Updated: May 31, 2009
Obsessive-compulsive disorder (OCD) is a relatively common, if not always recognized, disorder that is often associated with significant distress and impairment in functioning. Due to stigma and lack of recognition, individuals with OCD often must wait many years before they receive a correct diagnosis and indicated treatment. In severe presentations, this disorder is quite disabling and is appropriately characterized as an example of severe and persistent mental illness.
OCD is classified in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) as an anxiety disorder.1 It is characterized by distressing intrusive obsessive thoughts and/or repetitive compulsive actions (which may be physical or mental acts) that are clinically significant. The specific DSM-IV-TR criteria for OCD are as follows:
Obsessions and their related compulsions (the latter also referred to as rituals) often fall into 1 or more of several common categories.
Table. Categorizing Obsessions and Compulsions
Obsessions | Commonly Associated Compulsions |
| Fear of contamination | Washing, cleaning |
| Need for symmetry, precise arranging | Ordering, arranging, balancing, straightening until "just right" |
| Unwanted sexual or aggressive thoughts or images | Checking, praying, “undoing” actions, asking for reassurance |
| Doubts (eg, gas jets off, doors locked) | Repeated checking behaviors |
| Concerns about throwing away something valuable | Hoarding |
Although OCD is categorized as an anxiety disorder in DSM-IV-TR, Dr. Eric Hollander has proposed that it should instead be considered an impulse control disorder along with other disorders such as trichotillomania, kleptomania, and pathological gambling, which would comprise an O-C spectrum of disorders2,3 , although this remains a controversial proposal4 .
Case vignette
Ms. A is a 32-year old married mother of 2, living with her family in a suburban community. She comes to a psychiatrist’s office seeking help, with the strong encouragement of her husband, stating that she “just can’t cope anymore.”
In recent years, she has been spending increasing amounts of time, now at least 4 hours per day, in cleaning rituals. She will not allow anyone in the house to wear shoes, has declared the upstairs bathroom off limits, and will not let anyone else in the kitchen. She washes her hands with hot water and soap for at least 5 minutes after any occasion when she feels they have been contaminated and always wears gloves when outside. The skin on her hands is reddened and irritated. She spends up to an hour a day keeping items in the house in perfect placement (symmetrical and balanced), and she can become extremely angry if someone disturbs their placement. She spends approximately an hour every day arranging and rearranging her clothes in her closets, ordering each item on hangers in placement by size and color and correcting anything that is not hanging exactly symmetrically.
Over the last year she has also become phobic when seeing or hearing words pertaining to death, fearing that this could somehow lead to an untimely death for one of her children. If she reads such words or hears them on the radio or television, she will repeat the Lord’s Prayer in her own mind 100 times; if she loses count she will start again. This has led to her general avoidance of reading and listening to radio or television, except at times when she feels the content will be “safe.”
Initially rather clean, neat, fastidious, and cautious, these potentially adaptive tendencies have grown very trying for her husband and 2 young children, and an inordinate amount of time and attention is taken up related to her perceived needs for rules for cleaning and household items to be arranged “just so.” She recognizes the craziness of her fears of the word "death," but feels she cannot control her responses. She has become frustrated and unhappy coping with her fears and her burdensome responses, and although very reluctant to give up any of her protective rituals, she has agreed to seek professional advice, with the urging of an aunt who has confided her own successful struggles with similar problems.
