Delusions, illusions and hallucinations in epilepsy: 2. Complex phenomena and psychosis

Brent Elliott, Eileen Joyce, Simon Shorvon
Epilepsy Research 2009, 85 (2-3): 172-86
In this second paper the clinical features and electrophysiological underpinnings of more complex psychotic states associated with epilepsy are reviewed. (a) Complex partial status epilepticus, in particular of temporal lobe origin, may result in mental states remarkably similar to those seen in the primary psychoses. This non-convulsive state is associated with prolonged epileptic discharges on intracranial stereoelectroencephalography (SEEG) in hippocampal and other mesial temporal structures, sometimes without abnormalities on the scalp EEG. Where hallucinatory or psychotic symptomatology does occurs, it can be considered an examples of an ictal psychosis. The phenomenology and electrophysiological features of this condition are reviewed. (b) Postictal psychosis is noted for its similarity to schizophrenia-like/paranoid and affective psychoses and there is convincing SEEG evidence that, for some cases at least, the psychosis is not in fact postictal but rather an ictal psychosis due to ongoing limbic seizure activity and a form of non-convulsive status epilepticus. It has been suggested that postictal psychosis should be divided into two sub-groups: the classical 'nuclear' postictal type and an atypical periictal type. (c) Interictal hallucinosis in epilepsy has been poorly studied, but is probably commoner than appreciated. To what extent it represents subclinical epileptic discharges (i.e. auras) is not known. It may interestingly also be associated with abnormal affective states in epilepsy. (d) The interictal psychosis of epilepsy is often indistinguishable from primary schizophrenia. It occurs more commonly in temporal lobe (limbic) epilepsy, in those with frequent seizures and only in patients with a long history of epilepsy (usually over 10 years). There is convincing SEEG evidence of frequent, semi-continuous and sometimes continuous epileptic activity in limbic structures at the time of psychotic and hallucinatory ideation and behaviour, suggesting that in some cases at least, the epileptic activity is the cause of the symptoms. Whether the psychosis is directly 'driven' by subclinical electrographic activity or is indirectly a consequence of function change induced by such activity is not clear. An intriguing question also arises as to whether similar electrophysiological changes could underpin psychosis in patients without epilepsy but evidence on this point is sparse. The effects of temporal lobe surgery on the psychoses of epilepsy are described and these might throw light on the mechanisms of epileptic psychosis. The principles of pharmacological therapy of epileptic hallucinosis and psychosis are outlined.

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