Electroclinical - BMJable. Eachpatienthadat least onevideo-EEG or ambulatory recording with documentation of absences. In three patients repeat video-EEGrecording ofseizures wasobtained

Journal ofNeurology, Neurosurgery, and Psychiatry 1996;61:471-477

Electroclinical features of idiopathic generalisedepilepsy with persisting absences in adult life

Roberto Michelucci, Guido Rubboli, Daniela Passarelli, Patrizia Riguzzi, Lilia Volpi,Lucio Parmeggiani, Romana Rizzi, Elena Gardella, Carlo Alberto Tassinari

AbstractObjectives-To describe the electroclini-cal features of typical absences persistingin adult life.Methods-Twelve adult patients (aged 21to 56 years) with idiopathic generalisedepilepsy featuring typical absences as theprominent clinical feature were studied.All patients underwent a full clinical andneurophysiological investigation includ-ing ictal documentation of seizures.Results-Neurological examination andneuroradiological investigations werenormal in all cases. Clinical findingsincluded a median age at onset ofabsences of 14 (range 4-32) years, almostconstant tonic-clonic seizures (in 83% ofpatients), frequent episodes of absencestatus (in 33% of patients), and associatedcognitive or psychiatric disturbances.Interictal EEG findings showed normalbackground activity, generalised parox-ysms of spike waves or polyspike waves,and inconstant focal spikes (in fivepatients); runs of polyspikes were seenduring non-REM sleep. Ictal EEG find-ings showed generalised spike waves at3 Hz, sometimes preceded by multiplespikes, or more complex EEG patternswith sequences ofpolyspikes intermingledwith spike waves or polyspike waves,showing discharge fragmentation or varia-tion of intradischarge frequency.Conclusion-The results of the presentstudy show that absences persisting inadult life may show particular clinical andEEG patterns, distinct from those inchildhood or adolescence.

(i Neurol Neurosurg Psychiatry 1996;61:471-477)Department ofNeurology, Universityof Bologna, BellariaHospital, Bologna,ItalyR MichelucciG RubboliD PassarelliP RiguzziL VolpiL ParmeggianiR RizziE GardellaC A TassinariCorrespondence to:Dr Roberto Michelucci,Department of Neurology,Bellaria Hospital, Via Altura3, 40139 Bologna, Italy.Reeived 3 January 1996and in final revised form1 July 1996Accepted 1 July 1996

Keywords: idiopathic generalised epilepsy; typicalabsences; adults; polyspikes

It is widely ackowledged that idiopathic gener-alised epilepsy with absences may persist orrecur in adult life and many papers have beendevoted to the evolution and long term courseof "absence syndromes".'-3

However, little attention has been paid sofar to the clinical and neurophysiological semi-ology of such cases.

Gibberd4 reported 78 patients with petitmal persisting after the age of 20 years andGastaut et al 5 studied 26 patients withabsences continuing after the age of 30, eachfollowed clinically and by EEG for 20 to 37

years. Panayiotopoulos et al6 7 also described alarge population of adult patients with typicalabsences and provided an accurate syndromicclassification of their cases.We report the electroclinical patterns of 12

adult patients with idiopathic generalisedepilepsy, featuring typical absences as theprominent clinical manifestation.

Materials and methodsDuring the past five years we found 12patients meeting the following criteria: (a) ageover 20 years; (b) presence of typical absences,as defined by the Commission on Classifica-tion and Terminology of the InternationalLeague Against Epilepsy (ILAE)8; (c) clinicaland EEG features consistent with the diagnosisof idiopathic generalised epilepsy.9 Thesepatients were identified from 1000 consecutivereferrals from January 1991 to November1995 to our epilepsy clinic.

