RELATIONSHIP BETWEEN ATROPHY OF THE AMYGDALA AND ICTAL FEAR IN TEMPORAL-LOBE EPILEPSY

Citation
F. Cendes et al., RELATIONSHIP BETWEEN ATROPHY OF THE AMYGDALA AND ICTAL FEAR IN TEMPORAL-LOBE EPILEPSY, Brain, 117, 1994, pp. 739-746
Citations number
36
Categorie Soggetti
Neurosciences
Journal title
BrainACNP
ISSN journal
00068950
Volume
117
Year of publication
1994
Part
4
Pages
739 - 746
Database
ISI
SICI code
0006-8950(1994)117:<739:RBAOTA>2.0.ZU;2-U
Abstract
Viscerosensory and affective manifestations are often elicited by temp oral lobe seizure discharges. They have been reproduced by amygdaloid stimulation in awake patients during stereotaxic exploration or neuros urgical procedures. They are not exclusively reproduced by stimulation of the amygdala, though most commonly they are evoked from it. Ictal fear is frequently, but not invariably, associated with a rising epiga stric sensation, palpitations, mydriasis and pallor. We studied 50 pat ients (mean age 33 years) with intractable temporal lobe epilepsy (TLE ): MRI volumetric measurements of amygdala and hippocampus were perfor med using a protocol previously described by our group (Watson et al., Neurology 1992; 42: 1743-50). All patients had extensive EEG investig ation and at least two seizures recorded by video-EEG monitoring. Seve nteen patients (34%) had a clear history of fear accompanied by a risi ng epigastric sensation as the initial manifestation of their habitual attacks. The amygdala volumes in this group were significantly (P = 0 .001) smaller (mean 2131.6 mm(3)) compared with the volumes of the 33 patients without these symptoms (mean 2561.5 mm(3)). Both patient grou ps had smaller mean amygdala volumes compared with normal controls (me an 2828.2 mm(3)). Postoperative pathology correlated well with volumet ric atrophy. In addition, we found that patients with more pronounced amygdaloid atrophy more commonly had more frequently secondarily gener alized seizures. Results support the finding that ictal fear is relate d to pathology of the amygdala and that it, like the hippocampus, is a n important substrate of TLE.