Archives ofDisease in Childhood 1995; 73: 552-562

PERSONAL PRACTICE

The EEG and neuroimaging in the managementof the epilepsies

N V O'Donohoe

DiagnosisLennox wrote that 'every fresh case of epilepsyis an undiagnosed one'.1 Epilepsy is a recurringdisorder of brain function in which seizures,which may be convulsive or non-convulsive,partial or generalised, are the presentingsymptoms. The diagnostic pathway from thecomplaint of seizures to the verification ofepilepsy may be a difficult one. It is essentialthat misdiagnosis be avoided, recognising thatby no means all children with paroxysmalevents, spells, or 'funny turns' are sufferingfrom epilepsy.2 3

Apart from the need of a correct diagnosis,the other important diagnostic considerationsare seizure diagnosis, that is categorisation ofthe type or types of seizures occurring; aetio-logical diagnosis, recognising that it is now

possible to identify pathological, genetic,and biochemical abnormalities in a growingnumber of cases; and syndrome diagnosis,which consists of the identification of a par-ticular epileptic syndrome, if one can bedelineated.4 The cornerstones of diagnosis inall instances reside, as they have always done,in careful history taking and physical exami-nation.5 One might add that the wide-spread availability of the hand held camcorderprovides us with a new and convenient methodfor recording clinical seizures on videotape,either at home or in the clinic.

Diagnostic role of the EEGThe electroencephalogram (EEG) remainsthe single most valuable aid to the clinicaldiagnosis of epilepsy, a diagnosis for which itmay offer support but one which it will notnecessarily exclude. It is likely that the EEGwill retain a permanent place in the every-day measurement of brain function. EEGexaminations are painless, usually of shortduration, widely available, and relativelyinexpensive. Interictal epileptiform dischargesare generally more frequently seen in infantileand childhood epilepsy than in adult forms.6There are, however, considerable differencesin paediatric EEGs, as compared with adulttracings, and evolving changes in the EEG,both in the waking state and during sleep,occur from infancy through early childhoodand into late childhood.7 The interpreta-tion of paediatric EEGs requires specialknowledge and experience on the part of the

examiner and should preferably be doneby one well versed in the problems ofneuropaediatrics. It is recommended thatEEG departments specifically for childrenare essential as also, indeed, are EEG techni-cians familiar with the everyday problems ofobtaining good and reliable recordings inchildren.8

The EEG in the classification andmanagement of epilepsyIn addition to its value as a diagnostic aid, theEEG may:

* Help in classifying the epilepsies* Suggest an aetiology* Guide clinical management (choice ofdrugs, assessment of response to treatment,decisions about stopping treatment)* Provide evidence of localisation whenepilepsy surgery is contemplated.

The epilepsies and epileptic syndromesThe epilepsies are classified in two ways. First,a distinction is made between the generalisedepilepsies, in which seizures apparently arisesimultaneously in both hemispheres, andpartial (or localisation related) epilepsies, inwhich seizure onset is confined to a discreteregion of cortex. The second dichotomy distin-guishes primary or idiopathic epilepsies arisingin a structurally normal brain from secondaryor symptomatic epilepsies arising in patientswith structural brain disease and cryptogenicepilepsies caused by presumed but unprovedpathology.9

Various specific brain syndromes are now

recognised within the general framework ofthe epilepsies.10 Many of these have distinctclinical features, treatment, and prognosis.Primary epileptic syndromes with no demon-strable pathology, in which the seizures con-

stitute the disease, are distinguished fromsecondary or symptomatic epileptic syn-dromes, in which the seizures draw attention tothe existence of an underlying neurological dis-order. The primary syndromes are usually agerelated, have a strong genetic component, andoften respond well to treatment with a goodpossibility of permanent remission. The sec-

ondary syndromes include other evidence ofbrain dysfunction and response to treatmentand prognosis are uncertain.

The following two papersare the beginning ofanoccasional series where wehave asked two eminentexperts to tackle the sameclinical problem. ProfessorNiall O'Donohoe and DrChristopher Verity haveapproached the subject indifferent ways.

