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Cause of obsessive-compulsive disorder
The cause of obsessive-compulsive disorder is concerned with identifying the biological risk factors involved in the expression of obsessive-compulsive disorder (OCD) symptomology. The leading hypotheses propose the involvement of the orbitofrontal cortex, basal ganglia, and/or the limbic system, with discoveries being made in the fields of neuroanatomy, neurochemistry, neuroimmunology, neurogenetics, and neuroethology.
==Neuroanatomy==
Although there has been substantial debate regarding the assessment of OCD, current research has gravitated toward structural and functional neuroimaging. These technological innovations have provided a better understanding of the neuroanatomical risk factors of OCD. These studies can be divided into four basic categories: (1) resting studies that compare brain activity at rest in patients with OCD to controls, (2) symptom provocation studies that compare brain activity before and after incitement of symptoms, (3) treatment studies that compare brain activity before and after treatment with pharmacotherapy, and (4) cognitive activation studies that compare brain activity while performing a task in patients with OCD to controls.〔Maia, T. V., Cooney, R. E., & Peterson, B. S. (2008). The neural bases of obsessive-compulsive disorder in children and adults. Development and Psychopathology, 1251-1283.〕
Data obtained from this research suggests that three brain areas are involved with OCD: the orbitofrontal cortex (OFC), the anterior cingulate cortex (ACC), and the head of the caudate nucleus.〔 Several studies have found that in patients with OCD, these areas: (1) are hyperactive at rest relative to healthy control; (2) become increasingly active with symptom provocation; and (3) no longer exhibit hyperactivity following successful treatment with SRI pharmacotherapy or cognitive-based therapy.〔Whiteside, S.P., Port, J.D., & Abramowitz, J.S. (2004). A meta-analysis of functional neuroimaging in obsessive-compuslive disorder. Psychiatry Research, 132, 69-79.〕 This understanding is frequently cited as evidence that abnormality in these neuroanatomical regions may cause OCD.
The OFC and ACC are intricately connected to the basal ganglia via the cortico—basal ganglia—thalamocortical (CBGTC) loops.〔Alexander, G.E., DeLong, M. R., & Strick, P. L. (1986). Parallel organization of functionally segregated circuits linking basal ganglia and cortex. Annual review of Neuroscience, 9, 357-381.〕 Current theories suggests that OCD may be the result of an imbalance between the “direct” and “indirect” pathways through the basal ganglia. The direct pathways are described as running from the cortex to the striatum, then to the globus pallidus internal segment (GPi) and substantia nigra pars reticulate (SNr), then to the thalamus, and finally back to the cortex. The indirect pathways are described as running from the cortex to the striatum, then to the globus pallidus external segment (GPe), the subthalamic nucleus (STN), the GPi and SNr, then thalamus, and finally back to the cortex.〔Saxena, S., & Rauch, S. L. (2000). Functional neuroimaging and the neuroanatomy of obsessive-compulsive disorder. Psychiatric Clinics of North America, 23, 563-586.〕 While the net effect of the direct pathway is excitatory, the net effect of the indirect pathway is inhibitory. Thus, it has been hypothesized that excessive relative activity in the direct pathway in OFC/ACC CBGTC loops may result in a positive feedback loop whereby obsessive thoughts are trapped.〔 Although structural and functional neuroimaging studies have provided a strong basis for this supposition, it is still unclear why patients with OCD develop specific obsessions instead of a generalized obsessive behavior towards everything. While researchers have suggested that a response bias exists toward particular stimuli, such as contamination, the underlying cause is still unclear.〔Sasson, Y., Zohar, J., Chopra, M., Lustig, M., Iancu, I., & Hendler, T. (1997). Epidemiology of obsessive-compulsive disorder. Seminars in Clinical Neuropsychiatry, 6, 82-101〕
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