Blume's Atlas of Pediatric and Adult Electroencephalography, 1st Edition

Chapter 4

Epileptiform Phenomena

Epilepsy is a clinical diagnosis. Electroencephalographic (EEG) data play only a supporting role to the clinical impression. As an epileptic seizure is a relatively short-lived, unpredictable disturbance of cerebral function, a physician will actually witness a typical attack in only a minority of instances. Therefore, the most valuable diagnostic tool remains a full and accurate description of the attacks obtained by an attentive and experienced physician from the patient or observers. However, this description also falls short when the symptoms, signs, or circumstances are shared by one or more other causes of transient disturbances of central nervous system function or when the patient and/or observers do not give sufficiently precise or complete information. In these situations, one or more EEGs may help to establish the diagnosis. Because epilepsy is an intermittently recurring condition, so may be its electrographic correlates. Thus, the absence of such phenomena on a single recording does not exclude the possibility of their appearance on a subsequent EEG.

EEG may help to answer several questions: (a) Do the episodes represent a seizure disorder? (b) Are the seizures primary generalized, secondarily generalized, or focal? (c) If focal, from what part of the cerebral cortex do the seizures arise? and (d) What epilepsy syndrome do the seizures represent? The simultaneous occurrence of a clinical seizure (e.g., an absence attack) and EEG phenomena accepted as representing the cortical neuronal events constituting an epileptic seizure (e.g., generalized spike–waves) constitutes the only instance where the EEG establishes the diagnosis with certainty. In fact, EEG is the only means by which a diagnosis of epilepsy can be unequivocally established or a seizure accurately classified, and it does so within milliseconds of onset. Such EEG phenomena appearing in the absence of a clinically apparent seizure also give strong support to the clinical diagnosis of epilepsy but do not establish the diagnosis in itself.

More common than recorded seizures are spikes. Although these often represent interictal disturbances of neuronal function in epileptic patients, their correlation with epilepsy is imperfect. For example, Trojaborg (1968) reported that 82% of 242 children with spike foci had epilepsy. In contrast, Eeg-Olofsson et al. (1971) found focal spikes or sharp waves in 1.9% of their 743 normal children at rest. Cavazzuti et al. (1980) and Okubo et al. (1994) identified spikes in 3.5% and 4.5% of normal children; most were the spikes seen in benign partial epilepsies of childhood.

Thus, there is a good correlation between epileptiform activity in resting EEGs and seizure disorders in children. It is quite possible, however, for a patient to have focal spikes without a seizure disorder. On the other hand, demonstration of spikes is not required for diagnosis of a seizure disorder.

Epileptiform activity appears in 50% of single awake recordings among patients already known to have epilepsy, the proportion rising to 80% to 85% if sleep is included in the recording. Multiple recordings also increase the yield: two EEGs, 80% to 85%; four EEGs, 90% (Binnie & Stefan, 1999). Hyperventilation and photic stimulation also increase spike incidence.

Identifying EEG phenomena as spikes is facilitated in children by their greater abundance and usually more spectacular appearance than is seen in recordings of older patients. It is normal, however, for a greater number of waves in pediatric EEGs to be sharply contoured; overreading such features as epileptiform is a common error in clinical practice. Normal sharply contoured waves in pediatric awake recordings include mu rhythm, posterior slow of youth, sharply contoured temporal waves, and the buildup in hyperventilation. Any medication-induced beta creates sharply contoured waves in association with the already abundant diffuse theta. In drowsiness, normal bursts of 3 to 5 Hz high-voltage rhythmic waves can be indented by superimposed waveforms to create a notched spike–wave-like appearance. The normal apiculate V waves of children, comb-shaped spindles, and sharply contoured occipital delta are sleep potentials that can be mistaken for spikes. In addition, many of the clinically innocent spike phenomena commonly occur in children. The most historically famous of these is the 14 and 6 per-second positive-spike


phenomenon, which is a normal pattern seen in sleep recordings of many adolescents. The 6-per-second spike–wave phenomenon in its purest form likewise does not correlate with a seizure disorder. Although very spectacular in the rare instances in which it appears, the psychomotor variant phenomenon is likewise clinically insignificant. As shown later in the text, the several spike phenomena peculiar to children vary in their correlation with epileptic conditions.

Despite such reservations, spikes or spike-waves that are well identified and appear, at least occasionally, in the resting record not only give reasonable support to a clinical impression of a seizure disorder in children but also help the physician to determine whether the attacks represent focal and secondarily generalized or primary generalized seizure disorders.

Characteristics and clinical correlations of the major epileptiform patterns are presented in the following sections.

Focal Epileptiform Potentials

Focal epileptiform potentials are defined as involving one region of one hemisphere of the brain with occasional propagation to other ipsilateral zones and to the homotopic area of the opposite hemisphere.

“Rolandic” Spikes


Rolandic spikes are characteristically stereotyped, abundant, high-voltage discharges with three clearly defined phases and prominent aftercoming slow waves appearing singly or in groups in the central (rolandic) region (C3 or C4) using the 10–20 system. Usually there is a marked downward deflection of the principal phase of the spike in derivations F3–C3 or F4–C4, suggesting a dipole involving these leads. This dipole can occasionally be established using a distant reference. The principal parasagittal spread of the major deflection's negative electrical field is usually to the parietal region, as evidenced by the often minimal deflections in C3–P3 or C4–P4 derivations. The positive component of the aforementioned dipole involves the frontal region ipsilaterally or bilaterally. This may not always be demonstrable, however, even when other features of such spikes are present. Although the incidence of intractable seizures and other neurological abnormalities is lower when a dipole is demonstrable, these correlations remain incomplete.

In a given recording, the location of the electronegative component of these central spikes may vary in the inferior–superior axis. Recording with closely spaced electrodes, Legarda et al. (1994) disclosed two areas of maximum negative field: superior (C3,4) and inferior (C5,6) central, the latter appearing more commonly. The proportion of patients with seizure disorders was the same in both groups. Recording with the 10–20 system of electrode placement, Beaussart (1972) had shown earlier that such central spikes spread more commonly to the midtemporal (T3,4) region than the sagittal area (Cz). The spike location corresponds well with the lower rolandic region implicated by ictal symptoms and signs. Thus, motor seizures involving the contralateral hand occurred most commonly in the high central group and hypersalivation with motor involvement of the mouth and face occurred most commonly in the low central group (Legarda et al., 1994). However, there is no correlation between the laterality of ictal symptoms and that of the spikes (Beaumanoir et al., 1974)because laterality commonly shifts between EEG recordings or during the same recording. In 30% to 40% of patients, these spikes occur concurrently and asynchronously on each side. The spikes of higher voltage may spread homotopically. This characteristic may augment to a virtually synchronous and symmetrical appearance, approaching a morphology that resembles spike–waves. Indeed, about 5% of patients have independently occurring generalized spike–waves appearing spontaneously or, more commonly, with photic stimulation, hyperventilation, or sleep (Beaussart, 1972; Beaumanoir et al., 1974).

That spikes characteristic of the benign partial epilepsy of childhood may appear in association with other neurological diseases or in fully asymptomatic subjects indicates that their significance depends upon clinical correlation. For example, left rolandic spikes appeared in our 4-year-old patient, whose seizures implicated the right supplementary motor region where a tumor was lurking. Of 43 children with rolandic spikes, de Weerd and Arts (1993) found seizure disorders in only 26 (60%).

Spikes of similar morphology to rolandic spikes may appear in other regions, principally the parietal and posterior temporal areas. Gastaut and Broughton (1972) and Beaumanoir et al. (1974) emphasized the close association of rolandic spikes with the mu rhythm; distinction between prominent mu and rolandic spikes may be difficult.

The quantity of rolandic spikes and similar spikes in other locations augments during non-REM sleep, as may their bilateral synchrony. In 20% to 35% of patients, rolandic spikes may appear only in sleep (Lombroso, 1967; Blom & Heijbel, 1975). Therefore, a sleep recording should be obtained when benign rolandic epilepsy of childhood is clinically suspected


and awake recordings are normal. Hyperventilation and photic stimulation do not activate these discharges. They also may be abundant in REM sleep, but they remain unilateral. Although rolandic spikes may be absent for one or more recordings, they usually occur in abundance, in sharp contrast to the usual rarity of the clinical attacks. Aside from transient slowing during periods of abundant spikes, the background awake and sleep activity is characteristically normal. A persistently abnormal background in the same region would raise the possibility of an underlying structural lesion. No complete study of the EEG changes during an ictus exists because of the rarity of such an occurrence during waking hours. However, Dalla Bernardina and Tassinari (1975) reported one patient whose nocturnal seizure began as 20 to 30 µV, 12 Hz waves in the left central–parietal region. Such an attack is illustrated in this volume.

The age at appearance of the EEG pattern closely parallels that of the seizure disorder–that is, from 3 to 16 years. Rolandic spikes are rarely seen beyond adolescence.

Clinical Association

The incidence of seizures in association with rolandic spikes varies from 54% to 84% in various studies (Beaussart, 1972; Blom & Brorson, 1966; Smith & Kellaway, 1964).

Nocturnal generalized seizures, diurnal attacks implicating the lower rolandic region, and characteristic central spikes compose a self-limited syndrome occurring in otherwise healthy children. This disorder constitutes 15% of all childhood seizures excluding febrile seizures (Blom et al., 1972; Heijbel et al., 1975).

Heijbel et al. (1975) performed single EEGs on the siblings and parents; most included sleep recordings. Rolandic spikes appeared in recordings of 11 (34%) of 32 siblings and in 1 (3%) of 36 parents. Blom et al. (1972) found the seizure disorder associated with rolandic spikes to begin from 1 to 13 years of age and chiefly from 5 to 9 years.

Temporal Spikes


Anterior temporal spikes appear principally in adolescents and adults but may also arise in children after age 6 years. These are located at F7,8; T3,4; and Al,2. Mandibular notch electrodes as well as sphenoidal leads record them (Sadler & Goodwin, 1989). Hyperventilation and various levels of sleep may be required to elicit their presence. Temporal spikes may be associated with focal background abnormalities such as excessive delta or theta.

The electroencephalographer must distinguish temporal spikes from rolandic spikes, which also extend to temporal leads, particularly mid- and posterior–temporal regions (T3,4 and T5,6). The field of anterior–temporal spikes extends minimally and never principally above the sylvian fissure. A bipolar coronal montage can be used to measure the suprasylvian extension. However, the occasional associated frontal electropositivity of rolandic spikes, causing a downward deflection in the F4–F8 derivation, may create the false appearance of anterior–temporal electronegativity. Thus, both anterior–posterior and coronal bipolar montages may be needed to distinguish these two types of spikes.

The importance of this distinction lies in their markedly different clinical implications.

Clinical Association

Anterior–temporal spikes usually represent an identifiable structural lesion (Falconer et al., 1964). Eeg-Olofsson et al. (1971) found temporal spikes in only 2 of their 743 normal children. Temporal lobe seizures are not rare in childhood (Falconer, 1971). In most instances, the etiology is apparent from the clinical history and includes febrile seizures associated with mesial–temporal sclerosis and neocortical malformations (Aicardi, 1994).

Occipital Spikes


These well-defined surface-negative spikes appear unilaterally or bilaterally in synchronous or independent fashion. Spread to the ipsilateral parietal and posterior–temporal regions is common. Occipital spikes are most abundant with eyes closed; eye opening diminishes or abolishes their appearance. In this way, they may be distinguished readily from the occasionally electronegative lambda waves, which are present only when a complex field is being scanned. Patients with occipital spikes during wakefulness may develop posterior polyspikes in sleep.

Clinical Association

Eeg-Olofsson et al. (1971) found occipital spikes in only 2 of their 743 normal children. Among patients less than 4 years of age, spikes occur in the occipital region more commonly than in any other area. Conversely, occipital spikes appear more commonly in children less than 4 years old than at any other age (Trojaborg, 1968). Smith and Kellaway (1964) found seizures in only one third of patients with ocular abnormalities from infancy and


occipital spikes. Syndromes encompassing migraine, occipital seizure disorders, and occipital spikes have been described (Andermann, 1987). Occipital spikes associated with other focal occipital EEG abnormalities occur in children with epileptogenic lesions in this area, including tumors and cortical developmental abnormalities. Gobbi et al. (1991) described patients with occipital spikes, intractable epilepsy, and occipital calcifications in association with celiac disease. Patients with a progressive myoclonic epilepsy, such as Lafora body disease, may have occipital spikes and light-sensitive seizures (Tassinari et al., 1978).

Maher et al. (1995) reviewed all EEGs from the only laboratory serving Newfoundland and identified 31 children whose EEGs showed occipital spikes. Twenty-three (74%) had benign, nonlesional epilepsy; lesion-based seizures occurred in 5 (16%); and others had less defined conditions. No epilepsy occurred in 2 (6%).

The clinical significance of occipital spikes appears to hinge on associated EEG findings. An otherwise normal EEG suggests a condition such as a benign partial epilepsy of childhood. A unilateral alpha abnormality (slowing, low voltage) and focally excessive delta activity each raises the possibility of a lesion-based epilepsy. The migraine-based disorders may produce EEGs in either category. Blindness at birth or occurring in infancy may be associated with occipital spikes and bilateral absence of alpha.

Multiple Independent Spike Foci


Patients who have, on a single EEG, spikes that arise from at least three noncontiguous electrode positions with at least one focus in each hemisphere are considered to have the multiple independent spike foci pattern. Sixty-three (4%) of 1,500 children having recordings in our laboratory demonstrated this pattern (Blume, 1978). None of the normal children reported by Eeg-Olofsson et al. (1971) had multiple independent spikes.

Clinical Association

The following data are derived from two studies of this pattern by Noriega-Sanchez and Markand (1976) and Blume (1978). All patients in these studies were children except for 3.7% of the 1976 study. In previous EEGs, 16% of the patients in the 1976 study had hypsarrhythmia; 11% had slow spike–waves (SSW). Kotagal (1995) documented multifocal independent spikes as a transition pattern between hypsarrhythmia and SSW.

Seizures occurred in more than 90% of patients. Generalized motor seizures occurred in more than 80%, with generalized tonic–clonic being the most common single type. Half the patients had more than one type of seizure. Seizures occurred daily in 60% of those who had at least one spike every 10 seconds, but in only 33% of those whose spikes occurred less often. Only one third of patients were cognitively normal. However, intellect was normal in higher percentages of patients with infrequent spikes (52%), less than 10 spike foci (47%), and normal background activity (39%). Abnormalities were found on the neurological examination in about one half of the patients. The incidence of normal intelligence dropped from 47% of patients with normal neurological examinations to 16% with abnormal examinations.

Presumed etiologies included the majority of diseases that most commonly afflict the brain in early life, such as perinatal insult, central nervous system infection, neocortical malformations, degenerative conditions, trauma, and anoxia.

Periodic Phenomena


Periodically repetitive, relatively stereotyped focal, and/or diffuse EEG phenomena represent physiologically acute or subacute processes in both children and adults. Such phenomena may be spikes, polyspikes, or delta. Their location and distribution depend largely on that of an underlying structural lesion.

Clinical Association

A structural lesion can usually be identified in patients with periodic phenomena. It may be an acute process such as an infarct, contusion, encephalitis, or anoxic encephalopathy(Gross et al., 1999). Subacute lesions (such as subacute sclerosing panencephalitis and regionally accentuated chronic encephalitis) will produce periodic phenomena if they are progressive. Pathologically chronic nonprogressive abnormalities are associated with periodic EEG phenomena if recent and frequent epileptic seizures have occurred. However, periodic phenomena unassociated with acute lesions or seizures have been described (Westmoreland et al., 1986; Gross et al., 1999).

Structural lesions are either diffuse or multifocal, or they may occupy a substantial portion of one region. A small lesion produces periodic phenomena if an acute event such as a seizure occurs; the periodicity in this circumstance almost always is transient, lasting only seconds or a few


minutes postictally. Systemic metabolic disorders may be associated (Garg et al., 1995), but their role in generating periodicity remains unclear.

“Generalized” Epileptiform Potentials

“Generalized” is a misnomer, as no cerebral potential is expressed equally and diffusely in all recording electrode positions. As used, the term refers to phenomena appearing in widespread fashion simultaneously and usually synchronously in both hemispheres.

Generalized Spike–Wave Complexes


This phenomenon is also known as generalized spike-and-slow-wave complexes or generalized spike–waves. When more than one spike is present in each complex, the phenomenon is known as polyspike-and-waves.

The most prominent components of a generalized spike–wave complex are a bilaterally synchronous single spike or series of spikes (polyspikes) followed by a rhythmic slow wave. Both are surface-negative. Scrutiny of apparent monospike–wave complexes led Weir (1965) to discover that their morphology is considerably more complex. Within a series of spike–wave complexes, each 200- to 500-ms negative wave is preceded by a 100 to 150 ms positive trough. Interrupting this positive trough may be two negative spikes; the second, larger spike is the classical spike of the spike–wave complex. Usually maximal frontally, the amplitude of the spike waxes and wanes during a spike–wave series but is usually greatest at its onset. The succeeding negative wave is maximal in the frontal–parietal regions and minimal temporally. The first complex of a spike–wave series may consist of manifest polyspikes and waves apparently becoming single spike–wave complexes as the series proceeds.

Although classically bilaterally synchronous and symmetrical, spike–waves may begin 10 to 25 ms earlier and/or be maximally expressed in one hemisphere (Lemieux & Blume, 1986). However, this predominance should shift from side to side during a single recording or over several recordings. Rarely, a classical spike–wave series may be confined to a single hemisphere or region. Fragments of spike–waves appear, particularly on bipolar montages where the broad fields lead to partial cancellation of potentials. Such fragments can usually be distinguished from focal spikes by their morphological resemblance to components of the fully expressed spike–wave complexes and by their wider field. “Generalized” spike–wave complexes may be distributed diffusely over both hemispheres. In such cases, their voltage is usually greatest over the superior frontal regions. In other instances, the field may be more restricted and involve only the anterior head regions in synchronous fashion; less commonly, they may be confined to the posterior head regions.

