Dopaminergic hypersensitivity and cholinergic hypofunction in the pathophysiology of tardive dyskinesia

Gerlach, Jes; Reisby, N; Randrup, A.

doi:10.1007/bf00421217

Cited by 246 publications

(58 citation statements)

References 34 publications

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“…Choline chloride, an acetylcholine precursor, has been tried with some therapeutic benefit (Tamminga et al, 1977;Davis et a l, 1976). Consistent with the above observations, anti cholinergic agents aggravate TD (Klawans and Rubovits, 1974;Kiloh et al, 1973;Gerlacli et al, 1974;Birket-Smith, 1974) and in some cases elicit dyskinetic movements not previ ously apparent (Klawans and Rubovits, 1974;Gerlach et al, 1974). One possible explanation of these effects o f anticholinergic drugs is that they lower blood levels o f neuroleptics by one or another mechanism, for example, by im pairing gastrointestinal motility and subsequent neuroleptic absorption (Rivera-Calimlim et a l, 1973.…”

supporting

confidence: 62%

Adverse Effects of Anticholinergic Antiparkinsonian Drugs in Tardive Dyskinesia

et al. 1980

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10 long-term schizophrenic patients with tardive dyskinesia were studied over 14 weeks and maintained on their usual neuroleptic medications while anticholinergic antiparkinson drugs were employed and then discontinued, and the cycle then repeated. Discontinuation of anticholinergic medications resulted in improvement in dyskinetic movements and vice versa. Estimation of haloperidol equivalents in serum at four times suggested that changes in severity of tardive dyskinesia were not caused by changes in blood levels of neuroleptics. Levels of pituitary hormones were also estimated at four times. Prolactin levels tended to diminish in men over the course of the experiment. Growth hormone and thyrotropin values were mainly stable. However, the growth hormone levels peaked during the final ‘off anticholinergic’ condition and thyrotropin levels were consistently elevated.

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supporting

confidence: 62%

Adverse Effects of Anticholinergic Antiparkinsonian Drugs in Tardive Dyskinesia

et al. 1980

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“…TD is thought to be related to the predominance of an overactive dopaminergic as opposed to the choliner gic system within the basal ganglia [Gerlach et al, 1974], No generally satisfactory treatment has yet been demonstrated for the potentially irreversible symptoms of TD [Task Force Report, 1979;Woller and Tegeler, 1983], 1 Dedicated to the 60th birthday of Professor Dr. Hanns Hippius.…”

Section: Introductionmentioning

confidence: 99%

Tiapride: Effects on Tardive Dyskinesia and on Prolactin Plasma Concentrations

Greil¹,

Auberger²,

Haag³

et al. 1985

Neuropsychobiology

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In a placebo-controlled double-blind crossover study of 21 patients chronically treated with neuroleptics and suffering from tardive dyskinesia, tiapride (600 mg/day, mean plasma level: 682 ng/ml) exhibited a transient efficacy during 12 weeks of treatment, most distinct in the 6th week (p < 0.01). Tiapride induced an increase of prolactin plasma levels, on the average, from 1,195 to 2,179 µlU/ml (p < 0.01). Tiapride was well tolerated. Increase of parkinsonism was only mild and not significant. The results underline the difficulty in treating tardive dyskinesia and, thus, confirm the importance of prevention.

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“…Based on the finding that some parkinsonian patients receiving L-dopa therapy develop TD, it has been proposed [52][53][54] that TD is the result of dopamine receptor hypersensi tivity. Several clinical observations support this hypothesis: TD tends to worsen upon withdrawal of neuroleptic medications; Ldopa administration exacerbates drug-in duced TD, and in parkinsonian patients Ldopa may induce dyskinesia which closely resembles TD [55,56]. The fact that TD may be suppressed by treatment with drugs that deplete or block the action of dopamine such as tetrabenazine, neuroleptics as well as alpha-methyl-p-tyrosin [55] provides addi tional support for a state of relative dopamin ergic hypersensitivity.…”

Section: Dopaminementioning

confidence: 80%

Current Psychopathological Theories of Tardive Dyskinesia and Their Implications for Future Research

Ananth¹

1982

Neuropsychobiology

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An understanding of pathophysiology is essential for establishing an etiological relationship between the neuroleptics and tardive dyskinesia, for elucidating specific treatment methods and perhaps for synthesizing new neuroleptics which do not produce this side effect. Our current knowledge has been derived from clues obtained by drug-related factors, therapeutic agents assumed to improve tardive dyskinesia and by neuropathological findings. Among the many theories, dopaminergic hypersensitivity is the most favored and yet unproven. At present the etiology of tardive dyskinesia may be related to the interaction between the exogenous drugs and the endogenous predisposition, the nature of which is so far elusive.

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Dopaminergic hypersensitivity and cholinergic hypofunction in the pathophysiology of tardive dyskinesia

Cited by 246 publications

References 34 publications

Adverse Effects of Anticholinergic Antiparkinsonian Drugs in Tardive Dyskinesia

Adverse Effects of Anticholinergic Antiparkinsonian Drugs in Tardive Dyskinesia

Tiapride: Effects on Tardive Dyskinesia and on Prolactin Plasma Concentrations

Current Psychopathological Theories of Tardive Dyskinesia and Their Implications for Future Research

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