Seasonal Affective Disorder: Response to Light as Measured by Electroencephalogram, Melatonin Suppression, and Cerebral Blood Flow

• Published in: British journal of psychiatry Vol. 163; no. 3; pp. 327 - 331
• Main Authors: Murphy, D. G. M., Murphy, D. M., Abbas, M., Palazidou, E., Binnie, C., Arendt, J., Costa, D. Campos, Checkley, S. A.
• Format: Journal Article
• Language: English
• Published: Cambridge, UK Cambridge University Press 01.09.1993; RCP
• Subjects: Artificial; Bipolar Disorder - physiopathology; Bipolar Disorder - psychology; Bipolar Disorder - therapy; Blood flow; Brain - blood supply; Cerebral blood flow; Cerebral Cortex - blood supply; Circadian Rhythm - physiology; Contrast sensitivity; Contrast Sensitivity - physiology; Daylight; Depressive Disorder - physiopathology; Depressive Disorder - psychology; Depressive Disorder - therapy; EEG; Electroencephalography; Event-related potentials; Evoked Potentials, Visual - physiology; Humans; Latency; Light; Light effects; Melatonin; Melatonin - blood; Pathophysiology; Personality Inventory; Phototherapy; Physiology; Regional Blood Flow - physiology; Regional variations; Retina; Retina - physiopathology; Seasonal affective disorder; Seasonal Affective Disorder - physiopathology; Seasonal Affective Disorder - psychology; Seasonal Affective Disorder - therapy; Tomography, Emission-Computed, Single-Photon
• ISSN: 0007-1250; 1472-1465
• DOI: 10.1192/bjp.163.3.327

This study was designed to test the hypothesis that patients with SAD have significantly different physiological responses to light than healthy age- and sex-matched controls. We studied retinal contrast sensitivity, visual evoked EEG responses, and melatonin suppression by, and cerebral blood flow response to, full-spectrum artificial daylight. There was no significant difference between 10 patients and 11 controls in retinal contrast sensitivity, or amplitude or latency of N2, P2, P100 or P300 on EEG. We compared melatonin suppression in 12 SAD patients and 12 controls. During exposure to 500 lux and 1500 lux artificial daylight both the SAD patients and controls had a significant melatonin percentage suppression; however, the percentage suppression did not differ significantly between the SAD patients and the controls. In addition, we carried out a small pilot study into the effect of light on cerebral blood flow in four SAD patients and four controls. Before exposure to 1500 lux artificial daylight there was no significant difference between patients and controls in global, regional or cerebral hemispheric blood flow. After light exposure the SAD patients and controls had a significantly different percentage change in cerebral blood flow. We suggest that patients with SAD do not have significantly physiological responses to light than controls, except perhaps in cerebral blood flow. Furthermore, mechanisms other than supersensitivity of melatonin suppression must explain both the pathophysiology of the disorder and its response to treatment with light.