Obsessive-Compulsion Disorder: Etiology and Treatment

Traditional psychoanalytic theories posited psychogenic theories for what was once called obsessive-compulsive neurosis. These primarily involved early developmental experiences with perfectionistic, overly strict, and rigid parents who imposed unrealistic standards and stifled the child’s emerging autonomy. These theories likely do apply to the development of obsessive-compulsive personality, but not necessarily OCD.

In recent years, a number of findings from clinical practice and neurobiology have convincingly argued a ­biological basis for OCD. Let’s take a look at some of this evidence.

The disorder emerges early, often in late childhood, and maintains remarkable symptomatic stability throughout life. The incidence in the general population is 2.5 percent, yet it is seven percent in first-degree relatives, suggesting a possible genetic loading for the disorder.

Also, disease processes  such as certain types of encephalitis, that selectively damage areas of the basal ganglia (subcortical brain structures), have been shown to result in OCD-symptoms as have certain bacterial infections such as streptococcus.

Treatment with SSRI antidepressants

Probably most convincing are the findings from pharmacological and neuro-­imaging studies. A very large number of clinical studies have shown that OCD patients can be helped by treatment with SSRI antidepressants.

And this holds true even in OCD patients without co-existing depression. In addition, antidepressants that do not affect serotonin are not effective in alleviating OCD symptoms. The SSRI antidepressants selectively increase serotonin activity in the brain and probably more ­specifically in the basal ganglia, cingulate gyrus, and prefrontal cortex.

Finally, several studies of brain metabolic functioning reveal that in highly symptomatic OCD patients there is a significant increase in metabolic activity (thus increased activation) in the prefrontal cortex and basal ganglia. Furthermore, this abnormal metabolic activity becomes normalized when patients are treated with SSRI antidepressants.

Instinctual Behaviors Erupt

Two theories have emerged from these data. The first is that the frontal lobes normally act to inhibit or override the emergence of primitive instinctual urges. However, in OCD, this inhibition fails, and we see the eruption of innate urges, or behavioral routines, that resemble nest building, grooming, and the checking of territorial boundaries, instinctual behaviors associated with more primitive species.

In this model, ordering, straightening, cleaning, hand washing, checking door locks, and so forth may reflect human versions of a breakthrough of these more primitive urges.

A second theory holds that there are naturally existing neural pathways that typically serve adaptive purposes, especially when people are exposed to potentially dangerous situations. The frontal cortex serves as the launching site for worry. When exposed to dangerous stimuli, the frontal lobes guide and direct sustained perceptual focus and attention. In essence, arousal is passed through a feedback circuit.

Brain Senses Danger

In normal individuals, this serves to maintain alertness and vigilance until it is determined that there is no danger; then the inner reverberating loop shuts down. Presumably, this neural loop fails to inhibit itself in OCD. The brain continues to sense danger despite cognitive evidence to the contrary.

The patient gets caught in an on-going repetition of worry and engages in behavioral attempts to reduce the worry (the rituals). The caudate is richly innervated by 5-HT (serotonin) neurons. When these nerve cells are activated by 5-HT antidepressants, the inhibitory serotonergic cells reduce the excessive metabolic activity and shut down the maladaptive loop, and OCD symptoms diminish.

Standard psychotherapy is notoriously ineffective with OCD. To date, two approaches to treatment are, however, proving to be helpful in reducing symptoms in this truly devastating mental illness.

The first are behavioral techniques: exposure and response prevention. Exposure amounts to systematic, gradual exposure to anxiety-provoking stimuli; for example, for a patient afraid of contamination by germs, the exposure trial might involve having the patient clean a toilet without using gloves.

Although, because of the need to expose the patient gradually to anxiety-inducing stimuli, it is unlikely the patient with contamination based obsessions and ruminations would start with such an extreme behavioral intervention, but rather work towards this behavior in a stepwise fashion.

Response prevention amounts to helping the patient avoid rituals, such as avoiding excessive hand washing. The rituals, if carried out, usually reduce anxiety. The subsequent reduction in anxiety is highly reinforcing, which is why response prevention is so important and difficult.

Anxiety Diminishes with Exposure, Response Prevention

With response prevention, the initial experience is that the patient will encounter considerable anxiety as he or she avoids the ritualistic behavior. Yet with repeated exposures or response prevention, gradually the anxiety diminishes. This is an emotionally difficult treatment to embark upon but one shown to be successful in up to 75 to 80 percent of patients given an adequate number of trials, typically 20 to 25 sessions.

Medication treatment has become more successful with the advent of selective 5-HT antidepressants. These medications, as noted earlier, are given to OCD patients even if they are not clinically depressed. In addition to their antidepressant effects, these drugs reduce OCD symptoms directly.

Treatment with medications for OCD generally requires doses higher than those used to treat clinical depression. Aside from higher doses, treatment guidelines are the same as for treating depression. The high doses of serotonergic medications used in OCD should to be titrated up slowly and the patient should be monitored closely for negative side effects.

Psychotropic medications are believed to be effective in 50 to 65 percent of OCD cases, generally showing a 50 to 60 percent reduction in symptoms. Complete remission is not common. Unfortunately, if patients stop medications, there is a 95 percent relapse rate; thus chronic treatment is necessary.

In all likelihood, combined ­behavioral and pharmacologic treatment offers the best promise for successful outcome.


*This article is based on Dr. Moore’s latest book “Handbook of Clinical Psychopharmacology for Therapists” published by New Harbinger Press and coauthored by John Preston, John O’Neal, and Mary Talaga.

Preston, J., O’Neal, J., Talaga, M., & Moore, B. A. (in press). Handbook of Clinical Psychopharmacology for Therapists-Ninth Edition.  Oakland, CA: New Harbinger Press.


Obsessive-Compulsion Disorder: Etiology and Treatment

Bret Moore, Psy.D.

Dr. Moore is a board-certified clinical psychologist and prescribing psychologist in San Antonio, TX. His recent book Taking Control of Anxiety: Small Steps for Getting the Best of Worry, Stress, and Fear was developed as a self-help guide for people struggling with anxiety and for therapists to use with their patients. Dr. Moore is also coauthor of the Handbook of Clinical Psychopharmacology for Therapists-Ninth Edition and Child and Adolescent Psychopharmacology Made Simple-Fourth Edition.


APA Reference
Moore, B. (2020). Obsessive-Compulsion Disorder: Etiology and Treatment. Psych Central. Retrieved on September 19, 2020, from


Scientifically Reviewed
Last updated: 24 Mar 2020
Last reviewed: By John M. Grohol, Psy.D. on 24 Mar 2020
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