Distribution of basal ganglia lesions in Pick's disease with Pick bodies: A topographic neuropathological study of eight autopsy cases

Abstract

The distribution of the basal ganglia lesions, including the amygdala, striatum, and pallidum, were investigated neuropathologically in eight Japanese autopsy cases of Pick's disease with Pick bodies. The lesions were classified as mild, moderate or severe. The degree and distribution of basal ganglia lesions in all eight cases were uniform: the amygdala showed severe to moderate lesions, the caudate nucleus and putamen showed moderate to mild lesions, and the pallidum showed mild lesions. Furthermore, the lesions in the amygdala were more prominent in the basolateral group than in the corticomedial group. In Pick's disease with Pick bodies, the degree and distribution of the lesions within the basal ganglia differs from those reported in both ‘Pick's disease without Pick bodies’ and corticobasal degeneration (CBD), in which severe lesions were present in the pallidum. These neuropathological findings may contribute to the morphological differential diagnosis among Pick's disease with Pick bodies, ‘Pick's disease without Pick bodies’, and CBD.

Distribution of basal ganglia lesions in generalized variant of Pick's disease: a clinicopathological study of four autopsy cases

“…4); or severe, pronounced neuronal loss with rarefaction of the neuropil and/or prominent fibrillary gliosis (Fig. The classifi-cation of basal ganglia lesions described above, except for lesions of the substantia nigra, is fundamentally consistent with the classification of basal ganglia lesions in CBD and PDPB, as described by Tsuchiya et al [20,22], respectively. Substantia nigra lesions were judged compared with normal controls (Fig.…”

“…The generalized variant of Pick's disease, first proposed in 1984 by Munoz-Garcia and Ludwin [14], is not only a very rare dementing disease with a younger age at onset than in the other forms of Pick complex, but is also pathologically characterized by prominent atrophy of the basal ganglia, particularly the caudate nucleus, and the widespread presence of basophilic inclusion bodies, inconsistent with the pathology of Pick's disease with Pick bodies (PDPB) [6,7,13,15,22]. At least seven pathologically verified typical cases of the generalized variant of Pick's disease, in which clinical examination revealed obvious dementia and neuropathological findings showed the widespread appearance of basophilic inclusion bodies consistent with the light microscopic, immunocytochemical, and/or ultrastructural findings reported by not only Munoz-Garcia and Ludwin [14], but also by Munoz [13], have been reported [3,4,5,7,11,12,14,15].…”

“…In addition, the issue regarding the difference in basal ganglia lesions among this disorder, PDPB, and corticobasal degeneration (CBD) is discussed [20,21,22]. In addition, the issue regarding the difference in basal ganglia lesions among this disorder, PDPB, and corticobasal degeneration (CBD) is discussed [20,21,22].…”

FUS pathology defines the majority of tau- and TDP-43-negative frontotemporal lobar degeneration

“…We did not include NIFID and BIBD cases in this study as they have been described to have distinct clinical features to aFTLD-U cases, particularly prominent motor symptoms [3, 18, 19, 34, 51, 58]. In order to allow comparison of FTLD-FUS to other FTLD cases, we focussed on one subtype of FTLD-FUS (aFTLD-U), as it is possible that FTLD-FUS comprises a clinically heterogeneous group.…”

Impaired recognition of negative facial emotions in patients with frontotemporal dementia

“…Interestingly, the pattern of amygdalar atrophy appears to be different in the two diseases. FTD affects mostly the basolateral complex (Tsuchiya et al, 1999), which in the monkey has neurons that respond selectively to faces, and therefore is thought to be important for emotion recognition. Instead, AD affects mostly the corticomedial nuclei, which are phylogenetically older and modulate autonomic functions such as respiratory and cardiovascular control (Herzog & Kemper, 1980;Hooper & Vogel, 1976;LeDoux, 1996;Tsuchiya, & Kosaka, 1990).…”