Network Localization of Unconscious Visual Perception in Blindsight

Abstract

Objective: Blindsight is a disorder where brain injury causes loss of conscious but not unconscious visual perception. Prior studies have produced conflicting results regarding the neuroanatomical pathways involved in this unconscious perception. Methods: We performed a systematic literature search to identify lesion locations causing visual field loss in patients with blindsight (n = 34) and patients without blindsight (n = 35). Resting state functional connectivity between each lesion location and all other brain voxels was computed using a large connectome database (n = 1,000). Connections significantly associated with blindsight (vs no blindsight) were identified. Results: Functional connectivity between lesion locations and the ipsilesional medial pulvinar was significantly associated with blindsight (family wise error p = 0.029). No significant connectivity differences were found to other brain regions previously implicated in blindsight. This finding was independent of methods (eg, flipping lesions to the left or right) and stimulus type (moving vs static). Interpretation: Connectivity to the ipsilesional medial pulvinar best differentiates lesion locations associated with blindsight versus those without blindsight. Our results align with recent data from animal models and provide insight into the neuroanatomical substrate of unconscious visual abilities in patients.

A connectivity model of the anatomic substrates underlying Gerstmann syndrome

“…It may be advantageous for meta-analyses of the available literature which also include lesion-based studies to better derive clinical meaning to these results. 157 …”

Network Localization of Awareness in Visual and Motor Anosognosia

“…The functional connectivity data equivalent to that employed in this study is available online through the Harvard Dataverse at: https://doi.org/10.7910/DVN/ ILXIKS and the pipeline used to prepare the functional connectivity data is available at: https://github.com/ bchcohenlab/BIDS_to_CBIG_fMRI_Preproc2016. Lesion data used in this study is publicly available and obtained from published medical literature (see Supplementary Table S2, Kletenik et al 2022 11 and Pacella et al eLife 2019 1 ). Statistical neuroimaging analyses, specifically the voxelwise ANOVA was performed in MatLab (version 2019b) and FSL (version 5.0.10).…”

“…For this reason, we used a recently validated technique termed lesion network mapping to test whether these lesion-induced deficits map to specific brain networks. [11][12][13][14] We sought to identify (1) brain network connections associated with domain-specific anosognosia and (2) brain network connections associated with anosognosia in general, independent of the specific deficit.…”

Lesion network mapping for symptom localization: recent developments and future directions

“…In each of these conditions, prior neuroimaging studies have provided heterogeneous results and causal lesions are scattered throughout many different regions in the brain, leaving the neural substrate unknown. Using LNM, lesions causing tics mapped to a common circuit with the anterior putamen as the most sensitive and specific hub of the circuit [5 ▪ ], lesions causing blindsight were associated with connectivity to the medial pulvinar nucleus of the thalamus [22 ▪ ], and lesions causing pathological laughter and crying were characterized by connectivity to a complex network with positive connectivity to subcortical and medial cortical regions involved in emotional processing, and negative connectivity to sensorimotor cortex [13]. The identified circuits provide insight into the neural mechanisms of these symptoms and help to evaluate the link between patients’ symptoms and brain lesions.…”

“…Similarly, LNM has recently been applied to other long-standing neurological mysteries, including motor/vocal tics, blindsight, and pathological laughter and crying, characterized by inappropriate outbursts of laughter and/or weeping [5 ▪ ,13,22 ▪ ]. In each of these conditions, prior neuroimaging studies have provided heterogeneous results and causal lesions are scattered throughout many different regions in the brain, leaving the neural substrate unknown.…”