TY - JOUR
T1 - Subregional loss of putaminal efferents to the basal ganglia output nuclei may cause parkinsonism in striatonigral degeneration
AU - Goto, Satoshi
AU - Matsumoto, Sadayuki
AU - Ushio, Yukitaka
AU - Hirano, Asao
PY - 1996/10
Y1 - 1996/10
N2 - In this study, we examined the topographic involvement of the putaminal projection neurons and their axons in the globus pallidus and substantia nigra, which we visualized by calcineurin immunostaining, in the basal ganglia of patients with striatonigral degeneration (SND). In all cases examined, there was a marked decrease in number of calcineurin-immunopositive neurons in the caudal and lateral portion of the putamen. Also, marked depletion of calcineurin-immunoreactive putaminal efferents was consistently present in the posteroventrolateral portions of the globus pallidus interna (GPi) and externa, and in the ventrolateral portion of the substantia nigra pars reticulata (SNr) topographically corresponding to the putaminal lesion. In view of the functional model of the basal ganglia 'motor' circuit, these findings suggest that subregional deafferentation of the GPi/SNr (i.e., basal ganglia output nuclei/from putaminal inputs may be responsible for parkinsonism in patients with SND.
AB - In this study, we examined the topographic involvement of the putaminal projection neurons and their axons in the globus pallidus and substantia nigra, which we visualized by calcineurin immunostaining, in the basal ganglia of patients with striatonigral degeneration (SND). In all cases examined, there was a marked decrease in number of calcineurin-immunopositive neurons in the caudal and lateral portion of the putamen. Also, marked depletion of calcineurin-immunoreactive putaminal efferents was consistently present in the posteroventrolateral portions of the globus pallidus interna (GPi) and externa, and in the ventrolateral portion of the substantia nigra pars reticulata (SNr) topographically corresponding to the putaminal lesion. In view of the functional model of the basal ganglia 'motor' circuit, these findings suggest that subregional deafferentation of the GPi/SNr (i.e., basal ganglia output nuclei/from putaminal inputs may be responsible for parkinsonism in patients with SND.
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U2 - 10.1212/WNL.47.4.1032
DO - 10.1212/WNL.47.4.1032
M3 - Article
C2 - 8857740
AN - SCOPUS:0029805036
SN - 0028-3878
VL - 47
SP - 1032
EP - 1036
JO - Neurology
JF - Neurology
IS - 4
ER -