Treatment of progressive supranuclear palsy and corticobasal degeneration
Identifieur interne : 004D77 ( Main/Merge ); précédent : 004D76; suivant : 004D78Treatment of progressive supranuclear palsy and corticobasal degeneration
Auteurs : Anthony E. Lang [Canada]Source :
- Movement Disorders [ 0885-3185 ] ; 2005-08.
English descriptors
- KwdEn :
- Amantadine (therapeutic use), Cerebral Cortex (pathology), Cholinesterase Inhibitors (therapeutic use), Corpus Striatum (pathology), Dopamine Agents (therapeutic use), Dopamine Agonists (therapeutic use), Dystonia (drug therapy), Dystonia (pathology), Globus Pallidus (pathology), Humans, Indans (therapeutic use), Levodopa (therapeutic use), Nerve Degeneration (drug therapy), Nerve Degeneration (pathology), Piperidines (therapeutic use), Substantia Nigra (pathology), Supranuclear Palsy, Progressive (drug therapy), corticobasal degeneration, dopaminergic drugs, dystonia, myoclonus, progressive supranuclear palsy, tauopathy.
- MESH :
- chemical , therapeutic use : Amantadine, Cholinesterase Inhibitors, Dopamine Agents, Dopamine Agonists, Indans, Levodopa, Piperidines.
- drug therapy : Dystonia, Nerve Degeneration, Supranuclear Palsy, Progressive.
- pathology : Cerebral Cortex, Corpus Striatum, Dystonia, Globus Pallidus, Nerve Degeneration, Substantia Nigra.
- Humans.
Abstract
Success in treating patients with progressive supranuclear palsy and corticobasal degeneration remains exceedingly low. This finding probably relates to the widespread distribution of the pathological changes that account for the varied and complex spectrum of clinical manifestations. Dopaminergic drugs are regularly used for the parkinsonian features; however, these rarely result in more than modest benefit, and when better or sustained responses are obtained, as sometimes occurs in progressive supranuclear palsy, the clinical features are atypical and diagnosis is often delayed or not made in life. A variety of other treatments have been used in both disorders, sometimes directed at other specific features such as dystonia or myoclonus, and these treatments will be reviewed. Greater success in treating these disorders will require advances in our understanding of their cause(s) or the pathogenetic mechanisms underlying the neurodegenerative processes. The similarities in the molecular pathology of these four‐repeat tauopathies suggests that important advances in the management of one will have a definite impact on the treatment of the other. © 2005 Movement Disorder Society
Url:
DOI: 10.1002/mds.20545
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