Level 1 Explanation:
When the brain gets mixed up information a person can end up thinking the same things over and over which makes them feel anxious. A certain part of the brain tries to calm down the anxiety by telling the person to repeat rituals and behaviors. When the anxiety is reduced it reinforces the behaviors and a cycle begins- this is what we call OCD.
Level 2 Explanation:
There are specific areas of the brain associated with OCD, primarily the Cingulate Gyrus, which is located in the limbic system; it shares brain structures such as the amygdala, hippocampus and hypothalamus. Here are some of the ways that the Cingulate Gyrus interacts with other brain structures in the limbic system:
Cingulate gyrus + Amygdala = Fear conditioning. Sensory stimuli are linked with emotions.
Cingulate gyrus + hippocampus = Building of memories and storage of memories.
Dysfunction in the Cingulate Gyrus has been associated with many disorders such as Schizophrenia, OCD, anxiety, and depression.
The interaction of brain structures in the limbic system combines fear, anxiety, sensory information and memory. When there is miscommunication and translation of information to these parts of the brain, it can lead to obsessive thoughts and compulsive behaviors which happen in a cyclical manner which is difficult for a person to break.
Level 3 Explanation:
Despite the wealth of research on OCD, we still seem to be having a problem with integrating the neuroanatomical and psychological research in order to come up with a comprehensive understanding of the disorder. What we can say for certain is that there is a biological aspect to OCD which has been determined through the use of various research methodologies.
Aouizerate et al. (2007) summarized that obsessions can be caused by the brain confusing common behavioral situations with mistakes or errors, leading to compulsions, which is the brain’s attempt to try to relieve the anxiety brought on by the ‘errors/mistakes.’ If anxiety is reduced by performing the compulsions, it acts as a reward and reinforces the behavior. This creates the cyclical nature of obsessive compulsive disorder that becomes difficult to control. The researchers concluded that the main areas of the brain associated with OCD are the orbitofrontal and anterior cingulate cortices. These areas have been linked to how humans evaluate motivational, emotional and environmental information, which they then relate to prior experiences leading to decision-making choices.
A study conducted by Huey et al. (2008), adds validity to these findings by introducing the theory that structured event complexes (SECs) play a role in OCD by storing memories of previous behaviors. In summary, they propose that when anxiety produces obsessive thoughts the brain uses compulsions in order to relieve the anxiety, which is done by repeating a structured event complex (SEC). Essentially, when a SEC successfully reduces the anxiety of an obsessive thought, it reinforces the SEC and will more than likely be repeated as a coping mechanism for that particular anxiety trigger.
McGovern & Sheth (2017) reviewed 89 structural/functional neuroimaging as well as electrophysiology studies; they concluded and confirmed that the anterior cingulated cortex (ACC) plays a major role in OCD. In particular they confirmed that the area is related to error/mistake negativity networks that have been suggested by other research. Figee et al. (2011) added that OCD can resemble addictive behaviors due to the rewarding feeling after the anxiety is reduced by compulsive behaviors. They also concluded that the nucleus accumbens (typically known as the reward circuit) activation was significantly reduced in OCD patients compared to control subjects, and this may indicate that OCD is a disorder of addictive behavior and reward processing.
It is clear that there is not one singular neurological explanation for why OCD occurs in some people, but the findings have repeatedly shown that areas of the brain related to memory, emotion, judgment and reward are major players in the development and maintenance of OCD behaviors. More research is needed to determine the effectiveness of treatment modalities (i.e. CBT) on OCD, and to assess how treatment can affect the neural circuitry associated with obsessive compulsive behaviors.
References:
Aouizerate, B., Rotgé, J.Y., Bioulac, B., Tignol, J. (2007) Present Contribution of Neurosciences to a New Clinical Reading of Obsessive-Compulsive Disorder. Encephale 33(2): 203-10. https://pubmed.ncbi.nlm.nih.gov/17675916/
Figee, M. et al. (2011) Dysfunctional Reward Circuitry in Obsessive-Compulsive Disorder. Biol Psychiatry. May 1; 69(9): 867-74. https://pubmed.ncbi.nlm.nih.gov/21272861/
Huey, E.D., et al. (2008) A Psychological and Neuroanatomical Model of Obsessive-Compulsive Disorder. Journal of Neuropsychiatry and Clinical Neuroscience. Fall 20(4): 390-408. https:/www.ncbi.nlm.nih.gov/pmc/articles/PMC4476073/
McGovern, R.A., & Sheth S.A. (2017) Role of the Dorsal Anterior Cingulate Cortex in Obsessive-Compulsive Disorder: Converging Evidence from Cognitive Neuroscience and Psychiatric Neurosurgery. J Neurosurg. Jan; 126(1): 132-147. https://pubmed.ncbi.nlm.nih.gov/27035167/
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