What is the role of D2-like dopamine-receptors in the pathophysiology of Tourette syndrome (TS)?

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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Several groups have studied D2-like dopamine receptor binding in TS by using PET or SPECT. Four studies showed no meaningful differences between TS and control groups with the use of carbon-11 raclopride, [iodine-123]iodo-6-methoxybenzamide (IBZM), [123 I]iodo-2[beta]-carbomethoxy-3[beta]-(4-iodophenyl)tropane (beta-CIT), or11 C 3-N -methylspiperone. [28, 29, 30, 31] (However, a preliminary report from 1 of these studies did describe positive findings.)

Another study compared more severely affected monozygotic twins with TS to their less affected co-twins by using IBZM SPECT and found a correlation of severity with binding in the caudate but not the putamen. [32] This finding suggests that the caudate may play an important role in the pathogenesis of tics. [33]

Studies using a newer D2 ligand ([18 F] N -methylbenperidol) have concluded that D2-like receptor binding is probably normal in TS. However, a number of reports show that presynaptic markers of dopamine innervation may be abnormal in TS. Studies have shown consistently higher concentrations of presynaptic markers or activity in the ventral striatum. [34, 35, 28, 36, 37, 38, 39, 40, 41, 42]

These markers have been shown to appear to begin in childhood before treatment has been started. [43] Therefore, in TS, abnormal dopamine production (or abnormal regulation of dopamine production) may lead to abnormal movement and perhaps other altered behavior.

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