Obsessive-compulsive disorder (OCD) is characterized by either obsessions or compulsions. Obsessions are unwanted repetitive thoughts, images, or impulses that the patient has, often themes of threat or danger, and which cause significant distress. Common obsessional content includes fear of impurity, violence, forbidden sexual thoughts, disease, or religious blasphemy. Examples include thoughts of having contracted a deadly illness, or picking up germs, of having run someone over while driving, of having left the stove on, or having molested a child.
Compulsions are the repetitive behaviors that the sufferer performs either in response to the distress associated with the content of the obsessions, or in response to an unwanted drive . Common compulsive behaviors include excessive cleaning (e.g., hand washing), checking, ordering, rearranging, counting, repeating, and mental rituals..
Most patients with OCD have both obsessions and compulsions. In order to have the OCD diagnosis, the patient must find the obsessions or compulsions time-consuming (e.g., take more than 1 hour per day) or cause clinically significant distress or problems in social, occupational, or other important areas of functioning.
The new DSM-V published in 2013 has a new section titled “Obsessive-Compulsive and Related Disorders,” which encompasses the disorders OCD, hoarding disorder, body dysmorphic disorder, trichotillomania (hair-pulling disorder) and excoriation (skin-picking) disorder.
Obsessive-compulsive personality disorder (OCPD) is a separate condition, defined as a rigid, perfectionistic personality type. Although patients with OCPD display recurrent themes in their thinking such as over scrupulousness and inflexibility, they do not perceive their traits as being unwanted. Instead they identify with them, which is the opposite of what patients with OCD do.
The symptoms of OCD can occur in patients with other mental disorders, such as with patients depression who have ruminations, psychotic patients who have delusions, and in anxious patients preoccupied by their symptoms, and others. Psychiatric comorbidity is common in OCD,
The average age at onset of OCD is 21 years, with average onset age varying by gender (19 years for men; 22 years for women (Rasmussen and Eisen 1992). However, 21% of patients report symptoms before puberty. Although onset may occur during other periods of the life span, late-onset OCD is unusual and may be the result of an organic (non-psychiatric) illness
The clinical course of OCD is typically lifelong with waxing and waning symptomatology. Some patients with OCD may experience symptoms during phases, with periods of complete or partial remission in between. Women are at particular risk during pregnancy and the postpartum period. One report found that 57% of women experiencing postpartum depression also experienced obsessional thoughts (Wisner et al. 1999).
Rates of full remission over different time lengths (although all are over years, not months) in different studies have ranged from 6% to 43%. Rates of partial remission reported in these same studies have ranged from 17% to 75% (Eisen et al. 2010). The longest-term follow-up study ever conducted (mean follow-up period of 47 years) found that almost half (48%) of patients reported clinical recovery (defined as no clinically relevant symptoms for at least 5 years). However, only 20% experienced full remission (i.e., complete absence of symptoms for at least 5 years) (Skoog and Skoog 1999).
Although OCD was once considered a rare disorder, data from the ECA study found a lifetime prevalence of OCD of between 1.9% and 3.3% in a large sample of U.S. households (Goodman 1999). Epidemiological studies from other countries throughout the world have generally found comparable lifetime prevalence rates of OCD.
Psychiatric comorbidity (having an additional psychiatric diagnosis) is common in OCD, with the Epidemiologic Catchment Area study (1980-1985) finding that two-thirds of patients with OCD met criteria for at least one other psychiatric illness during their lifetime (Karno et al. 1988). The most common comorbid psychiatric diagnosis is major depressive disorder. Approximately one-third of individuals with OCD are currently experiencing a major depressive episode, and two-thirds will have a major depressive episode during their lifetime. Other commonly comorbid psychiatric illnesses include anxiety disorders, eating disorders, and substance abuse/dependence.(Hales et al. 2014)
The disability associated with OCD is severe enough that the World Health Organization has listed OCD among the 10 medical illnesses most likely to cause disability (Murray and Lopez 1996).
Freud (1909-1973) theorized that obsessions were defensive reactions to unconscious impulses, especially sexual and aggressive impulses. Obsessions functioned to mask these impulses and control them. However, even though psychodynamic therapy can reveal underlying origins to the obsessions, doing so has not been shown to relieve OCD symptoms.
The analysis of twin studies found that there is a strong inheritable component to OCD, including a concordance rate (odds of finding the disorder in both twins) of between 80% and 87% in monozygotic twins (genetically identical twins) and between 47%-50% in dizygotic twins (fraternal twins). (van Grootheest et al. 2005) OCD tends to run in families with a study of 1,209 first-degree relatives of an OCD subject (called the proband) showing an increased risk of OCD (8.2%) compared to control subjects (2%). (Hettema et al. 2001). Genetic studies have focused on a number of genes that may be associated with OCD, including serotonin, dopamine, and glutamate.