This was a retrospective study in which thepatients had a full clinical and neurophysiolog-ical investigation including detailed clinicalhistory, neurological and mental examination,CT or MRI of the head, routine EEG, video-EEG (six patients), ambulatory EEG (sixpatients), and sleep EEG (during afternoonnap). The clinical description of the seizureswas obtained by video recording in six patientswith daily absences and by witnesses in theremaining patients.EEGs were performed by using eight to 21

channels with a longitudinal montage. In sleeptracings, ECG, thoracic breathing, and deltoidsurface EMG were monitored. Patients wereasked to count aloud during hyperventilation,which allowed us to evaluate impairment ofconsciousness during generalised spike wavedischarges. In selected patients a more accu-rate neuropsychological assessment (includingreading and presentation of verbal or visualmemory tasks) was required. A Nihon Kohden21 channel polygraph or an eight channelMicromed Computerised EEG system wereused for all the recordings, both during wake-fulness and sleep. For video-EEG studies, asplit screen instrument combining the record-ing of the EEG waveforms with the synchro-nous TV pictures of the patient was used.Ambulatory EEG was accomplished with anOxford Medilog instrument using seven EEGchannels with a longitudinal montage supple-mented by ECG.We examined a total of 49 routine EEG

recordings performed at the time of referral atour Institute. In three patients 12 EEGs dating

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Clinicalfindings

Age of onset of seizures Frequency of seizuresFamily

Patient Sex history Age Abs GTCS 3terks Abs S Abs GTCS J7erks Abs S MelBe Therapy

1 F - 28 24 18 - 28 D SP - 2/life - VPA2 F - 25 4 14 - - D Mo - - - ETS,VPA,PB3 F - 49 23 23 - - W Mo - - ±Me CBZ,VPA,PB4 M - 56 16 20 - 41 SP 2/year - 2/year +Me PHT, PB5 M - 50 32 35 - - Mo 1/life - - - PB6 M - 55 17 27 - 55 D 4/year - 1/life +Me DZP, VPA, PB7 M + 23 11 12 - - D Mo - - ±Be LMT, VPA, PB, CNZ8 M 51 5 8 10 - D Mo D - - VPA9 F + 25 7 12 - 23 D Mo - 1/life +Be PHT, VPA, PB

10 F - 39 10 - - - W - - - - ETS11 M + 37 16 15 14 - W 1/life Mo - - VPA12 M + 21 17 - - - W - - - +Be VPA

Abs = absences; GTCS = generalised tonic-clonic seizures; Abs S = absences status; Me/Be = mental and behavioural status; D = daily; W = weekly; Mo =monthly; SP = sporadic; VPA = valproic acid; ETS = ethosuximide; PB = phenobarbitone; CBZ = carbamazepine; PHT = phenytoin; LMT = lamotrigine;DZP = diazepam; CNZ = clonazepam.

back to the time of onset of the epilepsy and atdifferent intervals thereafter were also avail-able. Each patient had at least one video-EEGor ambulatory recording with documentationof absences. In three patients repeat video-EEG recording of seizures was obtained. SleepEEG was performed in all patients at the timeof our study.

ResultsCLINICAL FINDINGSThese 12 patients represented 1 2% of the1000 unselected patients or 7% of the 170patients with a diagnosis of idiopathic gener-alised epilepsy referred to our epilepsy clinicduring a five year period. The table shows theclinical features of the patients included in thepresent study. The patients (seven men andfive women) had a median age at referral of 38(range 21-56) years. A positive family historyof epilepsy (of idiopathic generalised epilepsytype) or febrile convulsions was present in fourpatients (33%). A specific aetiological factor(birth hypoxia) was reported by two patients(16%). Absences began at a median age of 14(range 4-32) years but three patients had theirfirst absence after the age of 20.The absences were characterised by an

abrupt loss of contact in all patients associatedwith eye blinking in four and gestural automa-tisms in one. The absences were subjectivelyperceived as brief "blackouts" or momentary"loss of concentration". The degree of impair-ment of consciousness varied greatly amongthe patients; three patients were unaware oftheir absences and only neuropsychologicalassessment performed during the EEG dis-charges disclosed mild disruption of contactand mental slowing. Absences were one to sev-eral per day in six patients and occurred at alower frequency in the remaining patients(once a week in four and once a month intwo).

