients 'with this condi­ tion have some mechanical inefficiency of the extensor mechanism. In fact, it is now thought that this is not really a "disease," but a form of tendinitis of the kne tendon. In young athletes, the tendon is attached t prebone, which is w eaker than normal adult bone. With excessive stresses on the tendon from running and jumping, the structure becomes irritated and a tendinitis begins. Objective findings include: 1. A tender swelling over the tibial tubercle 2. Pain is reproduced on resisting quadriceps exten­ sion; squatting may also reproduce the pain. 3. Decreased flexibility. Most patients have signifi­ cant restriction in the hamstrings, triceps surae, and quadriceps muscles. The mechanical inefficiencies of the extensor mech­ anism should be treated by appropriate rehabilitative exercises. Inflexibility should be addressed through stretching and ankle dorsiflexion strengthening if weakness is found . This condition usually resolves without any significant additional treatment. Com­ plete immobilization is neither necessary nor practi­ cal. A simple patellar support, such as a Neoprene rubber knee sleeve, may help.

D

Osteoarthritis

Primary osteoarthritis has no known etiology; sec­ ondary osteoarthrosis can be traced to abnormal joint mechanks. Abnormal knee mechanics produce sec­ ondary changes in the articular cartilage, subchondral bone, and supportive structures of the knee. The knee is a common site of osteoarthritis of the femorotibial and patellofemoral joints, possibly because it is often subject to trauma. 140,183,251 Previous fractures of the joint surfaces, ligamentous instability, or tears of the meniscus may all be complicated by subsequent de­ generative changes. Osteoarthritis may be a physio­ logic response to repetitive, longitudinal impulse­ loading of the joint. Changes may involve either the medial or lateral tibiofemoral compartment, the patellofemoral joint, or any combination of these, or may be panarticular, invoiving all three areas. Osteoarthritis usually begins in the medial or lateral tibiofemoral compartment, where it may be related to the articular cartilage damage that foHows meniscal tears.107 One of the compartments is usually involved if there is any knee deformity (e.g., the medial com­ partment is associated with a varus deformity, the lat­ eral compartment with valgu s deformity). As the dis­

364

CHAPTER 13

•

The Knee

ease progresses, the d egenerative changes in either compartment tend to increase the degree of the exist­ ing deformity. If there is a leg-length disparity, the knee on the longer side is usually involved. 66 A flexed knee gai t often results on the longer side, if the shorter side is not comp ensated for with a built-up shoe. This results in increased patellofemoral forces , leading to excessive wear and degenerative changes in the joint. The most common alteration in alignment of the os­ teoarthritic knee is a varus deform ity. This results in increased forces in the medial compartment, which creates a degenerative lesion of the medial meniscus and subsequent degenerative changes of the medial compartment, and eventually becomes panarticular. Varus deformity is often associated with internal femoral torsion. Since these persons tend to walk with their feet pointed straight ahead by externally rotating the tibia, torsional malalignment also p roduces patellofemoral arthritis and subsequent abnormal me­ chanics of the extensor mechanism. Any condition resulting in a loss of rotation at the hip will eliminate the screw-h om e mechanism of the knee. This results in vastus medialis atrophy, lateral tibial rotation, increased ligamentous laxity of the knee, and eventual genu valgwn deformity and de­ generative changes in the knee. In the tibiofemoral compartment, the meniscus is also usually involved in the degenerative process. As the joint space narrows, increased pressure is carried by the weight-bearing surface of the meniscus, which develops increased degenerative changes and, occa­ sionally, a horizontal cleavage type of tear. The menis­ cus is slowly ground away, and the anterior part of the meniscus may actu ally disappear.255 PHYSI CAL EXAMINATION

The clinical features of primary and secondary os­ teoar thritis are the same. The major complaint is usu­ ally pain, which may be muscular, capsular, or per­ haps venous in origin. Morning stifhlesS is also a common complaint. This is relieved after mot.ion, but the knee becomes painful and stiff again once the weigh t-bearin g tolerance of the joint is exceeded by prolonged standing or walking. The muscles of the thigh, particularly the quadriceps, become painful as a fixed flexion contracture of the knee develops with re­ sulting instability. An insecure knee results in episodes of giving way, secondary to muscle fatigue, and transient severe pain, secondary to minor trauma (which may be the result of impingement of degener­ ated menisci, the presence loose bodies, or a misstep). Pain is aggravated by activity or weight-bearing, but may also be aggravated at rest, particularly if the knee is held in one position for a prolonged time.

Examjnation of the extensor mechanism may reveal quadriceps atrophy, parapatellar tenderness, retro­ patellar pain with compression, and retropatellar crepitation . If genu valgum is present, lateral subluxa­ tion of the patella is not unusual. In unicompartmen­ tal degenerative joint disease, joint compression with either a varus or valgus stress to the knee elicits pain. Marginal osteop hytes along the femoral condyles may be palpable and are sites of capsular tenderness re­ sulting from local irritation. MANAGEMENT

The general management of patients with osteoarthri­ tis of the knee is similar to that previously outlined for osteoarthritis of the hip and includes anti-inflamma­ tory drugs, rest, w eight loss, aids, and physical ther­ apy (see Chapter 12, The Hip). Salicylates act as an en­ zyme inhibitor that prevents chondromalacia and, when given early and in adequate doses, prevents fib­ rillation. Ice for pain and spasm relief and heat appli­ cations are usually beneficial (hot moist packs or diathermy).40 Patients also benefit from hydrother­ apy. With bilateral involvement of the knees, weight loss allows muscle strengthening and re-education of gait in the presence of pain relief, with resultant func­ tional improvement. Mobilization techniques aid in easing knee pain and stiffness. Small-amplitude stretching movements used at the limit of range are of most value. 49 One of the most common changes in the osteoarthritic knee is knee flexion contracture, so patients should be taught early how to avoid contracture. Stretching of the tight hamstrings may be as important as strengthening of the vastus medialis. Tight gastrocnemius muscles (common in women who wear shoes with heels higher than 1 inch) can also be detrirnental. 139 Al­ though it can be difficult to accomplish, stretching of the gastrocnemius often helps prevent ankle plantar­ flexion or knee fl exion contractures. Exercises to strengthen the quadriceps group should be a daily ritual, beginning with setting exer­ cises and increasing to full progressive resistive exer­ cises as tolerated. Biofeedback can be of great value in strengthening the vastus medialis. 148 A training regi­ men should incorporate several types of exercise and might include isotonic exercises (with eccentrics)5 and isometric and isokinetic training.6,1 63 Beneficial exer­ cises include closed kinetic chain hamstring exercises (the patient stands and flexes one knee, then holds th contraction to the point of fatigue) and gastrocne­ mius/ soleus exercises (the patient raises up on the toes bilaterally or unilaterally). Full-weight-bearing strengthening exercises should be used judiciously in subacute and chronic phases and avoided in the acut,

PART II

phase. Unloading 99 ,115 and weight-bearing in water 289 should be used as closed kinetic chain exer­ cises in the more acute phases. The patient's daily activities must be eva]uated and if necessary changed . In the morning, active flexion and extension exercises should be done before weight-bearing activities. Walking should be encour­ aged for daily activities but not forced. Deep knee bends, sitting in low chairs, and remaining in the same position for prolonged periods should be avoided. Faulty posture that strains the stance should be corrected.

•

PASSIVE TREATMENT TECHNIQUES

(For simplicity, the operator will be referred to as the male, the patient as the female. P-patient; O-opera­ tor; M-movement; MH- mobilizing hand.)

o Joint Mobilization Techniques I. Femorotibial Joint-Distraction A. Distraction in prone (Fig. 13-32A)

P-Prone with the thigh fixated with a belt O-Stands at the foot of the table and gen­ tly grasps the distal leg, proximal to the malleoli, with both hands. The pre­ sent neutral (resting) position is found. M-Distraction is applied on the long axis of the tibia by the backward leaning of the operator's trunk. This technique is particularly well-suited for treating pain but should not be used wi th forces beyond grade 2 traction.239 B. Distraction in sitting (Fig. 13-328) P-Sitting on the edge of the plinth, with several layers of toweling supporting the underside of the distal thigh O-Stands at the patient's side facing the patient's feet so as to direct his fore­ arms in the line of force. Both hands grasp the tibia proximal to the malleoli to gain a purchase on them. M-A long-axis distraction is produced by leaning forward with the trunk. This may be performed through varying de­ grees of flexion and extension. This technique is used as a general mobi­ lization to increase femorotibial joint play for pain control. Distraction at this joint tends to occur when moving into flexion

Clinical Applications-Peripheral Joints

365

(out of the close-packed position). As with any jOint, if normal distraction does not occur, premature compression of joint sur­ faces will result when moving toward the close-packed position. If conservative techniques are ind icated, the resting position of the tibiofemoral joint is used; if more aggressive techniques are indicated, a position approximating the re­ stricted range is used. An alternate tech­ nique is to use an ankle strap with a stirrup attachment for placement of the operator's foot to apply distraction (Fig. 13-320. 137,138 This allows the operator's hands to be free to palpate the joint space as the distraction is applied or to use soft-tissue techniques (i .e., to a restricted lateral retinaculum) . The operator may be either standing or sitting. Starting positions include neutral and inter­ nal and external rotation of the tibia, with various degrees of flexion or approaching extension of the knee. II. Femorotibial Joint- Posterior Glide A. Posterior glide-resting position (Fig. 13-33A) P-Supine, leg beyond the end of the table O-Stands facing the medial aspect of the leg and places his caudal hand around the distal end of the leg above the ankle. The cranial hand is placed on the proximal aspect of the tibia, with the ulnar aspect of the hand just distal to the joint line of ,the knee. The pre­ sent neutral (rest) position is found. M-With the elbow extended, the cranial hand applies a posterior glide by the operator leaning his body weight onto the tibia or by flexing his knees. Grade 1 traction may be applied concurrently with the caudal hand. This technique is used for assessment and pain control and to increase joint-play movement necessary for flexion. The neu­ tral position may change with the treat­ ment, requiring repositioning. B. Posterior glide-of tibia on femur with knee flexed (Fig. 13-338) P-Supine, with knee flexed 25° to 90°, foot flat on the plinth O-Stabilizes the anterior aspect of the dis­ tal femur by contacting it with his en­ tire left hand. The forearm is directed horizontally. The operator contacts the proximal tibia with his caudal hand. The forearm is directed horizontally. M-The caudal hand produces a posterior

366

CHAPTER 13

•

The Knee

A

B

FIG. 13-32. Distraction of femorotibial joint: (AJ in prone,

(8) in sitting, (CJ in sitting with use of an ankle strap.

c

glide of the tjbia while the cranial hand stabilizes the femur. This technique is used to increase joint-play movement necessary for knee flexion, This position is also used for the dra wer test (knee in about 90Q ) to evaluate the peL. e. Posterior glide-of tibia on femu r with knee approaching full ex tension (Fig, 13-33C) P-Supine, with knee slightly flexed from the limit of extension . A l-inch thick­ ness of towelin g may be placed under the posterior aspect of the distal fe mur.

O-Supports the proximal tibia with the cranial hand placed over the distal femur. He uses the forearm to support and control the femur . The caudal hand is placed on the proximal aspect of the tibia just distal to the joint space. M-A posterior glide is produced with the caudal hand by moving the lower leg dorsally, This technique is used to increase joint-play movement necessary for knee flexion. Since the knee is approaching full extension

PART II

Clinical Applications-Peripheral Joints

367

(close-packed position), it is consid ered more vigorous than Techniqu e IT,B.

A

B

~ct l

.

~e

reg

y Ke

Io n

C

FIG. 13-33. Techniques for posterior glide of the femorotibial joint, tibia on femur: (A) near the resting posi­ tion, (B) with the knee flexed (drawer test), and (e) with th e knee approaching full extension .

III. Femorotibial Joint-Anterior Glide A. Anterior glide-of tibia on femur in prone, near the resting position (Fig. 13-34A) P-Prone. A bolster may be placed under the distal femur for further stability and to prevent patellar compression O-Kneels on the table and su pports the patient's leg across his thigh. The cau­ dal hand grasps the proximal tibia. The distal thigh is stabilized with the cra­ nial hand. The present neutral position is found. M-Keeping the arm straight, the opera tor leans forward, gliding the tibia a nteri­ orly. This technique is used to increase joint-play movement necessary for k nee extension. The tibiofemoral joint is positioned in the resting position if conserva tive techniques are indicated or approximating the re­ stricted range of extension if a more aggres­ sive technique is indicated. If grade 1 trac­ tion is also desired, the operator remov s h is th igh, stand s facing the la teral aspect of the patient's leg, and places his cranial (mo­ bilizing) hand over the proximal tibia. The caudal hand grasps the distal a pect of th patient's leg. The cranial hand then glides the tibia in an anterior direction as the cau­ dal hand applies traction. B. Anterior glide-of tibia on fem ur with the knee flexed about 90° (Fig. 13-348) P-Supine, knee flexed about 90°, foot fl at on the plinth O-Stabilizes the foot and lower leg by partially sitting on the plinth, placing the proximal thigh over the dorsum of the patient's foot. H e grasps th e proxi­ mal tibia by wrapping the fingers of both hands around posteriorly and contacting the tibial tuberosity with both thumbs anteriorly. M-Anterior glide is p roduced by keeping the arms fixed and leaning backward with the trunk. This technique is used to increase joint-play movement necessary for knee extension. This position is also used for the dr awer test (knee in about 90°) to evaluate the ACL and as a technique to restore joint-p lay move­ ment for knee ex tension . The operator leans backward and glides the tib ia anteriorly. C. Posterior glide of femur-anterior tibia glide (Fig. 13-34C)

368

CHAPTER 13

•

The Knee

A

B

c FIG. 13-34. Technique for anterim glide of the femorotib­ ial joint tibia on femur: (A) in prone near the resting posi­ tion, (8) in supine with the knee flexed (drawer test), and (e) in extension (with posterior glide of the femurJ.

P-Supine, knee approximating the re­ stricted range of motion. The proximal aspect of the tibia is on a bolster. O-Grasps the distal femur with the radial aspect of the cranial hand. The caudal hand stabilizes the proximal tibia on the bolster. M-Keeping the arm straight, the operator leans down on the cranial hand, glid­ ing the femur posteriorly. This technique is used to increase joint-play movement for extension. This technique is particularly useful when the patient lacks the last few degrees of terminal knee exten­ sion. IV. Femorotibial Joint-Internal Rotation A. Internal rotation-with the knee flexed about 90° (Fig. 13-35A) P-Supine, knee flexed 90°, foot flat on the plinth O-One may stabilize the foot by sitting on the plinth, placing the proximal thigh over the dorsum of the patient's foot. The cranial hand grasps the proximal tibia laterally, with the fingers wrapped around posteriorly, the thumb contact­ ing the lateral aspect of the tibial tuberosity so as to gain a purchase against it. The caudal hand grasps the tibia anteriorly and medially, just distal to the cranial hand, gaining a purchase on the tibial crest. M- Both hands rotate the proximal tibia medially (internal rotation), gaining purchase on the tibial tuberosity and lateral tibial condyle with the cranial hand, and the tibial crest and medial tibial condyle with the caudal hand. This technique is used to increase a joint­ play movement necessary for knee flexion. B. Internal rotation-at varying degrees of flex­ ion and extension (Fig. 13-358) P-Supine O-Controls the distal thigh with the cra­ nial hand grasping from the lateral as­ pect, the thumb wrapping around pos­ teriorly and the fingers anteriorly. The caudal hand grasps the heel of the foot. He must place the ankle in the close­ packed position by fully dorsi flexing it so that the rotary force is transmitted to the tibia, not the ankle joint. Hi~ forearm is kept in close alignment with the patient's tibia. M-The caudal hand rotates the foot med i­ ally, transmitting the movement to th

A

PART /I

Clinical Applications-Peripheral Joints

369

v. Femorotibial Joint-External Rotation A. External rotation-with the knee flexed to abou t 90° (Fig. 13-36A) This is performed in the same manner as Technjque IV,A. The hand-holds are re­ versed, however, so that the cranial thumb

A

A

t-

r·

~x­

B

ra­

as­

; it ed 1.is ith ~i­

the

FIG. 13-35. Internal rotation of femorotibial Joint: rAJ with the knee flexed to about 90° and (8) at varying de­ grees of flexion-extension .

tibia through the dose-packed ankle. Starting with the knee slightly flexed, the movement can be applied at vari­ ous degrees of flexion and extension. Do not, however, rotate and simultane­ ously flex or extend. This technique is considered more vigorous than Technique IV,A. It increases joint-play movement necessary for flexion.

B

FIG. 13-36. External rotation of femorotibial joint: (A)

with knee flexed to 90 ° and (8) at varying degrees of flex­

ion-extension.

370

CHAPTER 13

•

The Knee

contacts the tibial tuberosity medially, while the caudal hand grasps the tibial crest and lateral aspect of the proximal tibia. This technique is used to increase joint-play movement necessary for knee extension. B. External rotation-applied in various posi­ tions approaching full extension (Fig. 13-36B)

P-Supine O-Supports the knee and distal end of the thigh with the cranial hand from the medial aspect, wrapping the fingers around anteriorly. The cranial hand primarily controls the position of the knee, keeping it from dropping into extension. He grasps the ankle and foot with the caudal hand, wrapping the fingers around the calcaneus. The ankle must be kept in the close-packed position so as to transmit the rotatory force to the tibia, not the ankle joint. M-The caudal hand and forearm rotate the foot and ankle externally (lateral rotation), keeping the ankle in the close-packed position. The cranial hand controls the position of the knee. This may be performed at various po­ sitions approaching full extension. Do not rotate and simultaneously flex or extend the knee. This technique is used to increase joint-play movement necessary for knee extension. It is considered more vigorous than Tech­ nique V,A. VI. Femorotibial Joint-lateral (Varus) Tilt (Fig.

FIG. 13-37. Lateral (valgus) tilt of the femorotibial joint.

the knee. As with any joint-play movement, it must not be moved past normal anatomic lim­ its. VII. Femorotibial Joint- Medial (Valgus) Tilt (Fig. 13-38)

This is performed in a similar manner to Tech­ nique VI. The hand-holds are reversed so that the caudal hand supports the proximal tibia and the knee. The cranial hand contacts the lateral

13-37)

P-Supine O- Supports the lower leg by resting the leg on the proximal thigh. His knee is placed on the plinth. He supports the proximal tibia and knee with his caudal hand from the lateral side, wrapping the fingers around posteriorly and the thumb anteriorly. The cranial forearm is supinated and in line with the direction of force. The cranial hand contacts the medial aspect of the femoral and tibial condyles. The fingers wrap around posteriorly for additional support. The patient's knee is kept slightly flexed. M-The cranial hand gently moves the knee into lateral tilt, taking care to avoid any flexion or extension of the knee. The opera­ tor's caudal hand supports the knee, but yields with the lateral movement. This technique is used to increase joint play at

'::I

FIG. 13-38. Medial (varus) tilt of the femorotibial joint.

PART" condyle. The cranial forearm comes around and is in line .vith the mobilizing hand, which moves the knee in a medial direction, thus ere· ating a medial gapping at the joint line. VIII. Femorotibial Joint-Medial-Lateral Glide A. Medial (lateral) glide-in supine (Fig. 13-39A)

A

'8 FIG. 13-39. Medial-lateral glide of the tibia: (A) medial glide, (B) lateral glide .

Clinical Applications-Peripheral Joints

371

P-Supine, leg extending over the edge of the table. The tibiofemoral joint is posi­ tioned in the resting position if conser­ vative treatment is indicated or ap­ proximating the restricted range if more aggressive techniques are indi­ cated. O-Stands at the foot of the table. The foot is held between his thighs or the lower leg is held between the arm and tho­ rax. The cranial hand stabilizes the dis­ tal femur from the medial aspect. The caudal hand grips the proximal tibia and fibula from the lateral side. M-The mobilizing hand gbdes the proxi­ mal tibia and fibula in a medial direc­ tion. This technique is used to increase joint play at the knee. To perform lateral glide the hand-holds are reversed-the stabilizing hand grips the distal femur from the lateral aspect and the mobilizing hand grips the proximal tibia from the medial side (Fig. 13-39B) . The mobilizing hand glides the tibia in a lateral direction while the trunk guides the motion. B. Medial (lntera/) glide-in sidelying (Fig. 13-40A) 137, 138 P-Sidelying on the uninvolved side, in­ volved leg extending over the edge of the table. A bolster is placed under the medial aspect of the distal thigh. O-Stands facing the dorsal aspect of the leg. The caudal hand grasps the distal leg above the ankle. The cranial hand grips the proximal tibia and fibula from the lateral aspect. The knee is maintained in the resting position and the leg is held against the operator's trunk. M-The tibia is glided in the medial direc­ tion indirectly through the fibula while the trunk guides the motion (by flexing the knees) . Lateral glide is performed in the same man­ ner as above, but the hand-holds are re­ versed and the patient lies on the involved side (Fig. 13-40B). These techniques are used to restore joint play for restricted flex­ ion or extension. IX. Patellofemoral Joint A. M edial-lateral glide (ti/O-in supine (Fig. 13-41A) P- Supine, knee slightly flexed over a firm support of toweling O-Contacts the lateral patellar border

372

CHAPTER 13

•

The Knee

A

A

,. B

FIG. 13-40. Medial-lateral glide of femorotibial joint: (A) medial glide in side!ying, (8) lateral glide in sidelying.

with the thumb pads or the heel of the hand. The remaining fingers rest over the anterior aspect of the pa tien t' s leg to help support the operator's hands. He keeps the elbows close to full exten­ sion. M-A medial glide of th e patella is pro­ duced with both hands. A lateral glide is produced by using the pads of the index fingers. Both hands glide the patella in a lateral direction. These techniques are used for general patellar mobiljzation in the presence of re­ stricted patellar movement. Grades I and II should be applied to highly irritable joints where pain is predominant. In less irritable joints, where pain is a result of tight struc­ tures, grades III and IV should be consid­ ered. B. Medial glide-in sidelying (Fig. 13-41B) P-Lying o n the unaffected side with the involved leg placed in hip and knee flexion . The affected patella is just over

B FIG. 13-41. (A) Medial-lateral tilt and (8) medial glide the patellofemoral joint in sidelying.

0

the edge of the table. A towel or bolster is placed under the knee. O-Stands facing the leg. The stabilizing hand contacts the proximal tibia or dis­ tal femur. The mobilizing hand is posi­ tioned with the heel of the hand on the lateral border of the patella. M-With the elbow extended, the mobiliz­ ing hand glides the patella in a med ial direction. The force is produced by th operator's body weight. In this position the lateral structures ar under some degree of tension, allowing a

PART II more effective stretch to the la teral struc­ tures. A void compression.

X. Patellofemocal Joint- Superioc-lnferior Glides A. Inferior glide-in sup ine (Fig. 13-42A) P-Supine, knee extended or in slight flex­ ion wi th a towel Wld er the kn ee O-Stands n ext to the pa tient's thigh, fac­ ing h er feet. The web space or heel of

A

of

ter

mg

r­

) i­ th

liz­ Ii.al the are

t)

a

B FIG. 13-42. Superior-inferior glide of patellofemoral joint (A) with the knee in extension and (B] with the knee in fJex­ ion.

Clinical Applications-Peripheral Joints

373

the near hand contacts the superior pole of the patella. M-The mobilizing hand glides the patella in an inferior direction, parallel to the femur. This technique is used to increase patellar mobility for knee flexion. Superior glide, to increase mobility for knee extension, is done in the reverse manner. The mobilizing hand is positioned with either the web space or the heel of the hand on the inferior pole of the patella. The patella is glided in the superior direction. Avoid compression of the patella into the femoral condyles. Grades I and II should be applied to highly irritable joints where pain is predominant. In less irritable joints, where pain is the re­ sult of tight structures, grades III and IV should be used. B. Inferior glide-in knee flexion (Fi.g. 13-42B) P-Supine, foot resting on the table, hip and knee in flexion O-Stands nex,t to the lower limb. The cau­ dal hand stabilizes the leg by grasping the lower tibia. The heel of the mobiliz­ ing hand contacts the superior pole of the patella. M -Glide the patella in a caudal direction, parallel to the femur. This technique is considered more vigorous than Technique X,A. To selectively stretch the lateral or medial retinaculum, caudal glide may be directed in a more medial caudal or lateral caudal direction. XI . Proximal Tibiofibular Joint (Fig. 13-43A) A. Anterior glide P-Assumes a half-kneeling position or stands at the side of the table, resting her leg on the table. The foot extends over the edge of the table. O-Places the heel of the mobiliz ing hand over the posterior aspect of the fibular head. The other hand may be used to support or reinforce the mobilizing hand or stabaize the ti.bia. The thigh supports the patient's foot in plantar­ flexion (10°). M-An anterior lateral glide of the fibula is produced by leaning forward with the trunk. The operator must prevent pain or fibular nerve compression. This technique is used to increase joint play in the proximal tibiofibular joint and to re­ duce a dorsal positional fault of the fibula. Lateral knee pain is often present when the proximal tibiofibular joint is affected 239

374

CHAPTER 13

•

The Knee

30.

