Abstract

Although this special issue is devoted to paroxysmal non-epileptic events, we think the inclusion of anoxicepileptic seizures (AES) is justified because almost all affected children do not have epilepsy. However, they do have epileptic seizures, but usually only when provoked by a syncope [1]. This chapter assumes that the reader knows that most syncopes are convulsive [2] and that this does not imply AES but rather that when there is acute cerebral hypoxia or ischemia, that leads to an anoxic (non-epileptic) seizure, with non-epileptic spasms, non-epileptic tonic extensions, non-epileptic myoclonus and so forth. The syncopes known to have been associated with AES are mainly neurally-mediated, in particular RAS (reflex anoxic seizures/reflex asystolic syncope), prolonged expiratory apnea (PEA – otherwise known as, cyanotic or blue breath-holding spells), mixed types with both cardiac inhibition and expiratory grunts, and more typical vasovagal syncope [1]. Compulsive Valsalva manoeuvres are also well known to trigger epileptic seizures [1] and obstructive apnea has been the mechanism in at least one child patient [3]. To date, AES have not been reported in the syncopes associated with long QT syndrome and other cardiac conduction defects, neonatal hyperekplexia, paroxysmal extreme pain disorder or imposed upper airways obstruction.

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