Tool use modulates somatosensory cortical processing in humans

Contains fulltext : 215844.pdf (Publisher’s version ) (Closed access)Tool use leads to plastic changes in sensorimotor body representations underlying tactile perception. The neural correlates of this tool-induced plasticity in humans have not been adequately characterized. This study used ERPs to investigate the stage of sensory processing modulated by tool use. Somatosensory evoked potentials, elicited by median nerve stimulation, were recorded before and after two forms of object interaction: tool use and hand use. Compared with baseline, tool use - but not use of the hand alone - modulated the amplitude of the P100. The P100 is a mid-latency component that indexes the construction of multisensory models of the body and has generators in secondary somatosensory and posterior parietal cortices. These results mark one of the first demonstrations of the neural correlates of tool-induced plasticity in humans and suggest that tool use modulates relatively late stages of somatosensory processing outside primary somatosensory cortex. This finding is consistent with what has been observed in tool-trained monkeys and suggests that the mechanisms underlying tool-induced plasticity have been preserved across primate evolution.14 p

A horizon for haptic perception

The spatial limits of sensory acquisition (its sensory horizon) is a fundamental property of any sensorimotor system. In the present study, we sought to determine whether there is a sensory horizon for the human haptic modality. At first blush, it seems obvious that the haptic system is bounded by the space where the body can interact with the environment (e.g., the arm span). However, the human somatosensory system is exquisitely tuned to sensing with tools-blind-cane navigation being a classic example of this. The horizon of haptic perception therefore extends beyond body space, but to what extent is unknown. We first used neuromechanical modelling to determine the theoretical horizon, which we pinpointed as six meters. We then used a psychophysical localization paradigm to behaviorally confirm that humans can haptically localize objects using a six-meter rod. This finding underscores the incredibly flexibility of the brain's sensorimotor representations, as they can be adapted to sense with an object many times longer than the user's own body

Tool use

Tool use is a defining feature of the human species. Tool-in-hand, humans can manipulate their environment in novel ways as well as process the sensory information arising during mechanical contact. This fact has led cognitive neuroscience researchers over the last few decades to explore how tool-based body augmentation impacts the behavior and neural processing of their users. In this chapter, we explore the findings of this research and draw some tentative conclusions about its implications for the sensorimotor system. We first survey research, conducted over the past decade, that has found that using a tool modulates body representations underlying action and somatosensory perception. This research includes both behavioral and neural approaches. We then focus on the sensory and functional underpinnings driving the tool-induced plasticity to body representations. Finally, we describe a novel means to evaluate the incorporation of tools into the sensorimotor system: The ability of humans to sense the locations of external objects with a tool. We will discuss how this research has already gained powerful insight into the relationship between tools and the body, as well as challenging our conception of the boundaries of the somatosensory system

Reach planning with someone else's hand

To investigate the relationship between the sense of body ownership and motor control, we capitalized on a rare bizarre disorder wherein another person's hand is misattributed to their own body, i.e., a pathological form of embodiment (E+). Importantly, despite E+ is usually associated with motor deficits, we had the opportunity to test two E+ patients with spared motor function, thus able to perform a reaching task. Crucially, these patients had proprioceptive deafferentation, allowing us to purely isolate the embodiment-dependent effect from proprioception-dependent ones that are usually associated in experimental manipulations of body ownership in healthy participants. Previous evidence suggests that the reaching movement vector is attracted towards an embodied hand during the rubber hand illusion (RHI). However, these results are confounded by the spared proprioception, whose modulation alone could explain the effects on reach planning. The neuropsychological approach employed here provides unambiguous evidence about the role of body ownership in reach planning. Indeed, three brain-damaged patients with proprioceptive deafferentation, two E+ and a well-matched control patient without pathological embodiment (E-), and 10 age-matched healthy controls underwent a reaching task wherein they had to reach for a target from a fixed starting point, while an alien hand (the co-experimenter's) was placed on the table. Irrespective of proprioception, damaged in all patients, only in E+ patients reaching errors were significantly more shifted consistently with the pathological belief, i.e., as if they planned movements from the position of the alien (embodied) hand, as compared to controls. Furthermore, with an additional experiment on healthy participants, we demonstrated that reaching errors observed during the RHI correlate with the changes in ownership. In conclusion, our neuropsychological approach suggests that when planning a reach, we do so from where our owned hand is and not from its physical location

Visual tests predict dementia risk in Parkinson disease

Objective: To assess the role of visual measures and retinal volume to predict the risk of Parkinson disease (PD) dementia. Methods: In this cohort study, we collected visual, cognitive, and motor data in people with PD. Participants underwent ophthalmic examination, retinal imaging using optical coherence tomography, and visual assessment including acuity and contrast sensitivity and high-level visuoperception measures of skew tolerance and biological motion. We assessed the risk of PD dementia using a recently described algorithm that combines age at onset, sex, depression, motor scores, and baseline cognition. Results: One hundred forty-six people were included in the study (112 with PD and 34 age-matched controls). The mean disease duration was 4.1 (±2·5) years. None of these participants had dementia. Higher risk of dementia was associated with poorer performance in visual measures (acuity: p = 0.29, p = 0.0024; contrast sensitivity: ρ = -0.37, p < 0.0001; skew tolerance: ρ = -0.25, p = 0.0073; and biological motion: p = -0.26, p = 0.0054). In addition, higher risk of PD dementia was associated with thinner retinal structure in layers containing dopaminergic cells, measured as ganglion cell layer (GCL) and inner plexiform layer (IPL) thinning (p = -0.29, p = 0.0021; p = -0.33, p = 0.00044). These relationships were not seen for the retinal nerve fiber layer that does not contain dopaminergic cells and were not seen in unaffected controls. Conclusion: Visual measures and retinal structure in dopaminergic layers were related to risk of PD dementia. Our findings suggest that visual measures and retinal GCL and IPL volumes may be useful to predict the risk of dementia in PD

Many Labs 5: Testing Pre-Data-Collection Peer Review as an Intervention to Increase Replicability

Replication studies in psychological science sometimes fail to reproduce prior findings. If these studies use methods that are unfaithful to the original study or ineffective in eliciting the phenomenon of interest, then a failure to replicate may be a failure of the protocol rather than a challenge to the original finding. Formal pre-data-collection peer review by experts may address shortcomings and increase replicability rates. We selected 10 replication studies from the Reproducibility Project: Psychology (RP:P; Open Science Collaboration, 2015) for which the original authors had expressed concerns about the replication designs before data collection; only one of these studies had yielded a statistically significant effect (p lt .05). Commenters suggested that lack of adherence to expert review and low-powered tests were the reasons that most of these RP:P studies failed to replicate the original effects. We revised the replication protocols and received formal peer review prior to conducting new replication studies. We administered the RP:P and revised protocols in multiple laboratories (median number of laboratories per original study = 6.5, range = 3–9; median total sample = 1,279.5, range = 276–3,512) for high-powered tests of each original finding with both protocols. Overall, following the preregistered analysis plan, we found that the revised protocols produced effect sizes similar to those of the RP:P protocols (Δr =.002 or.014, depending on analytic approach). The median effect size for the revised protocols (r =.05) was similar to that of the RP:P protocols (r =.04) and the original RP:P replications (r =.11), and smaller than that of the original studies (r =.37). Analysis of the cumulative evidence across the original studies and the corresponding three replication attempts provided very precise estimates of the 10 tested effects and indicated that their effect sizes (median r =.07, range =.00–.15) were 78% smaller, on average, than the original effect sizes (median r =.37, range =.19–.50)