Clinical Evidence Concise
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Am Fam Physician. 2004 Dec 1;70(11):2183-2184.
This clinical content conforms to AAFP criteria for evidence-based continuing medical education (EB CME). EB CME is clinical content presented with practice recommendations supported by evidence that has been systematically reviewed by an AAFP-approved source. The evidence is available at http://www.clinicalevidence.com/ceweb/conditions/meh/1004/1004.jsp.
What are the effects of initial treatments in adults?
Behavioral Therapy. We found no randomized controlled trials (RCTs) comparing behavioral therapy with no treatment. One systematic review and subsequent RCTs have found that behavioral therapy improves symptoms compared with relaxation. The review and one subsequent RCT found no significant difference in symptoms over four to 16 weeks between behavioral therapy and cognitive therapy. One subsequent RCT found limited evidence that group behavioral therapy improved symptoms after 12 weeks compared with group cognitive-behavioral therapy.
Cognitive or Cognitive-Behavioral Therapy. We found no RCTs comparing cognitive therapy with no treatment. One RCT found that group cognitive-behavioral therapy improved symptoms and quality of life compared with no treatment after 12 weeks. One systematic review and one subsequent RCT found no significant difference in symptoms over four to 16 weeks between behavioral therapy and cognitive therapy. Another subsequent RCT found limited evidence that group behavioral therapy improved symptoms over 12 weeks compared with group cognitive-behavioral therapy.
Serotonin Reuptake Inhibitors (Citalopram, Clomipramine, Fluoxetine, Fluvoxamine, Paroxetine, Sertraline). RCTs have found that selective and nonselective serotonin reuptake inhibitors (citalopram, clomipramine, fluoxetine, fluvoxamine, paroxetine) improve symptoms compared with placebo. Two systematic reviews found inconsistent results about the effects of sertraline compared with placebo. RCTs have found that selective and nonselective serotonin reuptake inhibitors (citalopram, clomipramine, fluoxetine, fluvoxamine, paroxetine, sertraline) improve symptoms compared with tricyclic antidepressants or monoamine oxidase inhibitors. RCTs have found no consistent evidence of a difference in efficacy among serotonin reuptake inhibitors, but have found that the nonselective serotonin reuptake inhibitor clomipramine is associated with more adverse effects than selective serotonin reuptake inhibitors.
Behavioral or Cognitive Therapy Plus Serotonin Reuptake Inhibitors (Compared with Behavioral or Cognitive Therapy Alone). RCTs provided insufficient evidence to assess the effects of adding serotonin reuptake inhibitors to behavioral or cognitive therapy.
Electroconvulsive Therapy. We found no RCTs of electroconvulsive therapy in people with obsessive-compulsive disorder.
Venlafaxine. One RCT provided insufficient evidence to compare venlafaxine with clomipramine.
What are the best forms of maintenance treatment in adults?
Optimum Duration of Treatment with Serotonin Reuptake Inhibitors. RCTs provided insufficient evidence to define the optimum duration of treatment with serotonin reuptake inhibitors.
What are the effects of treatments in adults who have not responded to initial treatment with serotonin reuptake inhibitors?
LIKELY TO BE BENEFICIAL
Addition of Antipsychotics to Serotonin Reuptake Inhibitors. Three small RCTs in people unresponsive to serotonin reuptake inhibitors found that the addition of antipsychotics improved symptoms compared with placebo.
Obsessive-compulsive disorder involves obsessions, compulsions, or both, that are not caused by drugs or a physical disorder, and that cause significant personal distress or social dysfunction.1,2 The disorder may have a chronic or an episodic course. Obsessions are recurrent and persistent ideas, images, or impulses that cause pronounced anxiety and that the person perceives to be self-produced. Compulsions are repetitive behaviors or mental acts performed in response to obsessions or according to certain rules, which are aimed at reducing distress or preventing certain imagined dreaded events. People with obsessive-compulsive disorder may have insight into their condition, in that obsessions and compulsions usually are recognized and resisted. There are minor differences in the criteria for obsessive-compulsive disorder between the third, revised-third, and fourth editions of the Diagnostic and Statistical Manual (DSM-III, DSM-III-R, and DSM-IV)1 and The ICD-10 Classification of Mental and Behavioural Disorders.2
