Leyton M, Bélanger C, Martial J, Beaulieu S, Corin E, Pecknold J, Kin N M, Meaney M, Thavundayil J, Larue S, Nair N P
Douglas Hospital Research Centre, Department of Psychiatry, McGill University, Verdun, Canada.
Biol Psychiatry. 1996 Sep 1;40(5):353-60. doi: 10.1016/0006-3223(95)00452-1.
Both clinical symptomatology and stress research suggest that panic attacks might be partially attributable to exaggerated psychophysiological responses to environmental stressors. In the present study, we aimed to explicitly test this idea by measuring the physiological responses to a mild psychological stressor in both healthy controls (n = 8) and fully remitted, medication-free panic disorder patients (n = 8). One hour before the stressor, former patients, compared to healthy controls, exhibited higher diastolic blood pressure. From a blood sample taken 30 min before the stressor, patients, compared to controls, had lower paroxetine platelet binding site densities. During the stressor, patients, compared to controls, had greater increases in plasma levels of cortisol. These preliminary findings suggest that remitted panic disorder patients might have disturbed physiological responses to mild psychological stressors. These disturbances might be related to the development of future episodes.
临床症状学和压力研究均表明,惊恐发作可能部分归因于对环境压力源的过度心理生理反应。在本研究中,我们旨在通过测量健康对照组(n = 8)和完全缓解且未服用药物的惊恐障碍患者(n = 8)对轻度心理压力源的生理反应,来明确验证这一观点。在压力源出现前一小时,与健康对照组相比,既往患者的舒张压更高。在压力源出现前30分钟采集的血样中,与对照组相比,患者的帕罗西汀血小板结合位点密度更低。在压力源作用期间,与对照组相比,患者的血浆皮质醇水平升高幅度更大。这些初步发现表明,缓解期惊恐障碍患者对轻度心理压力源的生理反应可能存在紊乱。这些紊乱可能与未来发作的发生有关。