The EEG Findings in Extratemporal Seizures

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1 Epilepsa, 39(Suppl. 4):Sl-W 1998 Lippincott-Raven Publishers, Philadelphia 0 International League Against Epilepsy The EEG Findings in Extratemporal Seizures Barbara F. Westmoreland Mayo Clinic, Rochester, Minnesota, U.S.A. Summary: Extratemporal seizures originate from the frontal, central, parietal, occipital, and midline regions of the brain. The scalp EEG can show various types of interictal and ictal discharges consisting of spikes, spike and wave sharp waves, paroxysmal fast activity, or rhythmic activity in the p, a, 8, or 6 frequency ranges. The discharges can occur as focal, regional, lateralized, or secondarily generalized discharges. Discharges arising from the frontal region are varied and at times complex. Centro-temporal spikes associated with benign epilepsy of childhood have a characteristic blunt spike and wave appearance. Centro-parietal spikes can occur in children with benign childhood epilepsy or in association with symptomatic epilep- sies at any age. Occipital spike discharges have been seen in young children with visual problems, benign occipital epilepsy of childhood, the Sturge-Weber syndrome, and other symptomatic or structural lesions involving the occipital lobe. There may be problems with detection of the source of origin of seizures secondary to the anatomy of the various regions, deep foci, small restricted foci, rapid spread of epileptiform discharges, and contaminating effects of muscle and movement artifact. Depth or intracranial recordings may help in further localization of foci. Key Words: Extratemporal seizures-eeg-frontal-central-parietal-occipital-midlinepileptiform. Extratemporal seizures arising from the frontal, central, parietal, and occipital regions can present with varied and at times complex epileptiform abnormalities on the EEG. FRONTAL EPILEPTIF ORM PATTERNS Next to temporal lobe-onset seizures, frontal lobeonset seizures are the most frequent type of focal or partial seizures. Frontal seizures can occur at any age, and Often there is some pa*ology e*g*3 mass lesion, vascular lesion, trauma, or congenital abnormalities, that gives rise to the seizures. Interictal patterns A variety of interictal patterns can be seen with frontal seizures. These include spikes, sharp waves, spike and wave, multiple spikes or multiple spike and wave, periodic sharp and slow-wave complexes, low-voltage fast rhythms, or paroxysmal fast activity (1-10) (Fig. 1). The interictal discharges can occur as focal discharges, unilateral discharges over one frontal lobe, multifocal discharges over one frontal lobe, lateralized hemispheric discharges, bifrontal spike or spike and wave discharges that are symmetric or asymmetric, bilaterally synchronous generalized spike and spike and wave discharges, or Address correspondence and reprint requests to Dr. B. F. Westmoreland at the Mayo Clinic, Rochester, MN 55905, U.S.A. secondary bilateral synchrony with a consistent focal onset in one region (1,4,8-13). On occasion, no epileptiform activity may be apparent (4). Other nonepileptiform EEG abnormalities that may be present and which may give a clue to the abnormal side are focal or lateralized slowing or an asymmetry of activity over the two hemispheres. Ictal patterns Ictal discharges can be complex and quite variable (4,6,9-14). These can present as low-voltage fast activity, an incrementing or a recruiting rhythm, repetitive spikes or spikes and slow waves, rhythmic slow waves, high-voltage sharp waves, or focal or widespread attenuation or a flattening of the background (Fig. 2). At times the seizure may be electrically silent, with no apparent change evident in the EEG (4). In contrast to seizures arising from the temporal lobe, spike and wave, paroxysmal fast, and P-frequency discharges with rapid spread are more likely to be seen with extratemporal and particularly with frontal seizures. As with interictal discharges, the ictal discharges may be focal, unilateral in onset, lateralized asymmetric, bilaterally synchronous, or secondarily generalized (Fig. 3). In contrast to temporal lobe seizures, the ictal discharges are frequently more widespread and may become evident later in the course of the clinical seizure. Precise localization of frontal lobe epilepsy is often s1

