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Obsessive-Compulsive Disorder (OCD) is an Axis I Anxiety Disorder in the American Psychiatric Association’s (APA) Diagnostic and Statistical Manual of Mental Disorders–Fourth Edition (DSM-IV). The primary diagnostic criteria are the existence of obsessions or compulsions, some degree of recognition of the irrationality of the behavior, and significant interference with everyday functioning. This article provides an up-to-date summary of the state of knowledge regarding obsessive-compulsive disorder.

OCD Research Paper Outline

I. Diagnosis and Symptoms

A. Epidemiology and Clinical Course

B. Comorbidity

II. Family and Patient Characteristics

A. Family Factors

B. Cognitive Characteristics

C. Information Processing in OCD

III. Theory and Treatment

A. Behavioral Models

B. Behavioral Treatments

C. Cognitive Models

D. Cognitive Treatments

E. Biological Models

F. Biological Treatments for OCD

IV. Future Directions

I. Diagnosis and Symptoms

Obsessions are recurring and persistent thoughts, images, or impulses that are experienced as intrusive, distressing, and, at least at times, unreasonable. Responding to these experiences, the individual may “neutralize” them, using some ritualistic thought or action, or attempt to ignore or suppress them. These repeated behaviors or mental acts are undertaken to relieve anxiety provoked by the obsessions and are called compulsions. Compulsions are usually applied rigidly or excessively. From the patient’s perspective, they restore safety or prevent a dreaded event. The intent of the compulsion is often hidden from the casual observer or even close family members. These symptoms consume at least an hour a day and interfere with the person’s normal activities. The symptoms of OCD are relatively common in the general population, but are not usually severe enough or do not interfere enough to meet diagnostic criteria. The content of clinical obsessive intrusions differs little from ordinary intrusive thoughts experienced by most people, but the former provoke much more anxiety and are more difficult to dismiss.

The content of obsessions and compulsions vary considerably from patient to patient, sharing only the disturbing nature of the intrusions and the ritualistic efforts to neutralize the obsessions. Often, patients report more than one type of obsession and ritual, and sometimes the content of the obsession or compulsion changes (e.g., cleaning to checking). The most common compulsions are checking rituals, which are usually designed to prevent catastrophes like fire, burglary, causing someone harm, or embarrassing oneself. Also common are washing rituals, which serve to remove “contamination” or “dirt” and thereby prevent a feared disaster (e.g., disease). Other common compulsions include repeating compulsions or magical rituals in which ordinary actions (such as crossing a threshold or lifting an object) are repeated to prevent harm from occurring (e.g., a loved one dying in an accident). Less common are ordering rituals, which involve arranging objects to produce symmetry or balance, and hoarding, the acquisition of and failure to discard seemingly useless objects like old magazines and receipts or empty containers.

The APA’s DSM-III defined obsessive-compulsive disorder (OCD) not only by the obsessions and compulsions, but by patients’ recognition of the irrationality of obsessions. Individuals who did not recognize the irrationality of their thoughts were considered either psychotic or “overvalued” in their ideas about the obsessions. Recent research demonstrates that patients vary on this characteristic from complete awareness to complete lack of awareness of the rationality of the symptoms, with most having at least some insight. This criterion has changed somewhat in DSM-IV in that patients must have insight at least at some point in the disorder. DSM-IV added a category of “poor insight” for patients with OCD who do not recognize the unreasonableness of their behavior.

Diagnostically, obsessions can be distinguished from symptoms of generalized anxiety disorder and hypochondriasis in that they are mental experiences that are not merely excessive worries about real-life problems (e.g., finances, family well-being, health, etc.). Also, obsessions are different in character from the guilty or depressive ruminations characteristic of people with major depression. Preoccupations with food, alcohol, drugs, gambling, and buying are readily distinguishable from obsessive fears of contamination, causing harm, preventing danger, and other anxiety-provoking concerns and rituals. The former symptoms are all appetitive preoccupations, while obsessive fears generally involve avoidance or escape responses.

A. Epidemiology and Clinical Course

Epidemiological studies of community samples estimate the annual and lifetime prevalence rates to be considerably higher than previously thought (annual, 0.8 to 2.3%; lifetime, 1.9 to 3.3%). Prevalence rates in this range have been replicated in a variety of studies throughout the world. While some studies have shown a slightly higher percentage of women than men with OCD, other studies have failed to find this difference. When examining childhood onset of OCD, however, males outnumber females by up to 2 to 1. For males, the mean age of onset is 14 to 19 years, while for females it is 21.7 to 22.0 years. Most patients develop symptoms before age 25 (65%), and only a small number (15%) develop symptoms after age 35. Patients typically wait 7 to 8 years after the onset of symptoms before seeking treatment. While 40% of those with OCD can identify no clear precipitant, some research suggests that changes in life roles and demands (i.e., pregnancy, childbirth, etc.) may be precipitants.

Recent prospective studies of the course of OCD indicate that despite significant advances in treatment, most OCD patients (at least 75 %) remain at least partially symptomatic over the long term. Between 43% and 75% of treated patients remain at least partially improved 2 to 5 years after treatment. Despite limited research on prediction of treatment outcome, mild or atypical symptoms, a short duration of symptoms, and a good premorbid personality appear to predict a good outcome. On the other hand, early onset in males, symmetry or exactness-related symptoms, symptoms of hopelessness, delusions or hallucinations, a family history of OCD, and the presence of tics suggest a poor prognosis.

