scholarly journals “Paralympic Brain”. Compensation and Reorganization of a Damaged Human Brain with Intensive Physical Training

Sports ◽  
2020 ◽  
Vol 8 (4) ◽  
pp. 46
Author(s):  
Kimitaka Nakazawa ◽  
Hiroki Obata ◽  
Daichi Nozaki ◽  
Shintaro Uehara ◽  
Pablo Celnik
Keyword(s):  
Evoked Potential ◽  
Motor Evoked Potential ◽  
Electromyographic Activity ◽  
Continuous Training ◽  
Intensive Training ◽  
Affected Side ◽  
Gold Medalist ◽  
Temporal Side ◽  
Spinal Excitability ◽  
The Brain

The main aim of the study was to evaluate how the brain of a Paralympic athlete with severe disability due to cerebral palsy has reorganized after continuous training geared to enhance performance. Both corticospinal excitability of upper-limb muscles and electromyographic activity during swimming were investigated for a Paralympic gold medalist in swimming competitions. Transcranial magnetic stimulation (TMS) to the affected and intact hand motor cortical area revealed that the affected side finger muscle cortical representation area shifted towards the temporal side, and cortico-spinal excitability of the target muscle was prominently facilitated, i.e., the maximum motor evoked potential in the affected side, 6.11 ± 0.19 mV was greater than that in the intact side, 4.52 ± 0.39 mV (mean ± standard error). Electromyographic activities during swimming demonstrated well-coordinated patterns as compared with rather spastic activities observed in the affected side during walking on land. These results suggest that the ability of the brain to reorganize through intensive training in Paralympic athletes can teach interesting lessons to the field neurorehabilitation.

scholarly journals The effects of forearm position and contraction intensity on cortical and spinal excitability during a submaximal force steadiness task of the elbow flexors

2020 ◽  
Vol 123 (2) ◽  
pp. 522-528
Author(s):  
Alexandra F. Yacyshyn ◽  
Samantha Kuzyk ◽  
Jennifer M. Jakobi ◽  
Chris J. McNeil
Keyword(s):  
Evoked Potential ◽  
Biceps Brachii ◽  
Cortical Excitability ◽  
Motor Evoked Potential ◽  
Elbow Flexor ◽  
Elbow Flexors ◽  
Neural Excitability ◽  
Force Steadiness ◽  
Maximal Force ◽  
Spinal Excitability

Elbow flexor force steadiness is less with the forearm pronated (PRO) compared with neutral (NEU) or supinated (SUP) and may relate to neural excitability. Although not tested in a force steadiness paradigm, lower spinal and cortical excitability was observed separately for biceps brachii in PRO, possibly dependent on contractile status at the time of assessment. This study aimed to investigate position-dependent changes in force steadiness as well as spinal and cortical excitability at a variety of contraction intensities. Thirteen males (26 ± 7 yr; means ± SD) performed three blocks (PRO, NEU, and SUP) of 24 brief (~6 s) isometric elbow flexor contractions (5, 10, 25 or 50% of maximal force). During each contraction, transcranial magnetic stimulation or transmastoid stimulation was delivered to elicit a motor-evoked potential (MEP) or cervicomedullary motor-evoked potential (CMEP), respectively. Force steadiness was lower in PRO compared with NEU and SUP ( P ≤ 0.001), with no difference between NEU and SUP. Similarly, spinal excitability (CMEP/maximal M wave) was lower in PRO than NEU (25 and 50% maximal force; P ≤ 0.010) and SUP (all force levels; P ≤ 0.004), with no difference between NEU and SUP. Cortical excitability (MEP/CMEP) did not change with forearm position ( P = 0.055); however, a priori post hoc testing for position showed excitability was 39.8 ± 38.3% lower for PRO than NEU at 25% maximal force ( P = 0.006). The data suggest that contraction intensity influences the effect of forearm position on neural excitability and that reduced spinal and, to a lesser extent, cortical excitability could contribute to lower force steadiness in PRO compared with NEU and SUP. NEW & NOTEWORTHY To address conflicting reports about the effect of forearm position on spinal and cortical excitability of the elbow flexors, we examine the influence of contraction intensity. For the first time, excitability data are considered in a force steadiness context. Motoneuronal excitability is lowest in pronation and this disparity increases with contraction intensity. Cortical excitability exhibits a similar pattern from 5 to 25% of maximal force. Lower corticospinal excitability likely contributes to relatively poor force steadiness in pronation.