The exact pathophysiologic process that underlies OCD has not been established. Research and treatment trials suggest that abnormalities in serotonin (5-HT) neurotransmission in the brain are meaningfully involved in this disorder. This is strongly supported by the efficacy of serotonin reuptake inhibitors (SRIs) in the treatment of OCD.5,6
Evidence also suggests abnormalities in dopaminergic transmission in at least some cases of OCD. In some cohorts, Tourette disorder (also known as Tourette syndrome) and multiple chronic tics genetically co-vary with OCD in an autosomal dominant pattern. OCD symptoms in this group of patients show a preferential response to a combination of serotonin specific reuptake inhibitors (SSRIs) and antipsychotics.7
Functional imaging studies in OCD have demonstrated some reproducible patterns of abnormality. Specifically, MRI and positron emission tomography (PET) scanning have shown increases in blood flow and metabolic activity in the orbitofrontal cortex, limbic structures, caudate, and thalamus, with a trend toward right-sided predominance. In some studies, these areas of overactivity have been shown to normalize following successful treatment with either SSRIs or cognitive-behavioral therapy (CBT).8 These findings suggest the hypothesis that the symptoms of OCD are driven by impaired intracortical inhibition of specific orbitofrontal-subcortical circuitry that mediates strong emotions and the autonomic responses to those emotions. Cingulotomy, a neurosurgical intervention sometimes used for severe and treatment-resistant OCD, interrupts this circuit (see Treatment).
Similar abnormalities of inhibition are observed in Tourette disorder, with a postulated abnormal modulation of basal ganglia activation.
More recently, attention has focused on glutamatergic abnormalities and possible glutamatergic treatments for OCD.9 Although modulated by serotonin and other neurotransmitters, the synapses in the cortico-striato-thalamo-cortical circuits thought to be centrally involved in the pathology of OCD principally employ the neurotransmitters glutamate and gamma-aminobutyric acid (GABA). Preclinical studies and several case reports and small clinical trials have provided some preliminary support for the therapeutic use of specific glutamatergic agents.10,11 However, these agents (eg, memantine, N-acetylcysteine, riluzole, topiramate, glycine) have varied glutamatergic and other pharmacological effects, so if they are demonstrated to be effective, clarifying any therapeutic mechanism of action will be important.
The fact that obsessive-compulsive symptoms seem to often take very stereotypic forms has led some to hypothesize that the pathological disturbance causing OCD may be disinhibiting and exaggerating some built-in behavioral potential that we have, which under other circumstances might have an adaptive function (eg, primate grooming rituals).
Once believed to be rare, OCD was found to have a lifetime prevalence of 2.5% in the Epidemiological Catchment Area study.12 Current estimates of lifetime prevalence are generally in the range of 1.7-4%. Discovery of effective treatments and education of patients and health care providers have significantly increased the identification of individuals with OCD over the past decade.
International studies have shown a similar incidence and prevalence of OCD worldwide.
OCD appears to have a similar prevalence in different races and ethnicities, although specific pathological preoccupations may vary with culture and religion (eg, concerns about blaspheming are more common in religious Catholics and Orthodox Jews).
The overall prevalence of OCD is equal in males and females, although the disorder more commonly presents in males in childhood or adolescence, and in females in their twenties. Childhood-onset OCD is more common in males and more likely to be comorbid with attention deficit hyperactivity disorder (ADHD) and Tourette disorder.
It is not uncommon for women to experience the onset of OCD during a pregnancy, although those who already have OCD will not necessarily experience worsening of their symptoms during pregnancy. However, women commonly experience worsening of their OCD symptoms during the premenstrual time of their periods. Women who are pregnant or breastfeeding should collaborate with their physicians in making decisions about starting or continuing OCD medications.
Symptoms usually begin in individuals aged 10-24 years. Childhood-onset OCD may have a higher rate of comorbidity with Tourette Disorder and ADHD.