There is some indication that the expression of OCD symptomatology is at least partially influenced by cultural factors. Similarities exist between OCD rituals and religious or cultural rituals, and certain religious practices are associated with OCD symptomatology. Culture-specific beliefs, as illustrated by koro (a fear of penile shrinkage found exclusively in Chinese cultures), also suggest the influence culture has on the expression of OCD symptoms. However, while these cultural variables may influence the symptom expression in OCD, there is little evidence to suggest they contribute to the development of the disorder. There is also little evidence to suggest that race or socioeconomic status are associated with OCD, although at least one study suggests that African-Americans may present with more severe OCD symptomatology. Given the lack of research in this area, however, any such conclusions must be tentative. Furthermore, different patterns of help-seeking among minority populations may mask potential differences between minority and nonminority groups.

B. Comorbidity

Comorbidity of OCD with other disorders is as high as 60% or more. Anxiety disorders, depression, alcohol abuse (dependence), eating disorders, Tourette’s syndrome, body dysmorphic disorder, hypochondriasis, and schizophrenia have all been found to be associated with OCD. Comorbidity with anxiety disorders is quite high, ranging from 25 to 60%, with the highest frequencies for specific phobias, followed by social phobia and panic disorder. Comorbidity and family study data have led some to suggest that OCD patients share a general genetic vulnerability with anxiety disorders.

There may be a shared vulnerability for various forms of depression as well, with studies indicating concurrent prevalence rates of 12 to 80%. At least one third of patients with OCD report histories of clinical depression, although 25 to 33 % do not report depression. An important question concerning the relationship of OCD and depression is whether the depression that accompanies OCD is primary or secondary. The majority of patients report an onset of depressive symptoms that occurred after the onset of OCD, and several investigators have found that successful treatment of OCD resulted in the reduction of depressive symptoms.

Despite a wide range in the degree of insight shown by OCD patients, OCD is relatively rarely accompanied by schizophrenia, although some research suggests a link. Patients with OCD may have more schizotypal traits and less cognitive inhibition than other anxiety disorder patients, similar to schizotypal and schizophrenic patients. Further research is necessary to test the hypothesis that obsessional thoughts (like schizophrenic thoughts) result from a failure in the cognitive inhibition of associations to ongoing stimulation.

Some impulse control disorders overlap with OCD and, consequently, they have been labeled as OC Spectrum Disorders. Tourette’s, Sydenham’s chorea, and other tic disorders have shown an association with OCD. One form of Tourette’s may be OCD-related and some OCD cases are Tourette’s-related. This has led to speculation that OCD and Tourette’s may be different expressions of a similar underlying genetic abnormality, for example, of the basal ganglia-frontal cortex pathway. Some investigators report associations between OCD and kleptomania, as well as exhibitionism. These reports are suggestive enough to warrant closer examination of a possible link with obsessive and compulsive symptoms.

As mentioned earlier, if the content of obsessions or compulsions concerns primary symptoms of eating disorders, body dysmorphic disorder, or hypochondriasis, a diagnosis of OCD is ruled out. In each of these cases, similarity of symptoms, comorbidity evidence, and response to treatment suggest that these disorders are closely related to OCD. Some have even suggested that they are actually forms of OCD.

Studies of comorbidity of OCD with Axis II disorders reveal that over one half of patients with OCD have at least one diagnosable personality disorder (PD). Unfortunately, the evidence fails to provide any clear indication of which co-occur most frequently. Despite its name, obsessive-compulsive personality disorder is no more closely related to OCD than avoidant, dependent, histrionic, or several other personality disorders. One observation from this literature deserves comment. Antisocial personality disorder often has the smallest overlap with OCD, which may reflect the importance of beliefs about excessive responsibility in patients with OCD. Questions remain about the role of personality disorders in OCD, as some evidence suggests that PD symptoms decline with successful treatment of OCD.

II. Family and Patient Characteristics

A. Family Factors

Although marital satisfaction among OCD patients resembles that of the general population, OCD patients (especially males who have an early onset) have higher celibacy rates than the general population. When OCD symptoms occur within a family context, family members often involve themselves in the rituals or avoidance behaviors of the patients. In families where households are restructured to adapt to OCD symptoms, greater family dysfunction and negative attitudes toward the patient have been observed.

A number of parental characteristics have been hypothesized to play a role in the development of OCD. The parents of OCD cleaners are hypothesized to be overcontrolling and overprotective and may model excessive cleaning behaviors. Parents of checkers are hypothesized to set higher standards for their children, to be overcontrolling and overcritical, as well as modeling meticulousness. Numerous cases report similar characteristics in the parents of OCD patients, including demanding or critical attitudes, overprotectiveness, perfectionism, and rejecting attitudes. Despite the frequency with which these characteristics have been informally observed, systematic research comparing parents of OCD patients and controls has been limited. A small number of controlled studies on this issue support the existence of these characteristics in the parents of OCD patients. In particular, parents of OCD patients and/or subclinical obsessive compulsives have been found to be overprotective, critical, perfectionistic, and risk aversive. In addition, the families of OCD patients show higher levels of expressed emotion (criticism and overinvolvement) than families of controls.

Clinical observation and preliminary evidence on these issues suggest that the parents of people who develop OCD are more likely to show a constellation of behaviors, including perfectionism, overprotectiveness, overcritical and demanding attitudes, and high levels of risk avoidance. Further research must establish that these characteristics are more prominent in the families of OCD patients than in controls; then, the question of their role in the development of the disorder can be addressed.

B. Cognitive Characteristics

Patients with OCD display a number of cognitive characteristics to a greater degree than other people. International experts have identified at least six such characteristics as being very important in OCD. These include overestimation of risk, excessive responsibility, controllability, overimportance of thoughts, intolerance of ambiguity, and perfectionism.