Spike–waves may occur as single complexes, brief bursts, or prolonged trains. They usually are of highest frequency at the onset of a series, when they repeat at a rate of 3 to 6 per second, usually 3 to 3.5 per second. The repetition rate then slows slightly. They begin and end abruptly, with an almost immediate return to the interictal EEG; rarely one or two frontally predominant rhythmic delta waves linger. If the spike–wave series is prolonged, as in absence status, the rate may slow to 2 per second. If the series is already in progress at the onset of the recording, differentiation from slow spike–waves (SSWs) may be difficult.

The major role of hyperventilation in children is to elicit spike–wave complexes that have not appeared in the “resting” record. Dalby (1969) reported that hyperventilation elicited spike–wave complexes in 50% of his patients who had absence attacks and 25% who had other forms of primary generalized seizures. Spike–wave complexes do not always appear within the first few minutes of hyperventilation. Therefore, when primary generalized epilepsy is clinically suspected and the resting record does not contain spike–waves, it may be necessary to ask the patient to hyperventilate for 3 to 4 min and repeat if spike–waves are absent.

The most clinically significant phenomenon with photic stimulation is the photoparoxysmal response, a bilaterally synchronous polyspike or polyspike–wave discharge that is not time locked to the flash rate and that may continue beyond the cessation of the flash stimulus (Reilly & Peters, 1973). This response is elicited most readily with flash rates of about 12 to 20 per second, particularly with eye closure. It appears in about 3% of all patients referred for EEG and of those with focal seizure disorders and in 20% to 50% of patients with generalized tonic–clonic, myoclonic, or absence attacks (Takahashi, 1987). The photoparoxysmal response suggests that seizures of patients with primary generalized epilepsy may be precipitated by light flashes. Spike–waves may be precipitated by eye closure in some of these patients). Widely synchronous spikes evoked by single flashes may indicate a progressive myoclonic epilepsy (Pampiglione & Harden, 1973).

As the photoparoxysmal response may be seen in normal subjects and in patients with metabolic or drug withdrawal conditions, the diagnosis of a seizure disorder cannot be made conclusively on this basis. Moreover, relatives of patients with primary generalized seizures may demonstrate a


photo-paroxysmal response without necessarily having a seizure disorder. On the other hand, such polyspike–waves may confirm questionable spike–wave discharges on the resting recording. A photoparoxysmal response in a child with febrile convulsions suggests that they may be the first manifestations of a myoclonic epilepsy of childhood (Dalla Bernardina et al., 1982; Dravet et al., 1984).

The incidence of spike–wave complexes usually augments in non-REM sleep, particularly in stages 3 to 4 (Sato et al., 1973). They may appear only in sleep; however, they are least common in REM sleep. Their morphology alters in non-REM sleep, particularly in deeper stages. The burst duration shortens, the complexes are less regular, polyspike–wave complexes become more abundant, and the repetition rate may slow to 1.5 to 2.5 Hz. In contrast, the spike–wave morphology in REM sleep resembles that of wakefulness. Arousal may precipitate spike–wave complexes.

Bursts of 2 to 4 Hz rhythmic waves (“projected” activity) and rhythmic occipital delta are two nondiagnostic phenomena that often occur in association with generalized spike–wave complexes. If clinically appropriate, their presence should encourage further measures to elicit spike–waves, such as longer recording, additional hyperventilation, and sleep.

Rarely, the electrographic accompaniment of absence attacks is 8 to 20 Hz rhythmic waves. Two such rhythms may become superimposed, one perhaps a multiple of the other, creating a saw-tooth appearance. Such phenomena may appear and recede subtly but frequently, masquerading as a drowsy pattern or beta. Unfortunately such patients tend to have frequent, therapy-resistant absence attacks.

Clinical Association

The presence of generalized spike–wave complexes on the resting record or with hyperventilation gives very strong support to a clinical impression that the patient has a primary generalized seizure disorder. However, the diagnosis cannot be made on the basis of EEG data alone. Four series of patients with such EEG findings (Dalby, 1969; Lundervold et al., 1959; Silverman, 1954; Blume et al., 1982) have found generalized seizure disorders in 97% to 98%. Conversely, Eeg-Olofsson et al. (1971) found no spike–waves in the resting recording of 743 normal children. Two of these children had spike–waves during hyperventilation.

Gibbs et al. (1935) first established the relationship between generalized spike–wave complexes and petit mal (absence) epilepsy. The incidence of clinically apparent absence attacks in subsequent series has ranged from 26% (Silverman, 1954) to 70% (Clark & Knott, 1955). Our study (Blume et al., 1982) found absence attacks in 58% of a group of 60 patients selected only on the basis of having generalized 3-per-second spike–waves. Dalby (1969) found a higher incidence of generalized tonic-clonic seizures (GTC) and myoclonic attacks among patients with polyspike-and-wave complexes. Despite such relationships, the EEG is unable to predict whether a patient with absence attacks will develop GTC (Dalby, 1969;Niedermeyer, 1972). The incidence of GTC also varies widely from study to study: from 37% (Dalby, 1969) to 86% (Jasper & Kershman, 1941). Sixty-five percent of our patients had GTC.

The EEG may be normal in patients with mild seizure disorders such as GTC in juvenile myoclonic epilepsy. In other cases, it may show diffuse bursts of theta or may contain sporadic 4 to 5 Hz spike–wave or polyspike–wave complexes. Asymmetrical or focal spike–waves, or both, may commonly appear; but these can be considered “fragments” or regional expressions of essentially bilaterally synchronous phenomena. During the rarely recorded GTC, 20 to 40 Hz diffuse waves, slowing to about 10 Hz, appear during the tonic phase followed by bilaterally synchronous and diffuse polyspike–waves during the clonic phase. Unfortunately, muscle artifact rapidly obscures the tracing during GTC. Postictally, diffuse delta and theta predominate, with a return toward a normal recording within several minutes. No regional postictal abnormalities should occur if the attack was a primary generalized GTC. In those patients with secondarily generalized GTC, the attack itself may predominate in one hemisphere and its postictal effects would reflect the side or area of most intense involvement.

Scrutiny of patients during bilaterally synchronous 3-per-second spike–waves has revealed several interesting features about absence attacks. Browne et al. (1974) studied reaction times to auditory stimuli before and during spike–waves. Reaction times most commonly were abnormal, from 0.5 to 1.5 s after the onset of spike–wave complexes; thereafter, some recovery took place, as 52% of reaction times obtained after 4 s of spike–wave discharges were normal. This finding parallels the common clinical observation that patients in absence status are more often partially responsive, whereas responsiveness is usually lost completely during a brief attack. Reaction times were more commonly impaired when the spike–waves involved all leads than when some regions were bilaterally free. This gives credence to the occasional patient's claim that he or she retains partial awareness during an absence attack. In practice, an absence attack is unlikely to be clinically detectable unless sequential spike–wave complexes last more than 5 s (Niedermeyer, 1987).



EEG is useful for monitoring the quantity of absence seizures and, therefore, the effectiveness of therapy. Both spike–wave incidence and duration correlate with absence quantity(Miller & Blume, 1993).

Penry et al. (1975) studied absence attacks with a multicamera videotape and found some motor accompaniment in 90% of attacks. Automatisms were detected in 63% and mild clonic components in 45%. Decreased postural tone occurred frequently (22%), but increased tone was rare (5%). The probability of an automatism occurring increased with increasing seizure duration, whereas clonic movements, usually of the eyelids, tended to occur early in the seizure. Two or more components commonly occurred in the same seizure (35%), but three or more components rarely appeared (5%). Klass and Daly (1961), Dalby (1969), and Blume et al. (1982) have noted occasional unilateral motor phenomena during seizures associated with generalized 3-per-second spike–waves. These include conjugate lateral ocular deviation or unilateral clonic jerks. Usually such motor phenomena do not consistently involve the same side.

Continuous spike–waves of sleep (electrographic status epilepticus of sleep) is a condition in which sequential bilaterally synchronous spike–waves are very abundant in non-REM sleep and, therefore, represent reiterative absence (Patry et al., 1971). Atypical absences with atonic components are among the seizure disorders present in wakefulness, as varying quantities of 3 Hz spike–wave discharges occur during the awake recording as well. Behavioral and mental deterioration, including a reduction in speech, occurs. Therefore, the syndrome shares clinical and electrographic properties with the Landau–Kleffner syndrome. The characteristic electrographic pattern and associated epilepsy generally disappear during adolescence; this is associated with an improvement in neuropsychological function (Jayakar & Seshia, 1991).

Bilaterally synchronous myoclonic seizures are usually associated with bilateral spike–waves or polyspike–waves. These may appear in an otherwise normal EEG, with SSWs in the Lennox–Gastaut syndrome, or with excess delta in degenerative central nervous system disorders and metabolic encephalopathies. Although the spike–wave complexes accompany the myoclonus, the specific timing between the spike and the myoclonic jerk varies (Gastaut et al., 1974). Some patients with generalized spike–wave complexes will have only febrile convulsions.

Paralleling the age of occurrence of the primary generalized epilepsies, Dalby (1969) found that the 5 to 14 year age group contained the highest number of patients with generalized spike–waves. However, such can be found in decreasing numbers before and after this age period, extending from 1 year to the elderly.

Generalized Slow Spike–Waves (SSWs)


SSWs classically consist of a spike followed by a 350- to 400-ms rhythmic wave. Generalized SSWs occur in prolonged bilaterally synchronous series with a repetition rate of 1 to 2 Hz. Three-per-second spike–waves may be intermixed sporadically with SSWs. The morphology, amplitude, and repetition rate of SSWs may vary moderately between bursts and within a burst. They are usually distributed diffusely but may be principally expressed in or confined to the anterior or posterior regions. Although usually bilaterally symmetrical, transient and shifting asymmetries may occur. SSWs characteristically occupy much greater portions of the awake recording than do 3 per second spike–wave complexes. Hyperventilation and photic stimulation have no effect on SSWs, but sleep increases their abundance. The interparoxysmal recording usually is abnormally slow for age. In sleep, polyspike–wave complexes, generalized polyspikes, rhythmic 10 to 20 Hz fast rhythmic waves (epileptic recruiting rhythm), and electrodecremental events may occur. Normal sleep potentials, such as spindles and V waves, may be absent.

The maximum incidence of SSWs occurs at 1 to 5 years, but their presence extends well into adulthood in some patients. SSWs also occur in the first year of life, when they may be intermixed with a hypsarrhythmic pattern.

Clinical Association

Clinically apparent seizures occur in 98% of patients with SSWs (Blume et al., 1973; Markand, 1977). Tonic seizures are the most common form in most studies (Chevrie & Aicardi, 1972; Gastaut et al., 1966). Atypical absences occur next in frequency; these consist of a gradual onset and termination of impaired awareness. Automatisms and diffuse increases or decreases in muscular tone also may occur during such absences. Atonic, myoclonic, and tonic–clonic seizures may also develop. Unfortunately, the majority of patients have more than one type of seizure, have daily attacks, and the seizures are resistant to therapy. One study showed that more than half of these patients were still having seizures after periods averaging 14.9 years (Blume et al., 1973).

The seizures usually begin earlier in life than in patients with 3-per-second spike–waves; the median age varies from 11 to 28 months (Blume et al., 1973; Markand, 1977; Chevrie & Aicardi, 1972). Chevrie and Aicardi also found that the type of seizure depended upon the age at seizure onset. Mean age of onset was 16 months for those with tonic seizures, 32 months


for atypical absences, 39 months for myoclonic attacks, 43 months for tonic–clonic seizures, and 48 months for atonic attacks.

In contrast to 3-per-second spike–waves, long series of SSWs are usually not accompanied by any discernible clinical alteration, although testing for subtle changes is often impeded by mental subnormality. Tonic seizures are most often accompanied by diffuse electrodecremental events, fast (10 to 25 Hz) rhythmic waves, and/or polyspikes (Blume et al., 1973;Markand, 1977). Atypical absence may be detected at the onset of generalized SSWs or may accompany any of the patterns of tonic seizures. Myoclonic attacks may be accompanied by high-voltage bisynchronous spikes superimposed on SSWs or without any EEG change.

All of the aforementioned studies have found cognitive impairment in the great majority of patients with SSWs. Not always evident at first, it becomes apparent in an increasing percentage of patients during follow-up. Thus, 30% of patients in the series of Chevrie and Aicardi were considered subnormal when the first seizure occurred (median age 11 months), 69% at the time of the first EEG with SSWs (median age 35 months), and 93% at follow-up (median age 4 years, 5 months). Similarly, 79% of the patients of Blume et al. had normal motor milestones; 35% had normal intelligence at a median age of 4 years, 7 months; and 24% were normal when followed at a median age of 16 years, 10 months. Patients with evidence of organic brain disease before the first seizure and those whose seizures began before the age of 2 years had a higher incidence of cognitive impairment and were more severely impaired.

The combination of intractable generalized seizures, SSWs, and fast (10 to 20 Hz) rhythmic waves constitutes the Lennox–Gastaut syndrome (LGS), which was originally outlined byLennox (1945) and detailed further by Gastaut et al. (1966). The initial manifestation of this syndrome is usually a seizure disorder. A minority of patients have had infantile spasms with hypsarrhythmia; with age, the seizure manifestations and EEG gradually become those of the LGS. Exceptionally, the first seizures may be absence and/or GTC with 3-per-second spike–waves.

Conditions presumably giving rise to a diffuse central nervous system insult in prenatal, perinatal, or early postnatal life had occurred in about half of the reported patients (Blume et al., 1973; Markand, 1977; Gastaut et al., 1966). Whether factors such as abnormal gestation, cerebral malformations, birth trauma and anoxia, meningitis, or trauma completely explain SSWs in each instance is conjectural. Moreover, up to 50% of patients in the aforementioned studies had no apparent cause for the SSWs. Identifiable degenerative diseases rarely occur in patients with LGS.

Hypsarrhythmia and Epileptic Spasms (Infantile Spasms)

Sudden brief, tonic muscular contractions producing flexion or extension of the trunk and extremities is a seizure disorder afflicting infants and young children; these attacks are known as epileptic spasms. The interictal EEG correlate is usually hypsarrhythmia. Unfortunately, most patients are cognitively subnormal at the time of the spasms and in later life.


Hypsarrhythmia, described by Gibbs and Gibbs (1952), consists of high-voltage, 1 to 3 Hz waves with multifocal asynchronous spikes and sharp waves in a chaotic mixture of varying morphology and amplitude. Although this pattern is almost continuous during wakefulness and light sleep, it may be discontinuous in deep sleep. This effect of sleep stage should be considered in comparing sequential recordings of the same patient.

Hypsarrhythmia may predominate in one hemisphere or even be associated with a consistent focal spike discharge. Such regional accentuation usually correlates with a focal lesion(Drury et al., 1995). Associated infantile spasms usually are accentuated in the contralateral limbs (Gaily et al., 1995). Epochs of attenuation may interrupt the hypsarrhythmic pattern. Asynchronous high-voltage delta activity with minimal epileptiform potentials can appear. The appearance of such varying EEG features depends on the duration of the recording, the clinical state of the patient, and the presence of structural abnormalities. For example, a large cystic defect in one hemisphere could impair the expression of hypsarrhythmia on that side, creating the asymmetrical form.

During a spasm, the EEG changes abruptly and diffusely. Initially, a high-voltage wave with or without a spike occurs. This usually is followed immediately by diffuse attenuation of activity, termed an “electrodecremental” event (EDE) (Bickford & Klass, 1960). Low-voltage high-frequency activity is occasionally superimposed upon these EDEs. The duration of the electrodecremental components varies from less than 1 s to more than 1 min. Following the spasm, the recording may appear more normal for a few seconds to minutes, with more regulated background activity. Subsequently, the hypsarrhythmic pattern resumes.

Clinical Association

Hypsarrhythmia is the most characteristic interictal EEG pattern seen in association with epileptic spasms. According to Jeavons and Bower (1974),


they appear in two thirds of first EEGs done for this condition. Other types of epileptiform discharges appeared in the initial recordings of 32% of their patients, leaving only 2% with normal or mildly abnormal recordings. Subsequent EEGs in these 2% showed either hypsarrhythmia or other types of epileptiform activity. Conversely, of 80 patients with hypsarrhythmia studied by Baird and Borofsky (1957), 51 had infantile spasms, 20 had other types of seizures, and 9 had no recognized seizure disorder.

Hypsarrhythmia is almost always confined to ages 3 months to 5 years, paralleling the time course of epileptic spasms. The evolution of hypsarrhythmia was studied by Watanabe et al. (1973). Initial EEGs in patients whose infantile spasms were thought to have a prenatal cause were normal or had focal spikes. These were occasionally followed by multifocal abnormalities before progressing to hypsarrhythmia. Among those with a perinatal central nervous system insult, the initial EEGs showed either a burst-suppression pattern (Ohtahara syndrome) or very low voltage activity. Follow-up EEGs before the development of hypsarrhythmia sequentially showed normal or near-normal activity, then focal or multifocal abnormality, and then hypsarrhythmia. For the group with a postnatal central nervous system event, the sequence was excess slow waves at the time of the insult; a subsequent EEG that was normal, slightly abnormal, or focally abnormal; and then hypsarrhythmia. Ohtahara (1978) described a syndrome of intractable tonic seizures beginning in the first few months of life with a burst-suppression EEG pattern. This often evolves to West syndrome. Cognitive impairment usually accompanies this syndrome.

As hypsarrhythmia resolves, the amplitude of its components declines and the spikes may become less multifocal and more synchronous (Hrachovy et al., 1984). This evolution to SSWs may occur at age 2 to 4 years. Jeavons et al. (1970) studied 68 patients at age 5 years or older who earlier had epileptic spasms: 34 had normal EEGs, 31 had focal or other abnormalities, and 3 continued with hypsarrhythmia.

