Posted by neuroscience on October 28, 2012, at 2:06:16
In reply to Re: question about tardive dyskinesia pathophysiology, posted by phidippus on October 27, 2012, at 18:22:13
> what does the neurotoxicity hypothesis state?
>
>
> Eric
Dopamine receptor blockade leads to an increase of dopamine turnover thus producing excessive free oxyradicals that damage striatal neurons.Also, there is this from Lerner, V. and C. Miodownik (2011). "Motor symptoms of schizophrenia: is tardive dyskinesia a symptom or side effect? A modern treatment." Curr Psychiatry Rep 13(4): 295-304.:
"To date, several neurochemical hypotheses have been proposed for the development of TD, including a disturbed balance between dopamine and cholinergic systems; dysfunctions of striatonigral, γ-aminobutric acid (GABA)ergic neurons; and excitotoxicity [38, 39]. Recently, the role of oxidative stress and structural abnormality in the pathophysiology of TD has gained impetus. Induction of free radicals by neuroleptic drugs leading to oxidative stress and resultant structural abnormality could be the key factor in the pathogenesis of TD. The studies by Lerner et al. [40] and Libov et al. [41] support the neurotoxicity hypothesis. It also has been supported by reports that chronic neuroleptic treatment increases free radical production and causes structural damage [37]. In 2005, Tan and colleagues [42] reported that brain-derived neurotrophic factor appears to exert a protective effect in the nervous system against TD in patients with schizophrenia.
Previously, it was suggested that only antipsychotic agents could cause TD. However, in recent years, many reports have suggested that various psychotropic medications, such as antihistamines, antidepressants, anticholinergics and other agents, can cause TD (Table 1)."you can read the whole thing here:
http://rd.springer.com/article/10.1007/s11920-011-0202-6/fulltext.html
poster:neuroscience
thread:1029742
URL: http://www.dr-bob.org/babble/20121018/msgs/1030034.html