Atlas of Pediatric EEG
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Atlas of Pediatric EEG Pramote Laoprasert, MD Assistant Professor University of Colorado School of Medicine Director of Surgical Epilepsy Program and Epilepsy Monitoring Unit Department of Pediatric Neurology The Children’s Hospital of Denver Aurora, Colorado
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Dedicated to my wife Nan, my children Maddy and Rick, and my parents Saman and Vilai For their unconditional love, enthusiastic support, encouragement, and long-suffering tolerance during preparation of this book. And to my patients and their families. Without them, this book would be impossible.
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CONTENTS Foreword . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix
3 Newborn . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 201
8 Generalized Epilepsy . . . . . . . . . . . . . . . . . . . . . . . . 613
Preface
xi
4 Focal Nonepileptoform Activity . . . . . . . . . . . . . . 275
9 Focal Epilepsy. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 675
Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xii
1 Normal and Benign Variants . . . . . . . . . . . . . . . . . . . 1
5 Generalized Nonepileptiform Activity . . . . . . . . 389 6 ICU . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 471
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 861
2 Artifacts . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125
7 Epileptic Encephalopathy . . . . . . . . . . . . . . . . . . . 529
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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FOREWORD Epilepsy is a common and frequently disabling disorder in children. Linking its clinical manifestations to electrographic and imaging changes is essential to correct diagnosis and management. This multimedia work provides an accessible, comprehensive, and timely tool for the child neurologist or epileptologist in training or in practice to become familiar with the extraordinary richness of the clinical and electrographic manifestations of childhood epilepsy. The text represents the distillation of an extraordinary body of clinical experience and painstaking attention to detail, which is characteristic of Dr. Laoprasert. I first had the privilege of making his acquaintance two decades ago, when he began his child neurology training at Mayo Clinic. Since that time, he has established himself as a first-class pediatric epileptologist and scholar. This
fine work is an appropriate testament to his diligence and skill. The text is laid out in a systematic and thoughtful fashion, beginning with common and not-so-common patterns and variants in the electroencephalogram, which can be a source of confusion and diagnostic error to the novice. Subsequently, pathological conditions are explored in a similarly logical and comprehensive fashion. Since most of us learn from our patients, I predict that this case-based approach will be extremely effective. I commend this work to anyone who wishes to improve his or her grasp of epilepsy in childhood. It will be essential reading for pediatric epilepsy trainees but will also be a frequently consulted resource for residents in training. By the same token, the child neurologist who is not an expert in epilepsy, and even
experienced pediatric epileptologists, will find a great deal of valuable material to enhance the care of their patients. Whether read cover-to-cover, used to review specific problems, or dipped into at random, this text makes learning about epilepsy in children a pleasure and will ultimately enhance the quality of their lives and those of their families. Marc C. Patterson, MD, FRACP, FAAN Professor of Neurology, Pediatrics and Medical Genetics Chair, Division of Child and Adolescent Neurology Mayo Clinic Rochester, Minnesota
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PREFACE EEG presents a tremendous challenge to the neurologist. Although EEG has been used for almost a century, it is still and will continue to be one of the most important diagnostic tools in neurology, especially in pediatric neurology and epilepsy. The rapid advances in digital and prolonged video-EEG as well as in epilepsy surgery enhance the usage of the EEG to the higher level. Atlas of Pediatric EEG presents both common and uncommon EEG diagnoses in a case-study-oriented
manner. Unlike other EEG atlases that catalog only the EEG patterns, this book stresses the viewpoint of the practicing neurologists and neurophysiologists. Integration of the EEG, clinical information, and neuroimaging is the heart of this book and is consistently presented throughout. Cited references for further study are extensive and up to date. This will help the readers to have a better understanding of the EEG and its applications.
Atlas of Pediatric EEG is designed for the electroencephalographer, child neurologist, EEG/ epilepsy fellow, neurology resident, pediatrician, and EEG technologist with an interest in pediatric EEG. Other healthcare providers, such as nurse practitioners and physician assistants who care for children with neurologic conditions, as well as medical students during the pediatric neurology clerkship who want to learn about the EEG in children, will also find this atlas valuable.
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ACKNOWLEDGMENTS I would like to acknowledge Dr. Marc Patterson for his extraordinary mentoring and for a very kind and thoughtful foreword. I thank Dr. Paul Moe and Dr. Andy White for their critical review and proofreading. I also thank my colleagues, epilepsy fellows, and neurology residents at the Denver Children’s Hospital in the preparation of this book.
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I am also deeply grateful to the editorial staff at McGraw-Hill, especially to Anne Sydor, Christine Diedrich, Sherri Souffrance and Priscilla Beer, as well as Sandeep Pannu and Aakriti Kathuria of Thomson Digital, for their generous support and competent assistance.
1
1
Alpha rhythm or posterior dominant rhythm (Figures 1-1 to 1-5, 1-11, and 1-16)
䡲
Normal and Benign Variants
Monomorphic either sinusoidal or having sharp points at the top or bottom, 8–13 Hz in older children and adults during relaxed wakefulness with eyes closed.
䡲
Eye opening attenuates alpha rhythm (AR) and eye closure accentuates AR.
䡲
AR also attenuates with:
䡲
䊳
Drowsiness
䊳
Concentration
䊳
Stimulation
䊳
Visual fixation
䊳
Anxiety
䊳
Eye closure with mental calculation
AR responsive to eye opening occurs in 75% of infants between 3rd and 4th months.
Frequency 䡲
䡲
Mean AR frequency: 䊳
4 months – 4 Hz
䊳
12 months – 6 Hz
䊳
36 months – 8 Hz
䊳
9 years – 9 Hz
䊳
10 years – 10 Hz
䊳
Elderly – above 9 Hz
Abnormal AR: 䊳
1 year: 50% is seen in 1.5% in all ages. Voltage asymmetry >20% is seen in 5% of normal children. Persistent asymmetry of 50% or more is considered abnormal. Persistent asymmetry of 35–50% is considered suspect if the lower voltage AR is on the right side. Symmetry is best measured in referential montage to avoid phase cancellation.
Effect of two separate alpha frequencies.
Bancaud phenomenon 䡲
䡲
䡲
When unilateral cerebral lesions or transient cerebral dysfunction (such as migraine or TIA) are present in the occipital or, less commonly, parietal or temporal lobes, the side of defective reactivity (eye opening and alerting) occurs ipsilateral to the side of the lesion. When both phenomena exist, the same side of the brain is affected.
䡲
≥ 13 Hz; most common 18–25 Hz; less common 14–16 Hz; rare 35–40 Hz. 䡲 First develops between 6 months and 2 years 䡲 䡲 䡲
Distribution: frontocentral >widespread>posterior. Voltage 35% is indicative of: 䊳 Cortical injury
䡲
䊳
䡲 䡲
The same rule is applied to mu and temporal theta activity.
Immediately after eye closure, alpha frequency may be accelerated for 0.5–1 sec. Therefore, alpha frequency assessment should not be done during this period.
Paradoxical AR 䡲
AR presents with eye opening if the environment is devoid of light as the result of partial alerting. Paradoxical AR is seen in drowsiness and sedation.
䊳
䊳
Transient conditions such as postictal state Subdural or epidural fluid collection
More sensitive than focal polymorphic delta activity (PDA) 䡲 Amplitude asymmetry of >35% is considered abnormal. 䡲 Focal increased amplitude is seen in: 䊳
Skull defect (breach rhythm)
Focal structural abnormality, especially focal cortical dysplasia 䡲 Presence of beta activity is almost always a good prognostic sign. 䊳
Slow alpha variant (Figures 1-6 to 1-7) 䡲
Beta activity
䡲
䡲
1
Normal and Benign Variants
䡲 䡲
䡲
䡲
䡲
A rare physiologic variant of AR (less than 1% of normal adults), seen during relaxed wakefulness, has a harmonic relationship and interspersed with the normal AR, and shows similar distribution and reactivity as a normal AR. Usually alternates with AR. Rhythmic sinusoidal, notched theta, or delta activities that have a harmonic relationship with the AR (one-third or, more commonly, one-half the frequency). Should not be misinterpreted as occipital intermittent rhythmic delta (OIRDA) or theta activity activities, and pathologic findings seen in children and adults. Slow alpha variant may be differentiated from pathologic slow waves by: 䊳 Morphology (notched appearance) 䊳 Frequency (subharmonic of normal AR) 䊳 Reactivity to eye opening 䊳 Disappearance with sleep Sometimes mimics rhythmic temporal theta bursts of drowsiness (RTTD), except that it occurs only over the posterior head regions.
Fast alpha variant pattern (Figures 1-8 to 1-10) 䡲
Harmonic of the AR that has a frequency approximately twice that of AR, usually within the range of 16–20 Hz, with a voltage of 20–40 μV. 䡲 Usually intermingled with AR and shows reactivity and a distribution similar to AR.
1 Posterior slow waves of youth (youth waves or polyphasic waves) (Figures 1-12 to 1-15)
Normal and Benign Variants
䡲
Amplitude varies, but is generally below 50 μV. Duration is 100–250 msec except in 1–3 years that can be up to 400 msec.
䡲
Most commonly seen in children aged 8–14 years and are uncommon in children under 2 years. 䡲 A 15% incidence in healthy individuals aged 16–20 years but rare in adults above 21 years of age.
Resemble positive occipital sharp transients of sleep (POSTS) and visual evoked potential. Subjects with prominent lambda waves also have prominent POSTS. 䡲 In children, highest amplitude and sharpest component is surface negative in the occipital region. 䡲 Random and isolated waveforms but may be recur at intervals of 200–500 msec.
