Human visual responses in the absence of the geniculo-calcarine projection

Barbur, Jl

doi:10.1093/neucas/3.5.395-g

Cited by 39 publications

(58 citation statements)

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“…V1 neurons, although predominantly linear in their contrast response, exhibit a degree of response saturation (Albrecht and Hamilton, 1982;Ohzawa et al, 1982;Sclar et al, 1990). Furthermore, the low spatial and higher temporal frequencies of stimuli used here, which are suggested to be "optimal" for blindsight (Barbur et al, 1980;Sahraie et al, 2003Sahraie et al, , 2008, are somewhat different from typical P channel preferences (Derrington and Lennie, 1984;Foster et al, 1985;Sclar et al, 1990).…”

Section: The Relationship Between Fmri and Neurophysiology In Contrasmentioning

confidence: 62%

Abnormal Contrast Responses in the Extrastriate Cortex of Blindsight Patients

et al. 2015

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When the human primary visual cortex (V1) is damaged, the dominant geniculo-striate pathway can no longer convey visual information to the occipital cortex. However, many patients with such damage retain some residual visual function that must rely on an alternative pathway directly to extrastriate occipital regions. This residual vision is most robust for moving stimuli, suggesting a role for motion area hMTϩ. However, residual vision also requires high-contrast stimuli, which is inconsistent with hMTϩ sensitivity to contrast in which even low-contrast levels elicit near-maximal neural activation. We sought to investigate this discrepancy by measuring behavioral and neural responses to increasing contrast in patients with V1 damage. Eight patients underwent behavioral testing and functional magnetic resonance imaging to record contrast sensitivity in hMTϩ of their damaged hemisphere, using Gabor stimuli with a spatial frequency of 1 cycle/°. The responses from hMTϩ of the blind hemisphere were compared with hMTϩ and V1 responses in the sighted hemisphere of patients and a group of age-matched controls. Unlike hMTϩ, neural responses in V1 tend to increase linearly with increasing contrast, likely reflecting a dominant parvocellular channel input. Across all patients, the responses in hMTϩ of the blind hemisphere no longer showed early saturation but increased linearly with contrast. Given the spatiotemporal parameters used in this study and the known direct subcortical projections from the koniocellular layers of the lateral geniculate nucleus to hMTϩ, we propose that this altered contrast sensitivity in hMTϩ could be consistent with input from the koniocellular pathway.

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Section: The Relationship Between Fmri and Neurophysiology In Contrasmentioning

confidence: 62%

Abnormal Contrast Responses in the Extrastriate Cortex of Blindsight Patients

et al. 2015

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“…Our test subject was G.Y., a 50-y-old man with blindsight arising from unilateral damage to his left medial occipital cortex that caused a right, homonymous hemianopia, with macular sparing extending 3.5°into what is an otherwise a blind hemifield (27) (Fig. 2).…”

Section: Resultsmentioning

confidence: 99%

Illusory motion perception in blindsight

Azzopardi

Hock

2010

Proc. Natl. Acad. Sci. U.S.A.

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Motion detection is typically spared in blindsight, which results from damage to the striate cortex (area V1) of the brain that is sufficient to eliminate conscious visual awareness and severely reduce sensitivity to luminance contrast, especially for high spatial and low temporal frequencies. Here we show that the discrimination of motion direction within cortically blind fields is not attributable to feature tracking (the detection of changes in position or shape), but is due instead to the detection of firstorder motion energy (spatiotemporal changes in luminance). The key to this finding was a version of the line motion illusion entailing reverse-phi motion in which opposing motion directions are simultaneously cued by motion energy and changes in stimulus shape. In forced-choice tests, a blindsighted test subject selected the direction cued by shape change when the stimulus was presented in his intact field, but reliably selected the direction cued by motion energy when the same stimulus was presented in his blind field, where relevant position information was either inaccessible or invalid. Motion energy has been characterized as objectless, so reliance on motion energy detection is consistent with impaired access to shape information in blindsight. The dissociation of motion direction by visual field (cortically blind vs. intact) provides evidence that two pathways from the retina to MT/V5 (the cortical area specialized for motion perception) are functionally distinct: the retinogeniculate pathway through V1 is specialized for feature-based motion perception, whereas the retinocollicular pathway, which bypasses V1, is specialized for detecting motion energy.superior colliculus | visual cortex | visual pathway | hemianopia B lindsight is a rare phenomenon caused by damage to the primary visual cortex (striate cortex, or V1) of the brain that is sufficient to eliminate conscious visual awareness (1, 2). Visual sensitivity to luminance contrast is reduced in the corresponding part of the visual field, most severely for high spatial and low temporal frequencies (3). The fact that it is not completely abolished for low spatial and high temporal frequencies accounts for many of the residual visual capacities that have been reported in blindsight, including, in forced-choice tests, the ability to detect and discriminate stimuli presented in the field defect (2, 4). Evidence obtained from monkeys with striate cortex lesions as well as from cortically blind patients suggests that these capacities are mediated by neural pathways that project from the retina to extrastriate visual cortex, which normally bypass the main visual pathway that projects from the retina to the striate cortex via the lateral geniculate nucleus (the retinogeniculate pathway) and involve the superior colliculus of the midbrain and the lateral geniculate and pulvinar nuclei of the thalamus (5-13).Blindsight is not merely normal vision without awareness. In addition to the loss of primary visual cortex, retrograde degeneration of relay neurons ...

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“…In fact, GY suffered a lesion strictly confined to his left V1 as a consequence of a traumatic brain injury during a traffic accident that occurred very early in his life, when he was only 7 years old (Barbur, Ruddock, & Waterfield, 1980;de Gelder et al, 2005;Morris et al, 2001;Sahraie et al, 1997). Thus, it has been proposed, and later on verified with different neuroimaging methods, that considerable post-lesion and experience-dependent plasticity has taken place in GY's brain (Bridge et al, 2008;Tamietto et al, 2012).…”

Section: What Could Be Mistaken About Affective Blindsight?mentioning

confidence: 99%

From affective blindsight to emotional consciousness

Celeghin

Gelder

Tamietto

2015

Consciousness and Cognition

111

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a b s t r a c tFollowing destruction or denervation of the primary visual cortex (V1) cortical blindness ensues. Affective blindsight refers to the uncanny ability of such patients to respond correctly, or above chance level, to visual emotional expressions presented to their blind fields. Fifteen years after its original discovery, affective blindsight still fascinates neuroscientists and philosophers alike, as it offers a unique window on the vestigial properties of our visual system that, though present in the intact brain, tend to be unnoticed or even actively inhibited by conscious processes. Here we review available studies on affective blindsight with the intent to clarify its functional properties, neural bases and theoretical implications. Evidence converges on the role of subcortical structures of old evolutionary origin such as the superior colliculus, the pulvinar and the amygdala in mediating affective blindsight and nonconscious perception of emotions. We conclude that approaching consciousness, and its absence, from the vantage point of emotion processing may uncover important relations between the two phenomena, as consciousness may have evolved as an evolutionary specialization to interact with others and become aware of their social and emotional expressions.

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Human visual responses in the absence of the geniculo-calcarine projection

Cited by 39 publications

References 0 publications

Abnormal Contrast Responses in the Extrastriate Cortex of Blindsight Patients

Abnormal Contrast Responses in the Extrastriate Cortex of Blindsight Patients

Illusory motion perception in blindsight

From affective blindsight to emotional consciousness

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