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Although damage to the primary visual cortex (V1) causes hemianopia, many patients retain some residual vision; known as blindsight. We show that blindsight may be facilitated by an intact white-matter pathway between the lateral geniculate nucleus and motion area hMT+. Visual psychophysics, diffusion-weighted magnetic resonance imaging and fibre tractography were applied in 17 patients with V1 damage acquired during adulthood and 9 age-matched controls. Individuals with V1 damage were subdivided into blindsight positive (preserved residual vision) and negative (no residual vision) according to psychophysical performance. All blindsight positive individuals showed intact geniculo-hMT+ pathways, while this pathway was significantly impaired or not measurable in blindsight negative individuals. Two white matter pathways previously implicated in blindsight: (i) superior colliculus to hMT+ and (ii) between hMT+ in each hemisphere were not consistently present in blindsight positive cases. Understanding the visual pathways crucial for residual vision may direct future rehabilitation strategies for hemianopia patients. Visual information from our eyes projects to a region at the back of the brain called the primary visual cortex, which is where the information is processed to allow us to see the world around us. If a person suffers a stroke that affects this primary visual cortex, he or she can become blind on one side. However, some people can still detect images within this ‘blind’ area, even if they are not consciously aware of it. This phenomenon is known as ‘blindsight’, but it remains unclear which pathways and structures in the brain might allow this information to be detected. Ajina et al. have now examined the brains of a large group of patients with damage to the visual cortex. The results for the patients with blindsight were compared to those without, and to a group of sighted control participants. This analysis identified a pathway that seems to underlie blindsight. This pathway (which runs between an area of the brain called the lateral geniculate nucleus and another called the motion area hMT+) was present in all patients with blindsight, but was missing or disrupted in those patients without blindsight. Ajina et al. then examined other pathways that had previously been suggested to support blindsight and revealed that they were unlikely to do so. This is because the suggested connections were not identifiable in all patients with blindsight, and were often intact in those patients without blindsight. So far, this work has addressed the structure of the pathways rather than their activity. Future work will attempt to determine whether it is possible to strengthen such pathways to improve visual ability.

Stereoscopic depth perception requires considerable neural computation, including the initial correspondence of the two retinal images, comparison across the local regions of the visual field and integration with other cues to depth. The most common cause for loss of stereoscopic vision is amblyopia, in which one eye has failed to form an adequate input to the visual cortex, usually due to strabismus (deviating eye) or anisometropia. However, the significant cortical processing required to produce the percept of depth means that, even when the retinal input is intact from both eyes, brain damage or dysfunction can interfere with stereoscopic vision. In this review, I examine the evidence for impairment of binocular vision and depth perception that can result from insults to the brain, including both discrete damage, temporal lobectomy and more systemic diseases such as posterior cortical atrophy. This article is part of the themed issue ‘Vision in our three-dimensional world’.

BACKGROUND:Increasing use of endoscopic endonasal surgery for suprasellar lesions with extension into the optic canal (OC) has necessitated a better endonasal description of the OC. OBJECTIVE:To identify the osseous OC transcranially and then investigate its anatomic relationship to the key endonasal intrasphenoidal landmarks. We also aimed to determine and describe the technical nuances for safely opening the falciform ligament and intracanalicular dura (surrounding the optic nerve [ON]) endonasally. METHODS:Ten fresh human head silicon-injected specimens underwent an endoscopic transtuberculum/transplanum approach followed by 2-piece orbitozygomatic craniotomy to allow identification of 20 OCs. After completing up to 270° of endonasal bony decompression of the OC, a dural incision started at the sella and continued superiorly across the superior intercavernous sinus. Subsequently the dural opening was extended anterolaterally across the dura of the prechiasmatic sulcus, limbus sphenoidale, and planum. RESULTS:Endonasally, the length of the osseous OC was approximately 6 mm and equivalent to the length of the lateral opticocarotid recess, as measured anteroposteriorly. The ophthalmic artery arose from the supraclinoidal carotid artery at approximately 2.5 mm from the medial osseous OC entrance. Transcranial correlation of the endonasal dural incision confirmed medial detachment of the falciform ligament and exposure of the preforaminal ON. CONCLUSION:The lateral opticocarotid recess allows distinction of the preforaminal ON, roofed by the falciform ligament from the intracanalicular segment in the osseous OC. This facilitates the preoperative surgical strategy regarding the extent of OC decompression and dural opening. Extensive endonasal decompression of the OC and division of the falciform ligament is feasible. ABBREVIATIONS:ICA, internal carotid arteryLOCR, lateral opticocarotid recessOC, optic canalOCI, optic canal invasionON, optic nerveMOCR, medial opticocarotid recess

One important, yet relatively unexplored question is whether blindsight, i.e., unconscious visually guided behavior in hemianopic patients, is endowed with basic perceptual properties such as detecting stimulus numerosity and overall configuration. Rather than a forced-choice procedure in which patients are supposed to guess about stimuli presented to the blind hemifield, we used a redundant signal effect paradigm, i.e., the speeding of simple reaction time (RT) when presenting multiple versus single similar stimuli. The presence of an effect of numerosity for the (unseen) stimuli presented to the blind field was indirectly assessed by measuring RT to bilateral versus unilateral stimuli presented to the intact hemifield. Chronic hemianopic patients were tested with unilateral or bilateral black dots, both of which could be either single or quadruple. The latter could either have a fixed spatial configuration representing a diamond or be randomly spatially assembled on every trial. Both configurations covered the same extent of visual field and had the overall same luminance. We found that a numerosity effect as a result of increasing the number of stimuli in the blind field was indeed present but only with the diamond configuration. This is a convincing evidence that this form of blindsight does not depend upon stimulus numerosity per se but is likely to be related to the presence of structured and memorized rather than meaningless changing stimuli.