䡲
䡲
Visual evoked potentials occur in association with saccadic eye movement.
䡲
Do not occur before 1 year of age. Most common during the middle years of childhood. The prevalence of lambda waves between 3 and 12 years of age is about 80%.
䡲
Physiologically high-voltage theta or delta waves accompanied by the AR and creating spike wave-like phenomenon
䡲
䡲
Typically seen both unilaterally and bilaterally in a single recording. They are always accompanied by the AR, attenuated with eye opening, disappear with the AR during drowsiness and light sleep, and may be accentuated by hyperventilation and stress. Characteristic findings: 䊳 Monorhythmic occipital rhythm attenuates with eye opening 䊳
Normal slower waveforms rarely >1.5 times the amplitude of AR.
䊳
Normal slower waveforms attenuate with AR during alerting. Slower waveforms has the same asymmetry in the ongoing AR
䊳
䡲
Index of abnormality of theta/delta slowing. 䊳 Complexity and variability of waveforms 䊳 Incidence (how often slow waves occur) 䊳
䊳 䊳
䡲
Lambda waves have been described as biphasic or triphasic; their predominant positive component is preceded and followed by a negative component.
䡲
Strictly bilateral synchronous although may be asymmetrical on the two sides. Rarely present only on one side.
䡲
Marked asymmetry indicates an abnormality on the side of lower amplitude. 䡲 The most important precipitating factor is voluntary scanning eye movements. 䡲 Lambda wave is attenuated by:
Voltage ratio (normal slow waves rarely >1.5 times the amplitude of AR) Persistence with eye opening Symmetry (consistently predominant on one side).
Lambda waves (Figures 1-17 to 1-19) 䡲
䡲
Sharp transients of sawtooth shape (biphasic or triphasic) occurring over the occipital region of waking subjects during visual exploration (scanning complex picture), mainly positive relative to other areas and time locked to saccadic eye movements.
䊳 䊳
Darkening room Staring at a blank card
Eye closure Lambda waves usually occur as random and isolated waveforms but may recur at intervals of 200–500 msec. 䡲 Accompanied by eye movement and eyeblink artifacts. 䡲 Sometimes, especially when present unilaterally, they may be mistaken for focal abnormalities, but the distinction can be made by replacing the geometric image with a blank surface. 䊳
3
䡲
Marked and persistent asymmetry indicates an abnormality on the side of lower amplitude.
Positive occipital sharp transients of Sleep (Figures 1-20 to 1-24) 䡲
Best seen at the age of 15–35 years and rarely 60 sec with gradual onset and offset. 䊳 The sharper component of the wave usually has a negative polarity in the anterior temporal region. 䊳 Unilaterally with shifting from side to side greater than bisynchronous. 䊳 Differentiated from ictal epileptiform activity by 앫 Monomorphic and monorhythmic (no evolution
into other frequencies although amplitude can vary) 앫 No alteration of background activity 앫 Occurrence in relaxed wakefulness and
drowsiness (most common) and disappearance in deeper levels of sleep. 䡲
Although it has no clinical significance, it was considered by some authors to be a pathologic finding in selected cases.
䡲
Electropositive of sharp component and electronegative of smooth component. 䡲 Widespread field lasting for 0.5–1 sec.
䡲
䡲
䡲
Occurs in children after age 3 to young adult but more common between 12 and 20 years with a peak at age 13–14 years. 䡲 Best seen in contralateral ear reference montage. 䡲 Appearance in diffuse encephalopathy EEG pattern in a wide variety of encephalopathies of childhood suggesting that they are epiphenomena or a resilient normal. Frequency is more variable and can be elicited by alerting stimuli.
Small sharp spike (SSS) or benign epileptiform transients of sleep (BETS) (Figures 1-93 to 1-96) 䡲 䡲
Benign variant of no clinical significance. 20–25% of a normal adult population.
䡲
Appearance in deep drowsiness and very light sleep and disappearance in deeper stages of sleep. 䡲 Usually low voltage, short duration, single monophasic, or biphasic spike with an abrupt ascending limb and a steep descending limb. 䡲
Fourteen and six per second positive spike discharge (Figures 1-83 to 1-92, 5-44 to 5-48, 6-44) 䡲 䡲
Benign variant of no clinical significance. Bursts of arch-shaped waves at 13–17 Hz and/or 5–7 Hz, most commonly at 14 and/or 6 Hz. The 14 Hz component is more commonly seen than 6 Hz.
䡲
Maximal over the posterior temporal and adjacent areas of one or both sides of the head.
䡲
Amplitude 150 μV), broad, biphasic transients (either negative–positive or positive–negative) with blunt configuration, seen maximally in frontal–prefrontal regions (Fp3–Fp4). They usually are isolated or occur in brief runs, alone or in combination with anterior slow dysrhythmia, symmetrically, bilaterally, and synchronously. They occur in transition from active to early quiet sleep. Although the premature form which is polyphasic and very high amplitude may appear very early at 26–31 weeks CA, the typical biphasic FST are maximally expressed at 35–36 weeks, are diminished in number and voltage after 44 weeks CA, are rarely seen during sleep after 46 weeks CA, and are absent at 48 weeks CA.17
230
Newborn
3
FIGURE 326. Eye Movement Artifact. A 38-week CA infant with apnea. EEG shows biphasic sharp theta activity in bilateral prefrontal regions that simulate frontal sharp transients. Eye lead channel can differentiate between these two conditions. When activity points in the different directions as in this EEG, it indicates that this is eye movement artifact rather than brain wave.
3
Newborn
231
FIGURE 327. Anterior Slow Dysrhythmia; (Anterior Dysrhythmia, Bifrontal Delta Activity). A 40 weeks CA infant with apnea and cyanosis. EEG shows “anterior slow dysrhythmia,” which is described as intermittent semirhythmic 1.5- to 2-Hz high-voltage delta activity (50- to 100 μV) in the frontal regions bilaterally. Anterior slow dysrhythmia is usually admixed with frontal sharp transients. It occurs most prominently during transitional sleep. It is a normal developmental EEG pattern. However, when it is abundant, persistently asymmetric, and high in amplitude or dysmorphic, it may be considered abnormal.2,4,5,10
232
Newborn
3
FIGURE 328. Anterior Slow Dysrhythmia & Frontal Sharp Transients. A 38-week CA baby girl with mild hypoxic ischemic encephalopathy and clinically suspected seizures. EEG shows bilateral synchronous, rhythmic 1.5-Hz sharp-contoured delta activity in bilateral frontal regions, intermixed with frontal sharp transients. Repetitive frontal sharp transients and anterior slow dysrhythmia is considered a normal, developmental EEG pattern.
3
Newborn
FIGURE 329. Frontal Sharp Waves; Intraventricular/Periventricular Hemorrhage. A 2-day-old full-term infant with intraventricular hemorrhage associated with congenital CMV infection and cardiomyopathy. EEG shows marked and persistent spike/sharp-wave activity in the right frontal region intermixed with focal theta and delta slowing in the same region. This spike/sharp wave activity is more likely to be epileptiform activity rather than anterior slow dysrhythmia. In the same recording (not shown), the patient also has focal electrographic seizures in the right frontal region.