2 s2 B. F. WESTMORELAND FPl -F3 F343 ; c3+3 2 p3-01 FP2-F4 FIG. 1. lnterictal focal right frontal spikes in a 25-yearold patient with right frontal seizures. F444 ; c4-p4 * p4-02 a l V 1 sec difficult and may be misleading (4,5,10-16). This is due to limitations of scalp recordings because of the anatomy of the frontal lobe and the network of projection pathways that allow the rapid spread of seizure activity within the frontal lobes or outside the temporal lobes (5,16). There may be widespread areas of epileptogenicity or multiple foci of seizure generators within the frontal lobe (5,12,16). The epileptic focus can be missed with scalp recordings, which may not show the focal onset or may not even show the seizure activity itself because of the inaccessibility of certain areas of the frontal lobe to scalp electrodes, such as the orbital and mesial frontal areas, the cingulum, and the supplementary motor area. The focus may be too distant from the scalp electrodes, or small localized foci may not be apparent on scalp recordings because a certain population size of neurons is required for a focus to be propagated to the surface. The spike discharges that may be present may not represent the primary focus because the lesion could be projected from a buried focus within deep cortical areas (4). In general, well-localized frontal foci are the exception ( 10,12). More often, the discharges occur in a regional or lateralized manner or as bilateral discharges with or without a lateralized predominance (lo). Bifrontal or generalized interical and ictal discharges are often seen with seizures originating from the mesial frontal region, the cingulum, or orbital frontal regions (1). Frontal lobe seizures are often manifested by widespread seizure discharges with poor localization or lateralization, because frontal lobe seizures commonly propagate to contralateral frontal regions and ipsilateral temporal regions, causing a problem with localization (15). Secondarily generalized discharges are a common occurrence with frontal lobe epilepsy. The EEG findings that suggest secondary bilateral synchrony or secondary generalized discharges include (a) focal spikes or sharp waves consistently occurring in one area, (b) focal spike discharges that precede or initiate more generalized bursts (Fig. 4), and (c) persistent lateralized abnormalities, such as slowing or an asymmetry over the involved area (17,18). Certain factors play a role in difficulty with localization. The focal onset may be obscured by the rapid spread to other areas, the seizures may be of brief dura- FIG. 2. Recorded right frontal seizure discharge characterized by repetitive spike discharges (paroxysmal fast activity) in the 25- year-old patient shown in Fig. 1. F4:c4 c4-p4 I Epilepsia, Vol. 39, Suppl

3 EEG IN EXTRATEMPORAL SEIZURES s3 FP1-F3 F3-C3 P c3-p3 p3-01 Fp2-F4 F444 c4-p4 p sec (1 50 VV FIG. 3. Example of right frontal spike discharges with secondary generalization in an 11 -year-old patient with right frontal seizures. tion, there may be little or no postictal change, and the discharge may be obscured by muscle artifact. In addition, the clinical seizure may occur before the ictal discharge is apparent on the EEG, or an ictal EEG discharge may occur without the patient being aware of the seizure. Intracranial or depth recording may be helpful in patients who may be candidates for surgery for more accurate localization of the seizure focus. (5,9-15,19). CENTRAL MIDTEMPORAL SPIKES The central midtemporal spikes are a characteristically present in children with benign Rolandic or Sylvian epilepsy of childhood (20-26). Usually, the centrotemporal spike discharges are seen in children between 5 and 10 years of age (27). The benign Rolandic seizures of childhood are characterized by focal twitching or paresthesias involving the hand or face on one side, and during the seizure the patient is unable to speak and exhibits excessive drooling or salivation. The seizures may spread and become generalized. Often they occur at night. The seizures are easily controlled with antiepileptic drugs (AEDs) and resolve after childhood. The children are usually otherwise normal and have no underlying lesion. Interictal discharges The characteristic EEG features consist of slow diphasic spikes with an aftercoming slow-wave component (20-27). The spike discharge is usually quite prominent and is high in amplitude. The spike discharges may vary in shape and amplitude, and at the other end of the spectrum one may see a small low-voltage spike discharge that is difficult to distinguish from background activity. The discharges can occur singly or in brief clusters of two to four in a row or at a frequency of 1-3 Hz. The spike discharges are maximal over the central midtemporal regions (Fig. 5). If extra electrodes are placed over the lower Rolandic area midway between the central and the midtemporal electrodes, the discharge is usually maximal in these electrodes. The discharge may occur unilaterally, bilaterally, asynchronously, or synchronously with an asymmetric amplitude (22-27). At times the EEG shows what appears to be generalized bursts, but these may merely represent a widespread reflection of the centro-temporal spike discharges (28). The discharges can shift from side to side and may vary in location in subsequent EEGs, or they may be absent in one record and reoccur in the next record. The centro-temporal spike often presents as a tangenital dipole across the Rolandic fissure, with a surface positivity over the frontal region and a surface negativity over the centro-temporal regions (22,23-26). p3-01 Pq- 4- FP1-h y F7-T3 T3-Ts T5-01 T 1SeC FIG. 5. Left central temporal spikes in a 9-year-old patient with benign Sylvian seizures.