~

6

- ====-­

~

1Q

FIG. 13-44. Femorotibial joint-forced (gentle) flexion.

u

u

u

A

B

FIG. 13-43. Proximal tibiofibular joint: (A) anterior glide,

(B) posterior glide.

Posterior mobilization may be performed in sidelying with the hip and knee slightly flexed (fig. 13-43B). Both anterior and infe­ rior glide m ay be performed in supine (see Fig. 14-40 in Chapter 14, The Lower Leg, Ankle, and Foot).

D

Se lf-Mobilizat.ion Tech nique s

I. Femorotibial Joint A. Forced (gentle) flexion (Fig. 13-44)

P-Supine, hip flexed slightly above 90°. The knee is flexed over a firm piIlow or towel roll, which acts as a fulcrum. MH-Both hands contact the lower leg over the ant.erior aspect, with the fingers in­ terlaced. M-Gentle flexion, with oscillations, is per­ formed. Note: Forced flexion may also be done ill a sitting position. The right hip is completely flexed so that the thigh is supported on the chest. The knee is flexed over the right forearm, which now acts as a fulcrum and gives additional support. The left MH contacts the lower leg over the anterior as­ pect and carries out gentle flexion of the knee. II. Pa,t ellofemoral Joint A. Medial-lateral glide P-Long-sitting on a firm cot or the floor, knee slightly flexed over a firm pillow or towel roll. (A sitting position in a chair may be used, with the leg ex­ tended, the knee slightly flexed, and the foot fixed to the floor.) MH-Both thumb pads contact the lateral or medial patellar border. The remaining fingers rest over the anterior aspect of the leg. The elbows are extended as much as possible. M-A medial or lateral glide of the patella can be produced by leaning the trunk forward and to one side. The glide is ef­ fected by moving the trunk ra ther than any part of the hand. Note: Superior-inferior glide may also be per­ formed by contact of the thumb pads on the supe­ rior or inferior borders of the patella, with the rest of the hand resting over the medial and lateral as­ pects of the knee.

REFERENCES 1, Abbott B, Bigland TI, Ritchc JM: The physiologiccd cost of negative work. J Physiai 117:380-390,19';2 2. Abern8thy PJ, Towns_e nd PR, H.osu RM, Radin EL: Is chondromalacia patellae a sep­ arate d inica! entity? ) Bone Joint Surg 608:205--210, 1978

u

Ii I

r

l'

~

Zl

': l

::­

::'l

PART 1/ Clinical Applications-Peripheral Joints 3. Adams A: Effect of exe rcise upon ligament s trength . Res Q 37:163-167. 1966

4. AhUdd SK, Larson RL, Collins HR: Anterior cnlci~h~ reco nstructio n in the chroni­

cally uns.t.lble knee using an expcmded polytetrafluo roethylene (PTFE) prosthetic

liga ment. Am J Sports Med 15:326-330, 1987

5. Albert M: Eccentri c Muscle Training in Sports and Orthopedics. London, Churchill

Livingstone, 1991

6. AJbert MS: Principles of exercist' progression. In Greenfield 81-1: Rehabilitation of the Knee: A Problem-Solving Approach. Philadelphia, FA Davis, 1993: 110--136 7. Amatuzzi M.M, Fazzi A, Vcuella MH: Pathologic synovia l plica of the knee. Am J

Sports Med 18:466-469, 1990

8. American Academy of Orthopaedic Surgeons: Knee Braces-Seminar Report Rose­ mont. It, The Academy, 1985

9. And erson AF, Lipscomb AB: Cliniccd diagnosis of meniscal tea rs--Description of a

new mi'l nipula ti\'e test. Am J Sports Med 14.:291-293, 1986

10. Andrews

JR,

Mc leod WD, Ward T, Howard K: The cutting mechanism. Am J

Sports Med 5:111 - 121,1977 11. Apley G: The did g nosis of meniscus injuries. J Bo ne Joint Surg 29A:78-84, 1947

12. Arno 5: The A nngle: A qurmtitative measurement of pat ~ lI.a a lignme nt ,md realign­

t

a

a

a

'"

n

ment. J Orthop Sports Phys Ther 12:237-242, 1990

13. Arnoczky SP: The blood supply of the meniscus and its ro le in hea ling and repair. In

Ame rica n Association of Orthopedic Surgeons: Symposium on S ports Medicine:

The Knee. St. Louis, CV Mosby. 1935

14. Arnoczky Sp, Toni.lli PA, \'V .uren RF, et al : Bio logic fi xat ivns of li ~a m e nt prostheses cl nd i' ugmen tati ons: An evaluation of bone ingrowth in the dog. Am J Sports Mc.d 16: 106- 112, 1988

15. Arnold JA, Coker TP, He(- Res llll ~ dfter ~lrthroscopic rt.' .

scclian Arc/1 Orthop Trouma Surg 108:282- 284, 1989

104. Hanten Wp, Sc.h ulthi es 55: Exercise's effect on t!iectromyogr.lphj( ilctivity of th e

li'astus m edia lis o bt iquea nd vastus la tera lis Ill uscl es. Phys Ther 70:661 ,.,565, 1990

105. Hardarkerw t WT, Wh ipple TL, Bassett FH: Dia g nosis a nd treatment of th e pliC'a syndrome of the knee. j Bo ne jocnt Su rg 62A:222- 225, 198() 106. Hil5tings DE: The' nunope.rat ive' tre.1 tme nt of co llate ral li ga men t injuri es of the knee joint. O in O rth()p 147:22-28, )980

l 07. Hclfct A: Disorders of the Knee. Philodelphi.l, JB Lippincott, 1974

108. 1leUebrand t FA, Houtz SJ, Kjrkorictn AM: Influence of bim(lnual exc rci~c o n u nililt­

eral w ork ca paci ly . J A ppl Phy,ioI2:452-466, 1950

109. J-Iellebrandt FA, HOllt z Sj, Partridge MJ, v\'nltel'S EC: Ton ic neck refll.?xes in L'Xi:'r Q $E'S

of s tress in man. Am j Phys Med 35:144--157, 1956

11 0. He Uebrilndt FA, Wa terla nd Je: lndi.rect {earninh- the influen ce of unimnnual e;'(e r­

cise on related muscle g rou ps of the sa m e il nd the opposite side. Am J Ph ys Med

41:45-55, 1962

In. H e nning eE, Lynch MA, C lick K: An ill vivo stTil in ga uge stud y of elongi1 tion of the

AC L. Am) Sport; Mod 13:22- 26, 1985

112. He n ning CE, Lynch M A, Glick K: Physica l examination of the knee. In Nkhol(ls JA,

Hc.rs llman n EB (ed s): Th e Lower Extre mity and Spine in Sport:. Mc·dkine, vol. 1. St.

Loui s. C\I M osby, 1986

113. Hoffa A: Th e infl ue nce of the Ildipos(' tissu e \v ith rega rd ~ to the pClthology oi thl'

knee joint. j Al'vtA 43:795-796, 1904

114. H old e n DL, Eggert AW, Butle r lE: The no nopemt.ive 1T• • lm e nt of gra de I and n me­

dial colla tEral liga men t injuries to the knee. Am J Sports M ed 1 l;,340- J 44 , 1983

115. Hol te n 0 : Medisinsk Trcn igsle.rd I ­ n.. jp

he

growth, inappropriate trimming, and in­ flammation of the nail beds. B. Soft tissue 1. Swelling (see under palpation) 2. Wasting of isolated or generalized muscle groups 3. General contours C. Bony structure and alignment 1. Note toe and metatarsal deformities such as claw toes, hammer toes, and varus-val­ gus deviations. 116 a. Claw toes are usually associated with a pes cavus deformity and may accom­ pany certain neurological disorders. The metatarsophalangeal joints are po­ sitioned in extension and the interpha­ langeal joints in flexion (Fig. 14-32A). Contracture of the long toe-extensors causes extension of the toes, which in­ creases the passive tension on the long toe-flexors. The intrinsic muscles are overbalanced, both actively and pas­ sively, by these muscle groups. b. Hammer toes are a result of capsular contracture of the proximal interpha­ langeal joints (Fig. 14-32B). The in­ volved joint or joints are fixed in some degree of flexion. Typically there is hyperextension of the metatarsophalangeal joint and dis­ tal interphalangeal joints and flexion of the proximal interphalangeal joint. It is usually only seen in one toe-the sec­ ond toe, occasionally the third. c. Mallet toe is associated with a flexion deformity of the distal interphalangeal joint (Fig. 14-32C). The metatarsopha­ langeal joint and proximal interpha­ langeal joints usually are normal. There is usually a callus formation under the tip of the toe or a deformity of the nail. d. Tailor's bunions ("bunionette") are caused by irritation and pressure of the fifth metatarsal head. There may be an overlapping fifth toe or quinti varus deformity (often congenital) of the fifth toe (Fig. 14-32D) . e. A hallux valgus is the most common deformity of the first metatarsopha­ langeal (M-P) joint. Pathologically it is a lateral deviation of the proximal pha­ lanx and medial deviation of the first metatarsal bone in relation to the center of the body (Fig. 14-32E). It may be as­ sociated with a pronated foot and is

Clinical Applications-Peripheral Joints

409

found most frequently in older women. The joint surfaces are no longer cong ru­ ent and some may even go on to ub­ luxation. Note the presence of any bursa over the M-P joint (bunion) and whether active inflammatory changes are present. The toe may be rota ted with the toe nail pointed inward. f. Assess the [ength of the metatarsals (Fig. 14-33). A line across the metatarsals should form a smooth parabola. The so-called Morton's, Gre­ cian, or atavistic foot is a hereditary type, in which the second toe is longer than the first. With this condition, nor­ mal balance is disturbed and weight stress falls toward the inside arch (prona­ tion).71 This tends to produce hyper­ mobility of the first ray, displacement of the sesamoid bones, and increased stress on the second metatarsal head. 2. If indicated, assess pronation of the foot, manifested by a flattening of the medial longitudinal arch. The relative position of the navicular tuberosity in the weight­ bearing and non-weight-bearing position is examined. A line (Feiss' line) is drawn from the tip of the medial malleolus to the plantar aspect of the first metatarsopha­ langeal joint. 133 The navicular tubercle should be within one third of ,the p erpen­ dicular distance between this line and the ground. If the navicular falls one third of the distance to the fioor, the condition is referred to as first-degree flatfoot; if it rests on the floor, a third-degree flatfoot. 3. The calcanei should be positioned verti­ cally with little or no inward or outward bowing of the Achilles tendon. 4. The general configuration of the foot should be assessed in standing and sitting positions. a. When standing, an untwisted foot is one in which the hindfoot is in prona­ tion and the forefoot is in supination. The calcaneus will be in valgus posi­ tion and the navicular tubercle will be sunken and often prominent. The talar head also becomes prominent medi­ ally, and the forefoot often assumes an abduoted position with respect to the hindfoot. There is often an associ­ ated valgus deformity of the first metatarsal-phalangeal joint. With excessive twisting of the foot

410

CHAPTER 14

•

The Lower Leg, Ankle, and Foot

1

A

---­

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

~'.

--~

D

B

I

,1 /

( E

c Toe deformities: (A) claw toes, IB) hammer toe, ICJ mallet toe (second toe), (D) an overlapping fifth toe or quinti varus deformity, and IE) hallux valgus with a bunion

and overlapped second toe.

FIG. 14-32.

(pes cavus) the calcaneus assumes a varus position and the medial arch is well formed, with the navicular tuber­ cle positioned well superiorly. There is often a tendency toward clawing of the toes in a cavus foot.

b. When sitting, the foot should relax into a position of plantar flexion, inversion, and adduction. A "supple" or "mobile" flat-foot will take on a more normal configuration in sitting with the force of weight-bearing relieved. A "fixed"

PART II Clinical Applications-Peripheral Joints

FIG. 14-33. Inspection of toes: Flex the toes and note the relative length of the metatarsals. Abnormally short first or fifth metatarsals are a potential cause of forefoot imbalance. When both are short, there is often a painful callus under the second metatarsal.

or "structural" flat-foot wiH maintain its planus (untwisted) state. 5. Perform a complete structural eXClmination of the remainder of the lower extremities, the pelvis, and the lower back, as dis­ cussed in Chapter 22, Lumbosacral-Lower Limb Scan Examination. Any structural deviations or asymmetries should be noted, and the possible effects on the bio­ mechanics of the foot considered. 6. Inspect the shoes, inside and out, for wear patterns that may offer clues as to the pres­ ence of persistent biomechanical distur­ bances and localized areas of pressure. Also inspect for other possible sources of pain arising from the shoe, such as nails protruding through the insole and promi­ nent seams. a. On the outer sole, the wear pattern should be displaced somewhat laterally at the heel. Over the front sole, the wear pattern should be spread fairly evenly across the area corresponding to the level of the first, second, and third metatarsophalangeal joints, with less wear laterally. There should be an even wear pattern across the rest of the me­ dial side of the sole. Areas of localized excessive wear should be noted as well as abnormal wear patterns. b. The upper portion of the shoe should show a gently curved transverse crease line at the level of the metatarsopha­ langeal joints. Excessive curling of the vamp of the shoe and the front part of the sole may occur in a shoe that is too long, too narrow, or both. A crease line that runs obliquely, from forward and

411

medial to backward and lateral, may arise from a stiff first metatarsopha­ langeal joint. Localized prominences of the vamp commonly occur medially in the pres­ ence of hallux valgus or dorsally w ith hammer toes or claw toes. Such promi­ nences should be noted. Inspect for excessive overhanging of the upper shoe with respect to the sole. This is likely to be observed mediaUy in shoes of patients with pronation of the hindfoot. When viewed from behind, the cup formed by the counter of the shoe should rise vertically and symmetri­ cally from the sole. Inclination of the counter medially, with bulging of the lateral lip of the counter, will be seen in shoes of patients with pronated feet. Areas of excessive scuffing of the upper shoe should be noted . Scuffing of the toe of the shoe may occur with weak dorsi flexors or restriction of mo­ tion toward dorsiflexion. c. When inspecting the inside of the shoe, feel along the inner surface of the seams for prominent areas that may give rise to pressure concentration. Also feel along the entire surface of the inner sole for prominent areas that might be caused by protruding nails. The wear pattern on the inside of the shoe should also be examined . There should be evidence of an even distribu­ tion of pressure over the medial and lateral sides of the heel counter, over the inner sole at the heel, and over the inner sole at the metatarsal heads. III. Selective Tissue Tension Tests A. Active movements (junc tional movements) 1. Barefoot walking a. Normal gait b. On toes. If unable to do so, determine whether it is because of pain, weak­ ness, or restriction of motion. The heel should invert and the arch should rise. c. On heels. If unable to do so, determine whether it is because of pain, weak­ ness, or restriction of motion. 2. Standing with feet fixed a. Externally rota te the leg with respect to the foot. This should cause some varus deviation of the heels and raising of the arches. Compare one foot to the other.

412

CHAPTER 14

•

The Lower Leg, Ankle, and Foot

b. Internally rotate the legs on the feet. This should result in some valgus devi­ ation of the heels and flattening of the arches. Compare one foot to the other. 3. Standing, keeping knees extended a. Evert the feet by standing on medial borders of feet. b. Invert the feet by standing on lateral borders of feet. 4. Sitting, with legs hanging freely. Compare range of motion of one foot to the other. Assess pain, range of motion, and crepitus. a. Dorsiflexion h. Plantar flexion c. Inversion d. Eversion e. Toe movements B. Passive physiological movements 1. Standing, before measurements are taken, determine the dynamic angle and base of walking using the patient's own line of progression as a reference.1 15 A paper walkway (approximately 20 to 24 feet long) on which the patient's footprints can be recorded (after walking in a normal fashion) is most convenient. ll ,U5,153 Using the line of progression as a reference, select one left and one right footprint from the middle of the progression to use to con­ struct a paper template of the footprints adjacent to each other. The dynamic foot angle and the distance between the middle of each heel are maintained (Fig. 14-34). Note: The paper walkway recording can be used for additional data collection such as stride length, velocity, and cadence in the gait analysis. 2. Measurement of subtalar joint in relaxed standing a. With a felt-tipped marking pen, bisect the middle one third of the posterior calcaneus.1 41 Extend the bisection line plantarly to the base of the supporting surface and from the middle one third of the calcaneus superiorly approxi­ mately 1 inch; the point of bifurcation is located at the junction of the proxi­ mal and middle one third of the bi­ sected calcaneus. b. Next, bisect the distal one third of the lower extremity just proximal to the malleoli. Extension of this line superi­ orly should bisect the knee joint within the popliteal space. Calipers may be used to determine the center of the

most proximal point of the lower one third of the leg and at the level of the malleoli. With a felt-tipped marking pen, these two points are then con­ nected to form the bisector of the lower one third of the leg. c. Measure the neutral calcaneus stance (a relaxed foot with the subtalar joint al­ lowed to pronate) (Fig. 14-35). i. Have the patient stand in a normal angle and base of gait (see B.1. above) and facing away from the examiner. 141 Using a goniometer or protractor, place the straight arm along the supporting surface (transverse plane). The center point of the goniometer or protractor is placed at the apex point of the angle created by the calcaneal bi­ section and the supporting surface (frontal plane). Rearfoot valgus is then measured to the nearest de­ gree. ii. The normal weight-bearing foot should demonstrate a mild amount of pronation but should still allow for additional pronation.12 If the patient is bearing weight or walk­ ing with the foot out of neutral po­ sition and near full pronation, an obligatory internal tibial rotation occurs and is prolonged, resulting in an increased force that is ab­ sorbed by the soft tissues of the knee?9,80 3. Measurement of tibia varum a. Measure tibia varum (tibiofibular varum), if indicated. If a lateral angula­

tion of the tibia-to-floor angle is 10° or

greater, the extremity requires an ex­ cessive amount of subtalar joint prona­ tion to produce a plantigrade foot (Fig. 14-36). i. Have the client stand in a normal angle and base of gait. With the feet in a resting calcaneal stance position, recheck the bisections of the calcaneus and lower leg. When the bisections are acceptable, mea­ sure the frontal plane relationship of the tibia to the transverse plane (or level grOlmd). If a gravity go­ niometer is used, the ang[e be­ tween the bisection of the leg and vertical is read on the face of the

.

PART"

Clinical Applications-Peripheral' Joints

413

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fA) Computation of foot angle fAS-longitudinal line bisecting each foot; CD-horizontal line through posterior third of foot perpendicular to line AS; EE-connecting line of intersectiol1S of CD and AS of two ipsilat­ eral feet [line of progressionJ; resulting angle is foot angle). fS) Computation of the base of support ISS- line drawn from intersection of CD and AS of contralateral foot perpendicular to line EEl. (C) Computation of dynamic angle and base of walking template. FIG. 14-34.

war

C

goniometer. Tibia varum is present when the distal end of the bisecting line of the leg is closer to the mid­ sagittal plane than the proximal end. Tibia valgum is present if the leg is angulated in the opposite di­ rection. Note: Tibia varum (tibiofibular varum) measurements can also be performed ''lith the foot positioned in subtalar neutral by palpating for talar congruency as the patient ro­ tates the trunk to the left and right,

allowing the tibia to externally and internally rotate, thus supinating and pronating the subtalar joint. Once subtalar neu tral is reached, the subject is then asked to main­ tain this position while measure­ ments are recorded. According to McPoil and co-workers the best pa­ tient position for clinical measure­ ment of tibiofibular varum is the neutral calcaneal s tance position. It would appear that the measure­ ment of true tibia varum cannot be

414

CHAPTER 14

•

The Lower Leg. Ankle. and Foot

FIG.

Measurement of neutral calcaneal stance ra relaxed foot with subtalar joint allowed to pronate).

FIG. 14-36. Measurement of tibia varum in the resting calcaneal stance position.

done without obtaining roentgeno­ grams of the lower extremities taken during weight-bearing. 115 4. Measurement of great toe extension a. Measurement of great toe extension can be made while the person is stand­ ing. The great toe is extended actively and assisted passively without dorsi­ flexing the first ray. Forty-five degrees has been found to be adequate for gen­ eral ambulation.104 b. Great toe extension test. Passive exten­ sion of the great toe at the metatar­ sophalangeal joint in the normal weight-bearing foot has two effects: el­ evation of the medial longitudinal arch (windlass effect) and lateral rotation of the tibia. The test is normal when both effects are seen (Fig. 14-37).1 43 5. Passive range of motion. The patient sits with ~egs hanging freely . Compare range of motion of one foot to the other. Note the presence of pain or crepitus. Note abnor­ malities or asymmetries in range of mo­ tion. Note the presence of pathological end feels. a. Hindfoot i. Plantar flexion ii. Inversion

iii. Eversion b. Transverse tarsal i. Plantar flexion li. Pronation (eversion) iii. Supination (inversion)

iv. Abduction

v. Adduction

6. Supine

a. Hip flexion-extension

b. Knee flexiolil-extension

c. First ray: position and mobility

i. Place the foot in a neutral subtalar position (see Fig. 14-27). Load the forefoot (see 7.c.i below). While maintaining the foot in neutral po­ sition, grasp the metatarsal heads (between the thumb and forefin­ ger) with the loading hand. Grasp the first metatarsal head with the other hand . ii. Assess the position of the first metatarsal head in relationship to its neutral position and assess the end-range position of the first metatarsal head in relationship to the second metatarsal head.142 iii. While maintaining the foot in neu­ tral subtalar position, manually plantar flex and dorsiflex the first

FIG. 14-35.

PART /I

FIG. 14-37.

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Clinical Applications-Peripheral Joints

415

Great toe extension test.

ray. Assess the motion of the first ray in relationship to its neutral po­ sition. iv. Limited range may result from a combination of biomechanical fac­ tors such as excessive pronation or a short tendon or from restriction of the joint proper. S1 7. Prone, with the feet over the edge of the table. a. Hip internal and external rotation with the knees flexed to 90°. h. Supination and pronation of the calca­ neus. The amOW1t of supination and pronation that is available can be mea­ sured by lining up the longitudinal axis of the lower limb and vertical axis of the calcaneus (Fig. 14-38).79,142 Passive movement of the calcaneus into inver­ sion (amoW1t of supination) is nor­ mally 20°.1 42 Conversely, the amount of eversion (pronation) is nor­ mally 10°.142 c. Forefoot valgus-forefoot varus. The subtalar should be positioned in subta­ lar neutral and the forefoot locked (Fig. 14-39). i. In order to accomplish locking of the forefoot in the open-chain posi­ tion the forefoot must be loaded against the neutral subtalar rear­ foot. This is accomplished by ap­ plying a dorsiflectory force against the fourth and fifth metatarsal heads so that the forefoot is fully pronated on a neutral rearfoot. In order to fully lock the forefoot, also called loading the forefoot, at the midtarsal joint the dorsiflectory

FIG. 14-38. Measurement of supination and pronation of the calcaneus (hindfoot inversion and eversion [non-weight .bearing]).

force should be applied only W1til resistance is appreciated. The rela­ tionship of the neutral subtalar po· sWon and a fully pronated forefoot against the rearfoot results in the neutral position of the foot in the open-chain position. It is not neces­ sary to dorsiflex the foot to 90° or lift the leg from the supporting sur­ face. Slightly adduct the forefoot to ensure complete midtarsal joint pronation. ii. Place one arm of the goniometer along the posterior calcaneal bisec­ tion and the other arm along the plantar aspect of the heel (see Fig. 14-39A). Align the latter arm with the plane of the forefoot (an imagi­ nary line from the head of the fifth metatarsal to the head of the first) and read the degrees of forefoot

4 16

CHAPTER 14

•

The Lower Leg, Ankle, and Foot

~

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B

A

FIG. 14-39. Measurement of forefoot valgus or varus (non-weight bearing I with niometer or (S) inclinometer.

deviation. An inclinometer may also be used with the knee in 90° of flexion (see Fig. 14-39B). Deviation from a normal perpendicular rela­ tionship with a line bisecting the calcaneus represents a difference between alignment of forefoot to hindfoot. iii. Forefoot valgus is commonly found in the varus foot. Forefoot varus may require increased pronation to adequately contact the surface while running or walk­ ing. 80,l66 iv. The calcaneal position, varus or valgus, can also be determined at this time. d. Dorsiflexion i. Position the patient prone with his foot over the edge of the table. Place a 4-inch roll underneath the distal anterior thigh to ensure full knee extension. Place the foot into

(AI

go­

subtalar neutraL While maintain­ ing subtalar neutral, manually assist dorsiflexion of the foot on the leg while the patient actively dorsi flexes the foot to its end range. ii. Repeat with the knee flexed to 90 0 • iii. Dorsiflexion is measured to the nearest degree. Note: The subtalar joint must be maintained in a neutral position during these motions. Pressure ap­ plied to the first ray win help pre­ vent pronation. 117 C. Resisted isometric movements. Resisted isomet­ rics are done in the supine or sitting position. Resisted isometric knee flexion should be in­ cluded because of the triceps surae action on the knee. With the patient's foot placed in the anatomical position, the movements tested are as follows. 1. Dorsiflexion. Pain may be due to a tendini­ tis. Painless weakness associated with a

PART II

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footdrop may be due to a lesion of the lat­ eral popliteal or the LS nerve root. Painful resisted dorsiflexion and inversion occurs in tendinitis of the anterior tibialis. 2. Plantar flexion. Test in weight-bearing. Pain may be due to a lesion of the AchiHes ten­ don or a tear in the gastrocnemius. A pain­ less weakness may be due to 51 nerve-root pressure. 3. Inversion. A painful weakness of inversion is usually due to tenosynovitis or tendini­ tis of the posterior tibialis muscle. Painless weakness may be due to a tendon rupture or L4 nerve root compression. 4. Extension of the great toe. A painful weak­ ness occurs with tenosynovitis of the ex­ tensor hallucis longus muscle. Painless weakness may indicate an LS nerve root compression. 5. Toe extension. A painful weakness may in­ dicate a tenosynovitis of the extensor digi­ torum longus; painless weakness occurs in an LS nerve root lesion. D. Joint-play movements. Assess for hypermobility or hypomobility and presence or absence of pain. 1. Distal tibiofibular joint-anteroposterior glide (see Fig. 14-41) 2. Ankle mortise (talocrural) joint a. Distraction of talus (see Fig. 14-42) b. Anterior and posterior glide of talus. Anterior glide is an important test for integrity of the anterior talofibular liga­ ment. The patient is supine. Place one hand over the dorsum of the distal tibia and cup the other hand around the back of the calcaneus. The talus by way of the calcaneus is pulled forward in the mortise, and the movement is com­ pared with the movement on the oppo­ site side. i. Hypermobility will be present in the case of a chromc anterior talofibular ligament rupture. ii. Pain will be reproduced from a talofibular ligament sprain or ad­ hesion. 3. 5ubtalar joint a. Distraction of calcaneus b. Dorsal rock of calcaneus, plantar rock of calcaneus (see Figs. 14-47 and 14-48) c. Varus-valgus tilts of calcaneus (see Figs. 14-45 and 14-46). The range of cal­ caneal inversion and eversion is as­ sessed and the two feet are compared.

