Stimulant withdrawal

The current paper is a review of the literature on abstinence symptomatology after stimulant use. The studies performed indicate biological and physical changes during abstinence. One outpatient study suggests a phasic model of stimulant abstinence which is characterized by a 'crash', 'withdrawal', and 'extinction' phase. However, two inpatient studies do not confirm these findings. In contrast, these latter two studies did not find a crash phase and reported a gradual improvement of mood during these 21-day and 28-day inpatient stays. Biological measures suggest changes in receptor, endocrinological and neurochemical activity. One study found hyperprolactinemia throughout the 4-week period, while another study using PET and FDG ([18F]-Fluorodeoxyglucose) found increased brain glucose metabolism in the dopamine-rich areas of the basal ganglia and orbitofrontal cortex. Another study using PET and F18-Methylspiroperidol found decreased dopamine D2 receptor binding during cocaine withdrawal and also a separate study using PET and F-18-Dopa discovered low dopaminergic brain activity. To date, few studies have been performed, and the lack of clear-cut physical withdrawal symptoms as seen in alcohol, sedative, and opiate withdrawal makes it difficult to demonstrate definitively the presence of withdrawal during stimulant abstinence. Amphetamine withdrawal has been less studied, but empirical data suggest that the symptoms are similar to cocaine withdrawal. Further studies are needed to better delineate the presence of acute versus chronic post-use symptoms.