The external globus pallidus in patients with Parkinson's disease and progressive supranuclear palsy

Underactivity of the external segment of the globus pallidus is thought to contribute to the generation of parkinsonian hypokinetic symptoms in association with striatal dopaminergic dysfunction and overactivity of the subthalamus. These symptoms can be corrected by neurosurgical techniques aimed at...

Full description

Saved in:
Bibliographic Details
Published inMovement disorders Vol. 14; no. 4; pp. 626 - 633
Main Authors Hardman, Craig D., Halliday, Glenda M.
Format Journal Article
LanguageEnglish
Published New York John Wiley & Sons, Inc 01.07.1999
Wiley
Subjects
Online AccessGet full text
ISSN0885-3185
1531-8257
DOI10.1002/1531-8257(199907)14:4<626::AID-MDS1012>3.0.CO;2-U

Cover

More Information
Summary:Underactivity of the external segment of the globus pallidus is thought to contribute to the generation of parkinsonian hypokinetic symptoms in association with striatal dopaminergic dysfunction and overactivity of the subthalamus. These symptoms can be corrected by neurosurgical techniques aimed at normalizing subthalamic overactivity. The aim of the present study was to compare the amount of neurodegeneration and changes in the calcium‐binding protein parvalbumin in the external segment of the globus pallidus in parkinsonian disorders. Cases with progressive supranuclear palsy were compared with cases with Parkinson's disease and control subjects. The number of neurones and neurofibrillary tangles was estimated using unbiased stereologic techniques. The external segment of the globus pallidus in Parkinson's disease was not significantly different from that in control subjects. In contrast, most patients with progressive supranuclear palsy had significant neurodegeneration of the external pallidum, particularly patients with significant degeneration of both the subthalamus and substantia nigra. These results suggest that the parkinsonian symptoms in progressive supranuclear palsy are caused by the degeneration of the external segment of the globus pallidus because such degeneration would increase thalamic inhibition through the basal ganglia output nuclei, particularly in patients with a loss of excitatory drive from the subthalamus.
Bibliography:National Health and Medical Research Council of Australia
istex:72FA56C6EA890A250DB504AC91AD1CC7F5459688
Clive and Vera Ramaciotti Foundation
ark:/67375/WNG-BS2C72GW-1
Parkinson's NSW Inc
ArticleID:MDS1012
Australian Brain Foundation
ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ObjectType-Article-1
ObjectType-Feature-2
ISSN:0885-3185
1531-8257
DOI:10.1002/1531-8257(199907)14:4<626::AID-MDS1012>3.0.CO;2-U