Simple Partial Seizures Versus Complex Partial Seizures

Partial seizures are further subdivided into simple partial seizures and complex partial seizures. A complex partial seizure is a partial seizure associated with diminished consciousness or responsiveness. Some of the partial seizures may be associated with completely retained responsiveness, such as a simple partial seizure involving clonic spasms of the face or hand—the patient may remain completely alert and aware during such a seizure. The majority of partial seizures, however, are associated with diminished responsiveness and are properly classified as complex partial seizures. Indeed, it is only during a minority of partial seizures that complete responsiveness is maintained. During complex partial seizures, the patient may appear awake but is unresponsive (or only minimally responsive) to stimulation. Staring behaviors frequently indicate reduced responsiveness during complex partial seizures. Only rarely does a patient appear to lose consciousness completely during a complex partial seizure.

Epileptic Auras

An epileptic aura is a subjective sensation that heralds the onset of a seizure. The sensations can be diverse, such as hearing a buzzing sound in the ears, experiencing déjà vu, or having a feeling of nausea immediately preceding a seizure. This initial, comparatively minor feature may then be followed by more dramatic seizure manifestations. Strictly speaking, an aura is not a preseizure warning or “prodrome.” Rather, it represents the onset of the seizure itself. The onset of the aura is coincident with the onset of the seizure discharge.

During the aura phase of a seizure, the epileptic seizure discharge is usually confined to a small area, often in the temporal lobe. As it spreads out of its confined area, the clinical seizure manifestations may become more dramatic. Because the aura should properly be considered the onset of a clinical seizure, a true epileptic aura can be counted as a seizure. In some cases, the aura may not progress and represents the seizure in its entirety.

Recordable EEG Patterns Associated With Partial Seizures

Partial seizures are distinguished by EEG patterns that involve only subsets of the brain. In comparison, the EEG patterns of generalized seizures involve all brain areas at once. Although most epileptic seizures can be recorded using standard scalp electrodes, in some cases a seizure discharge may occur in a cortical area that is not readily accessible to recording with conventional electrodes. These include such areas as the mesial surfaces of the frontal, parietal, and occipital lobes, the orbitofrontal surface of the frontal lobe, the basal occipital and temporal lobes, and the mesial surface of the temporal lobe and insula, among others (see Figures 10-5 through 10-9). Therefore, most, but not all partial seizures are well recorded at the scalp. For these reasons, a negative EEG recording cannot, in and of itself, exclude the diagnosis of an epileptic seizure. In these occasional cases of definite epileptic seizure with negative scalp recordings, other factors must be taken into account to make the correct diagnosis, such as the specific features of the patient event and the history. In cases of partial epileptic seizures associated with a negative EEG, the definition implies that there is some theoretical electrode placement that could record the seizure discharge, even if that placement location would have to be deep within the brain.

Figure 10-5 The basal surfaces of the brain are at some distance from the scalp and difficult to record well using routine techniques. The orbitofrontal surface of the brain lies on the floor of the anterior cranial fossa, above the eyes. The basal temporal lobe lies on the bone of the middle cranial fossa and the mesial temporal lobe, including the amygdala and hippocampus, also lie at some distance from the scalp electrodes.

Figure 10-6 A section through the sagittal midline of the brain shows the mesial surfaces of the frontal, parietal, occipital, and temporal lobes which can be difficult to record.

Figure 10-7 The insula (literally “island”) represents an infolding of cerebral cortex covered by the lips (opercula) of the Sylvian fissure. The frontal and temporal opercula are retracted to reveal this hidden area of cortex.

Figure 10-8 A coronal section of brain is seen on magnetic resonance imaging scan. The mesial frontal lobe, insula, and basal and mesial temporal lobes are highlighted.

Figure 10-9 The basal frontal and occipital lobes are highlighted on a sagittal MRI scan. The gyri of the mesial surface of the cerebral hemisphere (frontal, parietal, and occipital) are also visible.

The EEG patterns associated with partial seizures usually consist of a rhythmic, sharp discharge over the affected area (e.g., spike or spike-wave discharges) as shown in the previous figures. However, partial seizure recordings do not only appear as a train of spikes. Especially when seizure sources are located deeper in the brain and at some distance from the recording electrode, the seizure may only appear as a rhythmic focal slow wave without obvious sharp features when recorded from the scalp. In the case of partial seizures, the epileptic discharge is usually unilateral. Although a unilateral partial seizure discharge may spread incrementally through the primary involved hemisphere, at such time as the discharge might cross to the opposite hemisphere, both hemispheres become simultaneously engulfed with seizure activity; there is no incremental spread through the opposite hemisphere. This process is referred to as secondary generalization.

