Blind sight for recognition of facial expressions in a patient with cortical visual loss

Blindsight refers to the uncanny ability of cortically blind patients to respond correctly, or above chance level, to visual stimuli, despite having lesions in the primary visual cortex. Affective blindsight more specifically refers to the ability of correctly identifying emotional expressions presented to the patients' blind fields. This suggests that there may be alternate pathways for visual information processing in the brain, which can bypass the primary visual cortex and reach other areas that are involved in visual perception. One theory of affective blindsight posits that the amygdala, plays a key role in this phenomenon while another theory proposes that the phenomenon of affective blindsight can be explained by functional integrity of the extra-striate visual areas, via the projections from the superior colliculus and pulvinar. The posterior superior temporal sulcus (pSTS) is an extrastiate brain region that is involved in the processing of social and emotional information, such as facial expressions, gestures, and body language. Current research suggests that the pSTS may play a role in affective blindsight. However, there is limited literate on this. We report a rare case of affective blindsight for in whom we demonstrate a preserved pSTS with evidence for connectivity to pulvinar that bypass the primary visual cortex .

Methods: A 58 year old man developed sudden onset of seeing flashes of light across his entire visual filed that lasted for a few seconds. This was immediately followed by complete blackness and loss of vision. He presented to us 6months later with persistent visual loss. Based clinical evaluation and structural MRI he was found to have bilateral occipital lobe infarcts involving the primary visual cortices. On testing vision, he had no phenomenological vision in the central field but had a peripherally located island of vision in the right inferior visual field. Psychophysical testing, lesion mapping, lesion network mapping and resting state fMRI, were performed. The patient's structural MRI was spatially normalized to the MNI space, and the lesion location was manually mapped. We then used resting-state functional connectivity from a healthy cohort to identify the network of regions functionally connected to the lesion site. For this the lesion map was used as seed in a resting state functional connectivity analysis and a statistically thresholded map was defined as the lesion network. Results: Psychophysical testing revealed objective evidence of blindsight for color and facial expression recognition based on the 2-alternate forced choice paradigm. Lesion mapping showed that the lesion involved the region of the occipital face area(OFA). Lesion network mapping shows that the lesion network extended additionally to involve the fusiform face area(FFA) but spared the pSTS . Functional conncectivity analysis showed intact direct connectivity of the pulvinar nuclei to the pSTS without involving the lesioned lateral geniculate body to visual cortex pathway. There was no significant functional connectivity between the amygdala and pSTS.

Conclusions: In conclusion, our study adds to the literature of affective blindsight by demonstrating a role for the pSTS and its connections to the subcortical pathways via the pulvinar. As there is strong evidence for the pSTS in processing facial expressions, its preservation and its intact connections to the pulvinar are likely to be critical in the development of affective blindsight. The preserved island of vision were peripherally located in the visual field and are therefore unlikely to contribute to affective blindsight in our patient as the stimuli was presented in the central and blind fields. We did not find any significant connections between the amygdala and the pSTS in our study to support the amygdala theory of affective blindsight. We also show that connections from primary visual cortex to OFA and FFA are not necessary for affective blind sight.

Dr A.T. Prabhakar is a neurologist who is currently a professor of neurology in the department of neurological sciences, Christian medical college (CMC) Vellore.  He obtained his undergraduate and post graduate medical training from CMC Vellore. He joined as faculty in 2013 after completing his D.M in clinical neurology at CMC, Vellore. He was a visiting professor at the Montreal neurological institute Canada in 2017 and trained in lesion-symptom mapping. His areas of interest include clinical phenomenology, cognitive Neuroscience, Lesion based studies in cognitive  neuroscience,  CNS inflammatory disorders,  visual neuroscience, Consciousness studies, neuro-philosophy and Critical Care.

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