Absence status occurred in four patients(33%). In two of them, the status wasrecorded by video-EEG: in the early phase itconsisted of very frequent absence seizures,recurring every 20-30 seconds, and subse-quently, it took the form of "absence continu-ing", with a clinical picture of stupor andconfusion. Interestingly a status-like conditionwas found in the same patients due to hyper-

ammonaemia after the start of valproate treat-ment. A tonic-clonic seizure was sometimesreported at the end of the absence status.

Associated seizure types were described by10 patients: they consisted of generalisedtonic-clonic seizures (10), myoclonic jerks(two), and atonic seizures (one). Tonic-clonicseizures began at a mean age of 18 years.

At the time of referral, six patients were on asingle drug regimen, one was taking a combi-nation of two drugs, and five were taking threeor more drugs. Nine patients were receivingvalproic acid; seven phenobarbitone; two etho-suximide; two phenytoin; two benzodi-azepines; one carbamazepine; and onelamotrigine. Anticonvulsant treatment withphenytoin and carbamazepine (which are notusually effective in absence epilepsy) was justi-fied in three patients by the need to controlotherwise refractory tonic-clonic seizures.

Neurological examination was normal in allpatients. Some degree of cognitive impairmentconsisting of forgetfulness and mental slowingwas noted in three older (over 50 years)patients. Psychiatric disturbances (withaggressiveness, irritability, and impulsive reac-tions) were seen in three young patients. BrainCT and MRI were normal in all patients.

NEUROPHYSIOLOGICAL FINDINGSWaking interictalfeatures at the time of referralBackground activity was normal in all patients.Waking paroxysmal activity was invariablydetected in each patient: it consisted of gener-alised brief (0-5-2 s) and fast (3-5 Hz) bursts ofspike waves in six patients and of polyspikewaves in the remaining cases. Brief runs ofpolyspikes were also seen in two patients.Associated focal paroxysms were recorded infive. These were short transients of localisedsharp waves or spikes, or both. Focal spikesdid not precede the generalised paroxysms andcould occur in multiple locations in the sameor previous EEGs. Hyperventilation increasedthe generalised abnormalities in all patientswhereas intermittent photic stimulation waseffective in only three patients.

Sleep interictalfeatures at the time of referralNon-REM sleep phases were obtained in eachpatient. Paroxysmal abnormalities wereincreased compared with wakefulness in allpatients and consisted of generalised brief

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Electroclinicalfeatures of idiopathic generalised epilepsy with persisting absences in adult life

Figure 1 Sleep interictalparoxysms in two patients.Sleep phase 2: appearanceofgeneralised discharges ofmultiple spikes. Note theabsence ofany modificationof thoracic breathing,ECG, and deltoid surfaceEMG (right deltoid).

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(0-5-2 s) discharges of spike waves (four),polyspike waves (10), and polyspikes (eight)(fig 1). Associated focal abnormalities weredetected in two patients. Long lasting (up to7 s) runs of polyspikes followed by diffuseslowing (with a pattern similar to subclinicaltonic seizures) occurred in one patient. REMsleep was not recorded in any patients.

Ictalfindings at the time of referralA total of 40 absences were recorded duringvideo-EEG or ambulatory EEG sessions. Ineach patient 1 to 10 seizures were available foranalysis. The ictal patterns were subdividedinto the following categories: (type A) gener-alised spike wave discharge at 3-4 Hz withanterior predominance and abrupt onset andend (10 seizures in three patients); (type B)generalised spike wave or polyspike wave dis-charge at 3-4 Hz beginning with a brief(0-5-2-5 s) fast activity (polyspikes at 13-14Hz) (19 seizures in six patients) (fig 2); (typeC) generalised ictal event in which sequencesof polyspikes were intermingled with spikewaves or polyspike waves at 3-4 Hz, showingdischarge fragmentation and variation of

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Male aged 53 years 20 December 1993

intradischarge frequency (1 1 seizures in threepatients) (fig 2).