233
234
Newborn
3
FIGURE 330. Rhythmic Midline Central Theta Bursts. A 39-week CA infant with jitteriness. EEG shows bursts of rhythmic 4–5 Hz sharply-contoured theta activity in Cz and C4. The rest of the EEG recording was unremarkable. Note an electrode artifact at F7. Rhythmic midline central theta bursts are bursts of rhythmic 50- to 200 -μV, 5- to 9-Hz activity occurring in the midline central region. It can be either a normal variant or can occur in association with other abnormalities, especially central sharp waves, in patients with various CNS insults.5,20
3
Newborn
235
FIGURE 331. Transient Unilateral Attenuation of Background Activity During Sleep. A 41-week CA newborn with recurrent apneic episodes associated with cyanosis. The neurologic examination was normal. Head CT was unremarkable. A routine EEG during slow sleep shows intermittent attenuation of background activity over the left hemisphere lasting for 1–2 min. Transient unilateral attenuation of background activity during quiet sleep is seen in 3–4% of newborns and consists of a sudden flattening of the EEG activity occurring in one hemisphere. The asymmetry is transient, lasting from 1 to 5 min (less than 1.5 min in 75% of cases). It occurs at the beginning of quiet sleep. The EEG activity before and after the asymmetry is almost always normal. This EEG pattern may reflect the unusual functioning of mechanisms underlying the normal process of change from the low-voltage continuous EEG in REM sleep to the higher voltage discontinuous pattern of quiet sleep. This EEG phenomenon is of uncertain significance and must be differentiated from asymmetric background activity associated with structural abnormalities. The latter is usually shorter in duration, occurs in all states, and is associated with other EEG abnormalities such as sharp waves or delta slowing.5,20–22
236
Newborn
3
FIGURE 332. Transient Unilateral Attenuation of Background Activity During Sleep. A 41-week CA newborn with recurrent apneic episodes associated with cyanosis. The neurologic examination was normal. Head CT was unremarkable. A routine EEG during slow sleep shows intermittent attenuation of background activity over the left hemisphere lasting for 1–2 minutes. Faster paper speed enhances the “transient unilateral attenuation of background activity during sleep”. Transient unilateral attenuation of background activity during quiet sleep is seen in 3–4% of newborn and consists of a sudden flattening of the EEG activity occurring in one hemisphere. The asymmetry is transient, lasting from 1 to 5 min (less than 1.5 min in 75% of cases). It occurs at the beginning of quiet sleep. The EEG activity before and after the asymmetry is almost always normal. This EEG pattern may reflect the unusual functioning of mechanisms underlying the normal process of change from the low-voltage continuous EEG in REM sleep to the higher voltage discontinuous pattern of quiet sleep. This EEG phenomenon is of uncertain significance and must be differentiated from asymmetric background activity associated with structural abnormalities. The latter is usually shorter in duration, occurs in all states, and is associated with other EEG abnormalities such as sharp waves or delta slowing.5,20–22
3
Newborn
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FIGURE 333. Burst-Suppression Pattern; Severe Hypoxic-Ischemic Encephalopathy. (Same patient as in Figure 3-5 and 3-7) A 31-week CA infant with severe HIE. EEG shows a nonreactive burst suppression pattern. The burst of activity contains sharp waves and spikes intermixed with delta and faster frequencies. The interburst interval (IBI) is of very low amplitude. The patient died 1 day after this EEG. Burst suppression is the most extreme degree of discontinuity and represents an intermediate degree between depressed and undifferentiated EEG and electrocerebral inactivity. During the burst, activity contains intermixed components of poorly organized delta and theta frequencies, at times, with spikes or sharp waves. The IBI contains very low-voltage ( ictal pattern. Transient phenomenon (disappear within days to weeks). 䡲 Clinical: lethargic, focal seizures, focal neurological signs. 䡲 Occur at the rate of 1–2/sec and are commonly seen in posterior head region, especially in the parietal areas. 䡲
472
䡲 䡲 䡲
䡲
䡲 䡲 䡲 䡲
Sometimes associated with EPC. Related to an acute or subacute focal brain lesion involving gray matter. Chronic PLEDs were also reported in 9% of patients with intractable epilepsy who had structural abnormalities such as cortical dysplasia or severe remote cerebral injury. Etiology: 䊳 Acute stroke, tumor, and CNS infection were the most common etiologies. 䊳 Others included acute hemorrhage, TBI, PRES, familial hemiplegic migraine, and cerebral amyloidosis. PLEDs were more periodic when they were associated with acute viral encephalitis than with other etiologies. Most HSV encephalitides have PLEDs, maximal in the temporal region. Seizure activity occurred in 85%, with mortality rate of 27%. In one series, 50% of patients with PLEDs never developed clinical seizure.
Periodic epileptiform discharges in the midline (PEDIM) (Figures 6-10 and 6-11)
6
ICU
䡲
Most commonly caused by multifocal or diffuse cerebral injury, such as anoxic encephalopathy and CNS infection, as well as strokes and epileptic seizure disorders (especially complex partial SE). 䡲 Mortality of 52%, twice of patients with PLEDs. 䡲
Higher incidence of seizures. 䡲 BiPLEDs and GPEDs after an anoxic insult carried a poor prognosis for survival. Aggressive treatment of patients may not be warranted when these EEG patterns are seen after anoxic brain injury.
Generalized periodic epileptiform discharges (GPEDs) (Figures 6-19 to 6-21) 䡲
Subcortically triggered cortical excitation alternating with prolonged inhibitory events.
䡲
Periodic complexes that occur throughout the brain in a symmetric and synchronized manner.
䡲
Not consistently associated with a specific etiology including:
Hypoxic encephalopathy (HE) (Figures 6-5 and 6-16)
Bilateral independent periodic lateralized epileptiform discharges (BiPLEDs) (Figures 6-12 to 6-16) 䡲
Bilateral and asynchronous, and differ in amplitude, morphology, repetitive rate, and the location.
Severe anoxic encephalopathy
䊳
Post-SE
䊳
Toxic encephalopathy 앫 High doses of almost any drugs depressing
central nervous system function.
Poor prognosis for HE 䡲 䡲 䡲
앫 Lithium, baclofen, ifosphamide, and cefepime
Suppression. Burst-suppression. Alpha- and theta-pattern coma.
䡲
Generalized suppression to ≤20 μV.
䡲
Burst-suppression patterns with generalized epileptiform activity.
䡲
Generalized periodic complexes (GPEDs), especially on a flat background.
䡲
Nonreactive EEG.
Hemiconvulsion hemiplegia epilepsy syndrome (HHE) (Figures 6-17 and 6-18)
Metabolic encephalopathy
䊳
CJD
Whether GPEDs represent an EEG pattern of SE is debated. Many believe that the GPEDs represent brain damage rather than ongoing SE.
䡲
GPEDs with high amplitude (mean, 110 μV) and longer duration (mean, 0.5 sec), with preserved interGPED amplitude (mean, 34 μV), were more likely to be associated with SE, although these differences could not be used clinically in isolation to differentiate between SE and non-SE.
䡲
Patients with GPEDs whose clinical history and EEG are consistent with SE should be managed aggressively with antiepileptic drugs.
䡲
Other characteristics that favor a more optimistic outlook include:
䡲
Rare sequence comprising a sudden and prolonged hemiclonic seizure during febrile illness in an otherwise normal child, followed by permanent ipsilateral hemiplegia and focal epilepsy. 䡲 Caused by CNS infection and less commonly seen in TBI or cerebrovascular accident. 䡲 Ictal EEG shows high-voltage rhythmic slow waves intermingled with spikes, sharp waves, spike-wave complexes, or low-voltage fast activity. Higher amplitude and more abundant epileptiform activities with posterior predominance are noted in the affected hemisphere.
䊳
䡲
䡲
Same characteristics as PLEDs, except for location in midline vertex. 䡲 All had acute onset of partial motor seizures involving the lower extremity and sustained a cerebrovascular insult. 䡲 Origin from the watershed area involving predominantly the parasagittal, midline parietal, or midline central areas. 䡲 The location of the PEDIM corresponded to the seizure type and focal neurologic deficits.
䊳
䊳
Younger age
䊳
Higher level of alertness at the time of the EEG
䊳
History of seizures in the current illness
䊳
Higher inter-GPED amplitude
䡲
Independently associated with poor outcome in 90% of those with GPEDs versus 63% of those without.
䡲
GPEDs and BiPLEDs after an anoxic insult carried a poor prognosis for survival. Aggressive treatment
6 of patients may not be warranted when these EEG patterns are seen after anoxic brain injury.
Stimulus-induced rhythmic, periodic, or ictal discharges (SIRPIDs) (Figure 6-22)
ICU
䡲
Most common human transmissible subacute spongiform encephalopathy (TSSE).
䊳
䡲
Most CJD cases are sporadic (85%). The remaining 15% consist of genetic forms (genetic CJD, Gerstmann-Sträussler-Scheinker disease, fatal familial insomnia) and iatrogenic forms (cadaveric human growth hormone and dura mater, surgical or other invasive procedures, and transfusionassociated variant CJD infections). CJD has been reported in children.
䊳
䡲
Periodic, rhythmic, or ictal-appearing discharges that were consistently induced by alerting stimuli. 䡲 Quasiperiodic discharges (sharp waves, spikes, polyspikes, or sharply contoured delta waves) recurring at regular intervals are noted. 䡲
At times, the pattern became continuous and rhythmic rather than periodic.
䡲
The periodic or rhythmic nature of SIRPIDs may be a reflection of the oscillations generated by burst firing of the reticular thalamic nucleus. In the normal setting, the cortex inhibits thalamocortical bursting. In cortical dysfunction, disruption of this inhibitory feedback on the thalamus by cortical projections causes rhythmic activity.
䡲
These EEG patterns often qualify as electrographic seizures but are consistently elicited by stimulation.
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Common in encephalopathy, critically ill patients, and particularly those with acute brain injury.
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The relation between clinical seizures and SIRPIDs is unclear; therefore, there is no consensus on how aggressively SIRPIDs should be treated.
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In patients with cortical and subcortical dysfunction, alerting stimuli activate the arousal circuitry and, when combined with hyperexcitable cortex, result in epileptiform activity or seizures. This activity can be focal or generalized, and is usually nonconvulsive.
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EEG in CJD usually starts with PLEDs with atypical short interdischarge intervals of 0.5–2 sec.
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It usually takes several months to evolve into BiPLEDs or periodic sharp wave complexes (PSWCs).
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In the terminal stage when myoclonus subsides, EEG shows low-voltage EEG or continuously diffuse PDA.
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Generalized periodic discharges at approximately 1 Hz, with rapidly progressive dementia and myoclonus.
All patients showed PSWCs if serial recordings are performed in different stages of the disease. In another series, at the fully developed stage of the disease, 94% of the EEGs showed PSWCs. The sensitivity, specificity, and positive and negative predictive values of PSWC were 64%, 91%, 95%, and 49%, respectively. Alzheimer’s disease and vascular dementia were the underlying diseases in the falsely positive cases.
Subacute sclerosing panencephalitis (SSPE) (Figure 6-24) 䡲
Periodic high-amplitude complexes in almost all cases.
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The periodic complexes consist of two to four high-amplitude delta waves, polyspikes, and sharpand-slow wave complexes of 0.5–2 sec in duration, and are usually bisynchronous and symmetric and repeated at irregular intervals once in 5–7 sec but can last up to 15 sec.
If the electrographic seizure activity is adequately synchronized in a specific region involving motor pathways, focal motor seizures can occur.
Creutzfeldt-Jakob disease (CJD) (Figure 6-23)
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When both the clinical myoclonic jerks and the periodic EEG complexes were present, a one-to-one relationship existed between the two phenomena.
