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Self induced noogenic seizures in a photosensitive patient
  1. Department of Clinical Neurophysiology and Epilepsies, St Thomas’ Hospital, Lambeth Palace Road, London SE1 7EH, UK
  1. Dr M Koutroumanidis, Department of Clinical Neurophysiology and Epilepsies, St Thomas’ Hospital, Lambeth Palace Road, London SE1 7EH, UK.

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Self induced seizures are commonly encountered in photosensitive epileptic patients.1 Pattern,1musicogenic, and cheirogenic2 self induced seizures are rarely described. In all cases the manoeuvres employed by the patients implicate external stimuli. Self induced seizures with internal stimuli have not been reported.

In noogenic or thinking epilepsy seizures are precipitated by elaborate mental activity implicating decision complexity, sequential factors, and possibly related stress. In this condition a third of the patients also show photoparoxysmal discharges but not clinical photosensitivity.3

We report a photosensitive patient who induced absences by a specific noogenic process of predominant emotional character.

A 20 year old man of normal intelligence had a family history of seizures and a febrile convulsion at the age of 4. At the age of 11 he had generalised tonic-clonic seizures on three occasions while watching television. At that stage EEG showed frequent spontaneous generalised 3–4 Hz polyspike and wave discharges of up to five seconds and pronounced photosensitivity to frequencies from 10 to 50 Hz. Physical means for seizure prevention such as dispersion screens fitted on the TV screen, polaroid glasses, and monocular viewing had limited success. One year later, treatment with sodium valproate was initiated because of additional spontaneous clusters of absence seizures often followed by generalised tonic-clonic seizures. Absences consisted of brief repetitive episodes of “stopping his activities and looking vacant”. They would occur any time of the day but often in the morning after awakening. He could be taken out of this state by his mother shouting his name but if this was unsuccessful, absences would progress to generalised convulsions. This period coincided with the death of his father.

A typical absence seizure induced by 25 Hz intermittent photic stimulation at the age of 15. The patient is unresponsive and stares.

Seizures continued despite increasing sodium valproate to 2000 mg daily but poor compliance was confirmed on serial estimations of drug blood concentrations. Self induction was suspected but this was categorically denied by the patient and there was no evidence of recognisable relevant manoeuvres such as eyelid blinking, hand waving, or hyperventilation. Television, flickering lights, excitement, enjoyment, and concentration on previous emotional experiences were among the precipitating factors he listed on questioning at the age of 15. A video-EEG showed brief generalised polyspike and wave discharges only during intermittent photic stimulation (figure). There were no spontaneous or hyperventilation induced discharges. Neurological examination and brain MRI were normal.

Absences were dramatically reduced at the age of 18 when 50 mg lamotrigine given at night was added to sodium valproate, and ceased completely eight months later when the patient changed his lifestyle by starting university studies and limited self employment. One year later, he retrospectively admitted self induction by “concentrating on upsetting things in the school” and thinking of his father. “I know when I self induced the seizures. I could self induce the fits quite easily, if I thought about my father. Like the time I spent with him, also the time that he was in the hospital or things like that. This could induce the fits. I never did it to gain anything, I did it to get away from other people”. He also explained that he did not use light stimulation for self induction “because that would become obvious to others and betray my habit”. He employed self induction mainly at school and with the purpose of inducing absences. A new video-EEG at the age of 18 years showed only minor posterior photoparoxysmal responses and failed to induce abnormalities on thinking about his father.

Presently, the patient has only occasional generalised tonic-clonic seizures associated with alcohol excess or sleep deprivation. He also has a skin rash diagnosed as Darier’s disease.

This patient with typical absences, generalised tonic-clonic seizures, and clinical photosensitivity, presents two interesting features regarding his reflex seizures. Firstly, both flickering lights and complex internal noogenic stimuli were specific modes of seizure precipitation. Secondly, he self induced seizures by an emotional noogenic process and not by the common method of manipulating light stimulation. Like most of the patients with self induced seizures he concealed his habit for many years. Wilful confession was the only way to disclose it as no external stimuli were involved. Absences and self induction ceased due to conscious effort and appropriate medication.

Specific modes of precipitation in reflex epilepsies are simple and complex. Simple stimuli such as flickering lights are usually external, have a short time response, and are easy to identify.1Conversely, complex stimuli as in noogenic epilepsy are internal, have a longer time response, and are not discernible to the observer.3 The electroclinical characteristics of the generated response do not seem to be primarily determined by the type of the stimulus (simple or complex) and may be focal or generalised. In photosensitive epilepsy clinical seizures and EEG discharges may be restricted to the occipital regions or generalised1 and the underlying mechanisms seem to involve a non-uniform hyperexcitability of the occipital cortex and a critical mass of neuronal excitation and synchronisation. Similarly, seizures precipitated by higher cognitive processes such as thinking may be generated by hyperexcitable neurons in the relevant cortical areas— namely, the parietal lobes, are generalised, and the EEG phenomenology may vary.3 That in noogenic reflex seizures cortical hyperexcitability may expand to the occipital regions is implied by the fact that a third of the patients also show photoparoxysmal responses to intermittent photic simulation.3 The thought process that is linked with seizure precipitation does not seem to be uniform. Spatial processing,3 strategic or consequential thinking,4 and even prominently emotional processes have been proposed as decisively activating factors. In our patient the effective triggering stimuli are photic and complicated, primary emotional thinking processes. He elected the more elaborate noogenic trigger for self induction although photic manoeuvres would possibly be more provocative. This may suggest that the experience of the seizure itself was not the main objective as we previously suggested for another photosensitive patient who used patterns but never light for self induced seizures.5

A practical aspect of this report is that self induced noogenic seizures are difficult to discover, may escape detection for many years, and may not be as unique as this case may indicate.


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