An important exception to this rule is the example of temporal lobe seizures in which the seizure discharge may spread from one temporal lobe to the other without simultaneous involvement of the remainder of the hemispheres (see Figure 10-10). Therefore, in most cases, after the discharge becomes bilateral, the whole of both hemispheres is engulfed with the discharge and the discharge can be considered to have generalized. Complex partial seizures with bilateral temporal involvement represent the exception to this rule: the less typical example of a bilateral seizure discharge that is not truly generalized.

Figure 10-10 The beginning of the low-voltage sharp seizure discharge that is evident on the second half of the first page can be traced back to the right midtemporal area where the muscle artifact stops (1). After 3 seconds, the discharge spreads to the right parasagittal area (2) and then quickly to the midline (3). After 2 more seconds, the discharge has become bilateral and can be seen in the left parasagittal area (4). The sharp waves may be present simultaneously in the left temporal chain as well but would be difficult to discern because of the muscle and motion artifact in that area. As it nears its end, the seizure discharge increases in voltage and slows in frequency. The increased muscle and motion artifact is not unexpected as the clinical manifestation of seizures often includes muscle tensing and patient movement.

Partial Seizures With Secondary Generalization

As described earlier, a seizure discharge may start focally and subsequently spread to involve all brain areas (generalize). This flow of the discharge from a subset of cerebral cortex to all of cerebral cortex is reflected both by the spread of the recorded discharge from a subset of EEG channels to all EEG channels and also by an evolution of the patient’s seizure behavior from a partial manifestation to involvement of the whole body. For instance, in the classic example of the type of seizure referred to as a “Jacksonian march,” a patient’s seizure may begin with clonic contractions in the right hand and arm and subsequently spread to the right face and leg. Thereafter, it may spread to the opposite side of the body so that bilaterally synchronous clonic activity of the whole body is seen. This clinical progression is mirrored by an electrographic evolution of the discharge from a small area in the left hemisphere, which includes the portion of the motor strip that is associated with the left hand, to the whole of the left hemisphere and then, finally, to involvement of both hemispheres (see Figure 10-11).

Figures 10-11 A seizure in a child with severe myoclonic epilepsy of infancy (SMEI, or Dravet syndrome) is shown that begins in the left temporal chain (1) and quickly spreads to the left parasagittal chain (2). After a brief period of amplifier blocking (possibly related to patient movement), the discharge becomes bilateral (3). Although SMEI is related to the generalized epilepsies, this patient had similar focal seizure onsets arising from the opposite (right) side at other times.

Partial seizures that secondarily generalize are classified among the partial seizures rather than the generalized seizures for diagnostic reasons. Partial seizures that do not generalize and partial seizures that do secondarily generalize have the same list of possible causes. In comparison, the list of causes of generalized seizures is distinctly different from the list of causes of partial-onset seizures. The tendency to a partial seizure to secondarily generalize usually has little to do with the etiology of the seizure.

Automatisms

Especially during lengthier absence seizures, individuals can manifest automatic behaviors during the seizure discharge. The expression of such automatisms (which may also be seen during complex partial seizures) varies widely. Examples include fumbling of the hands, running the fingers through the hair, or making humming sounds. Unlike other clinical features of the seizure, such automatisms are not driven directly by a seizure discharge in the way that clonic jerking would be driven by repetitive spikes in the EEG. Rather, automatisms represent the release of automatic, preprogrammed behaviors. When the cerebral cortex is functioning normally, these automatic programs are suppressed. When the cerebral cortex is involved with seizure activity, however, as during an absence seizure, such preprogrammed behaviors may be released.

EEG

The most frequent EEG correlate to typical absence seizures is the “classic” 3-Hz generalized spike-wave discharge (see Figure 10-12). When these discharges are analyzed closely, the maximum voltage of the spike component of the spike-wave complexes is most commonly seen in the superior frontal electrodes (F3 and F4). Less often, the spike maximum is seen in the occipital area, and even less frequently in other locations.