Unfortunately, the role of EEG to assist in the diagnosis of epileptic spasms is limited. No aspect of the interictal or ictal pattern reliably correlates with etiology and course, prognosis for seizure relief, or mental evolution (Hoeffer et al., 1963; Jeavons et al., 1973). However, hypsarrhythmia and infantile spasms may reflect pyridoxine dependency. Therefore, if the etiology remains unclear, an infusion of 50 to 100 mg of pyridoxine intravenously during EEG monitoring would establish that diagnosis if the EEG and seizure quantity prominently improved within minutes (Holmes & Stafstrom, 1998).

Eeg Changes During Seizures

An EEG-recorded, clinically typical seizure would provide the best diagnostic confirmation of a seizure disorder and its classification (focal, generalized, or secondarily generalized).


A focal epileptic seizure consists of repetitive activity from one region that is dissimilar to its background rhythms and is not simply due to a change in state (Blume et al., 1984). The morphology of this sustained activity may be sequential spikes or sinusoidal waves. Such phenomena evolve, as progressive changes in morphology and/or frequency appear in almost all clinically apparent seizures. Thus, sinusoidal waves may evolve to repetitive spikes, or the reverse may occur. As the attack evolves, the repetition rate of its component phenomena may increase, decrease, or increase in some areas while decreasing in others. This evolution can help distinguish focal seizures electrographically from sequential, sharply contoured, clinically innocent phenomena such as psychomotor variant or subclinical rhythmic electrographic discharges in adults (SREDA) (Westmoreland, 1990). Unfortunately the morphology and sequencing of ictal phenomena can be bizarre, irregular, and slower when a diffuse encephalopathy is present.


In some instances, an electrographic seizure is manifested simply as sequential interictal potentials, such as a series of 3 Hz spike–wave discharges with absence attacks. Given the usual abundance of SSW discharges, it is sometimes difficult to determine whether the patient is having an atypical absence attack. Rhythmic waves of 10 to 20 Hz appearing diffusely may have absence or tonic seizures as the clinical correlate. Generalized myoclonic seizures have high-voltage diffuse, bilaterally synchronous spike–waves as the clinical correlate, even though the precise timing relationship between the EEG spike and the myoclonic jerk varies between patients and even in the same patient over time. Tonic–clonic (grand mal) seizures combine many of the aforementioned EEG features: very low-voltage high-frequency waves, 10 to 20 Hz rhythmic waves, or both appear during the tonic phase. These waves then are interrupted by 300 to 400 ms bilaterally synchronous slow waves to constitute polyspike–wave discharges during the clonic phase. The ictal


phase of infantile spasms and hypsarrhythmia has been described (see Gastaut and Broughton [1972] for a full discussion of these ictal EEG–clinical relationships).

Secondarily generalized seizures would combine one or more features of focal and generalized icti.

Focal Epileptiform Phenomena

Focal Spikes (Figs. 4-1.1 to 4-1.80)

  • Apiculate waveforms.
  • Clearly distinguished from juxtaposition of two or more normal background frequencies.
  • Interrupt background activity.
  • Have more than one phase with an abrupt change in polarity.
  • Largest phase usually electronegative.
  • Asymmetrical slopes.
  • Involve more than one electrode position but with a physiological field, that is, appropriate voltage gradients across scalp.
  • 70- to 200-ms slow wave.

“Rolandic” Spikes (Figs. 4-1.1134-1.1620)

  • High voltage at C3 or C4 using the 10–20 system.
  • Involve principally lower rolandic area (C5,6) using closely spaced electrodes.
  • Marked downward deflection at F3–C3 or F4–C4 suggests dipole.
  • Principal parasagittal spread of negative component usually parietal, occasionally frontal.
  • Abundant and stereotyped.
  • Unilateral, bilaterally independent, and/or bilaterally synchronous.
  • Background normal when spikes absent.
  • May increase or appear only in sleep.

Rolandic-like Spikes in Other Locations (Figs. 4-1.144-1.15, and 4-1.18)

  • Parietal, parietal–central sagittal, posterior temporal, or occipital.
  • Complex field possible.
  • Bilateral synchrony may occur.

Frontal Spikes (Figs. 4-1.21 to 4-1.42)

  • Usually electronegative.
  • Occasionally widespread.
  • Field may extend bilaterally.
  • May require periocular electrodes to distinguish from eye movement potentials.

Occipital Spikes (Figs. 4-1.43 to 4-1.56)

  • Electronegative.
  • Eyes closed.
  • Involve 01, 02, T5, T6.
  • May require ECG monitor for identification.
  • With or without loss of background (alpha).

Temporal Spikes (Figs. 4-1.57 to 4-1.78)

  • Major phase electronegative.
  • Involve principally mandibular notch (Ml,2), TI,2, A1,2, F7,8, T3,4 electrode positions.
  • Occasional involvement of homologous contralateral and frontopolar (FPl,2) regions.
  • Sharply defined field, steep voltage gradients, inferolateral maximum; or broader field, gradual gradient, greater suprasylvian extension.
  • Interspike variations in field common.
  • Associated with ipsilateral temporal delta and/or excess temporal theta.

Polyspikes (Figs. 4-1.53 to 4-1.564-1.67 to 4-1.68)

  • More apiculate than beta.
  • Onset and offset abrupt.
  • Delta waves may follow.

Multifocal Spikes (Figs. 4-1.79 and 4-1.80)

  • Three or more spike foci with at least one in each hemisphere.
  • Seizures in >90%.
  • Generalized tonic–clonic most common.
  • Many have more than one type of seizure.
  • Daily seizures common.



Generalized Epileptiform Phenomena

Generalized Spike–Wave and Polyspike–Wave Complexes (Figs. 4-2.1 to 4-2.84-2.10 to 4-2.254-2.28 to 4-2.35)

  • Bilaterally synchronous spike–wave complexes with repetition rate of 2.5 to 4 Hz.
  • Consist of spike, trough, and wave.
  • Bursts begin and end abruptly.
  • Repetition rate slows during long paroxysms.
  • Maximum amplitude usually at F3, F4; occasionally posterior (P3,4; O1,2).
  • Variable anterior–posterior extension.
  • May be maximally or exclusively expressed in one hemisphere; such asymmetry shifts.
  • Gradation between “generalized” and “focal” spike–waves occasionally occurs.
  • Incomplete forms are common.
  • In sleep, repetition rate slower, less regular.

Slow Spike–Wave (SSW) Complexes (Figs. 4-2.36 to 4-2.39)

  • Bilaterally synchronous sinusoidal waves, each accompanied by spike and trough forming a complex.
  • Repetition rate <2.5 per second.
  • Onset and offset less abrupt than spike–waves.
  • Occupy high percentage of recording.
  • Often no discernible clinical alteration in association.
  • Associated with a slow background.

6 Hz Spike–Waves (Figs. 4-2.26 and 4-2.27)

  • 5 to 7 Hz.
  • Diffuse, posterior- or anterior-accentuated.
  • Spike component is small, brief.
  • Morphology of anterior-predominant form merges with 3 Hz spike–waves; possibly more epileptogenic than posterior 6 Hz spike–waves.

Fast Rhythmic Waves and Polyspikes (Figs. 4-2.94-2.40 to 4-2.454-2.53 to 4-2.58)

  • Burst of rhythmic waves and/or sequential spikes repeating at 8 to 30 Hz.
  • Generalized, maximum frontally.
  • 40 to 350 µV.
  • Duration 1 to 8 s.
  • Tonic seizures or absence in association.
  • May occur on eye closure.

Hypsarrhythmia (Figs. 4-2.46 to 4-2.52)

  • Continuous (while awake) high-voltage, 1 to 3 Hz waves with multifocal asynchronous spikes.
  • Discontinuous in sleep.
  • Electrodecremental event (EDE): sudden attenuation of activity with or without low-voltage, high-frequency waves. Accompanied by infantile spasm, tonic seizure, or no discernible change.

PLEDs and Hemispheric Spikes (Figs. 4-2.58 to 4-2.62)

  • Widely distributed epileptiform discharges.
  • A “bridge” between focal and generalized phenomena.

Photoparoxysmal Response (Figs. 4-2.63 to 4-2.74)

  • Polyspikes, spike–waves.
  • Spike repetition rate varies within burst and is unrelated to flash rate.
  • May extend beyond flash stimuli.
  • Diffuse with anterior or posterior maximal expression.
  • Best depicted by combined ear reference and bipolar parasagittal montage.
  • Eye closure and eyes closed most easily elicit spike–waves.
  • Most frequently induced by 15 flashes per second with eyes closed, 20 per second with eyes open.
  • Threshold lowers with repeated flash stimuli.
  • Eye closure without flash may precipitate spike–waves in photic-sensitive patients.
  • Epileptiform response to single flash suggests progressive myoclonic epilepsy.

Photomyogenic (Photomyoclonic) Response (Figs. 4-2.75 and 4-2.76)

  • Muscle potentials from facial muscle contractions, principally orbicularis oculi and frontalis.
  • 50 ms latency.



  • Principally with eyes closed.
  • Increases gradually as flash continues; stops with flash.
  • May coexist with photoparoxysmal response.


Periodic Lateralized Epileptiform Discharges (PLEDs) (Figs. 4-3.14-3.24-3.4, and 4-3.5)

  • Diphasic or polyphasic spikes.
  • Usually electronegative.
  • Slow wave follows spike.
  • Duration of each complex about 200 to 500 ms.
  • Hemispheric or regional; not confined to single electrode position.
  • Recur every 0.5 to 2 s.
  • Abnormal background in area of PLEDs.
  • Acute or subacute cerebral process.
  • Synchronous contralateral myoclonic jerks in minority.

PLEDs Plus (Fig. 4-3.3)

Low-amplitude rhythmic, high-frequency discharge superimposed upon conventional PLEDs, usually the second slope.

BIPLEDs (Fig. 4-3.6))

Bilateral, asynchronous PLEDs.

Focal (Partial) Seizures (Figs. 4-3.7 to 4-3.55)

  • A new and sustained focal or regional phenomenon that cannot be ascribed to a change in state of alertness or to artifact.
  • Manifested by:
  1. Rhythmic waves from 2 to 40 Hz
  2. Sequential spikes
  3. Electrodecremental events
  • Gradual modification of morphology and/or frequency as seizure progresses.
  • Gradual spread to contiguous and/or homologous regions as seizure progresses.

Generalized Seizures (Figs. 4-3.56 to 4-3.72)

  • Bilaterally synchronous sequential spike–waves, spikes, or rhythmic waves.
  • Higher-frequency phenomena (fast rhythmic waves, polyspikes) usually appear earlier in the seizure than lower-frequency ones (spike–waves, rhythmic delta).
  • Usually an abrupt nonfocal onset and offset.

Non Epileptic Events (Figs. 4-3.73 to 4-3.79)

  • SREDA, rhythmic mid temporal discharges, non cerebral events.
  • Non evolving rhythmic phenomena.
  • Normal.

Fig. 4-1.1. “Rolandic spikes”. Patient's age, 9 years. Awake. The most characteristic feature of rolandic spikes is the prominent downward deflection in the superior frontal–central derivation (F4–C4 in this case). The morphology is characteristically triphasic, the most prominent phase being the second; however, note the variability. Almost equally characteristic in certain patients is the relatively minimal deflection in the central–parietal derivation (C4–P4 here); its peak usually is earlier than that of the frontal–central derivation. When these spikes are abundant, the associated background activity is slowed, but this usually returns to normal when spikes are absent, as in the last 2 s of this segment. Calibration signal 1 s, 100 µV.


Fig. 4-1.2. Central–temporal (rolandic) spikes. Patient's age, 11 years. Drowsy. Eyes closed. The striking downward deflection at F3–C3 derivation indicates bridging of an electropositive FP1–F3 field with an electronegative C3–P3 field parasagittally representing a radially orientated dipole. However, this dipole is not evident in the temporal run, which suggests a more vertically orientated dipole, negative at T3. Calibration signal 1 s, 150 µV.


Fig. 4-1.3. “Rolandic spikes” on coronal montage. Same illustration as previous. Having established that the left hemisphere is involved (and not the right), the coronal montage depicts the spike field more precisely and confirms the principally T3 involvement with considerable spread. Calibration signal 1 s, 150 µV.


Fig. 4-1.4. Mu rhythm resembling rolandic spikes. Patient's age, 10 years. Awake. When mu rhythm becomes very sharply contoured, it can resemble rolandic spikes to an extent that confident distinction is not always possible, as in this instance. The presence of a similar morphology in the derivations F4–C4 and C4–P4, and the fact that this mu rhythm exhibits all degrees of sharpness, suggest that all of these phenomena may be mu (*). Eyes closed. Calibration signal 1 s, 100 µV.


Fig. 4-1.5. V waves and right central spikes. Patient's age, 7 years. Sleep. Although apiculate, the V waves at CZ can be easily distinguished from the more brief right central (C4) spikes. Calibration signal 1 s, 150 µV.


Fig. 4-1.6. Parasagittal hints and sagittal surprise. Patient's age, 21 years. Awake. Eyes closed. This anterior–posterior bipolar montage only hints at epileptiform discharges centrally within the first 4 s. This obligate coronal montage clearly solves the riddle posed by the parasagittal portion as abundant CZ, PZ spikes appear. Calibration signal 1 s, 100 µV.


Fig. 4-1.7. Rolandic spikes. Patient's age, 5 years. Sleep. Although occurring moderately frequently, rolandic spikes can be hidden partially by normal sleep potentials. Distinction of the left rolandic spikes from the right-sided V waves is not difficult in this instance. A left-sided V wave appears in the next-to-last second. Calibration signal 1 s, 150 µV.


Figs. 4-1.8 and 4-1.9. Rolandic spikes. Patient's age, 9 years. Drowsy. This 16-channel recording has been divided into the two 8-channel sections shown in this and the following illustration. The first section suggests that the electronegative phase of this spike is primarily at T4 with principal spread to F8. However, the interhemispheric derivations (F7–F8, T3–T4) do not confirm this. It is possible that the prominent deflections at F4–F8 are due to electropositivity at F4. The low-amplitude upward deflections in channels 2 and 3 of the first illustration occurring synchronously with the downward deflections in channels 4 and 8 support this interpretation. Note the moderate electronegativity at T6 and the slight electronegativity at A2. Calibration signal 1 s, 70 µV.


Fig. 4-1.9. Rolandic spikes (continued). Patient's age, 9 years. Drowsy. This 16-channel recording has been divided into two 8-channel sections shown in this and the previous illustration. The first section suggests that the electronegative phase of this spike is primarily at T4 with principal spread to F8. However, the interhemispheric derivations (F7–F8, T3–T4) do not confirm this. It is possible that the prominent deflections at F4–F8 are due to electropositivity at F4. The low-amplitude upward deflections in channels 2 and 3 of the first illustration occurring synchronously with the downward deflections in channels 4 and 8 support this interpretation. Note the moderate electronegativity at T6 and the slight electronegativity at A2. Calibration signal 1 s, 70 µV.


Fig. 4-1.10. Rolandic spikes. Patient's age, 9 years. Same patient, same degree of drowsiness. The downward deflection in most even-numbered channels, together with data from the previous segments, suggests that A2 is slightly electronegative. The upward deflection in the bottom channel indicates strong electronegativity at T4. The possibility of a dipole is suggested by the prominent downward deflections in channels 4 and 2–i.e., possible electropositivity at F4 and FP2. Calibration signal 1 s, 70 µV.


Fig. 4-1.11. Rolandic spikes: referential and bipolar montage. Patient's age, 9 years. Sleep. Further analysis of these right rolandic spikes is afforded by combining a right-sided bipolar montage with a reference of the right-sided leads to the inactive left ear (A1). This shows prominent electronegativity at T4 with moderate spread to T6, and simultaneous electropositivity at F4 with minimal spread to FP2. This “dipole” explains the prominent downward deflection in the derivation F4–C4. Scrutiny of the left part of the segment suggests the possibility of a field moving in an anterior–posterior direction as the electropositivity at F4 and FP2 is preceded by brief electronegativity. Calibration signal 1 s, 100 µV.


Fig. 4-1.12. Rolandic spikes. Patient's age, 10 years. Awake. This referential recording demonstrates the almost simultaneous electronegativity of the principal component of such spikes in the left central–parietal (C3,P3) region with electropositivity bifrontally. This otherwise neurologically normal boy felt episodes of tingling around his mouth and drooling. Both clinical and electrographic features may represent benign rolandic epilepsy of childhood. Calibration signal 1 s, 100 µV.


Fig. 4-1.13. Rolandic spikes: Independent and bisynchronous. Patient's age, 3 years. Sleep. The rolandic spikes in this illustration occur either independently on each side or bisynchronously to create the appearance of a generalized spike wave. Sleep may have enhanced such bisynchrony. These spikes are electronegative in the superior frontal regions as well as at C3 and C4. Calibration signal 1 s, 150 µV.


Fig. 4-1.14. Left parietal spikes. Patient's age, 5 years. Awake. Spikes of similar morphology to rolandic spikes may appear in the parietal region. Calibration signal 1 s, 70 µV.


Fig. 4-1.15. Left parietal spikes. Patient's age, 5 years. Drowsy. Spikes similar to those on Figure 4-1.14 as seen on a coronal montage, with moderate spread to C3. Calibration 1 s, 100 µV.


Fig. 4-1.16. Right central spikes. Patient's age, 5 years. Awake. Two aspects of this recording suggest that these right central (C4) spikes do not represent benign rolandic spikes: (a) the relatively prominent deflections in the right central parietal (C4–P4) derivation, and (b) the excess right central parietal (C4–P4) delta and theta with a marked diminution of right-sided alpha. Calibration signal 1 s, 100 µV.