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Other atypical EEG findings included:
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Frontal rhythmic delta activity in intervals between periodic complexes. Electrodecremental periods following EEG complexes. Paroxysm of bisynchronous spike-wave activity.
Random spikes over frontal regions. Focal abnormalities, such as spike- and slowwave foci. 䡲 In the terminal stage, the background activity is suppressed, and the periodic complexes disappear. 䊳 䊳
Rhythmic coma (Figures 6-25 to 6-37) 䡲
Invariant, nonreactive, diffuse cortical activity of a specific frequency, such as alpha, beta, spindle, or theta, is called a rhythmic coma.
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The clinical outcome in rhythmic coma pattern depended on the underlying cause rather than the EEG finding.
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Beta coma is generally caused by intoxication and, thus, is often a reversible EEG abnormality. It may also be caused by acute brain stem lesions.
Alpha coma 䡲
Alpha frequency range (8–13 Hz) that occurs with a generalized distribution in a comatose patient. 䡲 Alpha coma can be distinguished from physiologic alpha rhythm by: 䊳 Monotonous, monophasic, symmetric, and most commonly anterior predominance (except alpha coma caused by brain stem lesion, which is posterior predominance) 䊳 Widespread distribution Highly persistent and nonreactive to stimuli May be caused by interruption of reticulothalamocortical pathways by metabolic or structural abnormalities. 䡲 Etiology and outcome of alpha coma patterns and other rhythmic coma patterns (beta, theta, and spindle) are similar. 䊳
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One type of rhythmic pattern can change to another. Sequential EEG recordings are required to detect the evolution of rhythmic coma patterns during childhood. 䡲 Monomorphic and no change to sensory stimuli. 䡲
Most commonly predominant in frontal region. 䡲 Most frequently seen in anoxic encephalopathy caused by cardiorespiratory arrest hypoxia. 䡲 Also seen in drug overdose, which is very similar to that seen with cardiorespiratory arrest, except with beta activity superimposed on the alpha activity.
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Other etiologies include head trauma, CJD, pontomesencephalic lesions, and encephalitis. 䡲 Prognosis depends on the underlying causes of coma. 䡲
Reactive rhythmic coma was associated with favorable outcome. 䡲 Prognosis is very poor in anoxic encephalopathy, especially if it develops after 24 hours of coma. 䡲
Alpha coma is replaced within 5–10 days by delta coma. EEG reactivity in subsequent patterns is relatively favorable, while a B-S pattern without reactivity is unfavorable in anoxic-ischemic encephalopathy.
Burst-suppression (B-S) (Figures 6-38 to 6-41) 䡲
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Complex wave forms (amplitudes of the bursts, multiple sharps, and spikes or regular/irregular rhythmic activity from delta to beta range, varying from 100 μV) alternating with completely attenuated background activity ( propofol > benzodiazepines. Common conditions: 䊳 Acute intoxication 䊳 Severe anoxic encephalopathy 䊳 Severe hypothermia 䊳 Anesthesia
Depression and lack of differentiation EEG (Figure 6-42)
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Electrocerebral inactivity (ECI) (Figures 6-43, 6-5) 䡲
Defined as “no cerebral activity over 2 μV when recording from scalp or referential electrode pairs, 10 or more centimeters apart with interelectrode resistances under 10,000 Ω (or impedances under 6000 Ω) but over 100 Ω.”
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Indicative of death only of the cortex, not the brain stem; therefore, a newborn can have prolonged survival despite having an EEG with ECI.
Fourteen- and 6-Hz positive spikes in encephalopathy (Figures 6-44, 5-44 to 5-48) 䡲
The 14- and 6-Hz positive spike pattern shows a similar incidence and morphology and topography to healthy children.
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The normal wave form is selectively preserved and more resistant to underlying structural or metabolic processes than other background features of drowsiness and sleep. 䡲 The positive spike bursts with continuous delta activity in comatose children are a rare but unique EEG pattern associated with hepatic, anoxic encephalopathy and other toxic/metabolic and primary cerebral insult. 䡲 In some subjects, 14- and 6-Hz positive spikes were provoked by auditory and somatosensory stimuli. 䡲
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Indicative of severe brain insult but is nonspecific in etiology and can be due to a wide variety of conditions, including severe HIE, severe metabolic disorders, meningitis or encephalitis, cerebral hemorrhage, and IVH. 䡲 A depressed and undifferentiated EEG within the first 24 hours after birth that persists indicates a poor prognosis.
All patients with HIE bilateral basal ganglia involvement have developmental delay.
Should not be misinterpreted as “paroxysmal fast activity (PFA).” The morphology, polarity, and distribution can differentiate between these two wave forms.
Refractory status epilepticus (RSE) (Figure 6-45 to 6-48) 䡲
Poor prognosis in children with mortality rate in one series of 32%.
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In seizures lasting >30 minutes, only 23% of the survivors were normal at follow-up; 34% showed developmental deterioration and 36% developed new-onset epilepsy.
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Mortality is related to etiology and is higher in younger children and with multifocal or generalized abnormalities on the initial EEG.
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RSE due to either an acute symptomatic etiology or a progressive encephalopathy were associated with highest mortality rates. Shorter duration of suppressive therapy, ultimately with the same outcome and possibly with fewer complications, was recommended. Continuous EEG monitoring detected seizure activity in 19% of patients, and the seizures were almost always NCSE. Coma, age 24 hours of monitoring to detect the first electrographic seizure. TBI (18–28%), ischemic stroke (11–26%), and CNS infection (29–33%) are the most common causes of NCSE. Neuronal cell loss in HS occurs as the result of prolonged severe seizure activity in humans.
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MRI change in the early stage of SE, in as little as 24 hours, is manifest by either asymmetrical or bilateral T2 signal hyperintensity in the hippocampi (HC) caused by focal transient cytotoxic and vasogenic edema. 䡲 Significant volume loss in both hippocampi between weeks 4 and 10, most likely representing neuronal loss and astrogliosis as the correlate of the later histologically proven hippocampal sclerosis. 䡲 HS can develop within 2 months of SE and may further progress during the following 3–4 years.
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TWs have been considered as a pathognomonic sign in severe hepatic encephalopathy, but they are also seen in encephalopathies associated with renal failure or electrolyte imbalance, as well as anoxia and intoxications (such as lithium, metrizamide, and levodopa).
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Occur most often in patients with metabolic encephalopathies but cannot be used to distinguish different causes.
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The most characteristic EEG feature in dialysis encephalopathy was paroxysmal high-voltage delta activity with anterior predominance and, less commonly, spike-and-wave activity and triphasic waves.
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Causes: hepatic encephalopathy, uremia, valproic encephalopathy, severe electrolyte imbalance, hypercalcemia, anoxia, hypoglycemia, hyperthyroidism, myxedema, Hashimoto’s encephalopathy, hypothermia, toxic encephalopathy (baclofen, levodopa, pentobarbital, lithium, ifosphamide, and serotonin syndrome)
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Also seen in NCSE.
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Poor prognosis in severe anoxic and metabolic encephalopathy.
Triphasic waves (TWs) (Figure 6-49) 䡲 䡲 䡲
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Never been reported in children except in lithium and ifosphamide toxicity. Rarely reported below the age of 20 years. Bursts of moderate- to high-amplitude complexes, usually at 1.5–2.5 Hz, with three (but sometimes two or four) negative-positive-negative phases, usually occurring in runs at 1.5–3/sec or more continuously. Fronto-occipital lag of 25–140 msec (bipolar montage) is unique but not a constant finding. Anterior (60%) > diffuse or posterior (40%) predominance.
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FIGURE 61. Posterior Reversible Encephalopathy Syndrome (PRES); Diffuse Polymorphic Delta Activity with Posterior Predominance. A 10-year-old girl with microscopic polyangiitis and chronic renal failure developed visual hallucinations, lethargy, and new-onset seizures. She was on cyclophosphamide. After the visual hallucination, she was found to have elevation of her blood pressure. EEG shows continuously diffuse polymorphic delta activity (PDA) with occipital predominance. Head CT and MRI show diffuse white matter involvement, maximally expressed in the watershed areas in the two hemispheres. The patient recovered after cyclophosphamide was stopped, and the blood pressure was well controlled. Diffuse slowing is the most common finding on the EEGs in posterior reversible leukoencephalopathy syndrome (PRES).1 The delta coma EEG pattern is usually seen with more advanced states of encephalopathy and coma. With progression to deeper stages of coma, it appears diffuse and is usually unreactive. Polymorphic delta comas are due to structural abnormalities involving subcortical white matter or profound metabolic coma.2–4 Posterior-predominant delta activity in this case is probably due to the predominant involvement of posterior head region in PRES.