Figure 10-12 This 3-Hz generalized spike-wave discharge shows the abrupt onset and termination that is characteristic of absence seizures. Note the frontal maximum of the waveforms.

Although the term 3-Hz generalized spike wave is well known and implies a consistent frequency, observed firing frequencies are not necessarily as consistent as the term implies. Often, the first few discharges fire at a frequency slightly faster than 3 Hz. After onset of the discharge, the firing frequency typically slows, often to 2.5 Hz and sometimes to 2 Hz before abruptly terminating (see Figure 10-13). One of the most characteristic attributes of the typical absence seizure is the abrupt onset and termination of the discharge. The classic 3-Hz generalized spike-wave discharge tends to occur against a normal background and has a clear time of onset and a fairly well demarcated termination. After termination, the EEG returns to the previous background after a few seconds or less.

Figure 10-13 Although the discharge associated with this typical absence seizure is classified as 3-Hz generalized spike-wave, note that the discharge’s firing frequency still evolves throughout its course. The first wavelength measured suggests a firing rate just above 4 Hz but (1), 1 second later at the time of the second measured wavelength, the firing rate has dropped to 3 Hz (2). Later in the discharge, the third measured wavelength implies a firing frequency of 2.5 Hz (3).

EEG

The EEG hallmark of atypical absence seizures is the slow spike-wave discharge. Slow spike-wave discharges differ from “classic” 3-Hz generalized spike-wave discharges in two important respects: slow spike-wave discharges, as their name implies, fire at a slower rate, usually 2.5 Hz or less at onset; see Figure 10-14). Slow spike-wave discharges also lack the clear-cut onset and termination characteristic of typical absence seizure discharges. Finally, whereas slow spike-wave discharges are often generalized, asymmetries, both between the left and the right hemispheres and the anterior and posterior head regions, are more common. There is no single characteristic location for the discharge maximum for the slow spike-wave discharges associated with atypical absence seizures, and the location of the voltage maximum may differ even within the same patient at different times. Atypical absence seizures often occur against the backdrop of an otherwise abnormal EEG, which may include scattered epileptiform activity or a slowed background.

Figure 10-14 Slow spike-wave discharges are seen in a young man with mixed seizures. Note the slowed firing rate of the train of spike-wave discharges on the second half of the page and the scattered, single discharges in multiple locations seen on the first half of the page.

Slow-spike wave discharges are often associated with atypical absence seizures, but this is not always the case. Although slow spike-wave discharges are expected as the EEG correlate of atypical absence seizures, the converse is often not true: most slow spike-wave discharges are not associated with clinical atypical absence seizures. In practice, slow spike-wave discharges are often seen as interictal abnormalities in the EEG. The simple observation of slow spike-wave discharges in the EEG is no guarantee that the patient is actually experiencing an atypical absence seizure, although the finding does raise suspicion that the patient has this seizure type. When this pattern is seen, the concurrent observation of associated staring or some form of decreased responsiveness or change in tone is necessary to establish the diagnosis of an electroclinical seizure. This same phenomenon of electrical discharge without clinical change may also occur with “classic” 3-Hz generalized spike-wave discharges as described in the previous section, although much less often.

Clonic Seizures

Clonic seizures are characterized by repetitive clonic jerks. These clonic jerks can occur in nearly any skeletal muscle group in the body depending on the cortical location of the discharge (usually including the motor strip). Clonic jerking from seizure activity tends to have a rhythmic quality. Because each clonic jerk is driven by an EEG discharge, a simultaneous spike or spike-wave discharge is expected with each clonic jerk. Therefore, the frequency of the EEG discharges typically matches the frequency of the jerks. Because clonic jerking is typically driven by discharges from the area of the motor strip, it is rare that scalp EEG electrodes will fail to record them, especially if they involve the face or hand.

Tonic Seizures

Tonic seizures cause tonic stiffening of a limb, several limbs, or the whole body. When the whole body is involved with a generalized tonic seizure, tonic stiffening in extension is most common; however, tonic stiffening with flexion of the hips, knees, or arms may also be seen. Especially with generalized tonic seizures, tonic contraction of the diaphragm may occur resulting in a forced inhalation or grunting sounds. Most often the EEG correlate of tonic seizures is a spray of rapid spikes in the affected area, often with an initial frequency of 10 to 25 Hz, which subsequently slows, similar to the onset of tonic-clonic seizures as described next. Other EEG correlates are not uncommon, including an abrupt desynchronization (flattening) of the EEG. When such flattening is seen, there is sometimes a suggestion of low voltage rapid spikes superimposed on the flattened pattern though these are not always identifiable (see Figure 10-17). Therefore, although most ictal patterns are dramatic and show high-voltage repetitive discharges, the electroencephalographer must also be alert to abrupt flattening of the EEG (an electrodecrement) as a seizure correlate. Other patterns are less common.

