Abstract
Background: Neurobiological abnormalities in the thalamus, particularly the dorsomedial nucleus of the thalamus, are believed to be involved in the pathophysiology of obsessive–compulsive disorder. Although obsessive–compulsive disorder commonly arises in childhood and adolescence, no prior study has examined the thalamus in pediatric obsessive–compulsive disorder patients. Methods: In this study, N-acetyl-aspartate, a putative marker of neuronal viability, creatine/phosphocreatine, and choline levels were measured in the lateral and medial subregions of the left and right thalami using a multislice proton magnetic resonance spectroscopic imaging sequence in 11 treatment-naive, nondepressed obsessive–compulsive disorder outpatients, 8–15 years old, and 11 case-matched control subjects. Results: A significant reduction in N-acetyl-aspartate/choline and N-acetyl-aspartate/(creatine/phosphocreatine + choline) was observed in both the right and left medial thalami in obsessive–compulsive disorder patients compared with control subjects. The N-acetyl-aspartate/choline and N-acetyl-aspartate/(creatine/phosphocreatine + choline) levels did not differ significantly between case–control pairs in either the left or the right lateral thalamus. Reduction in N-acetyl-aspartate levels in the left medial thalamus was inversely correlated with increased obsessive–compulsive disorder symptom severity. Conclusions: These findings provide new evidence of localized functional neurochemical marker abnormalities in the thalamus in pediatric obsessive–compulsive disorder. Our results must be considered preliminary, however, given the small sample size.
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