Clinical Applications-Peripheral Joints

417

Capsular restriction will result in a greater loss of inversion than eversion. 4. Transverse tarsal joint-dorsal-plantar glides (see Fig. 14-49) 5. Naviculocuneiform joint-dorsal-plantar glides (see Fig. 14-50) 6. Cuneiform-metatarsal joints a. Dorsal-plantar glides b. Pronation-supina tion (see Fig. 14-51) 7. Cuboid-fifth metatarsal joint-dorsal­ plantar glides 8. Intermetatarsal and tarsometatarsal joints-dorsal-plantar glides (see Fig. 14-53) 9. Metatarsophalangeal and interphalangeal joints a. Dorsal-plantar glides (see Fig. 14-55) b. Internal-external rotations c. Medial-lateral tilts d. Distraction (see Fig. 14-54) IV. Neuromuscular Tests There are few localized neurological problems that affect the foot. If a disorder affecting a rele­ vant nerve root (L4, LS, 51, or 52) is suspected, or if a problem affecting a peripheral nerve supply­ ing the foot is suspected, the necessary sensory, motor, and reflex testing should be performed. The segmental and peripheral nerve innervations, as well as the related reflexes, are listed in Chap­ ter 4, Assessment of Musculoskeletal Disorders and Concepts of Management. V. Palpation A. Skin 1. Moisture or dryness. Abnormal moisture, usually associated with pain and joint re­ striction, may accompany a reflex sympa­ thetic dystrophy. Vascular disorders may also cause changes in the moisture or tex­ ture of the skin. 2. Texture 3. Mobility. 5kin mobility may be restricted after prolonged immobilization, especially following a surgical procedure. 4. Temperature. Inflarrunatory lesions will often result in increased skin temperature over the site of the lesion. Fairly precise documentation of the degree of inflamma­ tion may be made by using a thermistor probe. This often offers a convenient guide as to the effect of treatment procedures on the state of the lesion as well as a guide to the state of the inflammatory process in general. For example, a baseline reading can be documented and measuremen taken before and after each treatment

418

CHAPTER 14

•

The Lower Leg, Ankle, and Foot

sion (these must be taken over precisely the same point and at the same time of day). A slight elevation of, say, 1DC can be expected after any treatment that imposes some mechanical stress, such as mobiliza­ tion, massage, or exercise. However, it is important that the elevation does not per­ sist over more than a few hours. If so, the treatment program may be too vigorous. If some decline in temperature is noted, it may be a sign that resolution is taking place. Thermistor readings, as with most tests, are significant when compared with a norma] side. B. Soft tissue 1. Swelling a. Localized extra-articular swelling may accompany ankle sprains, usually in­ volving the lateral aspect of the ankle below the lateral malleolus. b. Localized articular effusion of the ankle mortise joint manifests as a loss of defi­ nition over the malleolar regions. Sub­ tle joint effusion can be detected by ap­ plying firm pressure with the thumb and index fingers over the regions below the medial and lateral malleoli simultaneously. This will force the fluid into the anterior capsular region and cause a fullness over the dorsum of the ankle. c. Generalized edema of the foot may fol­ low major trauma, or it may accom­ pany systemic, more generalized vas­ cular or metabolic disorders. 2. Mobility 3. Consistency 4. Pulses a. The pulse of the dorsalis pedis artery may be palpated just lateral to the ten­ don of the extensor hallucis longus over the dorsum of the foot. b. The pulse of the posterior tibial artery is palpated behind the tendons of the flexor digitorum longus and flexor hal­ lucis longus posterosuperior to the me­ dial malleolus. 5. Other specific tendons, ligaments, and muscles should be palpated, as indicated by findings up to this point in the exami­ nation. A guide to palpation of these struc­ tures is included in the section on surface anatomy in this chapter. C. Bony structures and tendon and ligament attach­ ments 1. Palpate joint margins to assess structural

alignment and to note any hypertrophic changes. 2. Palpate tendon and ligament attadunents as indicated in the section on surface anatomy.

COMMON LESIONS AND THEIR MANAGEMENT Probably the most common lower limb problem in amateur and professional athletics is that of overuse syndromes. The frequency of overuse injuries ensures that they will be a significant portion of the practice of the sports medicine clinic and the general orthopedic clinic. Overuse injuries affect different anatomical sites and tissues and are usually secondary to training errors and accumu}ated microtrauma. In the lower leg group, specific syndromes include tibial stress syn­ drome, AchiUes tendinitis, shin splints, tibial stress fractures, and compartment syndromes. The common disorders affecting the foot are in the majority of cases the result of some biomechanical dis­ turbance. As indicated in the preceding section, such biomechanical disorders may be of local origin, or the primary problem may involve one of the other weight-bearing segments. For this reason, evaluation of chronic, subtle foot disorders requires that struc­ tural and functional assessments of the other weight­ bearing joints be made. Similarly, evaluation of pa­ tients with problems in these other regions may necessitate examination of the foot. In understanding the rationale of the evaluative and treatment proce­ dures related to foot disorders, it is essential that the practitioner have a basic knowledge of the biome­ chanics of the foot and how they relate to the biome­ chanics of the other weight-bearing joints. Because the numerous joints of the foot contribute to make it a very mobile structure as a whole, it has the ability to attenuate the energy of forces applied to it. For this reason, traumatic lesions affecting the foot are re]atively rare. On the other hand, the common le­ sions affecting the ankle are usually of traumatic ori­ gin.17 While the individual joints making up the ankle are relatively trackbound or uniaxial, the ankle com­ plex allows some movement in the sagittal, frontal, and transverse planes. However, transverse rotations are of limited range because they do not occur about a true vertical axis. Also, eversion is normally quite re­ stricted because the fibular malleolus extends distally to create an abutment that limits this movement. Forces that moVe the ankle past its physiological lim­ its of motion will tend to cause damage, usually to the osseus or ligamentous components of the ankle com­ plex, or to both. Excessive forces to the ankle produc­ ing such damage are often the result of forces from the

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ground acting over the lever-arm provided by the foot or forces of the center of gravity of the bod y acting over the lever-arm of the lower extr mity with the foot fixed. Because of these lever-aI ms over which forces acting on the ankle may be appli d and because certain ankle motions are normally limited, the ankle is often the site of acute traumatic injuries such as sprains and fractures. Except in situations in which there is mala lignm ent of bony constituents, such as after healing of a frac­ ture, or in situations in which there is marked restric­ tion of movement of one of the ankle joints, such as after arthrodesis of the subtalar joints, degenerative joint disease affecting the ankle is rare. Rheumatoid arthritis often affects the foot but less often the ankle. Both the foot and ankle may be the site of fatigue disorders. Such disorders result from abnormally high stresses occurring over relatively short periods of time or from mildly abnormal stresses occurring over a long period of time. The former situation usually oc­ curs in athletes or others who havt' undergone an abrupt increase in activity level. rn stich cases, the de­ gree of microtrauma affecting certain tissues exceeds the rate at which the body is able to repair itself; the result is a fatigue-induced yielding of th e involved tis­ sue. Examples are stress fractures, blisters, an d many of the tendinitis conditions aHecting this region. Milder stresses occurring over longer periods of time tend to result in tissue hypertrophy that may con­ tribute to certain painful disorders. Typical examples are heel spurs and various callus formations.

D

Overuse Syndromes of the Leg

The pathophysiology of overuse injuries i a local in­ flammatory response to stress. The causes of 0 eruse injuries are either intrinsic (malalignment syndromes, muscle imbalances) or extrinsic (training rror).65 A systematic musculoskeletal assessment is n ecessary in order to differentiate overuse injuries and to clarify the etiological factors. Effective trea tment is predi­ cated on recognizing and correcting th e underlying predisposing, precipitating or perpetuating etiological factors.

SHIN SPLINTS The term shin splints is considered by many to be a catch-all phrase applied to a number of different con­ ditions limited to the legs and has generated much confusion. 144,154,156 Shin splints (idiopathic compart­ ment syndrome) is used here to mean an etiological subset of exercise-induced pain: m echanical inflam­ mation due to repetitive stress of the broad proximal portion of any of the musculotendinous units origi-

Clinical Applications-Periph eral Joints

4 19

nating from the lo~er part of the leg or tibia dllIing weight-bearing.87,lo4,17S" This narrower d efini ti n is consi.stent w ith American Medical Association termi­ n Ology? Depending on the affected muscles, shi.n splints can be anterolateral or posteromediaI. 5,87,175 Anterolater al shin splints caus p ain a nd tenderness lateral to th e tibia over the anterior comp artment and invol e the pretibial m uscles, including th anterior tibialis, ex­ tensor hallucis longu , and extensor digitorum lon­ g u . Anterolater al shin splints may OCCllI second ary to heel contact on hard surfaces, or to w ear in g a shoe with a h ar d heel, or to biomechanical abnormalities such a forefoot val·us. 65 ,87 A muscle imbalance be­ tw een a weak pre-tibial muscle group and tight gas­ trocnemiu -soleus muscles m ay result in overactiva­ tion of these muscles d uring heel-strike and swing ph ase. Posteromedial shin splints cause symptoms along the posteromedial b order of the middle to lower tibia over th e posterior comrartment, which is ppreciated more during toe-of(1 2 Research has sho'wn a strong p o itive correlation betw een excessive pronation and p osteromed ial shin sp lints.171 In anterola teral an d posteromedial shin splints, there is typically weakness f the affected muscles and p ain reprodu ced by resi ted active motion.128

MEDIAL TIBIAL STRESS SYN DROME Med ial tibial stress syndrome (MTSS) or tibial perios­ titis presents as exercise-ind lIeed pa in localized to the distal po ter omedial b order of the tibia. According to Walker,T75 the clinical distinction between posterome­ dial shin p lints and MTSS is hazy, bu t the latter is usually more focal a nd more painfu l. The precise p athophysiology o f MTSS is controversial, but it is most likely perio teal inflammation (p riostitis) near the ori§1n of the p osterior tibialis or the medi.al sole us. 1 3 The soleus m uscle syndrome has been iden­ tified as a cause of posteriomedial shin splints through cada ver electromyograp hy (EMG) and open biopsy analysis b y M ichael and Holder.12° Exam ination reveals a well-localized 3- to 6-cm area of tenderness over the p osteromedial edge of the dis­ tal one third of the tibia. 82 Ac tive resisted p lantar flex­ ion and inversion of the foot repr duce the pain.

STRESS FRACTURE OF THE TIBIA Stress fractures of the lower limbs account for 95 p er­ cent of all s tres frac tmes in athletes. 131 Abou t one half occur in the tibia or fibula . Stres fractu res result from fatigue failu re w ithh' the bone, although the SllI­ rounding m uscle may actually fatigu e first. 175 In­ creased or different activity results in an altered rela­

420

CHAPTER J 4

•

The Lower Leg, Ankle, and Foot

tionship of bone growth and repair (Wolff's law). The resulting stress fracture ma y run the spectrum from a microfracture with simple cortical hypertrophy to rup ture of bony cortices with a fracture line.1 07 The factors that seem to be most clearly associated with the development of stress fractures are repeti­ tiveness of activity and muscle forces acting across the bone. The muscle forces, or torque, across the bone ma y stress that bone if an imbalance between antago­ nistic muscles exists.32 Sym p toms of stress fracture arE' usually gradual in onset over a 2- to 3-week period. 107 The patient com­ plains of pain which initially occurs during activity and is reli eved by rest. In the next stage the pain con­ tinues for hours, perhaps through the night, or it migh t become worse d uring th e nigh t, w hich is highly suggestive of bone pain.147 Swelling may occur partic­ ula rly after activi ty. On clinical examination, localized tenderness with or without swelling is almost always present over the fracture. Common sites are the medial aspect of the tibia and 2 to 3 inches above the tip of the fib ular malleolus above the joint line. S7 A positive percussion sign (transmission of pain to the fracture si te area on percussion of the bone at a distance) and the tuning fork test may help to add weight to the presumptive diagnosis of stress fracture. The use of ultrasound over a stress fracture often causes rather acute pain 1 to 2 hours after the patien t leaves a therapy session. This is felt to be secondary to increased hyperemia of the bone con taining the stress fracture. 87 A stress fracture may not be visible on ordinary x­ ray films for 2 to 8 w eeks after symptoms commence. Therefore, a tech netium-99 diphosp honate bone scan is the gold standard in diagnosing stress fracture.1 75 An increased uptake or "hot spot" on a positive bone scan can be seen within the first few days of the symp ­ toms presenting and false-positive scans are infre­ quent. 26 ,60,107,136

When overuse is a contributing factor, there will a characteristic history of gradual onset of pain that may be accentuated by excessive pronation or supina­ tion.1 63 Clement and coUeagues20 fOlmd that 56 per­ cent of 109 n mners with Achilles tendinitis displayed excessive pronation. Training errors, poor flexibility, and weakness of the Achilles tendon have also been implicated as predisposing factors in Achilles tendini­ ti s.65 The pain may also be associated with underlying hyperostosis of the posterior surface of the calcaneus (Haglund's deformity or "pump bump") or inflamma­ tion of the infra tendinous or supratendinous bursa Yl,1 63 Bursitis alone may be present and should be included in the differential diagnosis for posterior heel and ankle pain. One should also consider in the differential diagnosis os trigonum problems. 163 As ","ith other overuse injlUries, pain is aggravated by activity and relieved by rest. The patient presents with pain several centimeters proximal to the inser­ tion of the tendon into the calcaneus, the area of poor­ est blood suppiy.91 A presentation of considerable swelling and lumpiness of the Achilles tendon usually points to intratendinous damage. When there are su­ perficial, iso~ated areas of pain and crepitation that are palpable, one may be sure of the diagnosis of para ten­ onitis. Dorsiflexion causes pam, and crepitus may be felt along the tendon at the most tender area. 91 If there is pain on excessive plantar flexion, especially with palpation at the lateral posterior aspect of the ankle, an os trigonum injury should be suspected. 163 Treatment follows similar lines as that of other overuse injuries. Chronic paratenon lesions that do not respond to appropriate physical therapy, rest, and other adjunct measures will require a surgical tenoly­ sis. Tendinosis or intratendinous lesions may require surgical exploration. Necrotic tissue is cureted and the tendon is repaired. 163 A rupture of the Achil1es ten­ don requires immediate referral for consideration of a surgical repair.

TEN DINITIS

TREATMENT OF O VERUSE INJURI ES

Another common lower leg overuse injury about the ankle is tendinitis. Achilles tendinitis is the most com~ mon form of tendinitis seen in athletes.44 ,79,91 Because the Ad-lilies tendon does not have a synovial sheath, this condition cannot be considered to be tenosynovi­ tis. Inflammation, resulting from stress, often occurs in the loose cOrmedive tissue about the tendon known as the paratenon. Classification is based on whether this tissue, or the tendon itself, is involved. 146 Seen more often in men than women, Achilles tendinitis, w ith or without peritendinitis (involving the para tenon; see below) is often associated with repeti­ tive or high-in1pact sports such as running, basketball, or voileyba l1. 20

The principles of treatment and rehabilitation of overuse injuries are the same as those related to the management of abnormal foot pronation and supina­ tion (see pages 427 and 433) . Rest of the affected mus­ cle-tendon-bone unit is the mainstay of treatment in phase 1. Both shin splints and medial tibial stress syn­ drome can progress to stress fracture, and stress frac­ hues may progress to complete cortical break. I07 The duration of rest varies from 1 to 2 days for mild shin splints to seve.al months for severe stress fractures. In phase I, analogous to treatment of traumatic in­ juries (see management of ankle sprains, page 421), ice, compression, and elevation are used to reduce swelling and inflammation. Nonsteroidal anti-in flam-

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matory drugs (N5AIDs) are believed to be beneficial in most types of overuse injuryJ7S However, in stress fractures, they may have no advantage over simple analgesics. 1I I To prevent recurrence of overuse injury, it is imper­ ative to review and correct faulty training methods and to evaluate for biomechanical factors. Of all run­ ning injuries, 60 percent result from training errors such as running on hard, uneven, or inclined surfaces, improper footwear, and overzealous training.23

D

Ankle Sprain

The most common lesion affecting the ankle is a sprain or tear of one of the ligaments. 17,S2 The anterior talofibular ligament is the most commonly sprained ligament at the ankle and is probably the most com­ monly sprained ligament in the body. The next most frequently sprained ligaments at the ankle are the cal­ caneocuboid and the calcaneofibular ligaments. Por­ tions of the deltoid ligament may also be sprained, but more often a forceful eversion stress will result in an avulsion of the tibial malleolus rather than damage to the ligament. 18,31

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I. History A. Onset of pain. The patient will invariably recall the traumatic incident. The common mecha­ nism of injury for an anterior talofibular liga­ ment ~rain is a plantar flexion-inversion stress. S ,66,88,127 Typical examples include an athlete who lands from a jump on the lateral border of the plantarly flexed foot, a person wearing high-heeled shoes or walking on un­ even ground who catches a toe on the lateral side of the foot, or a person stepping off a curb or step who rolls over the lateral side of the plantarly flexed foot. If the forefoot is forced into supination or adduction, the calca­ neocuboid ligament may be injured instead or as well. The calcaneofibular ligament restricts inversion with the foot in a more neutral or dorsiflexed position. It may be injured along with the talofibular ligament if, at the time of injury, the person retains good contact of the foot with the ground but continues to force the foot into inversion. When torn, the deltoid ligament is usually injured because the foot is forced into external rotation and eversion with respect to the leg. As mentioned, it is more common for a por­ tion of the tibial malleolus to avulse with the deltoid ligament attachment. The anterior tibiofibular ligament may be torn with a simi­ lar mechanism, since as the talus rotates

CJinical Applications-Peripheral Joints

421

within the mortise, it tends to wedge the tibia and fibula apart, producing a diastasis. U8,31 In order for the talus to rotate enough to pro­ duce a diastasis and to tear the anterior tibiofibular ligament, the deltoid ligament is torn or the tibial malleolus is avulsed as well. 1 B. Site of pain . This usually corresponds well with the approximate location of the injury. Some pain may be referred distally into the foot or proximally into the lower leg. e. Nature of pain or disability. Similar to ligamen­ tous lesions at the knee, the degree of pain and disability immediately following an in­ jury to an ankle ligament does not necessarily correlate well with the severity of the lesion?8 A person sustaining a mild or moderate sprain may describe more pain and be more reluctant to continue a particular activity than one who completely ruptures a ligament. This is because in the event of a rupture there is complete loss of continuity of the structure and there are no longer intact fibers to be stressed and from which pain can be elicited. Repeated episodes of anterior talofibular ligament sprains are not uncommon. Usually the initial injury results in somewhat more pain and disability than with subsequent oc­ currences. These patients typically describe intermittent giving way of the ankle, often during athletic activities, followed by pain and effusion lasting for a few days.49,lS8 II. Physical Examination A. Observation. A patient seen soon after injury may hobble into the office walking with a characteristic "foot flat," short-stance gait; both heel-strike and push-off are lacking. If the pain is more severe, the patient may walk in with the aid of crutches or hop on one leg. B. Inspection. Locatized swelling over the region of the involved ligament is usually present within several hours after the injury. Since the anterior talofibular ligament and the deep fibers of the deltoid ligament blend with the ankle mortise joint capsule, there may be some associated articular effusion. Within a day or so following most ankle sprains, there is diffuse ecchymosis in the region of the in­ jury, which may extravasate distally into the foot.

e. Selective tissue tension tests 1. Active movements. In the acute stage there

is likely to be considerable difficulty in heel and toe walking and other weight­ bearing activities involving ankle move­ ments. The examiner mllst exercise judg­ ment in requesting the patient to perform

422

CHAPTER 14

•

The Lower Leg, Ankle, and Foot

these movements to avoid undue discom­ fort or stress to the part. 2. Passive movements and joint-play move­ ments (key objective tests) a. If the ankle mortise joint capsule has been stressed with subsequent articular effusion, the ankle movements will be limited in a capsular pattern; plantar flexion will be slightly more restricted than dorsiflexion. b. In the case of a mild or moderate liga­ mentous sprain, pain will be repro­ duced with movements that stress the involved ligament. There will usually be an associated muscle-spasm end feel. Painless hypermobility will be noted in the presence of chronic rup­ tures. Acu te ruptures will also demon­ strate hypermobility; however, a false­ negative finding may be elicited because of protective muscle spasm. Take care to ensure maximal relaxation of the part when performing passive movements. The common ligaments in­ jured and the passive movements used to test their integrity are as follows: i. Anterior talofibular ligament. Combined plantar f1exion-inver­ sion-adduction of the hindfoot and anterior glide of the talus on the tibia 17,97 ii. Calcaneocuboid ligament. Com­ bined supination-adduction of the forefoot iii. Calcaneofibular ligament. Inver­ sion of the hindfoot in a neu tral po­ sition of plantar flexion-dorsiflex­ ion iv. Deltoid ligament. Anterior fibers: combined plantar flexion-eversion­ abduction of the hindfoot; middle fibers: eversion of the hindfoot 3. Resisted movements. These should be strong and painless. Occasionally the per­ oneal tendons are strained in conjunction with an inversion ligamentous strain. In this case, isometric resistance to eversion w il1 be strong and painful. D. Neuromuscular tests . Results are noncontribu­ tory. E. Palpation 1. Tenderness w iU usually correspond to the site of the lesion in acute injuries. There is also likely to be diffuse tenderness in the presence of marked swelling from extrava­ sation of blood into the tissues. 2. Joint effusion from synovitis or extra-artic­

ular swelling will be palpable in the acute stages. 3. Skin temperature wiH be elevated over the region of the involved structure in the acute stages. III. Management A. Acute sprains-immediate measures. At this early stage, there is little that needs to be done to, or for, the patient that he cannot do on his own. Ice, elevation, compression, mobility ex­ ercises, and strengthening can be carried out easily at home by most patients. This does, however, require very clear and precise in­ struction by the therapist. Do not spare words or time in making sure that the patient under­ stands exactly what he should or should not be doing with the ankle. A follow-up visit after 2 or 3 days should be scheduled so that a reassessment can be made and the program appropriately progressed. At this point, there should be evidence of reduction of the acute inflammatory process; pain, temperature, and swelling should be decreased. It is important, in the subacute stage, to carefully reassess joint-play movements, since at this stage the therapist can determine more easily whether there has been some loss of integrity of the in­ volved structure. Often in the acute stage, muscle spasm precludes accurate determina­ tion of the extent of the damage. 1. Reduction of stress to the ligament to aJJow healing without undue lengthening. a. Ankle strapping will help reduce movement in response to mild (non­ weight-bearing) stresses. Swelling should have stabilized by the time of application. A felt or foam rubber horseshoe pad should be used to fin in the submalleolar depressions to obtain even compressions of the area with tape or an elastic bandage. b. Crutches should be used to relieve stress and pain during ambulation. A three-point, partial-weight-bearing crutd1 gait should be instituted; non­ weight-bearing is usually not necessary and should be avoided because of its nonfunctional nature. 2. Reduction of the acute inflammaton' process to reduce pain and to prevent undue tissue damage from localized pres­ sure and proteolytic ceBular responses a. Ice-To decrease blood flow and re­ duce capillary hydrostatic pressure, thus reducing extravasation of blood fluids b. Compression-Increased external pres­

