Early theories regarding the cause of this OCD-like condition stressed the role of distorted religious experience. English writers from the 18th and late 17th centuries attributed intrusive blasphemous images to the work of Satan. Even today, some patients with obsessions of “scrupulosity” still wonder about demonic possession and may seek exorcism.
The French 19th-century accounts of obsessions emphasized the central role of doubt and indecisiveness. In 1837, the French clinician Esquirol used the term “folie du doute,” or the doubting madness, to refer to this cluster of symptoms. Later French writers, including Pierre Janet in 1902, stressed the loss of will and low mental energy as underlying the formation of obsessive-compulsive symptoms.
The greater part of the 20th century was dominated by psychoanalytic theories of OCD. According to psychoanalytic theory, obsessions and compulsions reflect maladaptive responses to unresolved conflicts from early stages of psychological development. The symptoms of OCD symbolize the patient’s unconscious struggle for control over drives that are unacceptable at a conscious level.
Although often intuitively appealing, psychoanalytic theories of OCD lost favor in the last quarter of the 20th century. Psychoanalysis offers an elaborate metaphor for the mind, but it is not grounded in evidence based on studies of the brain. Psychoanalytic concepts may help explain the content of the patient’s obsessions, but they do little to improve understanding of the underlying processes and have not led to reliably effective treatments.
The psychoanalytic focus on the symbolic meaning of obsessions and compulsions has given way to an emphasis on the form of the symptoms: recurrent, distressing, and senseless forced thoughts and actions. The content of symptoms may reveal more about what is most important to or feared by an individual (e.g., moral rectitude, children in harm’s way) than why that particular individual developed OCD. Alternatively, the content (e.g., grooming and hoarding) may be related to the activation of fixed action patterns (i.e., innate complex behavioral subroutines) mediated by the brain areas involved in OCD.
In contrast to psychoanalysis, learning theory models of OCD have gained influence as a result of the success of behavior therapy. Behavior therapy does not concern itself with the psychological origins or meaning of obsessive-compulsive symptoms. The techniques of behavior therapy are built on the theory that obsessions and compulsions are the result of abnormal learned responses and actions. Obsessions are produced when a previously neutral object (e.g., chalk dust) is associated with a stimulus that produces fear (e.g., seeing a classmate have an epileptic fit). Chalk dust becomes connected with a fear of illness even though it played no causative role.
Compulsions (e.g., hand washing) are formed as the individual attempts to reduce the anxiety produced by the learned fearful stimulus (in this case, chalk dust). Avoidance of the object and performance of compulsions reinforces the fear and perpetuates the vicious cycle of OCD. The learned fears also begin to generalize to different stimuli. The fear of contamination with chalk dust may gradually spread to anything that can be found in a classroom, such as textbooks.
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 treatment has 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 Economo’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.