Multiple system atrophy: An update
Identifieur interne : 004032 ( Main/Exploration ); précédent : 004031; suivant : 004033Multiple system atrophy: An update
Auteurs : Gregor K. Wenning [Autriche] ; Felix Geser [Autriche] ; Michaela Stampfer-Kountchev [Autriche] ; François Tison [Autriche]Source :
- Movement Disorders [ 0885-3185 ] ; 2003-09.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Anatomic pathology, Animals, Benzothiazole, Brain (drug effects), Brain (pathology), Clinical Trials as Topic, Exploration, Human, Humans, Inclusion Bodies (drug effects), Inclusion Bodies (pathology), Levodopa (therapeutic use), Multiple System Atrophy (diagnosis), Multiple System Atrophy (drug therapy), Multiple System Atrophy (pathology), Multiple system atrophy, Nerve Tissue Proteins (metabolism), Neuroglia, Neurologic Examination (drug effects), Neurons (drug effects), Neurons (pathology), Neuroprotective Agents (therapeutic use), Parkinsonian Disorders (diagnosis), Parkinsonian Disorders (drug therapy), Parkinsonian Disorders (pathology), Review, Riluzole, Symptomatology, Synucleins, Treatment, alpha-Synuclein, glia, multiple system atrophy, riluzole, treatment.
- MESH :
- chemical , metabolism : Nerve Tissue Proteins.
- chemical , therapeutic use : Levodopa, Neuroprotective Agents.
- diagnosis : Multiple System Atrophy, Parkinsonian Disorders.
- drug effects : Brain, Inclusion Bodies, Neurologic Examination, Neurons.
- drug therapy : Multiple System Atrophy, Parkinsonian Disorders.
- pathology : Brain, Inclusion Bodies, Multiple System Atrophy, Neurons, Parkinsonian Disorders.
- Animals, Clinical Trials as Topic, Humans, Synucleins, alpha-Synuclein.
Abstract
Multiple system atrophy (MSA) is a sporadic neurodegenerative disorder that usually manifests in the early sixth decade of life and progresses relentlessly with a mean survival of 9 years. Clinically, MSA is dominated by autonomic/urogenital failure, which may be associated with either levodopa (L‐dopa) ‐unresponsive parkinsonism in 80% of cases (MSA‐P subtype) or with cerebellar ataxia in 20% of cases (MSA‐C subtype). Pathologically, MSA is characterized by a neuronal multisystem degeneration and abnormal glial cytoplasmic inclusions containing α‐synuclein aggregates. Pharmacological treatment of motor features is disappointing except for a transient L‐dopa response in a minority of MSA‐P patients. In contrast, autonomic and urogenital features of MSA should be identified early on, because they can be treated effectively in many instances. Neuroprotective strategies are presently unavailable, however, two multicentre European trials have been launched to evaluate the effects of riluzole and human recombinant growth hormone on disease progression in MSA. Clearly, further randomised, controlled trials are required to identify effective symptomatic or neuroprotective agents in MSA. Several in vivo models have become available to allow a careful preselection of candidate agents. Several research groups have been formed in Europe (EMSA‐SG, NNIPPS) and United States (NAMSA‐SG), providing a framework for coordinated trial activity in MSA. © 2003 Movement Disorder Society
Url:
DOI: 10.1002/mds.10561
Affiliations:
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Le document en format XML
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<term>Brain (pathology)</term>
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<front><div type="abstract" xml:lang="en">Multiple system atrophy (MSA) is a sporadic neurodegenerative disorder that usually manifests in the early sixth decade of life and progresses relentlessly with a mean survival of 9 years. Clinically, MSA is dominated by autonomic/urogenital failure, which may be associated with either levodopa (L‐dopa) ‐unresponsive parkinsonism in 80% of cases (MSA‐P subtype) or with cerebellar ataxia in 20% of cases (MSA‐C subtype). Pathologically, MSA is characterized by a neuronal multisystem degeneration and abnormal glial cytoplasmic inclusions containing α‐synuclein aggregates. Pharmacological treatment of motor features is disappointing except for a transient L‐dopa response in a minority of MSA‐P patients. In contrast, autonomic and urogenital features of MSA should be identified early on, because they can be treated effectively in many instances. Neuroprotective strategies are presently unavailable, however, two multicentre European trials have been launched to evaluate the effects of riluzole and human recombinant growth hormone on disease progression in MSA. Clearly, further randomised, controlled trials are required to identify effective symptomatic or neuroprotective agents in MSA. Several in vivo models have become available to allow a careful preselection of candidate agents. Several research groups have been formed in Europe (EMSA‐SG, NNIPPS) and United States (NAMSA‐SG), providing a framework for coordinated trial activity in MSA. © 2003 Movement Disorder Society</div>
</front>
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