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.