What is the role of dopaminergic function in the pathophysiology of Tourette syndrome (TS) and other tic disorders?

Updated: May 30, 2019
  • Author: William C Robertson, Jr, MD; Chief Editor: Stephen L Nelson, Jr, MD, PhD, FAACPDM, FAAN, FAAP  more...
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Substantial evidence indicates that neuroleptic and atypical antipsychotic agents reduce tic severity. Presynaptic dopamine-depleting agents also improve tics, and in some patients, tics may be worsened by neuroleptic withdrawal or, possibly, stimulant use. However, other data do not support a simple hypothesis that dopamine function is hyperactive in individuals with TS.

Tics are not abated with the subsequent development of Parkinson disease. [21] However, in Parkinson disease, dopamine loss is most evident in posterior putamen, [22] whereas caudate and ventral striatum are more implicated in TS.

Furthermore, dopamine receptor agonists have also been used to successfully treat tics, and patients whose tics improved with an agonist had evidence of prolactin inhibition, consistent with a postsynaptic effect. [23, 24, 25] With adequate carbidopa pretreatment, a single dose of levodopa was followed by diminished, not worsened, tic severity. [23]

In summary, clinical evidence suggests that dopaminergic function is abnormal in TS. However, the site of dopamine involvement within the pathway remains unknown.

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