The purpose of this study was to investigate the effects of light therapy on visual contrast sensitivity in patients with seasonal affective disorder (n=10) and healthy control subjects (n=10). Static and dynamic visual contrast sensitivity was measured using a Venus system before and after 4 weeks of light therapy (10 000 lux, 30 min, 5 times a week). Light therapy increased static visual contrast sensitivity in the patients. We found no significant difference between the patients and controls either before or after light therapy. These results raise the possibility that light therapy induces retinal sensitization in seasonal affective disorder.
In the last decade, light therapy became the first choice treatment of seasonal affective disorder (SAD). The antidepressant effect of light therapy is thought to be mediated by retinal phototransduction (Wehr et al., 1987). This therapeutic success raised the possibility that retinal factors may contribute to the pathophysiology of SAD. According to Remé et al. (1990), patients with SAD show retinal subsensitivity, failing to adapt to lower winter light intensity by increasing sensitivity. In contrast, Beersma (1990) hypothesized that patients with SAD display retinal supersensitivity in winter, leading to the abnormal regulation of circadian rhythms.
The available experimental data are not sufficient to determine which of these two assumptions is correct. Low electrooculographic (EOG) ratios have been consistently demonstrated in SAD, suggesting abnormal retinal pigment epithelium in winter (Lam et al., 1991 and Ozaki et al., 1995). Interestingly, light therapy does not seem to normalize this dysfunction (Ozaki et al., 1993). Lam et al. (1992) found lower amplitudes of the b-wave in the electroretinogram (ERG) of female SAD patients, whereas the opposite effect appeared in the case of male patients. The finding from the female patients, together with a recent ERG study conducted in 12 patients with subsyndromal SAD (Hébert et al., 2002), supports the retinal subsensitivity hypothesis.
Measuring the time course of dark adaptation, Oren (1991) demonstrated that SAD patients adapted to dim light more rapidly than controls. Similarly, lower cone threshold and faster rod recovery have also been found in SAD using a photopic and scotopic light detection paradigm (Terman and Terman, 1999). It is notable, however, that Oren et al. (1993) failed to find any evidence for ophthalmic pathology, despite the wide range of tests used.
In this study, we used visual contrast sensitivity (VCS) measurements to gain more insight into the potential visual pathophysiology of SAD. Luminance contrast is an essential parameter to detect a stimulus against its background on the basis of luminance difference. The minimal contrast that is indispensable for stimulus detection is called contrast threshold, and its reciprocal is VCS (Kelly, 1977). Therefore, lower contrast threshold is expressed as higher sensitivity. VCS is predominantly determined by retinal factors and neuronal mechanisms related to the lateral geniculate nucleus and primary visual cortex. Higher order visual cortices show lower VCS (Avidan et al., 2002). To explore the effect of light therapy, VCS was measured before and after 4 weeks of light therapy.
