Blindsight

Disease/Disorder

Anatomy or system affected: Visual perception, consciousness

Definition: The ability of some patients with occipital cortex damage to respond at above chance levels to stimuli presented in their blind visual field.

Key terms:

forced-choice alternative paradigms: experimental methodology for demonstrating blindsight; patients must “guess” from a range of options (i.e., make a forced choice from a range of alternatives) regarding a specific stimulus property (e.g., location, direction of motion, etc.)

geniculostriate pathway: primary pathway for vision from the retina via the lateral geniculate nucleus of the thalamus and optic radiations to primary visual cortex (occipital cortex)

homonymous hemianopia: blindness in one half of visual space due to unilateral occipital cortex damage; hemianopic field defects occur in contralesional space; "homonymous" refers to the uniform nature of the field defect seen in some patients

implicit processing: demonstration of altered behavioral responses to a stimulus in the absence of conscious reportage

occipital cortex: posterior portion of the cortex with a retinotopic representation of visual space

retinotopic map: a one-to-one representation of visual space mapped onto the occipital cortex; specific portions of the retina that respond to specific regions of space are mapped to a correspondingly specific region of the occipital cortex

Causes and Symptoms

Blindsight is a residual ability in some individuals who have suffered damage to the brain's occipital cortex, causing a corresponding region of blindness. The occipital cortex is organized retinotopically, with specific regions of space being represented in specific portions of the occipital cortex and beyond (often referred to as the striate and extrastriate cortex). Damage to left hemisphere occipital cortex will lead to blindness for the right visual space, and vice versa. The most common cause of such blindness is stroke, but any process that damages the occipital cortex will lead to blindness in a corresponding region of retinotopic space.

There are perhaps two common symptoms in cortically blind individuals that would hint at the presence of blindsight. The first is known as Riddoch's phenomenon, in which the patient reports having a “sense” of motion in their blind field. It is important to note that the patient does not routinely report conscious perception of motion but rather has a sense or “feeling” that something is moving in the blind field. Two-alternative forced-choice testing can then demonstrate the veracity of such blind-field motion processing. Second, cortically blind patients may show themselves to be adept at obstacle avoidance even for stimuli appearing in their blind field. Casual observation of such obstacle avoidance does not represent proof of blindsight, as in an uncontrolled environment the patient could simply be using learned strategies and eye movements to compensate for their blindness. As such, detailed testing that controls for a variety of factors, including eye movements, is needed to demonstrate true obstacle avoidance in the blind field.

Blindsight is categorized as either type 1 or type 2. In type 1 blindsight, the patient has no conscious awareness whatsoever of a visual stimulus but can nevertheless predict certain aspects of it at a significantly better-than-chance rate. In type 2 blindsight, the patient reports some awareness of visual change, such as movement, but still cannot consciously perceive it.

Treatment and Therapy

Blindsight is viewed not as a deficit but rather as a residual function. It has been used to demonstrate the presence of secondary visual pathways in the primate brain that transmit visual information from the retina to the extrastriate cortex without the need to first go through the occipital cortex. A variety of treatments have been tried for those suffering hemianopic field defects, with or without blindsight. These include the use of optical prisms to expand the patient's functional field of view and training to encourage patients to use intact abilities such as eye movements to compensate for their visual field loss.

Finally, and more controversially, there have been attempts at restitution of vision following stimulation of the blind field. Here the patient is presented with repetitive visual stimuli at the border of their sighted and blind fields with the assumption that neuroplasticity will expand the functional visual fields of neurons in this “transition” region. Two major restitution techniques are vision restoration therapy (VRT) and neuro-eye therapy (NeET). VRT involves presenting a light target within the boundaries of the patient's field defect with the intention of improving reaction time and detection rate over time. NeET involves presenting grating patterns (sets of black and white lines) with specific spatial frequencies at specific locations within the field defect and requiring the patient to choose in which of two time intervals the pattern was presented. Research on and results from restitution of this kind have been mixed.

Perspective and Prospects

Blindsight was first demonstrated by Lawrence Weiskrantz and colleagues in the early 1970s with a patient who could localize, by pointing or eye movements, targets presented to his blind field at better-than-chance levels. Since then, a wealth of research has demonstrated above-chance responses to a wide range of blind-field stimuli, although it should be noted that these responses have been evident in a relatively small number of patients. Residual capacities range from target localization and motion, form, and color discrimination to semantic priming and even affective responses to nonconscious stimuli. These results have been taken as evidence that there are multiple pathways for visual information to reach the cortex, some of which bypass the primary cortical target of the geniculostriate pathway—the primary occipital cortex (V1).

The notion that blindsight provided evidence for secondary visual pathways was initially challenged by Michael S. Gazzaniga and colleagues as instead reflecting the activity of spared “islands” of intact cortex within the damaged hemisphere. In addition, John Campion and colleagues suggested that light scatter—light from a blind-field stimulus scattering into the sighted field, or light within the orbit scattering to regions of the retina that process sighted-field stimuli—provided a more likely explanation for blindsight. However, more recent work using structural magnetic resonance imaging (MRI) and diffusion tensor imaging (DTI, which highlights white-matter tracts in the human brain), as well as behavioral studies with appropriate controls for light scatter, have conclusively shown that blindsight does indeed rely on secondary visual pathways that bypass V1.

The primary visual pathway, also called the geniculostriate visual pathway, is what provides people with a rich mental representation of the visual world. Blindsight allows researchers to explore the functionality of secondary pathways that rapidly transmit information to the cortex with little need for conscious processing. A person's ability to rapidly respond to moving stimuli, avoid obstacles in the periphery, or even formulate a rapid response to emotionally valenced stimuli may depend on these secondary networks to give a quick “first pass” neural analysis that can then be fed back to the slower-acting primary visual pathway.

Bibliography

Breitmeyer, Bruno. Blindspots: The Many Ways We Cannot See. New York: Oxford UP, 2010. Print.

Cowey, Alan. “The Blindsight Saga.” Experimental Brain Research 200.1 (2010): 3–24. Print.

Danckert, James, and Yves Rossetti. “Blindsight in Action: What Can the Different Sub-types of Blindsight Tell Us about the Control of Visually Guided Actions?” Neuroscience & Biobehavioral Reviews 29.7 (2005): 1035–46. Print.

Foley, Robert, and Robert W. Kentridge, eds. Type 2 Blindsight. Spec. issue of Consciousness and Cognition 32 (2015): 1–128. Print.

Grunda, Tomas, Petr Marsalek, and Pavla Sykorova. “Homonymous Hemianopia and Related Visual Defects: Restoration of Vision after a Stroke.” Acta Neurobiologiae Experimentalis 73.2 (2013): 237–49. Print.

Sahraie, Arash, and Ceri T. Trevethan. "Rehabilitation of Visual Field Impairment." Textbook of Neural Repair and Rehabilitation. Ed. Michael E. Selzer et al. 2nd ed. Vol. 2. Cambridge: Cambridge UP, 2014. 500–507. Print.

Striemer, Christopher L., Craig S. Chapman, and Melvyn A. Goodale. “ʻReal-Timeʼ Obstacle Avoidance in the Absence of Primary Visual Cortex.” Proceedings of the National Academy of Sciences of the United States of America 106.37 (2009): 15996–6001. Print.

Weiskrantz, Lawrence. Blindsight: A Case Study Spanning 35 Years and New Developments. New York: Oxford UP, 2009. Print.

Weiskrantz, Lawrence. “Blindsight Revisited.” Current Opinion in Neurobiology 6.2 (1996): 215–20. Print.