Editors

Department ofPaediatrics, TrinityColiege, Dublin

Correspondence to:Professor N V O'Donohoe,43 Orwell Park, Rathgar,Dublin 6, Ireland.

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The EEG and the classification of theepilepsiesSeizures, either generalised or partial, are theclinical events which draw attention to theexistence of various epilepsies and epilepticsyndromes. The EEG can be extremely valu-able in making a precise diagnosis of the typeof epilepsy that is present. In primary oridiopathic generalised epilepsies, both ictaland interictal discharges are generalised. Theclassical 3 Hz spike-wave discharges seeninterictally and during the absences of child-hood absence epilepsy (true petit mal) aretypical and represent the electrographic markerof the inherited predisposition to epilepsy.Equally important in such an EEG is thepresence of a normal background activity.Symptomatic generalised epilepsies, on theother hand, usually show a diffuse abnormalityof the background rhythm, reflecting thegeneralised cerebral pathology, and interictaland ictal discharges are of varied morphology.

In primary partial epilepsies as, for example,in the common benign partial epilepsy withcentrotemporal (rolandic) spike discharges,the location and morphology of the spikes areusually typical and, again, the backgroundactivity is normal. Symptomatic partialepilepsies are characterised by the presence offocal discharges, both at seizure onset and inthe interictal state. Secondary generalisation ofsuch discharges may occur and there areusually other associated abnormalities such asfocal slowing and disorganisation of the back-ground rhythm.6 8 It is of crucial diagnosticimportance to differentiate the rolandic spikedischarges seen in benign partial epilepsy ofchildhood from those discharges which arisedeep in the temporal lobes in children present-ing with complex partial seizures. The latterare propagated to the anterior or mid-temporalareas without suprasylvian extension. Theclinical presentations are, of course, quitedifferent in the two epilepsies. Curiously,however, sleep is a potent activator ofboth types of discharge and it should beremembered that the waking record may notreveal discharges in either epilepsy. In fact,sleep is the single most important activatingprocedure available for use during everydayEEG recordings. It should be utilised as muchas possible in the evaluation of suspectedepilepsy, especially when interictal epilepti-form activity is not well defined or even absentin the waking record. All night sleep recordingsare valuable in some cases and may help todifferentiate complex partial seizures arisingfrom the frontal lobes, often misdiagnosed asnon-epileptic sleep disorders.'1 Sleep depriva-tion, before a daytime EEG, can enhance thepossibility of obtaining spontaneous sleepduring the recording.

The EEG and aetiological diagnosisExact aetiological diagnosis remains difficult inthe epilepsies, despite great advances in theunderstanding of their physiological andmolecular basis.'2 Nevertheless, as aetiologyhas important implications for higher cortical

function in epilepsy, influences the naturalhistory and the response to treatment of thedisorder, and is closely linked to outcome andthe possibility of remission, it should be care-fully considered in each case. The EEG is ofvalue for identifying particular epilepticsyndromes (for example infantile spasms,Lennox-Gastaut syndrome) with consequentimplications for management and prognosis.Specific EEG patterns of abnormality are seenin subacute sclerosing panencephalitis, 13Batten's disease,'4 lissencephaly,'5 and thehappy puppet syndrome of Angelman,'6 in allof which clinical epilepsy may occur.

The EEG and clinical management:choice ofdrugsThe EEG can assist in the choice of drugs fortreating particular epilepsies but only to a verylimited extent. Perhaps only in childhoodabsence epilepsy with classical 3 Hz spike-wavedischarges does the EEG dictate the use ofethosuximide or sodium valproate or now, inresistant cases, a trial of lamotrigine.'7Contrariwise, typical or atypical spike-wavepatterns in children with other types of absenceseizure may prohibit the use of carbamazepinewhich can cause an exacerbation of epilepsy inthese seizure disorders.'8

