*Dept. of Biological Sciences,University of Surrey,UK.
Acta Neuropsychiatr. 1995 Jun;7(2):41-3. doi: 10.1017/S0924270800037522.
Seasonal affective disorder (SAD) is characterised by recurrent episodes in autumn and winter of depression, hypersomnia, augmented appetite with carbohydrate craving, and weight gain, and can be successfully treated with bright light. Circadian rhythm hypotheses (summarized in) have stimulated research into the pathophysiology of SAD, postulating that: 1.The illness is a consequence of delayed phase position, 2.It is correlated with diminished circadian amplitude, or 3.It results from changes in the nocturnal duration between dusk and dawn e.g. of low core body temperature or melatonin secretion. Light is considered to act directly on the circadian pacemaker ('Process C') and not on sleep dependent processes ('Process S'). Thus successful treatment of SAD must act via mechanisms within known retinohypothalamic pathways. Conversely, emergence of SAD symptoms may reflect inappropriate neurobiological response to decreasing daylength.
季节性情感障碍（SAD）的特征是在秋季和冬季反复发作抑郁、嗜睡、食欲增加伴碳水化合物渴求以及体重增加，可通过明亮的光线成功治疗。昼夜节律假说（总结在）刺激了对 SAD 病理生理学的研究，假设：1. 这种疾病是相位延迟的结果，2. 它与昼夜节律幅度减小有关，或 3. 它是由黄昏到黎明之间的夜间持续时间变化引起的，例如核心体温或褪黑激素分泌较低。光被认为直接作用于昼夜节律起搏器（“过程 C”），而不是作用于睡眠相关过程（“过程 S”）。因此，SAD 的成功治疗必须通过已知的视网膜-下丘脑途径内的机制来实现。相反，SAD 症状的出现可能反映了对白昼长度减少的不当神经生物学反应。
