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A growing body of evidence suggests that abnormalities within the cortico-striato-thalamic-cortical (CSTC) circuits are one of the key factors underlying the pathophysiology of OCD.25,26) Specifically, hyperactivity within the orbitofrontal cortex, anterior cingulate and ventromedial striatum has been associated with OCD behaviour.27,28) Glutamate is the primary neurotransmitter within the CSTC, and evidence suggests that abnormal glutamate metabolism is apparent in patients with OCD.29,30) Significantly higher levels of glutamate have been found in the cerebral spinal fluid and various regions of the brain including the right caudate and orbitofrontal cortex of treatment refractory OCD patients.15,31,32) However reduced concentrations were evident in the anterior cingulate in a sample of women with OCD, and were correlated with symptom severity.31) In addition, high levels of glutamate result in excitotoxicity and oxidative stress33) and oxidative stress has been detected in serum samples from those diagnosed with OCD, as evidenced by lipid peroxidation and alterations to antioxidant systems.17,18,34) In addition, higher levels of oxidative stress appear to correlate with symptom severity.35) Whether these findings are a cause or consequence of OCD pathophysiology, is yet to be identified
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Circadian control of many diurnally-expressed genes imposes temporal coordination on signaling and enzymatic pathways leading to optimal organismal functions