Ongoing managementThe EEG is of limited value as a reflection ofclinical improvement in epilepsy, exceptperhaps in some of the primary generalisedepilepsies, where clinical and EEG improve-ment may coincide. In the most commonepileptic syndrome of schoolchildren (benignpartial epilepsy with centrotemporal spikes),the frequency of the discharge bears no rela-tionship to the severity or otherwise of theclinical epilepsy and EEG discharges maypersist long after clinical remission hasoccurred. Furthermore, there is considerablediurnal and nocturnal variability in the EEGand a 30 minute recording provides only abrief window depicting the physiological stateof the brain at that time.8 The widespreadmisconception that the EEG will provide theclinician with information about the state ofthe patient's epilepsy leads to unnecessaryrequests for repeat EEG examinations, therebyadding to the burdens of EEG departments.Neither annual nor other periodic 'routine'EEGs add much to patient assessment, whichshould remain predominantly a clinicalexercise. However, if there has been a clear cutrecent deterioration in the clinical state, andthis is particularly true of a chronic epilepsy,evidence of associated marked deterioration inthe EEG may point to the need for a thoroughreview of the case and its management andperhaps the need for additional investigations.

Withdrawing treatmentClinical considerations should also determinedecisions about withdrawing medication andthese should include knowledge about the

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O 'Donohoe

natural history of the particular epilepsy andthe possibility ofremission. There is an unques-tionable correlation between individual epilep-tic syndromes and the success or failure of drugtreatment. Primary generalised epilepsies dobest while those epilepsies characterised by sec-ondary partial seizures, particularly complexpartial seizures, and cases with multiple seizuretypes, fare worst. In some syndromes, the EEGremains abnormal long after clinical remissionhas occurred. The example of benign partialepilepsy with centrotemporal spikes has beengiven. On the other hand, a normal EEGduring treatment of juvenile myoclonicepilepsy, in which the propensity to seizuresand the consequent need for antiepileptic drugsare life long, should not be used as an argumentfor stopping treatment.5

Nevertheless, despite these clinical consider-ations and caveats, the EEG can be a valuableadditional aid when deciding how and when towithdraw treatment, especially in difficultcases.19 Two definitive studies of the outcomeof childhood epilepsy, separated by an intervalof 12 years,20 21 both found that, in general, theotherwise normal child who had had a limitednumber of seizures and whose EEG wasnormal or only mildly abnormal was least likelyto relapse when treatment was stopped.

Contemplating epilepsy surgeryEpilepsy surgery is being considered moreoften in children and adolescents with medic-ally intractable seizures. Presurgical evaluationof such cases is necessarily very detailed. Inchildren who may require temporal lobe resec-tion because of intractable complex partialseizures, the non-invasive recording of ictalevents using simultaneous EEG and videomonitoring remains the most important pre-operative investigation.22 Invasive depth EEGrecordings using bilateral sphenoidal elec-trodes may additionally be necessary and canbe of invaluable agsistance in identifying deepseated mesial temporal epileptogenic foci.

Febrile convulsionsPaediatricians often are uncertain about therole of the EEG in the management of thechild with febrile convulsions. In the writer'sopinion, there is no benefit from routine EEGexamination in such children. A history toestablish the diagnosis, a physical examinationto find the source of fever and to excludemeningitis, and a lumbar puncture if there isdoubt about meningitis and especially ininfants under 1 year, are the only measures thatshould regularly be undertaken after mostfebrile seizures.23 24 The EEG is not a guide totreatment or prognosis and should certainlynot be undertaken after the initial convulsion.Bilateral slow wave changes will usually bepresent after the majority of attacks and willpersist for some days. Focal or asymmetricalslowing may be found after more prolongedseizures. Reversion ofthe EEG to normal is therule. A problem arises in children withrepeated febrile convulsions and in whom

reassurance for parents may be an issue. Again,the record will nearly always be normal or mayoccasionally show spike-wave paroxysms, par-ticularly in rather older children during drowsi-ness. This latter finding should be regarded asan expression of a genetic predisposition toepilepsy and certainly not as an indication thatepilepsy will develop in an individual patient.5However, it should be remembered thatseizures are sometimes provoked by fever inchildren who have genuine epilepsy. In these,the EEG will usually show unequivocal andfrequent epileptic abnormalities.

