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Blindsight, as the name implies, is a paradox—a sort of seeing without “seeing.” Ever since the term was first coined in the early 1970s it has raised profound and intriguing questions about what it means to “see,” and what it means to “guess.” For example, if you make 100 random guesses in a row and 90 of your guesses are correct, does it qualify as “guessing”? If you respond accurately (by guessing) to visual stimuli but deny having consciously seen anything, does this count as “seeing”? Barring a paranormal explanation, how could this be possible? By raising these and other questions, the phenomenon of blindsight has enriched our understanding of consciousness, vision, and the brain, and has been fodder for a rich scientific and philosophical debate. This entry will cover the essential concepts from neurology that are relevant to blindsight, provide a brief history of blindsight research, describe the defining characteristics of blindsight and how these might be explained by the architecture of the brain, and discuss the possibility of blindsight in normally sighted individuals as an emerging direction in blindsight research.

Hemianopia (“Cortical Blindness”)

To clearly understand what blindsight is, it is necessary to understand cortical blindness. Lesions in the primary visual cortex (called V1) of the occipital lobe, due to stroke or head trauma, normally lead to blindness in the corresponding region of the patient's field of view (FOV). For example, damage to the lower part of V1 in the left hemisphere will produce a “blind region” (or scotoma) in the upper-right quadrant of the FOV. Damage to the entirety of V1 in the left hemisphere will lead to blindness in the entire right-hand side of the FOV (called hemianopia, meaning “half-field blindness”). Note that in V1 the signals from the two eyes are combined into a single binocular view (you do not normally see two of everything, even though you have two eyes), so the blind area in this case is not specific to one eye or the other. The two eyes may continue to function normally, but the signals from the left side of each retina (in the latter example) are cut off at their main junction with the cerebral cortex (V1).

Just what do such patients experience when they look at the visual scene? One might suppose that these patients experience something like a large black stain in their visual field that occludes objects from view. In fact, what the patients experience in their scotoma is probably more like what you “see” behind your head. Most likely you do not feel that anything is missing from your field of view behind your head—it is simply not part of your field of view. Likewise these patients are usually unaware that anything is missing, even when they bump into something.

Normally the extent of such patients' scotomas is determined by asking the patients to fix their gaze and then recording their responses to brief flashes of light, presented one at a time at a broad array of points covering the normal extent of the visual field (a process called perimetry). The points that the patients consistently fail to detect are taken to delimit the scotoma(e), and thus concludes the test—or so it would seem.

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