In two patients, the coexistence of absencesof type B and C was found (fig 2). Theabsences lasted from three to 60 seconds, thelongest duration being found in one patientwith seizures of type C. Hyperventilation wasan effective activating procedure of absencesin 10 patients. Polygraphic variables (particu-larly surface EMG recording of deltoid mus-cle) did not show changes concomitant withabsences in any patients.

Absence status was recorded by video-EEGin two patients. The EEG features consisted ofeither short spacing absences of type B or along lasting condition of continuous spikewaves at 2-3 Hz.

Evolution ofEEG patternsThree patients showing absences of type B(with a brief run of polyspikes preceding thetypical discharge of spike waves at 3 Hz) at thetime of referral had EEG tracings dating backto the period of onset of epilepsy. Two ofthem, who had their onset of epilepsy at theages of 5 and 10 years, displayed absences of

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Figure 2 Typical absence seizures of type B and C in a 23 year old man. Upper strip: note the presence ofpolyspikes at the onset of the spike wavedischarge and the long duration of the seizure. Lower strip: a prolonged discharge ofpolyspikes is followed by polyspike waves and spike waves. Note thefragmentation of the paroxysms and the waxing and waning changes of discharge frequency.

type A (with the typical generalised dischargeof spike waves at 3-4 Hz) in the early phase ofthe disease (fig 3). Another patient, with anonset of epilepsy at the age of 16, showedabsences of type B also at the beginning of thedisease.

DIAGNOSTIC CONSIDERATIONSFrom the analysis of the clinical and neuro-physiological findings described above we havetried to classify our patients into syndromiccategories according to the proposal of theILAE.9 On the basis of the age of onset ofabsences, two patients (Nos 2 and 9 of thetable) had childhood absence epilepsy andfour patients (Nos 4, 6, 10, and 12 of thetable) were likely to have juvenile absenceepilepsy. Juvenile myoclonic epilepsy wasdiagnosed in two patients (Nos 8 and 11 of thetable) featuring myoclonic jerks as the promi-nent clinical feature. The remaining fourpatients had uncertain syndromic classifica-tion: indeed three (Nos 1, 3, and 5 of thetable) had late onset absences (after the age of

20) and an additional patient (No 7 of thetable), although reporting absences since ado-lescence, displayed high resistance to treat-ment, associated atonic seizures, andbehaviour disturbances, making the diagnosisof juvenile absence epilepsy difficult.

DiscussionWe suggest that our patients were true exam-ples of idiopathic generalised epilepsy. Indeedthe general criteria for the diagnosis of idio-pathic generalised epilepsy as defined by theCommission of the ILAE9 were met in each ofour patients: the generalised clinical expres-sion of the seizures, the generalised EEGpattern of the seizures, the absence of neuro-logical or neuroradiological signs, the interictalEEG findings (normal background activityand generalised discharges at 3 Hz or more),and the increase of the paroxysms during non-REM sleep. The diagnosis of a specific idio-pathic generalised epilepsy syndrome could bereliably made for most of our patients, juvenile

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Figure 3 Evolution ofEEG in one patient, with onset of absences at the age of lO.Note that the absences were characterised by generalised spike wavedischarges at 3-4 Hz at the age of 13 (left); 25 years later the absences consisted of a generalised spike wave discharge preceded by multiple spikes (right).

absence epilepsy being the most frequent con-dition encountered in the present series. Thisfinding is somewhat at variance with theresults described by Panayiotopoulos et at 6who reported a high incidence of juvenilemyoclonic epilepsy in adult patients with per-sisting absences. In our series, four patientscould not be classified with confidence, mostlybecause of an exceedingly late onset ofabsences. It may well be, however, that insome patients absences may escape detectionfor a long time due to their subtle clinical cor-relate (phantom absences).6 The prevalenceof 1 2% of typical absences found in adults inthis study is difficult to compare with otherpublished reports. The epidemiological datamainly reflect the type of population referredto our epilepsy clinic-that is, usually adultand drug resistant epileptic patients with along history of seizures, therapeutic, andsometimes diagnostic problems.

