Systematic Changes in Cerebral Glucose Metabolic Rate After Successful Behavior Modification Treatment of Obsessive-Compulsive Disorder

Abstract

These results replicate and extend previous findings of changes in caudate nucleus function with behavior therapy for obsessive-compulsive disorder. A prefrontal cortico-striato-thalamic brain system is implicated in mediation of symptoms of obsessive-compulsive disorder.

Rapid effects of brief intensive cognitive-behavioral therapy on brain glucose metabolism in obsessive-compulsive disorder

“…Thus, decreasing cingulate activity may sometimes be associated with improvement in OCD symptoms but does not appear to be a necessary mechanism of action for treatment response. Instead, the functional changes most strongly associated with treatment response in OCD are decreases in activity in the right OFC, 8,[10][11][12][13]36,37,42,43 right caudate 9,11,12,14,16,17,36,37,42 and thalamus. 9,11,15,36,37 In contrast to the effects of pharmacotherapy on brain function, enhancement of dACC activity may be a primary mechanism of action of CBT for OCD.…”

“…9,16,17 These findings and others have led to the theory that the symptomatic expression of OCD is mediated by hyperactivity along frontal-subcortical circuits connecting the OFC, caudate, globus pallidus and the medial dorsal nucleus of the thalamus. 18,19 Clinical response of OCD symptoms usually requires up to 12 weeks of treatment with SRI medications and standard, weekly outpatient CBT.…”

“…21 However, very little is known about the brain mediation of response to CBT in OCD. Baxter and colleagues 9,16 performed positron emission tomography (PET) scans on a total of 18 OCD patients before and after 8-12 weeks of weekly CBT and found that the 12 patients who responded to treatment showed significant, pre-to posttreatment decreases in normalized right caudate glucose metabolism. A study of 22 treatment-refractory OCD patients with Xenon-enhanced computerized tomography before and after 7-8 months of CBT also found significant reductions in right caudate blood flow, as well as smaller decreases in left frontal cortex and thalamus.…”

Animal Models of Deficient Sensorimotor Gating in Schizophrenia: Are They Still Relevant?

“…Others have reported aberrant limbic-cortical connectivity associated with both endogenous ) and drug-induced psychosis (Driesen et al 2013) in humans; similarly, excessive fronto-striatal metabolic correlation ["Brain Lock" (Schwartz 1997)] has been demonstrated in other disorders associated with the reduced PPI, such as OCD. Importantly, in OCD, therapeutic response to medication or psychotherapy is associated with a metabolic "uncoupling" of fronto-striatal regions (Schwartz et al 1996;Schwartz 1998). Perhaps, the most speculative but exciting concept to emerge from the NVHL/"hypercoupling model" is the possibility that an "uncoupling" of fronto-striatal circuitry might provide an avenue for early therapeutic interventions in schizophrenia.…”

“…Perhaps, the most speculative but exciting concept to emerge from the NVHL/"hypercoupling model" is the possibility that an "uncoupling" of fronto-striatal circuitry might provide an avenue for early therapeutic interventions in schizophrenia. That such an "uncoupling" can be produced in OCD via cognitive interventions (Schwartz et al 1996) may suggest such a therapeutic option in schizophrenia, as discussed below.…”