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Epileptic Disorders

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The Bancaud and Talairach view on the epileptogenic zone: a working hypothesis Volume 8, supplement 2, Supplement 2, September 2006

Figure 1 This 35-year-old, right-handed woman was suffering from drug-resistant, partial seizures associated with right hippocampal sclerosis. (A) Clinically, seizures were initiated by auditory illusions (1) followed by consciousness impairment (2), version of the head and eyes towards the left, left tonic-clonic brachio-facial motor signs with sialorhea (3), bilateral clonic jerks (4), and rapid recovery with a post-ictal motor deficit of the left arm. This sequence of symptoms strongly suggested the initial involvement of Heschl’s gyrus with spreading of the discharge to the suprasylvian opercular cortex and primary motor cortex. (B) The SEEG study was designed according to this hypothesis and also to understand whether mesio-temporal lobe structures could be initially involved without any initial accompaniment. Intracrebral recordings of spontaneous seizures confirmed that seizures arose from the posterior part of the first temporal gyrus (T1), quickly involved, almost simultaneously, the anterior part of T1 and the suprasylvian pre- and post-central operculum (Op), and then spread over the second temporal gyrus (T2) from its posterior to its anterior part, while the temporal pole and the hippocampus were tardily and only slightly involved.

Figure 2 Computer-assisted matching of a post-implantation CT-scan with a pre-implantation 3-D MRI (VOXIM, IVS Solution, Germany), showing how an electrode may investigate simultaneously the hippocampus (1-, the temporal neocortex (2), and the depth of the T4-T5 sulcus (3), or deep–seated cortical areas such as the insula (white arrow).

Figure 3 The Bancaud and Talairach definition of the epileptogenic zone includes the ictal onset zone (Amygdala, NA) and the zone of early spread (hippocampus, Hc; temporal pole, TP; parahippocampal gyrus, HcG). The temporal neocortex (TNcx) is only secondarily involved.

Figure 4 This 10-year-old boy was suffering from brief hypermotor seizures associated with left fronto-polar (Fpolar) focal cortical dysplasia (FCD). SEEG recordings demonstrated a number of subclinical discharges located well within the lesion (A). During clinical seizures (B), the cingulate cortex (CG) was also involved at the moment when the first symptom occurred.

Figure 5 In this 26-year-old, right-handed women who was suffering from drug-resistant partial epilepsy associated with left hippocampal sclerosis, SEEG recordings showed that seizures arose from the amygdalo-hippocampal complex (Amygd, Ant Hc, Post-Hc) (A). The temporo-basal cortex (T3, T4, T5), which was not involved, activated abruptly about 10 seconds later. Electrical stimulation of the fourth temporal convolution (T4) elicited an electroclinical seizure identical to the spontaneous ones, with an ictal onset in amygdalo-hippocampal structures without initial involvement of the temporo-basal cortex (B).