Fig. 4-1.17. Central temporal (rolandic) spikes. Patient's age, 3 years. Drowsy. The prominent downward principal deflection of these spikes indicates that they straddle a positive field (FP2–F4–F8) and a negative field (C4–P4–T6) and, therefore, occupy a wall of the central gyrus. Various quantities of delta activity may accompany these spikes without necessarily reflecting a lesion. In this instance, they may be a postictal phenomenon, as the child had a focal seizure 2 days prior to the recording. Calibration signal 1 s, 150 µV.


Fig. 4-1.18. Right central–parietal spikes. Patient's age, 3 years. Awake. Eyes open. The great abundance and morphology of these spikes resemble characteristics of benign “rolandic” spikes. However, the lack of an apparent dipole may suggest a right central–parietal lesion. The regularly repetitive nature of these abundant spikes suggests that the lesion may represent cortical dysplasia. In this patient, these spikes would not augment the likelihood that his staring spells represent seizures, as left sensory motor phenomena never occurred. Calibration signal 1 s, 100 µV.


Fig. 4-1.19. V-waves and right central spikes. Patient's age, 5 years. V waves, seen principally in the central–sagittal (CZ) region, contrast in morphology and location with the right central C4 spikes. Calibration signal 1 s, 150 µV.


Fig. 4-1.20. Right central spikes in drowsiness. Patient's age, 5 years. Right central (C4,F4) spikes appearing after a theta burst in drowsiness on this referential montage. Lack of any hint of a dipole suggests that these spikes represent a lesion. Calibration signal 1 s, 100 µV.


Fig. 4-1.21. Right frontal spikes. Patient's age, 8 years. Drowsy. The most prominent spikes occur in an electronegative fashion in the right frontal (FP2–F4) electrodes, as the negative F4 deflects upward to the right central (C4) electrode, while almost complete cancellation occurs between the frontal leads (FP2,F4). Note the moderate homologous spread. The prominent upward deflection of the spikes of F4–C4 derivation distinguishes them from benign rolandic discharges. Proof that these spikes of the bipolar montage arose from the right frontal (FP2,F4) region is afforded by the simultaneously recorded ear reference montage, in which the right ear (A2) is uninvolved. Calibration signal 1 s, 300 µV.


Fig. 4-1.22. Right frontal spikes. Patient's age, 11 years. Awake. F4 spikes occur repetitively. Their restricted right hemisphere spike field without obvious dipole suggests they are lesion-based. Calibration signal 1 s, 100 µV.


Fig. 4-1.23. Right frontal spikes. Patient's age, 8 years. Awake. Right superior frontal (F4) spikes are well depicted in both the bipolar and referential components of this montage. Calibration signal 1 s, 70 µV.


Fig. 4-1.24. Right frontal central spikes and ECG. Patient's age, 11 years. Drowsy. The regularly recurring right frontal central (F4,C4) spikes are clearly distinguished from ECG artifact by the accompanying monitor. Note the 14 and 6 per-second positive spikes at the right occipital parietal (O2,P4) region in the center of the segment. This patient is recovering from the Landau–Kleffner syndrome. Calibration signal 1 s, 100 µV.


Fig. 4-1.25. Sagittal spikes hidden from anterior–posterior montage. Patient's age, 24 years. Awake. Eyes closed. The parasagittal anterior–posterior montage (lower eight channels) discloses only a mixture of theta and delta activity at F4, with only a hint of epileptiform discharges at FP2–F4. These become astonishingly prominent on the coronal montage (top eight channels). Calibration signal 1 s, 70 µV.


Fig. 4-1.26. Sequential right frontal broad spikes (sharp waves). Patient's age, 63 years. Drowsy. These sequential right frontal spikes have a variable field. Although some of the later discharges are clearly electropositive at F4, the first definitive discharge (*) does not demonstrate a reversal of each phase, raising the possibility of a rapidly propagating focus from F4 to FP2 (in a manner similar to the occipital–frontal lag of triphasic waves). Spikes later in the sequence extend more posteriorly to engulf the entire right hemisphere. Involvement of the homologous regions on the left occurs commonly with frontal spikes; therefore the apiculate deflections at FP1 do not indicate an additional focus there. The left hemispheric delta appears only when that of the right hemisphere is of high voltage; therefore no definitely independent left hemisphere abnormality is demonstrated. A left ear reference montage or the common average reference (CAR) would depict the spike field better than this bipolar montage. Calibration signal 1 s, 100 µV.


Fig. 4-1.27. Right frontal spikes and right hemispheric delta. Patient's age, 63 years. Awake. Eyes closed. More than one type of epileptiform discharge appears in the right frontal region. The most frequent are electropositive broad spikes at FP2–F4. Electronegative spikes, at FP2 (*), are occasionally superimposed upon such electropositive spikes. The diffuse right-sided delta activity and the loss of right-sided alpha activity reflect widespread right hemisphere dysfunction. Although some of these broad spikes have a triphasic contour, these are not “triphasic waves” because of their unilateral (right) predominance with a normal awake background activity in the left hemisphere. The low-voltage left frontal delta likely reflects spread from the frontally accentuated right delta, as each wave on the left has a counterpart on the right. Calibration signal 1 s, 70 µV.


Fig. 4-1.28. Right frontal PLEDs and muscle. Patient's age, 67 years. Confused. With the high frequency filter (HFF) at 70 Hz (top eight channels), muscle artifact only partially obscures these repetitive discharges, which are moderately clarified by lowering the HFF filter to 15 Hz (bottom eight channels). Calibration signal 1 s, 100 µV.


Fig. 4-1.29. Right frontal “periodic” spikes. Patient's age, 13 years. Awake. Eyes open. Regularly repeating phenomena almost always represent an evolving central nervous system process as diverse as rapid dementia or a postictal phenomenon, as in this adolescent. The high-frequency, left hemisphere (maximum F3–FP1) rhythmic bursts are polyspikes. Muscle activity would produce less rhythmic and less discrete potentials. Calibration signal 1 s, 200 µV.


Fig. 4-1.30. Right frontal spikes. Right frontal polar, inferior frontal (FP2, F8) spikes are depicted on this bipolar montage. Prominent deflection in the F8–T4 derivation would be unusual with an anterior temporal spike, where cancellation in that derivation would have occurred. Calibration signal 1 s, 50 µV.


Fig. 4-1.31. Frontal spikes with common average reference (CAR). CAR depiction of spikes of the previous illustration demonstrates the principal inferior frontal (F8) involvement with spread to the right frontal polar region (FP2) and only minimal temporal (T4) spread. This confirms that the F8 position can represent inferior frontal as well as anterior temporal phenomena. Calibration signal 1 s, 50 µV.


Fig. 4-1.32. Prominent right frontal spikes and delta. Patient's age, 41 years. There should be little difficulty in identifying the right frontal polar (FP2) location of both the spikes and the delta activity, although the spikes spread more to the right superior frontal–region (F4) than does the delta. Note the 15 Hz breach rhythm at the C4–P4 and T4–T6 derivations. The second (right) segment illustrates the distinct bifrontal polar (FP1, FP2) electropositive deflection of eye movements and the initial electronegative deflection of the FP2 spike. Calibration signal 1 s, 50 µV.


Fig. 4-1.33. Frontal polar spikes. Patient's age, 14 years. Awake. The greater amplitude of the spikes and delta on the right suggests an FP2 origin with spread to FP1. Calibration signal 1 s, 100 µV.


Fig. 4-1.34. Three varieties of ocular flutter. Samples from three alert patients. Even without methods to reduce eye movement such as passive eye closure, eye opening or sleep and without infraorbital leads, one can distinguish this artifact from frontal delta-theta activity by the consistently identical morphologies at FP1 and FP2. Calibration signal 1 s, 70 µV.


Fig. 4-1.35. Bifrontal polar electropositive spikes. Patient's age, 76 years. Both the polarity and the morphology of these discharges resemble eye blinks, but the only eye movements in this recording during drowsiness are slow lateral eye movements, as seen in the F7, F8 derivations in the second to fourth seconds. Note the slightly earlier appearance of the spikes at FP2 than at FP1. The triphasic contour of some of these discharges would be distinctly unusual for eye blinks, as the initial negative component does not occur with eye blinks. Calibration signal 1 s, 70 µV.


Fig. 4-1.36. Bifrontal spikes, maximum right, with triphasic morphology. Patient's age, 63 years. Although these sequential primarily electropositive bifrontal polar (FP2, FP1) broad spikes resemble triphasic waves in their anterior location and morphology, their asymmetry and the normal left hemispheric background activity indicates that they are not triphasic waves. Eyeblinks (*) are distinguished by their location and morphology. Compare with Fig. 4-1.35. Calibration signal 1 s, 100 µV.


Fig. 4-1.37. Sequential right frontal spikes extending to infraorbital region. Although used to monitor extraocular movements, infraorbital leads may record potentials involving the anterior frontal regions. These derivations suggest a dipole with principal negativity at the right superior frontal region (F4) and principal positivity at the right frontal polar region (FP2, IOR). A referential recording would clarify this further. IOL, infraorbital left; IOR, infraorbital right. Calibration signal 1 s, 50 µV.


Fig. 4-1.38. Right frontal polar spikes with spread. Patient's age, 50 years. Awake. Eyes closed. As commonly occurs, these right frontal polar (FP2) spikes with accompanying delta spread moderately to the left frontal polar area but, on this occasion, moderately to the right anterior midtemporal region as well. Note the totally normal alpha activity bilaterally. Calibration signal 1 s, 100 µV.


Fig. 4-1.39. K complex and right frontal polar spikes. Patient's age, 6 years. Sleep. Do not let these classical sleep potentials (V waves and spindles) distract you from the clinically relevant right frontal spikes. Calibration signal 1 s, 150 µV.


Fig. 4-1.40. Low-voltage right frontal polar spikes. Patient's age, 23 years. Usually, low-amplitude, very brief spike-like forms in the frontal–polar leads are periocular muscle potentials. However, these (*) indicate right frontal polar (FP2) spikes. This should be suspected because of their spread to F4, as revealed by the F4–C4 derivation. These spikes did not propagate to FP1, as revealed by the FP1–F7 derivation, nor did they propagate to F3 (not shown). Calibration signal 1 s, 50 µV.


Fig. 4-1.41. Right frontal–polar spikes. Patient's age, 23 years. Same patient as in Fig. 4-1.40. The amplitude and field of these spikes increase in drowsiness, and the accompanying slow waves become considerably more prominent. Some propagation to the left frontal region (FP1, F7) is seen. Calibration signal 1 s, 70 µV.


Fig. 4-1.42. Frontal–polar spikes on an anterior coronal montage. Patient's age, 23 years. Same patient as in Figs. 4-1.40 and 4-1.41. This montage clearly depicts these spikes and their field as occurring in the right frontal polar region (FP2), with slight spread to the right inferior frontal region (F8) and the left frontal–polar region (FP1). Note the value of an ECG monitor as provided by the ear leads (A2–A1) in distinguishing these spikes, of nearly metronomic repetition, from cardiac potentials. Calibration signal 1 s, 70 µV.


Fig. 4-1.43. Right parietal–occipital polyspikes. Patient's age, 63 years. Awake. Diffuse abnormalities such as the right hemisphere–accentuated delta may partially obscure lower-amplitude focal abnormalities such as these right parietal (P4, O2) polyspikes (asterisks). Calibration signal 1 s, 50 µV.


Fig. 4-1.44. Right occipital spikes. Patient's age, 48 years. Awake. Eyes closed. These bisynchronous occipital spikes very principally involve the right occipital region (O2) as evidenced by greater propagation within the right hemisphere and the slower right posterior head background activity. Note the value of ECG in indicating that all these sharply contoured potentials are occipital spikes and not ECG “contamination.” Calibration signal 1 s, 150 µV.


Fig. 4-1.45. Occipital coronal montage. Same spikes as in the previous illustration. The coronal montage confirms O2 as the focus of these spikes, with rare, almost equal involvement of T6. Calibration signal 1 s, 150 µV.


Fig. 4-1.46. Right occipital spikes. Patient's age, 2 years. Light sleep. The degree of anterior (to P4) and contralateral spread of occipital spikes is variable but can be enhanced by sleep or hyperventilation. Calibration signal 1 s, 100 µV.


Fig. 4-1.47. Left occipital spike with alpha reduction. Patient's age, 7 years. Awake. That this left occipital (O1) spike represents a lesion is suggested by the lower alpha activity in the left occipital (O1) region as compared with the right (O2) and the greater delta activity in the left occipital parietal (P3) region. Calibration signal 1 s, 100 µV.


Fig. 4-1.48. Left occipital spikes and artifact. Patient's age, 2 years. Awake. The distinctive form of occipital spikes occasionally permits their identification in the midst of considerable artifact. Passive eye closure (c). Calibration signal 1 s, 100 µV.


Fig. 4-1.49. Bioccipital spikes. Patient's age, 3 years. Sleep. These have been termed “needle-like spikes of the blind” in that children with visual impairment from birth may have these without epilepsy (Smith & Kellaway, 1964). Note the brevity of these discharges, giving a superficial appearance of artifact. The following aspects indicate that they are indeed epileptiform potentials: (1) the spread to P3,P4, (2) the stereotypical waveform, and (3) the lack of other evidence of artifact. The posterior accentuated delta in sleep is a normal phenomenon at this age. Calibration signal 1 s, 100 µV (top 8 channels); 1 s, 150 µV (bottom 8 channels).


Fig. 4-1.50. Diffuse attenuation and artifact-like left occipital spikes. Patient's age, 15 months. Awake. Eyes open. The principal feature is a paucity of cerebral rhythms diffusely, whereas at this age, with eyes open, theta and delta should appear abundantly. Distinguishing the apiculate O1 waves between artifact and spikes could not be made without evidence that additional electrode positions are involved. Calibration signal 1 s, 50 µV.


Fig. 4-1.51. Diffuse attenuation and artifact-like left occipital spikes. Patient's age, 15 months. Awake. Same patient as previous illustration (Fig. 4-2.50). Awake. Eyes open. Involvement of OZ and neighboring electrodes confirms that these apiculate waves are epileptiform activity involving a small region. Thus, adjacent ten-twenty electrode positions (p3, T5) are only minimally involved. Note the addition of the electrodes (PO3, PO7 and OZ) outside of the ten-twenty system in bold. Calibration signal 1 s, 50 µV.


Fig. 4-1.52. Sequential right occipital broad spikes. Patient's age, 12 years. Awake. Eyes closed. Although they resemble V waves in morphology, their location identifies them as focal epileptiform discharges involving principally O2 with spread to T6 and slight spread to A2. A2 involvement (negative) is more likely than a dipole with F4–FP2 positivity. Calibration signal 1 s, 100 µV.


Fig. 4-1.53. Occipital spikes and polyspikes in sleep. Patient's age, 15 years. Abundant occipital spikes and polyspikes may appear only in non-REM sleep, as seen in the left occipital (O1) region. Note the slight spread to the left posterior temporal (T5) region and minimal spread to the left parietal (P3) and right occipital (O2) areas. Calibration signal 1 s, 100 µV.


Fig. 4-1.54. Posterior polyspikes. Patient's age, 6 years. Awake. Eye closure (*) precipitates left occipital (O1) polyspikes with spread to O2. Occipital spikes occur far more frequently with eye closed or with eye closure. Calibration signal 1 s, 70 µV.


Fig. 4-1.55. Left occipital polyspikes. Patient's age, 55 years. Confused. Occipital epilepsies frequently produce polyspike discharges in sleep, as in this segment. Their bizarre appearance may superficially suggest artifact, but their consistent propagation to T5–P3 indicates their genuine nature. Calibration signal 1 s, 100 µV.


Fig. 4-1.56. Left occipital polyspikes, left occipital–temporal attenuation. Patient's age, 55 years. Confused. In addition to the bizarre-appearing O1 polyspikes, a paucity of background activity is present at O1–T3. Calibration signal 1 s, 100 µV.


Fig. 4-1.57. Combined coronal and anterior–posterior bipolar montage illustrates temporal spikes. Patient's age, 38 years. The location of these frequent left temporal electronegative spikes is well depicted at M1 (left mandibular notch), T3, and F7 by this combined montage. The mandibular notch electrodes are placed 2.5 cm anterior to the tragus of the ear and immediately inferior to the zygoma (Sadler & Goodwin, 1989). Calibration signal 1 s, 200 µV.


Fig. 4-1.58. Right anterior mesial temporal spikes on common average reference montage. Patient's age, 35 years. A common average reference (CAR) clearly depicts the anterior mesial–temporal distribution of spikes with lesions in this region, such as mesial temporal sclerosis. In this instance, spikes appear principally at the right anterior mesial temporal (F8, M2) positions with moderate spread to the right midtemporal region (T4). Such spikes in some patients appear principally at M2 and T4 with relatively less involvement of F8. The right posterior temporal region may sporadically become involved. Note the minimal involvement of homotopic regions. Calibration signal 1 s, 30 µV.


Fig. 4-1.59. Right anterior–mesial temporal spikes and delta. Patient's age, 41 years. Awake. Eyes closed. Both the spikes and delta appear very principally at F8–T4, accounting for the relative cancellation of potentials in the 14th channel. However, the anterior–mesial temporal field extends below the 10–20 electrode placement system, thus requiring mandibular-notch electrodes for their complete depiction. Calibration signal 1 s, 150 µV.


Fig. 4-1.60. Anterior–mesial temporal spikes on standard coronal montage. Same epoch as in the previous illustration. Electronegative spikes appear almost equally at F8–T4–A2, as does the delta activity. Calibration signal 1 s, 150 µV.


Fig. 4-1.61. Anterior–mesial temporal spikes on an anterior frontal polar–central coronal montage. Same epoch as in the two previous illustrations. This montage helps to distinguish temporal spikes from frontal polar and inferior frontal ones. Note the principal involvement of F8–A2–T4. Calibration signal 1 s, 150 µV.


