Abstract
Introduction: More than half of psychiatric patients have comorbid substance use disorder (dual diagnosis) and this rate, confirmed by many epidemiological studies, is substantially higher compared to general population. Combined operation of self-medication mechanisms, common etiological factors, and mutually causative influences most likely accounts for comorbidity, which, despite its clinical prevalence, remains underrepresented in psychiatric research, especially in terms of neuroimaging. The current paper attempts to review and discuss all existing methodologically sustainable structural and functional neuroimaging studies in comorbid subjects published in the last 20 years. Methods: Performing a systematic PubMed/MEDLINE, Web of Science, and Cochrane databases search with predefined key-words and selection criteria, 43 structural and functional neuroimaging studies were analyzed. Results: Although markedly inconsistent and confounded by a variety of sources, available data suggest that structural brain changes are slightly more pronounced, yet not qualitatively different in comorbid patients compared to non-comorbid ones. In schizophrenia (SZ) patients, somewhat greater gray matter reduction is seen in cingulate cortex, dorsolateral prefrontal and frontotemporal cortex, limbic structures (hippocampus), and basal ganglia (striatum). The magnitude of structural changes is positively correlated to duration and severity of substance use, but it is important to note that at least in the beginning of the disease, dual diagnosis subjects tend to show less brain abnormalities and better cognitive functioning than pure SZ ones suggesting lower preexisting neuropathological burden. When analysing neuroimaging findings in SZ and bipolar disorder subjects, dorsolateral prefrontal, cingular, and insular cortex emerge as common affected areas in both groups which might indicate a shared endophenotypic (i.e., transdiagnostic) disruption of brain networks involved in executive functioning, emotional processing, and social cognition, rendering affected individuals susceptible to both mental disorder and substance misuse. In patients with anxiety disorders and substance misuse, a common neuroimaging finding is reduced volume of limbic structures (n. accumbens, hippocampus and amygdala). Whether this is a neuropathological marker of common predisposition to specific behavioral symptoms and drug addiction or a result from neuroadaptation changes secondary to substance misuse is unknown. Future neuroimaging studies with larger samples, longitudinal design, and genetic subtyping are warranted to enhance current knowledge on comorbidity.
Highlights
More than half of psychiatric patients have comorbid substance use disorder and this rate, confirmed by many epidemiological studies, is substantially higher compared to general population
PubMed/MEDLINE, Web of Science, and Cochrane databases were searched with the following keywords and word combinations: “Co-occurring disorders,” “Comorbidity,” “Dual diagnosis,” “Magnetic resonance imaging” (MRI) and “functional Magnetic resonance imaging,” “Schizophrenia and substance use disorder (SUD),” “Bipolar disorder and SUD,” “Depression and SUD,” “Anxiety disorder(s) and SUD”
Based on the duration of illness and the age of the included population, structural neuroimaging studies for schizophrenia are subdivided into two separate tables: Table 1 for studies including adolescent and young adult subjects with first episode or recent onset of the disease and Table 2 for subjects with chronic schizophrenia lasting more than 5 years
Summary
More than half of psychiatric patients have comorbid substance use disorder (dual diagnosis) and this rate, confirmed by many epidemiological studies, is substantially higher compared to general population. Most epidemiological studies indicate that in terms of occurrence, the mental disorder has a temporal priority [4, 5, 13, 17, 18], lending credibility to the so-called “self-medication” hypothesis [19, 20], considering SUD as a secondary result of repeating substance use in an attempt to alleviate mental disorder symptoms It is much more likely, that a combination of mechanisms acts for each pattern of comorbidity in each particular patient—for example, self-medication and bidirectional mechanisms are implicated in anxiety disorders–SUD association [21, 22], while in patients with schizophrenia and SUD, common neurobiological, neurodevelopmental, and genetic causal factors are intertwined with self-medication mechanisms [20, 23, 24]
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call