Neurology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Correspondence:
Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Correspondence are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by LÉAN, J. O.
Right arrow Articles by HORNYKIEWICZ, O.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by LÉAN, J. O.
Right arrow Articles by HORNYKIEWICZ, O.
NEUROLOGY 1976;26:863
© 1976 American Academy of Neurology

Beneficial effects of serotonin precursors in postanoxic action myoclonus

JACQUES OE LÉAN, M.D., MSc., J. CLIFFORD RICHARDSON, M.D., F.R.C.P. and OLEH HORNYKIEWICZ, M.D.

From the Division of Neurology, Toronto General Hospital (Dr. De Léan and Dr. Richardson), and the Department of Psychopharmacology, Clarke Institute of Psychiatry (Dr. Hornykiewicz), University of Toronto, Canada.

In two patients with postanoxic action myoclonus, L-tryptophan or a monoamine oxidase inhibitor induced a moderate improvement, but L-5-hydroxytryptophan had greater therapeutic effect. Methysergide, a potent blocker of serotonin receptors, consistently induced a marked deterioration in myoclonus. Pretreatment cerebrospinal fluid 5-hydroxyindoleacetic acid levels were reduced significantly in both patients. These findings suggest that postanoxic action myoclonus likely is associated with insufficient serotonergic activity in the central nervous system. Data are inadequate to determine whether this apparent insufficiency reflects structural changes in 5HT-containing raphe nuclei due to a direct anoxic damage to these structures or functional changes caused by a secondary reduction in the activity of intact serotonergic neurons.

Requests for reprints should be addressed to Dr. Richardson, Division of Neurology, 11 NUW, Toronto General Hospital, 101 College Street, Toronto, Ontario M5G 1L7.

A preliminary report of this study was read before the tenth Canadian Congress of Neurological Sciences, London, Ontario, June 20, 1975.

Received for publication September 24, 1975.






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1976 by AAN Enterprises, Inc.