In the early 1970s, it was first noted that patients with OCD exaggerate the probability and severity of negative outcomes. Clinical and empirical studies indicate that people with OCD are risk-aversive, that is, they are less likely to engage in behavior that they consider risky. Threat overestimation can be defined as the exaggeration of the probability or severity of harm believed to result from or follow intrusive internal experiences.

A second widely noted cognitive characteristic is an exaggerated sense of responsibility for harm that might befall oneself or others. Some investigators have argued that exaggerated responsibility is central to OCD. According to recent work on this issue by Salkovskis and others, obsessional responsibility refers to the belief that one has power to bring about or prevent subjectively crucial negative outcomes that may be actual (having real consequences) and/or moral.

In normal cognitive processing, irrelevant and intrusive thoughts are simply ignored, whereas in cognitive processing by people with OCD these thoughts are attended to, believed important, and attempts to suppress them are undertaken. Efforts at suppression typically provoke a paradoxical increase in the intrusions and associated discomfort. When efforts to suppress these thoughts fail, sensitization and vigilance to similar thoughts occurs, and this process escalates into an obsessional pattern. Individuals with OCD appear to have a need for control, which can be defined as an overvaluation of the importance of exerting complete control over intrusive thoughts, images, and impulses, and the belief that this is possible and desirable. Such efforts at control are hypothesized to be evident in hypervigilance for mental events, in a moral attitude toward control as a virtue, and in feared psychological and behavioral consequences of the failure to control thoughts.

People with OCD may believe that simply having an unwanted, objectionable thought is morally equivalent to engaging in the objectionable act, a form of moral “thought-action fusion.” Furthermore, when OCD patients imagine negative events, they may come to believe that the events are more likely to actually occur. Recent research on thought-action fusion supports the importance of this construct. Overimportance of thoughts can be defined as a belief that the mere presence of an intrusive thought gives it significance. Related to this concept are possible problems that people with OCD have with Cartesian reasoning and magical thinking.

Doubt about the veracity of one’s experience and the need for absolute certainty are commonly noted features of OCD. Some suggest that doubt stems from a belief that every situation has a perfect solution and the person with OCD will not feel comfortable unless that perfect solution is found. Others have suggested that because of their need for certainty, OCD patients repeat actions in an attempt to achieve perfect certainty. Such doubt may be central to the indecision seen in people with obsessive-compulsive tendencies. Intolerance for ambiguity is evident in obsessional beliefs about the necessity of being certain, about poor capacity to cope with unpredictable change, and about inadequate functioning in situations that are inherently ambiguous.

Perfectionism has been closely linked to OCD in both theory and clinical descriptions of the disorder. Recent research has found higher levels of perfectionism among OCD-diagnosed populations, as well as nonclinical populations, that exhibit obsessive-compulsive tendencies. Although it appears that high levels of perfectionism also characterize other disorders (e.g., social phobia, depression, and eating disorders), it appears to be important in shaping the course of OCD, and consequently international experts consider it a key cognitive component.

C. Information Processing in OCD

Several information processing capabilities, including memory, categorization, and attention, have been hypothesized to distinguish OCD patients from nonpatients. Four types of memory deficits have been hypothesized: (a) memory for actions, (b) general memory, (c) confidence in memory, and (d) reality monitoring (distinguishing actual from imagined actions). Among subclinical compulsive checkers, several studies reported deficits in memory for actions performed. Among clinical patients, this finding is less consistent, however, with one study supportive and another failing to replicate. Similar findings have emerged for general memory deficits. Nonclinical subjects showed poorer overall memory functioning, whereas findings for clinical patients were mixed, although most studies reported poorer memory functioning, especially with regard to visual memory. One consistent finding in this literature has been the lowered confidence in memory capacity shown by OCD subjects. No reality-monitoring deficits have been found.

Related to memory dysfunction in OCD, some argue that OCD patients also fail to categorize and integrate information properly. They categorize in an underinclusive way, such that many small categories are generated with narrow boundaries and overspecifled rules for category membership. Some clinical, as well as empirical, research supports this hypothesis. Because of a failure to recognize proper category boundaries, OCD patients create artificial structures that become rituals to determine the proper end of a sequence of behaviors.

A related hypothesis suggests that OCD patients fail to adequately inhibit irrelevant stimuli during normal processing, interfering with their focus on relevant stimuli. Consequently, processing ordinary information requires more conscious effort and active suppression of irrelevant or unwanted thoughts. A similar attention or cognitive inhibition deficit is hypothesized to characterize schizophrenia and schizotypal personality disorder. Several studies support this hypothesis having used a negative priming paradigm.

Another approach to studying attentional processes in OCD involves the use of the Stroop Color Word test. Subjects watch fearful and nonfearful words presented in different colors and are asked to name the color of the word. Fearful word meanings should be harder to inhibit and naming the color in which they are printed should take longer. Indeed, some studies have found that OCD washers take longer to name contamination words than neutral words, and that non-OCD patients do not. In other studies, OCD subjects have been found to attend selectively to negative OC-related words (e.g., disease, disaster) but to not show an attentional bias toward positive words (e.g., clean, precise). In another test of attentional processing, it has also been reported that after successful treatment, OCD patients no longer showed attentional bias toward contamination items in a dichotic listening task.

The research on memory and OCD provides some confirmation of deficits in memory for actions, general memory, decreased confidence in memory functioning, problems with overspecification in categorization, and problems in inhibiting attention to irrelevant information and in attending to relevant information. The findings fail to support any difficulties in distinguishing actual from imagined actions. Specific causes for these deficits will require further research.

III. Theory and Treatment

This section reviews the three major theoretical models for the development and maintenance of OCD and the treatment methods derived from these models, and summarizes evidence for the effectiveness of these treatments.