4 s4 B. F. WESTMORELAND The frequency of the spike discharges is significantly increased during drowsiness and sleep. The discharges are not significantly altered by hyperventilation or by photic stimulation. There is no correlation between the frequency and prominence of the spike discharge and the frequency of clinical seizures. The spike discharge can also be present in patients without seizures (27). The EEG background is usually otherwise normal (25). No anatomic or structural lesions are seen, and the child usually exhibits no abnormalities. Some children can have foci in other locations other than the centro-temporal area and may have seizures that are similar to the benign epilepsy of childhood and that resolve after childhood (25,29). There can be a variation on the location of EEG foci over time, and the spike discharge, despite its location, represents variants that can be seen with the benign epilepsies of childhood (29). As Luders et al. (28) have observed, it is the morphology of the spike discharge rather than the location that is the distinctive factor in identifying this type of spike discharge in association with the benign epilepsy of childhood. Ictal discharges Ictal discharges of patients with benign epilepsy of childhood have rarely been seen. When recorded, the ictal discharge consists of low-voltage fast activity, which initially occurs over the centro-temporal region and then evolves into higher-amplitude, slower frequencies over the temporal and centro-temporal regions (25-30) (Fig. 6). The seizure discharge may spread ipsilaterally or contralaterally and may secondarily generalize. CENTRO-PARIETAL SPIKES Centro-parietal spikes of childhood Centro-parietal spikes can be seen in childhood between the ages of 2 and 8 years, with a peak at 5 years of age (27). These can occur with benign seizures of childhood and may have similar characteristics to those of the centro-temporal spikes of childhood. However, the benign centro-temporal spikes of childhood may not necessarily be associated with seizures but can also be associated with cerebral palsy or some type of motor dysfunction. These can also occur in asymptomatic children without epilepsy (27). Centro-parietal spikes seen with other conditiods Symptomatic epilepsies arising from the central and parietal regions are associated with focal spikes or sharpwave discharges over the central and parietal regions (8,3 1,32). The centro-pariental spikes that occur in association with symptomatic seizures, in contrast to those seen in benign epilepsy of childhood, often occur as brief or rapid spikes (Fig. 7). These are usually a more epileptogenic spike and often are associated with some underlying pathology or disturbance of cerebral function affecting the central regions. As with other focal spikes, these also may have a more widespread reflection to adjacent areas (4,8,3 1,32). FIG. 0. A recorded left Sylvian seizure discharge in a 10-year-old boy with benign Sylvian seizures. Epilepsia, Vol. 39, Suppl '98

5 EEG IN EXTRATEMPORAL SEIZURES s5 p3-01 FIG. 7. Right central spike discharges in a 28-yearold man with a right central arteriovenous malforma- FPP-F4 tion and focal motor seizures. F444 a c4-p4 + 2 p4-02 Right central AVM 1- EPILEPSIA PARTIALIS CONTINUA Epilepsia partialis continua may occur in any location but is most often associated with spike discharges over the central regions. Often the discharges consist of lowamplitude rapid spikes. The spike discharges can occur as continuous repetitive spikes, in bursts or clusters, or in an intermittent fashion. Back-averaging from the clonic or myoclonic jerks may help to demonstrate the presence of an antecedent spike discharge (33). At times no spike discharges may be visible on surface recordings, and only focal slow-wave abnormality or an asymmetry of activity may be present over the involved region.(33). Corticography or intracranial recordings may be necessary to demonstrate the presence of the epileptiform discharges that are not apparent with scalp recordings (33). Vertex or midline spikes Vertex or midline epileptiform abnormalities can be seen with supplementary motor seizures or somatosensory seizures arising from the mesial surface of the brain (4,34,35). Interictal findings The interictal findings consist of focal spikes or sharp waves occurring focally in the central vertex or midline electrodes or with spread to adjacent parasagittal electrodes. More widespread spike and wave discharges, or bilaterally synchronous spike and spike and wave discharges, may also be present (34-36). The interictal discharges may be increased during sleep: However, there may be difficulty in distinguishing the spike discharges.from sleep activity. If the discharges are restricted to one or more midline electrodes, the distinction from normal sleep activity from spike activity can be made by the following observations (17,35): Different fields of distribution; The tendency for spikes to be lateralized to one side; Focal slowing in association with the spikes; Occurrence during wakefulness or drowsiness before V-waves are present; and Secondary generalization of epileptiform activity. If bilateral or widespread spikes or spike and wave discharges are present, it may be difficult to tell