Positron emission tomography measurement of cerebral metabolic correlates of yohimbine administration in combat-related posttraumatic stress disorder.

Positron emission tomography measurement of cerebral metabolic correlates of yohimbine administration in combat-related posttraumatic stress disorder.
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DOI:
10.1001/archpsyc.1997.01830150070011
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发表时间:
1997-03
影响因子:
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通讯作者:
Bremner Jd;R. Innis;C. Ng;L. Staib;R. Salomon;R. Bronen;J. Duncan;S. Southwick;J. Krystal;D. Rich;G. Zubal;H. Dey;R. Soufer;D. Charney
Bremner Jd;R. Innis;C. Ng;L. Staib;R. Salomon;R. Bronen;J. Duncan;S. Southwick;J. Krystal;D. Rich;G. Zubal;H. Dey;R. Soufer;D. Charney
中科院分区:
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文献类型:
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作者:
Bremner Jd;R. Innis;C. Ng;L. Staib;R. Salomon;R. Bronen;J. Duncan;S. Southwick;J. Krystal;D. Rich;G. Zubal;H. Dey;R. Soufer;D. Charney

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背景我们之前曾报道过,创伤后应激障碍(PTSD)患者在服用β2-拮抗剂育亨宾后,焦虑症状会增加,这种药物会刺激大脑去甲肾上腺素的释放。临床前研究表明,高剂量育亨宾诱导的去甲肾上腺素释放会降低新皮质和尾状核的代谢,但低水平的去甲肾上腺素释放会导致这些区域的代谢增加。方法 我们使用正电子发射断层扫描和氟脱氧葡萄糖 F 18 来测量患有 PTSD 的越南退伍军人 (n = 10) 和年龄匹配的健康对照受试者 (n = 10) 在以随机、双盲方式服用育亨宾 (0.4 mg/kg) 或安慰剂后的脑代谢。结果 育亨宾会导致 PTSD 患者的焦虑显着增加,但健康受试者则不会。与健康受试者相比,PTSD 患者的前额叶、颞叶、顶叶和眶额皮质对育亨宾的大脑代谢反应存在显着差异。服用育亨宾后,PTSD 患者的代谢趋于下降,健康受试者的代谢趋于增加。结论 这些发现与我们之前的假设一致,即育亨宾可增强 PTSD 患者大脑中去甲肾上腺素的释放。
BACKGROUND We have previously reported an increase in symptoms of anxiety in patients with posttraumatic stress disorder (PTSD) following administration of the beta 2-antagonist yohimbine, which stimulates brain norepinephrine release. Preclinical studies show decreased metabolism in the neocortex and the caudate nucleus with high-dose yohimbine-induced norepinephrine release, but low levels of norepinephrine release result in an increase in metabolism in these areas. METHODS We used positron emission tomography and fludeoxyglucose F 18 to measure brain metabolism in Vietnam combat veterans with PTSD (n = 10) and healthy age-matched control subjects (n = 10), following administration of yohimbine (0.4 mg/kg) or placebo in a randomized, double-blind fashion. RESULTS Yohimbine resulted in a significant increase in anxiety in the patients with PTSD, but not in healthy subjects. There was a significant difference in brain metabolic response to yohimbine in patients with PTSD compared with healthy subjects in prefrontal, temporal, parietal, and orbitofrontal cortexes. Metabolism tended to decrease in patients with PTSD and increase in healthy subjects following administration of yohimbine. CONCLUSION These findings are consistent with our previous hypothesis of enhanced norepinephrine release in the brain with yohimbine in patients with PTSD.