Figure 10-17 Electrodecremental seizure patterns consist of an abrupt flattening of the EEG, usually only lasting a few seconds. In some examples, low-voltage rapid spikes can be seen during the decrement (arrow), but in other cases spikes cannot be identified.

Generalized Tonic-Clonic Seizures

The generalized tonic-clonic seizure refers specifically to the sequence of whole-body tonic stiffening followed by clonic jerking. Unfortunately, this term is often used indiscriminately to refer to any generalized convulsion, a use which is technically incorrect; properly, the term generalized tonic-clonic seizure should be reserved exclusively for the sequence of whole-body stiffening followed by whole body clonic jerking. This distinction can be important as some clinical events which mimic seizures, such as convulsive syncope (nonepileptic stiffening and jerking body movements associated with brief episodes of significant hypotension, do not tend to manifest this specific sequence. The sequence of tonic body stiffening followed by clonic jerking, compared with other possible sequences of movements, is highly suggestive of epileptic seizure and should be duly noted.

The EEG correlate of the tonic-clonic seizure often begins with an abrupt onset of generalized rapid spikes which then slow in frequency over the course of the event. As the firing frequency of the spikes slows, the spikes may begin to manifest a clearer spike-wave morphology. From the clinical perspective, rapid spikes are often associated with tonic stiffening. At a certain point in the seizure, the firing rate of the spikes slows to a point that allows each spike or spike-wave discharge to generate a separate clonic jerk (see Figure 10-18). This is the reason that the progression from tonic stiffening to clonic jerking is so common. Over the course of a generalized tonic-clonic seizure the clonic jerking is seen to slow in frequency and blend into a slow-wave pattern: “postictal slowing.” Less commonly, a clonic-tonic-clonic seizure may occur in which clonic jerking speeds up and melds into tonic stiffening, followed by the usual progression back to clonic jerking. As expected, the EEG correlate of this type of seizure often consists of spike-wave discharges that speed up to become rapid spikes, and then slow down again (see Figure 10-19).

Figure 10-18 The classic evolution of a generalized tonic-clonic seizure is shown. There is abrupt onset of generalized rapid spikes at the start of the tonic phase. As the firing frequency of the spikes decreases the individual spikes become far enough apart from one another that each spike can generate a separate clonic jerk, representing the clonic phase of the seizure. In this case, there is a period of postictal suppression after cessation of the seizure discharge. After seconds or minutes, generalized slow-wave activity appears that may last from minutes to days depending on the duration of the seizure and the nature of the patient.

Figure 10-19 A clonic-tonic-clonic seizure discharge is shown. Note that, in comparison to the previous example, the initial rapid spikes appear in brief bursts (seconds 8–10 of panel A) each associated with a clonic jerk. After a few seconds, the rapid spikes consolidate and their firing frequency increases, corresponding to the tonic phase of the seizure. The seizure discharge then follows a pattern similar to that of the tonic-clonic seizure shown earlier, with slowing of the spike frequency associated with the clonic phase of the seizure. Postictal slowing is seen following this seizure discharge.

Atonic Seizures

As the name implies, atonic seizures consist of a loss of tone, usually of the truncal muscles. In its mild form, an atonic seizure may simply consist of a subtle slumping of the shoulders. More frequently, an atonic seizure may manifest as a head-drop spell in which the patient’s head slumps forward. The most dramatic version of an atonic seizure is the drop attack in which the patient collapses to the ground, possibly resulting in injury. An astatic seizure is a seizure resulting in a fall (discussed further in the section on seizure types in Lennox-Gastaut Syndrome). There are many possible EEG correlates to atonic seizures, including slow spike-wave discharges, EEG desynchronization (flattening), or polyspikes, sometimes followed by flattening.

