Amantadine hydrochloride treatment in heredodegenerative ataxias: a double blind study

OBJECTIVE: A group of 27 patients with Friedreich's ataxia and another group of 30 patients with olivopontocerebellar atrophies were each randomly divided into two subgroups, one receiving placebo and the other amantadine hydrochloride (AH; 200 mg daily) for three to four months. METHODS: The e...

Full description

Saved in:
Bibliographic Details
Published in:Journal of neurology, neurosurgery and psychiatry neurosurgery and psychiatry, 1996-09, Vol.61 (3), p.259-264
Main Authors: Botez, M I, Botez-Marquard, T, Elie, R, Pedraza, O L, Goyette, K, Lalonde, R
Format: Article
Language:English
Subjects:
Adult
Amantadine - pharmacology
Amantadine - therapeutic use
Analysis of Variance
Anticonvulsants. Antiepileptics. Antiparkinson agents
Antiparkinson Agents - administration & dosage
Antiparkinson Agents - pharmacology
Antiparkinson Agents - therapeutic use
Biological and medical sciences
Dopamine - metabolism
Double-Blind Method
Female
Friedreich Ataxia - drug therapy
Functional Laterality
Humans
Male
Medical sciences
Middle Aged
Neuropharmacology
Olivopontocerebellar Atrophies - drug therapy
Pharmacology. Drug treatments
Reaction Time
Treatment Outcome
Visual Perception
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:OBJECTIVE: A group of 27 patients with Friedreich's ataxia and another group of 30 patients with olivopontocerebellar atrophies were each randomly divided into two subgroups, one receiving placebo and the other amantadine hydrochloride (AH; 200 mg daily) for three to four months. METHODS: The effect of double blind treatment was evaluated by simple visual and auditory reaction time (RT) and movement time (MT) for both right and left hands. RESULTS: The subgroup with olivopontocerebellar atrophies receiving AH showed significant improvement on seven out of eight variables studied by analysis of covariance. In patients with Friedreich's ataxia, improvement was definitely less. Treatment remained contraindicated for those with cardiomyopathies or drug intolerance. CONCLUSION: The rationale of AH use in heredodegenerative ataxias can be explained by its replacement effect (dopamine release) and by direct involvement of N-methyl-D-aspartate (NMDA) in glutamate mediated neurotoxicity in cerebellar granular cells; memantine, an AH analogue, is a potent blocker of NMDA receptors.
ISSN:0022-3050
1468-330X
DOI:10.1136/jnnp.61.3.259