EEG abnormalities in normal childrenIt is important that paediatricians should beaware that epileptiform discharges may befound in about 3% ofnormal children7 25 and inup to a quarter of healthy siblings of childrenwith benign partial epilepsy. These dischargesare similar to those which occur in benignpartial epilepsy, are predominantly mid-tempo-ral and centrotemporal in situation, and vary inintensity and location from time to time, includ-ing moving from side to side. Unfortunately, afolklore has grown up over many years in con-nection with these fortuitous findings and termssuch as 'masked epilepsy' and 'epileptic equiva-lents' have been used. Children with a variety ofnon-epileptic complaints such as behaviourproblems, syncopal episodes, night terrors,headache, abdominal pain, tics, so-called mini-mal brain damage, specific or general (includingattentional) learning difficulties, etc, have beensubjected to unnecessary antiepileptic medica-tion and their parents made anxious aboutpossible epilepsy.2 Using the EEG to decidewhether a patient's symptoms are epileptic orpsychogenic or due to some non-cerebral causesuch as syncope is an improper use of the inves-tigation and can be misleading. A single normalEEG is not evidence against epilepsy nor is thefinding of epileptiform discharges in the EEGevidence that the patient's symptoms are neces-sarily epileptic in nature. The recognition of theepileptic nature of any symptoms or group ofsymptoms is a clinical task predominantly andshould remain so.26

Advent ofneuroimagingDuring the past 25 years, the advent of neuro-imaging techniques has revolutionised neurol-ogy, neuroradiology, and neurosurgery. In theevaluation and management of epilepsy,computed tomography and magnetic reso-nance imaging (MRI) now complement theelectrophysiological information provided inthe EEG by identifying structural brain diseasewhich may be causally related to the develop-ment of seizures. At present, computed tomog-raphy is much more widely available and alsoless expensive than MRI and this situation isunlikely to change in the immediate future.

Computed tomography and epilepsyA relatively early computed tomography studyof children with all types of seizures revealed

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The EEG and neuroimaging in the management of the epilepsies

an overall incidence of abnormalities in a thirdof cases.27 The presence of an abnormalneurological examination in any case doubledthe likelihood of finding an abnormality oncomputed tomography brain scan. Abnor-malities were demonstrated most frequently inpatients with secondary partial seizures andwith secondary generalised seizures but wererarely seen in children with partial or gener-alised seizures of primary type. In a morerecent study, at a north of England specialschool for children with epilepsy (and thereforea selected group with chronic epilepsy and withassociated handicaps in a proportion), an over-all incidence of abnormalities on computedtomography was again found in a third ofcases.28 The usual abnormality detected wassome degree of generalised or focal corticalatrophy.

MRI and epilepsyAmong the several advantages of MRI com-pared with computed tomography are highersensitivity, superior image quality, lack ofradiation exposure, and a capacity for multi-planar display. Visualisation of central nervoussystem anatomy has been revolutionised byMRI because it enables fine detail of the brainto be displayed and is capable of definingsubtle abnormalities of the cortical grey matterand hippocampus which are not visible oncomputed tomography.29 Rapid advances inMRI techniques have led especially toimprovements in the detection of brain lesionsin patients with epilepsy.30 New insights intothe aetiology of the epilepsies have been gainedand there have even been discoveries of newsyndromes characterised by epilepsy associatedwith mental handicap and developmentalabnormalities ofthe brain.31 MRI is superior tocomputed tomography in identifying abnor-malities of cortical architecture, especiallythose resulting from neuronal migration dis-orders, for detecting gliomas and vascular mal-formations, and in visualising the temporallobe structures.32 The information provided byMRI is extremely important both for the recog-nition of these disorders and for the planningof appropriate medical and surgical treatment.MRI scanning in the paediatric patient has

the disadvantage, however, that sedation oreven a general anaesthetic may be required toensure the degree of immobility necessary inorder to obtain clear interpretable images.Furthermore, as in the early years of computedtomography, considerable experience isrequired in the methodology and interpretationof paediatric MRI and the advice of a neuro-radiologist with a special interest in that subjectmay be essential.

