Learning theory does not account for all aspects of OCD. It does not adequately explain why some compulsions persist even when they produce, rather than reduce, anxiety. Because compulsions are viewed as a response to obsessions, learning theory does not account for cases in which only compulsions are present. It is also incompatible with obsessive-compulsive symptoms that develop directly as the result of brain injury. These limitations notwithstanding, the effectiveness of a behavior therapy technique referred to as exposure and response prevention has been confirmed in numerous studies.
The observation that medications referred to as serotonin reuptake inhibitors (SRIs) are preferentially effective in OCD led researchers to speculate that the brain chemical serotonin might be related to the cause of OCD. The immediate consequence of administering an SRI is to increase the levels of serotonin in the gap between nerve cells called the synapse. However, if this were the only factor involved in the treatment of OCD, one would expect symptoms to improve after the first dose of an SRI. That a response to an SRI takes weeks to develop suggests that the delayed effects of an SRI on brain chemistry are more relevant to OCD than its acute effects.
The effectiveness of SRIs in OCD furnishes important clues about serotonin, but additional research is needed to identify the precise role of this neurochemical in the treatment and cause of OCD.
For the first time, advances in technology are allowing researchers to investigate the activity of the waking human brain without causing significant discomfort or risk to the subject. Several of these techniques have been applied to the study of OCD with dramatic results. Lewis R. Baxter Jr. and colleagues of the University of California at Los Angeles and the University of Alabama in Birmingham were the first to use positron-emission tomography (PET) to study OCD.
PET scans produce color-coded images of the brain’s metabolic activity. Baxter’s study showed that patients with OCD had elevated brain activity in areas of the frontal lobes (particularly the orbital cortex) and the basal ganglia. Several other groups have since confirmed these findings. Other evidence for a causal role of the basal ganglia in OCD are accidents of nature, such as Sydenham’s chorea and von Ecomomo’s encephalitis that damage the basal ganglia and produce obsessive-compulsive symptoms.
The basal ganglia are a group of related brain regions housed deep within the substance of the brain. From an evolutionary standpoint, the basal ganglia are considered primitive structures. Because of their primitive status, until recently, the basal ganglia have been largely ignored in theories of psychiatric illness. Once thought to be a simple relay station in the control of motor behavior, it is now known that the basal ganglia function to integrate information converging from all over the brain.
Dr. Judith L. Rapoport of the National Institute of Mental Health has proposed an elegant neurological model of OCD that takes into account both anatomical and clinical evidence. According to this model, the basal ganglia and its connections are turned on inappropriately in OCD. The result is the emergence of self-protective behaviors such as grooming or checking. These primitive behaviors, which are stored as preprogrammed routines in the basal ganglia, unfold uncontrollably outside the reach of brain areas that command reason.
Abuse of stimulants such as amphetamine and cocaine may induce repetitive behaviors that resemble the rituals of OCD. “Punding” is a Swedish slang term that describes individuals who compulsively perform meaningless activities (e.g., assembling and disassembling household products) during intoxication with stimulants. Repetitive behaviors that mimic compulsions can be produced in laboratory animals by administration of stimulants.
Goodman, W. (2006). What Causes Obsessive-Compulsive Disorder (OCD)?. Psych Central. Retrieved on August 30, 2014, from http://psychcentral.com/lib/what-causes-obsessive-compulsive-disorder-ocd/000506
Last reviewed: By John M. Grohol, Psy.D. on 30 Jan 2013
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