Tardive Dystonia

Chiu, Helen F. K.; Lee, Paul

doi:10.3109/00048678909062626

Cited by 11 publications

(2 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Second, dopamine D2 receptor antagonists (e.g. neuroleptics and antiemetics) can cause both acute [36] and tardive [37] dystonias. If dystonia is a disorder of amplified activity in the postural control system, then it is not unreasonable to suggest, based on these observations, that the indirect pathway (which is mediated by D2 receptors) plays a role in controlling posture.…”

Section: Potential Role Of the Bg Indirect Pathway In Coordinating Mumentioning

confidence: 99%

New hypotheses about postural control support the notion that all dystonias are manifestations of excessive brain postural function

Blood¹

2008

Bioscience Hypotheses

View full text Add to dashboard Cite

This paper postulates that all forms of the neurological movement disorder, dystonia, can be argued to reflect excessive function of one or more components of the brain postural system. This is based on four central arguments. First, because some forms of postural control are already known to be dynamic, rather than static, it is suggested that hyperkinetic dystonias reflect excessive function of dynamic postures, rather than abnormal movements. Second, the range of functional roles served by the postural system is hypothesized to include direct control of movement, suggesting a postural basis for task-specific dystonias. Third, by defining posture as a neural system that maintains body stabilization, it can be shown that the range of mechanical means of implementing stabilization, including co-contraction of antagonistic muscles, matches the range of presentations of dystonia. Fourth, it is shown that the above premises are able to account for previously unexplained observations in dystonia. Based on the inhibitory influence that stabilizing mechanisms exert on movement, it is suggested that the broad functional role that is here referred to as posture may be the function served by the indirect pathway of the basal ganglia. Specifically, it is proposed that this pathway centrally coordinates function of the distributed network of brain regions controlling posture and, in conjunction with the direct pathway, coordinates posture and movement.

show abstract

Section: Potential Role Of the Bg Indirect Pathway In Coordinating Mumentioning

confidence: 99%

New hypotheses about postural control support the notion that all dystonias are manifestations of excessive brain postural function

Blood¹

2008

Bioscience Hypotheses

View full text Add to dashboard Cite

show abstract

“…As already mentioned, TDt is frequently co-occurring with other tardive syndromes, such as TDk, Tardive akathisia (TDa), Tardive myoclonous (TDm), and Tardive tourettism (TDr) ( Table 3). Patients with TDt are more aware of their movement disorders than patients with TDk [54].…”

Section: Diagnosis Clinical Presentation and Coursementioning

confidence: 99%

Tardive Dystonia due to D2 Antagonists and Other Agents

Σκώκου¹,

Tsermpini²,

Giamarelou³

et al. 2018

Dystonia - Different Prospects

View full text Add to dashboard Cite

Tardive dystonia due to D2 antagonists or other agents is a potentially severe extrapyramidal side effect emerging after long-term drug treatment, prevalent but not limited to psychiatric populations. Its course is often deteriorating, and available treatments are frequently far from satisfying. It presents with sustained muscle contractions, abnormal postures, and repetitive twisting movements and leads to increased psychiatric morbidity, mortality, and decline of quality of life. Inadequate clinical skill and awareness of tardive dystonia can lead to neglect or misdiagnoses, considered as conversion symptoms or of psychogenic origin. Since the syndrome is persistent and often treatment resistant, prevention should be a mainstay of clinical care. Emerging evidence supports positive effects of atypical antipsychotics, particularly quetiapine and clozapine. Therapies such as tetrabenazine, valbenazine, deutetrabenazine, anticholinergics, baclofen, benzodiazepines, vitamin E, or non-pharmacologic interventions, namely botulinum toxin A, deep-brain stimulation, have been found to be helpful in some cases of tardive dystonia. This chapter comprehensively illustrates multiple aspects of this entity, including recent advances on etiology, pathophysiology, clinical presentation, epidemiology, pharmacogenomics, and treatment, aiming to enhance and deepen clinicians' and researchers' awareness of tardive dystonia, with the final goal of ameliorating patients' prognosis and quality of life.

show abstract