PART II

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sure to the area will minimize capillary leakage by effectively reducing the vol­ ume of the tissue spaces. This can be maintained by appropriate application of an elastic bandage with a horseshoe pad below the malleolus. c. Elevation-Reduces capillary hydro­ static pressure to minimize fluid loss and assists the venous and lymphatic return. 3. Prevention of residual disability a. Motion of the part is instituted in planes that do not stress the healing lig­ ament to minimize residual loss of movement and optimize circulation in the area. b. Isometric exercises to the muscles in the area should be started as early as pain allows, to maintain strength of the muscles of the lower leg and foot. B. Acute sprains-subsequent measures 1. Mild sprains. In the case of a simple sprain, in which there is no hypermobility on the associated passive movement tests, gradual return to normal activities should be allowed as the inflammatory process re­ solves. Weight-bearing should be in­ creased and the crutches discarded, usu­ ally by the fifth day. Range of motion, strength, and joint play should be restored to normal. Most patients may regain nor­ mal motion and strength with careful in­ struction in home exercises. Before dis­ charging the patient from care, the therapist must ascertain tha't normal joint play has rehlrned . If it has not, the re­ stricted movements must be restored with passive joint mobilization techniques. Fric­ tion massage, initiated in the subacute stage, may promote healing of the liga­ ment in a mobile state and prevent adher­ ence to adjacent tissue. As the swelling subsides in the subacute stage, strapping should be substituted for the elastic bandage to provide support and to increase proprioceptive feedback as the patient resumes functional use of the part. Use of strapping should continue until good strength, range of motion, and joint play are restored. The athlete should con­ tinue to strap the ankle when participating in vigorous activities. Studies suggest that ankle strapping does playa role in pre­ venting ankle sprains. 37 This is probably not due to actual mechanical support pro­ vided by the tape, since movement of the bones within the skin (to which the tape is

Clinical Applications-Peripheral Joints

423

adhered) is probably still sufficient to allow a ligament to be stretched. However, the added proprioceptive input provided by the tape may enhance protective re­ flexes (such as contraction of the peroneal muscles) in response to forces tending to stress the ankle ligaments. Return to vigorous activity must be gradual. Clinical evidence of healing does not indicate that a ligament has regained normal strength. In fact, maturation of the new collagen laid down during healing may take weeks or months. The necessary stimulus for maturation and restoration of normal ligamentous strength is stress to the ligament produced by functional use of the part. This induces formation of the ap­ propriate collagen cross-links and realign­ ment of the new collagen fibers along the normal lines of stress. However, the liga­ ment must not be overstressed before nor­ mal strength is regained, since it is suscep­ tible at this point to reinjury. The athlete should begin by jogging, then running, in straight lines. When normal muscle strength and joint motion have been re­ gained, figure-of-eight patterns that im­ pose some lateral stress to the part may be initiated. Gradually, the patient should progress to sharp cutting drills. When these can be performed well and without pain, competitive activity may be re­ sumed. Also during the later stages of rehabili­ tation, balance drills should be instituted to facilitate the restoration of normal pro­ tective reflexes.48,SO Progression may pro­ ceed from challenging one-legged stand­ ing to one-legged standing on a rocking board to one-legged standing on a board supported on half a sphere (free to tilt in all planes). 2. Moderate sprains and complete ruptures. The related literature reflects some contro­ versy regarding the management of rup­ tured ligaments at the ankle. Most authori­ ties would agree that injuries involving extensive damage, with rupture of both the anterior talofibular and calcaneofibular ligaments, should be repaired surgically to restore passive stability to the ankle. 4,158 Good results are favored by early surgery, since the torn ends will tend to atrophy and retract with time, making app osition and suturing techni ally difficult or im po sible. Similar considera tions appl to rup­ ture of the deltoid ligament.

424

CHAPTER 14

•

The Lower Leg, Ankle, and Foot

There is more divergence of opmlOn, however, with respect to management of isolated ruptures, in which some hyper­ mobility of anterior glide of the talus in the mortise is demonstrable. While some clini­ cians favor early surgical intervention to suture the torn ends and minimize resid­ ual and structural instability, others favor early return to function following some period of restricted activity and immobi­ lization. There is evidence from studies by Freeman that suturing of the ligament does result in a more stable joint, but in the end, the functional status of those under­ going surgery is really no better than those treated "conservatively. ,,48-50 In fact, those patients treated conservatively returned to normal function significantly sooner than those undergoing surgery, if they were not immobilized in plaster for a prolonged pe­ riod of time. Of those treated conserva­ tively, there was very little difference in residual mechanical stability between those who were immobilized in plaster for 6 weeks and those treated with strapping and early mobilization. The incidence of residual pain and swelling several months following injury was highest in the surgi­ cal group. The only way to guarantee in­ creased mechanical stability following rupture of the anterior talofibular ligament is to reappose the torn ends with sutures. However, it seems that the residual dis­ ability resulting from prolonged immobi­ lization in those treated vvith surgery out­ weighs whatever advantage this form of management may have in producing a more stable ankle. Further studies by Free­ man suggest that there is no correlation be­ tween mechanical instability, as deter­ mined by stress roentgenograms, and the incidence of residual disability resulting from chronic swelling and pain. 48-50 Conservative (nonsurgical) management of patients in whom there is evidence of ac­ tualloss of integrity of the ligament should follow the same approach as management for Less serious injuries; the primary differ­ ence should be that those ankles with more extensive damage will need to be protected, by crutches and strapping, somewhat longer, perhaps as long as 2 weeks. How­ ever, early motion and strengthening at pain-free intensities should be initiated as resolution of the acute inflammatory process ensues. Also, in cases of more ex­

tensive damage, return to normal and, es­

pecially, to vigorous activity levels should

be more gradual. Again, it must be empha­

sized that although new collagen is laid

down within the first 1 or 2 weeks follow­

ing injury, it takes months for this new tis­

sue to mature to normal strength. During

the period of maturation, the ligament is

weaker than normal and, therefore, more

susceptible to rein jury .

C. Chronic recurrent ankle sprains. Following ini­ tial injury, especially to the anterior talofibu­ lar ligament, a certain number of patients wiU suffer recurrent giving way of the ankle, with subsequent pain and swelling. There are three possible causes of this to be considered and to which assessment should be directed. 1. Healing of the ]jgament with adherence to

adjacent tissues. In this situation, the

healed ligament does not allow the joint

play necessary for normal functioning of

the part. 31 With repetitive stress to the

tightened structure, pain and swelling will

result from a fatigue phenomenon. With

forceful stress to the structure, the adhe­

sion will rupture, producing another

sprain. This type of problem will present

as a painful, minor restriction on passive

plantar flexion-inversion of the hindfoot

and on anterior glide of the talus. Treat­

ment consists of deep, transverse friction

massage to the ]jgament and specific joint

mobilization in the directions of restric­

tion. Normal mobility to the ligament is

thus gradually restored .

2. Loss of protective reflex muscle stabiliza­

tion. Normally, stress to some aspect of a

joint capsule or to a joint ligament results

in firing of specific receptors in the struc­

ture, through a reflex arc, to produce con­

traction of the muscles overlying the

stressed structure. This "booster" mecha­

nism of dynamic joint stabilization pro­

tects joint ligaments from injury under

conditions of heavy loading. Thus, when

the anterior talofibular ligament is

stressed, the peroneus tertius is called to

reduce the load to the ligament. Damage to

a ligament w ith subsequent immobiliza­

tion may result in interference of this pro­

tective mechanism. Freeman has shown

good results in management of such cases

by instituting a program of balance train­

ing, as described.48 The therapist must also

make sure that good muscle strength has

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PART II 3. Gross mechanical instability of the joint. If

both the anterior talofibular ligament and the calcaneofibular ligament are ruptured, or if there has been extensive capsular dis­ ruption with an anterior talofibular liga­ ment rupture, the resultant mechanical in­ stability of the joint may not allow certain functional weight-bearing activities to be performed without giving way. Such pa­ tients will present with obvious hypermo­ bility on joint-play movement tests. If an aggressive muscle strengthening and bal­ ance training program is not sufficient to compensate for the instability, surgical re­ construction may be contemplated. Thus, the therapist should direct assess­ ment of the chronically unstable ankle to­ ward determining if there is some residual increase or decrease in joint play, if good muscle strength has been regained, and whether the person is able to balance well during one-legged standing t.mder various unstable conditions (e.g., on a tilt board) . It is important to realize that giving way of the joint is not necessarily the result of structural instability and that some degree of structural instability can be compen­ sated for by muscle strengthening or bal­ ance training.

o

Foot Injuries

CUBOID DYSFUNCTION

Cuboid dysfunction also may be referred to as sublux­ ation or the cuboid syndrome. The etiology is uncer­ tain but may be related to dysfunction of the calca­ neocuboid joint or abnormal pull of the peroneus longus tendon through a groove on the inferior aspect of the cuboid dorsally, causing the medial aspect of the cuboid to sublux plantarward. 126 Newell and Woodie 126 found that 80 percent of cuboid subluxa­ tions occur in pronated feet. The patient presents with fairly acute, severe pain and sometimes swelling local­ i.zed to the calcaneocuboid joint. He or she is unable to run, cut (do a 'lateral shift), jump, or dance without a marked increase in pain. There is localized tenderness to palpation in the plantar aspect of the foot and later­ ally over the joint. 144 Roentgenograms are negative. Treatment by manipulqtion of the cuboid using one of a number of methods, usually brings immediate re­ lief (see Fig. 14_52).29,54,91,100,108,109,118 Release of the long dorsiflexors and peroneals with deep massage should be performed prior to manipulation.1° 8 This should be followed by placement of a felt pad beneath

Clinical Applications-Peripheral Joints

425

the cuboid on the plantar surface of the foot, along with a low-dye strapping procedure (see Appendix B) to give the arch added support for 1 or 2 weeks. 91 In longstanding cases resistant to other forms of therapy, surgical exploration of the cuboid and peroneus longus tendon has been undertaken. 144 METATARSALG IA

Metatarsalgia is a syndrome describing pain over the metatarsal heads or in the metatarsophalangeal (MTP) joints. The cause may be vascular, avascular, neuro­ genic, or mechanical. 63 Scranton149 classifies metatar­ salgia according to whether a weight-bearing imbal­ ance exists between the metatarsals (primary) or whether the forefoot pain is due to other factors, such as stress fractures or rheumatoid arthritis (secondary). Both primary and secondary metatarsalgia have char­ acteristic associated keratosis. A third classification of forefoot pain is that wi.thout reactive keratosis such as neuromas, gout, and plantar fasciitis. 77 Many theories have been developed to attempt to explain the etiology of primary or generalized meta­ tarsalgia . One theory suggests that a short first metatarsal will cause the second to have to bear a dis­ proportionate amount of weight as the body propels over the foot and thereby result in ultimate dysfunc­ tion and the development of a painful callus. 77 A sub­ luxing second or third MTP joint, or failure of the transverse metatarsal arch to be maintained by the transverse metatarsal ligaments and the transverse head of the adductor haHucis muscle, may also be the cause of metatarsalgia. According to Kraeger,91 generalized metatarsalgia often occurs secondary to a tight Achilles tendon, which restricts dorsiflexion. The loss of full dorsiflex­ ion loads the weight onto the forefoot, thus applying pressure to the MTP joints. Any tendency toward ex­ cessive pronation will lead to hypermobile function­ ing of the first and fifth ray and thereby cause a rela­ tive depression of the transverse metatarsal arch. Metatarsalgia is common in middle-aged persons with a pronation tendency.14 Other extrinsic factors such as excessive weight gain and wearing high­ heeled shoes have been suggested as causes for, or ag­ gravating circumstances of the condition. The patient presents with an antalgic gait including diminished push-off. In some cases the patient may prevent any weight shift across the metatarsal heads by weight-bearing exclusively on the lateral border of the foot?7 Pain may occur at night, but the patient typically reports pain only on weight-bearing. Pre ­ sure to the involved metatarsal head will elicit pain. Treatment of the different causes of metatarsalgia are similar, although it must be individualized to the exact problem. Treatment should include heel cord

426

CHAPTER J 4

•

The Lower Leg, Ankle, and Foot

stretching and exercises to strengthen the intrinsic toe flexors. Mobilizati on is suggested in order to reduce secondary fibrositis from spasm and joint dysfunc­ tion. 29 Metatarsophalangeal d ecompression (traction) and manipulation of the metatarsals (metatarsal whip) are recommended treatments. Metatarsal pads just proximal to the second or third metatarsal head or an external metatarsal pad should be considered. An­ other option is to place a pad beneath the first metatarsal to allow it to bear m ore weight. 91 Or­ thotics, shoe modification, or a reduction in heel height should be considered. PLANTAR FASCHTIS

Plantar fasciitis is an inflammation of the plantar fas­ cia and the perifascial structures. Chronic stress to the origin of this fascia on the calcaneus may cause cal­ cium to deposit, forming a spur (plantar calcaneal spurs). Since plantar cak aneal spurs and plantar fasci­ itis involve basically the same symptoms, develop via similar mechanisms, and are treated in the same man­ ner, these common pathologies are often considered together. Frequently, heel spurs are not symptomatic. This has been shown to be the case with the discovery of calcanea ~ spurs on x-ray studies of nonsymptomatic heels. Roentgenograms may show big spurs without plantar fasciitis or no spurs in the patient with severe plantar fasciitis. As is typical of any overuse injury, plantar fasciitis can be caused by an acute injury (strain) from exces­ sive loading of the foot. More ofte n the mechanical cause is due to chronic irritation from an excessive amount of pronation or prolonged duration of prona­ tion, resulting in microtears at the plantar fa scial ori­ gin. A cav us or high-arched foot with its limited sub­ ta ~ ar excursion is also at risk, because a tight plantar fascia is usually present in this type of foot. A cavus foot may develop plantar fasciitis owing to its intrin­ sic inability to dissipate force (tack of prona tion) from heel-strike to mid stance, resulting in increased load in the plantar fascia. 92 Plantar fasciitis is a conunon cause of heel pain. It occurs in patients of either sex, usually over the age of 40 except in active sportsmen when the patient, usu­ ally male, may be in his twenties. 25 It is commonly found in people whose occupation involves pro­ longed standing or walking. Pain is made worse by activity, such as climbing stairs, walking, or running, may be present at night, and is often present when hrst getting out of the bed in the morning. It tends to be relieved by rest. Clinical examination usually localizes tenderness at the planta r fascial attachment of the calcaneus, just distal to this attachment, in the medial arch area and in the abductor hallucis muscle. Pa in to palpation of

the posterior inferior origin of the abductor hallucis muscle has been theorized to be the result of ov eruse of the abductor hallucis muscle in its role to aid in producing forefoot supination to decrease loading on the p lantar fascia. 19 Chronic partial ruptures have abundant scar tissue, which is palpable near the at­ tachment of the plantar fascia to the plantar tubercle of the calcaneus or more distally, toward the mid as­ pect of the foot.163 Pain may be reproduced by stretch­ ing the fascia on full dorsiflexion of the ankle or big toe. Range of motion of the great toe is usually limited in dorsiflexion, and ankle dorsjBexion is often less then 90°,9' Swelling is rare, but occasionally a small granuloma is palpated on the med,ial fascial origin. With increased pain, the patient changes his gait pat­ tern, keeping the foot in a rather supinated or inverted posture from foot-strike through to toe-off to mini­ mize pa in. 19 This injury must be differentiated from tarsal tunnel syndrome, and entrapment of the first lateral branch of the posterior tibialis nerve. Those with tarsal tunnel syndrome may also complain of burning pain with paresthesias of the heel. They usually have a positive Tinel sign and do not have pain to direct palpation of the plantar fascia. The etiology in younger patients, particularly when the symptoms are bilateral and are unresponsive to the usual conservative treatments, may be seropositive and seronegative collagen vascu­ lar disorders (e.g. , rheumatoid arthritis, spondylitis, and Reiter's syndrome ).13,58,59.1 51.1 70 The older pa tient with heel pain may have gout or osteomalacia.1 32 When dealing with a mechanical etiology, the treat­ ment p~an is directed at both a short-term goal (to con­ trol inflammation at the insertion of the fascia into the calcaneus in conjunction with relieving undue stress in the plantar fascia itself) and a long-term goal (cor­ rection of m echanical factors) . Ice-massage, rest, and anti-inflammatory medications should be used ini­ tially. Ultrasound and phonophoresis with 10 percent hydrocortisone has been used with limited success to control acute inflammation and pain?7 A period of non-weight-bearing is recommended until symptoms subside. Excessive pronation should be limited by use of low-dye strapping and, if this is beneficial, an in­ shoe orthotic device or over-the-counter arch support is recommended. The use of tension night splints has shown promising results. There are also an assort­ ment of heel pads made specifically for heel pain.w, In the case of a high-arched foot, a carefully selected in-shoe orthotic device with good shock absorbency can be used. Soft tissue techniques that stretch the plantar fascia, friction massage at the origin of the fas­ cia to break down the scar tissue, and joint mobiliza­ tions which mobilize the hind foot, subtalar joint, and inferior navicular are usually the most effective treat­ ment methods.25,29 Local corticosteroid injections

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PART II should be used judiciously. Surgery is rarely indi­ (ated.

o Problems Related to Abnormal Foot Pronation

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Pronation of the hindfoot with respect to the forefoot is a relatively common disorder that mayor may not give rise to foot pain. Also, because of the biomechani­ cal interplay between the foot and other weight-bear­ ing segments, the pronated foot may result in dys­ flmction in other regions of the lower extremity, especially the knee. Similarly, a pronated foot may be caused by some 10caI struchlral abnormality of the tarsal skeleton, or it may be caused by some struchlral deviation in segments either distal or proximal to the hindfoot. Pain resulting from a pronated foot is usually of the fatigue type from prolonged increased stress on the affected tissues. In some patients, pain may arise with normal activity levels, while others may get along well until they engage in some activity, such as jog­ ging, that involves increased stress 1evels or fre­ quency. Pain of local origin usually has its source in one of the plantar structures responsible for maintain­ ing the twisted configuration of the foot-the plantar aponeurosis, the short plantar ligament, or the long plantar ligament. Pain may also arise from fatigue of the intrinsic muscles of the foot, in which activity may be increased in an attempt to prevent undue stress to the plantar aponeurosis and ligaments. In association with increased tensile stress to the plantar aponeuro­ sis, a calcaneal periostitis may develop from the added pull to the proximal attachment of the aponeu­ rosis on the plantar surface of the calcaneus. Excessive pulling on the periosteum in this region occasionally results in a bony outcropping (heel spur) that in itself may give rise to localized pressure to the overlying soft tissue. Periostitis and eventually osteophyte for­ mation should be considered as resulting from in­ creased stress to the plantar aponeurosis. It must be emphasized that spurring can develop in the absence of pain and that a cartilaginous spur may be present that is not visible in roentgenograms. Another source of local pain occurring in association with a pronated foot is pressure from the shoes against the talar head or the navicular, which becomes prominent medially when the foot untwists. A pronated foot may be the cause of, or be associ­ ated with, pain in the forefoot, leg, or the knee. Pain from pressure over the first one or two metatarsal heads may result from increased weight-bearing over the medial side of the forefoot. This occurs if the talar head and navicular drop downward and inward, shifting the center of gravity line medially. Since hal-

Clinical Applications-Peripheral Joints

427

lux valgus often accompanies pronation of the hind­ foot, either as a cause or as a result, pressure over a prominent first metatarsophalangeal joint may also occur with increased pronation of the foot. Leg pain may result from increased tension on the anterior or posterior tibialis muscles, which are dynamic support­ ers of the arch of the foot. Chronic periostitis at the proximal attachment of these muscles may result and is often referred to as shin splints. The knee tends to assume a valgus pOSition when the foot pronate. Such an angulation tends to increase the lateral pull on the patella during loaded quadriceps contraction. This may predispose to pain from patellar tracking dysfunction at the knee (see Chapter 13, The Knee). As mentioned, pronation of the hindfoot may occur from some local structural disorder or from struchlral deviations elsewhere. The common local causes are capsuloligamentous laxity and bony abnormalities. CapsuloHgamentous laxity may be a hereditary condi­ tion, or it may accompany some specific disease state, such as rheumatoid arthritis. The common bony anom­ aly resulting in flatfoot is tarsal coalition, in which the talus and cak aneus are fixed to one another in a pronated orientation through fibrous or osseous union.43 The common malalignment problems affect­ ing other regions that predispose to abnormal prona­ tion of the hindfoot are femoral antetorsion, internal tibial torsion, a shortened Achilles tendon, and adduc­ tion of the first metatarsaL The excessive internal rota­ tion imposed by antetorsion of the femur or internal tibial torsion during stance phase is at least partially absorbed by the subtalar joint, bringing the hindfoot into pronation. In the presence of a short Achilles ten­ don, the midtarsal joint attempts to compensate for lack of dorsiflexion at the ankle; in order to do so, the foot must untwist to unlock the midtarsal joints. Be­ cause of the oblique orientation of the first cunei­ form-first metatarsal joint, adduction of the first metatarsal also involves a component of dorsiflexion. This effectively supinates the forefoot, which necessi­ tates a compensatory pronation of the hind foot in order to get the foot flat on the ground. Each of these possible causes must be considered when examining the patient with a pronated foot. Finally, it must be remembered that abnormal foot pronation during gait is not always associated with a "pronated foot" seen on structural examination with the patient standing. The typical example is a person with increased tibial varum. The foot usually app ars normal or even supinated during relaxed standing. However, when running or walking there is a ten­ dency to heel-strike on the lateral border of the heel, causing the foot to undergo increased hindfoot prona­ tion in order to press the heel flat on the ground. yen though the foot appears not to be pronated, it will be subject to increased prona tory stresses . Similar

428

CHAPTER 14

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The Lower Leg, Ankle, and Foot

considerations apply to the patient with either femoral retrotorsion or external tibial torsion, in which the cause of pronation is not localized to the foot itself. I. History A. Onset of pain is usually insidious, since the pathological tissue conditions associated w ith biomechanical abnormalities such as a pronated foot are typically fatigue phenom­ ena. Often the onset can be related to some in­ creased activity level, such as long-distance running. Another common predisposing fac­ tor is a period of disuse, such as immobiliza­ tion of the foot in a cast. In such cases, the muscles of the foot weaken, and when activity is resumed, they no longer contribute their share to stabilizing the arch of the foot . This results in increased stress to the capsuloliga­ mentous structures. Occasional1y, a change in footwear, for example, to a lower heel height, can be related to the onset. Lowering the heel height increases the tension on the Achilles tendon, which may in turn result in increased pronation of the hindfoot in the same way as described for a shortened Achilles tendon. A lowered heel also results in reduced dorsiflex­ ion of the toes during the stance, decreasing the windlass effect on the plantar aponeurosis and reducing the twisted configuration of the foot. B. Site of pain. Foot pain associated with abnor­ mal pronation usually is felt over the plantar aspect of the foot. Pain from calcaneal p erios­ titis and heel spurs is fairly well localized over the bottom of the heel, often more medi­ ally; it may be referred anteriorly into the sole of the foot. Pain from fatigue stress to the plantar ligament or aponeurosis is felt over the sole of the foot, usually more medially. Keep in mind that the bony and soft-tissue pathological processes referred to previously may occur concurrently. Forefoot pain arising secondary to a pronated foot condition may be felt in the re­ gion of the medial metatarsal heads, if due to abnormal weight distribution, or it may be felt over the medial aspect of the first metatar­ sophalangeal joint, if caused by pressure over the joint resulting from a hallux valgus defor­ mity. Knee pain related to a pronated foot is typi­ cally from patellofemoral joint problems (see section on patellar tracking dysfunction in Chapter 13, The Knee).