whether there is a midline focus or the side or site of origin of the discharges. Simultaneous video EEG monitoring, as well as intracranial monitoring may be helpful in documenting the seizures, indicating the site of origin, and distinguishing the seizures from pseudoseizures (35). Ictal patterns The ictal patterns consist of trains of spikes, sharp waves, spike and wave discharges, or rhythmic 8, a, p, or 6 activity occurring focally in the midline (Fig. 8). At times there may be an initial attenuation of the background followed by low-amplitude fast activity or spike and wave discharges (17,36). There may be spread to adjacent parasagittal regions or a more widespread and bisynchronous reflection of the ictal discharges (17,34-36). On the other hand, the ictal EEG may show no change or may be obscured by muscle artifact. OCCIPITAL SPIKES Occipital spikes can be seen at different ages and with a variety of entities, which include the following: Young children without seizures but with some type of visual impairment; Benign epilepsy of childhood with occipital spikes; Sturge-Weber syndrome; Epilepsy with bilateral occipital calcification; Late infantile neuronal ceroid lipofuscinosis; and Other symptomatic lesions. Occipital spikes with visual impairment Occipital spikes can be seen in young children (usually less than 4 years of age) with visual impairment but who do not have seizures (27,37). Needle sharp spikes have been seen in children who are blind or have retrolental fibroplasia (37,38). Usually the spikes resolve as the child grows older. It is believed that these spikes

6 with S6 B. F. WESTMORELAND F Age: 82 F7-F3 4 F3-Fz 4 FZ+4 1 F4-F8 T343 (234, ~ FIG. 8. Recorded focal seizure discharge manifested by repetitive spike discharges over the central vertex region which were associated with twitching movements a mesial of frontal the left infarct. leg in an 82-year-old patient cz-c4 C4-T4 w r - v Twitching of left leg represent a response to deprivation of visual afferent input that occurs before a critical age and leads to the development of spike discharges (27). Benign epilepsies of children with occipital paroxysms This entity was intially described by Gastaut in 1982 (39) and consists of a seizure disorder in children that is associated with elementary visual phenomena, such as scotomata, flashing lights, pr amaurosis. It may progress to hemiclonic seizures or secondarily generalized tonicclonic seizures. The child may have nocturnal seizures with head and eye deviation and nausea and vomiting (40-43). The seizures are sometimes followed by migraine headaches (25,39,41,42). The interictal EEG shows high-amplitude spike and spike and wave discharges over the occipital and adjacent head regions in a unilateral, bilaterally independent, or bilaterally synchronous manner. The discharges can occur singly or in rhythmic trains of 1-3 Hz and are usually maximal over the occipital head regions. However, they may also spread to the adjacent posterior temporal and parietal regions. The discharges are attenuated with eye opening and reoccur with eye closure (2539, 44) (Fig. 9). The epileptiform activity is increased during NREM sleep and decreased during REM sleep. Hyperventilation and photic stimulation usually do not enhance the spike discharges. The ictal discharges consist of low-voltage fast activity over one or both occipital regions which can spread more widely (25). There are also subclinical discharges that can occur during sleep (25). The EEG is otherwise normal. Usually there is no demonstrable lesion, and the child is otherwise normal and outgrows the seizures and the spike discharges (25,3946). The EEG pattern of occipital paroxysmal discharges suppressed by eye opening is not specific to benign epilepsy of childhood. It also can be seen with variants of the entity, including benign nocturnal occipital epilepsy, and in patients who have had basilar migraine associated with seizures (3 1,4 1,45). 1-15ow Sturge-Weber syndrome Epileptiform activity and seizures arising from the occipital region or adjacent posterior head regions are-seen with the Sturge-Weber syndrome. The other characteristic EEG findings in Sturge-Weber syndrome include a reduced amplitude of the activity on the side of the facial nevus and intracranial calcification (47). Epilepsy with bilateral occipital calcification An entity of epilepsy with bilateral occipital calcification has been described by Gobbi et al. (48). The EEG findings consist of posterior spike and wave discharges, which are attenuated with eye opening in the waking state, and posterior fast spikes and polyspikes during the sleep state. As the disease progresses, the seizures become more frequent and the EEG shows more diffuse slow and wave discharges and posterior dominant polyspike discharges. The ictal pattern consists of a diffuse recruiting rhythm that is maximal over the posterior head regions (48). Late infantile neuronal ceroid lipofuscinosis In late infantile neuronal ceroid lipofuscinosis, spike discharges are present over the occipital regions in the FP1 F3 bage 6yrs p t Eyes closed Eyes 0P~TIooyv 1 sec FIG. 9. Left occipital spike discharges attenuated by eye opening in a 6-year-old child with benign occipital epilepsy of childhood.