A. Behavioral Models

Early behavioral treatments for OCD (thought stopping, aversion therapy) were based on contingent reinforcement and punishment models and worked for only a limited number of patients. Efforts to use conditioning models alone (e.g., systematic desensitization) improved the situation only slightly. In the early 1970s, a refinement in the conditioning model led to the development of a more promising treatment. Exposure and response prevention (ERP), the standard and most effective of the behavioral techniques, is derived from the two-stage theory of fear and avoidance.

The first part of the two-stage theory posits that an otherwise neutral event acquires the capacity to provoke fear because of its pairing with an aversive stimulus, much as a dog phobia might develop in someone who has been bitten. While this can account for the onset of a number of cases, there is evidence that it does not account for all. Many patients cannot recall conditioning experiences associated with symptom onset. Also, although onset often follows stressful life events, it rarely does so immediately, as would be expected by the traumatic onset theory. Modifications of the acquisition portion of the two-stage theory suggest that stressful events sensitize some individuals to cues that have an innate tendency to elicit fear, were learned during early traumatic experiences, or have special cultural significance. Observational or informational learning also seems to account for the onset of some cases of OCD, particularly when patients report that their symptoms resemble their parents’ behavior.

In the second stage of this model, compulsions or escape/avoidance behaviors provide relief from the obsessional anxiety or discomfort. This relief negatively reinforces the compulsions. Thus, the frequency of compulsive actions increases in future situations, which triggers an obsessional concern. Both external cues (objects or situations) and internal triggers (thoughts, images, or impulses) serve as fear stimuli and can produce obsessional discomfort. Many of these cues or triggers cannot be avoided (e.g., closing the front door when leaving the house). Therefore, the passive avoidance which allows phobics to manage their fears is often insufficient to control anxiety for those with OCD. More active strategies like compulsive behaviors are needed to prevent harm or restore a feeling of safety.

Substantial evidence supports a behavioral account of OCD in which obsessions increase discomfort and compulsions reduce it. Obsessive thoughts increase heart rate and skin conductance more than normal thoughts, and contact with contaminants increases subjective and physiological anxiety reactions. In most instances, compulsions reduce anxiety in the short run. Although this model clearly accounts for the maintenance of OCD symptoms, it does not adequately account for many instances of onset, and expansion of this theory is necessary.

B. Behavioral Treatments

Treatment strategies based on the behavioral model attempt to disconnect obsessions from the associated discomfort and to eliminate rituals that prevent habituation of obsessional fears. Behavioral treatment for obsessions and compulsions involves exposure to overt and covert cues that provoke obsessions, followed by prevention of the compulsion. Because compulsions interfere with habituation of the negative mood generated by obsessions, blocking the rituals prevents the premature reduction of fear. This program of ERP has been widely studied and has been found to be highly effective.

Exposure and response prevention was developed by British researchers in the early 1970s to treat hospital patients who feared contamination and performed washing rituals. In the first attempt to use ERP, daily direct contact with contaminants and complete prevention of compulsions (turning off the plumbing in patients’ rooms, having nurses observe all washing) resulted in 10 of 15 patients being much improved or symptom-free, and the remaining 5 being moderately improved. After 5 to 6 years, only 2 patients relapsed. Since then, approximately 30 open trials and controlled studies, representing more than 600 patients with OCD, have reported good outcomes with ERP and its variants.

Numerous studies have shown that using from 10 to 20 sessions of ERP produces significant improvement in symptoms. After ERP, approximately 55% can be labeled “much” or “very much” improved, indicating that target symptoms improved by more than half; approximately 85 % show at least some degree of improvement. Improvement rates remain high at follow-up, with 50% of patients still in the “much” or “very much” improved categories and 75% in the “improved” category.

With regard to the amount of symptom improvement, the average degree of benefit from ERP ranges from 40 to 75 %. At follow-ups ranging from 3 months to 6 years, treatment gains remain high, in the 45 to 70% range for target symptoms. The degree of benefit and the consistency of ERP results from multiple treatment sites and countries are quite impressive and clearly indicate that exposure and response prevention is an effective intervention.

Support for the behavioral model from which ERP is derived can be found in studies examining the separate effects of exposure and response prevention on obsessions and compulsions. According to behavioral theory, exposure should reduce anxiety associated with obsessions, while response prevention should influence rituals more than obsessions. Several case series provide support for these hypotheses. When delivered independently, exposure reduces subjective anxiety more than rituals, although both decline. Response prevention reduces rituals more than it does obsessions. When exposure and response prevention are both given, patients show maximum improvement in symptoms.

Foa and Kozak suggested that ERP allows for the processing of emotional information which is prevented by compulsions. Compulsions circumvent this processing by allowing the patient to escape from a fearful situation before they have had a chance to habituate to it. These theorists hypothesize that fear-related memories are stored in fear structures that are activated by exposure to a fear stimulus. In the case of OCD, this may include any stimulus that prompts an obsession. Fear activated by exposure will dissipate unless neutralized by a compulsion. Exposure and response prevention activate the fear structure causing the patient to experience anxiety. When the ritual is prevented, habituation of anxiety will eventually occur. If habituation occurs within a session, then the fear structure is weakened and initial response to exposure should be lower at subsequent sessions. The new emotional information processed within such a session contains information about habituation, coping with anxiety, and so on, which is incompatible with a “fear” structure and therefore weakens the OC fear. Several parts of this process have been supported by research. As predicted by this model, attention-focusing instructions are associated with more anxiety during exposure and better habituation, whereas distracting instructions reduce initial anxiety and subsequent habituation, leading to poorer outcome. Therefore, standard clinical practice should focus attention on the exposure situation and avoid distracting conversation that might interfere with the processing of fearful information.