The effect of acetaminophen ingestion on cortico-spinal excitability

2013 ◽  
Vol 91 (2) ◽  
pp. 187-189 ◽  
Author(s):  
Alexis R. Mauger ◽  
James G. Hopker
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Magnetic Stimulation ◽  
Evoked Potential ◽  
Motor Evoked Potential ◽  
Silent Period ◽  
Sodium Currents ◽  
Cortical Silent Period ◽  
Voltage Gated ◽  
Spinal Excitability

Acetaminophen (ACT) facilitates the inhibition of voltage-gated calcium and sodium currents, which may effect cortico-spinal excitability. Twelve subjects ingested acetaminophen or a placebo and underwent transcranial magnetic stimulation to assess the motor evoked potential (MEP), and cortical silent period (CSP). ACT significantly increased MEP response (P > 0.05) but had no effect on CSP (P > 0.05). This indicates that ACT increases MEP and should be controlled for in studies where these measures are of interest.

scholarly journals Long-term motor deficit in brain tumour surgery with preserved intra-operative motor-evoked potentials

2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Davide Giampiccolo ◽  
Cristiano Parisi ◽  
Pietro Meneghelli ◽  
Vincenzo Tramontano ◽  
Federica Basaldella ◽  
...  
Keyword(s):  
Evoked Potentials ◽  
Brain Tumour ◽  
Evoked Potential ◽  
Corticospinal Tract ◽  
Motor Evoked Potentials ◽  
Motor Evoked Potential ◽  
Motor Deficit ◽  
Motor Deficits ◽  
Brain Tumour Surgery

Abstract Muscle motor-evoked potentials are commonly monitored during brain tumour surgery in motor areas, as these are assumed to reflect the integrity of descending motor pathways, including the corticospinal tract. However, while the loss of muscle motor-evoked potentials at the end of surgery is associated with long-term motor deficits (muscle motor-evoked potential-related deficits), there is increasing evidence that motor deficit can occur despite no change in muscle motor-evoked potentials (muscle motor-evoked potential-unrelated deficits), particularly after surgery of non-primary regions involved in motor control. In this study, we aimed to investigate the incidence of muscle motor-evoked potential-unrelated deficits and to identify the associated brain regions. We retrospectively reviewed 125 consecutive patients who underwent surgery for peri-Rolandic lesions using intra-operative neurophysiological monitoring. Intraoperative changes in muscle motor-evoked potentials were correlated with motor outcome, assessed by the Medical Research Council scale. We performed voxel–lesion–symptom mapping to identify which resected regions were associated with short- and long-term muscle motor-evoked potential-associated motor deficits. Muscle motor-evoked potentials reductions significantly predicted long-term motor deficits. However, in more than half of the patients who experienced long-term deficits (12/22 patients), no muscle motor-evoked potential reduction was reported during surgery. Lesion analysis showed that muscle motor-evoked potential-related long-term motor deficits were associated with direct or ischaemic damage to the corticospinal tract, whereas muscle motor-evoked potential-unrelated deficits occurred when supplementary motor areas were resected in conjunction with dorsal premotor regions and the anterior cingulate. Our results indicate that long-term motor deficits unrelated to the corticospinal tract can occur more often than currently reported. As these deficits cannot be predicted by muscle motor-evoked potentials, a combination of awake and/or novel asleep techniques other than muscle motor-evoked potentials monitoring should be implemented.

scholarly journals Designing a tangible solution to encourage playful hand usage for children with cerebral palsy