In our study, several clinical and neuro-physiological features deserve special empha-sis. Clinically, the semiology of absences, thefrequency of associated tonic-clonic seizures,the high incidence of petit mal status, and cog-nitive and psychiatric problems were distinc-tive findings.

Absences seemed to be typical from a clinicalpoint of view, as they were characterised by anabrupt loss of contact, sometimes accompa-nied by eye blinking. Their duration anddegree of impaired consciousness variedgreatly among patients. In several cases theduration did not exceed three to five secondsand the loss of contact could be detected only

after a neuropsychological assessment duringthe spike wave discharges. Panayiotopoulos etal6' also emphasised that absence seizures inadults are more difficult to recognise than inchildren, due to their short duration and milddegree of impaired consciousness.

Tonic-clonic seizures occurred in 83% ofour patients. A similar incidence was alreadyreported by other investigators in cases ofabsences persisting into adult life4-7; indeedmost of our patients began to have absencesafter the age of 10 years and this later onsetabsence epilepsy is more likely to be associatedwith generalised convulsions.' 3 On the otherhand the occurrence of this seizure type inpatients with absences is widely considered afactor forecasting the persistence of epilepsyand resistance to treatment.7 10

Absence status occurred at some time in athird of our patients and was recorded byvideo-EEG in two patients. It took the form of"absence continuing" often preceded by a pro-nounced increase of absences and followed by atonic-clonic seizure. Although absence statusmay occur at any age,"I it has been reported tooccur more often in adulthood,46 12 sometimesappearing de novo in previously non-epilepticpatients."I Panayiotopoulos et al 6 argued thatin cases of "late onset absence status" without aknown history of epilepsy, accurate clinicalobservation may disclose phantom absences.

Cognitive disturbances consisting of forget-fulness and mental slowing without evidenceof intellectual deterioration were noted inthree older patients, two of them exhibitingfrequent episodes of petit mal status and

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hyperammonaemia related stupor. Gastaut et

al7 have also reported a high incidence of lateonset psychomotor slowing in their series ofadults with persisting absences and noted thatthis finding was almost exclusively present infemale patients with long term treatment withcombined drugs. Conversely, in our experi-ence frequent absences and repeated episodesof absence status seem to predispose to mentalslowing; age and metabolic factors (hyperam-monaemia related to valproate treatment)could also play a part. Psychiatric and behav-ioural problems consisting of aggressiveness,impulsive reactions, and irritability were foundin three young patients. Psychiatric problemshave been reported to occur in 29% of patientswith absence epilepsy,2 which is similar to thatin our series. Recent data on psychosocialadjustment in young adults with absenceepilepsies indicate that even this medicallybenign condition has a great impact on

patients' lives. 3

Evaluation of EEG in our patients also dis-closed distinctive features including preserva-

tion of a normal background activity,persistence of interictal generalised paroxysms

increased by hyperventilation in routinerecords, independent focal spikes, activationof the abnormalities (mostly in the form ofpolyspikes or polyspike waves) during slowsleep, and peculiar ictal patterns.

Background activity has been reported toremain normal after many years of seizures inidiopathic generalised epilepsy.29 In our

patients interictal waking paroxysms were

identical to those found in typical idiopathicgeneralised epilepsy although an excess ofpolyspikes was often detected. Focal spikes,occurring as independent abnormalities with a

high tendency to change in location during thesame or following tracings, are not surprisingas they have been reported and accepted intrue generalised epilepsy.'4 The preponder-ance of fast paroxysmal activities during sleepis unusual in idiopathic generalised epilepsyand is classically reported in secondary gener-alised epilepsies. However, sleep patterns inadult idiopathic generalised epilepsy have notbeen reported so far.

