Pollack Mark H, Jensen J Eric, Simon Naomi M, Kaufman Rebecca E, Renshaw Perry F
Psychiatry Department, Massachusetts General Hospital, Boston, MA 02114, United States.
Prog Neuropsychopharmacol Biol Psychiatry. 2008 Apr 1;32(3):739-43. doi: 10.1016/j.pnpbp.2007.11.023. Epub 2007 Nov 28.
Abnormalities in brain gamma-aminobutyric acid (GABA) and glutamate may be relevant to the underlying pathophysiology of anxiety disorders including social anxiety disorder (SAD).
We used proton magnetic resonance spectroscopy (pMRS) to examine whole brain and regional GABA, glutamate and glutamine in patients (N=10) with SAD at baseline compared to a matched group of healthy controls (HC), and changes following 8 weeks of pharmacotherapy with levetiracetam.
For SAD subjects, there were significantly higher whole brain levels of glutamate and glutamine, though no significant differences in GABA. In the thalamus, glutamine was higher and GABA lower for SAD subjects. There was a significant reduction in thalamic glutamine with levetiracetam treatment.
Our findings provide preliminary support for impaired GABAergic and overactive glutamatergic function in social anxiety disorder and the potential relevance of changes in these systems for the anxiolytic response to levetiracetam.
大脑γ-氨基丁酸（GABA）和谷氨酸异常可能与包括社交焦虑障碍（SAD）在内的焦虑症的潜在病理生理学相关。
我们使用质子磁共振波谱（pMRS）检查了10例SAD患者在基线时与匹配的健康对照组（HC）相比全脑及区域的GABA、谷氨酸和谷氨酰胺情况，以及左乙拉西坦药物治疗8周后的变化。
对于SAD受试者，全脑谷氨酸和谷氨酰胺水平显著更高，而GABA无显著差异。在丘脑中，SAD受试者的谷氨酰胺更高而GABA更低。左乙拉西坦治疗后丘脑谷氨酰胺显著降低。
我们的研究结果为社交焦虑障碍中GABA能功能受损和谷氨酸能功能亢进提供了初步支持，以及这些系统变化与左乙拉西坦抗焦虑反应的潜在相关性。
