Gamma-vinyl-GABA treatment of tardive dyskinesia and other movement disorders

Stahl, Stephen M.; Thornton, Joe E.; Simpson, Mary; Berger, Philip A.; Napoliello, Michael J.

doi:10.1016/0006-3223(85)90214-8

Cited by 41 publications

(23 citation statements)

References 21 publications

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“…There was also a sedative effect of GVG which might unspecifically have contributed to the antidyskinetic effect. The relatively long-lasting antidyskinetic effect after GVG administration in two of the monkeys is in accordance with a study on human TD (Stahl et al 1985) where dyskinetic symptoms were still reduced 2 weeks after withdrawal of GVG.…”

Section: I)ise~onsupporting

confidence: 89%

“…In the human clinical studies with THIP (Korsgaard et al 1982;Thaker et al 1987), GAG (Casey et al 1980), and GVG (Korsgaard et al 1983;Stahl et al 1985;Thaker et al 1987) the patients received the test drugs orally for some weeks in doses much lower than in the present experiment. The patients also, as a rule, received concomitant neuroleptic medication.…”

Section: I)ise~onmentioning

confidence: 84%

“…As mentioned above, GAG and GVG have been tried on human TD and there are several reports of antidyskineric effects (Casey et al 1980;Tell et al 1981;Korsgaard et al 1983;Tamrninga et al 1983;Stahl et al 1985;Thaker et al 1987). In one of these studies (Korsgaard et al 1983), neuroleptics were administered concomitantly with GVG and a negative correlation was found between improvement rate in TD and parkinsonism, suggesting interactions between DA and GABA.…”

Section: I)ise~onmentioning

confidence: 97%

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GABA agonists in cebus monkeys with neuroleptic-induced persistent dyskinesias

Andersson

Häggström

1988

Psychopharmacology

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Tetrahydroisoxazolopyridinol (THIP), a GABA receptor agonist, gamma-acetylenic-GABA(GAG) and gamma-vinyl-GABA(GVG), two GABA transaminase inhibitors were given in single parenteral doses to three Cebus apella monkeys with persistent dyskinetic movements induced by earlier long-term administration of haloperidol. High doses of THIP temporarily abolished dyskinesias but also caused bradykinesia, ataxia, dystonia and myoclonic jerks. GAG and GVG reduced dyskinesias to a lesser extent and with fewer side effects. Whether the observed antidyskinetic effect is secondary to the concomitant general toxic effects or if these drugs have a specific antidyskinetic action remains an open question.

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Section: I)ise~onsupporting

confidence: 89%

Section: I)ise~onmentioning

confidence: 84%

Section: I)ise~onmentioning

confidence: 97%

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GABA agonists in cebus monkeys with neuroleptic-induced persistent dyskinesias

Andersson

Häggström

1988

Psychopharmacology

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“…It was seen to have a beneficial effect on tardive dyskinesias induced by neuroleptics, and there was conflicting evidence as to whether it ameliorated ataxia in degenerative cerebellar diseases. [9][10][11][12][13] There was one report of it having a positive effect on spasticity in metachromatic leukodystrophy. 14 There have been equivocal results in its use as a treatment of dyskinesias in Parkinson disease and spasticity in multiple sclerosis.…”

Section: Discussionmentioning

confidence: 99%

An investigation into the relationship between vigabatrin, movement disorders, and brain magnetic resonance imaging abnormalities in children with infantile spasms