Traditional ERP has been supplemented by varying the procedure to enhance benefits and reduce the cost of the treatment. Several investigations have found that imagery-based exposure is as effective as in vivo exposure. Furthermore, some evidence suggests that imaginal exposure may work better for patients with checking compulsions, perhaps because their fears can be more easily accessed by imagery. Other variants that have shown some promise include the use of therapist modeling and varying the duration of treatment and the spacing of ERP sessions. Additionally, several studies have found that self-controlled treatment is as effective as therapist directed, and may produce more durable gains. Recently, a number of self-help books have been published with background information and instructions to help in setting up self-directed ERP. Preliminary findings from one study suggest that using self-help texts can lead to significant improvement. Although it may be too early to tell whether completely self-directed ERP is effective, it may represent a significant development in the treatment of ERP.

Another recent advance in the application of modified versions of ERP is group administration. Only one controlled trial of group ERP has been reported in the literature, however. This study compared group ERP, with or without imagined exposure, to comparable individual treatment and to an individual relaxation control treatment. After 12 weeks, both exposure treatment conditions showed significant improvement in OCD symptoms, while the control group did not. Average posttest Yale-Brown OC Scale (YBOCS) scores fell below the clinical range. The group treatment led to changes comparable to those of individual therapy, although group benefits occurred somewhat more slowly. This study demonstrates the potential for group administration of ERP.

Several researchers have suggested the use of support groups for patients and family members. Some have used open-ended monthly group meetings for family members and patients to discuss the effect of OCD on the family and to plan coping strategies and rehearse behavioral exercises. Other reports have outlined psychoeducational groups for families that include sessions on diagnosis, assessment, theories of OCD, behavioral treatment, medications, and prevention of relapse. Goals for such groups include improving self-esteem, sharing feelings and experiences, accepting patients’ realistic limitations, and learning strategies for coping with OCD symptoms. Most of these studies reported high participant satisfaction, but no outcome data.

Further developments along these lines include using family members as treatment assistants. Evidence that spouse assistance in exposure treatment improves outcome, at least in the short run, has been reported by some investigators, although more research is needed to clarify the amount of added benefit over individual treatment. It appears that involving spouses and other family members in ERP leads to significant gains in OCD symptoms, mood state, and social and occupational functioning compared with unassisted treatment. Furthermore, family-treated patients continue to improve after treatment. Some studies suggest that nonanxious, consistent family members are more successful in providing support and supervision than anxious and inconsistent members, especially those who engage in argument and ridicule. Similar programs that teach relatives to reduce their involvement in rituals and to encourage self-exposure in noncritical ways have been found to be successful. Symptom decreases of 45% at discharge and 60% at 6-month follow-up indicate good success with family member involvement. Substantial reductions in YBOCS scores among patients in multiple family therapy groups that included spouses/partners, parents, and other relatives have been reported. The reductions are still significant 1 year later.

Research on predictors of success with ERP has failed to reveal consistent trends. Sex, age of onset, symptom severity, and duration have generally not been found to predict success in ERP. However, severity of avoidance behavior may be associated with poor ERP outcome. Some research also suggests that comorbid personality disorders, especially schizotypal personality disorder, are associated with poorer outcome in ERP. Greater insight regarding obsessions has been associated with positive ERP outcome in some studies, but not in others.

The studies on group, self-directed, and family-assisted behavioral treatments guide the way for the future of OCD treatment. Cost-effective applications of the behavioral treatments known to work for OCD are sorely needed. Further research in these areas is vital.

C. Cognitive Models

Models emphasizing the appraisal of threat form the backdrop for most of the cognitive theories of OCD. These models involve a two-step process. Identification of a potentially harmful situation (primary appraisal) creates an initial state of apprehension, and a secondary appraisal (of one’s ability to cope with the threat) determines whether the anxiety will rise or decline. As noted earlier in discussing cognitive characteristics of OCD, obsessive-compulsive patients are thought to make abnormally high estimates of the probability of bad things happening to them. That is, they anticipate danger or misfortune more readily than nonobsessionals and may believe in the need to be concerned about danger and to dwell on its possible occurrence in order to protect themselves. This overestimation of threat is part of an inaccurate appraisal process which contributes to the development of OCD. From a cognitive perspective, several types of beliefs or assumptions contribute to inaccurate appraisal. These include beliefs described by rational emotive therapists (RET) and by other cognitive theorists. Perfectionistic beliefs may take the form that one should be thoroughly competent, adequate, and achieving in all possible respects (i.e., perfect) to consider oneself worthwhile and to avoid criticism, and that perfect solutions to all problems are available and should be found. Other hypothesized OCD beliefs include the notion that making mistakes or failing to reach one’s ideals is unacceptable and should result in punishment, that one has the power to prevent disastrous outcomes by magical rituals, and that certain thoughts and feelings are unacceptable. Related to the cognitive features described earlier is the need for certainty to avoid criticism and reduce risk. Coping with threats generated by these beliefs is thought to be difficult for people with OCD. These early theories are similar with respect to the role and content of specific irrational beliefs, although they have been largely subsumed by more recent cognitive theorizing.