In most of our patients ictal patterns ofabsences were peculiar in that they showedeither a brief run of polyspikes preceding thetypical generalised discharge at 3-4 Hz or

more complex patterns with sequences ofpolyspikes intermingled with spike waves andchanges of frequency or discharge fragmenta-tion. Such EEG patterns in absences haverarely been mentioned in the medical litera-ture and have never been described in detail.De Castro et al'6 noted the loss of rhythm ofthe spikes and waves or the variable frequencyof the discharge during a single attack. Oller-Daurella'7 described the appearance of poly-spikes, either in the interictal tracing or beforethe spike wave disharge, in patients havingabsences at the time that grand mal attacksappeared. Similar findings were occasionallymentioned by Livingston et al,' Gastautand Tassinari,'5 Gastaut et al,) andPanayiotopoulos et a?' in adult patients with

idiopathic generalised epilepsy.The pathophysiology of these multiple

spikes in idiopathic generalised epilepsy isunknown. An excess of fast rhythms is some-times linked to treatment with benzodi-azepines but these were given to only twopatients in our series. We think that these ictalfeatures are typical of absences persisting inadult life and indicate resistance to treatmentor evolution toward grand mal epilepsy.

These clinical and neurophysiological find-ings may give rise to problems of differentialdiagnosis, mainly with frontal lobe epilepsy.'9It has been known for a long time that frontallobe epilepsy may at some stage of its evolu-tion mimic idiopathic generalised epilepsyboth from a clinical point of view and on EEG.Clinically the three seizure types encounteredin idiopathic generalised epilepsy (absences,tonic-clonic seizures, and massive myoclonias)have been found in frontal lobe epilepsy.20 22Electrically the ictal and interictal manifesta-tions of frontal lobe epilepsy may have thesame semiology as idiopathic generalisedepilepsy. 19 23 Roger and Bureau'9 suggestedthat, when unequivocal electroclinical signsare lacking, frontal lobe epilepsy may be sus-pected in patients who do not fit one of thespecific idiopathic generalised epilepsy syn-dromes classified in the IIAE proposal.9

In our patients a reliable diagnosis of idio-pathic generalised epilepsy specific syndromecould be made in eight patients and wasuncertain only in four. Abnormalities on EEGin patients with frontal lobe epilepsy, althoughapparently generalised, usually take the formof secondary bilateral synchrony- that is, focalepileptiform discharges followed by bursts ofbilateral synchronous spike wave complexes.24In five of our patients focal abnormalities onEEG occurred in combination with the gener-alised paroxysms. However, the focal spikesnever preceded the generalised discharges, ascommonly seen in secondary bilateral syn-chrony, but occurred as independent abnor-malities with a high tendency to change inlocation during the same or subsequent trac-ings. Moreover, isolated focal EEG abnormali-ties have been found in cases of true childhoodabsence epilepsy.'4 1'

In conclusion, we have reported the clinicaland EEG features of idiopathic generalisedepilepsy with absences persisting or recurringinto adult life, which seem to be different fromthose usually found in infancy or adolescence.We suggest that these findings are distinctiveand deserve consideration for proper diagnosisand treatment.

This work was partially made possible by grants from ProgettoTelethon E 109, Ministry of Health (40% funds), and CNR(grant No 942920).

1 Livingston S, Torres J, Pauli LL, Rider RV. Petit malepilepsy: results of a prolonged follow-up study of 117patients. _AAIA 1965;194:227-32.

2 Loiseau P, Pestre M, Dartigues JF, Commenges D,Barberger-Gateau C, Cohadon S. Long term prognosisin two forms of childhood epilepsy: typical absenceseizures and epilepsy with rolandic (centrotemporal)EEG foci. Ann Neurol 1983;13:642-8.