C. Nature of pain. Pain is from increased stress to

the plantar ligaments, fascia, capsules, or cal­ caneal periosteum under conditions in which increased untwisting of the foot takes place. This typically occurs in a person whose foot undergoes an abnormal degree of pronation during stance phase or whose foot remains in a pronated position during prolonged stand­ ing. The musdes controlling the twist, or arch, of the foot will protect these structures for a certain period of time. However, once the muscles fatigue, more stress is transmitted to the ligaments and fascia , which are responsi­ ble for the passive stabilization of the arched configuration of the foot. In some cases, this may occur with normal activity levels, such as after walking some distance or after standing for a long period of time. In others, increased activity, such as long-distance running, pro­ vides the added stress to bring on the pain. Once a low-grade inflammation develops, the pain is brought on with less stress and may be relatively continuous during weight-bearing. In these more severe cases, pain is typically pronounced on initial weight-bearing, subsid­ ing somewhat as the muscles contract more to protect the painful structures, then increasing again as the muscles fatigue. II. Physical Examination A. Observation and inspection of structural align­ ment. Evidence of excessive pronation of the foot and associated biomechanical abnormali­ ties may be noted when the patient walks or stands. 1. Flattening of the medial arch. The region of the navicular and the talar head may ap­ pear to be prominent medially and de­ pressed inferiorly. 2. Abduction of the forefoot on the rearfoot. 3. Adduction of the first metatarsal, perhaps with a valgus deformity of the first metatarsophalangeal joint. 4. Valgus position of the heel maintained throughout stance phase. 5. Internal tibial torsion. The feet may be pointed inward while the patellae face straight forward . 6. Femoral ante torsion. The patellae face in­ ward when the feet are in normal align­ ment. This must be differentiated from ex­ ternal tibial torsion, which may present similarly. External tibial torsion is evi­ denced by an increased external rotation of the intermalleolar line with respect to the frontal plane (in excess of about 25°).

PART ,II Femoral antetorsion is suggested when the total range of motion at the hip is about normal, but the range Df internal rotation is increased and the range of external rota­ tion is proportionally decreased. 7. Genu valgum. Th is often exists in conjunc­ tion with femoral anteversion.

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B. Inspection (sllpine) 1. Structural alignment a. Forefoot varus. This is the most com­ mon intrinsic deformity resulting from abnormal pronation. 33 ,142,167 Root and co~workers describe it as a frontal plane deformity that is compensated at the subtalar joint by ev ersion or a val­ gus position of the calcan eus in weight­ bearing. HI b. Dorsiflexed and hypermobile first ray producing hallux valgus, w hi ch is sub­ luxation of the metatarsophalangeal joint of the big toe in the sagittal and transverse plane. H I 2. Skin. Inspected for signs of pressure over the navicular tuberde, first metatarsopha­ langeal joint, and medial metatarsal head. As a result of firs t r ay insufficiency, callus or keratosis may d evelop under the head of the second metatar a1. 75 3. Soft tissue. Inspected for muscle a trophy that may relate to loss of dynamic support of the arch of the foot. 4. Inspection of shoes (see page 411). C. Selective tissue tension tests 1. Active movements. If inspection of struc­ tural alignment reveals a pronated posi­ tion of the hindfoot, the patient is observed while raising up on the toes and externally rotating the leg over the fixed foot. Both of these movements sho uld d ecrease the p rona­ tion and cause an increased twisting and arching of the foot. If not, a rigid flatfoot, caused by some fixed structural abnormality such as tarsal coalition, probably exists. 2. Passive movements. Unless a rigid flatfoot exists (a relatively rare condition), a pronated foot is usually a h ypermobile foot. Hypermobility, especially of the mid­ tarsal joints, may be noted. a. If a tight heel cord or restricted ankle mortise joint capsule is a contributing cause, d orsiflexion of the h indfoot will be restricted. One must lock the foot by supina tin g th e calcaneus and pronating the forefoot w h en testing ankle d or i­ flexion to avoid misinterpreting move-

Clinical Applications-Peripheral Joints

429

ment of the forefoot as b eing move­ m ent at the ankle. There hould be about 10° to 20° of dorsiflexion. [f dor­ siflexion and plantar fle xion are both restricted, the joint capsule is p robably a t faul t. If dorsiflexion is restricted with the knee straight, but not with the knee bent, the gastrocnemius is tight. If d or­ siflexion is restricted regardless of the postion of the knee, the soleus is p roba­ bly at fault. b. If ante torsion of the hip is a con tribu t­ ing factor, hip range of motion will be relatively normal but skewed toward internal rota tion with restriction of ex­ ternal rotation. c. Join t play. Movements of the tarsal joints are likely to be hyperm obile. Ex­ cessive arthrokinematic movements typically occur between four bones: ca l­ caneus, talus, navicular, and cuboid. 33 d. Pain from low-grade inflammation of the plantar fascia or ligaments, or from calcaneal periostitis, may be repro­ duced by passively everting the h eel, supinating the foot, and dorsiflexing the toes. 3. Resis ted movements. Results are usually noncon tributory. D. Neurom uscu lar tests. Determine whether weakness, either neurogenic or atrophic, of any of the muscles controllin g movement and stability of the foot exists. E. Palpation. Localized tender areas may exi.st that relate to areas of low-grad e inflammation occurring in r espon se to abnormal tissue tre es. As usual, the finding of local ized ten­ derness to palpation, in itself, m u st not be taken to be d iagnostic of any specific disorder because of the common p h enomenon of re­ ferred tenderness associated w ith lesions of d eep somatic tissue. Typica l areas of tend m ess associa ted w ith abnormal foot p ronation might include th e calcaneal attachment of the plantar fascia and long plantar ligament, especiaUy at the m dial tubercle; the p lantar fascia, us ua l y over the medial aspect of the sole o f the foot; the nav ic­ w ar tu bercle; the spring ligament, be tween the sustentaculum tali and the navi cular h l­ bercle; the m edial one or two m tatarsal heads; and the medial aspect of the first metatar sophalangeal joint. Areas of skin or subcutaneolls tissue hyper­ trophy may b e distingu ish ed on palpa tion as

430

CHAPTER 14

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The Lower Leg, Ankle, and Foot

localized indurated re gions. Such calluses, as­ socia ted with p ronation, might be foun d over the m edia l one or hvo me tatarsal heads or over the medial aspect of the first m e tatarsal­ phalangeal join t. III. M anagement Symptoms arising in associa tion with abnormal foot pronation are the resul t of increased stress to some pain-sen sitive tissue. Prop er m anagement, then, must involve selective red uctio n of abnor­ mal stresses. The approach used must be in accor­ dance with find ings on evalua tion, in cluding in­ forma tion relating to th e pab en t's activity level. In d @veloping a program of m anagemen t, it must be kept in mind that the tissue p athology resu lt­ ing in the painful condition m ay be due to n onnal stresses occurring at too great a freq u ency, to ab­ normally high stresses occurrin g at norm al fre­ quencies, or to som e combination thereof. Ei ther situation m ay resu lt in tissu e fa tigue in which the rate of tissue breakd own exceeds th e ra te at which the tissue is able to repair itself. However, the approach to management will differ, d epend­ ing on which condition prev ails. In gen eral, man­ agement of conditions associated with pron ation of the foot involves m easures to red u ce either the frequency or the magnitude of stresses, or b oth. In the case of the pron a ted foot, forces are ty pi­ cally increased by structural m alali gnments th at cause changes in the direction in which forces occur and changes in the degree of m ovem ent of skeletal parts durin g function al activi ties. The most common postural m alalignment causing ab­ normal foot pronation is p robably increased femoral antetorsion, w hich is usually accomp a­ nied by increased genu v alg um (knock knees). As men tioned earlier, the o ther common structural devia tions p redisposin g to increased prona tion of the foot a re ad duction of the firs t me tatarsal and increased in ternal tibial torsion . Each of these conditions results in un twisting of the tar sal skeleton durin g ambulation, such that a greater tensile stress is imposed on the plantar ligam ents, fascia, and joint cap sules. Under such conditions, the foo t loses the typical passiv e stabili ty nor­ m ally produce d by becoming twisted during stance phase. To comp ensa te, the intrinsic mus­ cles of the foot must con tract more to prepare the foot for push-off. Pain may arise from in creased stress to the pl an ta r caps uloliga men tou s struc­ tures, from fa tigue of the abnormally contracting muscles, or both . Persons with long-standing prona tiOll from a congenital s truc tural m ala lignment or from a malalignm ent acq uired early in life are likely to

have a permanent hypermobility of the joints of the foot. The ligaments and joint capsules will have been elongated from the chronic increased stresses applied to them throughout develop­ ment. By the time they are adults, these persons are not likely to have pain arising from the al­ ready le..'lgthened ligaments and fascia during normal activity levels. They are, however, likely to have feet that tire easily from increased activity of the intrinsics an d other muscles supporting the arch during gait. They are also more predisposed to developing prob lems elsewhere, such as metatarsalgia, hallux valgus, and patellofemoral joint dysfunction. Persons with m ore subtle structural deviations resulting in an increased tendency toward prona­ tion are likely to have problems only with in­ creased activity levels, such as long-distance run­ ni ng, that increase the magnitude and frequency of pronatory stresses. The mobility of the joints of the foot in these persons aUowed by the capsules and ligaments is likely to be fairly normal. It is es­ pecially important in patients experiencing pain suggestive of increased pronation, but who have relatively normal structural alignment, to con­ sider non::;.tructural causes. The most common of these would include a tight heel cord and inap­ propriate footwear. It is these patients, having subtle structura.l d eviations or nonstructural causes of increased pronation, who are likely to experience pain and develop pathological lesions associated with increased strain to specific tis· sues. The m ost common tissues involved are the sup porting p lantar structures of the foot, includ­ ing the periosteum of the plantar aspect of the cal­ caneus, and th e Achi lles tendon.

A. Techniques 1. Instruction in appropriate activity levels. As in any common musculoskeletal disor­ der, appropriate instruction in exactly what the patient should and should not do, and to what degree, is an essential component of the treatment program too often overlooked. Wrth respect to prob­ lems rela ted to increased foot pronation, this is especially important in the person experiencing problems primarily with in· creased activity levels. Treatment of the long-distance nmner experiencing pain from plantar fasciitis, Achilles tendinitis, or other pronation-related disorders sim­ ply involves advising the patient to not run so much. But this is not adequate man­ agement of the problem since, as with any disorder, the therapist must be concerned

PART II

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primarily with restoring optimal function. From the patient's standpoint, optimal function may be running long distances! The role of the therapist should be first to decide whether the patient's functional expectations are realistic. 111e patient with considerably increased femoral antetor­ sion, knock knees, and hypermobile flat feet probably should not be engaging in activities, such as long-distance running, that involve high-frequency, weight-bear­ ing stresses. However, this condition should not prevent the person from engag­ ing in other vigorous conditioning exer­ cise, such as swimming and bicycling. If there are no gross structural malalign­ ments predisposing to pronation-type problems, the therapist must then deter­ mine what can be done to reduce the stresses to the involved tissues, to allow th em to heal, and to prevent further p atho­ logical processes and pain. As far as heal­ ing is concerned, the most important step to be taken is to reduce the stresses that caused the problem. The most reliab~e method of doing this is to reduce the activ­ ity level. The long-distance runner experi­ encing chronic, persistent pain must be ad­ vised to markedly reduce or stop running for a period of 1 to 2 weeks to allow the tis­ sue to heal. Complete immobilization, however, is seldom, if ever, indicated for fatigue disorders such as these. During this period of relative rest the therapist should determine what can be done to re­ duce stresses when the activity is resumed. Other procedures to help restore the in­ volved tissue to its normal state may also be instituted. 2. Muscle strengthening and conditioning. Strengthening and endurance exercises for the intrinsic muscles of the foot as well as for the extrinsic muscles, such as the an­ terior and posterior tibialis that help main­ tain a twisted configuration of the foot, are important in the management of virtually all foot problems resulting from abnormal pronation. Improving the function of these muscles will allow the person with the hy­ permobile flat foot to stand or walk for longer periods of time before muscle fa­ tigue sets in. It will also help relieve strain on the plantar fascia and ligaments in pa­ tients suffering from strain of these struc­ tures by increasing the dynamic support of

Clinical Applications-Peripheral Joints

431

the arch, thus allowing the mu scle to take a greater portion of the load. 3. Proprioceptive balance training a. Because the peda~ intrinsic muscles ap­ pear to function similarly to the plantar fascia in stabilization of the foot, pedal intrinsic strengthening exercises should be prescribed. lOS Foot doming is a p ar­ ticularly beneficial exercise.36,lOS b. DorsiHexors are often found to be weak. Before strengtnening, according to Janda, it is better to stretch the tight structures (gastrocnemius­ soleus). Both eccentric and concentric exercises should be included. S1 c. The tibialis posterior, flexor digitorum longus, and flexor hallucis longus exert a supinatory force at the subtalar joint. These muscles help control pronation by working eccentrically. Marshall prefers to strengthen the supinators ec­ centrically by using the BAPS balance board (Camp International, Inc., Jack­ son, Michigan).108 4. Strapping. Strong muscles are of little use unless they contract with sufficient force and at the appropriate time to perform the desired function. Abnormal foot pronation can be controlled to varying degrees by contraction of the muscles that cause an in­ creased twisted configuration of the foot. Most important among these are the an­ terior and posterior tibialis muscles and the peroneus [ongus. Theoretically, muscle function can be enhanced by providing ad­ ditional input along the afferent limb of the reflex arcs that normally invoke muscle contraction during functional activities. One method of doing so is to strap the part in a manner that will cause increased ten­ sion to the straps, and therefore the skin, when movement occurs in the undesired direction. The added afferent input from the tension and pressure produced by the straps serves to enhance activity of mus­ cles that normally check the undesired movement. This is apparently the means by which ankle strapping helps to "stabi­ lize" the ankle against inversion sprains.52 Although empirically there seems to be ev­ idence for the efficacy of such procedures, electromyographical studies have yet to be performed to substantiate the proposed mechanism. For an excellent review of the litera ture,

432

CHAPTER 14

•

The Lower Leg, Ankle, and Foot

the reader is referred to the work of Met­ calf and Deneg ar.1 19 The low-dye strap­ p ing technique that was designed by Ralph Dye in an attempt to provide func­ tional mechanical support of the joints of the feet is recommended by Newell and Nutler 12S and by others3,6,39,71,90,1S0,177,179 to restrict abnormal foot pronation. The ability of low-dye strapping to modify forces on the medial arch during weight­ bearing has been clearly demonstrated by Scranton and colleagues. ISO It is meant to bring the ground up to the foot to ehmi­ nate the need for the foot to pronate to reach it. 177 It may be used to protect the passive stabilizing structures of the foot, such as the plantar fascia and associated structures, during the rehabilitation phase following injuries and to assess the effect of more permanent stabilizing measures, such as a biomechanical functional foot or­ thosis or shoe modification. A number of variations have been devel­ oped (modified low-dye, cross-X tech­ nique, Herzog taping) and used in rehabj]­ itating posterior tibial syndrome, posterior tibial tendinitis, peripatellar compression pain, Achilles tendon problems, and jumper's knee .80 ,125,176,1 77 James and asso­ ciates demonstrated effectiveness of this type of treatment for overuse injuries when combined with rehabilitation exer­ cises.80 These procedures pull the medial aspect of the foot toward the supportive surface and secure it in this position with tape (see Appendix B for one variation of this technique). 5. Ultrasound and friction massage. These may be importan t treatment measures in cases of plantar fasciitis, Achilles tendini­ tis, and tibialis per iostitis. The resultant in­ creased blood flow may assist in the heal­ ing process. Transverse frictions will promote the development of a mobile structure and help prevent adhesions as h ealing ensues. 6. Achilles tendon stretching. This is espe­ cially important when evaluation reveals a tight heel cord as a possible contributing cause of the patient's problem, and in cases of Achilles tend initis. McCluskey and co-workers were one of the first groups to report the beneficial ef­ fects of calf muscle stretching to reduce ankle injuries. H2 Ten degrees of dorsiflex­ ion with the knee extended and the subta­

lar in neutral is the amount considered necessary for normal walking,142 James suggests at least 15° talocrural joint dorsi­ flexion is required for running?9 One must take care to ensure that the stretching force is applied to the hindfoot, since using the forefoot as a lever to stretch the heel cord will result in dorsiflexion of the transverse tarsal joint in addition to dorsiflexion at the ankle mortise (talocrural) joint. This may result in hypermobility of the trans­ verse tarsal joint, which may add further to a tendency toward pronation of the foot. When stretching of the calf muscle is at­ tempted, it is important that the subtalar j,oint is maintained in a neutral position. To ensure that this position is maintained, the patient should either stretch out in a bio­ mechanical orthotic device or place a lift under the medial aspect of the bare foot during stretch. In the more acute stages of Achilles ten­ dinitis, the therapist must not be overly vigorous in restoring mobility to the heel cord, since the condition could be aggra­ vated. However, since most cases of Achilles tendinitis are fatigue disorders, an acute stage never exists. Some gentle stretching may be initiated carefully from the outset; the slow, short-termed stress produced by such stretching procedures in no way approximates the high-frequency, high strain-rate stresses that produce this type ,of disorder. In fact, early stretching, performed judiciously, will help prevent the fibers from healing in a shortened state. Increasing the load and speed of con­ traction with an emphasis on eccentric training has been found to be particularly heipful. I57 This can be carried out with the rear foot over the edge of a step to aHow for greater range of dorsiflexion-plantar flexion and eccentric control. To ensure normal weight-bearing alignment, a tennis ball can be placed between the patient's medial maUeoli; the patient is instructed not to lose contact with the ball through­ out the exercise, since this may invoke ex­ cessive supination or pronation.1 21 7. Shoe inserts and modifications. When ab­ normal foot pronation is due to some structural malalignment, whether marked or subtle, only surgery can remedy the true cause of the disorder. However, non­ surgical management is effective in the

PART II' d

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majority of cases. In order to optimize function, while at the same time prevent­ ing stresses sufficient to cause painful pathologic processes, the excessive un­ twisting of the foot must be reduced. This can be accomplished by altering the orien­ tation of the segments of the foot as they contact the ground during stance phase or by producing direct support to the arched configuration of the foot, or by both. If the joint capsules and ligaments of the foot are not elongated, as in the hypermo­ bile flat foot accompanying gross malalignment, the twist in the foot during stance phase can be increased by increas­ ing the pronatory orientation of the fore­ foot or by increasing the supinatory orien­ tation of the hindfoot. This can be done by providing a lateral wedge for the forefoot or a medial wedge for the heel. A trial, temporary insert can be made by cutting such a wedge from a piece of felt, l i s- to 3i}6-inch thick, to fit inside the shoe. How­ ever, if it is to be used on a permanent basis, the wedge should be incorporated mto the sole or heel of the shoe by one ex­ perienced in shoe modifications or should be incorporated into an orthosis. If the tarsal joints of the foot are lax, then the twisted configuration cannot be re­ stored by indirect means such as wedging, since these rely on taking up the slack in the joint capsules to effect a twisting of the tarsal skeleton. In the case of a hypermo­ bile, pronated foot, some direct support must be provided to prevent the head of the talus and navicular from dropping downward and medially in a pronatory fashion. for the severely pronated foot, an arch support may be used in conjunction with wedging of the sole or heel. Such wedging may be built into the orthosis or into the shoe. Regardless of the type of shoe modification or insert used, in order for the support to be effective the calca­ neus must be stabilized by a firm shoe counter or a calcaneal cup built into an or­ thosis. If the calcaneus is not held firmly, it will tend to compensate for attempts to in­ crease the twist of the foot by rolling far­ ther over into a valgus position (prona­ tion). Thus, many orthoses now in use have a heel cup incorporated into the or­ thosis itself, obviating the need for an extra-firm shoe counter. Such an orthosis can be used, for example, in athletic shoes,

Clinical Applications-Peripheral Joints

433

which often do not have very stiff coun­ ters. When chondromalacia of the knee oc­ curs as a result of abnormal pronation of the foot, the use of arch supports or shoe modification may be a necessary compo~ nent of the treatment program. The progression of a haHux valgus de­ formity may also be retarded by use of or­ thoses or shoe modifications, if the adduc­ tion of the first metatarsal is a result of abnormal foot pronation. In cases of metatarsalgia, if reducing the degree of pronation with appropriate or­ thotic devices or shoe modification does not adequately relieve the pressure over the metatarsal heads, a metatarsal insert may be used. This simply reduces the stress to the metatarsal heads by increas­ ing the weight-bearing surface area behind the heads. Metatarsal pads are available with an adhesive backing, or a metatarsal support may be incorporated into an arch­ supporting orthosis. To place the pad properly in the shoe, tape it to the patient's foot in place just behind the metatarsal heads with the widest dimension of the pad forward. Outline the bottom of the pad with lipstick or some substance that will leave a mark on the insole of the shoe when the patient steps down. The patient then puts on the shoes and walks about to make sure they are reasonably comfort­ able, realizing, of course, that they will at first feel somewhat peculiar. The shoes are then removed and the pad adhered to the insole of the shoe in the appropriate place as indicated by the marks left on the insole by the lipstick. Several devices designed to modify forces in the foot have been reported to be helpful for the patient with plantar heel pain. Heel pads have been used to reduce the shock of weight-bearing and to shift vertical forces forward and away from the heeI. 6,8,53 Some authors have suggested the use of a heel cup to prevent calcaneal eversion and thus reduce tension on the plantar fascia .15A1,85,l50

o Prob'ems Related

to Abnormal Foot Supination

Abnormal supination of the entire foot occurs when the subtalar joint functions in a supinated positionJ -I2

434

CHAPTER 14

•

The Lower Leg, Ankle, and Foot

There are three basic classifications for abnormal supination: pes equinovarus, pes cavus, and pes cavo­ varus.1°l,166 A pes equinovarus foot demonstrates a fixed plantar flexed forefoot and an inverted forefoot; the rear foot in weight-bearing is in neutral. 33 A pes cavovarus foot demonstrates a fixed medial column or first ray. In the weight-bearing position the calcaneus is in varus or inverted. 33 Root and co-workers define forefoot valgus as ever­ sion of the forefoot on the rear foot with the subtalar joint in neutra1. 142 The compensation for a forefoot valgus is inversion of the calcaneus in the weight­ bearing position.138,166 Forefoot valgus and a fixed plantar-flexed first ray are the most common intrinsic deformities resulting in abnormal supination of the subtalar joint. Functionally abnormal supination is a failure of the foot to pronate, resulting in a foot unable to compen­ sate normally. There is prolonged supination during the stance phase and a delayed pronation during the gait cycle. Stress fractures, metatarsalgia, plantar fasciitis, and Achilles tendinitis are common in this type of foot. In general, treatment consists of stretching, mobi­ lization, exercises, and orthoses. 167 The flexible cavus foot responds well to conventional biomechanical or­ thotic foot control. The rigid cavus foot requires a spe­ cial orthosis or a shoe with shock-absorbing materials such as Spenco Insoles (SpencoMedical Corp., Waco, Texas) and Sorbothane Inserts (Spectrum Sports, Twinsburg, Ohio) to lessen the strain on the lower ex­ tremities.

deformities. Softer flexible types of orthoses can be fabricated in the clinic as a temporary measure or may be made of flexible materials molded to a positive cast of the patient's foot. Most clinics are not equipped for fabrication of the rigid orthosis, which must be cus­ tom-made (from a positive model). There are a num­ ber of podiatry laboratories specializing in these types of orthotic appliances. Many excellent texts and arti­ cles have described orthotic fabrication and shoe modifications.* Shoe styles and features are constantly being changed by the manufacturers so that it is almost im­ possible for the clinician to keep abreast of current shoe models, particularly the athletic shoe. The basic functions of any quality shoes are to enhance shock absorption and foot control and to provide good trac­ tion and protection. Lasting or curve of the sole of the shoe should generally conform to the patient's own foot shape. In general, most patients will dO' well with a relatively straight last. Many manufacturers now provide information on shoes that have been selec­ tively designed to limit common foot abnormalities such as overpronation or oversupination of the subta­ lar joint. Sirnce foot problems and related disorders are com­ mon and because alteration of footwear is often an im­ portant component of management of these problems, it is important that the therapist develop a close work­ ing relationship with an orthotist, podiatrist, or other professional possessing these skills.

