ALS, Author Interviews, Neurological Disorders, Technology / 26.01.2018

MedicalResearch.com Interview with: [caption id="attachment_39652" align="alignleft" width="240"]Matthew McKee/BrainGate Collaboration New technique enables rapid calibration of the BrainGate brain-computer interface.[/caption] David Brandman, MD, PhD Postdoctoral research associate (neuroengineering), Brown University Senior neurosurgical resident Dalhousie University BrainGate Website MedicalResearch.com: What is the background for this study? Response: People with cervical spinal cord injuries, ALS, or brainstem stroke, may lose some or all of their ability to use their arms or hands. In some cases, they may even lose the ability to speak. One approach to restoring neurologic function is by using a brain computer interface (BCI). BCIs record information from the brain, and then translate the recorded brain signals into commands used to control external devices. Our research group and others have shown that intracortical BCIs can provide people with tetraplegia the ability to communicate via a typing interface, to control a robotic limb for self-feeding, and to move their own muscles using functional electrical stimulation. Use of a BCI generally requires the oversight of a trained technician, both for system setup and calibration, before users can begin using the system independently. An open question with intracortical BCIs is how long it takes people to get up and running before they can communicate independently with 2 dimensional cursor control. The goal of this study was to systematically examine this question in three people with paralysis. As part of the ongoing BrainGate2 clinical trial, each study participant (T5, T8, and T10) had tiny (4x4 mm) arrays of electrodes implanted into a part of their brain that coordinates arm control. Each participant used motor imagery – that is, attempted or imagined moving their body – to control a computer cursor in real time.
Author Interviews, Neurological Disorders / 21.07.2015

Dr Michael Lee  PhD MPhty MChiro BSc Discipline of Physiotherapy, Faculty of Health Sciences, The University of Sydney Clinical Neurophysiologist, The Brain & Mind Research Institute, The University of Sydney Research Affiliate, Neuroscience Research Australia Neurology Research Fellow, Institute of Neurological Sciences, Prince of Wales HospitalMedicalResearch.com Interview with: Dr Michael Lee PhD MPhty MChiro BSc Discipline of Physiotherapy, Faculty of Health Sciences, The University of Sydney Clinical Neurophysiologist, The Brain & Mind Research Institute, The University of Sydney Research Affiliate, Neuroscience Research Australia Neurology Research Fellow, Institute of Neurological Sciences, Prince of Wales Hospital Medical Research: What is the background for this study? Dr. Lee: Our research team at the University of Sydney has previously shown that the functioning of peripheral nerves deteriorate following spinal cord injury (SCI). Using novel, non-invasive electrophysiological techniques (nerve excitability testing), we showed in this study that peripheral nerves below the level of spinal cord injury underwent dramatic functional reorganization. Peripheral nerve dysfunction will not only contribute to a number of undesirable medical complications including peripheral neuropathy and pain, it exacerbates muscle atrophy and can potentially limit the effectiveness of rehabilitative therapies that drive central plasticity. In this study, we were interested to see whether this secondary peripheral nerve dysfunction could be reversed with a short-term targeted peripheral nerve stimulation therapy. Medical Research: What are the main findings? Dr. Lee: We studied peripheral nerve function in both the upper (median nerve at the wrist) and lower limbs (peroneal nerve near the fibular head) in 22 patients with acute spinal cord injury (all within 6 months of injury). We then randomly assigned one upper limb and one lower limb nerve to a daily regimen of 30-min peripheral nerve stimulation for 6 week. All study participants continued with standard rehabilitation. The results from our nerve excitability studies showed that 6-weeks of daily stimulation reversed a number of nerve excitability abnormalities secondary to spinal cord injury, and in some cases normalized it to a level comparable to healthy age-matched subjects. The peripheral nerves in the opposite limbs remained dysfunctional over the 6-week period. The results of our study showed convincingly that the addition of peripheral nerve stimulation in the early stages of spinal cord injury is beneficial by ameliorating the downstream effects of spinal cord injury. Spinal cord injuries can be an unfortunate effect of being a car accident, causing serious issues for those who suffer from it whether financial or physical. Those who find themselves in this type of situation may look into contacting someone like these car accident injury lawyers near Sacramento who might be able to help them to get compensation for their accident, which could help with phisyotherapy and medical bills.
Author Interviews, Case Western, Nature, Neurological Disorders / 26.12.2014

