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What Is Obsessive-Compulsive-Disorder (OCD)?

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What is OCD
Obsessive–compulsive disorder (OCD) is a mental disorder in which a person has certain thoughts repeatedly (called "obsessions") or feels the need to perform certain routines repeatedly (called "compulsions") to an extent that generates distress or impairs general functioning. The person is unable to control either the thoughts or activities for more than a short period of time. Common compulsions include hand washing, counting of things, and checking to see if a door is locked. These activities occur to such a degree that the person's daily life is negatively affected, often taking up more than an hour a day. Most adults realize that the behaviors do not make sense. The condition is associated with tics, anxiety disorder, and an increased risk of suicide.

The cause is unknown. There appear to be some genetic components, with both identical twins more often affected than both non-identical twins. Risk factors include a history of child abuse or other stress-inducing event. Some cases have been documented to occur following infections. The diagnosis is based on the symptoms and requires ruling out other drug-related or medical causes. Rating scales such as the Yale–Brown Obsessive Compulsive Scale (Y-BOCS) can be used to assess the severity. Other disorders with similar symptoms include anxiety disorder, major depressive disorder, eating disorders, tic disorders, and obsessive–compulsive personality disorder.

Treatment involves psychotherapy, such as cognitive behavioral therapy (CBT), and sometimes antidepressants, such as selective serotonin reuptake inhibitors (SSRIs) or clomipramine. CBT for OCD involves increasing exposure to fears and obsessions while preventing the compulsive behavior that would normally accompany the obsessions. Contrary to this, metacognitive therapy encourages the ritual behaviors in order to alter the relationship to one's thoughts about them. While clomipramine appears to work as well as do SSRIs, it has greater side effects and thus is typically reserved as a second-line treatment. Atypical antipsychotics may be useful when used in addition to an SSRI in treatment-resistant cases but are also associated with an increased risk of side effects. Without treatment, the condition often lasts decades.

Obsessive–compulsive disorder affects about 2.3% of people at some point in their lives while rates during any given year are about 1.2%. It is unusual for symptoms to begin after the age of 35, and half of people develop problems before 20. Males and females are affected about equally and OCD occurs worldwide. The phrase obsessive–compulsive is sometimes used in an informal manner unrelated to OCD to describe someone as being excessively meticulous, perfectionistic, absorbed, or otherwise fixated.

Signs and symptoms
OCD can present with a wide variety of symptoms. Certain groups of symptoms usually occur together. These groups are sometimes viewed as dimensions or clusters that may reflect an underlying process. The standard assessment tool for OCD, the Yale–Brown Obsessive Compulsive Scale (Y-BOCS), has 13 predefined categories of symptoms. These symptoms fit into three to five groupings. A meta-analytic review of symptom structures found a four-factor structure (grouping) to be most reliable. The observed groups included a "symmetry factor", a "forbidden thoughts factor", a "cleaning factor", and a "hoarding factor". The "symmetry factor" correlated highly with obsessions related to ordering, counting, and symmetry, as well as repeating compulsions. The "forbidden thoughts factor" correlated highly with intrusive and distressing thoughts of a violent, religious, or sexual nature. The "cleaning factor" correlated highly with obsessions about contamination and compulsions related to cleaning. The "hoarding factor" only involved hoarding-related obsessions and compulsions and was identified as being distinct from other symptom groupings.

While OCD has been considered a homogeneous disorder from a neuropsychological perspective, many of the putative neuropsychological deficits may be the result of comorbid disorders. Furthermore, some subtypes have been associated with improvement in performance on certain tasks such as pattern recognition (washing subtype) and spatial working memory (obsessive thought subtype). Subgroups have also been distinguished by neuroimaging findings and treatment response. Neuroimaging studies on this have been too few, and the subtypes examined have differed too much to draw any conclusions. On the other hand, subtype-dependent treatment response has been studied, and the hoarding subtype has consistently responded least to treatment.

Causes
The cause is unknown. Both environmental and genetic factors are believed to play a role. Risk factors include a history of child abuse or other stress-inducing event.

Drug-induced OCD
Many different types of medication can create/induce pure OCD in patients without previous symptoms. A new chapter about OCD in the DSM-5 (2013) now specifically includes drug-induced OCD.

