Post-traumatic stress and substance misuse; neurobiological and clinical pharmacological correlates

In post-traumatic stress disorder (PTSD) clients, the use of drugs and alcohol may be used as a self-prescribed treatment to both avoid trauma reminders and cope with the related distress. Conversely, substance misuse ‘per se’ might predispose to experience traumatic events. The present study aimed here at presenting an overview of most recent studies covering a range of issues relating to PTSD and substance misuse; namely: substances most frequently ingested by PTSD clients; neurobiological correlates; and treatment/management of these clients. Beyond the alcohol abuse/misuse, drugs most frequently misused are represented by opiates/opioids; sedatives; cannabis; and cocaine. PTSD-related khat misuse issues are here briefly discussed as well. From the neurobiological point of view, issues relating to amygdala and hippocampus dysfunction, with consequent altered levels of fear extinction/memory disruption, have been considered. Furthermore, PTSD may be characterized by imbalance of a range of neurotransmitter pathways, mainly cannabinoid-receptor (CB1); serotonin; and oxytocin. Although there is currently no effective pharmacotherapy for PTSD, most clients may be regularly prescribed with antidepressants; anxiolytics/sedative-hypnotics; and antipsychotics. Due to the heterogeneity of PTSD phenotype, focusing on the symptoms/signs of the PTSD client would allow for more personalized treatment. Although more research is needed, the development of chemoprophylactic treatments, e.g., intervening pharmacologically after trauma to prevent the occurrence of PTSD seems particularly promising.