약물사용 경험이 없는 강박증 환자에서 1H-MRSI를 이용한 N-acetylaspartate의 이상과 인지기능과의 관련성
Correlates of N-acetylaspartate and Cognitive Dysfunctions in Drug-naive Patients with Obsessive-compulsive Disorder：A Proton MRSI Study
Objectives：Reductions of N-acetylaspartate (NAA), a putative marker of neuronal viability, within the subcortical structures in patients with obsessive-compulsive disorder (OCD) are well documented. However, there has been no report of the NAA level in cortical structures. The authors used proton magnetic resonance spectroscopic imaging (1H-MRSI) to assess potential reductions of NAA in the frontal white matter, prefrontal gray matter, parietal gray and white matter, and the cingulate in drugnaive patients with OCD and explored the relationship between the brain metabolites and the degree to the dysfunction on the neuropsychological performances. Methods：Thirteen drug-naive patients who met DSM-IV criteria for OCD and 13 healthy age-, sex-, handness- matched control subjects were studied. Subjects underwent MRI and 1H-MRSI and the peaks of NAA, creatine+phosphocreatine (Cr), and choline-containing compounds (Cho) were measured. Differences between patients and control subjects were tested for each metabolite ratio, and the relations between metabolite ratios and clinical symptoms, neuropsychological performances were examined. Results：Upon comparison with normal controls, NAA/Cr ratio was significantly reduced in patients for the prefrontal gray matter, frontal white matter and anterior cingulate. There was no difference in Cho/Cr or NAA/Cho in any region. Also, a significant positive correlation was found between prefrontal NAA/Cr ratio and the delayed recall score of the Rey-Osterrieth Complex Figure Test in patients with OCD. Conclusion：The reduced NAA/Cr ratio in the prefrontal gray matter and frontal white matter suggests that OCD patients have lower neuronal viability than normal comparisons and it may be related to impaired organizational strategies in patients with OCD. These results support a role for the frontal-subcortical circuitry in a neurobiologic model of OCD.