Neuroanatomical studies have been focused on a major set of circuits in the brain connecting multiple brain centers, named the cortico-striato-thalamo-cortical (CSTC) circuits. These parallel circuits promote different functions from eye movement to cognitive function and affective functions. One of these CSTC circuits, termed the ventral cognitive loop, includes the orbitofrontal cortex, the caudate nucleus, and the dorsomedial thalamus. Functional neuroimaging studies have found functional abnormalities within all nodes of this circuit. These brain regions are hyperactive at rest in patients with OCD compared with healthy volunteers, this hyperactivity is amplified during OCD symptom exacerbation, and the hyperactivity is decreased with successful treatment (Dougherty et al. 2010).
A specific type of behavioral therapy, exposure and response prevention (ERP), has been developed since the 1960s for the treatment of OCD. Patients are first exposed to stimuli that trigger their specific OCD symptoms. For patients with contamination fears, this may involve touching a doorknob or a faucet handle that they perceive as being contaminated. Patients then prevent themselves from responding to the stimuli as they usually would (e.g., a patient who now feels contaminated will avoid washing his hands after touching the contaminated stimulus). Initially patients experience marked anxiety, and it can take a significant amount of time for the anxiety to decrease. As patients repeat their ERP exercises, both the intensity of the anxiety and the time required for it to diminish will gradually decrease until patients become habituated to the stimuli.
ERP is an effective treatment for some patients with OCD and is considered to be a first-line intervention for OCD. Meta-analysis of the many clinical trials for ERP has provided a general estimate of the response rates associated with ERP. Foa and Kozak (1996), using the cutoff for “response” as a 30% or more improvement of OCD symptoms found that across more than a dozen studies the response rate was 76%–83%.
It is worth noting that a few studies comparing ERP with pharmacotherapy have found that ERP is superior to pharmacotherapy (e.g., Foa et al. 2005). Additionally, some studies suggest that combining ERP and pharmacotherapy results in lower relapse rates in patients with OCD when they discontinue pharmacotherapy.
Cognitive therapy (CT) is a form of psychotherapy that seeks to identify and modify distortions and other maladaptive beliefs. A recent meta-analysis of psychotherapies in OCD (Rosa-Alcázar et al. 2008) found very similar effect size estimates for CT and ERP; however, the CT effect size was only based on three studies. Several recent CT studies not included in the meta-analysis (e.g., Wilhelm et al. 2009) also showed promising results. However, given that the number of CT studies is still relatively small, ERP is currently considered the psychotherapy of choice for OCD.
The serotonin reuptake inhibitors (SRIs) are usually the first-line medication treatment for OCD (Bandelow et al. 2008). The SRIs include all of the selective serotonin reuptake inhibitors (SSRIs) as well as clomipramine. Meta-analyses have generally found that 40%–60% of patients with OCD achieve response (defined as at least a 25%–35% decrease in OCD symptoms) when treated with SRIs (Greist et al. 1995).
When SRIs are used for treating OCD, it is important that high dosages be achieved (clomipramine up to 250 mg/day, fluoxetine up to 80 mg/day, paroxetine up to 60 mg/day, fluvoxamine up to 300 mg/day, sertraline up to 200 mg/day, citalopram up to 40 mg/day, and escitalopram up to 30 mg/day) because response rates are higher compared with treatment with low doses. Additionally, it is important to note that response may not be achieved until after 8–12 weeks of treatment, which is longer than the time necessary to see a response in treating depression.
Other potential monotherapy approaches to the treatment of OCD generally involve other classes of antidepressants that affect the serotonergic system. Serotonin-norepinephrine reuptake inhibitors (SNRIs) and, possibly, the monoamine oxidase inhibitors (MAOIs) although there is less data for their use. There is no evidence supporting the use of dopaminergic antidepressants (e.g., bupropion) for the treatment of OCD.
There have long been data supporting the use of dopaminergic antagonists to augment the effects of SRIs in the treatment of OCD. Although the initial studies, by included only conventional antipsychotics, newer studies since the advent of the atypical antipsychotics also support their use as augmenting agents with the SRIs.
Because of the lower extrapyramidal side-effect (movement disorder) burden, most clinicians now use the atypical antipsychotics to augment SRIs for the treatment of OCD rather than the older generation antipsychotics. However, it can be argued that the gains of lower extrapyramidal side-effect burden with the atypical antipsychotics are somewhat mitigated by the higher rates of metabolic syndrome (increase in glucose and lipid levels, and weight gain) with many of the atypical antipsychotics, so risks and benefits should be carefully discussed with the physician. Dosages are usually in the low to moderate range (e.g., risperidone 1–4 mg/day), and response after augmentation is typically seen within 1–4 weeks.
More recent pharmacological approaches to OCD treatment include agents that affect the glutamatergic system. Preliminary studies involving memantine, riluzole, and N-acetylcysteine show some promise.
Neurosurgical approaches may be effective for patients with severe, intractable OCD that have not responded to all conventional therapies. These approaches include ablative limbic system procedures such as anterior cingulotomy, anterior capsulotomy, subcaudate tractotomy, and limbic leucotomy as well as deep brain stimulation (DBS) electrodes placed at a number of different brain targets. The U.S. Food and Drug Administration (FDA) approved the use of DBS at the ventral capsule/ventral striatum target for treatment-refractory OCD in 2009.
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