Patients with lesions in the visual cortex are blind in corresponding regions of the visual field, but they still may process visual information, a phenomenon referred to as residual vision or \"blindsight\". Here we report behavioral and fMRI observations with a patient who reports conscious vision across an extended area of blindness for moving, but not for stationary stimuli. This completion effect is shown to be of perceptual and not of conceptual origin, most likely mediated by spared representations of the visual field in the striate cortex. The neural output to extra-striate areas from regions of the deafferented striate cortex is apparently still intact; this is, for instance, indicated by preserved size constancy of visually completed stimuli. Neural responses as measured with fMRI reveal an activation only for moving stimuli, but importantly on the ipsilateral side of the brain. In a conceptual model this shift of activation to the \"wrong\" hemisphere is explained on the basis of an imbalance of excitatory and inhibitory interactions within and between the striate cortices due to the brain injury. The observed neuroplasticity indicated by this shift together with the behavioral observations provide important new insights into the functional architecture of the human visual system and provide new insight into the concept of consciousness.

The primary visual cortex (V1) is one of the most studied regions of the brain and is characterized by its specialized and laminated layer 4 in human and non-human primates. However, studies aiming to harmonize the definition of the cortical layers and borders of V1 across rodents and primates are very limited. This article attempts to identify and harmonize the molecular markers and connectional patterns that can consistently link corresponding cortical layers of V1 and borders across mammalian species and ages. V1 in primates has at least two additional and unique layers (L3b2 and L3c) and two sublayers of layer 4 (L4a and L4b) compared to rodent V1. In all species examined, layers 4 and 3b of V1 receive strong inputs from the (dorsal) lateral geniculate nucleus, and V1 is mostly surrounded by the secondary visual cortex except for one location where V1 directly abuts area prostriata. The borders of primate V1 can also be clearly identified at mid-gestational ages using gene markers. In rodents, a novel posteromedial extension of V1 is identified, which expresses V1 marker genes and receives strong inputs from the lateral geniculate nucleus. This V1 extension was labeled as the posterior retrosplenial cortex and medial secondary visual cortex in the literature and brain atlases. Layer 6 of the rodent and primate V1 originates corticothalamic projections to the lateral geniculate, lateral dorsal, and reticular thalamic nuclei and the lateroposterior-pulvinar complex with topographic organization. Finally, the direct geniculo-extrastriate (particularly the strong geniculo-prostriata) projections are probably major contributors to blindsight after V1 lesions. Taken together, compared to rodents, primates, and humans, V1 has at least two unique middle layers, while other layers are comparable across species and display conserved molecular markers and similar connections with the visual thalamus with only subtle differences.

CONCLUSIONS: The Riddoch syndrome is thought to be caused by damage to the primary visual cortex (V1), usually following a vascular event. This study shows that damage to the anatomical input to V1, i.e., the optic radiations, can result in selective visual deficits that mimic the Riddoch syndrome. The results also highlight the differential susceptibility of the magnocellular and parvocellular visual systems to injury. Overall, this study offers new insights that will improve our understanding of the impact of brain injury and neurosurgery on the visual pathways. The Riddoch syndrome, characterised by the ability to perceive, consciously, moving visual stimuli but not static ones, has been associated with lesions of primary visual cortex (V1). We present here the case of patient YL who, after a tumour resection surgery that spared his V1, nevertheless showed symptoms of the Riddoch syndrome. Based on our testing, we postulated that the magnocellular (M) and parvocellular (P) inputs to his V1 may be differentially affected. In a first experiment, YL was presented with static and moving checkerboards in his blind field while undergoing multimodal magnetic resonance imaging (MRI), including structural, functional, and diffusion, acquired at 3 T. In a second experiment, we assessed YL\'s neural responses to M and P visual stimuli using psychophysics and high-resolution fMRI acquired at 7 T. YL\'s optic radiations were partially damaged but not severed. We found extensive activity in his visual cortex for moving, but not static, visual stimuli, while our psychophysical tests revealed that only low-spatial frequency moving checkerboards were perceived. High-resolution fMRI revealed strong responses in YL\'s V1 to M stimuli and very weak ones to P stimuli, indicating a functional P lesion affecting V1. In addition, YL frequently reported seeing moving stimuli and discriminating their direction of motion in the absence of visual stimulation, suggesting that he was experiencing visual hallucinations. Overall, this study highlights the possibility of a selective loss of P inputs to V1 resulting in the Riddoch syndrome and in hallucinations of visual motion.