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FIGURE 62. Posterior Reversible Encephalopathy Syndrome (PRES); Occipital Lobe Seizure. (Same patient as in Figure 6-1) The patient developed a new-onset seizure described as head and eyes deviating to the right side, associated with unconsciousness lasting for approximately 3 minutes. EEG shows ictal activity arising from the left occipital lobe during the seizure. Occipital lobe seizures have been described as a major clinical manifestation of PRES. This suggests that occipital lobe seizures may play a significant role in the anatomical location of the signal changes, offering an alternative explanation for the posterior location of the lesions, instead of the hypothesis that a paucity of sympathetic innervation in that region is the reason for this location.4 Status epilepticus (SE) can be the initial presenting symptom of PRES. Ictal EEG was obtained in six patients with SE in one series. Seizure focus was parieto-occipital in four patients and temporal in two. Seizures in PRES are often occipital in origin, which correlates well with imaging findings of predominant occipitoparietal involvement.6
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FIGURE 63. Cerebral Herniation Syndrome; Continuous Polymorphic Delta Activity and FIRDA. A 7-year-old comatose girl with severe TBI causing intraparenchymal hemorrhage required brain decompression. Cranial CT shows bilateral intraparenchymal hemorrhage, much greater in the left fronto-temporal region (open arrow and double arrows), with compression of midline structure and probable bilateral cerebellar infarction/edema (arrow), signs of cerebral herniation syndrome. EEG shows asymmetrically and continuously diffuse mono- and polymorphic delta activity (PDA) with superimposed frontal intermittent rhythmic delta activity (FIRDA). Note a persistent focal suppression of the left fronto-temporal region. Bilateral but lateralized PDA is characteristic of frontal lobe lesions. Functionally or structurally abnormal thalamocortical interactions, especially involving the dorsal medial nucleus of the thalamus, play a major role in IRDA.7–9 A combination of FIRDA or OIRDA and continuously focal PDA is the classic sign of impending cerebral herniation from a focal structural abnormality. However, the same combination of patterns can also be seen in patients with focal structural lesions and coexistent toxic or metabolic encephalopathies.10,11 Therefore, clinical correlation is required.
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FIGURE 64. Improvement of Right Hemispheric FIRDA and PDA; After Resection of Necrotic Tissues, Left Hemisphere. (Same patient as in Figure 6-3) The patient developed signs of cerebral herniation. He underwent another cerebral decompression with resection of necrotic tissues in the left fronto-temporal region. EEG performed after the surgery shows continuous high-voltage polymorphic delta activity (PDA) in the left hemisphere, caused by the surgery. In addition, there is improvement of PDA and FIRDA in the frontal central midline and the right hemisphere. Unfortunately, despite subsequent treatment with pentobarbital coma, the patient deteriorated and died 4 days after the surgery. Improvement of FIRDA and PDA in the right hemisphere may be due to decreased intracranial pressure after the surgery, which can affect the thalamocortical interactions.
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FIGURE 65. Electrocerebral Inactivity (ECI); Pulse Artifact. (Same patient as in Figure 6-3 and 6-4) The EEG shows electrocerebral inactivity before the cardiorespiratory support was discontinued. Note rhythmic delta activity, mainly at F3, time-locked with ECG indicating pulse artifact. Electrocerebral inactivity is defined as “no cerebral activity over 2 μV when recording from scalp or referential electrode pairs, 10 or more centimeters apart with interelectrode resistances under 10,000 Ω (or impedances under 6000 Ω) but over 100 Ω.”12
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FIGURE 66. Paradoxical Activation. EEG of a 20-month-old girl with nonaccidental trauma (NAT). There is a period of background attenuation more severe delta slowing following stimulation. This EEG reactivity is called “paradoxical activation.” In severe encephalopathy, the EEG does not show reactivity to any stimulation and is called “invariant EEG.” In milder encephalopathy, the EEG shows spontaneous variability, evidence of EEG reactivity to stimulation, typically attenuation of amplitude, reduction of delta activity, and increase in frequency. Paradoxical activation is a period of more severe delta slowing following painful stimulation. It is seen less commonly than a typical response to stimuli but is associated with a milder degree of encephalopathy compared to the invariant EEG.13
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FIGURE 67. EEG Reactivity in Coma; Diffuse Voltage Attenuation. (Same patient as in Figure 6-6) EEG of a 20-month-old girl with nonaccidental trauma (NAT). There is a period of background attenuation without delta slowing following stimulation. In severe encephalopathy, the EEG does not show reactivity to any stimulation and is called “invariant EEG.” In milder encephalopathy, the EEG shows spontaneous variability, evidence of EEG reactivity to stimulation, typically attenuation of amplitude, reduction of delta activity, and increase in frequency.13
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FIGURE 68. PLEDs (Periodic Lateralized Epileptiform Discharges); Ischemic Stroke Due to Cardiac Transplantation. A 2-year-old boy with bilateral parietal strokes, maximal in the right hemisphere (arrow) occurring after cardiac transplantation. He developed frequent seizures described as head and eyes deviating to the left side, followed by generalized tonic-clonic seizures. MRI shows bilateral watershed infarctions in the frontal parietal regions, much greater in the right hemisphere. EEG shows periodic lateralized epileptiform discharges (PLEDs) in the right parietal temporal region and polymorphic delta slowing in parietal temporal regions, greater on the right, corresponding to the strokes. Note pacemaker rhythm in the ECG channel. PLEDs usually occur at the rate of 1–2/sec and are commonly seen in the posterior head region, especially in the parietal areas.14 Seizures occurred in 85% of patients with a mortality rate of 27%.15 Acute stroke, tumor, and central nervous system infection were the most common etiologies of PLEDs.16
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FIGURE 69. Periodic Lateralized Epileptiform Discharges (PLEDs); Posterior Reversible Encephalopathy Syndrome (PRES). A 14-year-old boy with ALL s/p bone marrow transplantation who developed posterior reversible leukoencephalopathy syndrome (PRES). He developed a new-onset seizure described as left arm and facial clonic jerking with head and eyes deviating to the left side, followed by a generalized tonic clinic seizure. EEG shows periodic lateralized epileptiform discharges in the right centrotemporal region. PLEDs were first described by Chatrian et al. (1964) to define an EEG pattern consisting of sharp waves, spikes (alone or associated with slow waves), or more complex wave forms occurring at periodic intervals. They usually occur at the rate of 1–2/sec and are commonly seen in the posterior head region, especially in the parietal areas. It is sometimes associated with EPC.14 This EEG pattern is usually related to an acute or subacute focal brain lesion involving gray matter.17 Chronic PLEDs were also reported in 9% of patients with intractable epilepsy who had structural abnormalities such as cortical dysplasia or severe remote cerebral injury.15,16 In a recent review of 96 patients with PLEDs,19 acute stroke, tumor, and CNS infection were the most common etiologies. Others included acute hemorrhage, TBI, PRES, familial hemiplegic migraine, and cerebral amyloidosis. PLEDs were more periodic when they were associated with acute viral encephalitis than with other etiologies.20 Seizure activity occurred in 85% of patients, with mortality rate of 27%. However, 50% of patients with PLEDs never developed clinical seizures.15
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FIGURE 610. Periodic Epileptiform Discharges in the Mideline (PEDIM). A 2-month-old boy with anoxic encephalopathy due to SIDS. He had multifocal clonic seizures. MRI shows bilateral watershed infarction (arrows) as typically seen in anoxic encephalopathy. EEG shows quasiperiodic spikes and sharp waves the Cz electrode. This activity has the same characteristics as periodic lateralized epileptiform discharges (PLEDs) except for its location in midline vertex. All five patients had acute onset of partial motor seizures involving the lower extremity. All patients had sustained a cerebrovascular insult, either old or new. The PEDIM and seizures suggested an origin from the watershed area between the anterior, middle, and posterior cerebral arteries, involving predominantly the parasagittal region of the cerebral hemisphere. The location of the PEDIM corresponded to the seizure type and focal neurologic deficits.21
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FIGURE 611. Periodic Epileptiform Discharges in the Midline (PEDIM); Bilateral Mesial Frontal Infarction. A 9-month-old boy with fever, left facial twitching, and then generalized tonic clonic seizure. CSF findings showed 90 WBCs with 30 PMN, 69 lymphocytes, 1 monocyte; 46 glucose; 15 total protein; and 1000 RBCs. PCR for HSV type 2 was positive. MRI showed bilateral watershed infarction in the mesial frontal regions (arrows). EEG shows quasiperiodic spikes at the central vertex electrode consistent with the PEDIM. The PEDIM has the same characteristics as periodic lateralized epileptiform discharges (PLEDs) except the location. In one series, all five patients had acute onset of partial motor seizures involving the lower extremity. All patients had strokes. The PEDIM and seizures suggested an origin from the watershed area, involving predominantly the parasagittal, midline parietal, or midline central areas. The patients had partial motor seizures involving predominantly the leg, and EPC with continuous clonic jerks of the legs time-locked with the PEDIM in the EEG. The seizures and PEDIM resolved after initiation of treatment with antiepileptic drugs and treatment of the underlying disorder. The EEG characteristics of PEDIM, other than being in the midline, are similar to those of PLEDs. Similar to PLEDs, the PEDIM carries a poor prognosis, three out of five patients died and two were left with significant neurologic deficits.21
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FIGURE 612. Bilateral Independent Periodic Lateralized Epileptiform Discharges (BiPLEDs); Acute Herpes Simplex Encephalitis. A previously healthy 4-year-old girl who presented with high fever, lethargy, vomiting, and a new-onset seizure described as head and eyes deviating to the right side, followed by cyanosis. Initial CSF showed 22 WBCs (lymphocyte predominante) and 6 RBCs with normal glucose and protein. The CSF for HSV PCR was negative on three separated occasions. Brain biopsy was performed over the left occipital region. Pathology revealed numerous histocytes and inflammatory cells with early capillary proliferation scattered throughout the molecular layer. Leptomeninges showed histocytes and chronic inflammatory cells but no evidence of vasculitis. Brain tissue for herpes simplex type 1 DNA PCR was positive. (A) MRI with FLAIR sequence demonstrates hyperintense signal in bilateral temporo-occipital regions, greater on the left (arrow and open arrow). (B) Axial T1-weighted image with GAD shows increased enhancement in the left parieto-occipital regions (double arrows). EEG shows bilateral independent spikes and sharp wave complexes in the posterior temporal region with diffuse delta slowing (arrow head and asterisk). At the last follow-up 1 year later, the patient had moderate global developmental delay, visual anogsia, and well-controlled seizures. BiPLEDs are PLEDs that are bilateral, generally asynchronous, and differ in amplitude, morphology, repetitive rate, and location. They are most commonly caused by multifocal or diffuse cerebral injury, such as anoxic encephalopathy and CNS infection, and have a poorer prognosis with a mortality of 52%, twice that of patients with PLEDs. It may be classified as periodic short-interval diffuse discharges (PLIDDs).
