Destruction Of Primary Visual Cortex Research Articles

Blindsight is qualitatively degraded conscious vision.

Blindsight is a neuropsychological condition defined by residual visual function following destruction of primary visual cortex. This residual visual function is almost universally held to include capacities for voluntary discrimination in the total absence of awareness. So conceived, blindsight has had an enormous impact on the scientific study of consciousness. It is held to reveal a dramatic disconnect between performance and awareness and used to motivate diverse claims concerning the neural and cognitive basis of consciousness. Here I argue that this orthodox understanding of blindsight is fundamentally mistaken. Drawing on models from signal detection theory in conjunction with a wide range of behavioral and first-person evidence, I contend that blindsight is severely and qualitatively degraded but nonetheless conscious vision, unacknowledged due to conservative response biases. Psychophysical and functional arguments to the contrary are answered. A powerful positive case for the qualitatively degraded conscious vision hypothesis is then presented, detailing a set of distinctive predictions borne out by the data. Such data are further used to address the question of what it is like to have blindsight, as well as to explain the conservative and selectively unstable response criteria exhibited by blindsight subjects. On the view defended, blindsight does not reveal any dissociation between performance and awareness, nor does it speak to the neural or cognitive requirements for consciousness. A foundation stone of consciousness science requires radical reconsideration. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

Can IPS reach visual awareness without V1? Evidence from TMS in healthy subjects and hemianopic patients

TMS of the occipital cortex can elicit conscious visual percepts, the so-called phosphenes, i.e. the experience of flashes of light in the absence of an external stimulus. Previous evidence has shown that phosphenes can be elicited by TMS of the intraparietal sulcus (IPS). Here, we tested whether IPS-phosphenes are generated without any contribution from the occipital cortex. In Experiment 1, healthy subjects showed that parietal phosphenes were reliable different in terms of threshold, highly variable in size and, in contrast to the occipital ones, they did not change in lateralization within the visual field. Moreover, to strengthen these results and to ascertain whether feedback to primary visual cortex is necessary for visual awareness to emerge, in Experiment 2, we induced phosphenes by applying TMS over the parietal cortex of the lesioned hemisphere in two hemianopic patients with a complete destruction of primary visual cortex. For both patients we found that they could perceive phosphenes, that a psychophysical threshold function could be created and that this function was not different from that obtained with healthy subjects. In addition, they could reliably draw the phosphenes and position them within their blind field and they could reliably score the phenomenical characteristics of their phosphenes both in terms of vividness and brightness in a manner similar to healthy subjects. The two brain-damaged patients have thus shown that stimulation of visual areas within the intraparietal sulcus of their lesioned hemisphere, can, in fact, elicit conscious visual percepts. These results seem to demonstrate that TMS-induced visual phenomenology over IPS can generate conscious visual percepts and, more importantly, that it does so independently of any contributions from the primary visual cortex.

Evidence of a direct influence between the thalamus and hMT+ independent of V1 in the human brain as measured by fMRI

In the present study we employed Conditional Granger Causality (CGC) and Coherence analysis to investigate whether visual motion-related information reaches the human middle temporal complex (hMT+) directly from the Lateral Geniculate Nucleus (LGN) of the thalamus, by-passing the primary visual cortex (V1). Ten healthy human volunteers underwent brain scan examinations by functional magnetic resonance imaging (fMRI) during two optic flow experiments. In addition to the classical LGN-V1-hMT+ pathway, our results showed a significant direct influence of the blood oxygenation level dependent (BOLD) signal recorded in LGN over that in hMT+, not mediated by V1 activity, which strongly supports the existence of a bilateral pathway that connects LGN directly to hMT+ and serves visual motion processing. Furthermore, we evaluated the relative latencies among areas functionally connected in the processing of visual motion. Using LGN as a reference region, hMT+ exhibited a statistically significant earlier peak of activation as compared to V1. In conclusion, our findings suggest the co-existence of an alternative route that directly links LGN to hMT+, bypassing V1. This direct pathway may play a significant functional role for the faster detection of motion and may contribute to explain persistence of unconscious motion detection in individuals with severe destruction of primary visual cortex (blindsight).

Low-Level Phenomenal Vision Despite Unilateral Destruction of Primary Visual Cortex

GY, an extensively studied human hemianope, is aware of salient visual events in his cortically blind field but does not call this “vision.” To learn whether he has low-level conscious visual sensations or whether instead he has gained conscious knowledge about, or access to, visual information that does not produce a conscious phenomenal sensation, we attempted to image process a stimulus s presented to the impaired field so that when the transformed stimulus T(s) was presented to the normal hemifield it would cause a sensation similar to that caused by s in the impaired field. While degradation of contrast, spatio-temporal filtering, contrast reversal, and addition of smear and random blobs all failed to match the response to a flashed bar sf, moving textures of low contrast were accepted to match the response to a moving contrast-defined bar, sm. Orientation and motion direction discrimination of the perceptually matched stimuli [sm and T(sm)] was closely similar. We suggest that the existence of a satisfactory match indicates that GY has phenomenal vision.

Movement in the normal visual hemifield induces a percept in the ‘blind’ hemifisld of a human hemianope

We have investigated visual responses to moving stimuli presented to the normal hemifield of a hemianope, GY, who exhibits residual visual function in his right, 'blind' hemifield. Preliminary experiments established that his perception of moving stimuli localized in his 'blind' hemifield is retained when a similar stimulus is presented simultaneously in the normal hemifield. In response to a grating stimulus moving horizontally towards fixation in the non-foveal region of the normal, left hemifield, he perceives in addition to a normal motion percept in the left hemifield, a sensation of movement localized in the right hemifield. Qualitatively, this latter is indistinguishable from responses elicited by direct stimulation localized within his 'blind' hemifield by moving stimuli. We have investigated the characteristics of the mechanisms which induce the 'blind' field component of GY's responses to stimulation of the normal hemifield. We show that GY's sensitivity for detection of movement localized within his 'blind' hemifield is dependent on the direction of movement, the contrast and the velocity of a grating presented to the normal hemifield. No induced effects were recorded in response to colour or to non-moving, flickering stimuli. We examine the possible contribution of scattered light to our observations, and eliminate this factor by consideration of our experimental results. We discuss the neural mechanisms which may be involved in this response.

Imagery without perception—A case study of anosognosia for cortical blindness

A patient with complete cortical blindness after bilateral posterior cerebral artery infarctions denied her blindness. Her pretended visual experiences could frequently be traced back to synaesthetic translations of acoustic or tactile perceptions into mental visual images. Possibly, the belief to see resulted from a confusion of mental visual images with real percepts. The patient manifested preserved visual imagery also by correct responses to questions concerning the shapes of letters and the shapes and colours of objects. MRI showed an almost complete destruction of primary visual cortex with sparing of only small remainders of cortex at the occipital tip of the left upper calcarine lip. In the literature there are a few cases of denial of blindness with similarly severe damage to primary visual cortex but none with unequivocal evidence of complete destruction of primary visual cortex. We conclude that severe damage to primary visual cortex is compatible with visual imagery but that there is a possibility that islands of visual cortex must be spared to permit the generation of mental visual images.