7 EEG IN EXTRATEMPORAL SEIZURES s7 F Age: FIG. 10. Focal occipital seizure discharge characterized by repetitive spike discharges over the left occipital head region in a 22-year-old patient with a mitochondrial cytopathy. Sees red and blue colors in right visual field 1 sec 170 PV earlier stages of the disease. Later, these become more widespread. The most specific and diagnostic findings in this entity, however, are photic-induced spikes over the occipital head regions at low rates of flash stimuli (49,50). Structural lesions Various symptomatic conditions and structural lesions involving the posterior head regions can also be associated with occipital seizures and epileptiform abnormalities. These include, among others, head trauma, birth injury, porencephaly, congenital defects, cortical dysplasia, tumors, inflammatory processes, vascular lesions or malformations, mitochondrial encephalopathies, hematoma, and tuberous sclerosis (10,25,3 1,43,5 1). Interictal discharges that occur with symptomatic occipital epilepsies consist of focal spikes, sharp waves, spike and wave discharges, or polyspike and wave discharges (1,51). The discharges can occur focally over the occipital head regions or with a more widespread reflection over the posterior quadrant. Epileptiform discharges can also be seen over the temporal or centro-temporal region, or as wandering foci from one region to the other (10,52). The EEG may show other abnormalities, including slowing, asymmetry, or attenuation of activity over one or both occipital regions, in addition to the epileptiform abnormalities. Ictal discharges consist of repetitive spikes, sharp waves, and spike and wave or rhythmic fast activity (52) (Fig. 10). The ictal discharges from the occipital region have a lesser tendency to evolve into polymorphic seizure patterns than do seizure discharges from the other areas of the brain (F. W. Sharbrough, personal communication). Ictal discharges that occur focally over the occipital regions are usually associated with elementary visual symptoms or nystagmus (53,54). Occipital seizures can also spread to the temporal, parietal, and frontal lobes, to produce secondarily complex partial seizures or focal motor or sensory seizures (10,43,51,53,54). The ictal discharges that occur in a widespread manner over the posterior head regions with spread to the temporal and other regions may make it difficult to distinguish occipital from temporal or parietal lobe epilepsy (10,41,43,51). There also may be a problem in detecting occipital discharges on scalp recordings, particularly if the seizure focus originates from the mesooccipital region at a distance from scalp leads (51). Rapid spread of the discharges may also make it difficult to identify the origin from the occipital lobe. Muscle artifact can contaminate the recording, adding to the difficulty in detecting the onset of the seizure discharges. CONCLUSIONS Extratemporal seizures can be manifested by varied and complex epileptiform activity, both interictally and ictally. There may be problems with detecting the source of origin with scalp leads secondary to the anatomy of the various regions, deep foci, small restricted foci, foci that are distant from the recording electrodes, rapid spread of the epileptiform, and contaminating effects of muscle and movement artifact. Other means that may be helpful in detecting the site of origin of extratemporal seizures include the use of additional electrodes or special electrodes, digital recording, computer analysis, video.eeg monitoring, corticography, or intracranial or depth recording REFERENCES Ajmone-Marsan C, Ralston BL. The epileptic seizure: its functional morphology 'and diagnostic significance. Springfield, IL: Charles C Thomas, Fegersten