MRI and temporal lobe epilepsyEpilepsy originating from the temporal lobes isthe most important secondary partial epilepsyof childhood and may cause complex partialseizures to occur even from very earliestchildhood. The causative lesions are situateddeep in one or other temporal lobe.33

Developmental abnormalities includingneuronal migration disorders, vascular andneoplastic conditions, and, most importantly,hippocampal sclerosis (mesial temporal sclero-sis) are the main lesions found. MRI is muchmore sensitive to the localisation and lateralisa-tion of these lesions than are either conven-tional scalp EEG or computed tomographyscanning.34 This has important implicationsfor the management of this most disabling andchronic form of epilepsy as precise identifica-tion and early surgical removal of the offendinglesion may cure the epilepsy and also help toprevent the psychiatric, social, and cognitivemorbidity of severe uncontrolled epilepsy inchildhood.5

Functional neuroimagingThe EEG is helpful in diagnosis but is poor atlocalising functional changes in epilepsy.Computed tomography and MRI provide onlystructural information. Functional neuroimag-ing techniques can provide information aboutregional metabolic activity in the brain.Positron emission tomography (PET) islargely a research tool. Single photon emissiontomography (SPECT) uses a gamma cameraand is less expensive than PET and morewidely available. Both techniques showmetabolism and perfusion in the epileptogenicfocus to be decreased interictally and ictallyincreased and many help to localise a focuswhich is not visible on MRI.35 The recentdevelopment of non-invasive functional MRImethods is most exciting as they are capablenot only of demonstrating the structure of thebrain in fine detail, but also of providing infor-mation about the underlying metabolism ofbrain regions and of revealing the functionalactivity of the brain with high spatial and tem-poral resolution.36 They are already being usedto study cryptogenic generalised epileptic syn-dromes such as infantile spasms and Lennox-Gastaut syndrome in an attempt to locate areasof focal dysfunction which may be amenable tosurgical removal. It is important to emphasisethat these functional images do not make senseby themselves but only do so in the context ofthe whole clinical, EEG, neuropsychological,and neuroradiological information about thechild.

Indications for neuroimagingWhat should the paediatrician regard as indi-cations for neuroimaging when dealing withthe problem of an individual child's epilepsy(for most paediatricians, this will meancomputed tomography, at least in the firstinstance)? The following are the main indica-tions:

* Partial seizures (in all children), exceptthose with benign partial epilepsy* Abnormal neurological signs* Persistent and localised slow wavechanges (delta focus) and/or spike or sharpwave foci, either or both of which mayindicate the presence of a local structurallesion27 37

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556 O'Donohoe

* Manifestation of a sudden change inseizure pattern, in neurological examination,or in the EEG (any or all of which may indi-cate the presence of a progressive lesion).Patients with refractory seizures, even of

many years' duration, should be considered ascandidates for imaging, particularly MRI ifavailable, because of the possible presence of apotentially resectable epileptogenic lesion.Indolent gliomas, for example, may be an occultcause of chronic epilepsy.38 There is increasingrecognition of the importance of embryofetallesions, especially neuronal migration disorders,in children with moderate or severe mentalhandicap and epilepsy.32 Lissencephaly (agyria-pachygyria), for example, may be suspected bythe presence of excessive high amplitude fastactivity in the EEG and a computed tomo-graphy scan will show the typical smoothappearance of the cortex.'5 The importance ofsearching for the brain lesions of tuberosesclerosis by computed tomography in the severeepilepsies of infancy and early childhood is wellknown.39

