SAGE Journals Online
Advertisement
Sign In to gain access to subscriptions and/or personal tools.

 

Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Advertisement

Sign In to gain access to subscriptions and/or personal tools.
The Neuroscientist
This Article
Right arrow Full Text (PDF)
Right arrow References
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via Google Scholar
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Wichmann, T.
Right arrow Articles by DeLong, M. R.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Wichmann, T.
Right arrow Articles by DeLong, M. R.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Other

Parkinson's Disease and the Basal Ganglia: Lessons from the Laboratory and from Neurosurgery

Thomas Wichmann

Department of Neurology Emory University School of Medicine Atlanta, Georgia

Jerrold L. Vitek

Department of Neurology Emory University School of Medicine Atlanta, Georgia

Mahlon R. DeLong

Department of Neurology Emory University School of Medicine Atlanta, Georgia

During the last decade, a clearer understanding of the circuitry of the basal ganglia and their mode of operation has emerged. The basal ganglia are now viewed as parts of larger, segregated circuits that involve the thalamus and cerebral cortex. A pathophysiological model has been elaborated and tested in which Parkinsonian signs are viewed as resulting from increased activity of neurons in the "motor" portion of the internal pallidum, the major output nucleus of the basal ganglia, leading to increased inhibition of thalamocortical projection neurons and decreased activation of the precentral motor fields. Increased internal pallidal activity is thought to result from striatal dopamine loss, leading to decreased inhibition of the internal pallidum via a monosynaptic ("direct") striatopallidal pathway and to excessive excitatory glutamatergic drive via a polysynaptic ("indirect") striatopallidal pathway. Because current medical therapies for Parkinson's disease, aimed at systemically replacing dopamine, often lose their effectiveness after several years, with patients suffering from motor fluctuations and drug-induced dyski nesias, several new therapeutic strategies have been developed. In addition to the transplantation of dopaminergic tissue, other strategies attempt to reduce increased basal ganglia outflow directly by the placement of stereotactic lesions into the sensorimotor portion of the internal pallidum (pallidotomy) or by the chronic electric stimulation of the subthalamic nucleus. Preliminary results suggest that these new techniques may lead to significant improvement in Parkinsonian signs, motor fluctuations, and drug- induced dyskinesias. The Neuroscientist 1:236-244, 1995

Key Words: KEY WORDS Parkinson's disease • Basal ganglia • Stereotactic surgery • Pallidotomy • Globus pallidus • Subthalamic nucleus

The Neuroscientist, Vol. 1, No. 4, 236-244 (1995)
DOI: 10.1177/107385849500100407


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?




Advertisement