The present study has demonstrated that Tourette patients therapeutically respond to remarkably low levels of haloperidol. These results lend support to the hypothesis of a supersensitive dopaminergic receptor site as the pathophysiologic defect in Tourette syndrome. Of interest is the unusual sensitivity of the Tourette patient's receptors to butyrophenone blockade. This unique property produces both a therapeutic response as well as an increased tendency toward dysphoric side effects. Recent studies have demonstrated three separate dopaminergic receptor sites: Type 1, a haloperidol-insensitive adenylate-cyclase-related postynaptic receptor; Type 2, a haloperidol-sensitive postsynaptic receptor and a presynaptic autoreceptor. The authors speculate that the response of Tourette patients to drug therapy is based upon changes at the Type 2 receptor, although the possibility still exists that haloperidol might be altering dopaminergic transmission through blockade of presynaptic autoreceptors.
|Original language||English (US)|
|Number of pages||6|
|State||Published - Jan 1 1981|
ASJC Scopus subject areas
- Biological Psychiatry