Understanding OCD: Brain Differences

Obsessive-Compulsive Disorder (OCD) is a neuropsychiatric disorder characterised by uncontrollable and recurrent unwanted thoughts (obsessions), excessive and repeated behaviours (compulsions), or both. It's a common, disabling and chronic condition that affects about 1–3% of the population. Although OCD symptoms can appear at any moment, they often first appear in late childhood or early adulthood.

According to research, individuals with OCD frequently have anatomical and biochemical changes in their brains when compared to those without the disorder.

Biochemical Differences

• Glutamate: As an excitatory neurotransmitter, glutamate triggers neurons to send signals to the subsequent cell. Increased glutamate levels could be a biomarker of the illness.

• Gamma-aminobutyric acid (GABA): Since GABA inhibits specific alert signals, it may exert a soothing impact on the brain. GABA deficiency is linked to OCD.

• Serotonin: Serotonin: A neurotransmitter that controls mood, serotonin deficiency aids in mood regulation. Low levels of serotonin is frequently linked to OCD. 

Brain Circuit

The pathophysiology of OCD has been linked to several brain circuits, including the cortico-striato-thalamo-cortical (CSTC) circuit. The CSTC includes the orbitofrontal cortex (OFC), the anterior cingulate cortex, the basal ganglia, and the thalamus. Reward, habit development, and mobility are all influenced by the CSTC circuit. The overactive CSTC circuit in OCD might result in the facilitation of unwanted behaviours. 

Structural and Functional Differences 

One of the earliest mental illnesses to be identified by brain scans was OCD, which revealed abnormal activity in particular brain areas. Brain activity was measured through blood flow using Positron Emission Tomography imaging. 

Image 2: (top row) individual without any diagnosis; (bottom row) is from a patient with OCD

The most noticeable ‘overactive’ areas in the OCD brain are the caudate nucleus, a part of the basal ganglia located deep inside the brain, OFC—located at the front of the brain. Decision-making and reward processing are functions of the OFC, which interprets signals sent from the thalamus when an individual needs to ‘worry’ about something. OCD is brought on by a damaged caudate nucleus, which prevents it from suppressing OFC impulses and causes the thalamus to become overexcited. If this happens, the OFC receives powerful signals from the thalamus, which causes it to increase anxiety and obsessive conduct. This may help to explain why obsessive-compulsive people engage in repeating, seemingly unnecessary behaviours.

The striatum and amygdala are among the many additional brain areas contributing to OCD; the amygdala in emotional processing and fear conditioning, and the striatum in habit building and reward processing. 

A bigger pallidum—a region of the brain that aids in controlling voluntary motor movement—was more common in individuals with childhood-onset OCD, likely as a result of long-term compulsions or medication usage.

Reference list

Baxter, L.R. (1987). Local Cerebral Glucose Metabolic Rates in Obsessive-Compulsive Disorder. Archives of General Psychiatry, 44(3), p.211. doi:https://doi.org/10.1001/archpsyc.1987.01800150017003.

Bbc.co.uk. (2014). BBC - Science & Nature - Human Body and Mind - Root of obsession. [online] Available at: https://www.bbc.co.uk/science/humanbody/mind/articles/disorders/causesofocd.shtml.

Calzà, J., Gürsel, D.A., Schmitz-Koep, B., Bremer, B., Reinholz, L., Berberich, G. and Koch, K. (2019). Altered cortico–striatal functional connectivity during resting state in obsessive–compulsive disorder. Frontiers in Psychiatry, 10(319). doi:https://doi.org/10.3389/fpsyt.2019.00319.

Mayo Clinic (2023). Obsessive-Compulsive disorder (OCD). [online] Mayo Clinic. Available at: https://www.mayoclinic.org/diseases-conditions/obsessive-compulsive-disorder/symptoms-causes/syc-20354432.

National Institute of Mental Health (2024). Obsessive-Compulsive disorder. [online] National Institute of Mental Health. Available at: https://www.nimh.nih.gov/health/topics/obsessive-compulsive-disorder-ocd.

Pujol, J., Soriano-Mas, C., Alonso, P., ..., Vallejo, J. (2004). Mapping structural brain alterations in obsessive-compulsive disorder. Archives of General Psychiatry, 61, 720-30. 

Pittenger, C. (2014). What does an OCD brain look like? [online] medicine.yale.edu. Available at: https://medicine.yale.edu/news-article/what-does-an-ocd-brain-look-like/.

Psychiatrist.com. (2023). How Brain Chemical Imbalances May Contribute to OCD. [online] Available at: https://www.psychiatrist.com/news/how-brain-chemical-imbalances-may-contribute-to-ocd/.

Queensland Brain Institute (2017). Obsessive Compulsive Disorder (OCD). [online] qbi.uq.edu.au. Available at: https://qbi.uq.edu.au/brain/diseases-and-disorders/obsessive-compulsive-disorder-ocd.

Restoring Wellness Solutions (2024). Is an OCD Brain Different from a Normal Brain? [online] Restoring Wellness Solutions. Available at: https://restoringwellnesssolutions.com/is-an-ocd-brain-different-from-a-normal-brain/.

van den Heuvel, O.A., Vriend, C., Dzinalija, N., Simpson, B., M. Veer, I., Walter, H., Ivanov, I., Thompson, P.M. and Stein, D.J. (2022). How Disease and Medication Shape the Brain in OCD: Learning from Global Collaboration. [online] International OCD Foundation. Available at: https://iocdf.org/expert-opinions/how-disease-and-medication-shape-the-brain-in-ocd/.

Zhu, Y., Fan, Q., Zhang, H., Qiu, J., Tan, L., Xiao, Z., Tong, S., Chen, J. and Li, Y. (2016). Altered intrinsic insular activity predicts symptom severity in unmedicated obsessive-compulsive disorder patients: a resting state functional magnetic resonance imaging study. BMC Psychiatry, 16(1). doi:https://doi.org/10.1186/s12888-016-0806-9.