Sclerosis of the Amygdala

Although most of the attention has been given to the hippocampus, we must not forget that the amygdala (as well as the temporal pole and entorhinal cortex) is also involved in the pathologic process in mesial temporal sclerosis (9, 88,

115, 127). The amygdala sits on top of the hippocampal head at the level of the anterior commissure and it can be problematic to separate the hippocampal head from the lateral amygdaloid nucleus at that level (226). As pointed by Jack et al. (208, 265), disarticulating the uncus, amygdala, and hippocampus anteriorly sometimes requires arbitrary judgments. Using qualitative three-dimensional studies, atrophy of the amygdala can be diagnosed (161, 163). However, atrophy of the amygdala is uncommon without concomitant hippocampal atrophy.

The majority of quantitative MR studies using T2 relaxometry are focused on the hippocampus in patients with pathologically proven HS. Changes in other areas, particularly the amygdala, have also been documented (165-167, 171, 172, 178, 236, 334). Amygdaloid changes were assessed in a study of 29 patients with newly diagnosed and 54 patients with chronic temporal lobe epilepsy. In the newly diagnosed patients, the mean amygdaloid volume did not differ from that in controls. The mean T2 relaxation time in newly diagnosed or chronic patients did not differ from each other or from control values. However, unilateral T2 time of the amygdala was prolonged in 12% (171).

We have proposed that the amygdala can be best seen in tilted axial images in which clear separation of the hippocampus and amygdala is possible (Fig. 4.40), together with the standard coronal images (see top row of Fig. 4.19). Visual diagnosis of amygdaline sclerosis has proven to be very difficult except in rare cases. Because of the difficulty of using manual volume-based measurements, one effective way to assess the amygdala is with quantitative methods such as T2 relaxometry and volumetry (165-167, 171, 172, 178, 236, 334).

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