Effects of intensive cognitive-behavioral therapy on cingulate neurochemistry in obsessive–compulsive disorder

Abstract

The neurophysiological bases of cognitive-behavioral therapy (CBT) for obsessive–compulsive disorder (OCD) are incompletely understood. Previous studies, though sparse, implicate metabolic changes in pregenual anterior cingulate cortex (pACC) and anterior middle cingulate cortex (aMCC) as neural correlates of response to CBT. The goal of this pilot study was to determine the relationship between levels of the neurochemically interlinked metabolites glutamate + glutamine (Glx) and N-acetyl-aspartate + N-acetyl-aspartyl-glutamate (tNAA) in pACC and aMCC to pretreatment OCD diagnostic status and OCD response to CBT. Proton magnetic resonance spectroscopic imaging (1H MRSI) was acquired from pACC and aMCC in 10 OCD patients at baseline, 8 of whom had a repeat scan after 4 weeks of intensive CBT. pACC was also scanned (baseline only) in 8 age-matched healthy controls. OCD symptoms improved markedly in 8/8 patients after CBT. In right pACC, tNAA was significantly lower in OCD patients than controls at baseline and then increased significantly after CBT. Baseline tNAA also correlated with post-CBT change in OCD symptom severity. In left aMCC, Glx decreased significantly after intensive CBT. These findings add to evidence implicating the pACC and aMCC as loci of the metabolic effects of CBT in OCD, particularly effects on glutamatergic and N-acetyl compounds. Moreover, these metabolic responses occurred after just 4 weeks of intensive CBT, compared to 3 months for standard weekly CBT. Baseline levels of tNAA in the pACC may be associated with response to CBT for OCD. Lateralization of metabolite effects of CBT, previously observed in subcortical nuclei and white matter, may also occur in cingulate cortex. Tentative mechanisms for these effects are discussed. Comorbid depressive symptoms in OCD patients may have contributed to metabolite effects, although baseline and post-CBT change in depression ratings varied with choline-compounds and myo-inositol rather than Glx or tNAA.

Reductions in cortico-striatal hyperconnectivity accompany successful treatment of obsessive-compulsive disorder with dorsomedial prefrontal rTMS

“…One study has shown the opposite, corticostriatal hypoconnectivity, in a group of unmedicated patients (Posner et al, 2014). In addition, altered anterior cingulate cortex metabolic activity has been observed in OCD on fluorodeoxyglucose-positron emission tomography and magnetic resonance spectroscopy (Perani et al, 1995;Ebert et al, 1997;Saxena et al, 2004Saxena et al, , 2009O'Neill et al, 2013). Taken together, these observations delineate a possible neuroanatomical substrate for OCD symptomatology.…”

Risk Assessment and Manage- ment of Violence in Patients with Mental Disorders: A Re- view

“…In future, it is expected that some biological factors may be integrated into risk assessment procedures, following the development of this knowledge base. For example, a reduced risk after treatment could be visualized with functional brain imaging, similar to an attempt to evaluate cognitive behavioral therapy using measurements of brain metabolism [80]. However, we should always be aware that risk assessment has substantive uncertainty and that risk management has historically been biased to the deprivation of human rights.…”

Evidências de alterações neurais na Terapia Cognitivo-Comportamental: uma revisão da literatura

“…Em relação à concentração de glutamato no córtex cingulado medial anterior, observou-se redução em seus níveis após tratamento. Concentrações elevadas de NAA pré-tratamento apresentaram correlação com maiores índi-ces de melhora pós-tratamento (O'Neill et al, 2013). Já a concentração do metabólito (mio-) inositol no córtex orbito-frontal se mostrou fator preditor de boa resposta à TCC para o TOC.…”