Non-conscious visual processing of different object categories was investigated in a rare patient with bilateral destruction of the visual cortex (V1) and clinical blindness over the entire visual field. Images of biological and non-biological object categories were presented consisting of human bodies, faces, butterflies, cars, and scrambles. Behaviorally, only the body shape induced higher perceptual sensitivity, as revealed by signal detection analysis. Passive exposure to bodies and faces activated amygdala and superior temporal sulcus. In addition, bodies also activated the extrastriate body area, insula, orbitofrontal cortex (OFC) and cerebellum. The results show that following bilateral damage to the primary visual cortex and ensuing complete cortical blindness, the human visual system is able to process categorical properties of human body shapes. This residual vision may be based on V1-independent input to body-selective areas along the ventral stream, in concert with areas involved in the representation of bodily states, like insula, OFC, and cerebellum.
Facial expressions of emotions have been shown to modulate early ERP components, in particular the N170. The underlying anatomical structure producing these early effects are unclear. In this study, we examined the N170 enhancement for fearful expressions in healthy controls as well as epileptic patients after unilateral left or right amygdala resection. We observed a greater N170 for fearful faces in healthy participants as well as in individuals with left amygdala resections. By contrast, the effect was not observed in patients who had undergone surgery in which the right amygdala had been removed. This result demonstrates that the amygdala produces an early brain response to fearful faces. This early response relies specifically on the right amygdala and occurs at around 170 ms. It is likely that such increases are due to a heightened response of the extrastriate cortex that occurs through rapid amygdalofugal projections to the visual areas.
Fast and automatic behavioral responses are required to avoid collision with an approaching stimulus. Accordingly, looming stimuli have been found to be highly salient and efficient attractors of attention due to the implication of potential collision and potential threat. Here, we address the question of whether looming motion is processed in the absence of any functional primary visual cortex and consequently without awareness. For this, we investigated a patient (TN) suffering from complete, bilateral damage to his primary visual cortex. Using an fMRI paradigm, we measured TN's brain activation during the presentation of looming, receding, rotating, and static point lights, of which he was unaware. When contrasted with other conditions, looming was found to produce bilateral activation of the middle temporal areas, as well as the superior temporal sulcus and inferior parietal lobe (IPL). The latter are generally thought to be involved in multisensory processing of motion in extrapersonal space, as well as attentional capture and saliency. No activity was found close to the lesioned V1 area. This demonstrates that looming motion is processed in the absence of awareness through direct subcortical projections to areas involved in multisensory processing of motion and saliency that bypass V1.
Background: Olfactory hallucinations can be part of epileptic seizures of orbitofrontal origin. Olfactory hallucinations, however, are rare and therefore the semiology, localization and lateralization characteristics are underdetermined. In addition, many discrepancies are found in the literature regarding olfactory processing and orbitofrontal (OF) functions and olfactory function. Particularly, the questions of laterality and affective component in coding of odors in the OF cortex remain controversial. Aims: This study explored whether cortical electrical stimulation of the OF and mesiotemporal brain can trigger olfactory hallucinations with special focus on olfactory percepts in terms of laterality and hedonics. Materials and methods: Eight patients with temporal lobe epilepsy participated in the study, at the time of invasive exploration of their epilepsy. The most distal contact of the OF and anterior hippocampus depth electrodes were stimulated (50 Hz, 0.2 ms biphasic pulse; maximal stimulation 4 mA). Patients were instructed to report any kind of sensation they might experience. Intracranial depth electrodes were localized (iElectrodes): subject-specific brain mask, subcortical segmentation and cortical parcellation based on the Destrieux atlas (FreeSurfer) were superposed to the coregistered T1-weighted MRI and CT images (SPM). The center of mass of each electrode-artifact cluster determined the electrode localization. The electrode labeling was done in patient space. To obtain the electrode coordinates in Montreal Neurological Institute (MNI) space, the images obtained previously in the patient space were first segmented and normalized (SPM). Then, the localization procedure (iElectrodes) was run again with these new normalized images in MNI space. Results: No hallucination was evoked by stimulation, neither of the right nor the left hippocampus (8/8 patients). Pleasant olfactory hallucinations were evoked by OF stimulation in 5/8 patients in either hemisphere. Patients named the percept as the smell of lemon or coffee for example. Among those 5 patients, electrodes were localized in the cortex of the olfactory sulcus, medial orbital sulcus or medial OF gyrus. Increasing stimulation amplitude changed the olfactory percept identification in 3 out of those 5 patients. No affective judgement or change in perceived odor intensity was reported by the patients. No hallucination was evoked by the stimulation of the white matter of the medial OF brain in 3/8 patients independently of the hemisphere stimulated. Conclusions: This study demonstrated that stimulation of the cortex of the medial OF brain and not of its white matter elicits specific pleasant olfactory hallucinations independently of the hemisphere stimulated, supporting one symmetrical olfactory processing in human.
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