One national, community-based survey of obsessive-compulsive disorder in the United Kingdom (1993, 10,000 people) found that 1 percent of men and 1.5 percent of women reported symptoms in the past month.3 An epidemiologic catchment area survey carried out in the United States in 1984 (about 10,000 people) found age and sex standardized annual prevalence of obsessive-compulsive disorder in people 26 to 64 years of age of 1.3 percent, and lifetime prevalence of 2.3 percent.4 Subsequent cross-national surveys using methodology comparable with epidemiologic catchment areas found age and sex standardized annual and lifetime prevalence in people 26 to 64 years of age as follows: Canada (survey size about 2,200 people), annual prevalence 1.4 percent (standard error [SE] 0.25), and lifetime prevalence 2.3 percent (SE 0.32); Puerto Rico (survey size about 1,200 people), annual prevalence 1.8 percent (SE 0.39), and lifetime prevalence 2.5 percent (SE 0.46); Germany (survey size 4,811 people), annual prevalence 1.6 percent (SE 0.57), and lifetime prevalence 2.1 percent (SE 0.66); Taiwan (survey size about 7,400 people), annual prevalence 0.4 percent (SE 0.07), and lifetime prevalence 0.7 percent (SE 0.10); Korea (survey size about 4,000 people), annual prevalence 1.1 percent (SE 0.10), and lifetime prevalence 1.9 percent (SE 0.20); and New Zealand (survey size about 1,200 people), annual prevalence 1.1 percent (SE 0.31), and lifetime prevalence 2.2 percent (SE 0.42).4
The cause of obsessive-compulsive disorder is uncertain. Behavioral, cognitive, genetic, and neurobiologic factors have been implicated.5–11 Risk factors include a family history of obsessive-compulsive disorder, being single (which could be a consequence of the disorder), and belonging to a higher socioeconomic class.12 Other risk factors include cocaine abuse; female gender; not being in paid employment; and history of alcohol dependence, affective disorder, or phobic disorder.4
One study (144 people followed for a mean of 47 years) found that an episodic course of obsessive-compulsive disorder was more common during the initial years (about one to nine years), but a chronic course was more common afterwards.13 Over time, the study found that 39 to 48 percent of people had symptomatic improvement. A one-year prospective cohort study found 46 percent of people had an episodic course, and 54 percent had a chronic course.14
SEARCH DATE: September 2003
Adapted with permission from Soomro GM. Obsessive compulsive disorder. Clin Evid Concise 2004;11:1319–34.
1. American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th ed. Washington, DC: APA, 1994:669–73.
2. World Health Organization. The ICD-10 classification of mental and behavioural disorders. Geneva: World Health Organization, 1992.
3. Bebbington PE. Epidemiology of obsessive-compulsive disorder. Br J Psychiatry. 1998;35(suppl):2–6.
4. Horwath E, Weissman MM. The epidemiology and cross-national presentation of obsessive-compulsive disorder. Psychiatr Clin North Am. 2000;23:493–507.
5. Baer L, Minichiello WE. Behavior therapy for obsessive-compulsive disorder. In: Jenike MA, Baer L, Minichiello WE, eds. Obsessive-compulsive disorders. St Louis: Mosby, 1998:337–67.
6. Steketee GS, Frost RO, Rheaume J, et al. Cognitive theory and treatment of obsessive-compulsive disorder. In: Jenike MA, Baer L, Minichiello WE, eds. Obsessive-compulsive disorders. St. Louis: Mosby, 1998:368–99.
7. Alsobrook JP, Pauls DL. The genetics of obsessive-compulsive disorder. In: Jenike MA, Baer L, Minichiello WE, eds. Obsessive-compulsive disorders. St. Louis: Mosby, 1998:276–88.
8. Rauch SL, Whalen PJ, Dougherty D, et al. Neurobiologic models of obsessive compulsive disorder. In: Jenike MA, Baer L, Minichiello WE, eds. Obsessive-compulsive disorders. St. Louis: Mosby, 1998:222–53.
9. Delgado PL, Moreno FA. Different roles for serotonin in anti-obsessional drug action and the pathophysiology of obsessive-compulsive disorder. Br J Psychiatry. 1998;35(suppl):21–5.
10. Saxena S, Brody AL, Schwartz JM, et al. Neuroimaging and frontal-subcortical circuitry in obsessive-compulsive disorder. Br J Psychiatry. 1998;35(suppl):26–37.
11. Rauch SL, Baxter LR Jr. Neuroimaging in obsessive-compulsive disorder and related disorders. In: Jenike MA, Baer L, Minichiello WE, eds. Obsessive-compulsive disorders. St. Louis: Mosby, 1998:289–317.
12. Yaryura-Tobias JA, Neziroglu FA. Obsessive-compulsive disorder spectrum. Washington, DC: American Psychiatric Press, Inc., 1997.
13. Skoog G, Skoog I. A 40-year follow up of patients with obsessive-compulsive disorder. Arch Gen Psychiatry. 1999;56:121–7.
14. Ravizza L, Maina G, Bogetto F. Episodic and chronic obsessive-compulsive disorder. Depress Anxiety. 1997;6:154–8.
This is one in a series of chapters excerpted from Clinical Evidence Concise, published by the BMJ Publishing Group, Tavistock Square, London, United Kingdom. Clinical Evidence Concise is published in print twice a year and is updated monthly online. Each topic is revised every 12 months, and subscribers should view the most up-to-date version at http://www.clinicalevidence.com. If you are interested in contributing to Clinical Evidence, please contact Klara Brunnhuber (firstname.lastname@example.org). This series is part of the AFP’s CME. See “Clinical Quiz” on page 2067.
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