Neuronal loss and gliosis of the amygdaloid nucleus in temporal lobe epilepsy

Abstract

Although clinical and electrophysiological evidence indicates that the amygdaloid body plays an important role in the pathogenesis of temporal lobe epilepsy, there are very few detailed data on histopathological changes in this nucleus in epilepsy patients. In the present study we have examined the lateral nucleus of the amygdaloid body in 70 surgical specimens from patients with temporal lobe epilepsy and in 10 control specimens with respect to neuronal density and gliosis. The results were compared to the neuronal loss in the hippocampal formation. Our goal was to examine the pathological alterations of the amygdaloid body and their correlation with other morphological changes in temporal lobe epilepsy. In epilepsy patients with Ammon's horn sclerosis or focal lesions of the temporal lobe, the neuronal density of the lateral amygdaloid nucleus was significantly decreased as compared to normal controls (P < 0.001). Overall, the mean volumetric density in epilepsy patients was reduced to 59% of that in normal individuals. There was no correlation between the neuronal density in the lateral amygdaloid nucleus and that in the different segments of the hippocampal formation or to the age at onset or the duration of epilepsy. The neuronal loss of the amygdaloid nucleus correlated well with the presence of fibrillary gliosis. Our findings demonstrate that the amygdaloid body is severely altered in most patients with temporal lobe epilepsy and that these changes are independent of those in the hippocampus. The presence of neuronal loss and gliosis in the amygdaloid nucleus of patients with focal lesions but no Ammon's horn sclerosis is compatible with an involvement of the amygdala in secondary epileptogenesis.

Amygdala volumetry in "imaging-negative" temporal lobe epilepsy

“…In Wolf 's pathological examination of 70 temporal lobectomy specimens there were no cases of isolated amygdaloid sclerosis, attesting to the rarity of such an entity. 18 Previous authors studying the amygdala in TLE have not advocated the use of volumetry, because of an inter-rater repeatability of more than 20%. 4 19 In our institution amygdala volumetry has an intra-rater and inter-rater coefficient of repeatability of 13.0% and 14.5%, when using 1.5 mm slices and reformatting to correct for tilt.…”

Amygdala‐kindling induces alterations in neuronal density and in density of degenerated fibers

“…As in human TLE (Wolf et al, 1997), kindling led to a reduction of neuronal density in this area. Reduction of cell density in the medial nucleus of the amygdala has also been found in hippocampal-kindled rats (as well as reduced neuronal densities in the entorhinal cortex), however, this decline in neuronal density occurred only in hippocampalkindled rats which have had about 10 seizures per day (Bertram and Scott, 2000).…”

“…However, data concerning morphological changes are rare in other limbic structures involved in epilepsy, such as the amygdala and the entorhinal and perirhinal cortex. It is known that the amygdaloid nuclei may be damaged unilaterally or bilaterally in children and adults with temporal lobe epilepsy (TLE) or following status epilepticus (Wolf et al, 1997;Pitkänen et al, 1998). The volumes of the hippocampus and the amygdala were found to be smaller on the side of the focus in TLE patients compared with controls (Bernasconi et al, 1999).…”

Distribution of synaptic zinc in the macaque monkey amygdala

“…In addition, Zn is considered to play an important role in excitotoxicity and in epileptogenic pathology (Cuajungco and Lees, 1997;Coulter, 2000;Sensi and Jeng, 2004), and a natural question is whether inhomogeneities in Znϩ terminal distribution might correlate with known subnuclear vulnerability within the amygdala. Thhe amygdala is frequently damaged in patients with temporal lobe epilepsy (Gloor et al, 1992;Hudson et al, 1993;Wolf et al, 1997;Pitkannen et al, 1998), and ventral parts of the basolateral group (i.e., the ventral division of the lateral nucleus, the parvicellular division of the basal nucleus, and the paralaminar nucleus) are more vulnerable than other amygdaloid nuclei (Pitkannen et al, 1998;YilmazerHanke et al, 2000).…”