Epidemiological studies have shown that the prevalence in the general population of personality disorders is approximately 10 %. The rates vary between 4 % and 20 %, depending on the samples included. In individuals with a personality disorder, the risk of comorbid substance use disorder (SUD) is increased fivefold for alcohol use disorders and twelvefold for drug use disorder (Trull et al. 2010).

The comorbidity of personality disorders in patients with SUD is between 34 % and 73 % (Verheul 2001). These are most commonly cluster B personality disorders, particularly BPD (Walter et al. 2009). In a sample with BPD patients, half of the patients also exhibited an alcohol and/or a drug use disorder (McGlashan et al. 2000).

In patients with alcohol dependence, different specific personality disorders were identified, including BPD and narcissistic, compulsive, and paranoid personality disorders. The co-occurrence of one or more personality disorders was found to be positive correlated with the severity of addiction (Preuss et al. 2009). In patients with alcohol dependence and cannabis use disorders, BPD, ASPD, and schizotypal personality disorder were diagnosed most often (Hasin et al. 2011).

In a recent study, 46 % of patients with SUD also had a personality disorder—16 % ASPD and 13 % BPD (Langås et al. 2012).

Table 10.2 shows the prevalence rates for personality disorders and ASPD, as reported for patients being treated for SUD.

Thus, comorbidity between personality disorder and SUD is common; this comorbidity is mainly related to ASPD and BPD and is often associated with severe addiction problems. In addition, there are also clear indications that—even though the types of personality disorder in alcohol and drug dependence are similar—the prevalence of any specific comorbid personality disorder may be slightly higher in drug-dependent than in alcohol-dependent patients.

There are various different hypotheses to explain the frequent comorbidity of personality disorders and SUD, including secondary substance abuse in patients with a primary diagnosis of a personality disorder, the existence of common biological vulnerability factors such as problems with impulsivity and impulse control, and the possibility that repeated trauma cause personality changes that may be associated with the diagnosis of personality disorder.

The best current empirical model for the aetiology of comorbidity postulates a primary personality disorder, followed by the secondary development of a SUD. Especially in BPD, ASPD, and in the narcissistic personality disorder, the self-medication hypothesis is extended to the self-regulation of emotions hypothesis and thus provides a partial explanation of substance use. Patients with cluster B personality disorders such as BPD or ASPD usually begin early with excessive substance use. It was shown that these patients start using intravenous drugs significantly earlier than patients without comorbid personality disorder (Cohen et al. 2007).

It has also been proposed that there are common biological vulnerability factors, and indeed neuroimaging studies have shown similar findings for patients with personality disorders and with SUD. Current findings are primarily non-specific and are also found in other psychiatric disorders. One striking similarity between patients with ASPD, alcohol, cocaine, and heroin dependence is the reduction in the volume of grey matter in the brain areas of the limbic system such as the striatum and amygdala as well as in the prefrontal cortex (Makris et al. 2008). These areas are known to be involved in the regulation and control of emotions and craving (the desire to use drugs). In both disorders—personality disorders and SUD— these results may be linked to clinical deficits and difficulties in impulse control. Impulsivity in cocaine-dependent patients is positively correlated with the reduction in volume (Moreno-López et al. 2012). Family studies have shown that not only drug-dependent patients, but also their healthy family members had impulsive personality traits and deficits in executive functioning (Ersche et al. 2012).

In general, increased impulsivity is associated with lower dopamine autoreceptor binding and with greater stimulant-induced dopamine release in the striatum (Buckholtz et al. 2010). This result may provide an explanation of why patients with cluster B personality disorders are also more vulnerable to the consumption of psychotropic substances. Higher impulsivity in these patients leads to greater dopamine release in the brain, with corresponding positive substance effects after intake such as relaxation and euphoria (Blum et al. 2013).

In general, patients with personality disorders and comorbid SUDs differ from those without comorbid SUDs. They have earlier addiction problems, are younger at entry into an addiction-specific treatment, often consume illegal substances, and have more social problems and lower psychosocial functioning (Langås et al. 2012).

Moreover, the clinical course is, as expected, empirically worse for patients with personality disorder and comorbid SUD. Even when their clinical course had improved, patients with SUD and comorbid ASPD exhibited more severe addiction and mental health problems than those without comorbid personality disorder (Galen et al. 2000). Moreover, it was found that comorbid antisocial, borderline, or schizotypical personality disorder were a significant predictor for persistent drug use over several years, whereas other comorbid mental disorders had no influence on the course of drug problems (Fenton et al. 2012).

A further finding shows how important the diagnosis of a personality disorder for the course of addiction-specific treatment is: Comorbid personality disorder did not remit after treatment of SUD (Verheul et al. 2000). Conversely, comorbid SUD is associated with poorer outcome in patients with borderline personality disorder (Zanarini et al. 2004).

Overall, it can be assumed that treatment of SUD alone has little reciprocal effect on the course of the comorbid personality disorder, so addiction treatment should increasingly concentrate on the treatment of the specific concurrent personality disorder.