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To the Editor:
A recent AAN Practice Parameter concluded that postictal prolactin (PRL) elevation is useful in differentiating generalized tonic-clonic and complex partial seizures from psychogenic nonepileptic seizure.1 This observation was previously suggested by Trimble.2 An interesting finding is that serum PRL does not increase during status epilepticus (SE).3,4 As stated in the parameter, “on the basis of inconsistent studies, no conclusion can be established regarding serum PRL changes following termination of SE.” The purpose of this monograph is to shed light on this paradox and to suggest clues to the pathophysiology and treatment of SE.
Normally, seizures spontaneously stop as the cortical inhibitory mechanisms extinguish the abnormal neuronal electric activity.5 The postictal EEG slowing, Todd's paralysis, and postictal psychological depression are examples of manifestations of the cortical inhibition. Various mechanisms have been proposed to contribute to the postictal state.6 One hypothesis is that the cortical activity in SE does not reach the threshold to initiate …
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