Atypical antipsychotics (second-generation antipsychotics) such as olanzapine (Zyprexa) have been proven to induce de novo OCD in patients.

Genetics
There appear to be some genetic components with identical twins more often affected than non-identical twins. Further, individuals with OCD are more likely to have first-degree family members exhibiting the same disorders than do matched controls. In cases in which OCD develops during childhood, there is a much stronger familial link in the disorder than with cases in which OCD develops later in adulthood. In general, genetic factors account for 45–65% of the variability in OCD symptoms in children diagnosed with the disorder. A 2007 study found evidence supporting the possibility of a heritable risk for OCD.

A mutation has been found in the human serotonin transporter gene hSERT in unrelated families with OCD.

A systematic review found that while neither allele was associated with OCD overall, in Caucasians the L allele was associated with OCD. Another meta-analysis observed an increased risk in those with the homozygous S allele, but found the LS genotype to be inversely associated with OCD.

A genome-wide association study found OCD to be linked with SNPs near BTBD3 and two SNPs in DLGAP1 in a trio-based analysis, but no SNP reached significance when analyzed with case-control data.

One meta-analysis found a small but significant association between a polymorphism in SLC1A1 and OCD.

The relationship between OCD and COMT has been inconsistent, with one meta-analysis reporting a significant association, albeit only in men, and another meta analysis reporting no association.

It has been postulated by evolutionary psychologists that moderate versions of compulsive behavior may have had evolutionary advantages. Examples would be moderate constant checking of hygiene, the hearth or the environment for enemies. Similarly, hoarding may have had evolutionary advantages. In this view, OCD may be the extreme statistical "tail" of such behaviors, possibly the result of a high number of predisposing genes.

Autoimmune
A controversial hypothesis is that some cases of rapid onset of OCD in children and adolescents may be caused by a syndrome connected to Group A streptococcal infections known as pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS). OCD and tic disorders are hypothesized to arise in a subset of children as a result of a post-streptococcal autoimmune process. The PANDAS hypothesis is unconfirmed and unsupported by data, and two new categories have been proposed: PANS (pediatric acute-onset neuropsychiatric syndrome) and CANS (childhood acute neuropsychiatric syndrome). The CANS/PANS hypotheses include different possible mechanisms underlying acute-onset neuropsychiatric conditions, but do not exclude GABHS infections as a cause in a subset of individuals. PANDAS, PANS and CANS are the focus of clinical and laboratory research but remain unproven. Whether PANDAS is a distinct entity differing from other cases of tic disorders or OCD is debated.

A review of studies examining anti-basal ganglia antibodies in OCD found an increased risk of having anti-basal ganglia antibodies in those with OCD versus the general population.

Mechanics

Neuroimaging

Functional neuroimaging during symptom provocation has observed abnormal activity in the orbitofrontal cortex, left dorsolateral prefrontal cortex, right premotor cortex, left superior temporal gyrus, globus pallidus externus, hippocampus and right uncus. Weaker foci of abnormal activity were found in the left caudate, posterior cingulate cortex and superior parietal lobule. However, an older meta-analysis of functional neuroimaging in OCD reported that the only consistent functional neuroimaging finding was increased activity in the orbital gyrus and head of the caudate nucleus, while ACC activation abnormalities were too inconsistent. A meta-analysis comparing affective and nonaffective tasks observed differences with controls in regions implicated in salience, habit, goal-directed behavior, self-referential thinking and cognitive control. For nonaffective tasks, hyperactivity was observed in the insula, ACC, and head of the caudate/putamen, while hypoactivity was observed in the medial prefrontal cortex (mPFC) and posterior caudate. Affective tasks were observed to relate to increased activation in the precuneus and posterior cingulate cortex (PCC), while decreased activation was found in the pallidum, ventral anterior thalamus and posterior caudate. The involvement of the cortico-striato-thalamo-cortical loop in OCD as well as the high rates of comorbidity between OCD and ADHD have led some to draw a link in their mechanism. Observed similarities include dysfunction of the anterior cingulate cortex and prefrontal cortex, as well as shared deficits in executive functions.[78] The involvement of the orbitofrontal cortex and dorsolateral prefrontal cortex in OCD is shared with bipolar disorder and may explain the high degree of comorbidity.[79] Decreased volumes of the dorsolateral prefrontal cortex related to executive function has also been observed in OCD.

