The impulse control disorders can be conceptualized in addictive, affect-driven, and compulsive models (Figure 2). Targeted treatments of impulsivity in impulse control disorders can influence the motivational circuitry, or work via addictive, affect-driven, and compulsive systems. Treatments should also target comorbid bipolar spectrum, ADHD, and compulsive and addictive disorders for maximal anti-impulsive effects (Figure 3). There is some evidence that different symptom dimensions within the impulse control disorders are particularly responsive to different medication classes.11,12 It is therefore important to individualize treatment decisions based on the limited evidence base and the patient’s presenting problems, history, and comorbid conditions.
For example, a patient with borderline personality disorder with prominent cognitive/perceptual distortion may respond to neuroleptics, while a patient with depressed mood may respond best to antidepressants. Some symptom dimensions (eg, antisocial traits) may be less responsive to medication, and some classes of medication, including the benzodiazepines, do not appear particularly effective for the treatment of impulse control disorders and should generally be avoided.13
There may be several unique developmental trajectories to impulsivity and compulsivity (eg, ADHD, bipolar spectrum, trait impulsivity, obsessive-compulsive personality disorder) and various routes to altering motivational circuitry, such as modulators of cortico-striatal-limbic circuits. We suggest that core symptoms within disorders should be treated and appropriate outcome measures should be used to determine targeted treatment response. Interventions should be directed at the brain circuitry that modulates core symptoms, which may be shared across disorders rather than DSM diagnoses.14
Although the neurobiological basis of OCD (symptoms and related cognitive impairments) is unclear, lesion, functional neuroimaging, and neuropsychological studies have suggested that structural and functional dysfunction of limbic or affective cortico-striato-thalamocortical circuitry, which includes the orbitofrontal cortex, plays a key role.15-18 These circuits, first identified in nonhuman primates, have also been identified in human lesion and imaging studies of patients who have OCD.19-23
Intervention can occur at the symptom, syndrome, or behavioral level. Effective treatment of impulsivity and compulsivity depends on determining the cause(s) of these behaviors and selecting treatments accordingly. Pharmacological and nonpharmacological treatment, such as behavioral strategies aimed at reducing impulsive and compulsive behavior, may be most effective for the long-term treatment of the underlying chronic or recurrent illness.
There is no standardized treatment for complex disorders involving impulsivity, although a range of different medication classes have been investigated.13 Pharmacological treatments may reduce impulsivity and normalize arousal by decreasing dopamine(Drug information on dopamine)rgic activity, enhancing serotonergic activity, shifting the balance of amino acid neurotransmitter from excitatory (glutamatergic) toward inhibitory (GABAergic) transmission, lowering glutamatergic conduction, and/or reducing or stabilizing nonadrenergic effects. Medications used to treat disorders involving impulsivity, including impulse control disorders and cluster B personality disorders, which have been shown to be effective in some clinical trials, include SSRIs, lithium(Drug information on lithium), and anticonvulsants.14,24-31 Cognitive-behavioral therapy (CBT) and psychodynamically informed psychotherapy have a useful role in the management of a number of impulse control disorders. More specific details of the pharmacotherapeutic and psychotherapeutic approaches to each of the individual impulse control disorders can be found elsewhere.32
With regard to compulsive behavior, the most common treatment approaches for OCD are pharmacological and psychological. CBT was the first psychological treatment for which empirical support was obtained. A recent review compared psychological treatments with treatment as usual and found that psychological treatments derived from cognitive-behavioral models are effective for adults with OCD.33
On the basis of the hypothesized underlying neurobiology of OCD and observed treatment effects, SSRIs are considered first-line treatment for OCD. However, SSRIs are often associated with delayed onset of therapeutic effect (8 to 12 weeks), only partial symptom reduction, and response failure or intolerability in 40% to 60% of patients. Pharmacological options for SSRI-
refractory cases include increasing drug dosage, changing to another SSRI or clomipramine(Drug information on clomipramine), combining SSRIs, or changing the mode of drug delivery. Augmentation with second-generation
antipsychotics appears promising, as well as augmentation or monotherapy with some of the anticonvulsants.34-36
Some patients with OCD remain refractory to all standard pharmacological and psychological treatments. Several alternative medical interventions have been considered for these severe cases, including ablative neurosurgery and brain stimulation techniques such as electroconvulsive therapy, transcranial magnetic stimulation (TMS), and deep brain stimulation (DBS—the nonablative neurosurgical procedure). Studies that explore these techniques for OCD treatment are limited by small sample sizes and scarcity of double-blind trials, and none of these alternative interventions are FDA-approved for treatment of OCD. However, given the promising efficacy findings thus far, reversibility, noninvasiveness or minimal invasiveness, tolerability, and possibility of double-blind trials, additional research should be conducted with TMS and DBS to refine these techniques, better establish their efficacy, and offer more options to patients who have exhausted all other available treatments.37
Patients with comorbid disorders
Clinicians should also identify comorbid conditions and associated symptoms related to brain systems, because these can also influence treatment choice and response. For example, mood stabilizers, traditionally used to treat bipolar disorder, can be effective for other disorders, including impulse control disorders.
