caudate nucleus, while anterior cingulate cortex (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, 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. 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. 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 category involves deficits in executive dysfunction and is based on the observed structural and functional abnormalities in the dlpfc, striatum and thalamus. the second category involves dysfunctional modulatory control and 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. due to 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 or 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. 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. 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. ocd, like other mental and behavioral health disorders, cannot be diagnosed by a medical exam. nor are there any medical exams that can predict if one will fall victim to such illnesses. 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 dsm notes that there are multiple characteristics that can turn obsessions and compulsions from normalized behavior to "clinically significant". there has to be recurring and strong thoughts or impulsive that intrude on the day-to-day lives of the patients and cause noticeable levels of anxiousness. 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, suppress such obsessions, neutralize them with another thought or action, or try to rationalize their anxiety away. people with ocd tend to recognize their obsessions as 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 have 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 with 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, often 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). with measurements such as these, psychiatric consultation can be more appropriately determined, as it has been standardized. in regards to diagnosing, the health professional also looks to make sure that the signs of obsessions and compulsions are not the results of any drugs, prescription or recreational, that the patient may be taking. there are several types of obsessive thoughts that are found commonly in those with ocd. some of these include fear of germs, hurting loved ones, embarrassment, neatness, societally unacceptable sexual thoughts etc. within ocd, these specific categories are often diagnosed into their own type of ocd. ocd is sometimes placed in a group of disorders called the obsessive–compulsive spectrum. another criterion in the dsm is that a person's mental illness does not fit one of the other categories of a mental disorder better. that is to say, if the obsessions and compulsions of a patient could be better described by trichotillomania, it would not be diagnosed as ocd. that being said, ocd does often go hand in hand with other mental disorders. for this reason, one may be diagnosed with multiple mental disorders at once. a different aspect of the diagnoses is the degree of insight had by the individual in regards to the truth of the obsessions. there are three levels, good/fair, poor and absent/delusional. good/fair indicated that the patient is aware that the obsessions they have are not true or probably not true. poor indicates that the patient believes their obsessional beliefs are probably true. absent/delusional indicates that they fully believe their obsessional thoughts to be true. approximately 4% or fewer individuals with ocd will be diagnosed as absent/delusional. additionally, as many as 30% of those with ocd also have a lifetime tic disorder, meaning they have been diagnosed with a tic disorder at some point in their life. there are several different types of tics that have been observed in individuals with ocd. these include but are not limited to, "grunting", "jerking" or "shrugging" body parts, sniffling, and excessive blinking. there has been a significant amount of progress over the last few decades, and as of 2022 there is statically significant improvement in the diagnostic process for individuals with ocd. one study found that of two groups of individuals, one with participants under the age of 27.25 and one with participants over that age, those in the younger group experienced a significantly faster time between the onset of ocd tendencies and their formal diagnoses. 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 individual's self-concept. as 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 behaviors 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 cognitive behavioral therapy (cbt) and psychotropic medications are the first-line treatments for ocd. therapy one exposure and ritual prevention activity would be to check the lock only once and then leave. the specific cbt technique used is called exposure and response prevention (erp), which involves teaching the person to deliberately come into contact with situations that trigger obsessive thoughts and fears (exposure), without carrying out the usual compulsive acts associated with the obsession (response prevention). this technique causes patients to gradually learn to tolerate the discomfort and anxiety associated with not performing their compulsions. for many patients, erp is the add-on treatment of choice when selective serotonin reuptake inhibitors (ssris) or serotonin-norepinephrine reuptake inhibitors (snris) medication does not effectively treat ocd symptoms, or vice versa, for individuals who begin treatment with psychotherapy. modalities differ in erp treatment but both virtual reality based as well as unguided computer assisted treatment programs have shown effective results in treatment programs. for example, a patient might be asked to touch something very mildly contaminated (exposure), and wash their hands only once afterward (response prevention). another example might entail asking the patient to leave the house and check the lock only once (exposure), without going back to check again (response prevention). after succeeding at one stage of treatment, the patient's level of discomfort in the exposure phase can be increased. when this therapy is successful, the patient will quickly habituate to