OCD is diagnosed primarily by presentation and history. Once the diagnosis is suspected, the Yale-Brown Obsessive Compulsive Scale (Y-BOCS)13 is an important tool in defining the range and severity of symptoms and monitoring the response to treatment. The Y-BOCS is comprised of 10 items, 5 for obsessions and 5 for compulsions, each scored 0-4 (total score 0-40). For both obsessions and compulsions, these items rate the time spent, interference with functioning, distress, resistance, and control. Elements that should be covered when obtaining the history, including suggestions for typical interview questions, include the following:14
Information appropriate for a full evaluation is as follows:
The cause of OCD is not known; however, the following factors are relevant:
| Acute Respiratory Distress Syndrome | Huntington Disease Dementia |
| Anorexia Nervosa | Mental Retardation |
| Anxiety Disorders | Panic Disorder |
| Attention Deficit Hyperactivity Disorder | Phobic Disorders |
| Body Dysmorphic Disorder | Posttraumatic Stress Disorder |
| Bulimia | Rheumatic Fever |
| Cocaine-Related Psychiatric Disorders | Schizophrenia |
| Dementia Due to Head Trauma | Social Phobia |
| Depression | Somatoform Disorders |
| Hallucinogens | Tourette Syndrome |
Bipolar disorder (Manic-depressive illness)
Functional MRI and PET scanning have shown increases in blood flow and metabolic activity in the orbitofrontal cortex, limbic structures, caudate, and thalamus, with a trend toward right-sided predominance. In some studies, these areas of overactivity have been shown to normalize following successful treatment with either SSRIs or CBT.8 These imaging modalities, however, are of value for research, and not indicated for normal workups.
The mainstays of treatment of obsessive-compulsive disorder (OCD) include pharmacotherapy, particular forms of behavior therapy (exposure and response prevention and some forms of CBT), education and family interventions, and neurosurgical treatment in extremely refractory cases. A practice guideline for the treatment of OCD has recently been published by the American Psychiatric Association.22
Some clinicians feel that individuals with comorbid Tourette disorder or with hoarding as their principal OCD symptom may be more likely to be treatment resistant, although there is significant variation in treatment response, regardless of the particular presenting symptomatology.
Only antidepressants that potently inhibit presynaptic reuptake of serotonin appear to be effective in treating OCD. Clomipramine (Anafranil) is the only TCA with this quality. The SSRIs are also effective. SSRIs have the advantages of ease of dosing and low toxicity in overdose. Available SSRIs include fluoxetine (Prozac), fluvoxamine (Luvox), paroxetine (Paxil), citalopram (Celexa), escitalopram (Lexapro), and sertraline (Zoloft).
The dual serotonin-norepinephrine reuptake inhibitor antidepressants (SNRIs) venlafaxine (Effexor) and duloxetine (Cymbalta) may also have efficacy in OCD, and they have safety and tolerability profiles comparable to those of the SSRIs, but neither has yet been FDA-approved specifically for treatment of OCD.
SSRIs are generally preferred over clomipramine in treating OCD. The adverse effect profiles of SSRIs are less prominent, so improved compliance is promoted. SSRIs do not have the cardiac arrhythmia risk associated with TCAs. Arrhythmia risk is especially pertinent in overdose, and suicide risk must always be considered when treating a child or adolescent with mood disorder.
Physicians are advised to be aware of the following information and use appropriate caution when considering treatment with SSRIs in the pediatric population.
In December 2003, the UK Medicines and Healthcare Products Regulatory Agency (MHRA) issued an advisory that most SSRIs are not suitable for use by persons younger than 18 years for treatment of "depressive illness." After review, this agency decided that the risks to pediatric patients outweighed the benefits of treatment with SSRIs, except fluoxetine (Prozac), which appeared to have a positive risk-benefit ratio in the treatment of depressive illness in patients younger than 18 years.
In October 2003, the FDA issued a public health advisory regarding reports of suicidality in pediatric patients being treated with antidepressant medications for major depressive disorder. This advisory reported suicidality (both ideation and attempts) in clinical trials of various antidepressant drugs in pediatric patients. The FDA asked that additional studies be performed because suicidality occurred in both treated and untreated patients with major depression and thus could not be definitively linked to drug treatment.
Upon further analysis of pooled clinical trial data suicidality was reportedly increased in children and adolescents being treated with SSRIs for depression (approximately 2% for those treated with placebo vs 4% for those on SSRIs, although no actual suicides occurred in either group). These clinical trials were unfortunately not designed to specifically and clearly assess suicidal thoughts and behaviors, and therefore included events not readily classified. The FDA issued a public health advisory in October of 200428 , mandating a black box warning for antidepressants. Antidepressant treatment of children and adolescents with depression then significantly decreased over the next 2 years, although apparently so did suicides for this population. In 2007, the FDA extended its warning to young adults.29
Currently, evidence does not exist to associate an increased risk of suicide in patients with OCD and/or other anxiety disorders being treated with SSRIs. However, physicians should closely attend to whether treated patients have unusual uncomfortable adverse reactions (eg, akathisia), or if they might have comorbid bipolar disorder (which may involve only subtle hypomanic episodes), as occasionally antidepressant use seems to be associated with triggering dysphoria and sometimes manic episodes in such individuals. Children, adolescents, and young adults being treated with antidepressants should be closely and frequently monitored, particularly early in treatment, for any suicidal ideation or actions.
