Introduction
Obsessive-Compulsive Disorder (OCD) is a common disorder that appears in both children and adults. It consists of obsessions, compulsions, or both. Obsessions consist of recurring thoughts or impulses that are intrusive and unwarranted by the environment (but still perceived as originating from the patients own mind, distinguishing them from “though-insertion”), causing distress or anxiety, and compulsions are repetitive behaviors the obsessive-compulsive feels he/she must perform. Compulsions are often related to the obsessions, and are meant to neutralize the distress caused by such obsessions. Some of the most common obsessions include germaphobia, fear of causing harm to oneself or to others, and worrying that important tasks have been left undone, for example being unsure whether one has locked the door, and compulsions include behavior such as hand washing, counting, and checking. The patient is usually aware of the absurdity of their thoughts and actions, but nevertheless feels powerless to stop them (American Psychological Association, 2000).
In this paper, I will discuss the neurocognitive findings regarding OCD, particularly as they relate to the SEC/OCD model proposed by Huey et al (2008). I will begin with an overview of some of the brain studies of OCD, moving on to some popular models of the disorder. Finally, I will discuss the SEC/OCD model.
The Brain Regions Implicated in OCD and their Functions
Despite copious amounts of research, the precise neuropsychology of OCD is uncertain (Markarian et al, 2010). Different studies often provide different and even contradictory results. Despite this, there are some generally agreed upon neuroanatomical features of OCD. Specifically, it has been consistently found that obsessive-compulsives reveal anatomical and functional abnormalities in the orbitofrontal cortex and the anterior cingulate cortex, and also the basal ganglia, prefrontal cortex, and thalamus (Markarian et al, 2010; Huey et al, 2008).
Several studies have reported reduced bilateral orbitofrontal cortex volumes in obsessive-compulsives, and there seems to be a correlation between greater reductions and worse symptoms (Maia, Cooney, & Peterson, 2008). The orbitofrontal cortex seems to be involved in reward learning and emotions, and the regulation of complex behavior. It has been found that the orbitofrontal cortex responds to reward stimuli, but not when the desire for the stimuli has been satiated. Macaques with orbitofrontal have difficulty learning the reward value of stimuli, and are slow to change their behavior when reward conditions change (Huey et al, 2008).
There is evidence of increased anterior cingulate cortex activation in obsessive-compulsives (Fitzgerald et al, 2005). The anterior cingulate cortex is implicated in decision-making. In particular, it acts as a conflict and error detector, responding when there is a discrepancy between expected and actual events. Activation of the anterior cingulate cortex seems to lead to negative emotional states, such as anxiety (Huey et al, 2008).
It has been found that damage to the basal ganglia through infection can lead to obsessive-compulsive symptoms. The basal ganglia seem to play an important role in the generation and regulation of motor activities. Specifically, it has been suggested that the basal ganglia acts as a sort of gate for motor signals, facilitating certain motor actions while suppressing others (Huey et al, 2008).
The thalamus shows higher activation in subjects with OCD compared to controls, and has been reported to be larger in obsessive-compulsives (Maia, Cooney, & Peterson, 2008; Huey et al, 2008)). The thalamus seems to be a gateway for interactions between brain areas involved in OCD (Huey et al, 2008).
Some Models of Obsessive-Compulsive Disorder
Based on behavioral and neuroanatomical evidence, there have been numerous models proposed for OCD.
The Cognitive-Behavioral Model: According to this model, OCD arises from dysfunctional beliefs regarding the importance of thoughts. Almost everyone has had intrusive thoughts that are perceived as inappropriate: for example, the fleeting, unwarranted, and unwanted mental image of stabbing a loved one with a knife. Healthy subjects recognize this as just meaningless junk in the stream of consciousness. However, obsessive-compulsives, according to the cognitive-behavioral model, incorrectly view these thoughts as highly significant—for example, as evidence that one will, in fact, lose control and stab someone. Because of the importance attached to these thoughts, they develop into obsessions, and compulsions arise as a way to attempt to get rid of these unwanted thoughts and/or neutralize the danger associated with such thoughts. These compulsions are then reinforced by the temporary reduction in anxiety they cause and the fact that they prevent the obsessive-compulsive from learning that harmful consequences will not arise as the result of their thoughts (McKay & Abramowitz, 2010). This model has gathered a lot of support (with some exceptions), but does not provide a neuropsychological explanation.
The Standard Model: The standard neuroanatomical model of OCD proposes that the disorder arises as a dysfunction of elements of a post-frontal cortex-basal ganglia-thalamic loop. This model is consistent with most of the data collected on the neuroanatomy of OCD and forms the basis of many following models. However, it does not explain the psychological mechanisms of OCD (Huey et al, 2008).
