Revealing robust neural correlates of conscious and unconscious visual processing: Activation likelihood estimation meta-analyses.

Our ability to consciously perceive information from the visual scene relies on a myriad of intrinsic neural mechanisms. Functional neuroimaging studies have sought to identify the neural correlates of conscious visual processing and to further dissociate from those pertaining to preconscious and unconscious visual processing. However, delineating what core brain regions are involved in eliciting a conscious percept remains a challenge, particularly regarding the role of prefrontal-parietal regions. We performed a systematic search of the literature that yielded a total of 54 functional neuroimaging studies. We conducted two quantitative meta-analyses using activation likelihood estimation to identify reliable patterns of activation engaged by i. conscious (n = 45 studies, comprising 704 participants) and ii. unconscious (n = 16 studies, comprising 262 participants) visual processing during various task performances. Results of the meta-analysis specific to conscious percepts quantitatively revealed reliable activations across a constellation of regions comprising the bilateral inferior frontal junction, intraparietal sulcus, dorsal anterior cingulate, angular gyrus, temporo-occipital cortex and anterior insula. Neurosynth reverse inference revealed conscious visual processing to be intertwined with cognitive terms related to attention, cognitive control and working memory. Results of the meta-analysis on unconscious percepts revealed consistent activations in the lateral occipital complex, intraparietal sulcus and precuneus. These findings highlight the notion that conscious visual processing readily engages higher-level regions including the inferior frontal junction and unconscious processing reliably recruits posterior regions, mainly the lateral occipital complex.

The Impact of Early Deafness on Brain Plasticity: A Systematic Review of the White and Gray Matter Changes.

Background: Auditory deprivation alters cortical and subcortical brain regions, primarily linked to auditory and language processing, resulting in behavioral consequences. Neuroimaging studies have reported various degrees of structural changes, yet multiple variables in deafness profiles need to be considered for proper interpretation of results. To date, many inconsistencies are reported in the gray and white matter alterations following early profound deafness. The purpose of this study was to provide the first systematic review synthesizing gray and white matter changes in deaf individuals. Methods: We conducted a systematic review according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement in 27 studies comprising 626 deaf individuals. Results: Evidence shows that auditory deprivation significantly alters the white matter across the primary and secondary auditory cortices. The most consistent alteration across studies was in the bilateral superior temporal gyri. Furthermore, reductions in the fractional anisotropy of white matter fibers comprising in inferior fronto-occipital fasciculus, the superior longitudinal fasciculus, and the subcortical auditory pathway are reported. The reviewed studies also suggest that gray and white matter integrity is sensitive to early sign language acquisition, attenuating the effect of auditory deprivation on neurocognitive development. Conclusions: These findings suggest that understanding cortical reorganization through gray and white matter changes in auditory and non-auditory areas is an important factor in the development of auditory rehabilitation strategies in the deaf population.

Neuronal mechanisms of motion detection underlying blindsight assessed by functional magnetic resonance imaging (fMRI).

Brain imaging offers a valuable tool to observe functional brain plasticity by showing how sensory inputs reshape cortical activations after a visual impairment. Following a unilateral post-chiasmatic lesion affecting the visual cortex, patients may suffer a contralateral visual loss referred to homonymous hemianopia. Nevertheless, these patients preserve the ability to unconsciously detect, localize and discriminate visual stimuli presented in their impaired visual field. To investigate this paradox, known as blindsight, we conducted a study using functional magnetic resonance imaging (fMRI) to evaluate the structural and functional impact of such lesion in a 33-year old patient (ML), who suffers a complete right hemianopia without macular sparing and showing strong evidences of blindsight. We thus performed whole brain and sliced thalamic fMRI scan sequences during an event-related motion detection task. We provided evidence of the neuronal fingerprint of blindsight by acquiring and associating neural correlates, specific structures and functional networks of the midbrain during blindsight performances which may help to better understand this condition. Accurate performance demonstrated the presence of residual vision and the ability to unconsciously perceive motion presented in the blind hemifield, although her reaction time was significantly higher in her blind-field. When the normal hemifield was stimulated, we observed significant contralateral activations in primary and secondary visual areas as well as motion specific areas, such as the supramarginal gyrus and middle temporal area. We also demonstrated sub-thalamic activations within the superior colliculi (SC) and the pulvinar. These results suggest a role of secondary subcortical structures in normal spontaneous motion detection. In a similar way, when the lesioned hemifield was stimulated, we observed contralateral activity in extrastriate areas with no activation of the primary lesioned visual cortex. Moreover, we observed activations within the SC when the blind hemifield was stimulated. However, we observed unexpected ipsilateral activations within the same motion specific areas, as well as bilateral frontal activations. These results highlight the importance of abnormal secondary pathways bypassing the primary visual area (V1) in residual vision. This reorganization in the structure and function of the visual pathways correlates with behavioral changes, thus offering a plausible explanation for the blindsight phenomenon. Our results may potentially impact the development of rehabilitation strategies to target subcortical pathways.