People with OCD evince increased grey matter volumes in bilateral lenticular nuclei, extending to the caudate nuclei, with decreased grey matter volumes in bilateral dorsal medial frontal/anterior cingulate gyri. These findings contrast with those in people with other anxiety disorders, who evince decreased (rather than increased) grey matter volumes in bilateral lenticular/caudate nuclei, as well as decreased grey matter volumes in bilateral dorsal medial frontal/anterior cingulate gyri. Increased white matter volume and decreased fractional anisotropy in anterior midline tracts has been observed in OCD, possibly indicating increased fiber crossings.

Cognitive models
Generally two categories of models for OCD have been postulated, the first involving deficits in executive function, and the second involving deficits in modulatory control. The first category of executive dysfunction is based on the observed structural and functional abnormalities in the dlPFC, striatum and thalamus. The second category involving dysfunctional modulatory control primarily relies on observed functional and structural differences in the ACC, mPFC and OFC.

One proposed model suggests that dysfunction in the OFC leads to improper valuation of behaviors and decreased behavioral control, while the observed alterations in amygdala activations leads to exaggerated fears and representations of negative stimuli.

Because of the heterogeneity of OCD symptoms, studies differentiating various symptoms have been performed. Symptom-specific neuroimaging abnormalities include the hyperactivity of caudate and ACC in checking rituals, while finding increased activity of cortical and cerebellar regions in contamination-related symptoms. Neuroimaging differentiating content of intrusive thoughts has found differences between aggressive as opposed to taboo thoughts, finding increased connectivity of the amygdala, ventral striatum and ventromedial prefrontal cortex in aggressive symptoms while observing increased connectivity between the ventral striatum and insula in sexual/religious intrusive thoughts.

Another model proposes that affective dysregulation links excessive reliance on habit-based action selection with compulsions. This is supported by the observation that those with OCD demonstrate decreased activation of the ventral striatum when anticipating monetary reward, as well as increased functional connectivity between the VS and the OFC. Furthermore, those with OCD demonstrate reduced performance in Pavlovian fear-extinction tasks, hyperresponsiveness in the amygdala to fearful stimuli, and hyporesponsiveness in the amygdala when exposed to positively valanced stimuli. Stimulation of the nucleus accumbens has also been observed to effectively alleviate both obsessions and compulsions, supporting the role of affective dysregulation in generating both.[86]

Neurobiological
From the observation of the efficacy of antidepressants in OCD, a serotonin hypothesis of OCD has been formulated. Studies of peripheral markers of serotonin, as well as challenges with proserotonergic compounds have yielded inconsistent results, including evidence pointing towards basal hyperactivity of serotonergic systems. Serotonin receptor and transporter binding studies have yielded conflicting results, including higher and lower serotonin receptor 5-HT2A and serotonin transporter binding potentials that were normalized by treatment with SSRIs. Despite inconsistencies in the types of abnormalities found, evidence points towards dysfunction of serotonergic systems in OCD. Orbitofrontal cortex overactivity is attenuated in people who have successfully responded to SSRI medication, a result believed to be caused by increased stimulation of serotonin receptors 5-HT2A and 5-HT2C.

A complex relationship between dopamine and OCD has been observed. Although antipsychotics, which act by antagonizing dopamine receptors may improve some cases of OCD, they frequently exacerbate others. Antipsychotics, in the low doses used to treat OCD, may actually increase the release of dopamine in the prefrontal cortex, through inhibiting autoreceptors. Further complicating things is the efficacy of amphetamines, decreased dopamine transporter activity observed in OCD, and low levels of D2 binding in the striatum.[93] Furthermore, increased dopamine release in the nucleus accumbens after deep brain stimulation correlates with improvement in symptoms, pointing to reduced dopamine release in the striatum playing a role in generating symptoms.

Abnormalities in glutamatergic neurotransmission have implicated in OCD. Findings such as increased cerebrospinal glutamate, less consistent abnormalities observed in neuroimaging studies and the efficacy of some glutamatergic drugs such as the glutamate-inhibiting riluzole have implicated glutamate in OCD. OCD has been associated with reduced N-Acetylaspartic acid in the mPFC, which is thought to reflect neuron density or functionality, although the exact interpretation has not been established.

