title: Proton magnetic resonance spectroscopy reveals an abnormality in the anterior cingulate of a subgroup of obsessive-compulsive disorder patients.
abstract: Numerous neuroimaging studies have suggested that obsessive-compulsive disorder (OCD) patients had a neurobiological abnormality in the frontal-subcortical circuits. On the other hand, there are distinct differences in the responses to pharmacological treatment among OCD patients. In the present study, we measured the concentration of N-acetyl aspartate (NAA), a putative marker of neuronal viability, with proton magnetic resonance spectroscopy (MRS) in OCD patients with different pharmacological responses. Participants comprised 20 patients and 26 healthy control subjects. OCD patients were divided into three groups according to the pharmacological response; responders to a selective serotonin reuptake inhibitor (SSRI) (group A: n=7), responders to SSRI with an atypical antipsychotic (group B: n=8) and non-responders to either SSRI or SSRI with an atypical antipsychotic (group C: n=5). Short echo proton MRS was used to measure NAA concentrations in the anterior cingulate, the left basal ganglia and the left prefrontal lobe of subjects. A significantly lower NAA concentration was observed only in group B compared with control subjects in the anterior cingulate. Our results suggest that a subgroup of OCD patients who respond to an SSRI with an atypical antipsychotic have distinct biological abnormalities in the anterior cingulate.
authors.affiliation: Department of Psychiatry, Institute of Health Biosciences, University of Tokushima Graduate School, 18-15 Kuramoto-cho 3, Tokushima 770-8503, Japan. satsuki@clin.med.tokushima-u.ac.jp
authors.forename: Satsuki
authors.initials: S
authors.lastname: Sumitani
authors.forename: Masafumi
authors.initials: M
authors.lastname: Harada
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Kubo
authors.forename: Tetsuro
authors.initials: T
authors.lastname: Ohmori
mesh_terms: D000328:Adult; D014150:Antipsychotic Agents / Q000627:therapeutic use; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000378:metabolism; D001479:Basal Ganglia / Q000187:drug effects / Q000503:physiopathology; D001569:Benzodiazepines / Q000627:therapeutic use; D004292:Dominance, Cerebral / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004359:Drug Therapy, Combination; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology*; D005260:Female; D016666:Fluvoxamine / Q000627:therapeutic use; D005625:Frontal Lobe / Q000187:drug effects / Q000503:physiopathology; D006179:Gyrus Cinguli / Q000187:drug effects / Q000503:physiopathology*; D006801:Humans; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D009415:Nerve Net / Q000187:drug effects / Q000503:physiopathology; D009771:Obsessive-Compulsive Disorder / Q000175:diagnosis / Q000188:drug therapy / Q000503:physiopathology*; D000077152:Olanzapine; D017374:Paroxetine / Q000627:therapeutic use; D017397:Prefrontal Cortex / Q000187:drug effects / Q000503:physiopathology; D018967:Risperidone / Q000627:therapeutic use; D017367:Selective Serotonin Reuptake Inhibitors / Q000627:therapeutic use; D016896:Treatment Outcome
chemical_list: D014150:Antipsychotic Agents; D001224:Aspartic Acid; D001569:Benzodiazepines; D016666:Fluvoxamine; D000077152:Olanzapine; D017374:Paroxetine; D018967:Risperidone; D017367:Selective Serotonin Reuptake Inhibitors; C000179:N-acetylaspartate