When treating patients at risk for bipolar disorder, SSRI-induced manic behaviors could emerge in pathological gamblers who have a history of, or are at risk for, mania or hypomania.24 Thus, mood stabilizers such as lithium or valproate(Drug information on valproate) may be better treatment options for patients with comorbid impulse control disorder and bipolar disorder. Personality disorders with aggressive behavior and emotionally unstable character disorder with a disturbance of mood swings respond to lithium. A variety of personality factors and comorbid conditions such as premenstrual syndrome, bulimia, agoraphobia, major affective disorder (eg, bipolar II), and hypersomnia, which are overrepresented in patients with borderline personality disorder, often complicate the clinical picture. Depending on a mix of these factors, certain drugs may need to be avoided, nonstandard drug combinations may be needed, or safer but less effective drugs may need to replace more effective drugs whose abuse by suicidal patients may have more dangerous consequences.38
OCD is heterogeneous in terms of types of obsessions and compulsions, heritability, and comorbid conditions, which probably reflect heterogeneity in the underlying pathology.18 Accordingly, there are many disorders known as obsessive-compulsive spectrum disorders that share features with OCD, including trichotillomania and body dysmorphic disorder.39,40
The apparent association between altered serotonergic function and OCD has guided attention toward the possible role of serotonergic function in the underlying cause of trichotillomania.41 Some investigators have postulated that patients with trichotillomania who engage primarily in hair pulling, where their attention is focused on the hair pulling, are more phenomenologically similar to individuals with compulsions in OCD than those with automatic hair pulling that occurs outside conscious awareness, and thus they may be more responsive to pharmacological interventions found to be effective for OCD.42-43 A number of investigations of the use of antidepressants with specific inhibition of serotonin reuptake (ie, fluoxetine(Drug information on fluoxetine) and clomipramine) have yielded mixed results.44-48 Naltrexone(Drug information on naltrexone), an opioid antagonist, has been found to be superior to placebo in reducing trichotillomania symptoms.49 Also, augmentation of SSRIs with atypical neuroleptics may be beneficial, and olanzapine(Drug information on olanzapine) may be effective as a mono-therapy for trichotillomania, as well as CBT.50-55
Body dysmorphic disorder is a relatively common and often disabling somatoform disorder that may be an obsessive-compulsive spectrum disorder because of its similarity to OCD.40 There is some evidence for familial aggregation and genetic links with OCD.56 Although body dysmorphic disorder is still difficult to treat, success has been demonstrated for serotonin reuptake inhibitors and CBT.57 A clear role for the serotonin system is evidenced by the specificity of therapeutic response to serotonergic antidepressants.58 Higher doses of SSRIs and longer treatment trials than those used for many other psychiatric disorders, including depression, may be needed to effectively treat body dysmorphic disorder. CBT, using techniques such as cognitive restructuring, behavioral experiments, response (ritual) prevention, and exposure, also appears beneficial and is currently considered the psychotherapy of choice for body dysmorphic disorder.59
In general, evidence suggests that mood stabilizers appear to be effective for treating the symptom domains of impulsivity and compulsivity across a wide range of psychiatric disorders and for impulse control and cluster B personality disorders in particular. We suggest that clinicians target and treat core symptoms of impulsivity and compulsivity based on the underlying neurobiology of these behaviors instead of the overall diagnosis, while taking into account comorbid disorders, associated symptoms, developmental trajectory, and family history.