The “Feeling of Knowing” Model: Szechtman & Woody (2004) propose a model wherein OCD is caused by an inability to create the “feeling of knowing” that a task has been completed. Specifically, they argue that the common symptoms of OCD—washing, checking, fear of causing harm, etc.—are those that evolutionarily would have been related to the security of the organism and its fellows. This need for security leads to the evolution of a security-seeking system. Because there are no external stimuli that indicate the completion of a security-seeking task (for example, there could always a predator that the animal has missed), the completion of such tasks is indicated by an internally generated “feeling of knowing”. Obsessive-compulsives have a deficit in generating this subjective sensation, leading to the odd phenomena in which the obsessive-compulsive is perfectly aware, objectively, that, for example, their hands are perfectly clean, but they do not feel clean, leading to further washing.
The SEC/OCD Model
Huey et al’s (2008) model of OCD expands on Szechtman &Woody’s model and also on their own earlier work where they propose that complex behaviors with beginnings, middles, and ends are stored in the prefrontal cortex in the form of Structured Event Complexes, of SECs. For example, the knowledge of how to correctly eat dinner at a restaurant—finding a seat, ordering, eating, paying the bill, leaving—would be an SEC. SECs are usually implicitly recalled, and in this respect are similar to procedural memory. SECs are stored when a complex sequence of behavior leads to a reward, in order that such a sequence may be repeated. As evidence of these SECs, patients with damage to the prefrontal cortex have often reported difficulty with ordering and sequencing events and actions.
Just as the completion of an SEC can be rewarding, so too can the inability to complete an SEC can feel punishing. Furthermore, there are SECs that are themselves punishing but which bring about the removal of punishment: for example, few people feel good about doing their taxes, but most are relieved when their taxes are finally done.
In the SEC/OCD model, it is proposed that the initiation of an SEC is accompanied by a motivational signal, experienced as anxiety encouraging the animal to complete the SEC. In healthy subjects, the completion of the SEC is accompanied by a reward signal. According to the model, obsessive-compulsives have a deficiency in this latter process. Although the SEC is complete, the obsessive-compulsive does not have the sensation that it is done. This leads the anterior cingulate cortex to produce an error signal. The orbitofrontal cortex responds to this error as punishment, leading to a feeling of anxiety. This feeling is unconscious, leading the obsessive-compulsive to attempt to assign an explicit cause to it. This interpretation forms the basis of an obsession. The compulsion is caused by the fact that the completion of an SEC, for example hand washing, gives the obsessive-compulsives only partial relief, so that they feel they must repeat the SEC.
In regards to the basal ganglia, Huey et al suggest that just as it facilitates some motor actions while suppressing others, so too does it gate SECs. It is proposed that the basal ganglia sets thresholds for the activation of SECs, and when this threshold is lowered, for example by damage, it can lead to the overactivation of SECs, causing symptoms of OCD.
Conclusion
The cognitive neuroscience of OCD is still in its infancy. Much work is still to be done. However, Huey at al’s model provides a useful paradigm for further work. It shares and integrates elements from many of the previous models: along with expanding on Szechtman & Woody, it provides an explanation of why undue importance would be attached to fleeting thoughts as per the cognitive-behavioral model (the brain is looking for an explicit source of anxiety), and explains the possible psychological mechanisms of OCD that the standard model leaves out.
References
American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders: DSM-IV-TR, 4th ed Washington, DC: American Psychiatric Association Text Revision.
Fitzgerald, K., Welsh, R. C., Gehring, W. J., Abelson, J. L., Himle, J. A., Liberzon, I., & Taylor, S. F. (2005). Error-Related Hyperactivity of the Anterior Cingulate Cortex in Obsessive-Compulsive Disorder. Biological Psychiatry, 57(3), 287-294.
Huey, E. D., Zahn, R., Krueger, F., Moll, J., Kapogiannis, D., Wassermann, E. M., & Grafman, J. (2008). A psychological and neuroanatomical model of obsessive- compulsive disorder. The Journal of Neuropsychiatry and Clinical Neurosciences, 20(4), 390-408.
Maia, T. V., Cooney, R. E., & Peterson, B. S. (2008). The neural bases of obsessive- compulsive disorder in children and adults. Development and Psychopathology, 20(4), 1251-1283.
Markarian, Y., Larson, M. J., Aldea, M. A., Baldwin, S. A., Good, D., Berkeljon, A., & ... McKay, D. (2010). Multiple pathways to functional impairment in obsessive– compulsive disorder. Clinical Psychology Review, 30(1), 78-88.
McKay, D., Taylor, S., & Abramowitz, J. S. (2010). Obsessive-compulsive disorder. In D. McKay, J. S. Abramowitz, S. Taylor, D. McKay, J. S. Abramowitz, S. Taylor (Eds.) , Cognitive-behavioral therapy for refractory cases: Turning failure into success (pp. 89-109). Washington, DC US: American Psychological Association.
Szechtman, H., & Woody, E. (2004). Obsessive-Compulsive Disorder as a Disturbance of Security Motivation. Psychological Review, 111(1), 111-127.
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