The assessment of task-independent functional connectivity (FC) after a lesion causing hemianopia remains an uncovered topic and represents a crucial point to better understand the neural basis of blindsight (i.e. unconscious visually triggered behavior) and visual awareness. In this light, we evaluated functional connectivity (FC) in 10 hemianopic patients and 10 healthy controls in a resting state paradigm. The main aim of this study is twofold: first of all we focused on the description and assessment of density and intensity of functional connectivity and network topology with and without a lesion affecting the visual pathway, and then we extracted and statistically compared network metrics, focusing on functional segregation, integration and specialization. Moreover, a study of 3-cycle triangles with prominent connectivity was conducted to analyze functional segregation calculated as the area of each triangle created connecting three neighboring nodes. To achieve these purposes we applied a graph theory-based approach, starting from Pearson correlation coefficients extracted from pairs of regions of interest. In these analyses we focused on the FC extracted by the whole brain as well as by four resting state networks: The Visual (VN), Salience (SN), Attention (AN) and Default Mode Network (DMN), to assess brain functional reorganization following the injury. The results showed a general decrease in density and intensity of functional connections, that leads to a less compact structure characterized by decrease in functional integration, segregation and in the number of interconnected hubs in both the Visual Network and the whole brain, despite an increase in long-range inter-modules connections (occipito-frontal connections). Indeed, the VN was the most affected network, characterized by a decrease in intra- and inter-network connections and by a less compact topology, with less interconnected nodes. Surprisingly, we observed a higher functional integration in the DMN and in the AN regardless of the lesion extent, that may indicate a functional reorganization of the brain following the injury, trying to compensate for the general reduced connectivity. Finally we observed an increase in functional specialization (lower between-network connectivity) and in inter-networks functional segregation, which is reflected in a less compact network topology, highly organized in functional clusters. These descriptive findings provide new insight on the spontaneous brain activity in hemianopic patients by showing an alteration in the intrinsic architecture of a large-scale brain system that goes beyond the impairment of a single RSN.

In patients with visual hemifield defects residual visual functions may be present, a phenomenon called blindsight. The superior colliculus (SC) is part of the spared pathway that is considered to be responsible for this phenomenon. Given that the SC processes input from different modalities and is involved in the programming of saccadic eye movements, the aim of the present study was to examine whether multimodal integration can modulate oculomotor competition in the damaged hemifield. We conducted two experiments with eight patients who had visual field defects due to lesions that affected the retinogeniculate pathway but spared the retinotectal direct SC pathway. They had to make saccades to an auditory target that was presented alone or in combination with a visual stimulus. The visual stimulus could either be spatially coincident with the auditory target (possibly enhancing the auditory target signal), or spatially disparate to the auditory target (possibly competing with the auditory tar-get signal). For each patient we compared the saccade endpoint deviation in these two bi-modal conditions with the endpoint deviation in the unimodal condition (auditory target alone). In all seven hemianopic patients, saccade accuracy was affected only by visual stimuli in the intact, but not in the blind visual field. In one patient with a more limited quadrantano-pia, a facilitation effect of the spatially coincident visual stimulus was observed. We conclude that our results show that multisensory integration is infrequent in the blind field of patients with hemianopia.

Background The existence of transsynaptic retrograde degeneration (TRD) in the human visual system has been established, however the dependence of TRD on different factors such as lesion location, size and manner of lesion acquisition has yet to be quantified. Methods We obtained T1-weighted structural and diffusion-weighted images for 26 patients with adult-acquired or congenital hemianopia and 12 age-matched controls. The optic tract (OT) was defined and measured in the structural and diffusion-weighted images, and degeneration assessed by comparing the integrity of tracts in the lesioned and in the undamaged hemisphere. Results OT degeneration was found in all patients with established lesions, regardless of lesion location. In patients with acquired lesions, the larger the initial lesion, the greater is the resulting TRD. However, this was not the case for congenital patients, who generally showed greater degeneration than would be predicted by lesion size. A better predictor of TRD was the size of the visual field deficit, which was correlated with degeneration across all patients. Interestingly, although diffusion-weighted imaging (DWI) is more frequently used to examine white matter tracts, in this study the T1-weighted scans gave a better indication of the extent of tract degeneration. Conclusions We conclude that TRD of the OT occurs in acquired and congenital hemianopia, is correlated with visual field loss, and is most severe in congenital cases. Understanding the pattern of TRD may help to predict effects of any visual rehabilitation training.