Neuroleptic-mediated hypothalamic deregulation of central insulin and peripheral glucose metabolism in tardive dyskinesia: a hypothesis.

Abstract

In the following communication we discuss evidence that impaired peripheral and central glucose and insulin metabolism may be significant in the pathophysiology of neuroleptic-induced tardive dyskinesia. Such an association between alterations in glucose metabolism and pathophysiology of tardive dyskinesia may open new avenues in the prevention and pharmacological management of this often therapy-resistant chronic neurological disorder.