The existence of unconscious visually triggered behavior in patients with cortical blindness (e.g., homonymous hemianopia) has been amply demonstrated and the neural bases of this phenomenon have been thoroughly studied. However, a crosstalk between the two hemispheres as a possible mechanism of unconscious or partially conscious vision has not been so far considered. Thus, the aim of this study was to assess the relationship between structural and functional properties of the corpus callosum (CC), as shown by probabilistic tractography (PT), behavioral detection/discrimination performance and level of perceptual awareness in the blind field of patients with hemianopia. Twelve patients were tested in two tasks with black-and-white visual square-wave gratings, one task of movement and the other of orientation. The stimuli were lateralized to one hemifield either intact or blind. A PT analysis was carried out on MRI data to extract fiber properties along the CC (genu, body, and splenium). Compared with a control group of participants without brain damage, patients showed lower FA values in all three CC sections studied. For the intact hemifield we found a significant correlation between PT values and visual detection/discrimination accuracy. For the blind hemifield the level of perceptual awareness correlated with PT values for all three CC sections in the movement task. Importantly, significant differences in all three CC sections were found also between patients with above-vs. chance detection/discrimination performance while differences in the genu were found between patients with and without perceptual awareness. Overall, our study provides evidence that the properties of CC fibers are related to the presence of unconscious stimulus detection/discrimination and to hints of perceptual awareness for stimulus presentation to the blind hemifield. These results underline the importance of information exchange between the damaged and the healthy hemisphere for possible partial or full recovery from hemianopia.

Even when brain scans fail to detect a striate lesion, functional evidence for blindsight can be adduced. In the aftermath of an automobile accident, JK became blind. Results of ophthalmic exams indicated that the blindness must be cortical. Nevertheless, multiple MRI scans failed to detect structural damage to the striate cortex. Prior to the accident JK had been an athlete; after the accident he retained some athletic abilities, arousing suspicions that he might be engaged in fraud. His residual athletic abilities-e.g., hitting a handball or baseball, or catching a Frisbee-coupled with his experienced blindness, suggested blindsight. But due to the apparent absence of striate lesions, we designed a series of tasks for temporal and spatial dimensions in an attempt to detect functional evidence of his disability. Indeed, test results revealed compelling neural evidence that comport with his subjective reports. This spatiotemporal task-related method that includes contrasts with healthy controls, and detailed understanding of the patient\'s conscious experience, can be generalized for clinical, scientific and forensic investigations of blindsight.

The redundant target effect (RTE) is the well-known effect whereby a single target is detected faster when a second, redundant target is presented simultaneously. The RTE was shown in different experimental designs and applied in various clinical contexts. However, there are also studies showing non-effects or effects in the opposite direction. Our meta-analysis aims to investigate the replicability of the RTE. Herein, we focused on the clinical context within which the RTE has been applied most often and for which it gained particular prominence: The research on blindsight and other forms of residual vision in patients with damage to the neuronal visual system. The application of the RTE in clinical contexts assumes that whenever vision is present, an RTE will be found. Put differently, the RTE as a tool to uncover residual vision presumes that the RTE is a consistent feature of vision in the healthy population. We found a significant summary effect size of the RTE in healthy participants. The effect size depended on certain experimental features: task type, target configuration in the redundant condition, and how reaction times were computed in the single condition. A specific feature combination is typically used in blindsight research. Analyzing studies with this feature combination revealed a significant summary effect size in healthy participants predicting positive RTEs for future studies. A power-analysis revealed a required sample size of 14 participants to obtain an RTE with high reliability. However, the required sample size is rarely reached in blindsight research. Rather, blindsight research is mostly based on single-case studies. In summary, the RTE is a robust effect on group level but does not occur in every single individual. This means failure to obtain an RTE in a single patient should not be interpreted as evidence for the absence of residual vision in this patient.

