Neurological Basis of OCD

Hi all,

Our previous posts depict various aspects of obsessive-compulsive disorder.   Following the case studies and symptoms outlined below, I would like to present research findings that shed light on the neurological basis of the disorder.  The following list is of several areas in the brain that are understood to be involved in networks that perpetuate the symptomatic behaviours characteristic of this disorder.  The Orbitofrontal Cortex (OFC) is responsible for evaluation of consequences that underlie the decisions we make; the Anterior Cingulate Cortex (ACC) is actively engaged in situations that present a risk of making an error; The Dorsolateral Prefrontal Cortex (DLPC) is involved in cognitive processing of information relevant to making decisions; the caudate nucleus in the basal ganglia exerts control over programs of behaviour;  the Striatum receives input from the cerebral cortex; and the thalamus receives sensory signals from the external environment and relays them to the cortex.[1] Below is a diagram that will help you visualize the areas of the brain discussed.

Image courtesy of: dreamscience.org

So how do these parts of the brain work together to produce such intrusive and impairing symptoms that we associate with OCD?  To begin, let’s admit that everyone makes mistakes.  As it turns out, we have certain brain regions allocated to the evaluation of our potential risk of being wrong.   With the help of measurement devices like the Electroencephalogram (EEG) and functional Magnetic Resonance Imaging (fMRI) researchers have identified that caudal ACC is involved in producing something that is known as Error-Related Negativity. [2]  It has been documented that higher prevalence of OCD symptoms positively correlates with larger ERN.  Thus, an OCD patient may feel compelled to “fix” the error that is signalled by his/her brain, while an outside observer may not notice any cause for concern. [3] Peculiarly, OCD patients do not exhibit a higher level of ERN in all cases.  Whereas a hyperactivity of ERN is observed during a “response conflict task”, such as correctly labelling items, a hypo-activity of ERN is observed during tasks associated with reinforcement learning.  In other words, a person suffering from OCD is in a perpetual cycle of having an exaggerated sense of something being wrong, but not learning to abstain from the behaviours that trigger the distressing emotions he/she experiences, regardless of how irrational they may be.   Moreover, the OFC, striatum, and ACC are known to comprise a circuit, making it difficult for the patient to override the obsessions and compulsions. [4]

Okay, so the presence of brain circuitry and exaggerated error signals contribute to feelings of doubt and insecurity of OCD patients, leading to obsessions, and triggering responses that we label as compulsions.[5]   What is the basis for this inflexible and rigid network?  Rolls, E.T. has examined the relationship between the stability of cortical networks and elevated levels of glutamate in an attempt to get closer to the source of the problem.  There is indication that an increase of the neurotransmitter glutamate is linked to the increase of stability of these networks. Studies suggest that the neocortex and striatum in brains of patients with OCD contain greater levels of glutamate, accounting for increased stability. The glutamatergic activity is thought to cause decreased flexibility of thought about the action and maintain rigid motor activities that do not seem to be affected by cognitive analysis.  Interestingly, excessive levels of glutamate are not limited to specific areas and can be found in various regions of the brain which are associated with symptoms characteristic of the disorder.  It is known that OCD does not produce a uniformity of symptoms, as people seem to be affected differently.  It is therefore likely that the location in the brain affected by hyperglutamatergia (as it is known in scientific language), affects the nature of symptomatic behaviour exhibited by patients.   The cause of hyperglutamatergia is proposed to be linked to genetics, but not well known. [6]

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[1]Aouizerate, B., Bioulac, B., Burbaud, P., Cuny, E., Guehl, D., Rougier, A., Tignol, J. (2004). Physiology of obsessive-compulsive disorder: A necessary link between phenomenology, neuropsychology, imagery, and physiology.  Progress in Neurobiology, 72(3), 195-221.

[2]Allen, J.J.B., Cavanagh, J.F., Grundler, T.O.J., Figueroa, C.M., Frank, M.J. (2009). Task-related dissociation in ERN amplitude as function of obsessive-compulsive symptoms.  Neuropsychologia,  47(8-9), 1978-1987.

[3] Gehring, W., Himle, J., Nisenson, L. (2000). Action-Monitoring Dysfunction in Obsessive-Compulsive Disorder.  Psychological Science, 11(1), 1-6.

[4] Allen, J.J.B., Cavanagh, J.F., Grundler, T.O.J., Figueroa, C.M., Frank, M.J. (2009). Task-related dissociation in ERN amplitude as function of obsessive-compulsive symptoms.  Neuropsychologia,  47(8-9), 1978-1987.

[5] Falkai, P., Gruber, O., Melcher, T. (2008). Functional brain abnormalities in psychiatric disorders: Neural mechanisms to detect and resolve cognitive conflict and interference.  Brain Research Reviews, 59(1), 96-124.

[6] Rolls, E.T. (2012). Glutamate, obsessive-compulsive disorder, schizophrenia, and the stability of cortical attractor neuronal networks.  Pharmacology, Biochemistry and Behaviour, 100(4), 736-751.