L, Roger A. Frontal epileptogenic foci and their clinical correlations. Electroencephalogr Clin Neurophysiol 1961 ; 13: Ludwig B, Ajmone-Marsan C, Van Buren J. Cerebral seizures of probable orbitofrontal origin. Epilepsia 1975;16: Penfield W, Jasper H. Epilepsy and thefunctional anatomy of the human brain. Boston: Little, Brown, Company, Quesney LF, Krieger C, Leitner C, Gloor P, Olivier A. Frontal lobe epilepsy: clinical and electrographic presentation. In: Porter RJ, Mattson RH, Ward AA, Dam M, eds. XVth Epilepsy International Symposium New York: Raven Press, [Advances in epileptology, vol Rasmussen T. Characteristics of a pure culture of frontal lobe epilepsy. Epilepsia 1983; Tharp BR. Orbital frontal seizures: a unique electroencephalographic and clinical syndrome. Epilepsia 1972; 13: Epilepsia, Vol. 39, Suppl. 4, 1998

8 S8 B. F. WESTMORELAND 8. Van Ness PC. Frontal and parietal lobe epilepsy. In: Wyllie E, ed. The treatment of epilepsy: principles and practices. Philadelphia: Lea & Febiger, 1993: Williamson PD, Spencer DD, Spencer SS, Novelly RA, Mattson RH. Complex partial seizures of frontal lobe origin. Ann Neurol 1985;18: Williamson PD, Spencer SS. Clinical and EEG features of complex partial seizures of extratemporal origin. Epilepsia 1986;27(suppl 2):S I. Moms HH. Frontal lobe epilepsies. In: Liiders H, ed. Epilepsy surgery. New York: Raven Press, 1991: Quesney LF, Constain M, Rasmussen T, Stefan H, Olivier A. How large are frontal lobe epileptogenic zones? EEG, ECoG, and SEEG evidence. In: Chauvel P, Delgado-Escueta AV, Halgren E, Bancaud J, eds. Frontal lobe seizures and epilepsies. New York: Raven Press, 1992: [Advances in neurology, vol Williamson PD, Wieser HG, Delgado-Escueta AV. Clinical characteristics of partial seizures. In: Engel J Jr, ed. Surgical treatmenr of the epilepsies. New York Raven Press, 1987:lOl Quesney LF, Gloor P. Localization of epileptic foci. In: Gotman J, Ives JR, Gloor P, eds. Long-term monitoring in epilepsy. Amsterdam: Elsevier, 1985: Quesney LF. Electroencephalographic and clinical manifestations of frontal and temporal lobe epilepsy. Clin Neurol Neurosurg 1987;89: Quesney LF, Constain M, Fish DR, Rasmussen T. The clinical differentiation of seizures arising in the parasagittal and anterolaterodorsal frontal convexities. Arch Neurol 1990;47: Pedley TA. Interictal epileptiform discharges: discriminating characteristics and clinical correlation. Am J Electroencephalogr Techno1 1980; Tiikel K, Jasper H. The electr&ncephalogram in parasagittal lesions. Electroencephalogr Clin Neurophysiol I952; Sharbrough FW. Scalprecorded ictal patterns in focal epilepsy. J Clin Neurophysiol 1993;10: Beaumanoir A, Ballis T, Varfis G, Ansari K. Benign epilepsy of childhood with rolandic spikes. Epilepsia 1974;15: Blom S, Heijbel J, Bergfors PG. Benign epilepsy with centrotemporal foci. Prevalence and follow-up study of 40 patients. Epilepsia 1972; 13: Lerman P. Benign partial epilepsy with centrotemporal spikes. In: Roger J, Bureau M, Dravet C, Dreifuss FE, Perret A, Wolf P, eds. Epileptic syndromes in infancy, childhood and adolescence. 2nd ed. London: John Libbey Eurotext, 1992: Loiseau P, Beaussart M. The seizures of benign childhood epilepsy with rolandic paroxysmal discharges. Epilepsia 1973; Loiseau P, DuchC B. Benign childhood epilepsy with centrotemporal spikes. Cleve Clin J Med 1989;56(suppl I):S Loiseau P. Benign focal epilepsies of childhood. In: Wyllie E, ed. The treatment of epilepsy: principles and practices. Philadelphia: Lea & Febiger, Lornbroso CT. Sylvian seizures and mid-temporal spike foci in children. Arch Neurol 1967;17: Kellaway P. The incidence, significance and natural history of spike foci in children. In: Henry CE, ed. Current clinical neurophysiology. New