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FIGURE 613. Bilateral Periodic Lateralized Epileptiform Discharges (BiPLEDs); Pneumococcal Meningitis. A 5-month-old boy with pneumococcal meningitis who was in a comatose state and developed seizures. DWI MRIs are compatible with multifocal ischemic infarctions. EEG performed 4 hours after the seizure described as tonic posturing and nystagmus shows bilateral independent pseudoperiodic polymorphic sharp waves and spikes in the left temporal and right parieto-temporal regions. This finding is consistent with BiPLEDs. The patient subsequently developed NCSE. At 7 months of age, he started having infantile spasms. At a 26-month follow-up, he had severe developmental delay, microcephaly, intractable CPS, and left hemiparesis. BiPLEDs are PLEDs that are bilateral, generally asynchronous, and differ in amplitude, morphology, repetitive rate, and location. They are most commonly caused by multifocal or diffuse cerebral injury seen in patients with coma due to anoxic encephalopathy, strokes, epileptic seizure disorders, especially complex partial status epilepticus, and encephalitis.22,23 Stroke was the most frequent cause of PLEDs, while anoxic encephalopathy and CNS infection accounted for the majority of BiPLEDs.22 Patients with BiPLEDs have a poorer prognosis with a mortality of 52%, twice that of patients with PLEDs. BiPLEDs and GPEDs after an anoxic insult carried a poor prognosis for survival. Aggressive treatment of patients may not be warranted when these EEG patterns are seen after anoxic brain injury.24 BiPLEDs may be classified as periodic short-interval diffuse discharges (PLIDDs).
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FIGURE 614. Bilateral Independent Periodic Lateralized Epileptiform Discharges (BIPLEDs); Watershed Infarction Associated with Cardiomyopathy. A 9-yearold boy with dilated cardiomyopathy caused by viral myocarditis. He developed rhythmic shaking of his right arm and leg with eyes deviating to the right side as well as staring off with mouth movement. Examination and CXR were compatible with congestive heart failure. Axial FLAIR MR shows bilateral watershed infarction caused by hypoxic encephalopathy from poor cardiac function. EEG shows bilateral independent pseudoperiodic spikes and polymorphic sharp waves, maximum over the posterior head regions, consistent with BiPLEDs. There was no evolving pattern as seen in his electrographic seizures. The BiPLEDs persisted throughout the prolonged recording. BiPLEDs are PLEDs that are bilateral, generally asynchronous, and differ in amplitude, morphology, repetitive rate, and location. They are most commonly caused by multifocal or diffuse cerebral injury seen in patients with coma due to anoxic encephalopathy, strokes, epileptic seizure disorders, especially complex partial status epilepticus, and encephalitis.23,25 Stroke was the most frequent cause of PLEDs, while anoxic encephalopathy and CNS infection accounted for the majority of BiPLEDs.25 Patients with BiPLEDs have a poorer prognosis with a mortality of 52%, twice that of patients with PLEDs. BiPLEDs and GPEDs after an anoxic insult carried a poor prognosis for survival. Aggressive treatment of patients may not be warranted when these EEG patterns are seen after anoxic brain injury.24
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FIGURE 615. BIPLEDs; Bilateral Subdural Hematoma (Non-Accidental Trauma). A 4-month-old boy with a prolonged generalized tonic-clonic seizures due to nonaccidental trauma. Cranial CT and MRI show bilateral subdural hematoma and diffuse intracerebral hemorrhage. EEG during the comatose stage shows bilateral independent periodic lateralized epileptiform discharges in the bitemporal regions (BiPLEDS) (arrow and asterisk). This EEG pattern is commonly seen in patients with coma due to anoxic encephalopathy, strokes, epileptic seizure disorders, especially complex partial status epilepticus, and encephalitis.23,25
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FIGURE 616. Bilateral Independent Periodic Lateralized Epileptiform Discharges (BIPLEDs); Watershed Infarction Associated with Near Drowning. A 6-year-old boy with hypoplastic left ventricle with cardiac transplantation who developed anoxic encephalopathy due to near drowning. MRI shows a bilateral watershed infarction. EEG demonstrates BiPLEDs. The following EEG findings are associated with poor outcome in hypoxic encephalopathy (HE): (1) suppression; (2) burst-suppression; (3) alpha- and theta-pattern coma; (4) generalized combined periodic complexes; (4) generalized suppression to ≤20 μV; (5) burst-suppression patterns with generalized epileptiform activity; and (6) generalized periodic complexes on a flat background. BiPLEDs are usually caused by hypoxic encephalopathy or CNS infections and are typically associated with a poorer prognosis than PLEDs with a mortality of 52%, twice that of PLEDs patients. MRI in patients with BiPLEDs showed injury to the hippocampus bilaterally, bilateral infarction in the ACA territory or gray and white matter. Cortical involvement may be necessary in the pathogenesis in both BiPLEDs and GPEDs in patients with HE. Pathophysiology of PLEDs range from abnormal interactions between the “deranged cortex” and deeper “triggering” structures to increased local cortical irritability, possibly with involvement of normal and abnormal intracortical circuits.26 However, the pathophysiological mechanism responsible for periodicity in the EEG is unknown. GPEDs and BiPLEDs after an anoxic insult carried a poor prognosis for survival. Thus aggressive treatment of patients may not be warranted when these EEG patterns are seen after anoxic brain injury.24
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FIGURE 617. Hemiconvulsion Hemiplegia Epilepsy Syndrome (HHE); Refractory Nonconvulsive Status Epilepticus (NCSE). A 3-year-old boy with high fever, prolonged left hemiconvulsion, eye and head deviation to the left, and lethargy. Cranial CT shows diffuse hypodensity in the entire right hemisphere s/p decompression. EEG shows continuous ictal activity in the right hemisphere, maximally expressed in the fronto-central region. At times, the sharp waves are time-locked with the clonic jerks on the left side. He underwent surgical decompression and, subsequently, removal of necrotic tissue over the right hemisphere. A small focal cortical dysplasia was identified. The patient survived but was left with permanent left hemiparesis and intractable epilepsy. HHE is a rare sequence comprising a sudden and prolonged hemiclonic seizure during febrile illness in an otherwise normal child, followed by permanent ipsilateral hemiplegia and focal epilepsy. It is often due to CNS infection and less commonly seen in TBI or vascular. Ictal EEG shows high-voltage rhythmic slow waves intermingled with spikes, sharp waves, spike-wave complexes, or low-voltage fast activity. Higher-amplitude and more abundant epileptiform activity with posterior predominance is noted in the affected hemisphere.27
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FIGURE 618. Hemiconvulsion-Hemiplegia Epilepsy (HHE) Syndrome. (Same patient as in Figure 6-17) The EEG shows spike/polyspike-wave complexes time-locked with contralateral hemiclonic seizures of arm and face. Note muscle artifact, maximum in the left temporal region during the left facial twitching (open arrow). Axial and coronal T2 WI MRI shows increased signal intensity in the entire right hemisphere. The ictal EEG is characterized by bilaterally rhythmic slow waves, with higher amplitude on the hemisphere contralateral to the clinical seizure. The spike-wave complexes are periodically interrupted by a 1- to 2-sec background attenuation.28
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FIGURE 619. Generalized Periodic Epileptiform Discharges (GPEDs); Status Post Cardiopulmonary Resuscitation (CPR). A 4-year-old boy with cardiac arrest after rupture of coarctation of the aorta. Head CT shows bilateral massive cerebral edema. CXR shows congestive heart failure. EEG demonstrates generalized symmetric and synchronous periodic complexes consistent with GPEDs. Generalized periodic epileptiform discharges (GPEDs) are periodic complexes that occur throughout the brain in a symmetric and synchronized manner. They were not consistently associated with a specific etiology. Whether GPEDs represent an EEG pattern of SE is debated.29,30 Many believe that GPEDs represent brain damage rather than ongoing SE.31,32 GPEDs with high amplitude (mean, 110 μV) and longer duration (mean, 0.5 sec) with a preserved inter-GPED amplitude (mean, 34 μV) were more likely to be associated with SE, although these differences could not be used clinically to differentiate between SE and non-SE. Patients whose clinical history and EEG are consistent with SE should be managed aggressively with antiepileptic medications, despite GPEDs. Other characteristics that favor a more optimistic outlook include younger age, higher level of alertness at the time of the EEG, history of seizures in the current illness, and higher inter-GPED amplitude.33,34 Presence of any GPEDs was independently associated with poor outcome in 90% of those with PEDs versus 63% of those without.35 GPEDs and BiPLEDs after an anoxic insult carried a poor prognosis for survival than PLEDs. Aggressive treatment of patients may not be warranted when these EEG patterns are seen after anoxic brain injury.24
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FIGURE 620. Generalized Periodic Epileptiform Discharges (GPEDs); Refractory Status Epilepticus (RSE). A 9-year-old boy with refractory status epilepticus (RSE) of unknown etiology who was treated with pentobarbital coma but developed cardiorespiratory complications. He developed clinical seizures described as facial twitching and nystagmus while his pentobarbital dosage was decreased. EEG shows generalized periodic polyspikes and polyphasic sharp waves consistent with GPEDs superimposed on low-voltage background activity. The patient died after the cardiorespiratory support was withdrawn 3 days after this EEG.