3 Sato S, Dreifuss FE, Penry JK, Kirby DD, Palesch Y.Long-term follow-up of absence seizures. Neurology1 983;33: 1590-5.

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4 Gibberd FB. The prognosis of petit mal in adults. Epilepsia1972;13: 171-5.

5 Gastaut H, Zifkin BG, Mariani E, Salas Puig J. The long-term course of primary generalized epilepsy with persistingabsences. Neurology 1986;36: 1021-8.

6 Panayiotopoulos CP, Chroni E, Dascalopoulos C, Baker A,Rowlinson S, Walsh P. Typical absence seizures inadults: clinical, EEG, video-EEG findings and diagnosticsyndromic considerations. Neurol Neurosurg Psychiatry1992;55: 1002-8.

7 Panayiotopoulos CP, Giannakodimos S, Chroni E.Typicalabsences in adults. In: Duncan JS, Panayiotopoulos CP,eds. Typical absences and related epileptic syndromes.London: Churchill 1995:289-99.

8 Commission on Classification and Terminology of theInternational League Against Epilepsy. Proposal forrevised clinical and electroencephalographic classificationof epileptic seizures. Epilepsia 1981;22:489-501.

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Lorentz De Haas, eds. The epilepsies, handbook of clinicalneurology. Amsterdam: North-Holland PublishingCompany, 1974:130-44.

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16 De Castro P, Sacristan J, Moya G, Sanabra F. Phenomenesinterparoxystiques dans les traces EEG presentant desdecharges pointe onde bilaterales et synchrones. RevNeurol 1956;94:882-8.

17 Oller-Daurella L. Contribucion al estudio de las ausenciasepilepticas. Evolucion clinica y EEG de 109 casos de ausen-cias, seguidas a traves de un periodo de tiempo que oscila entre10 y 20 anos de observacion personal [thesis]. Barcelona:University of Barcelona, 1967.

18 Gastaut H, Tassinari CA. Epilepsies. In: Remond A, ed.Handbook of electroencephalography and clinical neurophysi-ology, Vol 13. Clinical EEG III, part A. Amsterdam:Elsevier, 1975:13A:1-13A:104.

19 Roger J, Bureau M. Distinctive characteristics of frontal lobeepilepsy versus idiopathic generalized epilepsy. In:Chauvel P, Delgado-Escueta AV, Halgren E, Bancaud J,eds. Frontal lobe seizures and epilepsies, Advances inNeurology. Vol 57. New York: Raven Press,1992:339-410.

20 Rasmussen T. Characteristics of a pure culture of frontallobe epilepsy. Epilepsia 1983;24:482-93.

21 Saint-Hilaire JM, Giard N, Bouvier G, Labrecque R.Anterior callosotomy in frontal lobe epilepsies. In: ReevesAG, ed. Epilepsy and the corpus callosum. New York:Plenum Press, 1985:303-14.

22 Swartz BE. Pseudo-absence seizures: a frontal lobe phe-nomenon. J7 Epilepsyl 992;5:80-93.

23 Bancaud J,Talairach J, Morel P, et al. "Generalized" epi-leptic seizures elicited by electrical stimulation of thefrontal lobe in man. Electroencephalogr Clin Neurophysiol1974;37:275-82.

24 Gastaut H, Zifkin B, Magaudda A, Mariani E.Symptomatic partial epilepsies with secondary bilateralsynchrony: differentiation from symptomatic generalizedepilepsies of the Lennox-Gastaut type. In: Wieser HG,Elger CE, eds. Presurgical evaluation of epileptics. Berlin:Springer Verlag, 1987:308-16.

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Documents

Electroclinical - BMJable. Eachpatienthadat least onevideo-EEG or ambulatory recording with documentation of absences. In three patients repeat video-EEGrecording ofseizures wasobtained