NEUROBIOLOGY OF SEASONAL AFFECTIVE DISORDER AND LIGHT THERAPY

尽管反复的研究已经证实，明亮的光线是一种 有效治疗SAD，其作用机制尚存 未知的，也是基本的生物异常 综合症。有充分的理由相信大脑5-羟色胺能 这些过程中可能涉及到系统。 在过去，我们进行了初步研究，以调查SAD 患者对输注阿司匹林的反应与正常对照组不同 选择性较强的5-羟色胺激动剂间氯苯基哌嗪 (M-CPP)。我们发现，如果在冬季不接受治疗，SAD 据报道，患者的活动程度比正常水平更高 对照组在输液后。有效的光治疗或即将到来 与这种激活的正常化有关 回应。我们早期的研究受到某些方法论的影响 不足之处。在本研究中，我们试图避免这些 通过增加我们的样本量，包括安慰剂输注，来弥补缺陷 状态和随机排序处理过的、开着灯的、未处理过的、关过的 灯光“，条件。符合冬季SAD标准的17名患者 15名健康对照组接受了m-CPP或安慰剂的输注。 分别在“关灯”和“开灯”的情况下工作。这个 “开灯”状态包括两周的每日治疗， 早上用10,000勒克司的白光照射45分钟，在 晚上；“关灯”状态包括至少两个星期 没有任何光处理。输液包括0.08毫克/公斤的 M-CPP生理盐水或单独生理盐水。在基线和90 在输液后几分钟，我们通过一种 24项NIMH自评量表、体温和抽血治疗 荷尔蒙测量。 正如我们之前所发现的，“兴奋-欣快感”分增加了 SAD患者在“熄灯”状态下的显著症状，如 与“亮灯”状态或与正常对照相比 任一条件(F=4.7；Df=3，90；温室-盖塞校正P为 少于.O5)。M-CPP输注后的激活增加 处于“熄灯”状态的患者与 用哈密尔顿抑郁指数测量光的抗抑郁反应 评级等级。因此，我们复制并加强了早期的 找到了。5-羟色胺能异常似乎与 SAD的病理生理学及其对光的反应。

Although repeated studies have established that bright light is an effective treatment for SAD, the mechanism of its actions remains unknown, as do the fundamental biological abnormalities responsible for the syndrome. There is ample reason to believe that brain serotonergic systems may be involved in these processes. In the past, we undertook preliminary studies to investigate whether SAD patients would respond differently from normal controls to infusions of the somewhat selective serotonin agonist, m-chlorophenylpiperazine (m-CPP). We found that when untreated during the winter months, SAD patients reported being activated to a greater degree than normal controls following the infusion. Effective light treatment or the advent of summer were associated with a normalization of this activation response. Our earlier studies suffered from certain methodological deficiencies. In the present study we have attempted to obviate these deficiencies by increasing our sample size, including a placebo infusion condition and randomly ordering treated, "on lights," and untreated, "off lights", conditions. Seventeen patients who met criteria for winter SAD and 15 healthy controls underwent infusions of either m-CPP or placebo on separate days in both "off lights" and "on-lights", conditions. The "on-lights" condition consisted of 2 weeks of daily treatments with 10,000 lux of white light for 45 minutes in the morning and 45 minutes in the evening; the "off-lights" condition consisted of at least two weeks without any light treatment. Infusions consisted of either 0.08 mg/kg of m-CPP in normal saline or the saline alone. At baseline and for 90 minutes following the infusion, we measured behavior by means of a 24-item NIMH self-rating scale, body temperature, and drew blood for hormonal measurements. As we had found previously, the "activation-euphoria" subscore increased significantly in SAD patients during the "off lights" condition, as compared with the "on-lights" condition or with the normal controls under either condition (F=4.7; df = 3, 90; Greenhouse-Geisser corrected P is less than .O5) . Increase in activation following m-CPP infusions in patients in the "off-lights" condition correlated significantly with antidepressant response to light, as measured by the Hamilton Depression Rating Scale. We therefore replicated and strengthened our earlier finding. Serotonergic abnormalities appear to related to the pathophysiology of SAD and its response to light.