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FIGURE 621. Asymmetrical Generalized Periodic Epileptiform Discharges (GPEDs); Refractory Status Epilepticus (RSE). (Same recording as in Figure 6-20) EEG consistently shows asymmetric GPEDs with no clinical accompaniment. At times, there are only periodic discharges in the right hemisphere, which simulate PLEDs (not shown).
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FIGURE 622. Stimulus-Induced Rhythmic, Periodic, or lctal Discharges (SIRPIDs); Refractory Status Epilepticus (RSE). (Same recording as in Figure 6-19 and 6-20) Phone ring induced a long burst of generalized polyspikes/sharp-wave and slow-wave activity in the EEG. SIRPIDs were defined as periodic, rhythmic, or ictal-appearing discharges that were consistently induced by alerting stimuli. Quasiperiodic discharges (sharp waves, spikes, polyspikes, or sharply contoured delta waves) recurring at regular intervals are noted. At times, the pattern became continuous and rhythmic rather than periodic.36 The periodic or rhythmic nature of SIRPIDs may be a reflection of the oscillations generated by burst firing of the reticular thalamic nucleus. In the normal setting, the cortex inhibits thalamocortical bursting. In cortical dysfunction, disruption of this inhibitory feedback on the thalamus by cortical projections causes rhythmic activity.37 The EEG patterns often qualify as electrographic seizures but are consistently elicited by stimulation. SIRPIDs are common in encephalopathic, critically ill patients, particularly those with acute brain injury. The relationship between clinical seizures and SIRPIDs is unclear; therefore, there is no consensus on how aggressively SIRPIDs should be treated.36 In patients with cortical and subcortical dysfunction, alerting stimuli activate the arousal circuitry and, when combined with hyperexcitable cortex, result in epileptiform activity or seizures. This activity can be focal or generalized, and is usually nonconvulsive. If the electrographic seizure activity is adequately synchronized in a specific region involving motor pathways, focal motor seizures can occur.38
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FIGURE 623. Periodic Sharp Wave Complexes (PSWCs); Creutzfeldt-Jakob Disease (CJD). A 75-year-old female with subacute progressive dementia and myoclonic jerks who was diagnosed with Creutzfeldt-Jakob disease (CJD) by postmortem examination. EEG shows bilateral synchronous periodic sharp waves occurring every 1.5–2 sec. CJD is the most common human transmissible subacute spongiform encephalopathy (TSSE). Most CJD cases are sporadic (85%). The remaining 15% consist of genetic forms (genetic CJD, Gerstmann-Sträussler-Scheinker disease, fatal familial insomnia) and iatrogenic forms (cadaveric human growth hormone and dura mater, surgical or other invasive procedures, and transfusion-associated variant CJD infections). CJD has been reported in children.39,40 EEG in CJD usually starts with PLEDs41 with atypical short interdischarge intervals of 0.5–2 sec. It usually takes several months to evolve into BiPLEDs or PSWCs. In the terminal stage when myoclonus subsides, EEG shows low-voltage or continuously diffuse polymorphic delta activity.42,43 All patients show PSWCs if serial recordings are performed in different stages of the disease.44 In another series, at the fully developed stage of the disease, 94% of the EEGs showed PSWCs.45 The sensitivity, specificity, and positive and negative predictive values of PSWCs were 64%, 91%, 95%, and 49%, respectively. Alzheimer’s disease and vascular dementia were the underlying diseases in the falsely positive cases.46
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FIGURE 624. Subacute Sclerosing Panencephalitis (SSPE). A 10-year-old boy with subacute deterioration of cognitive function and frequent myoclonus. He was diagnosed with SSPE. EEG shows bilateral synchronous pseudoperiodic sharp-wave complexes with interdischarge intervals of 3–4 sec. EEG in SSPE shows periodic high-amplitude complexes in almost all cases. The periodic complexes consist of two to four high-amplitude delta waves and polyspike-, sharp-, and slow-wave complexes of 0.5–2 sec in duration, are usually bisynchronous and symmetric, and repeated at irregular intervals once in 5–7 sec but can last up to 15 sec. When both the clinical myoclonic jerks and the periodic EEG complexes were present, a one-to-one relationship existed between the two phenomena. Besides periodic complexes, several atypical EEG findings were also noted that included frontal rhythmic delta activity in intervals between periodic complexes, electrodecremental periods following EEG complexes, paroxysms of bisynchronous spike-wave activity, random spikes over frontal regions, and focal abnormalities, such as spike- and slow-wave foci. In the terminal stage, the background activity is suppressed and the periodic complexes disappear.26,47 (Courtesy of Dr. Sorawit Viravan, Pediatric Neurology, Siriraj Hospital, Bangkok, Thailand.)
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FIGURE 625. Alpha Coma (AC); Hypoxic Encephalopathy During Midazolam Infusion. EEG of a 7-year-old boy with traumatic brain injury (TBI) who was on midazolam infusion for sedation. EEG shows continuously diffuse 10- to 12-Hz alpha activity, maximal anteriorly, throughout the whole recording. The EEG shows mild reactivity to external stimuli. The patient returned back to his baseline few days later. AC is an EEG pattern in the alpha frequency range (8–13 Hz) that occurs with a generalized distribution in a comatose patient. It is monomorphic and does not change in response to sensory stimuli and is predominant in the frontal region. The AC is most frequently seen in anoxic encephalopathy caused by cardiorespiratory arrest (CRA) 48,49 and associated with a very poor prognosis. AC can also be seen in drug overdose,50 which is very similar to that seen with CRA, except with beta activity superimposed on the alpha activity. Other etiologies include TBI, CJD, pontomesencephalic lesions,51 and encephalitis. The prognosis of AC depends on the underlying causes of coma. Etiology and outcome of AC and other rhythmic coma patterns (beta, theta, and spindle) were similar. One type of rhythmic pattern can change to another. Reactive rhythmic coma was associated with favorable outcome.5,34,52 Prognosis is very poor in anoxic encephalopathy, especially if it develops after 24 hours of coma.53
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FIGURE 626. Alpha Coma; Pontine Stroke. A 10-year-old boy with pontine stroke. He was in coma and died 4 days after this EEG recording. EEG shows broadly distributed alpha activity with anterior predominance and is nonreactive to external stimuli. This EEG pattern is termed “alpha coma.” Alpha coma is an EEG pattern in the alpha frequency range (8–13 Hz) that occurs with a generalized distribution in a comatose patient. It is monomorphic and does not change in response to sensory stimuli and is, most commonly, predominant in the frontal region. The alpha coma pattern is most frequently seen in anoxic encephalopathy caused by cardiorespiratory arrest and associated with a very poor prognosis. Alpha coma can also be seen in toxic encephalopathies that are very similar to that seen with cardiorespiratory arrest, except with beta activity superimposed on the alpha activity. Other etiologies include head trauma, CJD, brain stem lesions, especially pontomesencephalic, and encephalitis. Prognosis of alpha coma pattern depends on the underlying causes of coma. Etiology and outcome of alpha coma patterns and other rhythmic coma patterns (beta, theta, and spindle) were similar. One type of rhythmic pattern can change to another. Reactive rhythmic coma was associated with favorable outcome.5,52,54,55
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FIGURE 627. Alpha Coma. “Alpha coma” EEG pattern in an 18-year-old man who suffered from cardiac arrest after a severe motor vehicle accident occurring approximately 36 hours after the cardiopulmonary resuscitation. EEG shows continuously diffuse 10- to 11-Hz alpha activity, maximal posteriorly, throughout the whole recording. The EEG shows no reactivity to noxious stimuli. The alpha coma pattern has been reported in pontomesencephalic lesions,56 hypoxia,57,58 and drug overdose.50 The prognosis of alpha coma depends on the etiology. It is very poor in anoxic encephalopathy, especially if it develops after 24 hours of coma.53
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FIGURE 628. Comparison Between Alpha Coma and Physiological Alpha Rhythm. Alpha coma (B) can be distinguished from physiologic alpha rhythm (A) by (1) monotonous, monophasic, symmetric, and most commonly anterior predominance (except alpha coma caused by brain stem lesion, which is posterior predominance); (2) widespread distribution; and (3) highly persistent and nonreactive to stimuli.43 The clinical outcome in alpha coma depended on the underlying cause rather than the EEG finding. The prognosis of alpha coma as well as of rhythmic coma was better in children than in adults. Alpha coma may be caused by interruption of reticulothalamocortical pathways by metabolic or structural abnormalities.59 Alpha coma is replaced within 10 days by delta coma.60 In another study, alpha or theta coma change to a more definitive pattern by 5 days from coma onset. EEG reactivity in subsequent patterns is relatively favorable, while a burst-suppression pattern without reactivity is unfavorable in anoxicischemic encephalopathy.61
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FIGURE 629. Alpha-Theta Coma Pattern; Hypoxic Encephalopathy. EEG in a 5-year-old comatose boy with hypoxic ischemic encephalopathy due to near drowning shows widely distributed nonreactive alpha and theta activity with anterior predominance. This EEG is consistent with “alpha-theta coma.”
