Article Text

Postictal psychosis related regional cerebral hyperfusion
  1. Department of Neurology, New York University
  2. New York, NY, USA
    1. G C Y FONG
    1. Division of Neurology, Queen Mary Hospital
    2. 102 Pokfulam Road, Hong Kong
    3. cyfong.medicine{at}

      Statistics from

      I wish to comment on the postictal psychosis related regional cerebral hyperperfusion reported by Fong et al.1 Based on the their findings of hyperperfusion on SPECT within the time frame of postictal psychosis, the authors argue against the hypothesis that postictal psychosis is a psychic manifestation of a Todd's phenomenon. Two previous studies have shown a focal increase in cerebral blood flow on brain imaging during traditional motor Todd's paresis.2 3 An angiogram during a Todd's paresis may demonstrate a vascular “blush” perhaps representing loss of cerebrovascular autoregulation at the site of the epileptic focus.2 Hence, hyperperfusion may signal hypofunction, and the findings of Fong et alare indeed consistent with postictal psychosis as a Todd's equivalent.

      The strongest argument that postictal psychosis is not a Todd's equivalent is the delayed onset of psychosis compared with the decrescendo course of Todd's motor, cognitive, and visual phenomena.4 5


      Fong replies:

      We thank Boylan very much for the interesting letter provoking a second thought on the pathogenesis of postictal psychosis. Our data showed a definite increase in regional cerebral blood flow (rCBF) in both patients with postictal psychosis. As pointed out by Boylan, postictal psychosis may or may not be secondary to Todd's paralysis. In fact, the clinical features of postictal psychosis point against the hypothesis of Todd's phenomenon being the underlying pathophysiology.

      We think that the underlying mechanism of postictal psychosis is due to activation of a subcortical circuit. In our patients, the antiepileptic agents were restarted after a bout of secondary generalised tonic-clonic seizures. The re-institution of anticonvulsant drugs may cause a preferential suppression of abnormal cerebral cortical activities and hence normalise the surface EEG recording. In turn, it may result in a gradual build up of abnormal electrical activities propagating via subcortical neuronal networks which is shown by cerebral SPECT studies as areas of enhanced rCBF. This can explain the characteristic lucid interval of postictal psychosis1-1 and the activation of subcortical circuits may cause clinical psychosis.1-2

      To understand the pathophysiology of postictal psychosis, we wish to study the electrical activities of patients with postictal psychosis by intracranial electrodes and regional cerebral metabolism by cerebral PET.


      1. 1-1.
      2. 1-2.

      Request Permissions

      If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.