The most prominent cognitive theory of OCD was proposed by Salkovskis in 1985. He drew heavily from Beck’s cognitive theory of emotional disorders. Salkovskis noted that extensive research shows that intrusive cognitions are normal phenomena experienced by more than 90% of the population. What distinguishes people with OCD is not the experience of intrusive thoughts, but the way in which their occurrence and content are interpreted. People with OCD give special importance to their intrusions, whereas people not suffering from OCD simply ignore them. According to Salkovskis, the reaction to negative intrusive experiences in people with OCD depends on a set of underlying beliefs. These beliefs are characterized by an exaggerated sense that one is responsible for harm to oneself or to others and that one must act to prevent it. The OCD patient seeks to reduce the discomfort produced by these thoughts by engaging in neutralization (i.e., compulsion, suppression, or avoidance). The first step in the process is an appraisal of an intrusive thought as an indication that they are in some way responsible for harm or its prevention. In the second step, this appraisal elicits neutralizing behavior (overt or covert). If negative appraisal occurs without the appraisal of responsibility, neutralization will not take place and the result will be anxiety and/or depression, but not OCD. Thus, the core assumption of this model is that OCD symptoms are efforts to neutralize or ameliorate the appraisal of responsibility for harm.

Neutralization includes overt behaviors (washing, checking, etc.) as well as mental events, attempts to put things right, thought suppression, and reassurance seeking. Salkovskis suggests that neutralization effectively reduces the level of perceived responsibility in the short run, but increases the probability of intrusive thoughts in the longer term.

Research on the nature and measurement of obsessional responsibility, as well as experimental manipulations of responsibility, lend support to this theory, but there have been suggestions for modification. It has been proposed that in this theory, more emphasis should be given to dysfunctional beliefs about controlling thoughts and the costs of not doing so, as well as to the effect of depression in impairing the ability to control thoughts. Theorists also suggest that neutralization may develop only when other thought control efforts fail.

An alternate cognitive theory of OCD proposed recently is quite different from the appraisal model that has characterized previous cognitive theories. This model focuses on the inference process. It suggests that people with OCD do not react to an actual feared stimulus nor to its perceived consequences. Instead, they react to what they imagine might be there despite a lack of sensory evidence to support the belief. In this model, a faulty inference process is responsible for OCD beliefs. Rather than forming an hypothesis about an obsessional fear (the table is dirty) and testing it (feeling the table), the person with OCD changes the evidence to fit the hypothesis (the table must be dirty because I can imagine it dirty). The rituals are attempts to change this “fictional narrative” by changing what is real. The reliance on superstition, or on magical or pseudoscientific justifications for obsessional beliefs also reflects attempts to make the reality fit the fiction. This theory is quite interesting and deserves further research.

Although early cognitive treatments for OCD were not derived from these cognitive conceptualizations, more recently developed treatments have been. In particular, the use of rational emotive therapy (RET) and Beckian cognitive therapy tailored specifically for OCD have been investigated. Although still in the early stages of testing, these treatments show great promise.

D. Cognitive Treatments

Some investigators have observed cognitive changes after ERP treatment, especially with respect to the overestimation of risk. They suggest that ERP may reduce the overestimation of risk experienced by people with OCD. If exposure-based treatments can change cognitions associated with OCD, and if, as is suggested by the cognitive theories just reviewed, these cognitions are important components of the disorder, then perhaps other ways of changing cognitions exist. The assumption underlying cognitive therapy is that changing cognitions will lead to reductions in OCD symptomatology. Early studies of the effects of cognitive therapy on OCD were hampered by the fact that the therapies were generic and not specifically tied to OCD cognitions. Not surprisingly, these treatments were not very successful. Subsequent studies in which the cognitive therapy was tailored to OCD have met with considerably more success.

Several studies have compared RET focusing on OCD beliefs with self-controlled ERP. Both treatments led to substantial improvement in patient symptoms and RET was superior to ERP in improving mood. In subsequent studies, comparable improvement for RET and ERP treatments was seen among patients randomly assigned to treatment type and RET was also associated with a greater decline in irrational beliefs.

The other cognitive treatment model used in treating OCD is Beck’s cognitive model, in which faulty beliefs are identified, examined, and challenged. Case studies of the application of this type of therapy have been promising. Alternating cognitive therapy with response prevention resulted in improvement in a suicidal adolescent who previously refused exposure. Others have reported that this form of cognitive therapy altered unrealistic beliefs in a case with overvalued ideas. Furthermore, another investigation found that this type of therapy–focusing on excessive responsibility and without ERP improved successful in treating four patients with checking rituals.

The application of this model to OCD has been described by clinical researchers in the Netherlands and in Quebec, Canada. These researchers reported on two controlled trials that used this approach. The first of these studies compared cognitive therapy with exposure only in the context of behavioral experiments to an exposure-alone group. Both treatments resulted in substantially improved symptoms at posttest and follow-up. There was a trend for more favorable outcome for cognitive therapy, but the results were comparable to findings reported by others using ERP. A second study found cognitive therapy plus exposure significantly better than a waiting-list control for 29 obsessional ruminators. The treatment was successful for 85 % of the patients and the gains were maintained at 1-year follow-up.

Although to date only a small number of studies have been completed, cognitive therapy for OCD shows clear promise with or without ERP. It may also help in the reduction of relapse after treatment. In order for cognitive therapy to develop, however, research must identify which cognitions to target and how best to measure them. Research on the six cognitive characteristics associated with OCD identified by international experts in the field is an obvious place to start this process.

E. Biological Models

The discovery of the effectiveness of serotonin reuptake inhibitors (SRIs) in treating OCD produced a surge of speculation and theory about a biological basis for the disorder. Positron-emission tomography (PET) and related technology have generated dramatic advances in our knowledge of the biology of OCD. Two types of explanations have emerged. Neuropharmacological explanations have focused on the role of the serotonergic transmission system, and neuroanatomical explanations have concentrated on the orbitofrontal cortex, the basal ganglia, and their connections. These two types of explanations are by no means mutually exclusive.

Studies of the effects of administering SRIs as a treatment for OCD constitute the most consistent evidence for a neurochemical explanation. The evidence clearly shows that treatment with SRIs reduces OCD symptoms (see the following treatment section). Although this provides strong evidence for the role of serotonin in the biology of OCD, drug response studies are not the best source of evidence for neurochemical processes.