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FIGURE 630. Delta Coma. (Same patient as in Figure 6-29) EEG performed 6 days after the last EEG that showed “rhythmic coma” EEG pattern reveals continuously diffuse delta activity with suppression of sleep spindles. The patient developed moderate global developmental delay and focal epilepsy at 1-year follow-up after the near drowning. Alpha coma is replaced within 10 days by delta coma.60 In another study, alpha or theta coma changes to a more definitive pattern by 5 days from coma onset. EEG reactivity in subsequent patterns is relatively favorable, while a burst-suppression pattern without reactivity is unfavorable in anoxic-ischemic encephalopathy.5
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FIGURE 631. Beta Coma Pattern. (Same patient as in Figure 6-29 and 6-30) Prolonged EEG on the same day shows predominantly diffuse beta activity with anterior predominance. The patient received a low dose of midazolam for sedation. Invariant, nonreactive, diffuse cortical activity of a specific frequency, such as alpha, beta, spindle, or theta, is called “rhythmic coma.” The clinical outcome in a rhythmic coma pattern depended on the underlying cause rather than the EEG finding. The prognosis of alpha coma as well as of rhythmic coma was better in children than in adults. Alpha coma may be caused by interruption of reticulothalamocortical pathways by metabolic or structural abnormalities.59 Alpha coma is replaced within 10 days by delta coma.60 In another study, alpha or theta coma changes to a more definitive pattern by 5 days from coma onset. EEG reactivity in subsequent patterns is relatively favorable, while a burst-suppression pattern without reactivity is unfavorable in anoxic-ischemic encephalopathy.61
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FIGURE 632. Theta Coma (Reversible); Sedative Medication After NCSE. A 9-year-old boy with NCSE who received midazolam infusion. EEG shows anteriorly predominant theta activity intermixed with delta and beta activity. The patient was recovering after the treatment. Alpha or theta coma can also be seen in toxic encephalopathy. The EEG pattern is very similar to that seen with cardiorespiratory arrest, except that there is superimposed beta activity.62–64 Overdoses of many different drugs can produce this pattern.3 The outcome depends on the underlying causes. The prognosis of alpha-theta rhythmic coma as well as of other rhythmic coma is better in children than in adults.65
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FIGURE 633. Theta Coma (Irreversible) 15 Minutes Before the Patient Died; Anoxic Encephalopathy. A 9-year-old boy with anoxic encephalopathy after hanging. He underwent 45-minutes of CPR. Continuous EEG 15 minutes before he passed away shows nonreactive anteriorly dominant rhythmic 5-Hz theta activity. Diffuse theta patterns may occur on their own, or may be mixed with other frequencies such as alpha or delta in coma66,61 and may occur after cadiorespiratory arrest where theta activity is more prominent anteriorly, is nonreactive to external stimuli, and carries a poor prognosis similar to alpha coma.4,5 The prognosis of alpha coma (AC), theta coma (TC), or alpha-theta coma (ATC) patterns is poor in adults but better in children, especially if they are an incomplete (reactive) AC pattern. Based on the observation that etiology and outcome were similar in alpha, theta, spindle, and beta comas (“rhythmic coma” pattern), the pathophysiology of these patterns in children might be the same as AC in adults, interruption of the reticulothalamocortical pathways by structural or metabolic derangement and deafferentation. EEG patterns may be more variable in children (alpha, theta, spindle, and beta frequencies), possibly because of the difference in the response of the immature brain to such deafferentation.55 Whereas complete ATC is invariably associated with a poor outcome, full recovery is possible in patients with incomplete ATC.56 EEG in neonates may take longer to recover. Therefore, the first EEG should be waited until 24 hours after the CPR, unless seizures are suspected.68
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FIGURE 634. Evolving EEG Patterns in Anoxic Encephalopathy After Cardiopulmonary Resuscitation (CPR). A 9-year-old boy with anoxic encephalopathy from hanging. He underwent CPR 15 minutes after the incident when he was pulseless for 5 minutes. CPR was performed over 45 minutes. He was not noted to have hypothermia and severe metabolic disturbances, and was not on sedation. EEG evolves from electrocerebral inactivity to burst-suppression, GPEDs, and eventually theta coma before he passed away 15 minutes after the evidence of theta coma EEG pattern. EEG may evolve from one rhythmic pattern during a series of tests or may even occur in the same recording. The pathophysiology of rhythmic coma patterns (alpha, theta, spindle) in children might be the same as in adults, interruption of the reticulothalamocortical pathways by structural or metabolic derangement and deafferentation.65 In this patient, the theta coma pattern was most likely caused by the effect of central herniation syndrome on the brainstem. The risks of severe neurologic deficits or death are high among patients with alpha, theta, and alpha-theta coma patterns while in postanoxic coma. Seventy-three percent of patients with alpha coma after CPR died.3,64
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FIGURE 635. Asymmetric Spindle Coma During Midazolam Infusion; Embolic Stroke. A 6-year-old girl with acute lymphoblastic leukemia with febrile neutropenia complicated by left MCA stroke and small ischemia in the right occipital region. EEG during intubation and comatose state under midazolam IV infusion shows asymmetric 10- to 11-Hz spindle-like activity with suppression in the left hemisphere. Anterior predominance of spindle activity is noted. This finding is consistent with asymmetric spindle coma. Rhythmic coma patterns were found in 30.2% of recordings. Etiology, reactivity, and outcome of spindle, beta, alpha, and theta coma patterns are similar. The reactive pattern was associated with favorable outcome in 67%. The nonreactive rhythmic pattern was associated with unfavorable outcome in 60%. Sequential EEG recordings are required to detect the evolution of rhythmic coma patterns during childhood.55 The prognosis depends mainly on the primary disease process rather than the EEG finding. The prognosis of rhythmic coma pattern is better in children than in adults. The rhythmic coma pattern is probably caused by the interruption of reticulothalamocortical pathways by metabolic or structural abnormalities.59 An incomplete pattern has a better prognosis.64,61,67
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FIGURE 636. Asymmetric Spindle Coma; Acute Amoebic Meningoencephalitis with Herniation Syndrome. A 10-year-old boy with refractory status epilepticus and coma caused by amoeba Balamuthia mandrillaris. Axial MRI with FLAIR sequence and coronal T1-weighted image with GAD show an infarction of the right basal ganglion and midbrain (arrow) and Kernohan phenomenon in the opposite hemisphere (open arrow). EEG reveals asymmetrically diffuse spindle and delta coma with less abundant spindles and more pronounced polymorphic delta activity in the right hemisphere. In this patient, spindle and delta coma is most likely due to the lesions in the midbrain and basal ganglion caused by infarction and brain herniation syndrome. The patient died a few days after this EEG. Rhythmic coma patterns were found in 30.2% of recordings. Etiology, reactivity, and outcome of spindle, beta, alpha, and theta coma patterns are similar. The reactive pattern was associated with favorable outcome in 67%. The nonreactive rhythmic pattern was associated with unfavorable outcome in 60%. Sequential EEG recordings are required to detect the evolution of rhythmic coma patterns during childhood.52,55 The prognosis depends mainly on the primary disease process rather than the EEG finding. The prognosis of rhythmic coma pattern is better in children than in adults. The rhythmic coma pattern is probably caused by the interruption of reticulothalamocortical pathways by metabolic or structural abnormalities.65 Incomplete pattern has a better prognosis.4,61,67,69 More than 440 cases of severe central nervous system infections caused by Acanthamoeba spp., B. mandrillaris, and Naegleria fowleri have been reported.70 Balamuthia encephalitis may occur in any age group, may or may not be associated with immunosuppression, and usually has a subacute and fatal course from hematogenous dissemination of chronic skin or lung lesions. Common features that might be of value in diagnosis of Balamuthia encephalitis are high CSF protein, hydrocephalus, and Hispanic ethnicity.71 When purulent CSF is obtained and when no bacteria are noted in a patient with meningoencephalitis, the CSF should be examined specifically for other organisms, including amoeba. PCR assay and specific antibodies to Balamuthia are available. Brain biopsy should be considered in patients with encephalitis of unknown etiology whose condition deteriorates despite treatment with acyclovir.72 Chronic necrotizing vasculitis and focal hemorrhages are typical findings in Balamuthia infections.73,74 The prognosis is very poor due to delayed diagnosis, difficulty in isolation/identification of the organism, and lack of well-established treatment.75
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FIGURE 637. Beta Coma. A 10-year-old comatose boy following the treatment of convulsive status epilepticus with phenobarbital, fosphenytoin, and midazolam. Beta coma is generally caused by intoxication and thus is often a reversible EEG abnormality.50 It may also be caused by acute brain stem lesions.76
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FIGURE 638. Burst-Suppression Pattern; Cardiopulponary Arrest. A 15-month-old boy with anoxic encephalopathy caused by a complication of anesthesia. EEG shows very low-voltage background activity alternating with medium-voltage diffuse delta activity. The burst-suppression is characterized by their contrasting adjacent amplitude. The amplitudes of the bursts vary from 100 μV. Bursts contain multiple sharps and spikes or regular/irregular rhythmic activity from delta to beta range.43
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FIGURE 639. Burst-Suppression Pattern; Pentobarbital Coma. (Continue...) The EEG shows a burst-suppression (B-S) pattern with pentobarbital coma. A B-S pattern is a complex wave form alternating with complete attenuated background activity (