York EIsevierMorth Holland, LUders H, Lesser RP. Dinner DS, Moms HH. Benign focal epilepsy of childhood. In: Liiders H, Lesser RP, eds. Epilepsy: electroclinical syndromes. New York Springer-Verlag, 1987: Petersen L, Nielsen CJ, Gulmann NC. Atypical EEG abnormalities in children with benign partial (rolandic) epilepsy. Acra Neurol Scand 1983;67(suppl): Dalla Bemardina B, Tassinari CA. EEG of a nocturnal seizure in a patient with benign epilepsy of childhood with rolandic spikes. Epilepsia 197: Sveinbjomsdottir S, Duncan JS. Parietal and occipital lobe epilepsy: a review. Epilepsia 1993; I. 32. Williamson PD, Boon PA, Thadani VM, et al. Parietal lobe epilepsy: diagnostic considerations and results of surgery. Ann Neurol 1992;31: Thomas JE, Reagan TJ, mass DW. Epilepsia partialis continua. A review of 32 cases. Arch Neurol (Chicago) 1977;34:2& Moms HH, Dinner DS, Luders H, Wyllie E, Kramer R. Supplementary motor seizures: clinical and electroencephalographic findings. Neurology 1988;38: Moms HH. Supplementary motor seizures. In: Wyllie E, ed. The treatment of epilepsy: principles and practices. Philadelphia: Lea & Febiger, Pedley TA, Tharp BR, Herman KR. Electroencephalographic and clinical correlates of vertex spike foci. Elecrroencephalogr Clin Neurophysiol 1980;50: 153P. 37. Gibbs FA, Gibbs EL, Gibbs TJ. Relation between specific types of occipital dysrhythmia and visual defects. Johns Hopkins Bull 1968; Gibbs FA, Gibbs EL. Atlas of electroencephalography. Vol. 4. Reading, MA Addison-Wesley, Gastaut H. A new type of epilepsy: benign partial epilepsy of childhood with occipital spike-waves. Clin Electroencephalogr 1982;13: Feme CD, Beaumanoir A, Guemni R, et al. Early-onset benign occipital seizure susceptibility syndrome. Epilepsia 1997;38: Mahen J, Ronen GM, Ogunyemi AO, Goulden KJ. Occipital paroxysmal discharges suppressed by eye opening: variability in clinical and seizure manifestations in childhood. Epilepsia 1995; Panayiotopoulos CP. Benign nocturnal childhood occipital epilepsy: a new syndrome with nocturnal seizures, tonic deviation of the eyes, and vomiting. ChiM Neurol 1989;4: Salanova V, Andermann F, Rasmussen TB. Occipital lobe epilepsy. In: Wyllie E, ed. The treatment of epilepsy: principles and practice. Philadelphia: Lea & Febiger, 1993: Beaumanoir A. Infantile epilepsy with occipital focus and good prognosis. Eur Neurol l983;22: Beaumanoir A, Grandjean E. Occipital spikes, migraine and epilepsy. In: Andermann F, Lugaresi E, eds. Migraine and epilepsy. Boston: Butterworth, 1987: Panayiotopoulos CP. Benign childhood epilepsy with occipital paroxysms: a 15 years prospective study. Ann Neurol 1989;26: Brenner R, Sharbrough F. Electroencephalographic evaluation in Sturge-Weber syndrome. Neurology 1976;26: Gobbi G, Sorrenti G, Santucci M, et al. Epilepsy with bilateral occipital calcifications: a benign onset with progressive severity. Neurology 1988;38: Pampiglione G, Harden A. So-called neuronal ceroid lipofuscinosis: neurophysiological studies in 60 children. J Neurol Neurosurg Psychiatry 1977;40: Westmoreland BF, Groover RV, Sharbrough FW. Electrographic findings in three types of cerebromacular degeneration. Mayo Clin Proc 1979; Blume WT. Occipital lobe epilepsies. In: Liiders H, ed. Epilepsy surgery. New York: Raven Press, 1991: I. 52. Ludwig B, Ajmone-Marsan C. Clinical ictal patterns in epileptic patients with occipital electroencephalographic foci. Neurology 1975;25: Fois A, Malandrini F, Tomaccini D. Clinical findings in children with occipital paroxysmal discharges. Epilepsia 1988;29: Kaplan PW, Tusa RJ. Neurophysiologic and clinical correlations of epileptic nystagmus. Neurology 1993;43: Epilepsia. Vol. 39, Suppl. 4, 1998

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