Bradley T. Lang, PhD Researcher, Jerry Silver Lab Department of Neurosciences Case Western Reserve University School of MedicineMedicalResearch.com Interview with: Bradley T. Lang, PhD Researcher, Jerry Silver Lab Department of Neurosciences Case Western Reserve University School of Medicine Medical Research: What is the background for this study? What are the main findings? Dr. Lang: In the late 1980’s, Jerry Silver, PhD, discovered the presence of chondroitin sulfate proteoglycans in the developing nervous system, which form barriers to prevent aberrant growth. He has been building on this finding for more than 30 years, attempting to understand why the adult spinal cord is incapable of regenerating, or why axons don’t grow where they don’t. He has found that the glial scar, which surrounds the site of neural trauma, is incredibly rich in proteoglycans, which prevent regeneration in the spinal cord. In 2009 we collaborated with a group at Harvard to discover the very first receptor for chondroitin sulfate proteoglycans, protein tyrosine phosphatase-sigma, or PTPsigma. Medical Research: What are the main findings? Dr. Lang: The findings in this paper are twofold. We first describe a novel mechanism of regeneration failure, where regenerating axons become stabilized within a gradient of chondroitin sulfate proteoglycan, completely preventing motility. This finding helps explain why axons persist in the vicinity of the glial scar after injury indefinitely, with little to no regeneration potential—they are simply embedded within the scar. We were able to model this interaction in a petri dish to screen for drugs that were capable of promoting motility. The second finding in the manuscript is the discovery and characterization of a novel peptide therapeutic that binds to the receptor for chondroitin sulfate proteoglycans and releases inhibition. Most importantly, this drug was given systemically, similar to a daily insulin injection, avoiding complications due to direct nervous system infusion/injection. After several weeks of treatment (which began 1 day after injury), rats with severe spinal cord injury regained coordinated locomotion, bladder control, and/or balance. In total, 21/26 treated animals regained some function.
Author Interviews, Neurological Disorders, Stem Cells / 07.04.2014

Dr. Ivo Lieberam Lecturer, MRC Centre for Developmental Neurobiology King's College London New Hunt's House, Guy's Hospital Campus London, SE1 1UL UKMedicalResearch.com Interview with: Dr. Ivo Lieberam Lecturer, MRC Centre for Developmental Neurobiology King's College London New Hunt's House, Guy's Hospital Campus London, SE1 1UL UK  MedicalResearch.com: What are the main findings of the study? Dr. Lieberam: In this study, which my group undertook in collaboration with Linda Greensmith’s group at University College London, we found that we could artificially control muscle activity using transplanted stem cell-derived nerve cells as an interface between an opto-electronic pacemaker and paralysed muscle in mice. The nerve cells were equipped with a molecular photosensor, so that they could be activated by light. We think that long-term, this technology may be used in neural prosthesis designed to re-establish relatively simple motor functions, such as breathing or swallowing, in patients suffering from spinal cord injury or neuromuscular diseases such as Motor Neuron Disease.
Author Interviews, Lancet, Medical Imaging, MRI, Neurological Disorders / 03.07.2013

MedicalResearch.com Interview with: Dr Patrick Freund Spinal Cord Injury Center Balgrist University Hospital Zurich, University of Zurich Forchstrasse 380 8008 Zurich, SwitzerlandDr Patrick Freund Spinal Cord Injury Center Balgrist University Hospital Zurich, University of Zurich Forchstrasse 380 8008 Zurich, Switzerland MedicalResearch.com: What are the main findings of the study? Dr. Freund: Novel interventions targeting acute spinal cord injury (SCI) have entered clinical trials, but neuroimaging biomarkers reflecting structural changes within the central nervous system are still awaited. In chronic SCI, neuroimaging provided evidence of structural changes at spinal cord and brain level that could be related to disability. However, the pattern and time course of these structural changes and their potential to predict clinical outcomes is uncertain. In a prospective longitudinal study, thirteen patients with acute traumatic SCI were assessed clinically and by longitudinal MRI (within five weeks of injury, after two, six and twelve months) and were compared to eighteen healthy controls. Cross-sectional cord area, cranial white matter (CST) and grey matter (cortex) volume decrease was evident at baseline and progressed over twelve months. Multi-parametric mapping of myelin sensitive magnetization transfer (MT) and longitudinal relaxation rate (R1) was reduced both within and beyond the areas of atrophic changes. Better neurological and functional outcomes were associated with less atrophic changes of the CST in both cord and brain.