The nature of subjective conscious experience, which accompanies us throughout our waking lives, and how it is generated, remain elusive. One of the challenges in studying subjective experience is disentangling the brain activity related to the sensory stimulus processing and stimulus-guided behavior from those associated with subjective perception. Blindsight, a phenomenon characterized by the retained visual discrimination performance but impaired visual consciousness due to damage to the primary visual cortex, becomes a special entry point to address this question. However, to fully understand the underlying neural mechanism, relying on studies involving human patients alone is insufficient. In this paper, we tried to address this issue, by first introducing the well-known cases of blindsight, especially the reports on subjective experience in both human and monkey subjects. And then we described how the impaired visual awareness of blindsight monkeys has been discovered and further studied by specifically designed tasks, as verbal reporting is not possible for these animals. Our previous studies also demonstrated that many complex visually guided cognitive processes were still retained despite the impairment of visual awareness. Further investigation needs to be conducted to explore the relationship between visually guided behavior, visual awareness and brain activity in blindsight subjects.

The ability of the brain to recognize and orient attention to relevant stimuli appearing in the visual field is highlighted by a tuning process, which involves modulating the early visual system by both cortical and subcortical brain areas. Selective attention is coordinated not only by the output of stimulus-based saliency maps but is also influenced by top-down cognitive factors, such as internal states, goals, or previous experiences. The basal ganglia system plays a key role in implicitly modulating the underlying mechanisms of selective attention, favouring the formation and maintenance of implicit sensory-motor memories that are capable of automatically modifying the output of priority maps in sensory-motor structures of the midbrain, such as the superior colliculus. The article presents an overview of the recent literature outlining the crucial contribution of several subcortical structures to the processing of different sources of salient stimuli. In detail, we will focus on how the mesencephalic- basal ganglia closed loops contribute to implicitly addressing and modulating selective attention to prioritized stimuli. We conclude by discussing implicit behavioural responses observed in clinical populations in which awareness is compromised at some level. Implicit (emergent) awareness in clinical conditions that can be accompanied by manifest anosognosic symptomatology (i.e., hemiplegia) or involving abnormal conscious processing of visual information (i.e., unilateral spatial neglect and blindsight) represents interesting neurocognitive \"test cases\" for inferences about mesencephalicbasal ganglia closed-loops involvement in the formation of implicit sensory-motor memories.

Conscious visual motion information follows a cortical pathway from the retina to the lateral geniculate nucleus (LGN) and on to the primary visual cortex (V1) before arriving at the middle temporal visual area (MT/V5). Alternative subcortical pathways that bypass V1 are thought to convey unconscious visual information. One flows from the retina to the pulvinar (PUL) and on to medial temporal visual area (MT); while the other directly connects the LGN to MT. Evidence for these pathways comes from non-human primates and modest-sized studies in humans with brain lesions. Thus, the aim of the current study was to reconstruct these pathways in a large sample of neurotypical individuals and to determine the degree to which these pathways are myelinated, suggesting information flow is rapid. We used the publicly available 7T (N = 98; \'discovery\') and 3T (N = 381; \'validation\') diffusion magnetic resonance imaging datasets from the Human Connectome Project to reconstruct the PUL-MT (including all subcompartments of the PUL) and LGN-MT pathways. We found more fibre tracts with greater density in the left hemisphere. Although the left PUL-MT path was denser, the bilateral LGN-MT tracts were more heavily myelinated, suggesting faster signal transduction. We suggest that this apparent discrepancy may be due to \'adaptive myelination\' caused by more frequent use of the LGN-MT pathway that leads to greater myelination and faster overall signal transmission.

Convolutional Neural Networks (CNN) are a class of machine learning models predominately used in computer vision tasks and can achieve human-like performance through learning from experience. Their striking similarities to the structural and functional principles of the primate visual system allow for comparisons between these artificial networks and their biological counterparts, enabling exploration of how visual functions and neural representations may emerge in the real brain from a limited set of computational principles. After considering the basic features of CNNs, we discuss the opportunities and challenges of endorsing CNNs as in silico models of the primate visual system. Specifically, we highlight several emerging notions about the anatomical and physiological properties of the visual system that still need to be systematically integrated into current CNN models. These tenets include the implementation of parallel processing pathways from the early stages of retinal input and the reconsideration of several assumptions concerning the serial progression of information flow. We suggest design choices and architectural constraints that could facilitate a closer alignment with biology provide causal evidence of the predictive link between the artificial and biological visual systems. Adopting this principled perspective could potentially lead to new research questions and applications of CNNs beyond modeling object recognition.