Early Myoclonic Encephalopathy

Infants with EME present soon after birth with both fragmentary and massive myoclonic seizures. Other seizure types also occur. The magnetic resonance imaging (MRI) scan at birth is almost always normal, and a large fraction of these babies are eventually found to have a specific metabolic disorder, nonketotic hyperglycinemia (NKH). Those babies with EME who do not prove to have NKH may have other metabolic diagnoses, and it is felt that the remaining cases of EME may be caused by some metabolic entities yet to be defined. This belief is based on the observations that EME babies have anatomically normal brains by MRI, and there is usually no history of a previous neurological injury. Babies with EME have complete developmental failure, and the seizures tend to be refractory to treatment. The EEG shows an unremitting burst-suppression pattern that may continue unabated through childhood (see Figure 10-20).

Figure 10-20 A dramatic burst-suppression pattern is seen in the EEG of this newborn with early myoclonic epilepsy (EME). No sleep cycling occurred in this recording, and every page of the record showed the same burst-suppression pattern. In patients with EME, this discontinuous pattern may persist for years.

Early Infantile Epileptic Encephalopathy

EIEE, also known as Ohtahara syndrome, appears to be a “lesional” epilepsy syndrome and, in contrast to EME, is often associated with an abnormal MRI scan. Tonic seizures are more prominent in EIEE compared with EME. MRI abnormalities associated with this syndrome can include cerebral malformations, or cerebral injuries as may occur in babies with hypoxic-ischemic encephalopathy. Therefore, EIEE occurs as an epileptic syndrome that is believed to be symptomatic of a preexisting abnormality, be it a cerebral malformation or some type of brain injury. EIEE is more likely to evolve to West syndrome or the Lennox-Gastaut syndrome.

Like EME, EIEE is typically associated with a burst-suppression pattern on EEG. The EEG patterns of EIEE and EME are not easily distinguished without the benefit of the clinical history (see Figure 10-21). The burst-suppression pattern of EIEE is more likely to evolve into other EEG background patterns later in life, compared with the EME burst-suppression pattern, which may persist indefinitely.

Figure 10-21 The burst-suppression pattern of a newborn patient with EIEE shown in this figure is essentially indistinguishable from the patterns seen in EME. In EIEE, eventual evolution to other patterns over months or years is not uncommon.

Therefore, despite the many aspects they share in common (similar EEG pattern, intractable seizures, poor prognosis), EIEE distinguishes itself from EME in that EIEE is considered an acquired or lesional epileptic encephalopathy caused by a cerebral malformation or a cerebral injury. In contrast, children with EME are believed to have the disorder on a genetic or biochemical basis rather than from a postnatal event. In EME, MRI brain anatomy is typically normal.

Benign Neonatal Convulsions

The syndrome of benign neonatal convulsions is also known to as “fifth day fits,” a name that serves as a useful reminder that the fifth day of life is the most common age of onset for this syndrome. To some extent, the diagnosis of benign neonatal convulsions must be made in retrospect because a benign long-term course is a key part of the syndrome.

The expected presentation of benign neonatal convulsions consists of a newborn who appears normal at birth and who may have already been uneventfully discharged home from the hospital. The seizures begin in the first week of life, with the most common age of incidence being the fifth day of life; 90% of babies present between the fourth and sixth days of life. The seizures generally subside by the second month followed by continued normal development.

The family history for seizures is negative. There is no antecedent history of a difficult delivery or birth injury, and neuroimaging is normal. Apart from possible mild hypotonia, the interictal examination is normal. A search for central nervous system infection is negative, and no electrolyte or other metabolic disturbances are found. The clinician is left with a story of an otherwise perfectly well newborn with unexplained onset of seizures in whom all testing is normal.

In babies with benign neonatal convulsions, the EEG background pattern tends to be normal. A characteristic EEG finding has been described in such babies, termed théta pointu alternant. This is a pattern of sharpened theta waves occurring in brief runs, typically in each central area, and alternating sides (see Figure 10-22). Although this pattern is said to occur in the majority of patients with this seizure syndrome, it may be difficult to identify, and its presence is not necessarily diagnostic of benign neonatal convulsions.

Figure 10-22 Théta pointu alternant, or alternating sharp theta, may be seen in each central area in both the syndromes of benign neonatal convulsions and benign familial neonatal convulsions.

(Modified from Dehan M, Quillerou D, Navelet Y, et al. Convulsions in the fifth day of life: a new syndrome? Arch Fr Pediatr 1977;34:730 742).

