In my last post, I talked about the potential imbalance in the dopaminergic system as being part of the reason for compulsive behaviors. I loosely associated these behaviors to those found in OCD. I will continue to make this association in this post and the ones to come. This post will focus on studies that show differences in brain structure of people with and without OCD. We will see that much of the differences will correlate with regions involved in the dopaminergic system. Ultimately, my goal is to show that it is plausible that a deficiency in processing rewards, much of which takes place in the orbitofrontal cortex (OFC), is a major source of the dopamine imbalance and resulting compulsive behaviors.
Let me begin with describing some of the functionality believed to be related to the OFC. These functions include decision-making, judgements, planning, and reward processing. In this post I will focus on reward processing and goal pursuit. It is hard to fully separate these two from functions like decision-making and planning since choosing a goal is a decision-making process and then one constructs a plan for pursuing that goal. Nonetheless, I will focus here on goals and reward, and in my final post a few weeks from now I will go discuss decision-making.
Why do you pursue a goal? The goal must have some benefit, and that benefit manifests itself in the form of a reward. It the brain has difficulty in processing rewards, then it loses motivation to pursue the goal. Looking at the other side of the chicken and egg problem, if the brain is not able to focus on goal pursuit, then the benefit and reward for achieving the goal cannot be realized. It is unclear which is happening, but these are clearly linked. And naturally, the OFC is responsible for both goal pursuit and processing of rewards. Whether the problem in the OFC is related to the goal or the reward is still a mystery.
By now you may be asking if there is evidence that the OFC is different in people with and without OCD. There is actually a substantial amount of evidence using both positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) showing significantly more metabolism and activation in the OFC. Harris & Hoehn-Saric (1995) using MRI images found no structural differences between controls and those with OCD. However, the PET scans showed hypermetabolism in the OFC. More specifically, PET scans have shown increased metabolic rates for the right OFC (Kwon et al., 2003).
Tests with fMRI have shown similar results. In a comparison of patients with OCD and controls, while they are in a resting state, those with OCD presented increased amplitude of low-frequency fluctuation (ALFF) in the OFC. Additionally, the ALFF values were positively correlated with total Y-BOCS scores (Hou et al., 2012). (Y-BOCS is the Yale-Brown Obsessive Compulsive Scale, a standard test used for diagnosing OCD. Try it yourself at http://psychology-tools.com/yale-brown-obsessive-compulsive-scale/)
If the OFC is partially responsible for OCD, then after treatment (pharmacological or behavioral therapy), then one would hope that the hyperactivation of the OFC would be mitigated. Nakao et al. (2005) found that after such treatment, scores on the Y-BOCS test decreased and activation in the frontal lobe also decreased.
Hopefully, I have presented a good enough case that the OFC plays a significant role in OCD. Also, as I stated earlier, the OFC is related to goal pursuit and reward processing. Are these related? (Of course! Why else would I be asking the question?) A fascinating and recent study tested patients with OCD on their ability to use goal-directed behavior. The patients and the controls learned a new task, and both were able to learn the task at similar rates. However, the OCD patients performed poorly in their ability to adapt to changes in the task and instead fell into habits (Papmeyer et al., 2011). The authors relate this to resorting to compulsive behaviors like hand-washing and checking. I interpret this as a reward anticipation has been created, but the corresponding goal cannot be identified or selected and instead the person resorts to established behaviors in hopes of acquiring the reward. Unfortunately, the reward may be nonexistent or too little, and the cycle of reward anticipation and failed acquisition persists.
There are many brain regions the have been shown to be related to OCD, including the OFC, striatum, anterior cingulate, thalamus, and caudate nucleus (Saxena & Rauch, 2000). I focus here on the role of the OFC and its functioning for reward processing and goal pursuit. In my last post I began to make a case for an imbalance in the dopaminergic pathway, and this post I begin to provide evidence that malfunctioning of the OFC may be contributing to this imbalance. The striatum is releasing plenty (or too much) dopamine but perhaps the OFC is not able to metabolize it. The reward anticipation maintains but the reward is not fully realized. This is likely related to a deficiency in adapting and pursuing goals, and instead the ritualistic behaviors are repeated.
I will continue to look into this in my next post and look at the role of memory and learning. Reward is often related to learning, so we would expect to see an impact there.
Harris, G. J., & Hoehn-Saric, R. (1995). Functional neuroimaging in biological psychiatry. Advances in biological psychiatry, JAI Press, Greenwich, 113-160.
Hou, J., Wu, W., Lin, Y., Wang, J., Zhou, D., Guo, J., … & Li, H. (2012). Localization of cerebral functional deficits in patients with obsessive–compulsive disorder: A resting-state fMRI study. Journal of affective disorders,138(3), 313-321.
Kwon, J. S., Kim, J.-J., Lee, D. W., Lee, J. S., Lee, D. S., Kim, M.-S., … Lee, M. C. (2003). Neural correlates of clinical symptoms and cognitive dysfunctions in obsessive-compulsive disorder. Psychiatry Research, 122(1), 37–47.
Nakao, Tomohiro, et al. “Brain activation of patients with obsessive-compulsive disorder during neuropsychological and symptom provocation tasks before and after symptom improvement: a functional magnetic resonance imaging study.”Biological psychiatry 57.8 (2005): 901-910.
Saxena, S., & Rauch, S. L. (2000). Functional Neuroimaging and the Neuroanatomy of Obsessive-Compulsive Disorder. Psychiatric Clinics of North America, 23(3), 563–586.
Papmeyer, M., Morein-zamir, S., Ph, D., Sahakian, B. J., Ph, D., Fineberg, N. A., … Ph, D. (2011). Disruption in the Balance Between Goal-Directed Behavior and Habit Learning in Obsessive-Compulsive Disorder. American Journal of Psychiatry, 168(July), 718–726.