After testing positive for cocaine on a recent court-mandated urine drug screen, Mr. M, age 49, is referred by his parole officer for psychiatric and substance abuse treatment. Mr. M has bipolar I disorder and alcohol, cocaine, and opioid dependence. He says he has been hospitalized or incarcerated at least once each year for the past 22 years. Mr. M has seen numerous psychiatrists as an outpatient, but rarely for more than 2 to 3 months and has not taken any psychotropics for more than 5 months.
Approximately 1 week before his recent urine drug screen, Mr. M became euphoric, stopped sleeping for several days, and spent $2,000 on cocaine and “escorts.” He reports that each day he smokes 30 cigarettes and drinks 1 pint of liquor and prefers to use cocaine and opiates by IV injection. Several years ago Mr. M was diagnosed with hepatitis C virus (HCV) but received no further workup or treatment. Although he denies manic or psychotic symptoms, Mr. M is observed speaking to unseen others in the waiting room and has difficulty remaining still during his interview. His chief concern is insomnia, stating, “Doc, I just need something to help me sleep.”
The high prevalence of substance use disorders (SUDs) in persons with bipolar disorder (BD) is well documented.1,2 Up to 60% of bipolar patients develop an SUD at some point in their lives.3-5 Alcohol use disorders are particularly common among BD patients, with a lifetime prevalence of roughly 50%.2-5 Recent epidemiologic data indicate that 38% of persons with bipolar I disorder and 19% of those with bipolar II disorder meet criteria for alcohol dependence.5 Comorbid SUDs in patients with BD are associated with:
- poor treatment compliance
- longer and more frequent mood episodes
- more mixed episodes
- more hospitalizations
- more frequent suicide attempts.1,2
The impact of co-occurring SUDs on suicidality is particularly high among those with bipolar I disorder.6
Frequently referred to as “dual diagnosis” conditions, co-occurring BD and SUDs may be more accurately envisioned as multi-morbid, rather than comorbid, illnesses. Data from the Stanley Foundation Bipolar Network suggest that 42% of BD patients have a lifetime history of ≥2 comorbid axis I disorders.7 Rates of generalized anxiety disorder, panic disorder, and posttraumatic stress disorder are particularly high in BD patients with co-occurring SUDs.8,9 In addition, the presence of 1 SUD may mark the presence of other SUDs; for example, alcohol dependence is strongly associated with polysubstance abuse, especially in females with BD.8 Furthermore, medical comorbidities that impact treatment decisions also are highly prevalent in BD patients with comorbid SUDs.10 In particular, HCV rates are higher in persons with BD compared with the general population,11 and are >5 times as likely in bipolar patients with co-occurring SUDs.12
Unfortunately, limited treatment research guides clinical management of comorbid BD and SUDs.2,13,14 Clinical trials of medications for BD traditionally have excluded patients with SUDs, and persons with serious mental illness usually are ineligible for SUD treatment studies.13 Furthermore, the few randomized controlled trials (RCTs) conducted in persons with both illnesses have been constrained by relatively small sample sizes and low retention rates. In the absence of a definitive consensus for optimal treatment, this article outlines general clinical considerations and an integrated approach to assessing and managing this complex patient population.
Birds of a feather
Multiple hypotheses try to account for the high rate of SUDs in patients with BD (Table 1), but none fully explain the complex interaction observed clinically.14,15 Substance dependence and BD are chronic remitting/relapsing disorders with heterogeneous presentations and highly variable natural histories. As with SUDs, BD may go undiagnosed and untreated for years, coming to clinical attention only after substantial disease progression.16
The fluctuating illness course in BD and SUDs makes diagnosis and treatment difficult. Symptomatic periods often are interrupted by spontaneous remissions and longer—although usually temporary—periods of perceived control. Both BD and SUDs may be associated with profound mood instability, increased impulsivity, altered responsiveness to reward, and impaired executive function.17 Finally, the high degree of heritability in BD18 and many SUDs19 may make treatment engagement more difficult if either disorder is present in multiple family members because of:
- potential for greater clinical severity
- reduced psychosocial resources
- altered familial behavioral norms that may impede the patient’s recognition of illness.
Denial of illness is a critical symptom that may fluctuate with disease course in both disorders. Persons with BD or SUDs may be least likely to recognize that they are ill during periods of highest symptom severity. Accordingly, treatment adherence in patients with either disorder may be limited at baseline and decline further when the 2 illnesses co-occur.20