Epilepsy is a common disorder, beginningmost frequently during childhood and adoles-cence, and one which causes great parentalworry. It is not surprising, therefore, that acomputed tomography brain scan is oftenrequested for parental reassurance in the faceof marked and continuing anxiety. It should bepointed out to the family, however, thatcomputed tomography in young children canbe difficult and may require sedation or evenanaesthesia. It also involves a minimal amountof ocular irradiation. Furthermore, the reassur-ance provided by a normal computed tomo-graphy is not absolute as subsequent scansmonths or years later may reveal a lesion suchas a glioma or other tumour.38 There is simplyno justification for scanning all children withepilepsy and the investigation should be under-taken primarily on the basis of clinical historyand examination.37

Medicolegal problemsThe rising tide of medicolegal litigation allegingnegligence by doctors has inevitably led to thepractice of defensive medicine. This has meantthe overuse of investigation in order to prevent,at a later date, allegations ofnegligence becauseof failure to perform a particular test or radio-logical procedure. For paediatricians negli-gence means that they have failed to fulfil theirduty of care to the child. To succeed in such aclaim, the parents need to show that their childis damaged, they have to demonstrate the causeof that damage and then prove, on the balanceof probabilities, that the damage was due to thenegligence of the doctors.40A relevant dilemma for paediatricians in this

context is whether to choose a computedtomography or MRI scan when evaluating achild with seizures. Although MRI is techni-cally superior to computed tomography, itscurrent cost, lack of availability, and the factthat is a lengthy and rather frightening proce-dure for a child, prohibit its use as a 'screening'procedure, even if one accepts that it is

reasonable to screen for every eventuality.Paediatricians investigating a child withepilepsy may be anxious about missing a pro-gressive and potentially treatable lesion such asa neoplasm. In fact, neoplasms are relativelyrare causes of childhood epilepsy as most arisesubtentorially and are non-epileptogenic.Nevertheless, deep seated temporal lobetumours can cause intractable complex partialseizures33 and such tumours may be revealedby MRI, although invisible on computedtomography. If, therefore, the paediatricianremains concerned about the presence of atumour or other structural lesion after anormal computed tomogram in a child withcomplex partial seizures, MRI should beobtained. MRI should also be requested whenthere are equivocal lesions on computedtomography. Attention has already been drawnto the importance of considering patients withrefractory seizures for MRI, if available,because of the possible existence of a lesionwhich may be surgically treatable. Infants withunexplained seizures should be considered forcomputed tomography, especially if there is asuspicion of non-accidental trauma, as sub-dural haematoma not infrequently presents inthis manner.41

In conclusion, it must be emphasised thatthe surest means of avoiding error and also theaccusation of not having 'done everything' isone which applies to the investigation andmanagement of childhood epilepsy in general,that is, meticulous clinical assessment andregular review of the problem. Only thus canunnecessary and expensive investigativeprocedures be kept to a minimum.

1 Lennox WG. Epilepsy and related disorders. Vols 1, 2.London: J and A Churchill, 1960.

2 Stephenson JBP. Fits andfaints. Clinics in developmental med-icine. No 109. Oxford: Blackwell Scientific Publications,1990.

3 Brett EM. 'It isn't epilepsy is it, doctor?' BMJ 1990; 300:1604-5.

4 O'Donohoe NV. Delineation of epileptic syndromes.Current Paediatrics 1992; 2: 68-72.

5 O'Donohoe NV. Epilepsies of childhood. 3rd Ed. London:Butterworth-Heinemann, 1994.

6 Drury I. Epileptiform patterns of children. J ClinNeurophysiol 1989; 6: 1-39.

7 Peterson I, Eeg-Olofsson 0. The development of the elec-troencephalogram in normal children from the age of 1through 15 years. Non-paroxysmal activity. Neuropadiatrie1971; 2: 247-304.

8 Binnie CD. Neurophysiological investigations of epilepsy inchildren. In: Ross EM, Woody RC, eds. Epilepsy. Bailliere'sdinical paediatrics. International practice and research. Vol 2.No 3. London: Bailliere Tindall, 1994: 585-604.