Whether benign neonatal convulsions represents a single, distinct syndrome has been questioned. From one point of view, it should not be a surprise that the subgroup of newborns with seizures who have a negative history and normal testing would have a more favorable outcome than those newborns with seizures who have abnormal histories or abnormalities in neuroimaging or other testing. Whether or not benign neonatal convulsions represents a unique syndrome remains an open question. There is also a question as to whether the incidence of later epilepsy in these infants is somewhat higher than that of the unaffected population.

Benign Familial Neonatal Convulsions

The syndrome of benign familial neonatal convulsions (BFNC) has many elements in common with the previously described syndrome of benign neonatal convulsions. As the name implies, however, in such babies there is a positive family history of seizures in the newborn period. In this syndrome, the seizures tend to begin slightly earlier, typically on the second or third day of life, usually resolving by the second month. Unlike benign neonatal convulsions, in BFNC a 10% to 15% incidence of later epilepsy has been described. Also, mild developmental problems may occur with a slightly increased frequency compared with the unaffected population. A large proportion of affected individuals have been found to have linkage to the 20q13.3 gene locus corresponding to a mutation in the potassium channel gene KCNQ2. A smaller number of affected individuals have been found to have linkage to the 8q24 locus and a mutation in the KCNQ3 gene (both potassium channel genes). Still other kindreds appear to have no abnormality at either of these loci, suggesting that additional genetic abnormalities that cause this syndrome have yet to be identified.

The typical seizure in BFNC is the clonic seizure, preceded by tonic stiffening and apnea in some (Hirsch et al., 1993). Most commonly the interictal EEG is normal, however, the théta pointu alternant pattern, as has been described in benign neonatal convulsions, has been reported in some babies with this syndrome.

The Role of EEG in the Evaluation of Febrile Seizures

Despite the fact that EEG abnormalities may be seen in children with febrile seizures, the EEG has not proved to be a particularly useful tool in predicting later epilepsy in these children. The most common epileptiform abnormality found in children with febrile seizures is generalized spike-wave discharges. This pattern is, of course, nonspecific in that it is also seen in the generalized epilepsies. Its presence in the EEG of a child with febrile seizures has not been clearly shown to increase the risk of later epilepsy. Increased slowing, especially in the posterior quadrants, may be expected within a few days of a febrile seizure. In general, because the EEG has not been found to be useful in predicting later epilepsy in children with febrile seizures, EEG testing is not routinely indicated in the evaluation of uncomplicated febrile seizures. Also, because febrile seizures are rarely treated with daily antiepileptic medications, it is highly unlikely that an EEG result, whether or not it is abnormal, would prompt the use of daily seizure medication.

EEG in the Diagnosis of Infantile Spasms and West Syndrome

Because West syndrome has distinctive ictal and interictal EEG signatures, electroencephalography is a central tool in the diagnosis of infantile spasms and West syndrome. EEG helps establish the diagnosis of infantile spasms, either by identifying the characteristic interictal pattern of West syndrome (i.e., hypsarrhythmia) or by recording the spasms and demonstrating an ictal discharge during the events. EEG may also be used to monitor the success of treatment.

The EEG term hypsarrhythmia is derived from the Greek meaning “high” or “lofty” rhythm. In fact, some of the highest voltages measured in electroencephalography are seen in babies with hypsarrhythmia. Compared with adult EEGs in which voltages typically do not exceed 200 μV, hypsarrhythmia EEGs may exceed 1 mV (1000 μV). The essential features of the hypsarrhythmic pattern are high voltage and chaos. In this context, chaos refers to the opposite of synchrony. A completely chaotic EEG pattern is a pattern in which different electrical events and rhythms are occurring in different brain regions at different times in an unsynchronized and seemingly unrelated fashion. In contrast, the generalized spike-wave discharge, although abnormal, represents a pattern with a high degree of synchrony with all cortical areas acting in unison. In the chaotic hypsarrhythmia pattern, rapid spikes, high-voltage s low waves, and other abnormalities may occur in scattered locations at different times and in a seemingly random fashion (see Figure 10-23). Intermediate states between synchrony and complete chaos are also seen (see Figure 10-24).

Figure 10-23 The high-voltage, chaotic pattern of hypsarrhythmia is shown. Note the “random delta” activity and the scattered spikes, occurring both singly and in brief runs in a chaotic fashion.

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