SSRIs are used commonly. The tricyclic antidepressant clomipramine is also used, although often attended by more uncomfortable adverse effects.
Enhances serotonin activity due to selective reuptake inhibition at neuronal membrane. Highly protein-bound and metabolized by CYP450 2D6.
20-80 mg/d PO; not to exceed 80 mg/d PO; divide into 2 or more doses when >40 mg/d
<12 years: 1 mg/kg/d PO; not to exceed 40 mg/d
>12 years: 1 mg/kg/d PO; not to exceed 60-80 mg/d
May potentiate medications such as TCAs, SSRIs, phenothiazines, carbamazepine, flecainide, class 1C antiarrhythmics, and quinidine; serotonergic agents (eg, MAOI, tryptophan, sibutramine, other appetite suppressants) may induce serotonin syndrome
Documented hypersensitivity; concurrent MAOI therapy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in hepatic impairment and history of seizures; MAOIs should be discontinued at least 14 d before initiating fluoxetine therapy; common adverse effects include restlessness, sexual dysfunction, GI upset, sleep disturbance, and headache
Enhances serotonin activity due to selective reuptake inhibition at the neuronal membrane.
20-80 mg/d PO
Not established
Phenobarbital and phenytoin decrease effects of paroxetine; alcohol, cimetidine, sertraline, phenothiazines, and warfarin increase toxicity of paroxetine
Documented hypersensitivity; concurrent MAOI therapy; seizure disorder
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Cirrhosis; suicide attempt; SIADH; DM; breastfeeding; taper over 1-2 wk to avoid SSRI withdrawal syndrome; common adverse effects include fatigue, sexual dysfunction, and weight gain; caution in history of seizures, mania, renal disease, and cardiac disease
Enhances serotonin activity due to selective reuptake inhibition at the neuronal membrane.
50-200 mg/d PO
<6 years: Not established
6-12 years: 25 mg/d PO; if tolerated, may increase by 50 mg/wk; not to exceed 200 mg/d PO
>12 years: Administer as in adults
Increases toxicity of MAOIs, diazepam, tolbutamide, and warfarin
Documented hypersensitivity; concurrent MAOI therapy; seizure disorder
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Cirrhosis; suicide attempt; SIADH; DM; breastfeeding; common adverse effects include fatigue, sexual dysfunction, GI upset, and sleep disturbance; caution in preexisting seizure disorders; caution in those who have experienced a recent myocardial infarction and those who have unstable heart disease, hepatic impairment, or renal impairment
Enhances serotonin activity due to selective reuptake inhibition at the neuronal membrane. Also has the advantage of fewer potential drug interactions. Citalopram is a 50:50 racemate of r- and s-citalopram.
20-60 mg/d PO
Not established
May be potentiated by azole antifungals, omeprazole, and macrolides; serotonin syndrome may be induced by buspirone, tramadol, MAOIs, and nefazodone
Documented hypersensitivity; concurrent MAOI therapy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Cirrhosis; suicidal tendencies; SIADH; DM; breastfeeding; common adverse effects include fatigue and sexual dysfunction
Enhances serotonin activity because of selective reuptake inhibition at the neuronal membrane.