Fig. 4-1.62. Temporal spike with abnormal background. Patient's age, 63 years. Abnormal temporal spikes are accompanied by focal background abnormalities. Hyperventilation here elicited 3 to 5 Hz low to medium-voltage waves in the left anterior–midtemporal region (F7–T3) and rare low-voltage delta activity in the same area. Note the normal right temporal background activity; the only alteration is a mild fluctuation of its amplitude and some slow eye movements. Calibration signal 1 s, 50 µV.


Fig. 4-1.63. Left temporal spikes and theta with skull defect. Patient's age, 24 years. Skull defects are commonly associated with sharply contoured waveforms, creating difficulties in identifying spikes. The negative potentials of nonepileptiform rhythmic waves at skull defects are commonly sharply contoured, as seen here. However, two of these apiculate wave forms (*) clearly have steeper slopes and therefore sharper apices than the accompanying theta and can be identified as spikes. Calibration signal 1 s, 100 µV.


Fig. 4-1.64. Ultra-apiculate breach rhythm. Patient's age, 56 years. Awake. Eyes closed. The “seamless” range of sharpness of the T6 potentials could be interpreted as only a breach rhythm or a breach rhythm with intermingled spikes. The solution would be a sleep recording to eliminate the contribution of posterior alpha activity in creating the apiculate waveforms. The right central–parietal delta activity and spikes is unusual after posterior temporal lobectomy and may reflect a breach rhythm or a larger focality of this patient's cortical dysplasia. Calibration signal 1 s, 150 µV.


Fig. 4-1.65. Small sharp spike while awake with a burst of lateralized delta. Patient's age, 32 years. This normal phenomenon, which traditionally belongs to one state (light sleep), may appear in another. This widely distributed discharge (*) more resembles a small sharp spike than any other apiculate phenomenon. No “phase reversal” appears. Note its expression in most derivations. Its relationship to the burst of 1 Hz delta activity is not clear. The subsequent page illustrates other small sharp spikes to distinguish them from anterior temporal ones. Calibration 1 s, 50 µV.


Fig. 4-1.66. Small sharp spikes. Patient's age, 32 years. The small sharp spike (SSS), a normal phenomenon of light sleep, is briefer than most abnormal anterior–temporal spikes; it has steep slopes, a relatively brief aftercoming slow wave, and a particularly wide field. This latter attribute is particularly well displayed by coronal montages, as seen here, as the spike extends to the central, parietal, and frontal regions and well into the hemisphere contralateral to that of its principal expression. Calibration 1 s, 50 µV.


Fig. 4-1.67. Left temporal polyspikes on combined coronal and anterior–posterior bipolar montage. Patient's age, 40 years. Polyspikes may be slightly more difficult to recognize than single spikes, as they do not emerge as starkly from the background activity. These appear principally in the left midtemporal (T3) region with contiguous spread to the left anterior–inferior temporal area (F7, M1 [left mandibular notch]). Calibration signal 1 s, 70 µV.


Fig. 4-1.68. Left temporal polyspikes. Patient's age, 37 years. Polyspikes may escape detection by the electroencephalographer because they blend more with the background rhythms than do single spikes, and no aftercoming slow waves may occur. These polyspikes (*), appearing in light to moderate sleep, are progressively more difficult to detect going from the top tracing to the lower ones. The asterisks signify the center of each polyspike discharge. Calibration signal 1 s, 70 µV.


Fig. 4-1.69. Apiculate temporal alphoid rhythm. Patient's age, 51 years. This and the following figure, show a range of rhythmic-to-apiculate (sharply contoured) left temporal activity seen principally in the mandibular notch (M1) region with spread to F7–T3. Such gradations from nonepileptiform to epileptiform phenomena create difficulties in interpretation. Maintain a relatively high threshold for spike identification and seek areas with unequivocal spikes before making a positive identification of spikes. Sleep recordings that contain less or no alphoid rhythm may help in making this distinction. Calibration signal 1 s, 70 µV.


Fig. 4-1.70. Apiculate temporal alphoid rhythm. Patient's age, 51 years. Although they are apiculate, the morphology of none of these waves is clearly distinct from the waxing and waning temporal alphoid rhythm. Whether the slower left temporal waves reflect simply the waxing and waning of alphoid rhythm or an independent delta activity is difficult to determine on this and the previous illustration. Calibration signal 1 s, 70 µV.


Fig. 4-1.71. Wicket spikes. Patient's age, 44 years. Primarily electronegative arciform waves at T3 with principal spread to F7 occurring as part of a burst of more sinusoidal 7 Hz bitemporal waves. The slow waves at F7 and F8 represent lateral eye movements. Calibration signal 1 s, 70 µV.


Fig. 4-1.72. Wicket spikes. Patient's age, 21 years. Sequential electronegative wicket spikes at T3, T3–F7, and F7 with spread to T3. All of these wicket spikes appear as the sharply contoured negative components of 6 to 7 Hz rhythmic waves in the temporal region. Calibration signal 1 s, 50 µV.


Fig. 4-1.73. Left temporal wicket spikes. Patient's age, 50 years. The left temporal rhythms contain a variety of sharpness developing from an increase in the synchrony of ongoing background activity or the superimposition of background waveforms-i.e., the left temporal theta and alphoid rhythm. Thus, such isolated sharpness can be expected from this background. Single waveforms of identical morphology could be considered spikes if several of a similar morphology appeared and if the background activity were more amorphous than rhythmic. Calibration signal 1 s, 50 µV.


Fig. 4-1.74. Abrupt wicket spikes. Patient's age, 50 years. Wicket spikes may emerge gradually or appear abruptly, as here. Although none of these waves could be considered a spike, the phenomena likely indicate excess temporal theta for age and state (wakefulness). Calibration signal 1 s, 50 µV.


Fig. 4-1.75. Right anterior–temporal spikes and the mandibular notch electrode. Patient's age, 36 years. Mandibular notch and anterior–temporal electrode positions may depict temporal spikes better than the standard 10–20 system (Sadler & Goodwin, 1989). These stereotypical repetitive spikes appear principally at the mandibular notch electrode (M2) and at the inferior frontal–anterior temporal electrode (F8) with spread to the right midtemporal region (T4). Note their slightly greater amplitude on the coronal portion of this montage, involving M2, compared with the anterior–posterior portion. Right temporal delta activity accompanies these spikes. Calibration signal 1 s, 70 µV.


Fig. 4-1.76. Right temporal spikes on a coronal montage. Patient's age, 34 years. The field of these abundant right temporal spikes is well depicted by this coronal montage. Thus, such spikes appear principally in the inferior–anterior temporal (M2–F8) region with moderate spread to the right midtemporal (T4) region. Note the slightly varying field of such spikes. Calibration signal 1 s, 50 µV.


Fig. 4-1.77. Left midposterior temporal spikes and delta. Patient's age, 27 years. Awake. Eyes closed. Although these spikes and delta are prominent in the left hemisphere, no homotopic propagation to the right has occurred. Their repetitive nature and the prominence of associated delta suggest a relatively active process either as tumor growth, frequent seizures, or both. Contrast this T3–T5 maximum field with that of anterior mesial–temporal spikes (M1–F7–T3). Note the prominent P3 involvement, which is not a feature of anterior temporal spikes. Calibration signal 1 s, 150 µV.


Fig. 4-1.78. Left midposterior temporal spikes and delta. Patient's age, 27 years. Awake. Eyes closed. Same epoch as Fig. 4-1.77. To confirm that the moderate left parietal (P3) spike and delta spread did not indicate equal or even principal left parietal involvement, the coronal run, directly comparing T5 and P3, distinctly indicates principal T5 and also T3 involvement. Note the minimal involvement of the left anterior temporal region (A1,F7). Calibration signal 1 s, 150 µV.


Fig. 4-1.79. Spikes and aphasia. Patient's age, 4 years. Light sleep. These abundant spikes are located principally in the left posterior temporal–parietal–occipital and right central mid posterior temporal regions. Between ages 2 and 3 years, this boy lost all language and appeared not to understand what was said to him. Febrile convulsions and a grand mal seizure occurred in the past. This clinical EEG entity fits the syndrome of acquired aphasia or acquired epileptic aphasia of childhood (Landau–Kleffner syndrome). Calibration signal 1 s, 300 µV.


Fig. 4-1.80. Multifocal spikes. Patient's age, 29 years. Sleep. Note the widespread fields of each of these spikes, suggesting unbridled propagation. Calibration signal 1 s, 70 µV.


Fig. 4-2.1. 3-Hz spike–waves. Patient's age, 6 years. Sudden onset and termination of bilaterally synchronous spike–waves whose repetition rate slows slightly as the burst proceeds. Ultimately, the wave component becomes more prominent than the spike. Calibration signal 1 s, 500 µV.


Fig. 4-2.2. Three-Hz generalized spike–waves on ear reference montage. Patient's age, 5 years. Awake. Eyes closed. The slight asymmetries at onset do not indicate “secondary bilateral synchrony,” as some asymmetry is almost always found with bilateral spike–waves. Note the abrupt onset and reasonably abrupt offset, dominated by rhythmic waves. Calibration signal 1 s, 500 µV.


Fig. 4-2.3. 3 Hz generalized spike–waves, bipolar montage. Same patient as previous illustration. Awake. Eyes closed. Sudden bisymmetrical onset and offset of spike–waves with the wave component more prominent at onset and offset. Events are characterized by cessation of activity, eye flutter, walking about, at times bumping into objects. No recall of event or of number given during ictus. The low sensitivity attenuates depiction of background activity. Calibration signal 1 s, 500 µV.


Fig. 4-2.4. Generalized spike–waves. Patient's age, 9 years. Hyperventilation. In this spike–wave series, the spikes are less prominent than the waves. The attack begins as rhythmic waves before spikes appear. The patient opened his eyes slowly during the attack and rubbed his face at its termination. After the attack, he recalled a number given during the third second of the spike–wave series. The term “generalized” as used here refers to the bilaterally synchronous distribution of the spike–waves, even though they extend minimally to the occipital regions. The term relates more to the clinical correlate of the phenomenon—primary generalized epilepsy—than to its spread. Calibration signal 1 s, 500 µV.


Fig. 4-2.5. Generalized spike–waves, frontally predominant. Patient's age, 9 years. Awake. Eyes closed. Only after 3 to 4 s does the spike–wave discharge involve all parasagittal leads. Calibration signal 1 s, 300 µV.


Fig. 4-2.6. Three-Hz spike–waves on ear reference montage. Patient's age, 14 years. Awake. Eyes closed. These bilaterally synchronous “generalized” spike–waves are best expressed in the right hemisphere; such asymmetry appears commonly with spike–waves and usually shifts between hemispheres. Because the “lead-in” has the same morphology as full spike–waves and no focal right hemispheric spikes or delta appears, this does not qualify as “secondary bilateral synchrony.” Calibration signal 1 s, 200 µV.


Fig. 4-2.7. Left-hemispheric spike–wave onset. Patient's age, 9 years. Awake. 4 Hz spike–waves slowing to 3 Hz as the sequence proceeds. Calibration signal 1 s, 500 µV.


Fig. 4-2.8. Very asymmetrical “generalized” spike–waves. Patient's age, 14 years. Awake. Eyes closed. The marked asymmetry of this single spike–wave and spike–wave series, more clearly depicted on the bipolar portion of this montage, constitutes a morphological bridge between bisynchronous spike–waves of primary generalized epilepsy and “secondary bilateral synchrony” of secondarily generalized epilepsy. If this asymmetry were to persist in several recordings, it would support a diagnosis of “hemispheric epilepsy” (Blume, 1998). Calibration signal 1 s, 100 µV.


Fig. 4-2.9. Eye closure precipitates polyspikes. Patient's age, 24 years. Awake. The distinct appearance of each component of the posteriorly accentuated polyspike burst upon eye closure distinguishes them from muscle artifact and its high frequency with intermingled theta from fast alpha variant. Photic stimulation may elicit a photoparoxysmal response in this circumstance. Calibration signal 1 s, 100 µV.


Fig. 4-2.10. Bisynchronous posterior spike–waves. Patient's age, 9 years. Awake. Eyes closed. Bisynchronous spikes may appear in parietal–occipital association cortex. As is true with bilaterally synchronous spike–waves, the background activity is normal for age. Calibration signal 1 s, 150 µV (top 8 channels); 1 s, 200 µV (bottom 10 channels).


Fig. 4-2.11. Posteriorly situated bisynchronous and regional spike–waves. Patient's age, 8 years. Eyes closed. Although rhythmic delta predominates, the spike discharges appear sufficiently distinct to identify these as spike–waves. Note the regional expression (O2 and possibly O1) of these essentially bisynchronous discharges. Calibration signal 1 s, 300 µV.


Fig. 4-2.12. Hidden spike–waves within rhythmic delta bursts. Patient's age, 14 years. Sleep. An example of unilateral predominance of diffuse, rhythmic waves and spikes. Calibration signal 1 s, 200 µV.


Fig. 4-2.13. Believe it or not … there is a spike and wave in that drowsy pattern! Patient's age, 2 years. However, a better-expressed spike–wave would have to be identified before the record could be reported as such. Calibration signal 1 s, 200 µV.


Fig. 4-2.14. Sob artifact. Patient's age, 18 months. Awake. Eyes open. These repetitive spike-like potentials superficially resemble spike–waves, but the apparently diffuse field and patient observation (*) identify these as sob artifact. Calibration signal 1 s, 200 µV.


Fig. 4-2.15. 3 Hz spike–waves. Patient's age, 64 years. All of the components of spike–wave complexes described by Weir (1965) are difficult to identify on a bipolar montage, particularly when the spike–wave complex competes with background activity, as appears here. Instead, one sees single or multiple spikes of variable morphology preceding 300 ms, rhythmic or semirhythmic waves and appearing in a frontally dominant, bilaterally synchronous manner without a focal onset or offset. By placing a ruler along the presumed electrical baseline (from the mean of activity prior to and after the spike–wave complex), one can discern a considerable positive component, which represents the trough between the spike and the wave. Calibration signal 1 s, 50 µV.


Fig. 4-2.16. Generalized spike waves with posterior accentuation. Patient's age, 8 years. Awake. Although not conforming to the “classical” configuration of generalized spike–waves, this posteriorly accentuated generalized phenomenon is just that. Its onset as a right-sided rhythmic wave remains consistent with primary generalized epilepsy provided that this right-sided onset is not invariably present in other spike–wave complexes. Calibration signal 1 s, 150 µV.


Fig. 4-2.17. Generalized spike waves, maximal in the left and right hemispheres. Patient's age, 14 years. Awake. The spike–waves of patients with primary generalized epilepsy may be maximally or even exclusively expressed in one hemisphere, but the side of maximal expression will shift within the same recording or among several recordings. These examples of essentially generalized spike waves are obtained from the same recording. Calibration signal 1 s, 100 µV.


Fig. 4-2.18. Generalized spike–wave complexes with restricted field. Patient's age, 14 years. Awake. At times the spike–wave field may appear to be so restricted that it suggests a focal phenomenon. However, scrutiny of such events often reveals low-amplitude spikes in derivations that would be unaffected by a truly focal spike in the region in question. For example, in the segment on the left, there is greater expression of the spike–wave discharge in the right-sided leads than would be expected from a focal left parietal spike. The presence of similar spike–waves in other parts of the recording, which have a more widespread, shifting, or generalized distribution, are clues that such an apparently focal spike–wave is really a partial manifestation of a generalized phenomenon. On the other hand, a consistent localization of a spike–wave together with a corresponding background abnormality would indicate that the spike–wave represents a focal disturbance. In the right-hand segment (same recording), there are spike discharges in all right-sided derivations. Calibration signal 1 s, 70 µV.


Fig. 4-2.19. Different quantities of spike–waves. Patient's age, 8 years. Awake. Once you have identified spike–waves in a recording, look for minimal expressions of such complexes so that, on other recordings in which only such are present, they can be identified with confidence. Calibration signal 1 s, 200 µV.


Fig. 4-2.20. Spike–wave fragment. Patient's age, 36 years. Awake. Eyes closed. Same epoch, bipolar and referential montages. Although the bipolar montage suggests a focal right frontal spike, the ear reference montage with A2 clearly not involved indicates that this may be a “generalized” spike–wave fragment, as suggested by its morphology, the limited bisynchrony, and the lack of a right frontal focal background abnormality. Calibration signal 1 s, 150 µV.


Fig. 4-2.21. Hyperventilation elicits spike–waves. Patient's age, 9 years. Among the rhythmic 2 Hz bifrontal waves of hyperventilation are bisynchronous bifrontal spikes in the middle of this segment, constituting spike–waves. Patient has absence and rare generalized tonic–clonic seizures. Calibration signal 1 s, 150 µV.


Fig. 4-2.22. Absence status epilepticus. Patient's age, 11 years. The repetition rate of the spike–wave complexes during absence status usually is slower than that for briefer spike–wave series. The rate also varies considerably to the point of developing bisynchronous sequential spikes, as seen in the center of this illustration. Impairment of consciousness may not be as complete in absence status as in shorter attacks. When this patient was asked. “What time is it?” (at 1100 hours), he tardively responded, “Afternoon.” Calibration signal 1 s, 300 µV.


Figs. 4-2.23. Prolonged absence status epilepticus. Patient's age, 17 years. Obtunded. The amplitude and morphology of continuing spike–waves may diminish as this process continues, possibly lulling the clinician into falsely believing that the seizures have ceased. This and the following illustration show blunted bilaterally synchronous waves with accompanying polyspikes. This patient had intermittent episodes of absence for the previous 2 weeks. Calibration signal 1 s, 150 µV.


Fig. 4-2.24. Prolonged absence status epilepticus (continued). Same patient as previous illustration. Obtunded. The amplitude and morphology of continuing spike–waves may diminish as this process continues, possibly lulling the clinician into falsely believing that the seizures have ceased. This and Fig. 4-2.23 illustrate blunted bilaterally synchronous waves with accompanying polyspikes. This patient had intermittent episodes of absence for the previous 2 weeks. Calibration signal 1 s, 150 µV.


