The mechanism involved in the development of tardive dyskinesia (TD) is complicated. It now
seems that several neurotransmitter systems may be affected, including dopaminergic,
noradrenergic, gamma-amino-butyric acid (GABA) ergic, cholinergic and peptidergic pathways.
Piracetam (2-oxo-pyrrolidone) is a nootropic drug structurally related to GABA. It has been
used clinically to treat a wide range of diseases and conditions, mainly in treatment of
organic brain syndrome, myoclonus, memory impairment, post-concussional syndrome, vertigo,
alcohol withdrawal, cerebrovascular insufficiency, hypoxia, intoxications of different
origins or mechanic brain injures. Piracetam is cerebral homeostatic normalizer,
neuroprotectant, cerebral metabolic enhancer and brain integrative agent. It enhances brain
energy, especially under deficit condition: hypoxia, chemical toxicity or impaired cerebral
microcirculation; preserve, protect and enhance synaptic membrane and receptor structure and
plasticity. It has various effects on glutamate neurotransmission on micromolar levels
piracetam potentiates potassium-induced release of glutamate from hippocampal nerves. It is
an oxidant agent and may be useful for treatment TD. Piracetam is among the toxicologically
safest drugs ever developed even in mega doses.
Data derived from some clinical reports have suggested that piracetam can improve symptoms
and is effective agent for treatment of different movement disorders including acute
neuroleptic induced extrapyramidal symptoms and TD. The doses that used for TD treatment
varied from 800 mg/day to 24000 mg/day. According to these findings the symptoms of TD
disappeared in the period of 3-7 days.
To date there was only one double-blind crossover study regarding use of piracetam for
treatment TD that was conducted almost 20 years ago. The findings of this study were
impressive, but to our knowledge nobody reproduced these results.