And in a 2004 academic paper, "" (PDF), Dr. Ahmed Okashasummarizes studies of OCD in the Moslem, Jewish, Christian, and Hindu religions.(Scanned images of the pages in this paper were very kindly E-mailed to me byKristie in 2005 - thank you!)
All types and ages of people can develop OCD, and it can play a large role in how you go about your daily life, and the daily stresses that you run into.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.