The physiology of cocaine craving and 'crashing'.

Abstract

<h3>To the Editor.—</h3> In their article on abstinence symptomatology in cocaine abusers, Gawin and Kleber¹describe the cocaine "crashing" syndrome and other more protracted clinical manifestations of cocaine abstinence. They propose the term<i>neuroadaptation</i>for cocaine withdrawal, "if a physiologic basis for phase 2 symptoms is substantiated." We have already described crashing and other symptoms of cocaine withdrawal, hypothesized a physiological mechanism, and developed a specific pharmacotherapy,²and we believe that our previously reported research and new data support the findings by Gawin and Kleber. Our hypothesis states that symptoms of cocaine withdrawal and cocaine craving result largely from dopamine depletion.^2,3Cocaine withdrawal symptoms, such as hypersomnia, anergia, hyperphagia, depression, and psychomotor retardation, are consistent with dopamine depletion since they are commonly seen after neuroleptic treatment and are found in Parkinson's disease. Our hypothesis is primarily supported by the finding of hyperprolactinemia in human cocaine abusers,⁴