Feeling blue, seeing gray

Depression has long been associated with vision – and to colour perception in particular – and the link between them is evident in everyday language. Depression is, of course, often referred to as “feeling blue”, and those who suffer from it are sometimes told to “lighten up”. The link can be found in art, too – Picasso’s so-called “Blue Period,” for example, which was brought on by the suicide of his close friend Carlos Casagemas, is characterised by a series of striking paintings in shades of cold blue, which express the deep melancholy he felt at the time.

Although the association between depression and colour is largely metaphorical, there is actually some evidence that they are closely linked. The most recent comes from a new study by German researchers published in the journal Biological Psychiatry. The study shows that depressed people have reduced sensitivity to contrast, and therefore that they may perceive the world differently from others. It also suggests that depression can be diagnosed by objective measurements of electrical activity in the eye.

Earlier work has already shown that there is a physiological link between depression and vision. It has long been known, for example, that reserpine, a drug which is prescribed for psychosis and hypertension and which induces depression in humans, causes excessive sensitivity to light in various animals. Other studies have shown that patients with major depressive disorder (MDD) may also be supersensitive to light and that this can be reversed by anti-depressants; that depression causes changes in the electrical activity of the brain in response to visual stimuli; and that this change in activity can be altered by antidepressants.

Last year, neuropsychiatrist Ludger Tebartz van Elst of the University of Freiburg and his colleagues reported that patients with MDD exhibited a reduced sensitivity to contrast, while a team of researchers from Yale showed that visual motion perception is enhanced in depression. But these experiments could not establish whether the observed changes were due to alterations in the retina or the various parts of the brain through which visual information travels and is processed. And because they were based on the conscious experiences of the participants, the reported effects could have been modulated by attentional or other mechanisms.

For their latest study, van Elst’s group sought to confirm their previous findings using objective methods, and to determine if any observed changes in the contrast sensitivity of depressed patients are due to changes in the eye or brain. They recruited 40 patients diagnosed with MDD and 40 matched, healthy controls. They presented the participants with visual stimuli consisting of black and white checkerboard patterns, and used pattern electroretinography (PERG) to measure the response to the patterns. The PERG is evoked by viewing patterned stimuli and, in this case, its size is indicative of contrast gain. It is recorded at the cornea, and is thought to represent the activity of the retinal ganglion cells, which are involved in the early processing of visual information and whose axons form the optic nerve that carries the information into the brain.

Specifically, the researchers looked for differences between the two groups of participants in activity reflecting contrast gain, the process by which cells in the retina adapt to variance in the light intensity of the visual scene so that the amount of information extracted from it can be maximized. They found a significant difference in the contrast gain-related activity between the depressed patients and controls. The participants diagnosed with depression displayed a marked reduction in contrast gain when compared with the controls. The reduction was observed in both medicated and unmedicated patients. Those taking medication for their depression, however, had slightly lower depressivity scores and correspondingly better contrast gain than unmedicated patients.

Furthermore, the reduction in contrast gain was strongly correlated with the severity of depression – the more severe the depression, the greater was the observed reduction in contrast gain. No difference was observed between patients with recurrent depression and those experiencing their first episode of the condition, or between depressed patients taking selective serotonin uptake inhibitors such as fluoxetine (Prozac) and those taking tricyclic antidepressants such as imipramine. The intensity of the treatment, or dose being taken, did not affect the reduction in contrast gain observed in the depressed patients. Finally, the researchers could predict, with an accuracy of greater than 90%, which of the participants had been diagnosed with depression on the basis of their electroretinographic recordings.

This is a pilot study whose results need to be replicated. Nevertheless, it shows that processing of visual information related to contrast is altered in the retinae of depressed patients. A likely consequence of this is a reduced ability to perceive contrast – depressed people may indeed experience the world as being less colourful. The study further suggest that PERG could be useful in diagnosing and objectively measuring depression. It’s still unclear, however, whether reduced contrast processing is a specific marker of depression. The same effect could possibly occur in patients with other neuropsychiatric conditions such as schizophrenia, and this is could be investigated in future work.

Reference:

Bubl, E., et al. (2010). Seeing Gray When Feeling Blue? Depression Can Be Measured in the Eye of the Diseased. Biol. Psychiatry68: 205-208. DOI: 10.1016/j.biopsych.2010.02.009.