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OCD is separated from other mental health conditions by the presence of obsessions, compulsions, or both. The obsessions or compulsions cause marked distress, are time-consuming, and interfere with a person's normal function. Indications of OCD can occur in children and teenagers, with the disease usually beginning gradually and worsening with age. Symptoms of OCD can be mild or severe. Some people experience obsessive thoughts only, without engaging in compulsive behavior. Some people who experience OCD successfully hide their symptoms for fear of embarrassment or stigma.

Friends and family may, however, notice some of the more physical signs. Obsessions are more than the everyday worries experienced by most healthy people when thinking about real-life problems. Instead, people with OCD experience excessive thoughts and worries that prompt them to engage in particular actions or thoughts in an attempt to relieve or suppress the fear and anxiety. Not all "rituals" or forms of repetitive behavior are compulsions.

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Normal repetitive behaviors that feature in everyday life may include bedtime routines, religious practices, and learning a new skill. Behavior also depends on the context. For example, a person who works in a video store arranging DVDs for 8 hours a day is probably not acting out of compulsion. OCD is thought to have a neurobiological basis, with neuroimaging studies showing that the brain functions differently in people with the disorder.

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An abnormality, or an imbalance in neurotransmitters, is thought to be involved in OCD. OCD that begins in childhood is more common in boys than girls , with the usual time of onset of OCD later for females than males.

Obsessive-Compulsive Disorder: Diagnosis and Management - American Family Physician

The condition might be triggered by a combination of genetic, neurological, behavioral, cognitive, and environmental factors. OCD runs in families and can be considered a " familial disorder. Twin studies of adults suggest that obsessive-compulsive symptoms are moderately able to be inherited, with genetic factors contributing 27 to 47 percent variance in scores that measure obsessive-compulsive symptoms. However, no single gene has been identified as the "cause" of OCD.

Some rapid-onset cases of OCD in children might be consequences of Group A streptococcal infections, which cause inflammation and dysfunction in the basal ganglia. These cases are grouped and referred to as pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections PANDAS. In recent years, however, other pathogens, such as the bacteria responsible for Lyme disease and the H1N1 flu virus, have also been associated with the rapid onset of OCD in children. The behavioral theory suggests that people with OCD associate certain objects or situations with fear.

They learn to avoid those things or learn to perform "rituals" to help reduce the fear. This fear and avoidance or ritual cycle may begin during a period of intense stress , such as when starting a new job or just after an important relationship comes to an end. Once the connection between an object and the feeling of fear becomes established, people with OCD begin to avoid that object and the fear it generates, rather than confronting or tolerating the fear. The behavioral theory outlined above focuses on how people with OCD make an association between an object and fear.

The cognitive theory, however, focuses on how people with OCD misinterpret their thoughts. Most people have unwelcome or intrusive thoughts at certain times, but for individuals with OCD, the importance of those thoughts are exaggerated. For example, a person who is caring for an infant and who is under intense pressure may have an intrusive thought of harming the infant either deliberately or accidentally. Most people can shrug off and disregard the thought, but a person with OCD may exaggerate the importance of the thought and respond as though it signifies a threat.

As long as the individual with OCD interprets these intrusive thoughts as cataclysmic and true, they will continue the avoidance and ritual behaviors. Brain imaging techniques have allowed researchers to study the activity of specific areas of the brain, leading to the discovery that some parts of the brain are different in people with OCD when compared to those without. Despite this finding, it is not known exactly how these differences relate to the development of OCD. Imbalances in the brain chemicals serotonin and glutamate may play a part in OCD.

Environmental stressors may be a trigger for OCD in people with a tendency toward developing the condition. Traumatic brain injury TBI in adolescents and children has also been associated with an increased risk of onset of obsessive-compulsions.

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  6. One study found that 30 percent of children aged 6 to 18 years who experienced a TBI developed symptoms of OCD within 12 months of the injury. Overall, studies indicate that people with OCD frequently report stressful and traumatic life events before the illness begins. A number of other psychiatric and neurological disorders , such as depression and anxiety, have similar features to OCD and can occur alongside the condition.

    OCD usually develops into a chronic condition if left untreated, with episodes where symptoms seem to improve. Without treatment, remission rates are low, at around 20 percent. However, around 40 percent of people who develop OCD in childhood or adolescence experience remission by early adulthood. Treatment for OCD will depend on how much the condition affects the person's ability to function. First-line treatments for OCD will often include:. CBT is a type of psychotherapy talking therapy that aims to help the individual change the way they think, feel, and behave.

    It refers to two distinct treatments :. Research has shown that 75 percent of people with OCD are significantly helped by cognitive behavioral therapy. Treatment techniques include exposure and response prevention ERP , this involves the following:. Other techniques focus solely on cognitive therapy.

    People who participate in this type of therapy work toward eliminating the compulsive behavior. This is done by identifying and re-evaluating their beliefs about the consequences of engaging, or not engaging, in the compulsive behavior. Once these intrusive thoughts and the meanings the person applies to them are acknowledged, the therapist will then encourage the person to:. These studies have, however, found CT to be effective.

    It might take up to 3 months for results to be noticed.

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    About half of all people with OCD do not respond to SSRI treatment alone, with atypical antipsychotic medications often added to the treatment. Successful treatment can significantly improve and even cure OCD. However, the condition can return later on. Article last updated by Adam Felman on Thu 18 January All references are available in the References tab. American Psychiatric Association. American Psychiatric Pub. Abramowitz, J. Obsessive-compulsive disorder.

    The Lancet, , Arnold, P. Glutamate transporter gene SLC1A1 associated with obsessive-compulsive disorder.

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    Archives of General Psychiatry, 63 7 , Fontenelle, L. Role of stressful and traumatic life events in obsessive—compulsive disorder. Neuropsychiatry, 1 1 , Grados, M. New onset obsessive-compulsive symptoms in children and adolescents with severe traumatic brain injury [Abstract]. Hollander, E. Kellner, M.

    Drug treatment of obsessive-compulsive disorder. Dialogues in Clinical Neuroscience, 12 2 , Markarian, Y. Multiple pathways to functional impairment in obsessive-compulsive disorder. Clinical Psychology Review, 30 1 , Moretti, G. Murphy, D.

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    Obsessive-compulsive disorder and its related disorders: a reappraisal of obsessive-compulsive spectrum concepts. Dialogues Clinical Neuroscience, 12 2 , Nestadt, G. A family study of obsessive-compulsive disorder. Archive of General Psychiatry , 57 4 , OCD at school - a primer for educators. Parmet, S. The different types of obsessive-compulsive disorder.

    Treatments for OCD: Medications. What causes OCD? 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 increased 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, [68] and low levels of D2 binding in the striatum.

    Abnormalities in glutaminergic neurotransmission have implicated in OCD.