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Increased discharge threshold after an interictal spike in human focal epilepsy
Author(s) -
Curtis Marco,
Tassi Laura,
Russo Giorgio,
Mai Roberto,
Cossu Massimo,
Francione Stefano
Publication year - 2005
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2005.04458.x
Subject(s) - ictal , spike (software development) , epilepsy , neuroscience , psychology , medicine , computer science , software engineering
Abstract It is commonly assumed that interictal spikes (ISs) in focal epilepsies set off a period of inhibition that transiently reduces tissue excitability. Post‐spike inhibition was described in experimental models but was never demonstrated in the human epileptic cortex. In the present study post‐spike excitability was retrospectively evaluated on intracerebral stereo‐electroencephalographic recordings performed in the epileptogenic cortex of five patients suffering from drug‐resistant focal epilepsy secondary to Taylor‐type neocortical dysplasias. Patients typically presented with highly periodic interictal spiking activity at 2.33 ± 0.87 Hz (mean ± SD) in the dysplastic region. During the stereo‐electroencephalographic procedure, low‐frequency stimulation at 1 Hz was systematically performed for diagnostic purposes to identify the epileptogenic zone. The probability of evoking an IS during the interspike period in response to 1‐Hz stimuli delivered close to the ictal‐onset zone was examined. Stimuli that occurred early after a spontaneous IS (within 70% of the inter‐IS period) had a very low probability of generating a further IS. On the contrary, stimuli delivered during the late inter‐IS period had the highest probability of evoking a further IS. The generation of stimulus‐evoked ISs is occluded for several hundred milliseconds after the occurrence of a preceding spike discharge. As previously shown in animal models, these findings suggest that, during focal, periodic interictal spiking, human neocortical excitability is phasically controlled by post‐spike inhibition.