Fig. 4-2.25. Absence status arrested by intravenous diazepam. Patient's age, 17 years. The blunted spike–waves of the previous two illustrations have ceased with 10 mg of diazepam intravenously, leaving low-voltage delta and beta activity. Calibration signal 1 s, 150 µV.


Fig. 4-2.26. 6 Hz spike–waves. Patient's age, 34 years. These diffuse but often posteriorly accentuated spike–waves repeat at about 6 Hz in these samples. Note the brevity of each spike. The right-sided accentuation of some of these has no clinical significance. Posteriorly accentuated 6 Hz spike–waves are not thought to correlate with a seizure disorder (Hughes, 1980; Westmoreland, 1990). However, the morphology of the more diffuse or anterior-predominant 6 Hz spike-waves may merge with the more clearly epileptogenic 3 Hz spike–waves and therefore correlate more highly with a seizure disorder. Such prominent anterior accentuation and merging of morphologies are illustrated in the first and last examples, which may be more epileptogenic than the middle examples. Calibration signal 1 s, 70 µV.


Fig. 4-2.27. 6 Hz spike–waves. Patient's age, 20 years. Drowsy. Several studies have indicated the intermediate position of this epileptiform phenomenon in terms of its epileptogenicity, as about 35% to 50% of these patients have generalized seizures. Note their principal expression posteriorly (P3,4; O1,2). Distinction of this phenomenon between 6 Hz spike–waves and 14/6-per-second positive spikes is often difficult and arbitrary, as in this example. Calibration signal 1 s, 70 µV.


Fig. 4-2.28. Polyspike–waves. Patient's age, 24 years. Sleep. Each segment demonstrates very high frequency polyspikes with lower frequency polyspike–waves. The discrete nature of the discharges, their bursting quality, and their presence in non-REM sleep distinguish these from bursts of muscle potentials. Calibration signal 1 s, 300 µV.


Fig. 4-2.29. Generalized polyspike–waves. Patient's age, 22 years. Awake. Eyes closed. The discrete appearance of each individual spike is the feature of polyspikes distinguishing them from bursts of muscle artifact. Note the instantaneous onset and offset of each paroxysm. Calibration signal 1 s, 300 µV.


Fig. 4-2.30. Generalized polyspike–waves and spike–waves. Patient's age, 29 years. Awake. Eyes open. These frontally predominant, diffuse, bilaterally synchronous polyspike–waves are preceded and followed by low-voltage single spike–waves. Note the normal background activity. Calibration signal 1 s, 400 µV.


Fig. 4-2.31. Polyspike bursts in wakefulness. Patient's age, 27 years. Such bursts are more difficult to discern in wakefulness than in sleep because of the greater prominence of background rhythms whose frequencies approach or overlap that of the polyspikes. However, the onset (*) can be clearly discerned from the ongoing background activity; the offset is characterized by bisynchronous 200 to 300 ms waves. Note the brief burst of muscle potentials in the first second of this sample and persistent muscle potentials at FP2. A glossokinetic potential consisting of bisynchronous delta activity with a burst of muscle potentials appears in the last second of the sample. Calibration signal 1 s, 50 µV.


Fig. 4-2.32. (Almost) unilateral polyspike waves. Patient's age, 20 years. Epileptiform discharges of a morphology usually associated with a bilaterally synchronous distribution may appear unilaterally or even regionally (Gastaut & Broughton, 1972; Blume & Kaibara, 1999). The morphology of these bursts, their widespread distribution throughout the right hemisphere, the moderate expression in the contralateral (left) hemisphere, and the lack of a focal interparoxysmal abnormality all suggest that these spikes do not represent a focal cortical lesion. Nonetheless, recording with parasagittal and sagittal leads during both wakefulness and sleep should be done to seek secondary bilateral synchrony. Note the distinction in frequency between the polyspikes (multiple spikes) and the diffuse background of alpha-beta range. Calibration signal 1 s, 50 µV.


Fig. 4-2.33. Right, then left hemisphere–predominant polyspike–waves. Patient's age, 45 years. Sleep. The discrete appearance of these spikes constituting a polyspike burst distinguishes them from muscle artifact. A dissimilar metals artifact would be unlikely to have such regional accentuation and would more likely be a single potential as opposed to bursts. Calibration signal 1 s, 200 µV.


Fig. 4-2.34. Right hemispheric accentuated polyspike–waves at arousal. Patient's age, 45 years. The discrete presence of each individual potential distinguishes this polyspike burst from glossokinetic or other muscle artifact. Whether arousal “evoked” the polyspike waves or vice versa is unclear. Calibration signal 1 s, 150 µV.


Fig. 4-2.35. Left hemispheric polyspike–waves. Patient's age, 45 years. Sleep. Same recording as in the previous illustration. Essentially “generalized” epileptiform potentials commonly shift hemispheres in the course of one or more recordings, as occurred here. Calibration signal 1 s, 150 µV.


Fig. 4-2.36. Slow spike–waves. Patient's age, 3 years. Awake. There was no discernible clinical alteration at this time. The patient is cognitively impaired and has tonic seizures. Calibration signal 1 s, 500 µV.


Fig. 4-2.37. Slow spike–waves. Patient's age, 55 years. Awake. Eyes open. These 2 Hz bilaterally synchronous spike–waves are characteristically more abundant in a single recording than are higher-frequency spike–waves, and carry a greater epileptogenicity. Note the prominent electropositive “troughs” between the spike and wave components. The third slow spike–waves somewhat resembles a triphasic wave except for the sharpness of the first component. The “slow” of slow spike–waves refers principally to repetition rate of the complex, not to the duration of the spike component, which can be as brief as that of 3 Hz spike–waves. Calibration signal 1 s, 200 µV.


Fig. 4-2.38. Slow spike–waves. Patient's age, 55 years. Awake. Eyes open. The ipsilateral ear montage depicts the morphology of these slow spike–waves much better than does the bipolar montage. Note that slow spike–waves (as well as spike–waves) consist of bisynchronous spikes, troughs, and waves. Calibration signal 1 s, 100 µV. (bipolar); 1 s, 150 µV (referential).


Fig. 4-2.39. Slow waves with spikes. Patient's age, 27 years. Awake. Eyes closed. In patients with intractable generalized epilepsy, this combination often appears-i.e., both waves and spikes, only sporadically appearing together as a complex. Calibration signal 1 s, 70 µV.


Fig. 4-2.40. Bisynchronous spikes and electrodecremental events (EDE). Patient's age, 37 years. Awake. Eyes closed. Sudden, diffuse attenuations lasting about 1 s are interspersed within delta and bisynchronous spikes. Such EDEs usually accompany active physiological processes such as frequent seizures but are unusual in an apparently awake patient. Calibration signal 1 s, 100 µV.


Fig. 4-2.41. Runs of polyspikes. Patient's age, 21 years. Sleep recording. A burst of bisynchronous spikes at 10 to 25 Hz is an epileptiform pattern associated with primary generalized epilepsy. Other aspects of the Lennox–Gastaut syndrome may be present (Gastaut & Broughton, 1972; Brenner & Atkinson, 1982). This pattern may appear in patients of any age with tonic or absence seizures. Calibration signal 1 s, 70 µV.


Fig. 4-2.42. Multifocal spikes, fast rhythmic waves (epileptic recruiting rhythm) and abnormal drowsy pattern. Patient's age, 13 years. Drowsy. The diffuse 3 s burst of 15 to 20 Hz fast rhythmic waves is preceded by multifocal spikes. Moreover, the delta-dominated background activity in this drowsy patient also indicates a diffuse encephalopathy, as theta is the only normal-range drowsy pattern. Note the attenuated background after the burst. This phenomenon, together with slow spike–waves and tonic seizures, constitutes the Lennox–Gastaut syndrome. Calibration signal 1 s, 150 µV.


Fig. 4-2.43. Fast rhythmic waves (epileptic recruiting rhythm). Patient's age, 11 years. Sleep. The high frequency of the waves (P4,P3,C4,C3), together with their sudden onset and abrupt offset, distinguish this phenomenon from beta activity. Calibration signal 1 s, 150 µV.


Fig. 4-2.44. Bilateral polyspikes. Patient's age, 18 years. Awake. Eyes open. Although superficially resembling several types of artifact, these diffuse, posteriorly accentuated polyspikes are commonly epileptogenic and may suggest relative intractability. Calibration signal 1 s, 200 µV.


Fig. 4-2.45. Fast rhythmic waves and multiple independent spikes. Patient's age, 8 years. Awake. Eyes open. Although the excess delta and plentiful spikes in the left hemisphere reflect a moderately severe encephalopathy there, the prolonged train of higher-frequency waves in the right hemisphere with preceding and proceeding attenuation indicate an even greater encephalopathy on the right. Calibration signal 1 s, 200 µV.


Fig. 4-2.46. Hypsarrhythmia. Patient's age, 8 months. Awake. High-voltage 1 to 3 Hz, arrhythmic waves with profuse multifocal spikes constitute the hypsarrhythmic pattern. In wakefulness and light sleep, this pattern is continuous. Calibration signal 1 s, 300 µV.


Fig. 4-2.47. Hypsarrhythmia. Patient's age, 11 months. Awake. Eyes open. The high-voltage, multifocal, posteriorly accentuated spikes and delta constitute this interictal pattern. Calibration signal 1 s, 300 µV.


Fig. 4-2.48. Hypsarrhythmia and electrodecremental event. Patient's age, 11 months. Awake. Eyes open. An auditory stimulus (*) provoked an epileptic spasm (note tonic muscle artifact at T6) with an accompanying electrodecremental event. Calibration signal 1 s, 300 µV.


Fig. 4-2.49. Bihemispheric polyspikes and excess delta. Patient's age, 6 months. Drowsy. This can be considered a modified hypsarrhythmic pattern accentuated in the posterior head because of the spikes and polyspikes associated with excess delta activity for age and state. Calibration signal 1 s, 200 µV.


Fig. 4-2.50. Hypsarrhythmia becoming slow spike–waves. Patient's age, 3 years. Awake. This segment illustrates the transition from the multifocality and asynchrony of hypsarrhythmia to the bilateral synchrony of slow spike–waves. Calibration signal 1 s, 300 µV.


Fig. 4-2.51. Hypsarrhythmia in deep sleep. Patient's age, 4 months. Spikes become clustered into brief bursts in deep sleep. The asymmetry seen in this segment was transient, a common finding at this age. Calibration signal 1 s, 200 µV.


Fig. 4-2.52. Electrodecremental event. Patient's age, 5 months. Sleep. Electrodecremental events vary in degree. This infantile spasm (*) was associated with (a) a less-than-usual decrease in voltage of delta activity for 2 s, followed by a gradual return, and (b) cessation of multifocal spikes for 5 to 6 s. Hypsarrhythmia surrounds the event. Calibration signal 1 s, 150 µV.


Fig. 4-2.53. Fast rhythmic waves. Patient's age, 5 months. Awake. The patient's eyes opened partially and all limbs extended tonically at the onset of the burst of high-frequency (about 18 Hz) rhythmic waves. Calibration signal 1 s, 150 µV.


Fig. 4-2.54a. Fast rhythmic waves. Patient's age, 8 months. A similar phenomenon to that shown in Fig. 4-2.53 but unilateral. No clinical change. Calibration signal 1 s, 150 µV.


Fig. 4-2.54b. Fast rhythmic waves. Same patient as in Fig. 4-2.54a. These high-frequency rhythmic waves in the right hemisphere were associated with slow opening and closing of the eyes coincident with slow conjugate vertical (upward and downward) ocular deviation. These persisted until the early part of the second electrographic phase of the attack, when the amplitude of the rhythmic waves diminished slightly and a 30 Hz rhythm also appeared. The only modification in the left hemisphere was a transient further slowing of the abnormally excessive delta activity. Calibration 1 s, 150 µV.


Fig. 4-2.55. Fast rhythmic waves. Patient's age, 7 months. Awake. Conjugate upward ocular deviation (*) was the only apparent clinical accompaniment to these generalized high-frequency rhythmic waves. However, the bifrontal muscle artifact (c) near the end of the burst may indicate the tonic component extended beyond the extraocular muscles. This severely disabled child had frequent tonic seizures in extension. Calibration signal 1 s, 150 µV.


Fig. 4-2.56. Left hemispheric polyspikes. Patient's age, 16 years. Awake. Eyes closed. This group of illustrations (Fig. 4-2.56 to 4-2.62) displays large fields or hemispheric expression of epileptiform phenomena of this chapter. Although these polyspikes appear principally in left temporal leads, their parasagittal extension reflects a widespread left hemispheric involvement. The frequency, abruptness of onset and offset, and aftercoming delta activity all distinguish them from spindles. Calibration signal 1 s, 100 µV.


Fig. 4-2.57. Left hemispheric polyspikes. Patient's age, 8 years. Awake. Eyes open. Paradoxically, localization of the delta and theta, principally in the left hemisphere, suggests that the polyspikes arise ipsilaterally and are not regional expression of “generalized” epileptiform discharges. Such left hemispheric accentuation of both polyspikes and delta/theta persisted throughout the recording, supporting this conclusion. Calibration signal 1 s, 150 µV.


Fig. 4-2.58. Left hemispheric polyspikes and bihemispheric delta. Patient's age, 8 years. Sleep. In this post–corpus callosotomy recording, polyspikes predominate in the left hemisphere with rare independent ones in the right hemisphere. Note the lack of normal sleep potentials such as V waves and spindles. Calibration signal 1 s, 100 µV.


Fig. 4-2.59. Right hemisphere PLEDs. Patient's age, 48 years. Awake. Eyes closed. These F4–P4 regularly repeating spikes suggest a physiologically evolving condition with a high incidence of associated seizures, although a stereotypic relationship with contralateral clonic seizures may not always occur. Calibration signal 1 s, 100 µV.


Fig. 4-2.60. Right hemispheric PLEDs plus and reduced right hemisphere sleep potentials. Patient's age, 6 months. Sleep. Repetitive or periodic epileptiform or nonepileptiform phenomena suggests physiologically evolving processes including recent seizures, as is the case here. Spindles were reduced in the right hemisphere and minimally present in this segment. Note the well-defined spindle in the left hemisphere at the beginning of the segment. Calibration signal 1 s, 150 µV.


Fig. 4-2.61. Shifting spike–waves. Patient's age, 7 years. Awake. Eyes closed. Note the left hemispheric and then right hemispheric predominance of these generalized spike waves. Calibration signal 1 s, 500 µV.


Fig. 4-2.62. Hemispheric epilepsy. Patient's age, 15 years. Sleep. Some epilepsies have intermediate positions between focal and generalized; this segment illustrates that concept (Blume, 1998). Calibration signal 1 s, 200 µV.


Fig. 4-2.63. Polyspikes upon eye closure. Patient's age, 39 years. Because they merge somewhat with background activity, these diffuse or posteriorly accentuated discharges occurring upon eye closure may be overlooked. Compare background activity with eyes open (first 2 s) and eyes closed (last 4 s) with that of the first second after eye closure, which contains widely synchronous sequential 15 Hz spikes. Perform photic stimulation carefully in such patients, as a photoparoxysmal response may occur. Calibration signal 1 s, 70 µV.


Fig. 4-2.64. Bisynchronous polyspike–waves; photoparoxysmal response. Patient's age, 11 years. Awake. Eyes open. Abnormal responses to photic stimulation (13 Hz here) may have several morphologies ranging from rhythmic waves to spike–waves with poor intraburst stereotypy, i.e. inconsistent morphology of a complex within a burst. Calibration signal 1 s, 200 µV. (top 8 channels), 1 s, 300 µV (bottom 8 channels).


Fig. 4-2.65. Photoparoxysmal response. Patient's age, 11 years. Awake. Eyes closed. Flash rate 13 Hz. Note its multiple morphologies, better expressed on the ear reference portion of this montage. Calibration signal 1 s, 200 µV. (bipolar); 1 s, 300 µV (referential).


Fig. 4-2.66. Subtle photoparoxysmal response. Patient's age, 16 years. The enlarged boxes (A,B) illustrate in two of the derivations (P3–O1, O1–A1) the generalized sequential spikes elicited by photic stimulation. Note the delayed appearance of photically induced polyspikes in the right segment. Calibration signal 1 s, 70 µV.


Fig. 4-2.67. Photoparoxysmal response with eye closure. Patient's age, 28 years. Awake. After several seconds lacking any photoparoxysmal response from a 15 Hz flash rate, eye closure on two occasions evokes spike–waves. Calibration signal 1 s, 150 µV.


Fig. 4-2.68. Photic stimulation with eyes closed and with eye closure elicits spikes. 39 years. Photic stimulation (15 Hz) with eyes closed (beginning of photic stimulation) and with eye closure (*) elicits polyspikes. Flash stimuli usually elicit polyspikes when eye closure on the resting record does so. Calibration signal 1 s, 70 µV.


Fig. 4-2.69. Photoparoxysmal responses. Patient's age, 20 years. Awake. Eyes closed. Bisynchronous epileptiform potentials linked to photic stimulation (PS) may have varying morphologies from sequential spikes to spike–waves ending during the PS or extending beyond it. Note the larger amplitude response at 20 Hz flash rate (right) as opposed to 9 Hz flash rate (left). Calibration signal 1 s, 100 µV. (left), 1 s, 150 µV (right).


Fig. 4-2.70. Photic responses at different flash rates. Patient's age, 37 years. Awake. Eyes closed. Upper left (12 Hz): Transient driving at a subharmonic of the flash rate. Upper right (15 Hz): Minimal photic driving. Lower left (25 Hz): High-voltage polyspike–wave discharges terminating before the flash rate ends. Lower right (30 Hz): Single polyspike–wave near photic onset. Calibration signal 1 s, 100 µV.


