Posted by neuroscience on October 15, 2012, at 10:38:53
In reply to Re: Lou's response-knrvehyjentz, posted by neuroscience on October 15, 2012, at 6:55:24
> I can understand your desire to warn people about TD Lou.
>
> On the topic of pathophysiology, there is something I just read from Motor Symptoms of Schizophrenia: Is Tardive Dyskinesia a Symptom or Side Effect? A Modern Treatment:
>
> "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."
>
> The neurotoxicity hypothesis seems promising.Libov, I., et al. (2007). "Efficacy of piracetam in the treatment of tardive dyskinesia in schizophrenic patients: a randomized, double-blind, placebo-controlled crossover study." J Clin Psychiatry 68(7): 1031-1037.
The above article I cited is extremely interesting to me. It supports the neurotoxicity hypothesis.
Piracetam is a potent antioxidant and a cerebral neuroprotector.
poster:neuroscience
thread:1028704
URL: http://www.dr-bob.org/babble/20121009/msgs/1028720.html