Brain : a journal of neurology
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Central pain below the injury level after spinal cord injury is excruciating, chronic and resistive to treatment. Animal studies suggest that pretreatment may prevent central pain, but to date there are no measures to predict its development. Our aim was to monitor changes in the sensory profile below the lesion prior to the development of below-level central pain in order to search for a parameter that could predict its risk and to further explore its pathophysiology. ⋯ Furthermore, it appears that below-level central pain develops after a substantial build-up of hyperexcitability. To the best of our knowledge, this is the first systematic report establishing that neuronal hyperexcitability precedes central pain. Predicting the risk for central pain can be utilized to initiate early treatment in order to prevent its development.
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Post-mortem ganglion cell dropout has been observed in multiple sclerosis; however, longitudinal in vivo assessment of retinal neuronal layers following acute optic neuritis remains largely unexplored. Peripapillary retinal nerve fibre layer thickness, measured by optical coherence tomography, has been proposed as an outcome measure in studies of neuroprotective agents in multiple sclerosis, yet potential swelling during the acute stages of optic neuritis may confound baseline measurements. The objective of this study was to ascertain whether patients with multiple sclerosis or neuromyelitis optica develop retinal neuronal layer pathology following acute optic neuritis, and to systematically characterize such changes in vivo over time. ⋯ Further, these data provide evidence of subclinical disease activity, in both participants with multiple sclerosis and with neuromyelitis optica without a history of optic neuritis, a disease in which subclinical disease activity has not been widely appreciated. No pathology was seen in the inner or outer nuclear layers of eyes with optic neuritis, suggesting that retrograde degeneration after optic neuritis may not extend into the deeper retinal layers. The subsequent thinning of the ganglion cell layer following acute optic neuritis, in the absence of evidence of baseline swelling, suggests the potential utility of quantitative optical coherence tomography retinal layer segmentation to monitor neuroprotective effects of novel agents in therapeutic trials.
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Parietofrontal integrity determines neural modulation associated with grasping imagery after stroke.
Chronic stroke patients with heterogeneous lesions, but no direct damage to the primary sensorimotor cortex, are capable of longitudinally acquiring the ability to modulate sensorimotor rhythms using grasping imagery of the affected hand. Volitional modulation of neural activity can be used to drive grasping functions of the paralyzed hand through a brain-computer interface. The neural substrates underlying this skill are not known. ⋯ Finally, estimated white matter microstructure integrity in regions of the contralesional superior longitudinal fascicle adjacent to primary sensorimotor and posterior parietal cortex, as well as grey matter volume co-localized to these specific regions, positively correlated with sensorimotor rhythm modulation leading to successful brain-computer interface control. Thus, volitional modulation of ipsilesional neural activity leading to control of paralyzed hand grasping function through a brain-computer interface after longitudinal training relies on structural and functional connectivity in both ipsilesional and contralesional parietofrontal pathways involved in visuomotor information processing. Extant integrity of this structural network may serve as a future predictor of response to longitudinal therapeutic interventions geared towards training sensorimotor rhythms in the lesioned brain, secondarily improving grasping function through brain-computer interface applications.
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Cross-modal reorganization in the auditory cortex has been reported in deaf individuals. However, it is not well understood whether this compensatory reorganization induced by auditory deprivation recedes once the sensation of hearing is partially restored through a cochlear implant. The current study used electroencephalography source localization to examine cross-modal reorganization in the auditory cortex of post-lingually deafened cochlear implant users. ⋯ At the P100 latency, cochlear implant users also showed activation in the right auditory cortex, which was inversely related to speech recognition ability with the cochlear implant. These results confirm a visual take-over in the auditory cortex of cochlear implant users. Incomplete reversal of this deafness-induced cortical reorganization might limit clinical benefit from a cochlear implant and help explain the high inter-subject variability in auditory speech comprehension.
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Amputees can move their phantom limb at will. These 'movements without movements' have generally been considered as motor imagery rather than motor execution, but amputees can in fact perform both executed and imagined movements with their phantom and they report distinct perceptions during each task. Behavioural evidence for this dual ability comes from the fact that executed movements are associated with stump muscle contractions whereas imagined movements are not, and that phantom executed movements are slower than intact hand executed movements whereas the speed of imagined movements is identical for both hands. ⋯ The dynamic causal modelling analysis further confirmed the presence of a clear neurophysiological distinction between imagination and execution, as motor imagery and motor execution had opposite effects on the supplementary motor area-primary motor cortex network. This is the first imaging evidence that the neurophysiological network activated during phantom limb movements is similar to that of executed movements of intact limbs and differs from the phantom limb imagination network. The dual ability of amputees to execute and imagine movements of their phantom limb and the fact that these two tasks activate distinct cortical networks are important factors to consider when designing rehabilitation programmes for the treatment of phantom limb pain.