Diagnosis
Formal diagnosis may be performed by a psychologist, psychiatrist, clinical social worker, or other licensed mental health professional. To be diagnosed with OCD, a person must have obsessions, compulsions, or both, according to the Diagnostic and Statistical Manual of Mental Disorders (DSM). The Quick Reference to the 2000 edition of the DSM states that several features characterize clinically significant obsessions and compulsions, and that such obsessions are recurrent and persistent thoughts, impulses or images that are experienced as intrusive and that cause marked anxiety or distress. These thoughts, impulses or images are of a degree or type that lies outside the normal range of worries about conventional problems. A person may attempt to ignore or suppress such obsessions, or to neutralize them with some other thought or action, and will tend to recognize the obsessions as idiosyncratic or irrational.

Compulsions become clinically significant when a person feels driven to perform them in response to an obsession, or according to rules that must be applied rigidly, and when the person consequently feels or causes significant distress. Therefore, while many people who do not suffer from OCD may perform actions often associated with OCD (such as ordering items in a pantry by height), the distinction with clinically significant OCD lies in the fact that the person who suffers from OCD must perform these actions to avoid significant psychological distress. These behaviors or mental acts are aimed at preventing or reducing distress or preventing some dreaded event or situation; however, these activities are not logically or practically connected to the issue, or they are excessive. In addition, at some point during the course of the disorder, the individual must realize that his or her obsessions or compulsions are unreasonable or excessive.

Moreover, the obsessions or compulsions must be time-consuming (taking up more than one hour per day) or cause impairment in social, occupational or scholastic functioning. It is helpful to quantify the severity of symptoms and impairment before and during treatment for OCD. In addition to the person's estimate of the time spent each day harboring obsessive-compulsive thoughts or behaviors, concrete tools can be used to gauge the person's condition. This may be done with rating scales, such as the Yale–Brown Obsessive Compulsive Scale (Y-BOCS; expert rating) or the obsessive-compulsive inventory (OCI-R; self-rating).[98] With measurements such as these, psychiatric consultation can be more appropriately determined because it has been standardized.

OCD is sometimes placed in a group of disorders called the obsessive–compulsive spectrum.

Differential diagnosis
OCD is often confused with the separate condition obsessive–compulsive personality disorder (OCPD). OCD is egodystonic, meaning that the disorder is incompatible with the sufferer's self-concept. Because egodystonic disorders go against a person's self-concept, they tend to cause much distress. OCPD, on the other hand, is egosyntonic—marked by the person's acceptance that the characteristics and behaviours displayed as a result are compatible with their self-image, or are otherwise appropriate, correct or reasonable.

As a result, people with OCD are often aware that their behavior is not rational and are unhappy about their obsessions but nevertheless feel compelled by them. By contrast, people with OCPD are not aware of anything abnormal; they will readily explain why their actions are rational. It is usually impossible to convince them otherwise, and they tend to derive pleasure from their obsessions or compulsions.

Management
A form of psychotherapy called "cognitive behavioral therapy" (CBT) and psychotropic medications are first-line treatments for OCD. Other forms of psychotherapy, such as psychodynamic and psychoanalysis may help in managing some aspects of the disorder, but in 2007 the American Psychiatric Association (APA) noted a lack of controlled studies showing their effectiveness "in dealing with the core symptoms of OCD".

Therapy
The specific technique used in CBT is called exposure and response prevention (ERP), which involves teaching the person to deliberately come into contact with the situations that trigger the obsessive thoughts and fears ("exposure") without carrying out the usual compulsive acts associated with the obsession ("response prevention"), thus gradually learning to tolerate the discomfort and anxiety associated with not performing the ritualistic behavior. At first, for example, someone might touch something only very mildly "contaminated" (such as a tissue that has been touched by another tissue that has been touched by the end of a toothpick that has touched a book that came from a "contaminated" location, such as a school). That is the "exposure". The "ritual prevention" is not washing. Another example might be leaving the house and checking the lock only once (exposure) without going back and checking again (ritual prevention). The person fairly quickly habituates to the anxiety-producing situation and discovers that his or her anxiety level drops considerably; he or she can then progress to touching something more "contaminated" or not checking the lock at all—again, without performing the ritual behavior of washing or checking.

