Neural correlates of visual and spatial awareness

This PhD thesis focuses on attempting to experimentally investigate the neural correlates of awareness related to visual and spatial perception in humans. Specifically, this project aimed at looking into the electrophysiological markers of awareness in normal conditions and when awareness is lost due to a real or a “virtual” lesion. In both the studies conducted we adopted a causal multimodal approach, namely Transcranial Magnetic Stimulation and EEG (TMS-EEG) co-registration, which can provide insights into the neural correlates of visual and spatial awareness. The first study focuses on spatial awareness and specifically on the investigation of the mechanisms underlying neglect syndrome. Neglect is defined as a disorder of consciousness in which patients fail to report, respond to, or orient to stimuli presented on the opposite side of the brain lesion. One of the most influential models to explain the dysfunction underlying this syndrome takes into account the concept of inter-hemispheric rivalry, which postulates a pathological hyperactivation of the unaffected hemisphere due to the reduced inhibitory influences from the lesioned hemisphere. The aim of the present study is to test these models analyzing the effect that low frequency repetitive TMS (rTMS) exerts on the stimulated and contralateral hemispheres in the processing of visual stimuli. Specifically we aim at assessing the contribution of left and right parietal cortices in an impaired neglect-like functioning induced by means of low frequency rTMS in healthy participants. Fourteen healthy volunteers performed a Line Bisection task and a simple detection task of unilateral checkerboards stimuli. Both tasks were performed either before and after 30 minutes of low frequency rTMS (1 Hz) over the right posterior parietal cortex. The EEG signal was continuously recorded throughout the experiment. The efficacy of rTMS in inducing neglect-like phenomena was confirmed by the results of the Line Bisection task where participants showed a rightward deviation after rTMS, a performance comparable to that of neglect patients. Detection task results showed that the effect of rTMS was a lengthening of reaction times for both left and right visual stimuli and a reduction of the amplitude of P200 component registered both on left and right parietal sites. TMS-evoked potentials recorded during 30 minutes of stimulation, showed that low frequency rTMS induced a reduction of cortical excitability both of the stimulated right parietal cortex and of the left contralateral homologous area. Therefore, our results did not show a hyperactivation of the left hemisphere due to the inhibition of the right hemisphere (as theorized by “rivalry models”). Conversely, the inhibition of the right parietal cortex induced a spreading of the inhibition to the homologous area of the left hemisphere. The second study focuses on visual awareness and specifically aimed at investigating the neural correlates of phosphene perception. Single-pulse TMS of the visual cortex is known to induce visual sensations, i.e. phosphenes, which appear as brief flashes of light without light actually entering the eyes. Recent studies have shown that TMS can produce visual sensations not only when it is applied over early visual areas but also when parietal cortex is stimulated. As the pivotal neural basis involved in the perception of parietal phosphenes still remain unknown, the main question is whether parietal phosphenes are generated directly by local mechanisms or emerge through indirect activation of other visual areas. To characterize the electrophysiological correlates of occipital and parietal phosphene perception we investigated TMS-evoked potentials in a sample of healthy participants by comparing trials in which a phosphene was perceived with trials in which no visual percept was reported. When the left occipital cortex was stimulated, phosphene perception started to affect TMS-evoked potentials at a late latency, whereas phosphenes elicited by left parietal cortex stimulation modulated TMS-evoked potentials at an earlier latency. This difference in the time-course of cortical activation between occipital and parietal phosphenes could underlie a different mechanism in their generation. The early latency of the phosphene effect observed when TMS was applied over the parietal cortex might suggest that parietal phosphenes should be considered as the direct result of the activation of the stimulated area, rather than the consequence of a feedback activation of the early visual cortex. Furthermore, we investigated electrophysiological correlates of parietal phosphene perception in a hemianopic patient (SL) who suffered from a complete destruction of the left primary visual cortex. Ipsilesional parietal phosphene perception in patient SL showed a similar pattern of results to that of parietal phosphene perception in healthy participants, starting to affect TMS-evoked potentials at an early stage of latency. This evidence might thus support the idea of parietal cortex as an independent generator of magnetically induced conscious visual experiences.