Blindsight

There's quite a frightening wealth of neurological conditions that could possibly befall you. I've chosen to devote this section to a phenomenon called blindsight which arises from one such disorder. Blindsight is both fascinating to think about in itself, and it adds another layer to the sections on the ventral and dorsal streams of vision.

A person with blindsight has damage in their primary visual cortex, V1. This leads to areas of blindness in some parts of their visual field, a condition called an -anopsia. In Greek, an means 'without', and opsia means 'seeing'. Depending on where the blind area is located, a person may have right or left hemianopsia (half of a visual field is gone) or quadrantanopia (a quarter of it is gone). For example, a person with binasal hemianopsia would see the following image:

Blindsight is the name given to a phenomenon in which people afflicted in the way described above can actually detect moving visual stimuli presented inside their blind area. This awareness is so strong that they can even catch objects thrown at them without warning. Furthermore, it's been shown that their blind areas retain some degree of sensitivity to luminance and color. These findings are an important part of neuroscience because they offer evidence that at least some aspects of visual stimuli don't have to enter our consciousness in order to play a part in our behavior. We've already seen hints of such non-conscious action in the dorsal stream, which is a concept that actually arose largely as a hypothesis to explain blindsight.

(As an aside, the findings above lead to a hypothesis curious to think about - that consciousness is not a property all parts of the brain share equally, but may instead be the product of a select few areas within it. At the very least, it's clear that individual brain circuits impinge on consciousness to varying degrees).

To get a firm hold on what blindsight really means, let's consider the kind of experiments done to investigate it. In one study, subjects were placed in front of a monitor and asked to guess whether any stationary object was present or not within their blind area after a tone was played. The results showed clearly that these people couldn't register the presence of an immobile object; they were wholly blind to it.

The same subjects were then shown stimuli that would start in the center of their blind area and move in some direction - up, down, right, or left. They were asked to 'guess' at the direction each stimulus had moved in. The results indicated that there was very little true guesswork involved, as the responses were nearly perfectly accurate. The subjects stubbornly insisted that these results were wholly due to luck, a hallmark of this phenomenon.

Another study played videos of the faces of people expressing particular emotions inside the blind areas of subjects' visual fields. Given options, the subjects could guess the correct emotion (most of the time). This has been shown to occur in people with normal vision, too, when emotional faces have been flashed onto a screen at a rate too fast to be consciously perceived. Though unable to consciously perceive these flashing, grimacing faces, subjects still showed appropriate reactionary emotional responses in subcortical brain areas and were able to 'guess' at the locations in which the faces had appeared at a better-than-chance rate.

The list goes on; blindsight experiments come up with pretty wild findings. The eye-pupils of cortically damaged patients continue to behave normally, adjusting to light intensity and contrast. Some patients adjust their grip shape and size to reach for objects they can't see. Others are able to glean and use the meanings of words flashed in their blind areas to make choices between pairs of words afterward presented in their intact visual fields. The perception of color, too, is not completely lost in some cases, though unfortunately the conscious experience of it is.

Given a deeper knowledge of neuroanatomy, these phenomena should actually not come as much of a surprise. This is because not all the RGC axons traveling out of the retina are restricted to the central visual pathway that I've focused on until now. Some connect to other targets in the brain, and can be either visual or non-visual - I made a small list of them in the optic nerve section.

Which of these secondary visual pathways make blindsight possible? Most often, the tecto-pulvinar pathway is invoked to explain the phenomenon. This pathway bypasses V1, connecting the retina to the superior colliculi and then to the extrastriate visual area V2 through a different thalamic nucleus, the pulvinar.

The superior colliculi form the upper pair of the tectum, which is the name given to two paired, ball-like extrusions jutting from the back of the midbrain. Like the LGN, the pulvinar is a nucleus positioned posteriorly on the thalamic egg.

Approximately 10% of RGCs leave the retina of the eye and end up in the contralateral superior colliculus. Most of these RGCs are parasol cells and hence form a magnocellular pathway focused on movement but not on fine visual discrimination. It's an old pathway, predating its LGN-V1 counterpart. Fish, amphibians, and reptiles have only this one circuit to guide them visually.

The superior colliculus (SC) is an essential component of a functional visual system. When you look at a scene, your eyes are never fixed on one spot. Both eyeballs make incessant tiny jumps, or fixations, together around the scene. They're on a constant lookout for important information while at the same time constructing your 3-D notion of the environment. It's in part the SC that guides the saccades of the eye. These movements, occurring at a rate of 2 or 3 per second, are among the fastest your body can make, second only to eye-blinks.

A cool evolutionary feature of saccades is that the eyes move further apart when performing an upward saccade, and closer together when jumping downward. Try this as you sit. Look straight on, and then jump your gaze upward. You'll probably have felt your eyes moving further apart. The reason for this has a statistical basis rooted in a 3-D perception of the environment. Your eyes diverge when looking upward in order to maximize the probability of an accurate fixation - an inaccurate alignment of your eyes would lead to double-vision. For your eyes to align properly, there's normally a need for slight corrections. Through the convergence or divergence of your eyes caused by their saccades, you maximize reaction time and minimize the energy you need to expend when changing what you're looking at.

Saccades also play a big part in the act of reading. Especially when you're reading quickly, your eyes jump across sentences and skip over words you don't perceive as important, in the way you're going to skip the second 'the' in the phrase 'Paris in the the Spring' right now.

In the tecto-pulvinar visual pathway and therefore in blindsight, the SC seems to be involved in directing attention to movement, enabling the eyes to pick out a target. It has also been contended that it plays a part in arm-reaching movements, which reminds us of the dorsal stream of vision.

Such visuomotor activity is a characteristic of the pulvinar nucleus of the thalamus, the next stop along this pathway. The pulvinar is actually a collection of nuclei - there are four distinct cell body groups within it - and so it's more accurately called a nuclear complex. The SC supplies the inferior, medial, and lateral sections of the pulvinar. From these nuclei the neural information proceeds to structures implicated in the dorsal visual stream, like the posterior parietal cortex.

In recent years (2017), a case study was published of a boy (called B.I.) who suffered extensive damage in both V1 cortices just after birth. He was the victim of a genetic disorder called MCAD, in which the body can't break down certain key fats into energy and problematically low sugar levels can result. When he was tested at 7 years of age, however, he showed remarkable visual capability. The consensus arrived at was the B.I. is not blind, nor merely adept at using blindsight - he could consciously identify colors and facial emotions, which are tasks associated with ventral stream processing that should not be able to bypass an absence of V1 cortical function.

To explain this, it was suggested that B.I.'s brain had re-routed its visual neural circuitry. MRI technology was employed to ascertain whether this was in fact the case, and a version of the tecto-pulvinar route I've outlined above came to the fore. In the circuit B.I. had formed to overcome his occipital damage, the inferior pulvinar nucleus played a leading role, forming an enhanced connection with the MT area, or V5. Thus, anecdotally at least, it appears that the V1 area can in some cases be circumvented.