ERP has a strong evidence base, and it is considered the most effective treatment for OCD. However, this claim was doubted by some researchers in 2000, who criticized the quality of many studies. A 2018 review found that self-help metacognitive training improved symptoms in OCD. A 2007 Cochrane review also found that psychological interventions derived from CBT models were more effective than treatment as usual consisting of no treatment, waiting list or non-CBT interventions. For body-focused repetitive behaviors (BFRB), behavioral interventions are recommended by reviews such as habit-reversal training[31] and decoupling.

It has generally been accepted that psychotherapy in combination with psychiatric medication is more effective than either option alone.

Medications
The medications most frequently used are the selective serotonin reuptake inhibitors (SSRIs). Clomipramine, a medication belonging to the class of tricyclic antidepressants, appears to work as well as SSRIs but has a higher rate of side effects.

SSRIs are a second-line treatment of adult obsessive compulsive disorder with mild functional impairment and as first-line treatment for those with moderate or severe impairment. In children, SSRIs can be considered as a second-line therapy in those with moderate to severe impairment, with close monitoring for psychiatric adverse effects. SSRIs are efficacious in the treatment of OCD; people treated with SSRIs are about twice as likely to respond to treatment as are those treated with placebo. Efficacy has been demonstrated both in short-term (6–24 weeks) treatment trials and in discontinuation trials with durations of 28–52 weeks.

In 2006, the National Institute of Clinical and Health Excellence (NICE) guidelines recommended antipsychotics for OCD that does not improve with SSRI treatment. For OCD there is tentative evidence for risperidone and insufficient evidence for olanzapine. Quetiapine is no better than placebo with regard to primary outcomes, but small effects were found in terms of YBOCS score. The efficacy of quetiapine and olanzapine are limited by an insufficient number of studies. A 2014 review article found two studies that indicated that aripiprazole was "effective in the short-term" and found that "[t]here was a small effect-size for risperidone or anti-psychotics in general in the short-term"; however, the study authors found "no evidence for the effectiveness of quetiapine or olanzapine in comparison to placebo." While quetiapine may be useful when used in addition to an SSRI in treatment-resistant OCD, these drugs are often poorly tolerated, and have metabolic side effects that limit their use. None of the atypical antipsychotics appear to be useful when used alone. Another review reported that no evidence supports the use of first-generation antipsychotics in OCD.

A guideline by the APA suggested that dextroamphetamine may be considered by itself after more well-supported treatments have been tried.

Procedures
Electroconvulsive therapy (ECT) has been found to have effectiveness in some severe and refractory cases.

Surgery may be used as a last resort in people who do not improve with other treatments. In this procedure, a surgical lesion is made in an area of the brain (the cingulate cortex). In one study, 30% of participants benefitted significantly from this procedure. Deep-brain stimulation and vagus nerve stimulation are possible surgical options that do not require destruction of brain tissue. In the United States, the Food and Drug Administration approved deep-brain stimulation for the treatment of OCD under a humanitarian device exemption requiring that the procedure be performed only in a hospital with special qualifications to do so.

In the United States, psychosurgery for OCD is a treatment of last resort and will not be performed until the person has failed several attempts at medication (at the full dosage) with augmentation, and many months of intensive cognitive–behavioral therapy with exposure and ritual/response prevention. Likewise, in the United Kingdom, psychosurgery cannot be performed unless a course of treatment from a suitably qualified cognitive–behavioral therapist has been carried out.
Children

Therapeutic treatment may be effective in reducing ritual behaviors of OCD for children and adolescents. Similar to the treatment of adults with OCD, CBT stands as an effective and validated first line of treatment of OCD in children. Family involvement, in the form of behavioral observations and reports, is a key component to the success of such treatments. Parental interventions also provide positive reinforcement for a child who exhibits appropriate behaviors as alternatives to compulsive responses. In a recent meta-analysis of evidenced-based treatment of OCD in children, family-focused individual CBT was labeled as "probably efficacious", establishing it as one of the leading psychosocial treatments for youth with OCD. After one or two years of therapy, in which a child learns the nature of his or her obsession and acquires strategies for coping, that child may acquire a larger circle of friends, exhibit less shyness, and become less self-critical.

Although the causes of OCD in younger age groups range from brain abnormalities to psychological preoccupations, life stress such as bullying and traumatic familial deaths may also contribute to childhood cases of OCD, and acknowledging these stressors can play a role in treating the disorder.
 
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