Direct evidence of the role of serotonin in OCD comes from two types of studies. First, concentrations of known metabolites of serotonin (5-hydroxyindoleacetic acid: 5-HIAA)in the blood or cerebrospinal fluid provide peripheral markers of serotonin in the brain. Administration of serotonin agonists provoke serotonergic responses in people whose serotonergic system is dysregulated. These pharmacologic challenge studies provide a second direct way of testing the role of serotonin in OCD. Unfortunately, peripheral marker studies have been inconsistent in establishing the role of serotonin function in OCD. It is possible that compensatory mechanisms in the body mask peripheral markers that would indicate serotonin dysregulation. Although the effectiveness of SRIs in treating OCD suggest that patients suffer from a functional deficit in serotonin, surprisingly, pharmacologic challenge studies have suggested the opposite. Administration of serotonin agonists produce exacerbated OCD symptoms, suggesting that OCD patients have heightened sensitivity to serotonergic stimulation. Furthermore, administration of serotonin receptor antagonists reverses this effect. There is some inconsistency in the findings of these challenge studies, however. Neuroendocrine responses to pharmacologic challenge suggest a hyposensitivity, whereas behavioral responses suggest a hypersensitivity. This suggests that dysregulation of the serotonergic system is probable, but the nature of the dysregulation is not clear. A number of investigators suggest taking multiple transmitter systems into account in developing a more complex model of OCD.

The basal ganglia, frontal cortex, and the limbic structures which connect them have been the focus of anatomical models of OCD. The basal ganglia assist in the regulation of movement and cognitive functioning. Within the basal ganglia, the three structures that make up the corpus striatum (caudate nucleus, putamen, and globus pallidus) have been the focus of attention with respect to OCD. The volume of the caudate nucleus appears to be smaller in OCD patients than in controls, as measured by computerized tomography (CT) studies. Increased metabolic activity has also been observed in the caudate nucleus of OCD patients during rest. Other PET scan studies have found increased metabolic activity in the striatum during exposure among OCD cleaners, but reduced metabolic activity among OCD checkers. The latter finding may reflect the ability of checkers to engage in covert neutralization during the PET scan procedure. In any case, there is clear evidence of a striatal abnormality in OCD, but whether it is primary or secondary is not clear.

On the basis of evidence for basal ganglia involvement, some investigators postulate that OCD is a basal ganglia disorder. The function of the basal ganglia is to detect stimuli that activate fixed-action patterns and to allow their release. These fixed-action patterns are innate species-specific responses that are motor programs for action and take the form of grooming and safety rituals. The basal ganglia stores these programs and provides a gating mechanism for their release. In OCD patients, basal ganglia dysfunction allows the inappropriate release of fixed-action patterns (i.e., compulsive rituals).

Neuropsychological testing and electroencephalogram (EEG) studies suggest that deficits in frontal lobe functioning also play a role in OCD. In addition, PET scan studies and single-photon-emission computed tomography (SPECT) studies have shown increased metabolic activity in the frontal cortex of OCD patients compared with controls. Increased metabolic activity in response to provocative stimulation (obsessional rumination) has been found in OCD patients and in normal controls. This suggests that the mental activity associated with obsessional thinking can be localized in the frontal lobe. Furthermore, elevations in metabolic activity in the frontal lobes are no longer present after successful treatment with medication or behavior therapy. Based on this evidence and that of basal ganglia involvement, in 1992, Insel suggested a hyperactive cortical-striatal-thalamic-corticalcircuit in OCD. According to this theory, the caudate nucleus sends erroneous inhibitory signals to the globus pallidus. As a result, the globus pallidus fails to inhibit the thalamus from sending signals to the cortex. Thus, the cortex receives signals that it would not have received if the circuit operated normally. Further erroneous signals from the caudate nucleus inhibit the interruption of the circuit and messages continue to reverberate.

Baxter and colleagues suggested that the gating and screening activities of the striatum fail to inhibit impulses or thoughts that “leak” into consciousness and are experienced as obsessions. Fixed-action patterns (obsessions) occur automatically in response to obsessions and require effortful suppression and/or neutralization. This produces hyperactivity in the basal ganglia and frontal lobes. Similar models postulate a problem with the “comparator mechanism” in the limbic system or in the basal ganglia which matches sensory information with what is anticipated. When a mismatch occurs, arousal and corrective procedures are undertaken. A defective comparator mechanism might result in faulty evaluation of sensory input (i.e., hands feel dirty when they are not) and ineffective corrective action (washing hands to remove dirt that is not there). The dirt can only be felt but not removed.

There is strong evidence for frontal-striatal circuit involvement in OCD. The etiologic significance of this circuit is unclear, however. It may cause the disorder or may simply be the biological expression of it. Future research along these lines will clarify the mechanisms and roles of biochemical substances and structures in OCD.

Studies of genetic involvement in OCD have been inconsistent. Those using strict diagnostic criteria to define concordance have found only weak or inconsistent evidence for genetic transmission. Studies using subclinical OCD symptoms to establish concordance have found strong evidence of genetic involvement in OCD. However, some have suggested that what is transmitted is a diathesis for anxiety disorders rather than OCD specifically. Also along these lines, some researchers suggest that at least a subtype of OCD and Gilles de la Tourette’s syndrome are different phenotypic expressions of a common underlying genotype.

