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Treatment of Heredo-Degenerative Ataxias with Amantadine Hydrochloride

Published online by Cambridge University Press:  18 September 2015

M.I. Botez
Affiliation:
Laboratory of Clinical Neuropsychology and Behavioral Neurology, Neurology Service, Hôtel-Dieu Hospital, Université de Montréal and the Department of Psychiatry, McGill University, Montréal
Simon N. Young
Affiliation:
Laboratory of Clinical Neuropsychology and Behavioral Neurology, Neurology Service, Hôtel-Dieu Hospital, Université de Montréal and the Department of Psychiatry, McGill University, Montréal
Thérèse Botez*
Affiliation:
Laboratory of Clinical Neuropsychology and Behavioral Neurology, Neurology Service, Hôtel-Dieu Hospital, Université de Montréal and the Department of Psychiatry, McGill University, Montréal
Olga L. Pedraza
Affiliation:
Laboratory of Clinical Neuropsychology and Behavioral Neurology, Neurology Service, Hôtel-Dieu Hospital, Université de Montréal and the Department of Psychiatry, McGill University, Montréal
*
Neurology Service, Hôtel-Dieu de Montréal, 3840 St-Urbain Street, Montréal, Québec, Canada H2W IT8
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Abstract:

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Amantadine hydrochloride (AH) was administered (200 mg/day) for more than three months to 17 patients with Friedreich's ataxia (FA) and to 12 patients with olivopontocerebellar atrophies (OPCA) in an open clinical trial. Reaction time (RT) and movement time (MT) with the right and left hand were measured before and after treatment. A striking improvement on both RT and MT was observed in the OPCA group (on seven out of eight measures), whereas in the FA patients improvement was seen only in two out of four MT measures with no improvement in RT. Both groups had low levels of homovanillic acid (HVA) in their cerebrospinal fluid before treatment, relative to their controls. However, improvement with AH was not related to HVA levels.

Type
Original Articles
Copyright
Copyright © Canadian Neurological Sciences Federation 1991

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