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Ataxia in Institutionalized Patients with Epilepsy

Published online by Cambridge University Press:  18 September 2015

G.B. Young ,
S.R. Oppenheimer ,
B.A. Gordon ,
G.A. Wells ,
L.P.A. Assis ,
J.H. Kreeft ,
N.A. Lohuis  and
W.T. Blume
G.B. Young*
Affiliation:
Department of Clinical Neurological Sciences
S.R. Oppenheimer
Affiliation:
Department of Clinical Neurological Sciences
B.A. Gordon
Affiliation:
Department of Biochemistry
G.A. Wells
Affiliation:
Department of Faculty of Medicine, the University of Western Ontario; the Department of Biostatistics and Epidemiology
L.P.A. Assis
Affiliation:
Department of Radiology
J.H. Kreeft
Affiliation:
Department of Medicine
N.A. Lohuis
Affiliation:
Department of Faculty of Medicine, the University of Ottawa and the University of Toronto
W.T. Blume
Affiliation:
Department of Clinical Neurological Sciences
*
Department of Clinical Neurological Sciences, Victoria Hospital, London, Ontario, Canada N6A 4G5
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Abstract:

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Fifty-four per cent of 41 chronically institutionalized adult patients with epilepsy had ataxia of gait (wide mean stride width). None of the following correlated with stride width: serum phenytoin, previous phenytoin toxicity, seizure frequency, or status epilepticus. Seventeen of the 41 patients had computed tomographic head scans. Patients with radiological evidence of cerebellar atrophy had a wider mean stride width, later age of onset of seizures, greater peak serum concentrations of phenytoin than did those without cerebellar atrophy. Ataxia of gait was inconsistently associated with cerebellar atrophy. Elevated serum/plasma concentrations of phenytoin may be a risk factor for cerebellar atrophy, but seizure frequency or status epilepticus are not independently related to this complication.

Type
Original Articles
Information
Canadian Journal of Neurological Sciences , Volume 21 , Issue 3 , August 1994 , pp. 252 - 258
Copyright
Copyright © Canadian Neurological Sciences Federation 1994

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