F. Biological Treatments for OCD

A substantial number of clinical and placebo controlled trials have now been conducted with the serotonin reuptake inhibitors, including clomipramine (Anafranil), fluvoxamine (Luvox), fluoxetine (Prozac), and sertraline (Zoloft). Qualitative and quantitative reviews of the treatment outcome literature generally conclude that all SRIs are effective in the treatment of OCD. Recent studies have also shown promise for a newer SRI, paroxetine (Paxil). At least moderate improvement occurs with SRIs in 55 to 70% of previously untreated patients. Although these drugs are also considered antidepressants, the SRIs appear to work for OCD patients whether or not they are depressed.

Meta-analytic comparisons among the SRIs show a preference for clomipramine, although at least one such study was equivocal on this issue. More large-scale direct comparisons of treatment efficacy are needed before drawing conclusions regarding differential effectiveness of these drugs. More research is also needed on the effects of method of administration. Intravenously administered clomipramine may work significantly faster than oral administration, as has been seen in several clinical series, and it may be effective for patients who do not respond to standard treatment. Dosage ranges have been partly tested for fluoxetine, with higher doses (up to 60 mg) producing better results, but additional research is needed to identify optimal dosage ranges for the SRIs.

Despite the effectiveness of SRIs in the treatment of OCD, there are some drawbacks to their use. Patients treated with SRIs show only a modest (30 to 60%) reduction in their symptoms, and a significant number (30% or more) show no improvement at all. While the side effects of newer SRIs are less severe than those of tricyclic antidepressants and clomipramine, they still represent a problem. The major side effects include sedation, sexual dysfunction, and weight changes. Although many patients may be willing to tolerate the side effects for the symptom relief they provide, these side effects can be a major cause of treatment dropout. Unfortunately, few studies report dropout or noncompliance rates for SRIs. In recent reports, from 10 to 27% of patients drop out of SRI treatment. Little information is available regarding relapse rates for the SRIs. Cessation of SRIs resulted in 89% and 90% relapse, respectively, in two studies. Relapse during continued SRI treatment has ranged from 18 to 23 %.

Predictors of treatment response have been examined in a recent multicenter trial of more than 500 patients. Only age of onset predicted outcome. Later age of onset was associated with better response to SRIs. Other research suggests that patients with schizotypal personality disorder respond poorly to SRI treatment for OCD. There is some evidence that augmenting SRI treatment with neuroleptics may benefit those patients with schizotypal personality disorder and comorbid tic disorders.

The development of sophisticated instrumentation, more precise lesion placement, and the increasing safety record make psychosurgery a viable treatment option for patients who have failed to respond to multiple medication trials and behavior therapy. Four types of such surgery are in use: cingulotomy, capsulotomy, limbic leucotomy, and subcaudate tractotomy. Few studies of psychosurgery outcome for patients who have failed to respond to medication or behavior therapy exist. One such study reported that 45% of cingulotomy patients who had failed at adequate trials of medication and behavior therapy were at least partial treatment responders. Reviews of the available literature have recommended cingulotomy as the first choice for psychosurgery with these patients. A newer method of psychosurgery, gamma knife, may also show promise for intractable OCD.

Few studies offer a direct comparison of behavior therapy, SRIs, or a combination of the two. The first such comparison, in the early 1980s, found greater average improvement with exposure treatment compared with clomipramine. In a later study, 75 to 80% of ERP patients improved compared with 22 to 23 % of clomipramine patients. The combination of clomipramine and ERP resulted in more subjects in the “much” improved category after 1 year (73%). Others have reported a slight advantage for the combination of fluoxetine and behavior therapy at 6 months, but after 1 year the effects are minimal. Preliminary results from a multicenter trial suggests that ERP alone may be more effective than clomipramine and the combination of clomipramine and ERP.

Reviews of combined ERP and SRI efficacy are hampered by the small number of studies using both treatments and by the inconsistencies in outcome measures. Nonetheless, they provide some pertinent information. In a comprehensive 1993 review, Abel concludes that ERP is more effective than clomipramine, especially in the treatment of rituals. For patients with severe depression, obsessions only, and overvalued ideas about obsessions, however, clomipramine appears to be more effective. While SRIs have the advantage of less time and effort by therapist and patient, ERP has fewer dropouts, side effects, and risks, and better maintenance. Meta-analytic reviews have provided additional information about comparative efficacy. These reviews have found behavioral and pharmacologic treatments equivalent, or that ERP alone and ERP in combination with medication were both more effective than SRIs alone, according to self-report measures. No differences among the treatments have been observed when assessor-rated measures were used. So far, no studies examining the efficacy of SRIs compared to or combined with cognitive treatments have been reported.

IV. Future Directions

Although our knowledge of the nature and treatment of this disorder is far greater than it was a decade ago, there remain significant gaps. For example, the level of insight into obsessions varies both between and within OCD patients. It is not yet understood how insight influences treatment or whether some treatments (e.g., cognitive therapy) can change insight. In addition to level of insight, other issues remain unsolved. A number of other disorders appear to be closely associated with OCD, including hypochondriasis, eating disorders, impulsive disorders, and more. Research is needed to identify the core overlapping features of these disorders.

There may be some utility to identifying subtypes of OCD. One subtype may be those with early onset (especially males), tics, and/or schizotypal traits. These patients have been found to respond poorly to treatment. Similarly, identification of cultural influences on symptomatology and treatment response is needed. The influence of family members on the maintenance of OCD symptoms also remains largely unexplored. Efforts to incorporate family members into the treatment process must be guided by such research.

Attempts to develop cognitive treatments for OCD developed out of the realization of the importance of belief structures and cognitive processing in the disorder. Progress in this endeavor depends on the conceptualization and measurement of these phenomena. Thoughtful progression from conceptual models to treatment strategies is needed to ensure that newly developed treatments will be effective. Cooperative investigation offers the potential for speeding this process along.

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