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Increased Plasma Catecholamines in Patients with Friedreich’s Ataxia

Published online by Cambridge University Press:  18 September 2015

A. Pasternac ,
P. Wagniart ,
R. Olivenstein ,
R. Petitclerc ,
R. Krol ,
E. Andermann ,
S. Melancon ,
G. Geoffroy ,
J. de Champlain  and
A. Barbeau
A. Pasternac
Affiliation:
Department of Medicine of the Montreal Heart Institute, and the Clinical Research Institute, Departments of Medicine and Physiology. University of Montreal and the Department of Neurogenetics, the Montreal Neurological Hospital and Institute, McGill University, Montreal, Quebec, Canada
P. Wagniart
Affiliation:
Department of Medicine of the Montreal Heart Institute, and the Clinical Research Institute, Departments of Medicine and Physiology. University of Montreal and the Department of Neurogenetics, the Montreal Neurological Hospital and Institute, McGill University, Montreal, Quebec, Canada
R. Olivenstein
Affiliation:
Department of Medicine of the Montreal Heart Institute, and the Clinical Research Institute, Departments of Medicine and Physiology. University of Montreal and the Department of Neurogenetics, the Montreal Neurological Hospital and Institute, McGill University, Montreal, Quebec, Canada
R. Petitclerc
Affiliation:
Department of Medicine of the Montreal Heart Institute, and the Clinical Research Institute, Departments of Medicine and Physiology. University of Montreal and the Department of Neurogenetics, the Montreal Neurological Hospital and Institute, McGill University, Montreal, Quebec, Canada
R. Krol
Affiliation:
Department of Medicine of the Montreal Heart Institute, and the Clinical Research Institute, Departments of Medicine and Physiology. University of Montreal and the Department of Neurogenetics, the Montreal Neurological Hospital and Institute, McGill University, Montreal, Quebec, Canada
E. Andermann
Affiliation:
Department of Medicine of the Montreal Heart Institute, and the Clinical Research Institute, Departments of Medicine and Physiology. University of Montreal and the Department of Neurogenetics, the Montreal Neurological Hospital and Institute, McGill University, Montreal, Quebec, Canada
S. Melancon
Affiliation:
Department of Medicine of the Montreal Heart Institute, and the Clinical Research Institute, Departments of Medicine and Physiology. University of Montreal and the Department of Neurogenetics, the Montreal Neurological Hospital and Institute, McGill University, Montreal, Quebec, Canada
G. Geoffroy
Affiliation:
Department of Medicine of the Montreal Heart Institute, and the Clinical Research Institute, Departments of Medicine and Physiology. University of Montreal and the Department of Neurogenetics, the Montreal Neurological Hospital and Institute, McGill University, Montreal, Quebec, Canada
J. de Champlain
Affiliation:
Department of Medicine of the Montreal Heart Institute, and the Clinical Research Institute, Departments of Medicine and Physiology. University of Montreal and the Department of Neurogenetics, the Montreal Neurological Hospital and Institute, McGill University, Montreal, Quebec, Canada
A. Barbeau*
Affiliation:
Department of Medicine of the Montreal Heart Institute, and the Clinical Research Institute, Departments of Medicine and Physiology. University of Montreal and the Department of Neurogenetics, the Montreal Neurological Hospital and Institute, McGill University, Montreal, Quebec, Canada
*
Clinical Research Institute of Montreal, 110 West Pine Avenue West, Montréal, Quebec, Canada H2W 1R7
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We studied free plasma catecholamines in 23 patients with Friedreich’s ataxia, having a mean age of 22 ± 9.6 (SD) years. Conjugated catecholamines were also studied in 10 patients. Mean plasma norepinephrine and epinephrine were significantly higher than controls both in the supine and standing positions. In total 15 out of 23 patients (65%) had increased free and/or conjugated plasma catecholamines. The increase in plasma catecholamines was more marked in patients with severe neuromotor impairment. Among the patients with left ventricular concentric hypertrophy (wall thickness >12 mm), only 3 had no demonstrable sympathetic hyperfunction.

Since the high local concentrations of norepinephrine at the site of release from sympathetic nerve terminals may serve as a trigger for the hypertrophic response of the myocardial cell, it is suggested that early pharmacological intervention could prevent or limit the cardiomyopathic process or its clinical consequences.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 9 , Issue 2 , May 1982 , pp. 195 - 203
Copyright
Copyright © Canadian Neurological Sciences Federation 1982

References

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