100-300 mg/d PO divided bid/tid
<8 years: Not established
>8 years: 25 mg PO qhs; if tolerated, increase by 25 mg PO q4-7d; not to exceed 200 mg/d PO; if total daily dose >50 mg, administer in divided doses
Potentiates triazolam, alprazolam, theophylline, warfarin, carbamazepine, methadone, beta-blockers, and diltiazem effects; smoking may increase serum levels
Documented hypersensitivity; concurrent MAOI therapy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Cirrhosis; suicide attempt; SIADH; DM; breastfeeding; history of seizures; common adverse effects include fatigue, drowsiness, sexual dysfunction, sleep disturbance, and GI distress
Tricyclic antidepressant with potent NE and 5-HT reuptake inhibition.
75-250 mg PO qhs or in divided doses
<10 years: Not established
>10 years: 25 mg/d PO, advancing over 2 wk to 3 mg/kg/d or 100 mg/d PO in divided doses, whichever is smaller; if tolerated, advance to maximum dose of 3 mg/kg/d or 200 mg/d PO, whichever is smaller; after titration to a therapeutic dose, may administer hs
Potentiates CNS depressants, anticholinergics, sympathomimetics, and other protein-bound drugs; potentiated by CYP2D6 inhibitors; SSRIs
Documented hypersensitivity; concurrent use of MAOI or other TCA
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Suicidal tendencies or risk of overdose; seizure disorder; cardiac disease; glaucoma; urinary retention
SSRI and S-enantiomer of citalopram. Used for the treatment of depression. Mechanism of action is thought to be potentiation of serotonergic activity in CNS resulting from inhibition of CNS neuronal reuptake of serotonin. Onset of depression relief may be obtained after 1-2 wk, which is sooner than other antidepressants.
10 mg PO qd initially; if needed, may increase to 20 mg/d after 1 wk
Not established
Primarily metabolized by CYP450 3A4 and 2C19; coadministration with alcohol or other centrally acting drugs increases CNS depression; cimetidine increases AUC and maximum serum concentration; coadministration with sumatriptan and SSRIs has caused weakness and hyperreflexia
Documented hypersensitivity; administration within 14 d of receiving MAOI
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution with history of seizures, mania, suicide; common adverse effects include insomnia, ejaculation disorder (primarily ejaculatory delay), nausea, sweating, fatigue, and somnolence
If a patient has symptoms of sufficient severity to warrant hospitalization, consider transfer to a psychiatric unit with expertise in treating OCD.
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OCD, obsessive-compulsive disorder, obsessions, anxiety, obsessive compulsive disorder treatment, symptoms, cognitive-behavioral therapy, CBT, anxiety, behavior therapy, exposure and response prevention
William M Greenberg, MD, Associate Director, Clinical Development, Forest Research Institute, Forest Laboratories, Inc; Visiting Scientist, Nathan S Kline Institute for Psychiatric Research; Private Practice
William M Greenberg, MD is a member of the following medical societies: American Orthopsychiatric Association and American Psychiatric Association
Disclosure: Forest Laboratories, Inc. Salary Employment
Mohammed A Memon, MD, Medical Director of Geriatric Psychiatry, Department of Psychiatry, Spartanburg Regional Hospital System
Mohammed A Memon, MD is a member of the following medical societies: American Association for Geriatric Psychiatry, American Medical Association, and American Psychiatric Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
David Bienenfeld, MD, Vice-Chair, Program Director, Professor, Department of Psychiatry, Wright State University School of Medicine
David Bienenfeld, MD is a member of the following medical societies: American Medical Association, American Psychiatric Association, and Association for Academic Psychiatry
Disclosure: Nothing to disclose.
Harold H Harsch, MD, Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin
Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: lilly Honoraria Speaking and teaching; Forest Labs Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; Pfizer Grant/research funds Speaking and teaching; Northstar Grant/research funds Research; Novartis Grant/research funds research; Pfizer Speaking and teaching; Sanofi-avetis Grant/research funds research; Otsuke Grant/research funds reseach; GlaxoSmithKline Grant/research funds research
Stephen Soreff, MD, President of Education Initiatives, Nottingham, NH; Faculty, Metropolitan College of Boston University, Boston, MA
Stephen Soreff, MD is a member of the following medical societies: American College of Mental Health Administration and American Psychosomatic Society
Disclosure: Nothing to disclose.