Book contents
- Frontmatter
- Contents
- Contributors
- Preface
- Part I Historical perspective
- Part II Clinical aspects of tardive dyskinesia
- Part III Mechanisms underlying tardive dyskinesia
- 11 Neurochemistry of the basal ganglia
- 12 A reanalysis of the dopamine theory of tardive dyskinesia: the hypothesis of dopamine D1/D2 imbalance
- 13 Tardive dyskinesia and phenylalanine metabolism: risk-factor studies
- 14 Neuroendocrinological studies of tardive dyskinesia
- 15 Cognitive deficits and tardive dyskinesia
- 16 Studies of tardive dyskinesia using computed tomography and magnetic-resonance imaging
- 17 Rodent and other animal models of tardive dyskinesia during long-term neuroleptic-drug administration: controversies and implications for the clinical syndrome
- Part IV Measurement of tardive dyskinesia
- Part V Tardive dyskinesia in different populations
- Part VI Other neuroleptic-induced movement disorders
- Part VII Treatment of tardive dyskinesia
- Index
13 - Tardive dyskinesia and phenylalanine metabolism: risk-factor studies
from Part III - Mechanisms underlying tardive dyskinesia
Published online by Cambridge University Press: 09 October 2009
- Frontmatter
- Contents
- Contributors
- Preface
- Part I Historical perspective
- Part II Clinical aspects of tardive dyskinesia
- Part III Mechanisms underlying tardive dyskinesia
- 11 Neurochemistry of the basal ganglia
- 12 A reanalysis of the dopamine theory of tardive dyskinesia: the hypothesis of dopamine D1/D2 imbalance
- 13 Tardive dyskinesia and phenylalanine metabolism: risk-factor studies
- 14 Neuroendocrinological studies of tardive dyskinesia
- 15 Cognitive deficits and tardive dyskinesia
- 16 Studies of tardive dyskinesia using computed tomography and magnetic-resonance imaging
- 17 Rodent and other animal models of tardive dyskinesia during long-term neuroleptic-drug administration: controversies and implications for the clinical syndrome
- Part IV Measurement of tardive dyskinesia
- Part V Tardive dyskinesia in different populations
- Part VI Other neuroleptic-induced movement disorders
- Part VII Treatment of tardive dyskinesia
- Index
Summary
Continuing research on tardive dyskinesia has considerably broadened the classic hypothesis of dopamine-receptor supersensitivity, proposed more than 20 years ago (Klawans, 1973). Roles for other neurotransmitter systems (GABA and norepinephrine) have been postulated (Tamminga, Crayton, & Chase, 1979; Wagner et al., 1982; Fibiger & Lloyd, 1984; Gunne, Haggstrom, & Sjoquist, 1984; Jeste, Doongaji, & Linnoila, 1984; Stahl et al., 1985; Kaufman et al., 1986; Thaker et al., 1987; Andersson et al., 1989; Thaker, Nguyen, & Tamminga, 1989), and there is a newer hypothesis suggesting that cellular damage mediated by free radicals underlies tardive dyskinesia (Lohr et al., 1988, 1990; Cadet & Lohr, 1989). Demographic and psychiatric variables, such as gender, age, and concomitant affective disorder, have also been identified as risk factors (Smith & Baldessarini, 1980; Jeste & Wyatt, 1982; Kane & Smith, 1982; Richardson et al., 1985; Kane et al., 1986; Weiner & Lang, 1989). Increasingly, these disparate variables support the concept that tardive dyskinesia, like most brain dysfunctions, may involve multiple abnormalities and that vulnerability to it may be multifactorial. In this chapter we summarize our findings concerning risk factors for tardive dyskinesia that suggest that amino acid metabolism – particularly that of the large neutral amino acid phenylalanine (Phe) – may play a role in vulnerability to tardive dyskinesia.
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- Neuroleptic-induced Movement DisordersA Comprehensive Survey, pp. 161 - 174Publisher: Cambridge University PressPrint publication year: 1996