Chronic Psychosis in Dual Disorder Heroin Use Disorder Patients

Abstract

In bipolar disorder, manic or depressive episodes and mixed states are frequently marked by psychotic symptoms. Moreover, psychosis may occur after substance use disorder, often intervening with the effect of making the clinical picture indistinguishable from that of a primary psychosis. Cannabinoids, stimulants, hallucinogens, alcohol and poly-use most commonly develop psychosis induced by the non-medical use of substances. Among substance use disorder users, it has not yet been ascertained whether opioids exert a psychotic effect. Still, some authors have supported the view that opioids have antidepressant, antipanic and antipsychotic effects. It has also been hypothesized that affective disorders, coupled with genetic disposition rather than affective disturbance or psychosis, result in bipolar psychosis or schizoaffective disorder, respectively. In the history of chronic psychotics, heroin use is relatively infrequent. Chronic use of psychotogenic substances and autonomous chronicity of psychotic symptoms may root in a bipolar substrate. Substance use among people with schizophrenia cannot always be justified in terms of dysphoria. Still, the number of depressive symptoms can significantly influence the risk rate for alcohol, cannabinoid use or poly-use. Dual disorder psychotic heroin-addicted patients usually enter treatment with more severe psychopathological aspects and a shorter, less severe addiction history than their non-psychotic peers suggesting that these patients are likely to benefit from opioid medication. These data indirectly confirm the antipsychotic effects of opioids and Khantzian’s self-medication hypothesis. For further confirmation, patients affected by chronic psychosis and anxiety disorders tend to progress from a psychiatric disorder to a substance use disorder. In contrast, patients with mood disorders are initially affected by drug addiction. As far as dual disorder is concerned, it is advisable to employ agents that do not heavily affect dopamine metabolism in an inhibitory way since the worsening of use hampers the effectiveness upon psychotic symptoms. On the other hand, when the tie with substances is more robust, their use may amplify as a direct consequence of dopamine antagonism, as a compensatory mechanism effective throughout the reward pathway. Novel antipsychotics seem to permit equivalent effectiveness on psychotic symptoms without promoting drug use, at least to the same extent, and might have anticraving properties.