Drug Induced Movement Disorders 2005
DOI: 10.1002/9780470753217.ch9
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Tardive Dyskinesia

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Cited by 8 publications
(15 citation statements)
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“…These striatal neurons are primarily GABAergic but other neuropeptides and neurotransmitters such as dynorphin, substance P, neurotensin, CCK (cholecystokinin), and NMDA (N-methyl D-aspartate, a glutamate receptor), and opioid receptors may also contribute to the development of TD (Hyde et al, 2005;Margolese et al, 2005). We discuss two hypotheses, the dopamine supersensitivity hypothesis, including the related D2 binding affinity theory, because they explain at least some of the characteristics of TD, and the neurotoxicity theory which hypothesis is also linked to movement disorders found in neurology.…”
Section: Pathophysiologymentioning
confidence: 99%
See 1 more Smart Citation
“…These striatal neurons are primarily GABAergic but other neuropeptides and neurotransmitters such as dynorphin, substance P, neurotensin, CCK (cholecystokinin), and NMDA (N-methyl D-aspartate, a glutamate receptor), and opioid receptors may also contribute to the development of TD (Hyde et al, 2005;Margolese et al, 2005). We discuss two hypotheses, the dopamine supersensitivity hypothesis, including the related D2 binding affinity theory, because they explain at least some of the characteristics of TD, and the neurotoxicity theory which hypothesis is also linked to movement disorders found in neurology.…”
Section: Pathophysiologymentioning
confidence: 99%
“…However, several arguments challenge this hypothesis: (i) supersensitivity of the receptor is already present after a few weeks of antipsychotic use while TD often develops much later, (ii) almost all patients on antipsychotics develop dopamine supersensitivity but not all develop TD, and (iii) after cessation of antipsychotics, the dopamine supersensitivity disappears but TD often persists for years (Hyde et al, 2005).…”
Section: A Dopamine Supersensitivity Theorymentioning
confidence: 99%
“…However, this hypothesis provides an incomplete picture [ 1 , 25 , 33 ]. Evidence on dopamine D2-receptor supersensitvity associated with dyskinesias in animals, which develop quickly and resolve rapidly after drug discontinuation, has been questioned as an inexact model for TD in humans.…”
Section: Pharmacotherapy Of Tardive Dyskinesiamentioning
confidence: 99%
“…Specific treatments for TD are best prescribed within a comprehensive management strategy including preven-tive screening for early signs, differential diagnosis, and informed discussion with patients and caregivers ( Table 1 ) [ 1 , 16 - 20 ]. Numerous agents have been tested as treatments for TD based on competing theories of pathophysiology [ 21 - 26 ]. The statistical designs of these clinical trials have been extensively reviewed [ 18 , 26 - 32 ].…”
Section: Introductionmentioning
confidence: 99%
“…TSs are generally thought to be reversible to some degree; the rate of resolution is often quoted to be approximately 30% overall and possibly lower in elderly people. 14 16 While many studies examining reversibility have been conducted in psychotic patients who continue treatment with DRBAs, few studies have examined the remission rate of TSs in patients in whom the offending agents are permanently discontinued. 17 – 21 Remission rates in these studies range from 2% to 33% with follow-up as long as 6.7 years.…”
Section: Introductionmentioning
confidence: 99%