Nonetheless, the only statistically significant cognitive finding was a correlation of hippocampal volume and performance on one of the four tasks. This finding is the basis for the claim that methamphetamine users had memory impairments, because the hippocampus is known to play a role in some long-term memory; but other brain areas are also involved in processing long-term memory. The size of these other areas was not different between the groups.
Deterioration of intelligence in methamphetamine-induced psychosis: Comparison with alcohol dependence on WAIS-IIIpcn_2
Long-term use of methamphetamine could also lead to the emergence of psychotic symptoms, such as paranoid ideation, persecutory delusion, auditory and visual hallucination and thereby to a diagnosis of methamphetamine-induced psychosis(MIP), which sometimes is difficult to differentiate from paranoid schizophrenia. Clinically, MIP is not an uncommon disorder in epidemic areas, and management is mainly focused on the amelioration of psychosis using antipsychotics, yet the complication of cognitive deterioration of the addicts is seldom noted.
In a well-designed study of the neuropsychological function of 78 amphetamine users, McKetin and Mattick reported that the severity of amphetamine dependence was found to be associated with poorer performance on both memory and attention/concentration indices of the Wechsler Memory Scale–Revised.
Chronic intake of ethanol both in human and rat results in a substantial impairment in memory function associated with a reduction in the number of cholinergic neurons in the basal forebrain that give rise to the cholinergic afferentation of the cortical
mantle. Neuropsychological studies have demonstrated poor functioning on tests of visuospatial, executive, and memory functioning in alcohol dependent (AD) adults compared with demographically matched controls.
Some of the neurobiological effects of chronic methamphetamine abuse appear to be at least partially reversible. In the aforementioned study, abstinence from methamphetamine resulted in less excess microglial activation over time, and abusers who had remained methamphetamine- free for 2 years exhibited microglial activation levels similar to the study’s control subjects. Another neuroimaging study showed neuronal recovery in some brain regions following prolonged abstinence (14 but not 6 months). This recovery was associated with improved performance on motor and verbal memory tests. But function in other brain regions did not recover even after 14 months of abstinence, indicating that some methamphetamineinduced changes are very long lasting. Moreover, methamphetamine use can increase one’s risk of stroke, which can cause irreversible damage to the brain. A recent study even showed higher incidence of Parkinson’s disease among past users of methamphetamine.
METH dependent individuals who were abstinent for longer periods of time exhibited better decision-making than those who were abstinent for shorter periods of time. And self-reported emotional symptoms improved with abstinence. METH abusers’ ratings of craving decreased with the duration of abstinence, while cue-induced craving increased until 3 months of abstinence and decreased at 6 months and 1 year of abstinence.
.Importantly, although methamphetamine abusers performed significantly worse than controls on some cognitive tasks, their performance remained within the age- and education-matched normal range. Furthermore, previous discussions of the impact of methamphetamine-related effects on human cognition have neglected data from research assessing the immediate effects of the drug on cognitive performance. These studies can provide crucial complementary information because they assess cognitive performance immediately before and after administration of the drug. The rationale for this approach is that if methamphetamine produces cognitive deficits, one might predict that methamphetamine-induced disruptions would be observed following acute administration of large doses.