Etiology, pathophysiology, and imaging of tardive dyskinesia

This chapter summarizes the current data concerning the etiology, pathophysiology, and results of imaging studies: computed tomography, magnetic resonance imaging, positron emission tomography and dopamine transporter scan. Tardive dyskinesia may be caused by medications from a variety of chemical groups and classes with sundry therapeutic purposes. The pathophysiology of tardive dyskinesia is complicated, only partly explained and remains unclear. Multiple models have been suggested to explain this unpleasant and sometimes disabling side effect. To date, several neurochemical hypotheses have been proposed for the explanation of TD development. These theories include: dopamine postsynaptic hypersensitivity; a disturbed balance between dopamine and cholinergic systems; noradrenergic dysfunction; dysfunctions of striatonigral, γ-aminobutric acid (GABA)ergic neurons; neurodegenerative hypothesis; synaptic plasticity, and genetic predisposition. The results of imaging studies concerning TD are not consistent and need further investigation.