Obsessive-Compulsive Disorder (OCD)
Conventional treatment for OCD includes both pharmacological and non-pharmacological therapy. These therapies, alone or in combination, can be successful in managing OCD symptoms. However, complete remission of symptoms is rare, and approximately 25% of patients with OCD will receive little if any benefit from conventional OCD therapies (Pittenger 2011).
Cognitive behavioral therapy (CBT), a specific type of psychotherapy, appears to be roughly as effective for OCD as medication. A rigorous analysis of many studies on behavioral and pharmacotherapy did not find evidence for superiority of pharmacotherapy over behavioral treatment. Importantly, this analysis also did not find that addition of medication to behavioral treatment was associated with an improvement in outcomes, compared with behavioral treatment alone (Romanelli 2014).
Some important limitations to CBT are difficulty accessing treatment (BPS 2006b), patient aversion to the indicated methods, and a high dropout rate. Additionally, the methods are not equally applicable to all symptom dimensions (subtypes). CBT for OCD encompasses two approaches: exposure with response prevention and cognitive therapy (Hebbar 2013; Bonchek 2009; McKay 2015; Ponniah 2013; Grant 2014; Romanelli 2014).
Exposure with response prevention. In this therapy, the patient is guided through exposure to fear- and anxiety-producing situations and stimuli, progressing from least to most distressing. At the same time, the patient refrains from the compulsive behaviors that temporarily relieve anxiety and distress. An important part of this treatment is for the patient to learn that the anxiety and fear pass on their own, and to develop tolerance for this distress (Grant 2014; McKay 2015). Sixty to eighty-five percent of patients improve with exposure-response prevention treatment, although for up to 30% of patients this treatment is not effective, or patients refuse or discontinue treatment due to the anxiety associated with the exposure (Grant 2014; Veale 2014; Yip 2014). Contamination and washing obsessions are the most responsive to this therapy, while hoarding obsession responds poorly (Veale 2014; Yip 2014).
Cognitive therapy. Cognitive therapy helps patients correct their obsessions and compulsions by identifying unrealistic thoughts and beliefs. Unlike exposure-response prevention, cognitive therapy is not aimed at reducing the anxiety associated with a specific situation (eg, handling a dirty object without washing), but rather at challenging the belief that not washing will lead to negative consequences (Grant 2014). Cognitive therapy may be used independently as a therapy for OCD, or as an adjunct to exposure-response prevention. As an adjunct, cognitive therapy may help increase the patient’s ability to tolerate distress, help address dysfunctional beliefs, and help the patient adhere to and remain in treatment (McKay 2015; Whittal 2005; Ponniah 2013).
Serotonin reuptake inhibitors. Selective serotonin reuptake inhibitors (SSRIs) and the tricyclic antidepressant clomipramine (Anafranil) (a non-selective serotonin reuptake inhibitor, or SRI) are both considered first-line pharmacotherapy for OCD. However, SSRIs have a more favorable side effect profile than clomipramine, so they are usually the preferred primary medications (Seibell 2013; Kellner 2010; Grant 2014).
The SSRI medications fluvoxamine (Luvox), paroxetine (Paxil), fluoxetine (Prozac), and sertraline (Zoloft) are approved by the Food and Drug Administration (FDA) for use in OCD patients (Sudak 2012), though they have comparable efficacy (Soomro 2012). Although drug treatment of OCD is not proven more effective than behavioral therapy, it is sometimes used as the sole treatment, including in patients who find the idea of behavioral therapy intimidating (Grant 2014).
Roughly 40–65% of OCD patients respond to treatment with clomipramine or an SSRI, with an average improvement in symptom severity of 20–40%. Relatively few patients experience complete remission with drug treatment alone. Also, OCD patients usually need to undergo drug treatment for longer duration and at a higher dose to achieve benefit, compared with patients using these drugs to treat depression. Symptoms of OCD tend to relapse when medication is discontinued, particularly in those on medication for less than two years (Grant 2014). Most studies of pharmacotherapy for OCD have only lasted 8‒12 weeks, though some studies lasting longer than 12 months demonstrated efficacy. Uncertainty remains, however, about adverse effects and the long-term efficacy of SSRIs for OCD, as well as the ideal duration of treatment (NLM 2014; Soomro 2008).
The side effect profile of SSRIs, while better than the tricyclic antidepressant clomipramine, is significant. Almost a quarter of patients taking SSRIs report adverse effects on sexual function, and other commonly reported side effects include sleep problems, tiredness and fatigue, restlessness, dry mouth, nausea, constipation, dizziness, and weight gain (Bet 2013).
Augmentation therapy. Augmentation is the use of additional medications in patients who do not respond to initial therapy with an SRI. This might include the addition of the tricyclic antidepressant clomipramine to treatment with fluoxetine; or the use of second-generation antipsychotic agents such as risperidone (Risperdal) or haloperidol (Haldol), stimulants, and glutamate receptor modulators such as memantine (Namenda) (Pittenger 2011; Walsh 2011; Seibell 2013). Though there are conflicting data on the efficacy of augmentation therapy, and there are no FDA-approved drugs for this purpose, this medication strategy is often part of clinical practice for OCD (Pittenger 2005; Grant 2014; Soomro 2012; Seibell 2013).
Deep-brain stimulation involves the surgical implantation of electrodes within specific areas of the brain, and electrical stimulation to produce changes in these regions (Hammond 2008; Lapidus 2014; Malaty 2014; Denys 2009). Deep-brain stimulation is FDA approved to treat chronic and severe cases of OCD (Grant 2014), with reports of successful treatment from case reports and small trials (de Koning 2011; Kisely 2014). Deep-brain stimulation is an invasive procedure in which probes are inserted directly into brain tissue, and carries a risk of adverse effects including infection, intracerebral hemorrhage, acute mood changes, and seizures (de Koning 2011).