FI

ric

JOINT MOBILIZATION TECHNIQUES

D

Orthoses

Ultimately, the patient exhibiting a true intrinsic bio­ mechanical fault should be fitted with a custom-made functional biomechanical orthosis to correctly balance the foot during weight-bearing activities. Orthotic de­ vices are most often used to correct excessive prona­ tion and thus may be effective in the management of related shin splints, chondromalacia, and, occasion­ ally, trochanteric bursitis. The orthosis made from a positive mold of the foot in its neutral position is designed for restoration of normal alignment of the subtalar and midtarsal joint by controlling excessive pronation and supination and reducing the abnormal forces through the kinetic chain. In basic terms, it is directed toward preventing the foot from compensating and allowing normal mo­ tion to take place in its proper sequence. When the orthosis is in place, the foot should func­ tion near its neutral position. It is important to evalu­ ate muscle imbalances extrinsic and intrinsic to the foot, in addition to evaluating forefoot and rear foot

Note: For the sake of simplicity, the operator will be referred to as the male, and the patient as the female. All of the techniques described apply to the patient's left extremity except where indicated. (P "" patient; 0= operator; M = movement)

D

Tibiofibular J'o int

1. The Proximal Tibiofibular Joint-Anteroposterior glide (Fig. 14-40) P-Supine, with knee flexed about 90°, the foot flat on the plinth O-Stabilizes the knee with the right hand contact­ ing the medial aspect of the knee area. He grasps the head and neck of the proximal fibula with the left hand, the thumb contacting anteriorly, the index and iong finger pads con­ 'See references 10, 12,1 5, 22, 24, 27, 28,37,38,47,68,80,92,94, 108, 114,139,160, and 176.

2.

PART II

r-

Clinical Applications-Peripheral Joints

435

FIG. 1 4 ·40. The proximal tibiofibular joint: anteroposte­ rior glide.

FIG. 14-41. The distal tibiofibular joint: anteroposterior glide.

tacting posteriorly. He takes care to avoid di­ rect pressure to the common peroneal nerve. M-The left hand may move the proximal fibula posteriorly or anteriorly. This ' should be per­ formed through a movement of flexion and ex­ tension at the shoulder, rather than through finger or wrist movements. This technique is used to increase joint play at the tibiofemoral joint. The fibular head must move for­ ward on knee flexion and backward on knee exten­ sion. Dysfunction at the proximal tibiofibular joint commonly causes symptoms distally in the leg or ankle rather then proximally. 2. The Distal Tibiofibular joint-Anteroposterior glide (Fig. 14-41) P-Supine O-Cradles the ankle in his right hand, fixing it to the plinth, so that the fingers wrap around the heel posteriorly. The medial malleolus rests over the palmar aspect of his dorsiflexed wrist. The left hand contacts the lateral malleolus an­ teriorly with the heel of the hand. M-While the operator's right hand prevents downward movement of the medial malleolus, the left hand glides the lateral malleolus pos­ teriorly in relation to the medial malleolus. The hand holds may be reversed to move the medial malleolus posteriorly on the lateral malleolus. These techniques are used to increase joint play at the distal tibiofibular joint. This joint must spread slightly during ankle dorsiflexion, since the talus is wider anteriorly than posteriorly. AIthough spreading cannot be performed passively by the

operator, increasing anteroposterior movement is likely to increase other joint-play movements such as spreading.

D

The Ankle

1. The Tnlocrural joint-Distraction (Fig. 14-42) P-Supine, with the knee flexed about 90°, the hip flexed and somewhat abducted O-Half-sits on the edge of the plinth, with his back to the patient. He wraps the patient's leg around his right side to support the knee on his iliac crest, tucking the lower leg between his elbow and side (Fig. 14-42A) . The operator grasps the ankle with both hands so that the thumbs wrap around medially and the fingers laterally. The web of his right hand contacts the neck of the talus dorsally; the web of h.is left hand contacts the calcaneus posteriorly. The forearms are kept in line with the direc­ tion of force (Fig. 14-428). M-A distraction is imparted with both hands. The ankle may be shghtly everted to help ~oc k the subtalar join t. This technique is used to increase joint play at the ankle mortise joint. Distraction must occur here during plantar flexion, and is necessary for full movement toward the close-packed position, which is dorsiflexion. 2. The Talocrural joint~ Posterior glide of tibia on talus (or anterior glide of talus on tibia) (Fig. 14-43) P- Supine O-Stabilizes the talus and foot by grasping

436

CHAPTER 14

•

The Lower Leg, Ankle, and Foot

The talocrural joint (left foot): posterior glide of tibia on talus.

FIG. 14·43.

FIG. 14·42. The talocrural joint. Distraction: (Aj position of the operator; (S) view of the operator's grip at the ankle.

around medially to the posterior aspect of the calcaneus with the left hand. He contacts the distal tibia by placing his right hand over the anteri.or distal aspect of the tibia, just prox­ imal to the malleoli. M-The tibia is glided posteriorly on the talus with the right hand. Note: An anterior glide of the talus on the tibia may be performed by stabilizing the tibia with the right hand and moving the talus anteriorly. When this technique is used, it is important to keep the subtalar joint slightly everted to lock the calcaneus on the talus. The talus is glided anteriorly on the tibia via the calcaneus at the ankle mortise. This is a slightly more difficult technique, because the oper­ ator must work against gravity. Both of these techniques are used to increase joint-play movements necessary for plantar flexion at the ankle mortise joint. 3. The Talocrural Joint-Posterior glide of the talus on the tibia (Fig. 14-44) P-Supine, with the calcaneus hanging over the end of the plinth O-Stabilizes the distal tibia against the plinth by grasping it with the left hand, wrapping the fingers around posteriorly. The left forearm rests over the dorsum of the patient's lower leg to prevent it from rising up from the plinth

during the movement. He contacts the neck of the talus dorsally with the web of the right hand, bringing the thumb around laterally and the index finger medially. The remaining three fingers of the right hand wrap around the sole of the foot for support and control of the de· gree of plantar flexion. M-The right hand moves the talus posteriorly on the tibia. This technique is used to increase a joint-play movement necessary for ankle dorsiflexion. 4. The Subtalar Joint-Distraction (not illustrated) This is performed in the same manner as distrac­ tion at the talocrural (refer to technique 1), except that the dorsal handhold moves distally to contact

\

FIG. 14·44.

tibia.

The talocrural joint: posterior glide of talus on

PART" Clinical Applications-Peripheral Joints

--

437

FIG. 14-45. The subta/ar joint: valgus tilt (eversion).

FIG. 14-47. Dorsal rock of the calcaneus on the talus.

the navicular. In thi s way the calcaneus is dis­ tracted from the talus by the nav icular and cuboid. =>. The Subta/ar Joint-Valgus til t (eversion) (Fig. 14-45) P-Supine, with the knee flexed about 90°, the hip flexed and somewhat abducted O-Assumes the same position as for distraction (see Fig. 14-42A) and grasps the ankle so that the thumb pads contact the medial aspect of the calcaneus and the remaining finger pads contact laterally, just proximal to the calcaneus and level with the sinus tarsi. M-A valgus tilt of the calcaneus is produced by ulnar deviation of the wrists, transmitting the force through the thumb pads. The finger pads act as a fulcrum about wh ich the movement occurs. This technique is used to increase ever­ sion at the subtalar joint. 6. The Subta/ar Joint-Varu s tilt (inversion) (Fig. 14-46) Thi~ is carried out in the same manner as valgus tilt (refer to teclmique 5). The operator's thumb pads move just proximal to the calcaneus; the fin­ ger pads move distally to contact the calcaneus lat­ erally. The finger pads move the calcaneus into in­ version about a fulcrum created by the thumb pads.

This technique is used to increase inversion at the subtalar joint. 7. The Subtalar Joint-Dorsal rock of the calcaneus on the talus (Fig. 14-47) P-Supine, with the knee flexed about 90°, the hip flexed and somewhat abducted O-Assumes the same position as for distraction (see Fig. 14-42A) and stabilizes the talus dor­ sally with the web of the right hand, wrapping the thumb around medially and the fingers lat­ erally. He contacts the upper border of the cal­ caneus posteriorly with the web of his left hand in a similar fashion. M-While the right hand stabilizes the talus, the left hand rocks the calcaneus forward and dor­ sally. Note: According to Memwll, a small amount of movement must occur at the subtalar joint at the extremes of plantar flexion and dorsiflexion . This technique, and the one that follows, have been de­ veloped to restore that m ovemen t. 11S 8. The Subta/a/" Joint-Plantar rock of the calcaneus on the talus (Fig. 14-48) This is carried out in the same manner as dorsal

FIG. 14-46. The subtal ar joint: varus tilt (inversion).

FIG. 14-48. Plantar rock of the calcaneus on the talus.

n

438

CHAPTER l' 4

•

The Lower Leg. Ankle. and Foot

rock (refer to technique 7), except the handholds are changed so that the right hand moves down to contact the navicular. The navicular tubercle is used as a landmark. The left hand moves just prox­ imal to the posterior aspect of the calcaneus. The right hand rocks the calcaneus backward and plan­ tarly via the navicular and cuboid. The web of the left hand acts as a fulcrum about which movement occurs.

D

The Foot

1. The Transverse Tarsal Joints (talonavicular alld calca­ neocuboid joints)-Dorsal-plantar g]ide (Fig. 14-49) P-Supine, with the knee bent about 60°, the heel

resting on the plinth 0-The left hand fixes the calcaneus and talus to the plinth by grasping dorsally at the level of the talar neck, the thumb wrapping around laterally and the rest of the fingers medially. The right hand grasps the navicular, using the navicular tubercle as a landmark. The web and the thumb contact dorsally, and the hand and fingers wrap around the foot medially and plantarly. M-As the left hand stabilizes and prevents move­ ment at the ankle, the right hand may move the navicuJar dorsally or plantarly on the talus. The cuboid is moved in a similar manner, with one hand fixating the cakaneus and talus whiJe the other hand moves the cuboid dorsally or plantarly on the calcaneus. These techniques are used to in­ crease joint play at the forefoot. 2. The Naviculocuneiform Join t-Dorsal-plantar glide (Fig. 14-50) This is performed in the same manner as dorsal­ plantar glid e at the talonavicular joint (refer to technique 1), with the handholds moved distally.

FIG. 14-49. The glide.

transverse

tarsal joints: dorsal-plantar

FIG. 14-50. The naviculocuneiform joint: dorsal-plantar glide.

The left hand stabilizes the navicular while the right hand moves the cuneiforrns. This technique is used to increase joint play at the forefoot. 3. The Cuneiform-Metatarsal Joints-Dorsal-plan­ tar glide (not illustrated) This technique is also performed in the same manner as for the talonavicular joint, with the handholds shjfted distally. The right hand grasps the cuneiforms and provides stabilization while the left hand moves the metatarsal joints. This technique, like techniques 1 and 2 for the talonavicu~ar and naviculocuneiform joints, is used to increase joint play of the forefoot. 4. The Cuneiform-Metatarsal and Cuboid-Meta­ tarsal Joints-Rotation (pronation and supination) (Fig. 14-51) P-Supine, with the knee bent about 70°, the heel resting on the plinth O-Stabilizes the cuneiforms and cuboid with the left hand, the thumb wrapping around the foot dorsally, the fingers plantarly. For pronation the operator's right hand grasps the proximal metatarsal shafts from the lateral aspect, with the thumb contacting dorsally and the finger:... plantarly. His forearm is supinated (see Fig 14-51A). For supination, the operator's righ hand grasps the proximal metatarsal shafu from the medial aspect, with the thumb con­ tacting dorsally and the fingers plantarly. lib forearm is pronated (see Fig. 14-51B). M-Th e right hand rotates the metatarsals, a ~ _ unit, into pronation or supination. These techniques are used to restore pronation a n,~ supination to the forefoot. 5. The Cuboid-Metatarsal Joint: Dorsal-plantar gli This technique is performed as dorsal-plant,

PART II

Clinical Applications-Peripheral Joints

439

B FIG. 14-51. Rotation of cuneiform-metatarsal and cubometatarsal joints: .(A) pronation and (8) supination .

ta­

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glide at the calcaneocuboid joint (refer to technique

I), with the handholds moved distally. The proxi­

mal hand stabilizes the cuboid while the distal

hand moves the fourth and fifth metatarsal

joints. This technique, like technique 3 for the

cuneiform-metatarsal joints, is used to increase

joint play of the forefoot.

6. Manipulation of the Cuboid and Navicular

Joints: Whip and squeeze techniques (Fig. 14-52)

P-Prone with the thigh and leg beyond the table

and flexed at 30° or, even better, standing and

leaning forward on the table (see Fig. 14-52A).

O-Standing at the foot end of the table, the opera­ tor holds the foot, pressing on the cuboid with both thumbs superimposed (see Fig. 14-52B). M-The arms of the operator are extended so that

the pressure on the cuboid causes knee flexion

and dorsiflexion. Finally when the foot is re­

laxed, a thrusting movement similar to crack­

ing a whip, is performed (tractional plantar­

flexion thrust) laterally at a 45° angle.

This action usually allows the subluxed cuboid (in­

ferolateral) to move dorsally back into place. Treat­

ment is identical to that of the cuboid for manipu­

lation of an inferior navicular when present in the

pronated foot. Dorsal glide of the cuboid or navicu­

lar joints can be effectively applied in the prone po­

sition. Marshall and Harnilton 109 believe that a

technique called the "cuboid squeeze" is far more

effective than the cuboid whip. To perform the

squeeze technique, the clinician gradually stretches

the foot and ankle into maximum plantar flexion.

When the operator feels the soft tissues· relax, the

B cuboid is reduced with a fina~ squeeze of the thumbs. FIG. 14-52. Manipulation of the cuboid and navicular These techniques should be followed with a lowjoints: IA) whip and (B) squeeze techniques.

440

CHAPTER 14

•

The Lower Leg, Ankle, and Foot metatarsal with the thumb on the dorsal aspect and the index finger on the plantar aspect. M-The mobilizing hand grips the midshaft of the adjacent metatarsal in the same manner as the stabilizing hand. While the stabilizing hand holds one metatarsal in position, the mobiliz­ ing hand glides the metatarsal in a dorsal or plantar direction. Movements can be performed between the second and first, the third and the fourth, and the fourth and fifth metatarsal bones. The purpose is to re­ store or increase joint play in the intermetatarsal articulations in the presence of hypomobility and to decrease pain in the forefoot. Movements will si­ multaneously take place in the tarsometatarsal joints and between the MTP joints.

D FIG. 14-53. Intermetatarsal and tarsometatarsal joints: dorsal-plantar glide.

dye strapping procedure to give added arch sup­ port for 1 to 2 weeks. 175 The management of chronic subluxations should include instruction in self-mobilization techniques. 7. Intermetatarsal and Tarsometatarsal Joints: Dor­ sal-medial glide (Fig. 14-53) P-Supine, \-vith the foot in a neutral position O-Facing the dorsal surface of the foot, the stabi­ lizing hand grips the midshaft of one

The Toes

Note: The use of a surgical glove, athletic underwrap used in adhesive taping, or a tongue blade taped to the toe may assist the operator in obtaining a stronger grip by reducing slippage and in directing a more pre­ cise mobilization of the toes. 1. Metatarsophalangeal (MTP) Joints-Distraction (Fig. 14-54) P-Supine O-Facing the dorsal aspect of the foot, the stabi­ lizing hand holds the midfoot securely, while the thumb and forefinger of the mobilizing hand grasp the first phalanx at the MTP joint. The MTP joint is positioned in the resting posi-

FIG. 14-54. Metatarsophala joints: distraction.

PART II

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tion if conservative techniques are indicated or near the restricted end range if more aggres­ sive techniques are indicated. M-The mobilizing hand moves the base of the proximal phalanx distally. This is a useful technique in increasing joint play in the MTP joint and overall range of motion. A hal­ lux valgus deformity is usually caused by improp­ erly fitting shoes or has a genetic origin. Because of this, the treatment of choice is mechanical, such as orthotics or surgery. However, along with this, mo­ bilization should be used in order to help increase the abduction of the first MTP joint. 29 Mobilization of the MTP joint-with oscillatory movements in dorsal-plantar glide, medial-lateral glide, abduc­ tion, adduction, rotation and compression-may provide pain relief. 1. Metatarsophalangeal Joints: Dorsal-plantar glide (Fig 14-55) P-Prone or supine with the forefoot supported on the table or with a sandbag or wedge, toes extended over the edge of the table O-Standing beside the patient and facing the foot, the stabilizing hand grips the head of the metatarsal between the thumb and index fin­ ger. M-The mobilizing hand grips the proximal pha­ lanx (dorsal and plantar aspect) between the thumb and index fingers. The MTP joint is po­

/

441

Clinical Applications- Peripheral Joints

sitioned in the resting position or approximat­ ing the restricted range if more aggressive techniques are indicated. The mobilizing hand glides the proximal phalanx in a dorsal direc­ tion (Fig. 14-55A, patient prone) or plantar di­ rection (Fig. 14-55B, patient supine) while em­ ploying grade 1 traction. The purpose of these techniques is to increase joint play in the MTP joints; plantar glide for restricted flexion and dorsal glide for restr,icted extension. As to the remaining joints of the foot, the interpha­ langeal joints may be mobilized in the same manner as that described for the corresponding joints of the hand. Self-mobihzation should be considered in chronic conditions.

REFERENCES 1. Alldrl?dg(' RH: Diastases of tht::' di stal tibiofibular jOint a nd a ssociat (~ les ions . JA)AA 115:21 36-2140,1940 2. American Medic:li Association, Subco mmittee on C lass ificl ltury­

Crol",, 1976

74. Hunt GC: ExamiTU:i tion of lo '\,\,(' r ~X" tTe m.Hy d ysfun ctio n . In Gould JA, Da vies G] (eels): O rthopac'
484

CHAPTER 15

•

The Temporomandibular Joint

59. Forsberg 0 \'1, HeUsin g E. Li n d l'.r~A ronson 5, et a l: EMG activity in the neck and maslit Jtory muscles in re la bon to extension and flexion of the head. Eur J Orthod 7:"1 77.1985 60. l:riction J, H massete.r and a nt erior te mpor.Jlis muscle in the open-close-d ench cycle in the temporomand ibula r joint d ysfun ction. Monogr Ora l Sci 4:117-1 23, 1975 132. Pa ris SV: Th. Spina l Les ion. Ch ri5lchurch, New Zealand. Pegasus Press. 1965 133. Peck C, Kra ft G: El ectrom yograp hic biofeedback fo r pain relMed to m uscle tC1'\s ion: A stu dy of tension hea d. che. back. and jaw pain . A reh Surg 112:88'Hl95. 1977 134. PelJegrino MJ: Atypical chest pain as an initial p resentati on o f prinTilIJ' hbromyal­ gi•. Arch l'hys Med Rehabil 71 :52fr528, 1990 135. Perry C Neuromuscular control of mandibular movem en ts. J Prosthet Dent 30:714-720.1973 136. Pin to OF: A n £ \\' Structure related to the temporo mandibular joint .:lnd the middle eo r. J Prosthct Den t 12(1):95- 103, 1962 137. Plunkett GAl, "'-lest, VC: Systemic joint laxity a.nd m,mdibllJ nr nm gc of movement. J Craniomandib Pr"ct 6:320-326. 1988 138. Parler M.R: Th e at ta chment of ti'le JJ lerru pterygo id mu scle of the meniscu s. J Pros­ thet Dent 24 :55~56 2, 1970 139. PrieskeJ HW: Some obsc rvBtions o n the postural pos ition of the mandible, J Prost.het Den t 15:625-633. ]965 140. Profitt WR Equ alizati on theory revis ited : Fe

h

DISK PRESSURES The young healthy disk maintains a positive pres­ sure within the nucleus pulposus at rest, which in­ creases as loads are applied to the spine. This pressure approximates 1.5 times the mean applied pressure over the entire area of the end-plate.1 63 These pres­ sures have importance therapeuticaHy when activity and exercise programs for patients with disk prob­ lems are being designed. Disk pressures have been ex­ tensively studied in various poshlres and seating con­ figurations. A more detailed description can be found in other sources and will not be covered here.* The "preloaded" spinal colunm in the healthy nucleus maintains a continuous pressure to separate the adja­ cent vertebrae. This preloaded condition and the in­ 'See references 5,7-15,82, 84, 85,88,89,147,150,1 52,155,157-161, and 163.

Clinical Applications-The Spine

503

compressibility of the nucleus serve to form a self­ righting system: with a compressive force or angular movement in any direction, .the resultant intradiskal pressure changes are such that the disk favors move­ ment back to the "neutral" position. Note, however, that this self-righting system also depends on the ten­ sile strength and the elasticity of the annulus. Tensile strength or stiffness must be provided in the horizon­ tal direction in order to withstand the intermittent stresses applied to it from the nucleus. Elasticity of the annulus or movement between adjacent planes of an­ nular fibers is necessary in a vertical direction to allow angular movement between adjacent vertebral bodies. Loss of a balance between this extensibility and stabil­ ity of the annular fibers is probably a contributing fac­ tor in disk disorders. In axial compression, the increased intradiskal pres­ sure is counteracted by annular fiber tension and disk bulge, rather analogous to inflating a tire (Fig. 16-13A).179 Some disk-space narrowing also occurs. Because of the incompressibility of the fluid-like nu­ cleus, forces acting on the nucleus will act to move it, change its shape, or both. In flexion, extension, and lateral bending, the same process occurs. Because the annular fibers are somewhat elastic and because the annulus allows vertical and tangential movements be­ tween vertebral bodies, the nucleus in the healthy disk may either change in shape or move within the limits allowed by the annulus. 197 Its volume, how­ ever, must remain the same. Displacement of the nu­ cleus within the disk has been disputed more re­ cently.84,118 Because the nucleus is roughly spherical, some have considered it as a ball that allows one ver­ tebra to rotate over its neighbor. The nucleus is said to move backward during flexion and forward during extension. However, others have not confirmed this observation, and Krag and associates found little mo­ tion of the nucleus.1 18 In the consideration of an angular movement for­ ward (flexion) of one vertebral body on another in a weight-bearing situation, the forward shift of weight will result in an increased compressive force on the anterior aspect of the disk. This causes the anterior an­ nular fibers to bulge backward and causes the nucleus to shift backward, transferring the vertical compres­ sive force to a horizontaHy directed force backward against the posterior annulus (Fig. 16-13B). Because the healthy nucleus is fluid-like, an even distribution of pressure results across the inner annular layers. The posterior annular fibers, which are normally bulged somewhat backward in the neutral position, tend to straighten because of the increase in distance beh-veen the posterior vertebral bodies. However, because of the pressure against the posterior annulus by the nu­ cleus, there is also a tendency to maintain this poster­ ior bulge and thus bring the vertebrae back to a neu­

504

CHAPTER 16

•

The Spine-General Structure and Biomechanical Considerations 5

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FIG. 16·13. Nucleus pulposus: (A) during axial compres­ sion. (B) in spine flexion, (e) in spine extension, (D) in lat­ eral bending, and (E.) during axial rotation.

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c, tral relationship (the self-righting mechanism dis­ cussed earlier). Looking at it from another perspec­ tive, the straightening of the annular fibers tends to increase the counterpressure against the posteriorly bulging nucleus, which effects a counterforce against the original vertical compressive force . In this wayan equilibrium must be reached between the transforma­ tion of the vertical loading to a horizontal pressure against the annulus and the tendency for the annulus to reconvert this pressure, in a self-righting manner, to counter the compressive loading. In extension

and lateral bending, the same process occurs (Fig. 16-13C,D). Of clinical significance is the fact that

changes in this equilibrium favor pathological changes in the related tissues, while, conversely, pathological tissue changes result in a change in the equilibrium; the resultant cycle of events should be obvious. For example, a ,·veakening of the annular fibers results in less tendency to resist the horizontal forces exerted by the nucleus, which will result in fur­ ther weakening of the annulus. Osteoporosis of the vertebral bodies results in a decreased ability to with­

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PART III

stand reactive vertical forces with erosion of disk ma­ terial into the vertebral bodies; the so-called vacuum phenomenon. In axial rotation, a compressive force causes an in­ crease in intradiskal pressure and tends to narrow the joint space (Fig. 16-13E). When rotation occurs, the an­ nular fibers-which are oriented in the direction of ro­ tary movement-become taut, while the fibers ori­ ented in the opposite direction tend to slacken. Mathematical models based on the geometry of the disk demonstrate that torsion produces stress concen­ trated on the region of the posterior lateral annulus, which is a common site of disk herniation.]21,204 Tor­ sionalloading of spinal segments in vitro produces fis­ sures in the annulus in the same posterolateral loca­ tion and is thought to be one of the common early causes of acute low back painJ80 During daily activi­ ties the disk is loaded in a complex manner, usually by a combination of compression, bending, and tor­ sion. Flexion, extension, and lateral flexion of the spine produce mainly tensile and compressive stresses in the disk, whereas rotation produces shear stress. The tensile stress in the posterior part of the an­ nulus fibrosus in the lumbar spine has been estimated to be four to five times the applied axial 10ad?O,155 The thoracic annu]i fibrosi are subjected to less tensile stress than the lumbar annu]i fibrosi because of their geometric difference. The ratio of disk diameter to height is higher in the thoracic disk than the lumbar diskJ24 The entire intervertebral disk in the adult is avascu­ lar. Up to the time of skeletal maturity, blood vessels do enter the disk from the vertebral bodies through the cartilaginous end-plates. These vessels are gradu­ ally obliterated, leaving scars in the end-plate where they penetrated.