Fig. 4-2.71. Photic responses at different flash rates. Patient's age, 28 years. Awake. Eyes closed. Upper left (1 Hz): It is doubtful that the single spike–wave relates only to the flash itself as subsequent single flashes do not evoke it. Thus, it could be considered as an abnormal epileptiform initial response. Upper right (12 Hz): As did the single flash, the onset of 12 Hz flash rate evoked a single spike–wave followed by a driving response, suggesting a similarity between the initiation of higher-frequency photic stimulation to that of single flashes. Lower left (15 Hz): The initiation of a 15 Hz flash rate also evokes a bisynchronous epileptiform phenomenon as single and polyspikes, followed by photic driving subsequently interrupted by posteriorly situated polyspike–waves. Lower right (18 Hz): It is not clear whether the ongoing polyspike–wave discharge in response to 18 Hz is specific for that frequency or represents a gradual lowering of photoparoxysmal response threshold as the photic procedure continues. Calibration signal 1 s, 70 µV.


Fig. 4-2.72. Variations of photoparoxysmal (photoconvulsive) response. Patient's age, 8 years. As with spontaneously occurring spike–waves, those in response to photic stimulation may be expressed in various degrees. When a minimal response occurs, the technologist should present other flash frequencies to determine the Hz of maximum response. In this instance, a clear response occurred at 16 and 12 Hz and a minimal response at 8 and 13 Hz. Calibration signal 1 s, 70 µV.


Fig. 4-2.73. Spike–waves: spontaneous or evoked? Patient's age, 18 years. Awake. Eyes open/closed. As the morphology of these spike–waves closely resemble those of the resting record (not shown), it is not clear that the photic stimulation actually evokes these discharges. Flash rates at 20 Hz except lower right at 25 Hz. Top segments, eyes open. Bottom segments, eyes closed. Calibration signal 1 s, 100 µV.


Fig. 4-2.74. Widely synchronous spikes evoked by single flashes, then myoclonus in neuronal ceroid lipofuscinosis. Patient's age, 5 years. Awake. This polygraph recording illustrates the consistent occurrence of widely synchronous bilateral spikes to single flashes. Bilaterally synchronous myoclonus followed each event, recorded unilaterally as movement potentials of the proximal left limbs and neck. Note the fast paper speed. Calibration signal 0.5 s, 200 µV.


Fig. 4-2.75. Photomyogenic response. Patient's age, 76 years. Repetitive muscle spikes appear and gradually augment during photic stimulation at 15 flashes per second and subside promptly with the flash, leaving some muscle artifact. Extending posteriorly, the muscle spikes intermingle with photic driving to resemble a photoparoxysmal response. The simultaneous termination of the muscle potentials with flash is more suggestive of a photomyogenic response. Calibration 1 s, 50 µV.


Fig. 4-2.76. Photomyogenic response. Patient's age, 68 years. Awake. Eyes open. No clinical significance can be ascribed to these purely muscle potentials involving supraocular and other cranial musculature in response to photic stimulation at 20 Hz flash rate. Importantly, no distinct spikes or waves appear. Note that the photomyogenic response does not outlast the flash stimulus and even responds to the single, erroneously-timed flash at termination. Calibration signal 1 s, 200 µV.


Fig. 4-3.1. Right temporal periodic lateralized epileptiform discharges (PLEDs). Patient's age, 81 years. Although PLEDs may not always equate with clinical seizures but as possible harbingers of such, they are placed first in this seizure section. These polyphasic PLEDs are clearly depicted by this coronal montage along with the right hemispheric delta activity. Both the periodicity and the delta activity represent a physiologically evolving process such as a postictal or preictal condition, a cerebral viral infection, or a recent stroke. Calibration signal 1 s, 70 µV.


Fig. 4-3.2. Right parietal PLEDs. Patient's age, 75 years. These biphasic, principally negative right parietal (P4) spikes spread moderately to the right occipital (O2) region. The diffuse delta activity is accentuated in the right hemisphere while the more sustained and higher frequency background activity appears principally in the left hemisphere. Calibration signal 1 s, 70 µV.


Fig. 4-3.3. PLEDs plus. Patient's age, 76 years. Periodic lateralized epileptiform discharges (PLEDs) accompanied (preceded or followed) by low-voltage high-frequency rhythms constitute “PLEDs plus” which is associated with a high likelihood of a seizure occurring within the next 15 to 30 min of recording (Reiher et al., 1992). This activity is accompanied by diffuse delta, more prominent in the right hemisphere, the side of the “PLEDs plus.” Note the diffuse right hemispheric electrodecremental events. Calibration signal 1 s, 50 µV.


Fig. 4-3.4. Periodic left temporal sharp waves and diffuse delta with herpes simplex encephalitis. Patient's age, 67 years. Regularly repetitive, sharply contoured diphasic delta waves appear over the left anterior–midtemporal (F7, T3) area in association with left temporally accentuated diffuse continuous delta. This combination of EEG features in association with an encephalitic-like clinical picture suggests herpes simplex as its cause–as was the case here. Note the sporadically appearing low-voltage right temporal (F8, T4) spikes. Calibration signal 1 s, 50 µV.


Fig. 4-3.5. Repetitive temporal complexes in herpes simplex encephalitis at slower sweep speed. Patient's age, 67 years. The regular repetition of these stereotyped left anterior midtemporal (F7–T3) diphasic, sharply contoured delta waves is even more evident at 15 mm/s sweep speed. Diffuse delta activity is accentuated in the left temporal region and left hemisphere. Bursts of spindle-like alphoid activity are lower in the left hemisphere as compared to the right. Calibration signal 1 s, 50 µV.


Fig. 4-3.6. BiPLEDs. Patient's age, 66 years. Bilateral periodic lateralized epileptiform discharges (BiPLEDs) consist of asynchronously and independently occurring complexes in each hemisphere which differ in morphology, rate, and site of maximal involvement. BiPLEDs may be produced by anoxic encephalopathy or encephalitis and are commonly associated with coma (de la Paz & Brenner, 1981; Walsh & Brenner, 1987). Note the faster repetition rate in the left hemisphere, which also has the higher voltage and more sustained background activity. This tracing would therefore indicate severe bihemispheric abnormalities, principally right. Transformer artifact at FP1,2. Calibration signal 1 s, 50 µV.


Fig. 4-3.7. Focal seizure. Seizure being as repetitive spikes and broader spikes at F4–C4. Calibration signal 1 s, 70 µV.


Fig. 4-3.8. Focal seizure (continued). About 3 s later, frequency of sequential spikes has increased moderately and are transiently joined by 15–20 Hz semi-rhythmic waves. Calibration signal 1 s, 70 µV.


Fig. 4-3.9. Focal seizure (continued). Within 2–3 s, principal manifestation gradually shifts to about 10 Hz rhythmic waves, again at F4–C4 with minimal ipsilateral spread and no homotopic spread. Calibration signal 1 s, 70 µV.


Fig. 4-3.10. Focal seizure (continued). Frequency slows to 7–8 Hz semi rhythmic waves remaining at C4–F4. Note the principally left-sided chewing artifact on this and other pages. Calibration signal 1 s, 70 µV.


Fig. 4-3.11. Focal seizure (continued). Seizure morphology has again changed to irregularly sequential spikes at C4–F4 with slight right hemisphere spread. Calibration signal 1 s, 70 µV.


Fig. 4-3.12. Focal seizure termination. Note the gradual offset of this focal seizure. Calibration signal 1 s, 70 µV.


Fig. 4-3.13. Right anterior temporal seizure, anterior–posterior bipolar montage. Patient's age, 50 years. Sleep. Scrutiny of this seizure discloses its propagation to the ipsilateral frontal–polar region. Calibration signal 1 s, 50 µV.


Fig. 4-3.14. Right anterior temporal seizure (continued). Further evidence of this right frontal polar propagation. Calibration signal 1 s, 50 µV.


Fig. 4-3.15. Right anterior temporal seizure (continued). A morphological change occurs at the fourth second, principally as an increase in the rate of some components. Calibration signal 1 s, 50 µV.


Fig. 4-3.16. Right anterior temporal seizure, termination. Focal right temporal–frontal delta activity dominates this phase, suggesting that the seizure has ended or is in the process of doing so. Calibration signal 1 s, 50 µV.


Fig. 4-3.17. Right anterior mesial temporal seizure. Same seizure on coronal, anterior-posterior montage. Patient's age, 50 years. Sleep. The location and morphology of this seizure is typical for patients with anterior mesial temporal epileptogenesis. The onset as 12 to 13 Hz, very low voltage M2–T4–F8 waves followed by 7 Hz rhythmic waves, then about 11 Hz rhythmic waves constitute the significant morphology and frequency change that defines a recorded seizure. Calibration signal 1 s, 50 µV.


Fig. 4-3.18. Right anterior mesial temporal seizure, further evolution. The rhythmic waves change to sequential 5 to 6 Hz then 7 to 8 Hz spikes and remain confined to the right temporal region with only minimal left temporal reflection. Calibration signal 1 s, 50 µV.


Fig. 4-3.19. Right anterior mesial temporal seizure, further evolution. Calibration signal 1 s, 50 µV.


Fig. 4-3.20. Right anterior mesial temporal seizure, termination. Lack of any measurable left temporal involvement implies minimal to no epileptogenic potential there. Calibration signal 1 s, 50 µV.


Fig. 4-3.21. Left temporal neocortical seizure. Patient's age, 40 years. Awake. Eyes open. Seizure begins ambiguously as a conversion from semirhythmic 2 Hz delta activity to rhythmic 3 Hz waves at T3–T5 without A1, F7 initial involvement. In subsequent illustrations this increases to 6 Hz and spreads to C3,P3 and minimally to F7. This frequency increases to 10 Hz, again with principal involvement of T3–T5. Gradually, this pattern evolves to 6-Hz sequential spikes at T3–T5 with spread to C3,P3 but with minimal involvement of F7 and A1. Such spikes ultimately slow to about 2 Hz without changing field as the seizure abruptly stops. Postictal delta appears principally in the region of maximal ictal involvement-i.e., T5,T3. Calibration signal 1 s, 200 µV.


Fig. 4-3.22. Left temporal neocortical seizure (continued). Calibration signal 1 s, 200 µV.


Fig. 4-3.23. Left temporal neocortical seizure (continued). Calibration signal 1 s, 200 µV.


Fig. 4-3.24. Left temporal neocortical seizure (continued). Calibration signal 1 s, 200 µV.


Fig. 4-3.25. Left temporal neocortical seizure (continued). Calibration signal 1 s, 200 µV.


Fig. 4-3.26. Left temporal neocortical seizure (continued). Calibration signal 1 s, 200 µV.


Fig. 4-3.27. Left temporal neocortical seizure (continued). Calibration signal 1 s, 200 µV.


Fig. 4-3.28. Left temporal neocortical seizure, termination. Calibration signal 1 s, 200 µV.


Fig. 4-3.29. Left temporal neocortical seizure. Same seizure on coronal montage. Patient's age, 40 years. Awake. Eyes open. This confirms principal involvement of T3 and T5 with spread to C3,P3 but with minimal to no involvement at F7,A1. Calibration signal 1 s, 200 µV.


Fig. 4-3.30. Left temporal neocortical seizure (continued). Calibration signal 1 s, 200 µV.


Fig. 4-3.31. Left temporal neocortical seizure (continued). Calibration signal 1 s, 200 µV.


Fig. 4-3.32. Left temporal neocortical seizure (continued). Calibration signal 1 s, 200 µV.


Fig. 4-3.33. Left temporal neocortical seizure (continued). Calibration signal 1 s, 200 µV.


Fig. 4-3.34. Left temporal neocortical seizure (continued). Calibration signal 1 s, 200 µV.


Fig. 4-3.35. Left temporal neocortical seizure (continued). Calibration signal 1 s, 200 µV.


Fig. 4-3.36. Left temporal neocortical seizure (continued). Calibration signal 1 s, 200 µV.


Fig. 4-3.37. Left temporal neocortical seizure, termination. Calibration signal 1 s, 200 µV.


Fig. 4-3.38. Right central–temporal seizure. Patient's age, 9 years, awake, eyes closed. In this patient with benign rolandic epilepsy, a clinically typical seizure was recorded. This is an extreme rare occurrence as the vast majority occur nocturnally. Its initial manifestation is sequential spike–waves at C4 with sequential spikes at T4, each with contiguous spread. Note the coexistence of simultaneous, distinct ictal morphologies in the parasagittal and temporal leads. Calibration signal 1 s, 200 µV.


Fig. 4-3.39. Right central–temporal seizure (continued). This evolves to high frequency rhythmic waves at C4–P4 with spread to T4–T6. Calibration signal 1 s, 200 µV.


Fig. 4-3.40. Right central–temporal seizure (continued). The rhythmic waves spread to the left hemisphere and are joined by left temporal–frontal clonic muscle artifact of the seizure with slight right-sided muscle involvement in the temporal and frontal leads. Calibration signal 1 s, 200 µV.


Fig. 4-3.41. Right central–temporal seizure, termination. The frequency of the sequential spikes and clonic movements slows and is accompanied by diffuse, rhythmic delta activity as the seizure terminates. Note the postictal diffuse attenuation. Calibration signal 1 s, 200 µV.


Fig. 4-3.42. Right central–parietal–temporal seizure. Patient's age, 82 years. Confused. Abrupt onset as 1- to 1.5-Hz sequential polyspike–waves at C4–P4–T4–T6. Calibration signal 1 s, 100 µV.


Fig. 4-3.43. Right central–parietal–temporal seizure (continued). Gradual replacement by about 5 and 15 Hz semirhythmic waves intermingling with declining sequential polyspike–waves. Calibration signal 1 s, 100 µV.


Fig. 4-3.44. Right central–parietal–temporal seizure (continued). These evolve relatively abruptly to 2 Hz rhythmic waves at C4–P4–T6–T4. Calibration signal 1 s, 100 µV.


Fig. 4-3.45. Right central–parietal–temporal seizure (continued). These elements gradually abate. Calibration signal 1 s, 100 µV.


Fig. 4-3.46. Right central–parietal–temporal seizure (continued). 2 Hz right hemispheric rhythmic waves predominate with minimal intermingled spikes. Calibration signal 1 s, 100 µV.


Fig. 4-3.47. Right central–parietal–temporal seizure (continued). Similar to previous illustration. Calibration signal 1 s, 100 µV.


Fig. 4-3.48. Right central–parietal–temporal seizure, termination. Seizure ends with a right hemispheric burst-suppression pattern. Calibration signal 1 s, 100 µV.


Fig. 4-3.49. Tonic seizure: Frontal polar origin. Patient's age, 23 years. Sleep. 3 Hz, irregularly sequential spikes at FPI, 2, with spread to F4,F8 and later to F7 and diffusely. Calibration signal 1 s, 150 µV.


Fig. 4-3.50. Tonic seizure: Frontal polar origin (continued). Spikes spread slightly posteriorly in the right hemisphere and then the left, culminating in a tonic seizure whose muscle artifact dominates the latter half of the illustration and constituted the remainder of this seizure. Calibration signal 1 s, 150 µV.


Fig. 4-3.51. Tonic seizure: Frontal polar origin (continued). Calibration signal 1 s, 150 µV.


Fig. 4-3.52. Tonic seizure: Frontal polar origin (continued). Calibration signal 1 s, 150 µV.


Fig. 4-3.53. Tonic seizure: Frontal polar origin (continued). Calibration signal 1 s, 150 µV.


Fig. 4-3.54. Tonic seizure: Frontal polar origin, termination. Calibration signal 1 s, 150 µV.


Fig. 4-3.55. Frontal polar subclinical seizure. Patient's age, 32 years. Awake. Eyes closed. The only abnormality on this recording is sequential 3 to 4 Hz spikes at FP1,2 with spread to F3,4 and F7,8 and slight spread to T6. The seizure terminates abruptly after only 9 s. Calibration signal 1 s, 70 µV.


Fig. 4-3.56. Typical absence seizure. Patient's age, 14 years. Awake. Eyes closed. Note the initial polyspike–waves, more prominent in the left hemisphere. Such initial asymmetry is common in generalized bisynchronous epileptiform potentials that ultimately become more symmetrical. Calibration signal 1 s, 200 µV.


Fig. 4-3.57. Typical absence seizure (continued). The spike–waves have slowed from an initial 3.5 Hz to 2.5 Hz. Calibration signal 1 s, 200 µV.


Fig. 4-3.58. Typical absence seizure, termination. The instantaneous return to normal background rhythms completes the classical manifestations of this recorded absence attack. Such abrupt termination also distinguishes this clinical seizure from temporal lobe dyscognitive seizures and excessive daytime sleep. Calibration signal 1 s, 200 µV.


Fig. 4-3.59. Clonic–tonic–clonic seizure (grand mal). Patient's age, 29 years. Awake. Eyes closed. The attack begins as 10 Hz rhythmic diffuse waves upon eye closure for 1 s joined by 3 to 4 Hz rhythmic waves for about 1 s. Subsequently, the EEG is largely obscured by muscle potentials typical for generalized tonic–clonic seizures: the initial manifestations are bilaterally synchronous clonic movements. At the termination of this illustration, these are partially replaced by left-sided tonic movements with minimal expression on the right. Calibration signal 1 s, 150 µV.


Fig. 4-3.60. Clonic–tonic–clonic seizure (grand mal) (continued). EEG is entirely obscured by the diffuse tonic phase. Calibration signal 1 s, 150 µV.


Fig. 4-3.61. Clonic–tonic–clonic seizure (grand mal) (continued). Tonic phase continues. Calibration signal 1 s, 150 µV.


Fig. 4-3.62. Clonic–tonic–clonic seizure (grand mal) (continued). Tonic phase becomes interrupted. EEG activity remains occluded. Calibration signal 1 s, 150 µV.


Fig. 4-3.63. Clonic–tonic–clonic seizure (grand mal) (continued). Greater interruptions of the tonic phase to form clonic-like sequential movements. Calibration signal 1 s, 150 µV.


