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Ward, N. S.

Publications and source records attributed to Ward, N. S..

4 recordsLinked to original sources

Use of the non-paretic arm reflects a habitual behaviour in chronic stroke

BackgroundA proportion of stroke survivors use their affected arm less than might be expected based on their level of impairment. The resulting non-use of the affected arm has a negative impact on participation in neurorehabilitation and functional independence. However, non-use remains poorly understood. One possibility is that prioritising the non-paretic arm reflects a habit, despite residual functional capacity in the paretic arm. Methods30 chronic stroke survivors (Mean FM: 28.9 {+/-} 11.3) participated in a simplified version of the forced response paradigm, which reliably identifies the presence of a habit. Participants were asked to choose which arm to use to maximise points scored during a reaching task. During half of the trials, the presumed habit of using the non-paretic arm yielded more points, whereas in the other half using the non-paretic arm incurred a loss of points. Participants completed two versions of this task, once with unlimited response time available and once without. ResultsParticipants scored fewer points in the limited response condition compared to the unlimited response conditions. This difference was driven by a selective increase in the use of the non-paretic arm in trials where the paretic arm yielded more points. The results were not mediated by former hand dominance. ConclusionsOur results demonstrate that not using the non-paretic arm may reflect a habit response that is more readily triggered in demanding (e.g. time-limited) situations. This may explain why successful neurorehabilitation does not always result in a more functionally useful arm. Our results pave the way for targeted interventions such as habit breaking techniques to be included in clinical practise.

neuroscience↗

Spatiotemporal organization of human sensorimotor beta burst activity

Beta oscillations in human sensorimotor cortex are hallmark signatures of healthy and pathological movement. In single trials, beta oscillations include bursts of intermittent, transient periods of high-power activity. These burst events have been linked to a range of sensory and motor processes, but their precise spatial, spectral, and temporal structure remains unclear. Specifically, a role for beta burst activity in information coding and communication suggests spatiotemporal patterns, or travelling wave activity, along specific anatomical gradients. We here show in human magnetoencephalography recordings that burst activity in sensorimotor cortex occurs in planar spatiotemporal wave-like patterns that dominate along two axes either parallel or perpendicular to the central sulcus. Moreover, we find that the two propagation directions are characterised by distinct anatomical and physiological features. Finally, our results suggest that sensorimotor beta bursts occurring before and after a movement share the same generator but can be distinguished by their anatomical, spectral and spatiotemporal characteristics, indicating distinct functional roles.

neuroscience↗

The impact of brain lesions on tDCS-induced electric field magnitude

BackgroundTranscranial direct current stimulation (tDCS) has been used to enhance motor and language rehabilitation following a stroke. However, improving the effectiveness of clinical tDCS protocols depends on understanding how lesions may influence tDCS-induced current flow through the brain. ObjectiveWe systematically investigated the effect of brain lesions on the magnitude of electric fields (e-mag) induced by tDCS, and how to overcome lesion-induced inter-individual variability in e-mag. MethodsWe simulated the effect of 630 different lesions - by varying lesion location, distance from the target region of interest (ROI), size and conductivity - on tDCS-induced e-mag in the brains of two participants. Current flow modelling was conducted for two tDCS montages commonly used in clinical applications, which target either primary motor cortex (M1) or Brocas area (BA44), respectively. We further explored how the inherent variability in e-mag that is introduced by inter-lesion differences can be overcome by individualising tDCS protocols. ResultsThe effect on absolute e-mag was highly dependent on lesion size, conductance and the distance from the target ROI. Larger lesions, with high conductivity, closer to the ROI caused e-mag changes of more than 30%. The sign of this change was determined by the location of the lesion. Specifically, lesions located in-line with the predominant direction of current flow increased e-mag in the ROI, whereas lesions located in the opposite direction caused a decrease. Lesions had a large impact on the optimal electrode configuration if attempting to maximise for the total e-mag in the ROI, but little impact if only the component of e-mag flowing radially inward to the cortex was maximised. Knowing the effect of a given lesion on e-mag also allows for individualising tDCS intensity to reduce variability. ConclusionsThese results demonstrate that tDCS-induced electric fields are profoundly influenced by lesion characteristics, and further exacerbate the known variability in e-mag across individuals. Additionally, the dependence of these results on the assigned conductance of the lesion underlines the need for improved estimates of lesion conductivity for current flow models. Our results highlight the need for individualised dose control of tDCS in the lesioned brain to overcome the substantial inter-individual variability in electric fields delivered to a cortical target region. Highlights- Lesions can alter tDCS-induced electric field magnitude (e-mag) in a target by 30% - Lesions can cause increases or decreases to e-mag - Direction of change depends on the position of the lesion relative to current flow - Lesion conductivity - the true value for which is unknown - also impacts change - E-mag variability can be reduced by individualising montage and stimulation intensity

neuroscience↗

Welcoming back my arm: Affective touch increases body ownership following right hemisphere stroke

Right hemisphere stroke can impair the ability to recognise ones contralesional body parts as belonging to ones self. The study of this so-called disturbed sense of limb ownership (DSO) can provide unique insights into the neurocognitive mechanisms of body ownership. Here, we address a hypothesis built upon experimental studies on body ownership in healthy volunteers. These studies have shown that affective (pleasant) touch, an interoceptive modality associated with unmyelinated, slow-conducting C tactile afferents, has a unique role in the sense of body ownership. Here we systematically investigated whether affective touch stimulation could increase body ownership in patients with DSO following right hemisphere stroke. An initial feasibility study in 16 adult, acute stroke patients enabled us to optimise and calibrate an affective touch protocol to be administered by the bedside. The main experiment, conducted with a different sample of 26 right hemisphere patients, assessed changes in limb ownership elicited following self-(patient) versus other-(experimenter) generated tactile stimulation, using a velocity known to optimally activate C-tactile fibres (i.e. 3cm/s), and a second velocity that is suboptimal for C-tactile activation (i.e. 18cm/s). We further examined the specificity and mechanism of observed changes in limb ownership in secondary analyses looking at (1) the influence of perceived intensity and pleasantness of touch, (2) touch laterality, and (3) level of DSO on ownership change, as well as (4) changes in unilateral neglect arising from touch. Findings indicated a significant increase in limb ownership following experimenter-administered, CT-optimal touch. Voxel-based Lesion-Symptom Mapping (VLSM) identified damage to the right insula and, more substantially, the right corpus callosum, associated with a failure to increase body ownership following experimenter-administered, affective touch. Our findings suggest that affective touch can increase the sense of body-part ownership following right hemisphere stroke, potentially due to its unique role in the multisensory integration processes that underlie the sense of body ownership.

neuroscience↗