OCD is a complex disorder with multiple aetiological theories. Recent research points to role of autoimmunity as well as hyperactivity of glutaminergic pathways in aetiopathogenesis of the disorder. It is possible that autoimmune mechanisms may modulate excitatory neurotransmission resulting in OCD.

This study aimed to study the association between serum anti-basal ganglia autoantibodies (ABGA) and Glx (glutamate + glutamine) levels in caudate nucleus and anterior cingulate cortex as demonstrated by 1H-MRS (proton magnetic resonance spectroscopy).

Thirty psychotropic-naive OCD patients and an equal number of age, gender matched healthy controls were studied using 1H-MRS and levels of Glx were obtained. ABGA was measured using ELISA (enzyme linked immunosorbent assay) technique and categorised as present or absent in the serum.

ABGA was present in significantly higher proportion of patients as compared to controls (P < 0.05). Glx level was significantly higher (as measured by 1H-MRS) in patients with ABGA as compared to those without ABGA (P = 0.02). The study results did not differ based on age, gender, disease severity and illness duration.

The study demonstrates presence of ABGA in at least a subset of OCD population. The significant correlation between brain Glx levels and presence of ABGA provides a putative neurobiological framework for OCD. The strengths of the study include psychotropic-naive patients, blinded investigators and use of standardized instruments. The limitations include small sample size, use of Glx as proxy measure of glutamate and lack of other disorder controls. Similar studies on a larger sample are warranted for a better understanding.

The authors have not supplied their declaration of competing interest.