Fong

Osborne

Edwards

et al. 2013

Develop Med Child Neuro

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AIM We aimed to investigate the relationship between movement disorders, changes on brain magnetic resonance imaging (MRI), and vigabatrin therapy in children with infantile spasms. METHOD Retrospective review and brain MRI analysis of children enrolled in the InternationalCollaborative Infantile Spasms Study (ICISS) who developed a movement disorder on vigabatrin therapy. Comparisons were made with controls within ICISS who had no movement disorder. RESULTSTen of 124 infants had a movement disorder and in eight it had developed on vigabatrin therapy. Two had a movement disorder that resolved on dose-reduction of vigabatrin, one had improvement on withdrawing vigabatrin, two had resolution without any dose change, and in three it persisted despite vigabatrin withdrawal. The typical brain MRI changes associated with vigabatrin therapy were noted in two infants. Ten control infants were identified. Typical MRI changes noted with vigabatrin were noted in three controls.INTERPRETATION It is possible that in two out of eight cases, vigabatrin was associated with the development of a movement disorder. In six out of eight cases a causal relationship was less plausible. The majority of infants treated with vigabatrin did not develop a movement disorder. MRI changes associated with vigabatrin do not appear to be specifically related to the movement disorder.Infantile spasms are an age-related epileptic encephalopathy that occurs in children, usually between the ages of 3 months and 18 months. The seizures manifest typically as clusters of either flexor or extensor epileptic spasms, which are often coincident with an arrest or regression of neurodevelopment. The electroencephalograph characteristically, but not always, shows a chaotic high voltage interictal pattern known as hypsarrhythmia. Many underlying aetiologies, such as tuberous sclerosis complex, trisomy 21, neuronal migration disorders, and hypoxic-ischaemic encephalopathy, have been associated with infantile spasms but in a significant minority of cases no cause is found. There has been much debate about the most effective treatment modality for these patients but there appears to be a relatively wide consensus that the two most effective therapies are either the GABA-ergic anticonvulsant, vigabatrin, or hormonal therapies (prednisolone, adrenocorticotrophin hormone [ACTH], or synthetic ACTH). 1It has been known since the 1980s that vigabatrin usage in animals was associated with the development of intramyelinic oedema in the central nervous system, most notably in the cerebellum, reticular formation and optic tracts in rats, and columns of the fornix and the optic tracts in dogs. 2,3 Recently reports have surfaced in the literature linking vigabatrin usage in humans with characteristic magnetic resonance imaging (MRI) changes in the globus pallidus, thalamus, brain stem, and dentate nuclei of the cerebellum. 4,5 These changes appear to be dose-dependent

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“…Gamma acetylene GABA suppresses oral movements induced by chronically administered haloperidol in humans (Casey et al 1980), and injections of GABA receptor antagonists into the substantia nigra precipitate oral dyskinesias in rats (Arnt and Scheel-Kriiger 1980). Clinical trials with drugs that modify the functions of GABA-containing systems, such as muscimol (Tamminga et al 1979), sodium valproate (Nair et al 1980), gamma-vinyl GABA (Tamminga et al 1983 ;Stahl et al 1985) and baclofen (Simpson et al 1978), have further implicated a role for GABA in tardive dyskinesia. Repeated administration of neuroleptics in rats has been reported to increase GABA turnover rates in the caudate nucleus and nucleus accumbens, and decrease turnover in the substantia nigra (Mao et al 1977;Marco et al 1978).…”

mentioning

confidence: 99%

Neuroleptic-induced oral dyskinesias: effects of progabide and lack of correlation with regional changes in glutamic acid decarboxylase and choline acetyltransferase activities

Mithani¹,

Atmadja²,

Baimbridge

et al. 1987

Psychopharmacology

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The development of vacuous chewing movements (VCMs), and changes in glutamic acid decarboxylase (GAD) and choline acetyltransferase (ChAT) activities in extrapyramidal nuclei were examined in rats treated chronically with neuroleptics. Animals were injected with flupenthixol (FLU) or haloperidol (HAL) decanoate for 16, 40 or 48 weeks and were then sacrificed. Another group of rats was treated with FLU or HAL for 48 weeks, and then withdrawn from the neuroleptics for 16 weeks before sacrifice. VCMs were assessed weekly, and the effects of the GABA agonist progabide on VCMs and locomotor activity were examined. GAD and ChAT activities were determined at death. The concentrations of Calbindin D28K (CaBP) and parvalbumin (PV) were determined in rats receiving 48 weeks of neuroleptic treatment. VCMs first appeared after 8-10 weeks of neuroleptic administration, reached asymptotic rates after 18-20 weeks, and then remained stable for the remainder of the chronic drug administration period. During withdrawal, there was a steady decline in the VCM rate. The GABA receptor agonist progabide reduced VCMs and locomotor activity. Significant decreases in nigral GAD activity were observed after 40, but not after either 16 or 48 weeks of neuroleptic administration. CaBP and PV were unchanged after 48 weeks of neuroleptic treatment. In addition, ChAT activities in 16, 40 or 48 week treated animals did not show consistent changes after either neuroleptic. Chronic neuroleptic administration followed by 16 weeks of withdrawal also did not have any significant effects on GAD or ChAT activity in any of the brain areas examined.(ABSTRACT TRUNCATED AT 250 WORDS)

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Gamma-vinyl-GABA treatment of tardive dyskinesia and other movement disorders

Cited by 41 publications

References 21 publications

GABA agonists in cebus monkeys with neuroleptic-induced persistent dyskinesias

GABA agonists in cebus monkeys with neuroleptic-induced persistent dyskinesias

An investigation into the relationship between vigabatrin, movement disorders, and brain magnetic resonance imaging abnormalities in children with infantile spasms

Neuroleptic-induced oral dyskinesias: effects of progabide and lack of correlation with regional changes in glutamic acid decarboxylase and choline acetyltransferase activities

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