2020 ◽  
Vol 6 (2) ◽  
Author(s):  
Christina Mittag ◽  
Regina Leiss ◽  
Katharina Lorenz ◽  
Dagmar Siebold
Keyword(s):  
Cerebral Palsy ◽  
Support System ◽  
Functional Test ◽  
Intensive Training ◽  
Affected Side ◽  
Motivational Support ◽  
Children With Cerebral Palsy ◽  
Unilateral Cerebral Palsy ◽  
Arm Function ◽  
Inertial Measurements

AbstractChildren with unilateral cerebral palsy (CCP) benefit from intensive training with the affected side. The SHArKi project strives for a motivational support system, using wristbands with inertial measurements units (IMU) to measure arm function, providing biofeedback as well as motivating stimuli. To consider finger and wrist movements as well, this paper covers concepts for a tangible solution and its first implementation including the gamification development. Finalizations of the demonstrator, an overall functional test as well as concluding feedback from CCP are pending.

scholarly journals GPR110 ligands reduce chronic optic tract gliosis and visual deficit following repetitive mild traumatic brain injury in mice

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Huazhen Chen ◽  
Karl Kevala ◽  
Elma Aflaki ◽  
Juan Marugan ◽  
Hee-Yong Kim
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Visual Evoked Potential ◽  
Evoked Potential ◽  
Optic Tract ◽  
Primary Microglia ◽  
Visual Dysfunction ◽  
The Brain

Abstract Background Repetitive mild traumatic brain injury (mTBI) can result in chronic visual dysfunction. G-protein receptor 110 (GPR110, ADGRF1) is the target receptor of N-docosahexaenoylethanolamine (synaptamide) mediating the anti-neuroinflammatory function of synaptamide. In this study, we evaluated the effect of an endogenous and a synthetic ligand of GPR110, synaptamide and (4Z,7Z,10Z,13Z,16Z,19Z)-N-(2-hydroxy-2-methylpropyl) docosa-4,7,10,13,16,19-hexaenamide (dimethylsynaptamide, A8), on the mTBI-induced long-term optic tract histopathology and visual dysfunction using Closed-Head Impact Model of Engineered Rotational Acceleration (CHIMERA), a clinically relevant model of mTBI. Methods The brain injury in wild-type (WT) and GPR110 knockout (KO) mice was induced by CHIMERA applied daily for 3 days, and GPR110 ligands were intraperitoneally injected immediately following each impact. The expression of GPR110 and proinflammatory mediator tumor necrosis factor (TNF) in the brain was measured by using real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) in an acute phase. Chronic inflammatory responses in the optic tract and visual dysfunction were assessed by immunostaining for Iba-1 and GFAP and visual evoked potential (VEP), respectively. The effect of GPR110 ligands in vitro was evaluated by the cyclic adenosine monophosphate (cAMP) production in primary microglia isolated from adult WT or KO mouse brains. Results CHIMERA injury acutely upregulated the GPR110 and TNF gene level in mouse brain. Repetitive CHIMERA (rCHIMERA) increased the GFAP and Iba-1 immunostaining of glia cells and silver staining of degenerating axons in the optic tract with significant reduction of N1 amplitude of visual evoked potential at up to 3.5 months after injury. Both GPR110 ligands dose- and GPR110-dependently increased cAMP in cultured primary microglia with A8, a ligand with improved stability, being more effective than synaptamide. Intraperitoneal injection of A8 at 1 mg/kg or synaptamide at 5 mg/kg significantly reduced the acute expression of TNF mRNA in the brain and ameliorated chronic optic tract microgliosis, astrogliosis, and axonal degeneration as well as visual deficit caused by injury in WT but not in GPR110 KO mice. Conclusion Our data demonstrate that ligand-induced activation of the GPR110/cAMP system upregulated after injury ameliorates the long-term optic tract histopathology and visual impairment caused by rCHIMERA. Based on the anti-inflammatory nature of GPR110 activation, we suggest that GPR110 ligands may have therapeutic potential for chronic visual dysfunction associated with mTBI.

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