Editing Blindsight (section)

== Brain regions involved ==
{{More medical citations needed|section|reason=only final sentence appears to be inline referenced|date=August 2015}}

Visual processing in the brain goes through a series of stages. Destruction of the primary visual cortex leads to blindness in the part of the visual field that corresponds to the damaged cortical representation. The area of blindness – known as a [[scotoma]] – is in the visual field opposite the damaged hemisphere and can vary from a small area up to the entire hemifield. Visual processing occurs in the brain in a hierarchical series of stages (with much [[Crosstalk (biology)|crosstalk]] and feedback between areas). The route from the [[retina]] through V1 is not the only visual pathway into the cortex, though it is by far the largest; it is commonly thought that the residual performance of people exhibiting blindsight is due to preserved pathways into the extrastriate cortex that bypass V1. However both physiological evidence<ref>{{cite journal|vauthors = Rodman HR, Gross CG, Albright TD|title = Afferent basis of visual response properties in area MT of the macaque. I. Effects of striate cortex removal|journal = The Journal of Neuroscience|volume = 9|issue = 6|pages = 2033–50|date = June 1989|pmid = 2723765|pmc = 6569731|doi = 10.1523/JNEUROSCI.09-06-02033.1989}}</ref> in monkeys and behavioral and imaging evidence in humans<ref name=":2" /><ref name=":3" /><ref name=":6" /><ref name="ncbi.nlm.nih.gov" /> shows that activity in these extrastriate areas, and especially in V5, is apparently sufficient to support visual awareness in the absence of V1.

To put it in a more complex way, recent physiological findings suggest that [[visual processing]] takes place along several independent, parallel pathways. One system processes information about shape, one about color, and one about movement, location and spatial organization. This information moves through an area of the brain called the [[lateral geniculate nucleus]], located in the [[thalamus]], and on to be processed in the primary visual cortex, area V1 (also known as the [[striate cortex]] because of its striped appearance). People with damage to V1 report no conscious vision, no visual imagery, and no visual images in their dreams. However, some of these people still experience the blindsight phenomenon,<ref name=":0" /> though this too is controversial, with some studies showing a limited amount of consciousness without V1 or projections relating to it.<ref>{{cite journal|vauthors = Ffytche DH, Zeki S|title = The primary visual cortex, and feedback to it, are not necessary for conscious vision|journal = Brain|volume = 134|issue = Pt 1|pages = 247–57|date = January 2011|pmid = 21097490|pmc = 3159156|doi = 10.1093/brain/awq305|doi-access = free}}</ref>

The superior colliculus and prefrontal cortex also have a major role in awareness of a visual stimulus.<ref name=":1">{{cite journal|vauthors = Hall NJ, Colby CL|year=2009|title=Response to blue visual stimuli in the macaque superior colliculus|journal=Society for Neuroscience|volume=19|pages=520–533}}</ref>

=== Lateral geniculate nucleus ===
{{Main|Lateral geniculate nucleus}}

[[Mosby's Dictionary of Medicine, Nursing & Health Professions]] defines the LGN as "one of two elevations of the lateral posterior thalamus receiving visual impulses from the retina via the optic nerves and tracts and relaying the impulses to the calcarine (visual) cortex".<ref>{{Cite book|title=Mosby's Dictionary of Medicine, Nursing & Health Professions|date=2009|publisher=Mosby/Elsevier|others=Mosby, Inc.|isbn=9780323049375|edition=8th|location=St. Louis, Missouri|oclc=226911727|title-link=Mosby's Dictionary of Medicine, Nursing & Health Professions}}</ref>

What is seen in the left and right visual field is taken in by each eye and brought back to the [[optic disc]] via the nerve fibres of the retina.<ref name="neuroscience.uth.tmc.edu">{{cite web|url=http://nba.uth.tmc.edu/neuroscience/s2/chapter15.html|title=Chapter 15: Visual Processing: Cortical Pathways|vauthors=Dragoi V|date=1997|work=Neuroscience Online|publisher=The University of Texas Health Science Center at Houston|access-date=November 3, 2013|archive-date=July 26, 2024|archive-url=https://web.archive.org/web/20240726180038/https://nba.uth.tmc.edu/favicon.ico|url-status=live}}</ref> From the optic disc, visual information travels through the optic nerve and into the [[optic chiasm]]. Visual information then enters the optic tract and travels to four different areas of the brain including the [[superior colliculus]], [[pretectum]] of the mid brain, the suprachiasmatic nucleus of the [[hypothalamus]], and the [[lateral geniculate nucleus]] (LGN). Most axons from the LGN will then travel to the primary visual cortex.<ref name="neuroscience.uth.tmc.edu" />

