Search

Comprehending the nature of tactile disorders following brain damage is crucial to understand how the brain constructs sensory awareness. Stroke patients may be unaware of being touched on the affected hand if, simultaneously, they are touched on the unaffected hand (i.e., tactile extinction). More rarely, they feel touches on the two hands, when they are solely touched on the unaffected hand (i.e., synchiria). Using a novel assessment tool, we investigated whether in stroke patients with apparent intact tactile awareness on standard evaluation, tactile extinction might be possibly masked by phantom (synchiric) sensations (i.e., elicited by ipsilesional stimulation) arising exclusively during Double Simultaneous Stimulation (DSS). Patients with right (n = 17) and left (n = 8) hemisphere lesions and age-matched healthy controls (n = 13) were tested with the Tactile Quadrant Stimulation test, consisting in delivering unilateral or bilateral touches to one of four quadrants, identified on the participants' hands. In DSS trials, stimuli were applied to asymmetric quadrants. Participants reported the side(s) and then pointed to the site(s) of stimulation. We found that, with the exception of one patient who showed tactile extinction, about 50% of patients with overall intact tactile perception on classical evaluation, although reporting two stimuli in DSS, failed in pointing to the correct contralesional stimulated site. They reported the felt sensation in positions that corresponded to the ipsilesional stimulated sites. Thus apparent detections of contralesional touches in DSS were accounted for by 'phantom' sensations of ipsilesional stimulation that masked unawareness of contralesional touches when classic assessment was applied. Preliminary lesion analyses indicate that the symptom was associated with damage to structures often affected in tactile extinction. These findings, while unveiling important underestimation of the patients' neurological condition, provide a framework for investigating bihemispheric contributions to altered tactile perception following stroke., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Rightward prismatic adaptation (RPA) can reduce neglect symptoms in patients whereas adaptation to leftward deviating prisms (LPA) can induce neglect-like behavior in healthy subjects. One influential anatomo-functional model of prismatic adaptation (PA) postulates that it inhibits activity of the posterior parietal cortex (PPC) contralateral to the prismatic deviation. By hypo-activating the PPC and thus eventually acting on interhemispheric balance, both LPA and RPA could possibly affect visuospatial perception in healthy subjects, however, such behavioral modulation has seldom been reported after RPA. In the light of recent evidence showing that LPA-induced visuospatial shift need time to develop we hypothesized that RPA might induce significant changes in visuospatial cognition on a longer time scale. We thus assessed the Landmark task, as well as sensorimotor aftereffects, several times over 8 h after a single session of either LPA or RPA. In agreement with previous reports, sensorimotor effects were symmetrical and long-lasting, with both LPA and RPA inducing shifts of comparable amplitudes in the direction opposite to the deviation that lasted up to 8 h. Visuospatial cognition assessed by Landmark performance, was also significantly modulated for up to 8 h, but only after LPA. Interestingly, the timing and direction of this modulation differed according to participants' baseline bias. An initial leftward bias led to a rapid, but short-lasting rightward shift, whereas an initial rightward bias led to a slower-developing and longer-lasting leftward shift. These findings shed new light on a so-far relatively overlooked feature of spatial cognition that may interact with the effect of PA: the state of the visuospatial system prior to PA should be taken into account when attempting to understand and modulate visuospatial cognition in healthy and brain-damaged populations. This highlights the need for refining current models of PA's mechanisms of action., (Published by Elsevier Ltd.)