9 O'Donohoe NV. Classification of epilepsies in infancy,childhood and adolescence. In: Ross EM, Woody RC,eds. Epilepsy. Bailliere's dinical paediatrics. Internationalpractice and research. Vol 2, No 3. London: BailliereTindall, 1994: 471-84.

10 Roger J, Bureau M, Dravet C, Driefuss FE, Perret A, WolfP. Epileptic syndromes in infancy, childhood and adolescence.2nd Ed. London, Paris: John Libbey, 1992.

11 Stores G. Confusions concerning sleep disorders and theepilepsies in children and adolescents. Br J Psychiatry1991; 158: 1-7.

12 Schwartzkroin PA, ed. Epilepsy. Models, mechanisms and con-cepts. Cambridge: Cambridge University Press, 1993.

13 Ibrahim MM, Jeavons PM. The value of electroencephalog-raphy in the diagnosis of subacute sclerosing panenephali-tis. Dev Med Child Neurol 1974; 16: 295-307.

14 Pampiglione G, Harden A. So-called neuronal ceroid lipo-fuscinosis. Neurophysiological studies of 60 children. JfNeurol Neurosurg Psychiatr 1977; 40: 323-30.

15 Gastaut H, Pinsard N, Raybaud C, Aicardi J, Zifikin B.Lissencephaly (agyria-pachygyria). Clinical findings andserial EEG studies. Dev Med Child Neurol 1987; 29:167-80.

16 Boyd SG, Harden A, Patton MA. The EEG in early diag-nosis of Angelman's (happy puppet) syndrome. Eur JPediatr 1988; 147: 503-13.

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17 Besag FMC. Difficult-to-treat childhood epilepsies. In:Reynolds EH, ed. Lamotrigine - a new advance in thetreatment of epilepsy. London: Royal Society of MedicineServices, 1993: 53-64.

18 Snead OC, Hosey LC. Exacerbation of seizures in childrenby carbamazepine. NEnglJ Med 1985; 313: 916-21.

19 Shinnar S, Berg AT, Moshe SL, et al. Discontinuingantiepileptic drugs in children with epilepsy: a prospectivestudy. Ann Neurol 1994; 35: 534-45.

20 Emerson E, D'Souza BJ, Vining EP, Holden KR, MellitsED, Freeman JM. Stopping medication in children withepilepsy. Predictors of outcome. NEnglJ Med 1981; 304:1125-9.

21 Camfield C, Camfield P, Gordon K, Smith P, Dooley J.Outcome of childhood epilepsy. A population-basedstudy with a simple predictive scoring system for thosetreated with medication. JPediatr 1993; 122: 861-8.

22 Holmes GL. Surgery for intractable seizures in infancy andearly childhood. Neurology 1993; 43 (suppl 5): S28-37.

23 Joint Working Group of the Royal College of Physicians andthe British Paediatric Association. Guidelines for themanagement of convulsions with fever. BMJ 1991; 303:634-6.

24 Camfield PR, Camfield CS. Febrile seizures. In: Ross EM,Woody RC, eds. Epilepsy. Bailliere's clinical paediatrics.International practice and research. Vol 2, No 3. London:Bailliere Tindall, 1994: 547-59.

25 Cavazzuti GB, Capella L, Nalin A. Longitudinal study ofepileptiform EEG patterns in normal children. Epilepsia1980; 21: 43-55.

26 Lerman P, Kivity S. Focal epileptic EEG discharges inchildren not suffering from clinical epilepsy. In: Degan R,Dreifuss FE, eds. Benign localized and generalized epilepsiesof early childhood. Amsterdam, London: Elsevier, 1992:99-103.

27 Yang PJ, Berger PE, Cohen ME, Duffner PK. Computedtomography and childhood seizure disorders. Neurology1979; 29: 1084-8.

28 Gordon N. Computed tomography in childhood epilepsy.

Arch Dis Child 1988; 63: 1114.29 Barnes PD. Imaging of the central nervous system in pedi-

atrics and adolescence. Pediatr Clin North Am 1992; 39:743-76.

