RESIDENT: Neuroinflammation in OCD

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Presenting Author(s): Dr. Bohan Yang

Co-Author(s): Dr. Glen Baker & Dr. Serdar Dursun

Date and time: 25 Mar 2023 from 13:00 to 13:15

Location: Hawthorn B  Floor Map

Learning Objectives

  1. Discuss limitations of current pathophysiological models and current treatments for OCD;
  2. Identify recent studies that suggest inflammatory processes as a potential contributor to the development of OCD;
  3. List potential inflammatory markers in OCD;
  4. Give examples of OCD comorbid conditions that are associated with inflammatory responses;
  5. Identify anti-inflammatory therapeutics currently under investigation for OCD.



The idea of exploring neuroinflammatory mechanisms underlying OCD is motivated by the limitations of current treatments for OCD, the observation of OCD being highly associated with autoimmune disorders, the well-known syndromes of PANS/PANDAS often characterised by OCD-like behaviors which are thought to have an autoimmune etiology, and accruing evidence in recent literature demonstrating neuroinflammation underlying other mental disorders including depression and schizophrenia.


Through an explorative literature review, we provided a broad overview of the evidence so far in the literature that supports or refutes a neuroinflammatory model of OCD.


We conducted an exploratory literature review following PRISMA guidelines with a focus on primary research articles within the past 5 years, but did not exclude older articles in the case of landmark findings or if there is a lack of recent research in a particular area.


We identified numerous studies providing support for inflammatory and autoimmune processes taking place in CNS structures, CSF, serum, and the gut microbiome in OCD patients. We found the prevalence of OCD to be greater in patients with conditions characterized by heightened inflammatory states, such as autoimmune disorders, infections, metabolic disorders, and even pregnancy. There is also evidence to suggest that treatments with anti-inflammatory properties – such as antibiotics and NSAIDS – can have benefit in OCD.


Our review is supportive of a neuroinflammatory model of OCD. Future studies on developing treatments that target neuroinflammation would be helpful to determine the clinical translatability of this model.

Literature References

Only the first 7 references are listed. For the full list of references, please contact the presenting author directly.

  1. Abramowitz JS, Taylor S, McKay D. Obsessive-compulsive disorder. The Lancet. 2009;374(9688):491-499. doi:10.1016/S0140-6736(09)60240-3
  2. Raviv N, Staudt MD, Rock AK, MacDonell J, Slyer J, Pilitsis JG. A systematic review of deep brain stimulation targets for obsessive compulsive disorder. Neurosurgery. 2020;87(6):1098-1110. doi:10.1093/neuros/nyaa249 
  3. Pittenger C. Pharmacotherapeutic Strategies and New Targets in OCD. In: Current Topics in Behavioral Neurosciences. Vol 49. Springer Science and Business Media Deutschland GmbH; 2021:331-384. doi:10.1007/7854_2020_204
  4. Attwells S, Setiawan E, Wilson AA, et al. Inflammation in the neurocircuitry of obsessive-compulsive disorder. JAMA Psychiatry. 2017;74(8):833-840. doi:10.1001/jamapsychiatry.2017.1567
  5. Zarghami M, Kaveh M, Yazdani-Charati J. The Efficacy of Ketamine Augmentation on Treatment-Refractory Obsessive-Compulsive Disorder: A Double-Blind Placebo-Controlled Clinical Trial. Int J Behav Sci. 2022;16(3):170-176. doi:10.30491/IJBS.2022.333954.1770
  6. Liu X, Cui H, Wei Q, et al. Electroconvulsive therapy on severe obsessive-compulsive disorder comorbid depressive symptoms. Psychiatry Investig. 2014;11(2):210-213. doi:10.4306/pi.2014.11.2.210
  7. Najjar S, Pearlman DM, Alper K, Najjar A, Devinsky O. Neuroinflammation and Psychiatric Illness.; 2013.

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