Haloperidol cognitive impairment

Tourette s syndrome is a well-studied condition, characterized by motor and phonic tics and by behavioral and psychological problems. While many neurotransmitters were implicated in the etiology of this disorder, it is now believed that the dopaminergic system and noradrenergic systems are involved. Two major clinical trials (Shapiro et ah, 1989 Sallee et al, 1997) indicated that haloperidol and pimozide reduced the severity of tics by 65%. However, these medications are associated with side effects (including possible cognitive impairment, sedation, dysphoria, and tardive dyskinesia) that may limit their effectiveness in children with MR. 

Harvey, P. D., Rabinowitz, J., Eerdekens, M., Davidson, M. 2005, Treatment of cognitive impairment in early psychosis a comparison of risperidone and haloperidol in a large long-term trial, Am.J.Psychiatry, vol. 162, no. 10, pp. 1888-1895. 

Allain H, Dautzenberg PH, Maurer K, Schuck S, Bonhomme D, Gerard D. Double blind study of tiapride versus haloperidol and placebo in agitation and aggressiveness in elderly patients with cognitive impairment. Psychopharmacology (Berl) 2000 148(4) 361-6. 

Williams SA, Wesnes K, Oliver SD, Rapeport WG. Absence of effect of sertraline on time-based sensitization of cognitive impairment with haloperidol. J Clin Psychiatry (1996) 57 (Suppl 1), 7-11. 

The interaction of the dopamine antagonist haloperidol 5 mg orally with subanesthetic doses of ketamine has been studied in a placebo-controlled study in 20 healthy volunteers over 4 days (53). Haloperidol pretreatment reduced impairment of executive cognitive functions produced by ketamine and reduced the anxiogenic effects of ketamine. However, it failed to block the ability of ketamine to produce psychosis, perceptual changes, negative symptoms, or euphoria, and it increased the sedative and prolactin responses to ketamine. These results imply that ketamine may impair executive cognitive functions via dopamine receptor activation in the frontal cortex, but that the psychoactive effects of ketamine are not mediated via dopamine receptors, but rather via NMDA receptor antagonism. 

---