INTERVERTEBRAL FORAMINA

The intervertebral foramen is the aperture that gives exit to the segmental spinal nerves and entrance to the vessel and nerve branches that supply the bone and soft tissues of the vertebral canal. This aperture or cana] is superiorly and inferiorly bounded by the re­ spective pedicles of the adjacent vertebrae (see Fig. 16-2). Its ventral and dorsal relations involve the two major intervertebral articulations. Ventrally it is bounded by the dorsum of the intervertebral disk, covered by the posterior longitudinal ligament, and dorsally by the capsule of the articular facet and liga­ mentum flavum (see Fig. 16-8). Spur formation within the foramen can decrease the available space and cre­ ate compression forces on the spinal nerves exiting through the foramen or on the structures that reenter the foramen, such as the sinu-vertebral nerve, which

Clinical Applications-The Spine

505

innervates the posterior longitudinal ligament (see later, Vertebral Innervation, page 509). Nerve-root entrapment may also result from clo­ sure or narrowing of the vertebral foramen, through any of the following mechanisms: (1) approximation of the pedicles resulting from narrowing of the inter­ vertebral disk; (2) hypertrophic degenerative arthritic changes of the articular facet joints; and (3) thickening of the ligamentum flavum. The existence of additional ligamentous elements in relation to the intervertebral foramen (e.g., the transforaminalligaments, found fre­ quently in the lumbar region) could be criti­ cal. 33,19U92 The transforaminal ligaments are strong, unyielding cords of collagenous tissue that pass ante­ riody from various parts of the neural arch to the body of the same or adjacent vertebra.

D

The Control System:

Noncontractile Soft Tissues

LIGAMENTS

The ligaments are vital for the structural stability of the spinal system. Their principle role is to prevent ex­ cessive motion. The ligaments are also the principal tensile load-bearing elements and, along with the apophyseal capsules, provide the central nervous sys­ tem with information in regard to posture and move­ ment. 225 Unlike muscles, ligaments are passive struc­ tures so that their tension depends on their length. Ligaments are viscoelastic in nature, with their defor­ mation and type of failure being dependent on the rate of loading. Like all materials, lifsaments fatigue and can fail with repetitive 10adingJ 9,216 They read­ ily resist tensile forces but buckle when subject to compression. The ligaments that connect the anterior elements of the spine are the broad anterior longitudinal ligament, which extends from the basiocciput to the sacrum, and the posterior longitudinal ligament, which also ex­ tends from the basiocciput to the sacrum on the an­ terior aspect of the neural canal, behind the vertebral bodies. These ligaments are interlinked at each level by the disk, which adds support to the disk and verte­ bral body network (see Fig. 16-8). The annulus fibro­ sus of the intervertebral disk may be considered a part of the ligamentous structure. These ligaments deform with separation of the vertebrae and bulging of the disk. 220 Richly supported by nerve fibers, they re­ spond to painful stimuli. The remaining ligaments of the spine support and link the posterior elements. ANTERIOR LONGITUDINAL LIGAMENT

The anterior longitudinal ligament is one ligamen­ tous structure placed anterior to the center of rotation of the intervertebral joint. It thus acts to prevent hy­

506

CHAPTER J 6

•

The Spine-General Structure and Biomechanical Considerations

perextension, along with the capsular ligament of the articular facet joint (see Fig. 16-S). It begins as a rather narrow band from the basi occiput and broadens as it descends from C3 to the sacrum. It consists of long fibers along its length and short, arched fibers cours­ ing between individual vertebrae and inserting into the anterior aspect of the intervertebral disk (see Fig. 16-10C).!09 Considered perhaps the strongest liga­ ment in the body (with a tensile strength of nearly 3000 pounds per square inch), the anterior longitudi­ nalligament, along with the muscles about the spine, keeps a preload beam condition in the spine that helps to strengthen the spine during lifting.59 In the lumbar spine it also resists the weight of the spine in its ten­ dency to slip into the pelvic cavity.173 Because of its breadth and tensile strength, this ligament provides strong support and reinforcement to the anterior disk during lifting, and Harrington and others have used the strength of the anterior ligament combined with Harrington rods to apply traction to fracture disloca­ tions of the low back. 220 POSTERIOR LONGITUDINAL LIGAMENT

The posterior longitudinal ligament extends from the basiocciput to the sacrum on the anterior aspect of the neural canal behind the vertebral bodies (see Fig. 16-SA,B,0). It is densely attached to the posterior an­ nulus fibrosus at each level, with both vertical and transverse fibers that spread across the posterior an­ nulus; however, as the posterior longitudinal ligament passes the vertebral bodies, it narrows and is not at­ tached to them except at their margins.191 ,192 This al­ lows entrant arteries, veins, and lymphatics to pass in and out of the posterior portion of the vertebral bod­ ies. In flexion the posterior longitudinal ligament be­ comes taut and serves as a valve on these vessels, which do not have a valve mechanism of their own. It, like the anterior longitudinal ligament, is thickest in the thoracic (dorsal) spine. It is often reduced to a cord-shaped filament in the lumbar spine. The lateral expansions over the disks are thin, whereas the cen­ tral portions are much thicker. This is presumably why most posterior protrusions of the disk soon move laterally to become posterolateral protrusions. Al­ though the posterior longitudinal ligament is not as massive as the anterior longitudinal ligament in terms of cross-sectional area, the tensile strength per unit area seems to be the same for both structures. 209 Func­ tionally, the ligament litmits forward bending and gives support to the disks except in the lumbar region. Of interest is that in the midline the ligament does have a small amount of elastic tissueY3 In the cervical spine the ligament is a broad band on the entire pos­ terior aspect of the bodies, but because it is attached only in the region of the disk, with disk degeneration it produces folds that can press into the spinal canal

on backward bending; this movement is therefore to be avoided in such conditions. SEGMENTAL LIGAMENTS

The segmental ligaments of the spine include the liga­ mentum f/avum, the interspinous and intertransverse liga­ ments, and the anterior and posterior capsular ligaments of the articular facet joints. The biomechanical signifi­ cance of these structures depends on their strength, stiffness, and distance from the axis of rotation of the joints they span. 220 LIGAMENTUM FLAVUM

The ligamentum flavum extends from the anteroin­ ferior border of the laminae above to the posterior border of the laminae below (see Fig. 16-SB,C,0). It connects the laminae from C2 to S1. The medial edges fuse with the contralateral ligament in midline and completely close the vertebral canal (a slight septum is provided for the passage of arteries and veins). At its lateral border, the ligamentum flavum blends with the capsules of the articular facets, particularly in the lum­ bar region (see Fig. 16-SB,C).96 Histologically, the liga­ mentum flavum has the highest percentage of elastic fibers of any tissue in the body.31,162 It checks the movement of the articular facet joints by exerting a constant pun on the capsule and thus assists in pre­ venting the synovial lining and intra-articular menisci from being painfully nipped between the articular joint surfaces.!73 It owes much of this function to its yellow elastic fibers (hence,f/avum, meaning yellow). During forward bending the ligamentum flavum permits considerable range and assists in return to neutral or the resting position of the spinal segments without the development of folds. It thus serves to protect the spinal canal from encroachment by soft tis­ sues on flexion and extension. Nachemson and Evans found that in neutral the ligamentum flavum is pre­ strained by about 15 percent and that full physiologi­ cal flexion can stretch it an additional 30 to 35 percent, while it retains a 5 percent stretch in full physiological extension. 162 This elasticity is lost to some extent in normal aging, but if the instant axis of rotation for flexion is in the region of the posterior annulus, the flexion-extension torque resistance in the ligamentum flavum is significant. There is appreciable strain of the ligamentum flavum on sidebending or lateral flex­ ion. 171 The ligamentum flavum also provides some pre loading of the disk (leading to disk nucleus pres­ sures greater than atmospheric), even when there is no external load on the spine, which may reduce slack in the motion segment. In patients with severe spine degeneration, the ligamentum flavum may be thick­ ened and less elastic and may produce narrowing of the spinal canal in extension. This narrowing occurs

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INTERTRANSVERSE AND INTERSPINOUS LIGAMENTS The inter transverse ligaments are well developed in the thoracic spine and are intimately connected with the deep muscles of the back.220 They pass between the transverse processes and are characterized a. rounded cords These ligaments are barely mentioned in many texts on functional anatomy, particularly w ith respec t to the lumbar spine, as being significant. Functionally, they tend to lim it sidebending and ro ta­ tion. The interspinous ligaments, which connect the spin­ ous processes, are important for the stability of the spinal column. They are r inforced, especially at the level of the thoracic and lumba r spine, by the supraspinous ligaments (see Fig. 16-8C,0). Their at­ tachments extend from the root to the apex of each spinous process, proceeding in an upward and back­ ward direction, not an upward and foreword d irec­ tion, as often illustrated.173 This upward and back­ ward orientation permits increased range of motion during flexion while still resisting excess ive range. Panjabi and associates found high strain in both the interspinous and supraspinous ligaments with flexion while these were relatively unstrained in rotation. l71 The interspinous ligament are narrow and elonga ted in the thoracic region, only 'lightly developed in the cervical spi.ne, and thicker in the lumbar spine.220 In 90 percent of cadavers over 40 years of age, RissaJlen noted that the interspinous ligament between L4 and L5 had degenerated or was comp~ete ly ruptured. 187 The supraspinous ligament is a strong fibrous cord that connects the apices of the spines from the C7 to L4, and occasionally to L5 (see Fig. 16-8C,0).173 At this level it is replaced by the interlocking fibers of the somewhat stronger erector spinae t ndons of inser­ tion. The supraspinous ligament is thicker and broader in the lumbar region than the thorac,ic, and it is intimately blended in both areas with the neighbor­ ing fa scia. Between the spine of C7 and the external occipital protube rance, it is much expanded and called the ligamentum nuchae (see Fig. 17-4).212 In the cervical region the spinous processes are buried deeply between the heavy muscles on the back of the neck so that the supraspinous ligament is represented by a thin septum between the musculature of the two sides. In quadruped s with heavy heads, the ligamen­ tum nuchae is a strong, thick band of elastic tissue which aids the muscles in holding up the head.97 In humans, however, the supraspinous and interspinous ligaments and the ligamentum nuchae a re largely col­ lagenous tissue, relatively inelastic and of little

Clinical Applications-The Spine

507

strength; in the cervical and lumbar regions, where they shou ld be most important in limiting seg·.11ental flexion, the interspinous ligamen ts ar frequ en tly de­ fective or lacking in one or several inter p aces. 97 Be­ cause the suprasp inous ligament is the mos t superfi­ cial of the spinal ligaments and fa rthe t from the axis of flexion, it has a greater potentia l for sprains.109 FASCIAL ANATOMY THORACOLUMBAR REGION Although not technically a ligament, the thora­ columbar (lumbod orsa l) fa scia has a tensile ·trength of nearly 2000 pounds p er square inch and serves as one of th mo t important noncon tractile structu res in the lumbar spine ( ig. 16-14A) .60 The thoracolumbar fascia consists of three layers (anterior, middle an d post rior) that arise from the transverse and spinous pro s es and blend with other tissu es. The aJlterio r layer is derived from the fascia of the quadratus lumborum muscle. The m iddle layer lies posterior to it. The posterior layer consists of two laminae, one with fibers oriented caudomedially and the other oriented caudola terally.2 5 The two lami­ nae of the p osterior layers fuse with th transversus abdominus m uscle to the lumbar spinous processes. Gracovet ky, Farfan, and Helleur78 have designated the anterior p art of the thoracolumbar fascia as the "passive" p art aJld the posterio r layer as the "active" part. The passive part serves to transmit tension from con tra ti on of the hip fle xors to the spinous processes. The active part is activat d by the transversus ,ab­ d mi nu muscle, w hich tightens the fascia. The teni n in the fa cia transmit I ngitudinal tension to the tips of th spinou p r 'e es of U - L4 and may help the spinal ext nsor mus les to resist an ap plied load. In the lower thoracic and lu mbar regi ns this fasc.ia is m uch thicker than the rest of the spinal area, for it represents not only fa scia l tissue but the fused aponeuroses of several muscle , .97 It functions in many respects as a ligament, because it invests epaxial m uscles tha t course along the spinous processes and is reinforced by the ap oneuro tic origin of the latis­ simus dorsi cranially and by the attachment of the erector spinae (epaxial paravertebral) muscle mass caudally into the sacrum and sacral ligaments. It spans the area from the iliac crest and sacrum up to the thoracic cage. The posterior layer is reinforced by the la tissimus dorsi superficia lly and by the attach­ ill nt of the sacrosp inalis to its deep su rface. The fas­ cial aponeur otic heet encl se. the erector spinae muscle mass between the thoracic spines and the in ­ tersp ino us ligamen ts med ially, and the laminae and ligamentum flavum anteriorly. Because the thorocolumbar fascia encloses a space on each side of the spine, contraction of the erector

508

CHAPTER 16

•

The Spine-General Structure and Biomechanical Considerations

I Superiicial layer

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fascia Pretracheal layer of the cervical fascia

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ing layer (superiiciall) of cervical fascia B

spinae muscle mass (with a consequent increase in the transverse muscle area) tends to greatly tighten the thoracolumbar fascia, so that it functions as part of an active mechanism for pulling the vertebrae posteriorly and controlling shear and flexion during lifting. On full flexion, as the muscles become electrically silent, the thoracolumbar fascia becomes the major force against further flexion. 134 On extension from a fully flexed position th e gluteus maximus and hamstrings act in concert with the thoracolumbar fascia to initiate extension?6 With increased activity of these muscles the fascia serves to increase their efficiency?9 It also serves as a protective ligament against excessive flex­ Ion, and as the muscle mass contracts, the increased diameter of the muscle exerts a wedging effect on the aponeurosis, which may relieve some of the shear load on the articular facet joints and disks in flexion-extension movements of the spine. 61 It ha s been further demonstrated on the basis of dis­ sections and histological observations that the mus­ cles of the abdomen have the potential to stabilize the vertebral column through the action of the thora­ columbar fascia. This can be brought about, according to Tesh and associates, by (1) the intrinsic nature of the fascia without direct involvement of the vertebral

ligaments; (2) muscle contraction modifying longitu­ dinalligament tension by the thoracolumbar fascia; or (3) a combination of both mechanisms. 2G8 CERVICAL REGION

The cervical spine, with its investing musculature, is housed within the vertebral compartment, situated centrally and posteriorly. The contents of this com­ partment provide points of anchorage and suspension for fascia] layers defining all remaining compartments (see Fig. 16-148).125 The superficial (investing) layer embeds all the muscles of the neck except the platysm a. The primary layers of the deep cervical fascia are the pretrachial layer and prevertebraJ fascia. The pretrachial layer is connected with the connective tissue sheath around the neurovascular bundle (common car otid artery, i.n­ ternal jugular vein, and vagus nerve as the carotid sheath) and embeds the infra- and suprahyoid mus­ cles. It is firmly adherent to the cla vicle and deeper still to the layer or lam.iJ1a of the prevertebral fascia. Although these fascial layers provide stabilization to their contents, they are normally sufficiently lax to permit motion of the neck as a unit, as well as motion of one c.ompartment relative to another.

p n

PART 111 PREVERTEBRAL FASCIA

The prevertebral fascia (see Fig. 16-14B,C) is a firm membrane lying anteriorly to the prevertebral mus­ cles (longus colli; longus capitis; anterior, middle, and posterior scalenes; and rectus capitis). It is attached to the base of the skull just anterior to the capitis muscles and descends downward and laterally to ultimately blend with the fascia of the trapezius muscles. In its course it covers the scalene muscles and also binds down the subclavian artery and the three trunks of the brachial plexus. The prevertebral fascia crosses medi­ ally to the transverse processes of the cervical verte­ brae and covers all the cervical nerve roots. The fascia does not ensheath the subclavian or axillary veins, and therefore does not cause venous congestion. The fascia is firmly adherent to the anterior aspects of the cervical vertebrae. In the posture causing scapulocostal syndrome symptoms, the depressed scapula places strain on the fascia as well as the scapular musculature. 33 Oblitera­ tion of the radial pulse, as observed in Adson's ma­ neuver, can be attributed to the tension of the cervical fascia on rotation of the head and neck. Traction on the lower trunk of the brachial plexus may well cause pain and numbness in the ulnar distribution of the hand, which is common in this syndrome. 211 CAPSULES

The joint capsule of the spinal articular facet joint is composed of two layers, an outer layer known as the stratum fibrosum and an inner layer called the stratum synovium. The outer layer is attached to the perios­ teum of the component bone by Sharpey's fibers and is reinforced by musculotendinous and ligamentous structures that cross the joint. The outer layer is poorly vascularized but richly innervated. The nerve endings that are located in and around the joint cap­ sule are sensitive to the rate and direction of motion, tension and to compression and vibration. 86 In contrast to the outer layer, the inner layer of the capsule is highly vascularized but poorly inner­ vated. 94 The stratum synovium is insensitive to pain but undergoes vasodilatation and vasoconstriction in response to heat and cold. It produces the hyaluronic acid component of the synovial fluid and serves as an entry point for nutrients and an exit pOint for waste materia1. 94 The capsules of the articutar facet joints possess two noteworthy recesses, one superior and one inferior, through which the synovium may dis­ tend during effusion or backward bending.52,136 The superior recess is the weaker, and effusion here may protrude sufficiently to press on the mixed spinal nerve as it enters the intervertebral foramen. 52 Capsuies encompass all the articular facet joints in

Clinical

Applications~The

Spine

509

the spine including the articulation of the head with the atlas.1 50 The capsules include separate thickenings which have different functional roles. The capsules and their ligaments guide and restrict the motion seg­ ments. Because they are far from the disks and there­ fore act on long moment arms, these ligaments have an important functional role in resisting spinal flex­ ion.1 79 In full flexion of the lumbar spine, the capsules support 40 percent of the body weight?6 These fibers are generally oriented in a direction perpendicular to the plane of the articular facet joints. They are broader and more taut in the cervical region than the rest of the spine. 171 The capsules of the lumbar spine, which are often illustrated as being short and bunchy, in fact have a considerable medial extent and are quite fi­ brous, possessing an upward and medial direction that ideally suits them to restricting forward bending.173 The capsular ligaments, along with the anterior longitudinal ligament, also act to prevent hy­ perextensi.on of the spine. 60 Capsules are an important consideration with re­ spect to the Ioose- and close-packed positions of the articular facet joints of the spine.46,76 The concept of loose- and close-packed positions is useful in under­ standing when a joint may be less stable and more vulnerable. Loose-packed positions are those posi­ tions in a joint's range of motion in which the liga­ ments and capsules are slack; the area of contact with the articular surfaces is generally low and the joints are more vulnerable and less able to resist an external force. Close-packed positions, on the other hand, are those in which there is maximum contact between ar­ ticular surfaces and maximum tautness of the liga­ ments. 2 The close-packed position of the articular facet joints from C3 to L5 is extension, whereas the close-packed position for the atlas and axis is full flex­ ion 76 The close-packed position is often lost following a pathological process, trauma, or prolonged periods of poor posture. Inability to assume a fun close­ packed position results in the potential for increased dysfunction, and as a result a more unstable, loose­ packed position is maintained. VERTEBRAL INNERVATION

Because of the high frequency of patients presenting clinically with complaints of spinal pain or pain ap­ pearing to be of spinal origin, it is necessary for the clinician to have a thorough knowledge of spinal in­ nervation. More specifically, the clinician must be aware of what structures appear to lack innervation totally. This information must be combined with an understanding of common pathological processes and their clinical manifestations. In this way a more reli­ able understanding may be acquired as to the nature

510

CHAPTER 16

•

The Spine-General Structure and Biomechanical Considerations

and extent of various disorders and perhaps a better understanding of the often bizarre symptoms and signs that result. Information relating to spinal innervation and pain­ sensitive spinal tissues has come from two types of in­ vestigations: (1) actual experiments with human sub­ jects in which attempts are made to isolate noxious stimuli to a particular tissue; and (2) laboratory tissue studies in which sensory endings are identjfied and attempts are made to trace the afferent pathways from these endings to central connections. For obvious rea­ sons, those studies belonging to the first category of investigation are relatively few and results have at times been inconsistent or highly criticized . There have been numerous studies of the second type, how­ ever, and the results, for the most part, seem to be consistent. One must realize, however, that there is a limit as to how much can be inferred from tissue stud­ ies with respect to clinical significance. This is espe­ cially true when considering pain-sensitive tissue, be­ cause there is no direct correlation between the type of ending found within a particular tissue and the capac­ ity for the tissue, when stimulated, to send signals to higher centers, which result in the perception of pain (see Chapter 4, Pain). Presented here will be a summary of what seem to be reasonably well-accepted findings relating to spinal neurology. Spinal structures receive innervation largely from two sources, the sinu-vertebral (recurrent meningeal) nerves and the medial branches of the pos­ terior primary divisions of the segmental spinal nerves (Fig. 16-15A,B). Endings found in the dura mater and blood vessels are primarily of the free nerve plexus type (see Chapter 3, Arthrology). Endings found in the posterior longitudinal ligament and periosteum in­ clude free nerve endings and plexuses as well as encap­ sulated and nonencapsulated nerve endings. It is as­ sumed that the larger encapsulated nerve endings act primarily as mechanoreceptors. It is important to real­ ize that each sinu-vertebral nerve tends to innervate the tissues at its own level as well as send ascending and descending branches to levels above and below (Fig. 16-15A). It follows that stimulation of endings supplied by a particular sinu-vertebra] nerve may result in the perception of pain or in reflex changes in muscle tone at levels of the spine other than the level at which the le­ sion lies. Also, because it is well documented that stim­ ulation of deep somatic tissues often results in segmen­ tally referred pain, one may assllme that pain may be referred into a segment not corresponding to the verte­ bral segment (level) at which the lesion lies. The posterior division of the spinal nerve divides into lateral, intermediate, and medial branches (Fig. 16-16). The lateral branch innervates the skin and deep muscles of the back segmentally, while the me­ dial branch innervates the articular facet joint cap­

sules, the posterior aspect of the ligamentum flavum, the interspinous ligaments, the supraspinous liga­ ments, and the blood vessels supplying the vertebrae. The medial branches of the posterior division also send ascending and descending branches to (usually) one level above and one level below, with the same clinical implications as discussed for the overlapping sinu-vertebral nerves. Receptors found in the facet j.oint capsules, sending signals along the medial branch of the posterior division, include all four of the receptors discussed in the section on joint neurology (see Chapter 3, Arthrology). Afferent fibers from both the sinu-vertebral nerve and the medial branch of the posterior primary divi­ sion approach the spinal cord through the dorsal roots. In the dorsal roots the small unmyelinated fibers, thought to be largely responsible for transmis­ sion of noxious stimuli, aggregate toward the anterior aspect of the dorsal root. These enter the spinal cord and send branches to Lissauer's tract, where they may ascend or descend for a few segments before sending fibers to the substantia gelatinosa at the tip of the dor­ sal horn (see Chapter 4, Pain). Other fibers may pass directly to the base of the dorsal hom of the gray mat­ ter. From here they may ascend along the spinoreticu­ Iothalamic tract or through internuncial neurons and synapse w ~ th alpha motor neurons of segmentally re­ lated muscles (see Fig. 16-15A). In this way, noxious stimulation of sensitive spinal tissues may result in re­ flex muscle spasm (or perhaps inhibition) of segmen­ tally related muscles. Thus, muscle spasms-'which are often a part of this clinical syndrome-may result from this proposed pathway or by yet an undeter­ mined sensory or motor-reflex pathway.69 Note again that because of the overlapping distribution of sen­ sory fibers, muscles of more than one segment are likely to be affected. The previously mentioned as­ cending tract tends to cross within a few segments be­ fore ascending, with only a few ascending ipsilater­ ally. Signals traveling along this tract are thought to contribute to the conscious awareness of pain. The larger-diameter afferent fibers reach the spinal cord through the posterior rami of the dorsal roots. These contribute to the dorsal columns of the spinal cord, which supply information to higher centers, in­ cluding proprioceptive and "fast-pain" input. Other large fibers synapse at the tip of the dorsal born of the gray matter, the substantia gelatinosa, to contribute to modulation of afferent input to higher centers, as dis­ cussed in Chapter 4, Pain. Recall, however, that ulti­ mate perception of pain is, in part, determined by the relative balance of large-fiber and small-fiber input to the substantia gelatinosa, and that an imbalance in favor of small-fiber input tends to facilitate pain per­ ception. Selective stimulation of spinal structures has been