Injury to the primary visual cortex, including lesions and other trauma, leads to the loss of visual experience.<ref name="Schmid, M. Mrowka 2010" /> However, the residual vision that is left cannot be attributed to V1. According to Schmid et al., "thalamic lateral geniculate nucleus has a causal role in V1-independent processing of visual information".<ref name="Schmid, M. Mrowka 2010" /> This information was found through experiments using fMRI during activation and inactivation of the LGN and the contribution the LGN has on visual experience in monkeys with a V1 lesion. These researchers concluded that the [[Magnocellular pathway|magnocellular system]] of the LGN is less affected by the removal of V1, which suggests that it is because of this system in the LGN that blindsight occurs.<ref name="Schmid, M. Mrowka 2010">{{cite journal|vauthors = Schmid MC, Mrowka SW, Turchi J, Saunders RC, Wilke M, Peters AJ, Ye FQ, Leopold DA|display-authors = 6|title = Blindsight depends on the lateral geniculate nucleus|journal = Nature|volume = 466|issue = 7304|pages = 373–7|date = July 2010|pmid = 20574422|pmc = 2904843|doi = 10.1038/nature09179|bibcode = 2010Natur.466..373S}}</ref> Furthermore, once the LGN was inactivated, virtually all of the extrastriate areas of the brain no longer showed a response on the fMRI.<ref name="Schmid, M. Mrowka 2010" /> The information leads to a qualitative assessment that included "scotoma stimulation, with the LGN intact had fMRI activation of ~20% of that under normal conditions".<ref name="Schmid, M. Mrowka 2010" /> This finding agrees with the information obtained from, and fMRI images of, patients with blindsight.<ref name="Schmid, M. Mrowka 2010" /> The same study<ref name="Schmid, M. Mrowka 2010" /> also supported the conclusion that the LGN plays a substantial role in blindsight. Specifically, while injury to V1 does create a loss of vision, the LGN is less affected and may result in the residual vision that remains, causing the "sight" in blindsight.<ref name="Schmid, M. Mrowka 2010" />

[[Functional magnetic resonance imaging]] has launched has also been employed to conduct brain scans in normal, healthy human volunteers to attempt to demonstrate that visual motion can bypass V1, through a connection from the LGN to the human middle temporal complex.<ref name=":2" /><ref name="ncbi.nlm.nih.gov">{{cite journal|vauthors = Gaglianese A, Costagli M, Bernardi G, Ricciardi E, Pietrini P|title = Evidence of a direct influence between the thalamus and hMT+ independent of V1 in the human brain as measured by fMRI|journal = NeuroImage|volume = 60|issue = 2|pages = 1440–7|date = April 2012|pmid = 22300813|doi = 10.1016/j.neuroimage.2012.01.093|s2cid = 937762}}</ref> Their findings concluded that there was an indeed a connection of visual motion information that went directly from the LGN to the V5/hMT+ bypassing V1 completely.<ref name="ncbi.nlm.nih.gov" /> Evidence also suggests that, following a traumatic injury to V1, there is still a direct pathway from the retina through the LGN to the extrastriate visual areas.<ref name="cns.nyu.edu">{{cite journal|vauthors = Cowey A|title = Visual system: how does blindsight arise?|journal = Current Biology|volume = 20|issue = 17|pages = R702-4|date = September 2010|pmid = 20833309|doi = 10.1016/j.cub.2010.07.014|s2cid = 17351599|doi-access = free|bibcode = 2010CBio...20.R702C}}</ref> The extrastriate visual areas include parts of the [[occipital lobe]] that surround V1.<ref name="neuroscience.uth.tmc.edu" /> In non-human primates, these often include V2, V3, and V4.<ref name="neuroscience.uth.tmc.edu" />

In a study conducted in [[primate]]s, after partial [[ablation]] of area V1, areas V2 and V3 were still excited by visual stimulus.<ref name="cns.nyu.edu" /> Other evidence suggests that "the LGN projections that survive V1 removal are relatively sparse in density, but are nevertheless widespread and probably encompass all extrastriate visual areas," including V2, V4, V5 and the inferotemporal cortex region.<ref name="Weiskrantz, L. 1996">{{cite journal|vauthors = Weiskrantz L|title = Blindsight revisited|journal = Current Opinion in Neurobiology|volume = 6|issue = 2|pages = 215–20|date = April 1996|pmid = 8725963|doi = 10.1016/s0959-4388(96)80075-4|s2cid = 1833570}}</ref>