The association between risk factors for tardive dyskinesia and phenylalanine-induced abnormal movements in schizophrenia

We examined whether an oral challenge dose of the amino acid phenylalanine (a dopamine precursor) exacerbates the abnormal movements of tardive dyskinesia (TD). We also examined age, gender, treatment duration, and baseline movement severity in relation to phenylalanine‐induced changes in movements....

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Published in:Human psychopharmacology Vol. 16; no. 3; pp. 273 - 277
Main Authors: Schultz, S. K., Ellingrod, V., Fleming, F. W., Andreasen, N. C.
Format: Journal Article
Language:English
Published: Chichester, UK John Wiley & Sons, Ltd 01-04-2001
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Summary:We examined whether an oral challenge dose of the amino acid phenylalanine (a dopamine precursor) exacerbates the abnormal movements of tardive dyskinesia (TD). We also examined age, gender, treatment duration, and baseline movement severity in relation to phenylalanine‐induced changes in movements. Lastly, we assessed the influence of fasting amino acid levels on phenylalanine‐induced movements. In a placebo‐controlled fashion, the abnormal involuntary movement scale (AIMS) was obtained on 25 patients before and after a phenylalanine challenge drink. A general linear model determined the relative effects of age, gender, treatment duration, and fasting amino acid levels on the magnitude of induced movements. Age and treatment duration did not affect phenylalanine‐induced movements. Lower fasting levels of phenylalanine were associated with greater movements after controlling for age, F = 11.89, p < 0.003. The severity of abnormal movements at baseline also predicted response to phenylalanine, F = 8.62, p = 0.0079. Brain amino acid and neurotransmitter pools are influenced by changes in dietary protein, which may have implications in the development and prevention of movement disorders. This study suggests that fasting amino acid levels may predict differences in vulnerability to movements during an influx of neurotransmitter precursors, perhaps due to long‐term compensatory changes in receptor sensitivity. Copyright © 2001 John Wiley & Sons, Ltd.
Bibliography:ark:/67375/WNG-J6VRM76G-1
ArticleID:HUP245
istex:C6C451FA056AE5EBE3CA727B297F377D5201E19C
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0885-6222
1099-1077
DOI:10.1002/hup.245