C~

II'

nl

Je

IT

Jil

51

c;

PART III

Clinical Applications-The Spine

511

Sympathetic chain Ascending branch of sinuvertebralis Branch ,to ligamentum flava and facet off sinuvertebralis

Recurrent grey rami to anterior longitudinal ligament Branch from grey rami to disk

III:-+-------I--Sinuvertebralis to disk f---II---\IIi1 L.6;""-~t;.-----r- Direct branch off mixed spinal nerves to facet

"";==-7'~-Local branch to facet and multifidus t.a-- -

Medial branch of posterior primary ramus to facet Lateral branch to facet and

Descending facet branch

rA

Nerve branches

of posterior

primary ramus

to muscles

#;~-"tsky S. Farfa n Hr. L1I11)' C: Th mechan ism of lu mbar spine. Spine

6:249-262, 1981

'n,c

'n,C

Clinical Applications-The Spine

525

80. Gra.tl t JCB: G rilnt'~ At las of Ana tulTI Y. Baltimo re, \Nilli.a ms a nd \tVilkins, 1972

81. G regCTSeIl GG Lucas D B: An in v ivo stud y of the axial rota ti on o f the. human thora ­ co lumba r sp one. ) Bone JOint Surg 49(11):247- 262, 1967 82. G r w D: tntra-a bdom ina] pressure response to 1.:1d rt pplicd to th e torso in no nnal

su bjects. p ine 5:149-155, 1980

83. G rie ve CPoManip ul.ti on the rapy for neck pain. Physiothern py 65:13 146, 1979

84. G ri ve C P: Comm on Vl-:.' rteb ral Joint Proble.ms, 2nd e.d . e w Yo rk, Ch u rchjJj living­

s tone, 1988

85. Grie " e C p , Diagn osis. Phys io ther Pract 4:73-77, 1988 86. Guyton A C: &1sic Hu man Physi ology: o rmal Function i1 nd Mechanisms of Dis­

ease, 2nd ed. Philadelphja, WB S., un d rs, 1977

87. Ha ll Me The Locomo tor System : Functi onal J\ nJ tomy. Springfield, IL, Ch;.ules C TIlOmas,19 88. HanuIton WJ (ed ): Tex tbook of H u m. n Ana tomy, 2nd ed . 5t Lo uis, CV Mosby, 1976

89. He mborg B, Moritz \I: Intra-abdo mina l p ressu re a nd trunk muscle actIvity durin g

lifting. n. Ch ron ic low-back p" 'ie n ts. Sc U1S liftin g. Scand) Rehabil Mod 16:103-111. 1984

]66. Norkin ee, Levengie DK:JOin t Structure and Function: A Comp re hensive Analysis,

2nd ed . Phil .delphi" FA Dal' "'. 1992

167. Okada M: ElectroOlyogro phic assessDl"" t o( the m uscu lar loael 111 fon~ard bending

post-ures. joumal of the l'.cul ty 01Science, Unil'crslty of Tokyo 3:311-336. 1970

168. Obda M : An clcclTomyograph ic examinati on of tile relative muscula r 10Dd in dif~ feren t human postll rt>S. J Hwn Urgol 1:75-93. 19n 169. b rtengren R. Ande rsson GB): EJoctromyogrnphic studies of trunk m uscles with spe­

dal rde""". to the (uncti onal nnotomy 01 the Iwnbar sp ine. Spino 2:44-52. 1977

170. Panjabi MM, Brand RA, ","hite AA: Mechanical properties or the hu man th oracic

sp ine as shownhy thret..;o...d imensionalload -disp lnc{·rnent curves. J Bone Joi.nt SUTg

8(A):642--652. 1976

171. P;mjil b i MM, Goo l VK, f dknta K: Phys'io logic strains in thl'. lumb.::tr Ii garrlcnts: An in

v itro biomcchnni ca l stud y. Spine 7: 1Q2- 203, 1983

172. l'anj. bi MM. Krag MM" W~ l e AA. e l .1: Effect of prcJond 0 11 luod d is pl-81 . 1975

191. Roth m an RH, Si ml.'One FA: Th e Sp in e.. Zno cd, vo lt. Philadel phiil, WO Sa und ers,

1982

192. ROlnm ClI1 RH, Simeone FA : TIle Sp ine, 2nd ed. \'01 2. Philadc.lph io. \'VB S
48:863-868, 1973

206. Stoddard A: Manual o( Osteopathic Technique. London. Hutchinson. 1962

207. Tauber ): An unn.rthodox look at backaches.. ) Occu p Mod 12:12S-130. 1970

208. Tesh JH. Evans J, Sh,l\vdu nn J, O'Bri ~n JP: ' n1 ~ mechanica l interact ion b e twccil lhe

thon'l.co lllnlbllr £a s l~ i a and the conn~ctive tissue of th e pos terior spine. In Buege.r AA,

Greenm an PE (eds): Empiric., 1 Approadl to th. Validation of SpillaJ M,,,,jpulatiun.

Springfield. IL. O,arlJlS C Thomas. 1985

209. Tkaczuk H: Tensile p ropert,ies of human lumbar longi tud ina l hga ment. Acta Orthop

Scand SuppI1 15:9-{;9, 1968

210. Trou p JDG, Hood CA, Chap man AT;:: tvieaslIre.mcn ts of the sag ittlt l m o bility of lum­ b. r ' pine nnd hips. Ann Phy>Med 9:30&-321 . 1976

211. Urschel I,C, Razzu k MA. Wood RE. Parckn M. P. ulson D1.: Objective d lagl10sis

(ul nar nerve cond uct ion vel oci ty) and current th.€' rtlpy of the th oracic outlet syn ~

dromc. Ann Tho rae Surg 12:608-620. 1971

212. Warn'ick R, \tV ilharns P: Gray 's Ana tomy, 36th ed (Sr). Ph Lltldelphia, JB lippincot t,

1980

213. VVa tnnabe K: A study on tht.' po:-> tl.l re; The function of the human e rector sl:>inae. jpn

J Ph)'s Ed uc 21:69-76. 1976

214 . Weisl H: TI,e ~ r t icul a r su rfuces of the sacro-ilia c joint and their rela tion to the mov e­ men t of the snCTUIn. Acta Anat 22:1- 14, 19.54­ 215. Weisl H: 711(' m ovements o r the sacro-i.l ioc joinL Acta Anftt 23:~9 1, 1955

216. \l\Ic ism 3 n G, Pope MH , Johnson RJ: Cy(.uc l o~ding in knee liga me nt inju ri es. Am J

Sport ML~i 8:24-30, 1980

:1 :1 :i

PART III 217. Weism.l ntc l A: Eva lu at ion and tr(.'ntmcn t o f sacroili,lC jo int problems . Bull Ortl u) p Sect APTA 3:5-9, 1982. 21B. White AA: Analysis of the mechanics of the thoracic sp ine ;n ma n. Acta Orthop

Sca nd (Supp l) 127:S-105, 1969

219. ~VhHe AA, rlirch C: The significan ce o f th e vertebra l posterior elements i.n the me­

ehonies of the th o rac ic sp ine. C lin O rthop 81:2- 20, 1971

220. White I\A, Panjabi M.M: Clinica l Biomechanics o f the Spine, 2nd ed. Philadelphia, J8

Lippmcott, 1990

221. White AA, Southwi ck WQ,Pa nj abi M, ct al: Practica l bi omc h:mics of the spine

for orthop.,edic su<seons. lns tr Cow-se Leet 23:62- 78, 1974

222. Wilder DC, Msrne, Pope MH, Fry moyer JW: The funct-ional topog raphy of the sacroil iac joint. Spine 5:575-579,1980

Clinical Applications-The Spine

52 7

223. Wo lf SL, & smajian JV: Assessment o f parasp i.nn l e'll~c t rom)'og raphic activity in nor­

ma l subjects il nd in chronic back p nin patien t us ing muscle biofeedback d evice. In

As m ussen E, GorgcnS
&Itimort!, Unive rs ity Pur-is Press, 1977

224. Wolf SL, Bosm ajicln JV, Russe erc, Kutna M: Norma tive d.Jta o n low back mobility

and acti vity levels. Am J Ph)'s Mod 58:217- 229, 1979

225. Wyke DO: 1110, neu rology o f joi nts. Ann R CoUSurg Eng I41 :25-50, 1967. 226. Wy kc 8: Receptor syste ms in lumbosncra l tissues in relation to the prod uction of

low bock pain. In White AA, Gordon SL (ed$): American Aca demy of Orthopaedic

Surgeons Sy mpos ium o n Idi op;lth ic Lo w Bac k Pain. St Louis, CV Mosby, 1982

The Cervical Spine MITCHELL BlAKNEY AND DARLENE HERTLING

• Review of Functional Anatomy

Osseous Structures

Joints and Ligaments

Muscle Groups

Innervation

Blood Supply

Joint Mechanics

Lower Cervical Spine (C2-Tl) Upper Cervical Spine (Occiput-C l-C21 Head-Righting Mechanism • Examination

History

Observation

Inspection

REVIEW OF FUN·C TIONAL

ANATOMY

D

Osseous Structures

The seven vertebrae of the cervical spine can be di­ vided into two groups, according to structure and function. The vertebrae of the lower cervical spine (C2-C7) are similar in structure to the vertebrae of the thoracic and lumbar spine with clearly defined verte­ bral bodies and spinous processes (Fig. 17-1).11 The transverse processes are abbreviated to allow better mobility, and there is a foramen to allow passage of the vertebral artery. The lateral portions of the verte­ bral bodies form the joints of Luschka, which also fa­ cilitate mobility of the lower cervical spine. l1 The facet joints of the lower cervical spine are in the sagittal plane and incline forward at approximately 45°. This

528

Selective Tissue Tension Neurological Testing Palpation Roentgenographlcal Analysis • Common Disorders

Acceleration Injury Cervical Instability Acute Disk Bulge Degenerative Joint Disease • Treatment Techniques

Manual Techniques-Muscles Manual Techniques-Joints Positional Traction

forward inclination allows the facet joints to bear weight and guides the motion of the segment. The bony structure of the upper cervical spine (oc­ ciput-C1-C2) is specialized to allow a great deal of mobility and to protect the medulla oblongata (Fig. 17-2A,B). The inferior facet of C2 has the same form and function as the facets of the lower cervical spine. The joint surfaces of the superior facet of C2 are aligned in the horizontal plane to allow approxi­ mately 90° rotation. The dens portion of C2 is a verti­ cal pin of bone that acts as a pivot around which the atlas rotates (Fig. 17-2C,D).11 The atlas is a wide, thin ring of bone with a well-developed transverse process but no spinous process. There is no intervertebral disk beh"leen the C1 and C2 because the atlas, with con­ cave joint surfaces above and below, serves the func­ tion of the disk. The anterior portion of the transverse ligament of the atlas forms a socket for the dens. Darlene Hertling en d Randolph M . Kessler: MANAGEMENT OF COMMON MUSCULOSKELETAL DISORDERS: Physicel Therapy Principles and Methods, 3rd ed . «.'l 1996 Uppincott-Raven Publishers .

c of co tht

gt'

OC 1

PART 1,11

Clinical Applications-The Spine

529

Spinous process Vertebral body Inferior facet

/1-1----ir-Uncinate process

Transverse -+--process

A

Vertebral body

C

FIG. 17-1. A typical lower cervical vertebra: (AJ inferior, (B) anterior, and (e) sagittal views.

The atlanto-occipital joint is the one true convex-on­ concave joint in the spine. The superior facet surfaces of the atlas are oval, concave, and toed-in slightly. The convex condyles of the occiput are slightly larger than the joint surfaces of the atlas, making maximal con­ gruence possible on only one side at a time, when the occiput is laterally bent on the atlas. The anterior

placement of the center of rotation of the atlas causes a lateral movement to the opposite side whenever the atlas is rotated (Fig. 17-3). This can be palpated as the transverse process becoming more ,p rominent on the side opposite rotation. When viewed from the side, the superior facet joint of C2 is rounded as the atlas rotates. It rolls down the shoulder of the side of

Transverse foramen Transverse process

Superior articular facet Posterior arch of alias

Body---.,I"";;

c

Spinous process of axis

o FIG. 17-2. The upper cervical spine: (AJ superior view of atlas, (B) inferior view of axis, (CJ lateral view of axis, and (DJ lateral view of atlantoaxial articulation.

530

CHAPTER 17

•

The CeNical Spine Fovea for dens

Superior articular facet Transverse ,ligament of atlas

IntersPinous ~~ ligament ,

Nuchal ligament

IlltV,l//;t///h

FIG. 17-3. The atlantoaxial joint from a superior view, showing the dens and the transverse ligament of the atlas.

rotation and climbs up the shoulder of the side oppo­ site rotation. This can be palpated as the transverse process of the atlas becoming higher and farther for­ ward on the side opposite rotation and lower and more posterior on the side of rotation.1 8 The atlanto-occipital, atlantoaxial, and, arguably, the Luschka joint surfaces are lined with articular car­ tilage; they have synovial membranes and, like other synovial joints, have rich proprioceptive and nocicep­ tive innervation. 23

D

Supraspinous ligament

'C

FIG. 17-4. A lateral view of the cervical spine, showing the interspinous, supraspinous, and nuchal ligaments.

Joints and Ligaments

The anterior and posterior longitudinal ligaments and the ligamentum flavum are present in the cervical spine from C2 through C7 and perform the same functions as in the thoracic and lumbar spine (see Fig. 16-10). The interspinous and supraspinous ligaments blend with the nuchal ligament of the cervical spine (Fig. 17-4). The nuchal ligament has its origins on the spin­ ous processes of the cervical spine and its insertion on the occiput. Its function in quadruped animals is to support the head. Its function in humans is to prevent overflexion of the neck. The nuchal ligament tightens at the extreme of neck flexion. It also becomes tight, flattening out the cervical lordosis, with approxi­ mately 15° of nodding of the upper cervical spine.1 8 The posterior longitudinal ligament ends at C2. The tectorial membrane, which is thin and diaphanous through the rest of the spine, thickens into the tectorial ligament arising from C2, bypasses the atlas, and in­ serts on the occiput (Fig. 17-5). The tectorial ligament becomes tight with flexion of the head. Deep to the tectorial ligament is the cruciform liga­ ment, which has both vertical and transverse portions (see Fig. 17-5). The vertical portion of the cruciform ligament has its origin on C2 and has the same inser­ tion and function as the tectorial ligament. It also by-

passes C1. The horizontal portion of the cruciform lig­ ament has its origin and insertion on the interior sur­ face of the anterior ring of the atlas. It encircles the dens to reinforce the transverse ligament of the atlas (see Fig. 17-3). The transverse ligament of the atlas has its origin and insertion on the interior surface of the anterior ring of the atlas. It encloses the dens and is lined with a synovial membrane and articular cartilage to pro­ vide lubrication as the atlas rotates around the dens. If the transverse ligament of the atlas and the horizontal portion of the cruciform ligament are weakened by systemic inflammatory disease or injured in an acci­ dent, there is danger of damage to the medulla oblon­ gata by dislocation of the dens. If this is suspected, traction or mobilization of the cervical spine should be considered gravely dangerous. The alar ligament is a winglike structure that has its origin on the lateral borders of the dens and its inser­ tion on the occiput (see Fig. 17-5). It is a major portion of the stabilization system of the upper cervical spine. The configuration of the atlanto-occipital joints could allow considerable lateral flexion, which would dam­ age the medulla oblongata. This lateral flexion is checked by the alar ligament. If the alar ligament is congenitally absent or damaged or if the dens is frac­


. C I " ~" ific(1tio n , D i a~;Tl os i s, Management.

icago. Yea, Book Med ical P,lblishers, 1986 3. C ria x J: Textbook of O rlho!"'di Merlit:inc, Diilg'nostks. Nt-'w York , Georg Thieme Ver­

IClg, Thieme Medical Publis hers, 1990

43. Edmund Sl: Manipu loltion "nd Mobil izatjon: E>. tre mity and Spinal Techniques. St.

Louis, C V rvlosb\', 1993

44, EdHf.ud s BC: Combi.ned mov\.' ments o f th c lumb.lf spine: Examination and clinic..,1

s ig ni fica nce. Aust J Physiot.her 25:147-152, 197Q

~5. EdwClId s Be Comb ined m ovem~n t s in the c~rvic,1 l spine (C2-7): TIlt-ir \,;1 Iu \? in ex­

amination d Approach. San Diego,

Singula r Publishing Gro up, 1992

47. El vey Rl.; Pa infuJ restrict.ion of should er movement: A clin ical ()bsen~.... tio n stu dy.

In: Proceedings, Disor ders of the Knee, Ank le and Shoulder, Perth, Western A us­

tr. liilll Institvte of Technology, 1979

48. Elvey RL: Trea tment o f arm pain associa ted with abno rmal brt1chia l pl ex us ten sion.

Aust J PhySiother 32:224-229, 1986

49. Elvey RL, Quin hle r JL, Thomas AN: A cli ni cal study of RSI. Aust F.l m Phys 15:1314-1322, 1986

SO. Evans 1': The he.li ng process at a cellula r level. PhysioU,erapy 66;256-259, 1980

51 . Ev.ns RC: Ulus trnted Essent ials in Orthopedic Ph ysica l Assessmen t. St, Lo ui s, CV

Mosby, 1994

52. E"jen th 0, H amberg J: Muscle Stretching in Man ua l Therapy: A Clinic. 1 M,ln un l,

Vol. 2: 'n ,e Spinal Colu mn and tho TMJ. Al It., Sweden, Alfln Rehab Forlag, 1984

53. Fari1dy JA: Current pri ncip les in the non ope rat.ive n13n agement o f s tructural adoles­

cent scoliosis, Phvs Ther 63:512- 523, 1983

54. Forlan H, Graco;etsky S: T he n. ture of inst.l bility. Spi ne 9:714-719, 1984

55. Feldenkrais M: Body an d Matu re Behav ior: A Stud y of Anxi.ty, Sex, Gravi ty and

Learning . New Yo rk, l nte m a fJonn l U ni v crsitl~ Press, 1949

56. Fcldenkrais M: Awareness Through Movement-Hea lth Exercises (ur Personal Growth. N ew York, Harper & Row, 19n 57. Feldenkrais M: The Potential Self: The Dyna mi cs of Body and the Min d. San Fro n­

cisco, Harper & Row, 1985

5B. I:ord OM, Bagnall KM, Clements CA, et al: Muscle sp indles in the paras pinal mus­

culature of patien ts WIth adol escent idiopa thic scoliosis. Spine 13:461-465, 1988

59. Ford OM, Bagrurll KM, McFadden, KD, ot al: Par.spina l m uscle im ba lance in adoles,

cent idiopathic sco liosis. SpiM 9:373-376, 1984

60. Fr.lnk C, Akeson WH, Woo 5, e t a l: Physiology and thera peutic v"lu e of passive join t mo tion. C1in Orthop 185;1 13-125,1 984 61. Fryette HH: Pnnclples of Osteopa th.c Technique. Carmel. Calif., Academy of Ap­

plied Os teopa thy, 1954

62. Ce1b M ; An Int'rodu ction to the A leXi1 n dcr Techn iqu ~ . New York, H en ry Holt &

Co mpan y, 1987

63. Ge.rha.rdt· JJ: Docu mentation o f JOint Mo ti on: Tnte.mati o nnl Standa rd Ne utra l-Ze ro

Measuring S.F.T.R. Reco rding and Applica tio n of Goniomct"ers, Inclinometers nnd

Calipers. Portland, Onegon, lSOMIOD Inc., 1992

64. Gonnella C, Paris 5, Kutner M: Reliab ili ty in evaJunting passive in tcJ"\'crtebra J mo­

tion. Phys Ther 62:437-444, 1982

65. Greenman PE: Principles of Man uC'l1 i\k-d i(.'i ne. B.... ltimo re, \'Villiams & Wilkins, 1989

66. Grieve GP: Mobil.isation o f the Sp inc: No tes o n E>.a m ination, Assessment and Clini­

cal Method, 4th ed . Edinburg h, Churchill Lh>ings tone, 1984

67. G rieve GP: 'nornclc joint prob lems and s imulated viscem l ctisea.se.. In G rieve GP

(ed ): Modem Manua l Therapy of the Vertebral Column New York, Churchill Li\,­ ingstone, 1986:3n-395 68. GriD1Shy 0; Lumbar-Thorad c Spine. Continu ing ed uca ti on course, In!o>titutc oi

Grad uate Health Sdencos, Nashville, Tenn" 1976

69. Gustavsen R: Fra a kti" .,'spenning til trening. Oslo, Norlis, 19n 70. Gustav.sen R: Traini ng Therapy: Prop hy laxi.s and R('habililcltion. New York, Th iem

1993

71 . Hllll CD: Clinical Concept..; in RegIon a l !"l u5culn~kddd.1 Illn ~ss. l ondun, Grunt..' & St rat ton, 1987:227-24·j Hartman L: Class ificatio n ,md .l pp li cnti~'n of os k'opathi c m",lOlpli lati\'c tC'thniquc:­ In Glasgo' .... EF, TW(l OlCy LT, Scull FR, ('t a l (eds): Aspects. of ~vfi)n i pui ll ti \'e Tht:'r.lpy 2nd 00. Ed inbu rg h, Churchi ll Li,·ini;s.ton('!t idiop.:lt hlc sct) Ji l)~ i s ~x ioal Arts, 1988

153. Saliba VL, Jo hnson GS: Lumba r protlJ.Ctiv e rnecha n ism. In Whitp J\f-f, And e rson R

(ed s): Conserva tive Care of Lo\-v Ba k Pa in . B..l lrimore" Willi a ms &: Wil kins , 1991

154. Sa unde rs HD: EV'al uAt ion, T reatment an d Preve ntion of Mu&:ulosk.ele ta! Di.:;orders.

Minneapoli', Vi king. 1985

155. She.rring ton C: The Integ rated Action of the Nervo us 5ysrem~ 2nd ed~ e \o\,>' H ,wen ,

Y,l k Unj ve.rs ity Press, 1947

156. Sina ki M, Ke nne th P, O ffo rd MS: Ph y-sicrli tlCliv ity in p ostml? n 0 p au ~ 1 wumen: Effect On b rt~bral disc degeneration cL)nsidered ilS a press ure 'ltTophy. J

Bone JOint Surg 39A:933-945, 1957

Linton 51: The relationship between activity and chronic pain. Pain 21 :289-294, 1985

Lippi! AS: The facet joint and its role in s p ine pain mnnaSE:.' m ent with fac(,t joint in­ jections. Spine 9:746-750,19114 Lipson S1. Muir H: Protcoglycans in experiment.. 1 intern.'.rlebral disc d('gcn er;)tinn .

Spine 6:194-210, 1981

Liston CB: Back schools and ergonomics. In Twomey LT, Ta y lor IR (cd s): Physic.,1 Therapy of the Low Bot k. New York, Churchill Livings tone, 19 87:279-303

353. Liyang D, Yi.nkiln X, W~nming Z, C't al: nl(~ effe ct l)f fl('xion -(ixlP;n s ion motion of th

lumbar spine on the capacity of the spinal c,mnl. Spine 14::;23-525, 1989

354. Ljung,gren AE, Eldevik P: AutotrJction in lumbJr disk hemiation with CT eX.;'lmin
Scand I Rehabil Mod 5: 186-190, 1973

370. Magora A: Investigation of the relation between low back pain and occupation: 7. Neu rologi c and orthopedic conditions. Scilnd Rehabil Med 7(4): 146-151 , 1975

371. Mugora A, Schwartz A: Relation bet..veen the low back pain syndrom e and X-raj

fi.ndings: 1. Degenerativ e osteonrthritis. Scnnd J Rehabil Med 8:115-125, 1976

372. Maigne R: OrthopaediC Medicine. Springfield, Ilo, Charles C. Th omas, 1976

373. Maigne R: Manipulation of the spine. In Rogoff JB (ed): M.;"Inipulations, Traction an d Massage, 2nd ed. Baltimo re, Williams & Wilkins, 1980:59-120 374. Maitland GD: Movement of pain-scosi tive structures in the vertebral canal in a group of physi otherapy students. S Afr J Phys iotber 36:4-12, 1980

375. Maitland GO: Vertebral Manipulati on, 5th ed. Boston, Butterworths, 1986

376. Maitlan d G O: The Maitland concept: A ssessment, examin.ltiol1 and treatment bv pass iv e movem ents. In Twomey LT, Taylor JR (c.ds): PhYSical Therapy of the 1..0\~ . Back. N ew York, Churchill Livingstone, 1987:135- 156 377. Mandai AC: The rorrect height of school furniture. Physiothernp), 70:41l-53, 1984

378. MannheinlC'r lS, Lampe GN: Cl inical Tr