It’s hard not to take all the complexities of our visual perception for granted. Human vision generally allows us to simultaneously perceive many attributes of an object, like colour, shape, and texture. We can perceive features and recognize people, differentiate them from one another, understand their facial expressions, and associate them with how they might feel. But when these modes of perception are impaired, they can create similarly complex effects.
In An Anthropologist on Mars, neurologist Oliver Sacks writes about a case of a painter completely unable to perceive colour. In another case explored in Melvyn Goodale & David Milner’s Sight Unseen, detailed by Sacks, that of patient DF, a woman wakes up from a coma and realizes she can no longer see shapes. Aimee Bender — a surrealist fiction writer — writes about a boy who cannot recognize faces and expressions.
Although that last case is fictional, these stories all talk about real impairments in visual perception that some people actually experience. The Varsity interviewed Jonathan Cant, an associate professor in the Department of Psychology at UTSC who studies cognitive neuroscience and visual perception, about what causes all of these visual impairments — and what they can tell us about the human brain.
Cerebral achromatopsia: the case of the colourblind painter
A painter, Mr. I, had been driving when he was hit by a truck on the passenger side of his car. After the accident, he saw the world in greyscale. This had been a strange case for the late 1980s because colourblindness was understood as genetic and congenital, not a condition acquired later in life.
Also, most colourblind cases were characterized by an inability to distinguish between red and green, which was due to defects in the cones, the photoreceptor cells that allow us to perceive colour. And because cones are part of the retina, this is called retinal colourblindness. As such, colourblindness had been attributed to defects in the retina, not to lesions of brain regions that process colour.
What made this case different was that not only was the painter unable to see colour, he was also no longer able to imagine it. It was unclear whether the damage was to his brain or eyes. However, his inability to even imagine colour pointed to the brain as the damaged structure.
Mr. I was a professional painter — he knew the colours of everything. But he couldn’t see or imagine the colours that he once knew; after the accident, he only knew colours by their names. Imagine how frustrating this must feel: you are certain you know something, but you can’t see it or remember it; you absolutely no longer have access to it, even in the form of memory or imagination.
Total colourblindness, like the case described in The Case of the Colourblind Painter, is called cerebral achromatopsia and is caused by bilateral cortical damage — damage of the colour-processing areas in both hemispheres of the brain.
In the interview, Cant said that the region of the brain most commonly affected in cerebral achromatopsia is the lingual gyrus and fusiform gyri in the occipito-temporal cortex.
Such was the case for the colourblind painter: the secondary visual cortex in both hemispheres, specifically visual area four, which is in the fusiform gyrus, was bilaterally impaired. The occipital cortex is at the back of your brain and the temporal cortex is near your temples. The lingual and fusiform gyrus are regions that span from the back of the brain to the bottom sides of the brain, near your temples.
Cant added that cerebral achromatopsia is acquired — in contrast to retinal colourblindness, which is genetic — and occurs after a lesion to the cortex caused by stroke, head injury, epileptic seizure, or any incident that might disrupt certain regions of the brain. Cant added, “If the lesion to a brain is to the right hemisphere near the lingual and fusiform gyrus, the patient would lose colour vision for the opposite visual field,” and vice versa. Cant continued, “If you have bilateral lesions in the same general region on both sides of the brain, you would acquire full cerebral achromatopsia.”
It is also not always the case that full cerebral achromatopsia patients lose their ability to imagine colour. But some patients with full cerebral achromatopsia do lose visual imagery for colour. And this was the case for the colourblind painter.
Bender, who writes surrealist fiction, wrote a short story called “Faceless” in The Colour Master, a short story collection. The story is about a boy who cannot see the faces of the people around him. Until my interview with Cant, I thought this had been a surrealist fiction story with a case that Bender had made up, but to my surprise, face blindness is a real neurological disorder!
This impairment in recognizing facial features is called prosopagnosia. The common area lesioned in cases of prosopagnosia is the ventromedial — front and middle — region of the occipito-temporal cortex, including the lingual and fusiform gyri — similar to the regions commonly lesioned in cerebral achromatopsia.
Visual form agnosia
Cant also mentioned the case of patient DF as the one that spurred his interest in visual perception. After carbon monoxide poisoning, patient DF woke up from a coma and couldn’t see shapes anymore but could see colour just fine, implying that shape and colour are processed independently in the visual system. This agnosia was caused by damage to the occipital cortex of patient DF.
U of T courses on vision perception and impairment
If these cases interest you, there are some courses about vision perception offered at the Scarborough campus of U of T. Most relevant to this topic is PSYC51 — Cognitive Neuroscience of Vision, which covers visual cognitive impairments like cerebral achromatopsia, visual form agnosia, higher-level perception of features, and defects in this perception like prosopagnosia. Also at UTSC, PSYC75 — Cognitive Psychology Laboratory covers classic cognitive psychology experiments and visual processing.
Editor’s note (February 25): A previous version of this article mistakenly referred to patient DF as a man, when, in fact, patient DF was a woman.