Six month evaluation of thiopropazate hydrochloride in tardive dyskinesia.

Smith, J. Lawton; Kiloh, L. G.

doi:10.1136/jnnp.42.6.576

Cited by 13 publications

(2 citation statements)

References 11 publications

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“…This design may be a better measure of the neuroleptics’ ability to suppress withdrawal dyskinesias than persistent TD. Other studies were either unblinded or did not use appropriate control groups (Roxburgh 1970; Curran 1973; Jus et al 1979; Smith and Kiloh 1979). Of three particularly well-controlled studies, two found significant long-term suppression (Frangos and Christodoulides 1975; Gerlach and Casey 1983), while the third did not (Korsgaard et al 1984).…”

Section: Suppressive Therapies For Tdmentioning

confidence: 99%

Treatment of Tardive Dyskinesia

Egan

Apud

Wyatt

1997

Schizophrenia Bulletin

136

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Although the new generation of atypical antipsychotic agents could some day eliminate concerns about tardive dyskinesia (TD), this disorder remains a significant clinical problem for both patients and physicians. Fortunately, many, if not most, cases of TD are mild. For patients with mild to moderate TD, therapeutic efforts are primarily directed at minimizing neuroleptic exposure or, when possible, changing to atypical agents. Most cases of TD do not seem to progress, suggesting that the risk of remaining on typical neuroleptics is probably small. Patients with moderate to severe forms of TD present greater challenges. These patients frequently require medication to suppress their dyskinesias. A variety of suppressive agents have been tried with limited success. No treatment strategy has emerged that is clearly superior or even successful in most patients. Increasing doses of typical neuroleptics may be useful for short-term suppression; however, the long-term efficacy and risk of this strategy have not been studied carefully. Data on atypical neuroleptics are scant. Clozapine's short-term suppressive effects seem, at best, weak, but patients may improve with long-term treatment. Medications with relatively few side effects that may have suppressive efficacy for some patients include calcium channel blockers, adrenergic antagonists, and vitamin E. Gamma-amino-butyric acid agonists agents and dopamine depleters are frequently useful, but have troubling side effects of their own. A variety of other medications have been employed, but are not well studied. For patients with tardive dystonia, anticholinergic agents or botulinum toxin has been particularly effective. Efforts to understand the neurobiology of TD may shed light on this persistent clinical conundrum.

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Section: Suppressive Therapies For Tdmentioning

confidence: 99%

Treatment of Tardive Dyskinesia

Egan

Apud

Wyatt

1997

Schizophrenia Bulletin

136

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“…Dopamin-Antagonisten Apomorphin in niedriger Dosis (25,222,235) ButYrophenone (32,89,137,142) Clozapin (101,208,246) Oxiperomid (28) Papaverin (43) Phenothiazin-Derivate (158,212,219) Pimozide (41,88) Sulpirid (29) Tiaprid (40,47) Monoamin-entspeichernde Substanzen Reserpin (123) Tetrabenazin (32,142) Katecholaminsynthese-Blocker Alpha-Methyldopa (123) AI~ha-MethYltYrosin (105) Cholinergika Deanol (76,171) Cholin, Lezithin (100,111,162) Physostigmin (63,229) GABAerge Substanzen 7Baclofen (104,154,174) Benzodiazepine (18,115,213) Valproinsäure ( Literatur…”

Section: Therapeutische Strategienmentioning

confidence: 99%

Die Spätdyskinesien - eine Übersicht über Klinik, Pathogenese, Prophylaxe und Therapie eines späten neuroleptischen Seiteneffekts

K¹

1983

Fortschr Neurol Psychiatr

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Tardive dyskinesia (t.d.) is a disorder of the extrapyramidal motor system occurring as a late harmful side-effect long-term therapy with neuroleptic drugs. Prevalence rates, for a variety of causes not easily obtainable, are apparently rising and, according to new studies that also take into account borderline or doubtful cases, may reach 30% for both hospitalized and non-hospitalized chronically schizophrenic patients. Very pronounced forms and complications of tardive dyskinesia are rare. Tardive dyskinesia does not present as a single well defined disorder; rather, several types of t.d. may be distinguished either clinically with regard to localisation, manifestation and the course of the disease, or pharmacologically with regard to susceptibility to provocation or therapy. Reversibility remains the most important practical criterion for differentiation. In addition to long-term treatment with neuroleptics old age, and an ill-defined "individual disposition" are of particular importance in the multiconditional model of t.d.. In terms of pathophysiology t.d. is conceived to be a hypersensitivity of postsynaptic-dopamine-receptors of the nigrostriatal pathways. While therapeutic guidelines may be derived from this model, an effective and generally accepted therapeutic regimen for t.d. does not exist. Therefore, prevention or, secondarily, early diagnosis must receive proper emphasis and attention.

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Therapeutic Strategies Against Tardive Dyskinesia

Jeste¹

1982

Arch Gen Psychiatry

157

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Six month evaluation of thiopropazate hydrochloride in tardive dyskinesia.

Cited by 13 publications

References 11 publications

Treatment of Tardive Dyskinesia

Treatment of Tardive Dyskinesia

Die Spätdyskinesien - eine Übersicht über Klinik, Pathogenese, Prophylaxe und Therapie eines späten neuroleptischen Seiteneffekts

Therapeutic Strategies Against Tardive Dyskinesia

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