Benkelfat C, Bradwejn J, Meyer E, Ellenbogen M, Milot S, Gjedde A, Evans A
McConnell Brain Imaging Center, Department of Neurology and Neurosurgery, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.
Am J Psychiatry. 1995 Aug;152(8):1180-4. doi: 10.1176/ajp.152.8.1180.
The authors tested the prediction of temporal cortex activation during experimentally induced anxiety by using positron emission tomography and the [15O]H2O bolus-subtraction method to determine regional cerebral blood flow (CBF) changes in normal volunteers challenged with a bolus injection of cholecystokinin tetrapeptide (CCK4).
Eight right-handed healthy subjects (five male, three female; mean age, 26.4 years) underwent four 60-second [15O]H2O scans separated by 15-minute intervals; each scan followed an intravenous bolus injection of either saline (placebo) or CCK4 (50 micrograms). Each subject received CCK4 once, as the first or second bolus, in a random-order, placebo-controlled, double-blind fashion. Two of the three placebo conditions were nominally identical, and the remaining placebo was used to control for anticipatory anxiety. Magnetic resonance imaging scans were obtained for subsequent anatomical correlation of blood flow changes.
CCK4, but not placebo, elicited a marked anxiogenic response, reflected by robust increases in subjective anxiety ratings and heart rate. CCK4-induced anxiety was associated with 1) robust and bilateral increases in extracerebral blood flow in the vicinity of the superficial temporal artery territory and 2) CBF increases in the anterior cingulate gyrus, the claustrum-insular-amygdala region, and the cerebellar vermis.
Some of the temporopolar cortex CBF activation peaks previously reported in humans in association with drug- and non-drug-induced anxiety, as well as the increase in regional CBF in the claustrum-insular-amygdala region, may be of vascular and/or muscular origin.
作者使用正电子发射断层扫描和[15O]H2O团注减法来测定区域脑血流量（CBF）变化，以此测试在实验诱导的焦虑期间颞叶皮质激活的预测情况，实验对象为接受团注注射四肽胆囊收缩素（CCK4）的正常志愿者。
八名右利手健康受试者（五名男性，三名女性；平均年龄26.4岁）接受了四次60秒的[15O]H2O扫描，间隔15分钟；每次扫描前静脉团注注射生理盐水（安慰剂）或CCK4（50微克）。每位受试者以随机顺序、安慰剂对照、双盲方式接受一次CCK4注射，作为第一次或第二次团注。三个安慰剂条件中的两个名义上相同，其余安慰剂用于控制预期焦虑。进行磁共振成像扫描以用于后续血流变化的解剖学关联。
CCK4而非安慰剂引发了明显的致焦虑反应，表现为主观焦虑评分和心率显著增加。CCK4诱导的焦虑与1）颞浅动脉区域附近脑外血流的双侧显著增加以及2）前扣带回、屏状核-岛叶-杏仁核区域和小脑蚓部的CBF增加有关。
先前在人类中报道的与药物和非药物诱导的焦虑相关的一些颞极皮质CBF激活峰值，以及屏状核-岛叶-杏仁核区域区域CBF的增加，可能起源于血管和/或肌肉。