30 Anonymous. Magnetic resonance imaging in epilepsy[Editorial]. Lancet 1992; 340: 343-4.

31 Kuzniecky R, Andermann F, Guerrini R, and theCongenital Bilateral Perisylvian Syndrome (CBPS)Multicenter Collaborative Study. Congenital bilateralperisylvian syndrome: study of 31 patients. Lancet 1993;341: 608-12.

32 Kuzniecky R. Magnetic resonance imaging in developmen-tal disorders of the cerebral cortex. Epilepsia 1994; 35(suppl 6): S44-56.

33 Wyllie E, Luders H. Complex partial seizures in children:clinical manifestations and identification of surgical candi-dates. Cleve Clin J Med 1989; 56 (suppl (pediatric epilep-tology) part I): S43-52.

34 Cross JH, Jackson GD, Neville BGR, et al. Early detectionof abnormalities in partial epilepsy using magnetic reso-nance. Arch Dis Child 1993; 69: 104-9.

35 Anonymous. SPECT and PET in epilepsy [Editorial].Lancet 19891 333: 135-7.

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37 Gibbs J, Appleton RE, Carty H, Beirne M, Acomb BA.Focal electroencephalographic abnormalities and com-puterised tomographic findings in children with seizures. JfNeurol Neursurg Psychiatry 1993; 56: 369-71.

38 Lee TKY, Nakusa Y, Jeffree MA, Molyneaux AJ, AdamsCBT. Indolent glioma: a cause of epilepsy. Arch Dis Child1989; 64: 1666-71.

39 Riikonen R, Simell 0. Tuberose sclerosis and infantilespasms. Dev Med Child Neurol 1990; 32: 203-9.

40 Hull D. A question of negligence. Current Paediatnics 1993;3: 52-5.

41 Aoki N. Chronic subdural haematoma in infancy: clinicalanalysis of 30 cases in the CT era. J Neurosurg 1990; 73:201-5.

The place of the EEG and imaging in themanagement of seizures

Child DevelopmentCentre, Addenbrooke'sHospital, Hills Road,Cambridge CB2 2QQ

Correspondence to:Dr Verity.

C M Verity

'Most diagnostic investigations are open toabuse, but none more so than the EEG'.(Binnie 1994.1)'There is considerable debate in the literatureabout whether all patients with seizures requireCT scans.' (Holmes 1989.2)

This paper discusses the choice of appro-priate investigations for children with seizuresand takes the form of a series of questions forwhich answers are suggested. The word seizureis used rather than fit and the term febrileconvulsion rather than febrile seizure. Epilepsy isdefined as recurrent (more than one) afebrileseizures.

General considerationsWHAT TYPES OF SEIZURE OCCUR INCHILDHOOD AND WHY DOES IT MATTER?When considering a general approach tochildren with seizures it helps to know the fre-quency of seizure types in the population. Thetable shows some of the findings of the ChildHealth and Education Study, which followedup a national cohort of children for the first 10years of life.3 4 Some of the important observa-tions were as follows: febrile convulsions wererelatively common - they affected 2/7% ofchildren. The majority were simple febrile

convulsions, but 22% were complex (that islonger than 15 minutes' duration, focal ormultiple during one episode of fever). Afebrileseizures were much less common - about 0-4%of children in the study had epilepsy. Thecommonest afebrile seizure type was tonic-clonic, but complex partial seizures were thenext and classical childhood absence seizures('petit mal') were the least common of all (justone child in the cohort).The cause of seizures and the prognosis

varies with the seizure type. When consideringappropriate investigations for the individualchild it makes sense to consider which seizuretypes occur most commonly - children with'blank spells' are more likely to be having com-plex partial seizures or atypical absences thantrue 'petit mal' (see the table).

WHEN SHOULD INVESTIGATIONS BEPERFORMED?Not too soon. The most important step is toobtain a good history. The parents may be ableto record attacks at home using their ownvideo.5 The diagnosis of epilepsy is clinical andshould not be made without 'incontrovertibleclinical evidence'.6 Such evidence is usuallyprovided by the patient's description and by