May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Electroretinography in Patients with Winter Seasonal Affective Disorder
Author Affiliations & Notes
  • M. Hebert
    Dept Ophthalmology, Pavillon CHUL/University Laval, Quebec, PQ, Canada
  • C.W. Beattie
    Dept Ophthalmology,
    University of British Columbia, Vancouver, BC, Canada
  • E.M. Tam
    Division of Clinical Neurosciences/Depart of Psychiatry,
    University of British Columbia, Vancouver, BC, Canada
  • L.N. Yatham
    Division of Clinical Neurosciences/Depart of Psychiatry,
    University of British Columbia, Vancouver, BC, Canada
  • R.W. Lam
    Division of Clinical Neurosciences/Depart of Psychiatry,
    University of British Columbia, Vancouver, BC, Canada
  • Footnotes
    Commercial Relationships  M. Hebert, None; C.W. Beattie, None; E.M. Tam, None; L.N. Yatham, None; R.W. Lam, None.
  • Footnotes
    Support  MRC Grant
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 794. doi:
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    • Get Citation

      M. Hebert, C.W. Beattie, E.M. Tam, L.N. Yatham, R.W. Lam; Electroretinography in Patients with Winter Seasonal Affective Disorder . Invest. Ophthalmol. Vis. Sci. 2004;45(13):794.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: A retinal sensitivity abnormality has been hypothesized in seasonal affective disorder (SAD). The electroretinogram (ERG) was used to objectively assess retinal sensitivity at the level of the rod photoreceptor system. Methods:23 normal control subjects were age–paired and sex–matched as much as possible with 27 depressed patients meeting DSM–III–R criteria for major depression, recurrent, with a seasonal (winter) pattern. Scotopic ERG testing was performed in dark–adapted dilated eyes in winter between 10:00 and 15:00 h. Retinal sensitivity was based on the light stimulus intensity (blue–green) necessary to reach a 50µV amplitude threshold. Results: Retinal sensitivity was significantly lower (0.21 log units; p<0.05) in SAD patients compared to normal control subjects (that is a higher intensity was needed to reach the 50µV amplitude criteria in SAD patients). 55% of the patients had a retinal sensitivity value one standard deviation lower than the mean value of the control subjects. Conclusions: These results are consistent with a retinal hyposensitivity hypothesis for SAD, but the explanation for lower rod photoreceptor sensitivity in SAD is not known. We hypothesize that a brain neurotransmitter dysregulation may be at the origin of both the mood disorder and retinal sensitivity change. Since retinal sensitivity has been shown to be modulated by melatonin and dopamine, we propose that serotonin (precursor of melatonin) and/or dopamine could be good candidates to explain both the depressive symptoms and the retinal sensitivity change observed in our patients. A cone ERG assessment might be helpful to further investigate the role of dopamine in SAD.

Keywords: electroretinography: non–clinical • dopamine • melatonin 
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