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Significance of the EEG after the first afebrile seizure
  1. RICHARD E APPLETON, Consultant Paediatric Neurologist
  1. The Roald Dahl EEG Unit
  2. Alder Hey Children’s Hospital
  3. Liverpool L12 2AP, UK

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    Editor,—Although Panayiotopoulos in his personal practice article and Cross in her accompanying commentary1debate an interesting topic, they do not adequately address some important issues when discussing the role and implications of electroencephalography.

    First, the EEG is not necessarily a “harmless” investigation. Although it may be relatively non-invasive and therefore physically harmless, it may be harmful in terms of its interpretation. An unsatisfactorily recorded EEG, undertaken by technical staff who have never been trained to perform such investigations in children, which is reported by a clinician who has not been taught the normal maturational as well as abnormal appearances of children’s EEGs, may result in inaccurate diagnoses of both epilepsy and the specific epilepsy syndrome. Clearly, this may have serious medical, psychological, and social consequences. Unfortunately, appropriately trained technical staff and paediatric neurologists or clinical neurophysiologists are not ubiquitous, particularly within the UK.

    Second, epilepsy is a clinical diagnosis and is defined on the basis of not one but recurrent seizures, as clearly emphasised by Cross. The finding of an abnormal EEG, including the demonstration of characteristic features of a specific epilepsy syndrome, does not imply that the child will inevitably have a further seizure. Most parents are likely to elect not to give their child antiepileptic medication after a first seizure (even if it was a tonic–clonic convulsion), if they are told truthfully that it is possible that there will be no recurrence. Understandably, much depends on how parents are given this information. In my experience, their decision is usually made irrespective of the finding of an abnormal even “syndrome diagnostic” EEG, and the potentially high predictive risk of a further seizure. If there is any chance, no matter how small, that their child may not have a second seizure, most parents would prefer to adopt a wait and see approach.

    Third, much of the discussion was clearly adult oriented. Importantly, the implications of a diagnosis of epilepsy and even an epileptiform EEG (as intimated by Panayiotopoulos’s argument) may be very different for a child and an adult, specifically in areas of career/employment and leisure/driving. Epilepsy in children is not, and never should be, regarded as simply a downward extrapolation of epilepsy in adulthood.

    These issues must be considered when interpreting EEG findings in relation not just to the seizure history but to the overall clinical situation.2 It must also be remembered that most children with epilepsy are managed outside teaching hospitals or tertiary epilepsy centres and do not necessarily have access to the technical and clinical personnel who should be undertaking and reporting their EEGs.


    Dr Panayiotopoulos comments:

    Dr Cross partly accepts and Dr Appleton partly rejects the significance of the EEG after the first afebrile seizure. My reaction to their views is on clinical, not EEG, matters. They rely on an unhelpful definition of epilepsy—two or more recurrent seizures—instead of emphasising that epilepsies are hundreds of seizure disorders with different and often diverse causes, manifestations, and prognoses that frequently mandate different short and long term management.1-1 Any further discussion would be pointless if our aim was to diagnose epilepsy and not a specific epileptic condition.

    The inclusive term “epilepsy” or the simplistic rules “to treat or not to treat”, “wait and see”, “start with sodium valproate or carbamazepine after the second seizure” are detrimental to the diagnosis and management of epilepsies. It is because of these problems that in a recent report from London nearly half of children with typical absence seizures are inappropriately treated with carbamazepine and vigabatrin.1-2

    Regarding EEG after the first afebrile seizure none of my four arguments was debated:

    • It is possible to recognise children with features of specific epileptic syndromes

    • Minor seizures such as absences and myoclonic jerks that often escape clinical detection may be recorded

    • EEG is imperative in establishing seizure precipitating factors

    • An EEG in an untreated stage of an epileptic syndrome is imperative.

    Instead, the responders insist on the significance of to treat or not to treat, which I emphasised “is not a convincing argument: the prime aim in medicine is the diagnosis that determines prognosis and treatment strategies”.

    Appleton has four arguments that I reply to in order:

    • Anything in medicine, clinical or laboratory, may be harmful if misinterpreted—raising standards, not abandoning the practice, is the answer

    • Clinical diagnosis may often be incorrect without EEG—see, for example absences versus complex partial seizures, visual seizures versus migraine or unreported myoclonic jerks

    • There is nothing adult oriented in my text

    • It is because most children are managed outside teaching hospitals that awareness of the various aspects of epilepsies should be improved and standards raised above “epilepsy is more than two seizures” or “the treatment of epilepsy is with drug A or drug B”.

    The message of my paper was that, as in all other fields of paediatrics, children with epilepsies are entitled to a diagnosis, prognosis, and management that is specific and precise. I should add that this is possible for most of the children with one or more seizures based on skilful clinical and EEG evaluation.


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