Fig. 4-3.64. Clonic–tonic–clonic seizure (grand mal), termination. Postictal EEG attenuation associated with bursts of decerebrate or decorticate posturing. Calibration signal 1 s, 150 µV.


Fig. 4-3.65. Tonic seizure. Patient's age, 7 years, sedated. Following a rhythmic, bisynchronous diphasic delta wave, diffuse, high-frequency, rhythmic waves begin, decrease slightly for 1 to 2 s, then begin in earnest as incrementing very high frequency potentials. The gradually augmenting sequential spikes and the lack of associated movement artifact distinguish this from muscle activity despite the considerable frequency overlap between these two phenomena. Calibration signal 1 s, 200 µV.


Fig. 4-3.66. Tonic seizure (continued). Further evolution as high-frequency rhythmic waves gradually replace sequential spikes along with diffuse theta. Calibration signal 1 s, 200 µV.


Fig. 4-3.67. Tonic seizure (continued). Multiple phenomena now appear: sequential spikes, rhythmic waves, theta and delta activity, the latter principally in the right hemisphere posteriorly. Calibration signal 1 s, 200 µV.


Fig. 4-3.68. Tonic seizure (continued). Rhythmic waves persist as a “start-stop-start phenomenon” principally in the left hemisphere, while delta activity predominates in the right hemisphere. Calibration signal 1 s, 200 µV.


Fig. 4-3.69. Tonic seizure (continued). Same pattern as in the previous illustration except that delta becomes more prominent bilaterally. Calibration signal 1 s, 200 µV.


Fig. 4-3.70. Tonic seizure, termination. Only a fragment of ictal activity remains (in the left hemisphere) while the recording is dominated by diffuse delta activity that is maximal anteriorly. The T3 and T4 potentials are muscle artifact. Calibration signal 1 s, 200 µV.


Fig. 4-3.71. Hemispheric seizure. Patient's age, 6 years. Drowsy. This seizure dominated by rhythmic waves morphologically resembles many “generalized seizures”, but is very predominant in the left hemisphere. Seizures of this nature blur the distinction between “focal” and “generalized” events. Note that the frequency of these waves increase as the seizure progresses. Calibration signal 1 s, 150 µV.


Fig. 4-3.72. Hemispheric seizure, later phase. The rhythmic potentials have decreased in frequency but remain virtually confined to the left hemisphere with only slight spread to the right frontal region. Calibration signal 1 s, 150 µV.


Fig. 4-3.73. Nonepileptic event. Patient's age, 49 years. Awake. Eyes closed. Rhythmic 3 Hz head movements manifested as rhythmic waves and posterior head muscle bursts. Calibration signal 1 s, 150 µV.


Fig. 4-3.74. Nonepileptic event (continued). Event continues without evolution. Calibration signal 1 s, 150 µV.


Fig. 4-3.75. Nonepileptic event, termination. Event terminates with immediate return to normal background activity. Calibration signal 1 s, 150 µV.


Fig. 4-3.76. SREDA, onset. Patient's age, 73 years. Awake. Eyes closed. In contradistinction to epileptic seizures, the new appearance of right temporal (T4–T6) theta fails to significantly evolve (no distinct morphological or frequency change, no propagation) in this and the next two illustrations, thus constituting the “subclinical rhythmic EEG discharges of adults” (Westmoreland, 1990). Calibration signal 1 s, 50 µV.


Fig. 4-3.77. SREDA, middle. Same patient as in the previous illustration. Calibration signal 1 s, 50 µV.


Fig. 4-3.78. SREDA, termination. Same patient as in previous two illustrations. Calibration signal 1 s, 50 µV.


Fig. 4-3.79. Rhythmic midtemporal discharges (psychomotor variant). Patient's age, 29 years. Awake. Eyes open. The monorhythmic nature of this sharply contoured theta and beta activity is a normal phenomenon anything maintaining an invariably regular frequency is likely to be normal. (Engel, 1984). There is minimal, if any, morphological distinction between psychomotor variant and SREDA. Calibration signal 1 s, 100 µV.


Aicardi J. Epilepsy in Children. New York: Raven Press; 1994:168.

Andermann F. Clinical features of migraine–epilepsy syndromes. In: Andermann F, Lugaresi E, eds. Migraine and epilepsy. Boston: Butterworth–Heinemann; 1987:3–30.

Baird HW, Borofsky LG. Infantile myoclonic seizures. J Pediatr. 1957;50:332–339.

Beaumanoir A, Ballis T, Varfis G, et al. Benign epilepsy of childhood with rolandic spikes. A clinical EEG and telencephalographic study. Epilepsia. 1974;15:301–315.

Beaussart M. Benign epilepsy of children with rolandic (centro-temporal) paroxysmal foci. A clinical entity. Study of 221 cases. Epilepsia. 1972;13:795–811.

Bickford RG, Klass DW. Scalp and depth electrographic studies of electrodecremental seizures. Electroencephalogr Clin Neurophysiol. 1960;12:263(P).

Binnie CD, Stefan H. Modern electroencephalography: its role in epilepsy management. Clin Neurophysiol. 1999;110:1671–1697.

Blom S, Brorson LO. Central spikes or sharp waves (rolandic spikes) in children's EEG and their clinical significance. Acta Pediatr Scand. 1966;55:385–393.

Blom S, Heijbel J. Benign epilepsy of children with centro-temporal EEG foci. Discharge rate during sleep. Epilepsia. 1975;16:133–140.

Blom S, Heijbel J, Bergfors PG. Benign epilepsy of children with centro-temporal EEG foci. Prevalence and follow-up study of 40 patients. Epilepsia. 1972;13: 609–619.

Blume WT. Clinical and electrographic correlates of the multiple independent spike foci pattern in children. Ann Neurol. 1978;4:541–547.

Blume WT. Hemispheric epilepsy. Brain. 1998;121:1937–1949.

Blume WT, David RB, Gomez MR. Generalized sharp and slow wave complexes. Associated clinical features and long-term follow-up. Brain. 1973;96:289–306.



Blume WT, Kaibara M. In Blume WT, ed. Atlas of Pediatric Encephalography, 2nd ed. Philadelphia: Lippincott–Raven; 1999.

Blume WT, Klass DW, Daly DD. In: Blume WT, ed. Atlas of Pediatric Electroencephalography. New York: Raven Press; 1982:140.

Blume WT, Young GB, Lemieux JF. EEG morphology of partial epileptic seizures. Electroencephalogr Clin Neurophysiol. 1984;57:295–302.

Brenner RP, Atkinson R. Generalized paroxysmal fast activity: electroencephalographic and clinical features. Ann Neurol. 1982;11:386–390.

Browne TR, Penry JK, Porter RJ, et al. Responsiveness before, during and after spike–wave paroxysms. Neurology. 1974;24:659–665.

Cavazzuti V, Winston K, Baker R, et al. Psychological changes following surgery for tumours in the temporal lobe. J Neurosurg. 1980;53:618–626.

Chevrie JJ, Aicardi J. Childhood epileptic encephalopathy with slow spike–wave. A statistical study of 80 cases. Epilepsia. 1972;13:259–271.

Clark EC, Knott JR. Paroxysmal wave and spike activity and diagnostic subclassification. Electroencephalogr Clin Neurophysiol. 1955;7:161–164.

Dalby MA. Epilepsy and 3 per second spike and wave rhythms. A clinical, electroencephalographic and prognostic analysis of 346 patients. Acta Neurol Scand Suppl. 1969;45:1–180.

Dalla Bernardina B, Capovilla G, Gattoni MB, et al. Epilepsie myoclonique grave de la premiere annee. Rev Electroencephalogr Neurophysiol Clin. 1982;12:21–25.

Dalla Bernardina B, Tassinari CA. EEG of a nocturnal seizure in a patient with “benign epilepsy of childhood with rolandic spikes.” Epilepsia. 1975;16:497–501.

de la Paz D, Brenner RP. Bilateral independent periodic lateralized epileptiform discharges. Arch Neurol. 1981;38:713–715.

de Weerd AW, Arts WF. Significance of centro-temporal spikes on the EEG. Acta Neurol Scand. 1993;87:429–433.

Dravet C, Roger J, Bureau M. L'epilepsie myoclonique severe du nourrisson. In: Roger J, Dravet C, Bureau M, Dreifuss FE, Wolf P, eds. Les syndromes epileptiques de l'enfant et de l'adolescent. London: John Libbey, 1984;58–66.

Drury I, Beydoun A, Garofalo LA, Henry TR, eds. Asymmetric hypsarrhythmia: Clinical electroencephalographic and radiological findings. Epilepsia. 1995;36: 41–47.

Eeg-Olofsson O, Petersen I, Sellden U. The development of the electroencephalogram in normal children from the age of 1 through 15 years. Paroxysmal activity. Neuropadiatrie. 1971;2:375–404.

Engel J Jr. A practical guide for routine EEG studies in epilepsy. J Clin Neurophysiol. 1984;1(2):109–142.

Falconer MA. Genetic and related aetiological factors in temporal lobe epilepsy. A review. Epilepsia. 1971;12:13–31.

Falconer MA, Serafetinides EA, Corsellis JAN. Etiology and pathogenesis of temporal lobe epilepsy. Arch Neurol. 1964;10:233–248.

Gaily EK, Shewmon DA, Chugani HT, et al. Asymmetric and asynchronous infantile spasms. Epilepsia. 1995;36:873–882.

Garg BP, Patel H, Markand ON. Clinical correlation of periodic lateralized epileptiform discharges in children. Pediatr Neurol. 1995;12:225–229.

Gastaut H, Broughton R. Epileptic Seizures. Clinical and Electrographic Features, Diagnosis and Treatment. Springfield: Charles C. Thomas; 1972.

Gastaut H, Broughton R, Roger J, et al. Generalized convulsive seizures without local onset. In: Vinken PJ, Bruyn GW, eds. Handbook of Clinical Neurology. Amsterdam: Elsevier; 1974;107–129.

Gastaut H, Roger J, Soulayrol R, et al. Childhood epileptic encephalopathy with diffuse slow spike–waves (otherwise known as “petit mal variant”) or Lennox syndrome. Epilepsia. 1966;7:139–179.

Gibbs FA, Davis H, Lennox WG. The electroencephalogram in epilepsy and in conditions of impaired consciousness. Arch Neurol Psychiatry. 1935;34:1133–1148.

Gibbs FA, Gibbs EL. Atlas of Electroencephalography. Vol 2: Epilepsy. Reading, PA: Addison–Wesley, 1952:24.

Gobbi G, Ambrosetto G, Parmeggiani A, et al. The malignant variant of partial epilepsy with occipital spikes in childhood. Epilepsia. 1991;32(Suppl 1):16–17.

Gross DW, Wiebe S, Blume WT. The periodicity of lateralized epileptiform discharges (PLEDs). Clin Neurophysiol. 1999;110(9):1516–1520.

Heijbel J, Blom S, Rasmuson M. Benign epilepsy of children with centrotemporal EEG foci: A genetic study. Epilepsia. 1975;16:285–293.

Hoeffer PFA, de Napoli RA, Lesse S. Periodicity and hypsarrhythmia in the EEG. Arch Neurol. 1963;9:424–436.

Holmes GL, Stafstrom CE. The epilepsies. In: David RB, ed. Child and Adolescent Neurology. St. Louis: Mosby–Year Book; 1998:218.

Hrachovy RA, Frost JD Jr, Kellaway P. Hypsarrhythmia: Variations on the theme. Epilepsia. 1984;25:317–325.

Hughes JR. Two forms of the 6/sec spike and wave complex. Electroencephalogr Clin Neurophysiol. 1980;48:535–550.

Jasper H, Kershman J. Electroencephalographic classification of the epilepsies. Arch Neurol Psychiatry. 1941;45:903–943.

Jayakar PB, Seshia SS. Electrical status epilepticus during slow-wave sleep: A review. J Clin Neurophysiol. 1991;8:299–311.

Jeavons PM, Bower BD. Infantile spasms. In: Vinken PJ, Bruyn GW, eds. Handbook of Clinical Neurology. Vol. 15: The Epilepsies. New York: Elsevier; 1974: 219–234.

Jeavons PM, Bower BD, Dimitrakoudi M. Long-term prognosis of 150 cases of “West syndrome.” Epilepsia. 1973;14:153–164.

Jeavons PM, Harper JR, Bower BD. Long-term prognosis in infantile spasms: A follow-up report on 112 cases. Dev Med Child Neurol. 1970;12:413–421.

Klass DW, Daly D. Petit mal seizures [sound movie recording]. Electroencephalogr Clin Neurophysiol. 1961;13:824(P).

Kotagal P. Multifocal independent spike syndrome: Relationship to hypsarrhythmia and the slow spike–wave (Lennox–Gastaut) syndrome. Clin Electroencephalogr. 1995;26:23–29.



Legarda S, Jayakar P, Duchowny M, et al. Benign rolandic epilepsy: High central and low central subgroups. Epilepsia. 1994;35:1125–1129.

Lemieux JF, Blume WT. Topographical evolution of spike–wave complexes. Brain Res. 1986;373:275–287.

Lennox WG. The petit mal epilepsies, their treatment with tridione. JAMA. 1945; 129:1069–1074.

Lombroso CT. Sylvian seizures and midtemporal spike foci in children. Arch Neurol. 1967;17:52–59.

Lundervold A, Henriksen GE, Fegersten L. The spike and wave complex: A clinical correlation. Electroencephalogr Clin Neurophysiol. 1959;11:13–22.

Maher J, Ronen GM, Ogunyemi AO, et al. Occipital paroxysmal discharges suppressed by eye opening: Variability in clinical and seizure manifestations in childhood. Epilepsia. 1995;36:52–57.

Markand ON. Slow spike–wave activity in EEG and associated clinical features: Often called “Lennox” or “Lennox–Gastaut” syndrome. Neurology. 1977;27:746–757.

Miller H, Blume WT. Primary generalized seizure disorder: Correlation of epileptiform discharges with seizure frequency. Epilepsia. 1993;34:128–132.

Niedermeyer E. Epileptic seizure disorders. In: Niedermeyer E, Lopes da Silva F, eds. Electroencephalography: Basic Principles, Clinical Applications and Related Fields. Baltimore: Urban & Schwarzenberg; 1987:415–416.

Niedermeyer E. The Generalized Epilepsies. A Clinical Electroencephalographic Study. Springfield, IL: Charles C. Thomas; 1972:18.

Noriega-Sanchez A, Markand ON. Clinical and electroencephalographic correlation of independent multifocal spike discharges. Neurology. 1976;26:667–672.

Ohtahara S. Clinico-electrical delineation of epileptic encephalopathies in childhood. Asian Med J. 1978;21:7–17.

Okubo Y, Matsuura M, Asai T, et al. Epileptiform EEG discharges in healthy children: Prevalence, emotional and behavioral correlates, and genetic influences. Epilepsia. 1994;35:832–841.

Pampiglione G, Harden A. Neurophysiological identification of a late infantile form of “neuronal lipidosis.” J Neurol Neurosurg Psychiatry. 1973;36:68–74.

Patry G, Lyagoubi S, Tassinari CA. Subclinical “electrical status epilepticus” induced by sleep in children. Arch Neurol. 1971;24:242–252.

Penry JK, Porter RJ, Dreifuss FE. Simultaneous recording of absence seizures with video tape and electroencephalography: A study of 374 seizures in 48 patients. Brain. 1975;98:427–440.

Reiher J, Grand'Maison F, Leduc CP. Partial status epilepticus; Short-term prediction of seizure outcome from on-line EEG analysis. Electroencephalogr Clin Neurophysiol. 1992;82:17–22.

Reilly EL, Peters JF. Relationship of some varieties of electroencephalographic photosensitivity to clinical convulsive disorders. Neurology. 1973;23: 1050–1057.

Sadler RM, Goodwin J. Multiple electrodes for detecting spikes in partial complex seizures. Can J Neurol Sci. 1989;16:326–329.

Sato S, Dreifuss FE, Penry JK. The effect of sleep on spike–wave discharges in absence seizures. Neurology. 1973;23:1335–1345.

Silverman D. Clinical correlates of the spike–wave complex. Electroencephalogr Clin Neurophysiol. 1954;6:663–669.

Smith JMB, Kellaway P. The natural history and clinical correlates of occipital foci in children. In: Kellaway P, Petersen I, eds. Neurological and Electroencephalographic Correlative Studies in Infancy. New York: Grune & Stratton; 1964: 230–249.

Takahashi T. Activation methods. In: Niedermeyer E, Lopes da Silva F, eds. Electroencephalography: Basic Principles, Clinical Applications and Related Fields. Baltimore: Urban & Schwarzenberg; 1987:212.

Tassinari CA, Bureau-Paillas M, Dalla Bernardina B, et al. La maladie de Lafora. Rev EEG Neurophysiol. 1978;8:107–122.

Trojaborg W. Changes of spike foci in children. In: Kellaway P, Petersen I, eds. Clinical Electroencephalography of Children. New York: Grune & Stratton; 1968: 213–225.

Walsh JM, Brenner RP. Periodic lateralized epileptiform discharges: Long-term outcome in adults. Epilepsia. 1987;28:533–536.

Watanabe K, lwasc K, Hara H. The evolution of EEG features in infantile spasms: A prospective study. Dev Med Child Neurol. 1973;15:584–596.

Weir B. The morphology of the spike–wave complex. Electroencephalogr Clin Neurophysiol. 1965;19:284–290.

Westmoreland BF, Klass DW, Sharbrough FW. Chronic periodic lateralized epileptiform discharges. Arch Neurol. 1986;43:494–496.

Westmoreland BF. Benign EEG variants and patterns of uncertain clinical significance. In: Daly DD, Pedley TA, eds. Current Practice of Clinical Electroencephalography. New York: Raven Press; 1990:243–252.