STRIATAL D2 RECEPTOR-BINDING IN SLEEP BRUXISM - A CONTROLLED-STUDY WITH IODINE-123-IODOBENZAMIDE AND SINGLE-PHOTON-EMISSION COMPUTED-TOMOGRAPHY

The neurochemical mechanisms underlying sleep bruxism are little under stood at present. However, recent pharmacologic evidence suggests that the central dopaminergic system may be involved in the pathophysiolog y of sleep bruxism. This possibility was further assessed by means of functional neuroimaging of dopamine D2 receptors with single-photon-em ission computed tomography (SPECT). Ten controls and ten patients with polysomnographically confirmed sleep bruxism were injected intravenou sly with 185 MBq (5 mCi) iodine-123-iodobenzamide, a specific D2 recep tor antagonist radioligand, and data acquisition was performed 90 min post-injection. Following image reconstruction, it was found that stri atal D2 receptor binding potential (basal ganglia/background ratio) di d not differ significantly between bruxism patients and controls. Howe ver, side-to-side differences between unilateral values of the striata l D2 binding potential (''highest side'' values minus ''lowest side'' values) were significantly larger for the bruxism patients (p < 0.001, by two-independent-samples t test with pooled variances). It was conc luded that an abnormal side imbalance in striatal D2 receptor expressi on can be associated with sleep bruxism. This reinforces the possibili ty that the central dopaminergic system plays a role in the pathophysi ology of this disorder.