Primary Motor Cortex In Patients Research Articles

Repetitive transcranial magnetic stimulation focusing on patients with neuropathic pain in the upper limb: a randomized sham-controlled parallel trial

This study aimed to evaluate the efficacy and safety of navigation-guided repetitive transcranial magnetic stimulation (rTMS) over the primary motor cortex in patients with neuropathic pain in the upper limb. This randomized, blinded, sham-controlled, parallel trial included a rTMS protocol (10-Hz, 2000 pulses/session) consisting of five daily sessions, followed by one session per week for the next seven weeks. Pain intensity, as well as pain-related disability, quality of life, and psychological status, were assessed. For the primary outcome, pain intensity was measured daily using a numerical rating scale as a pain diary. Thirty patients were randomly assigned to the active rTMS or sham-stimulation groups. In the primary outcome, the decrease (least square [LS] mean ± standard error) in the weekly average of a pain diary at week 9 compared to the baseline was 0.84 ± 0.31 in the active rTMS group and 0.58 ± 0.29 in the sham group (LS mean difference, 0.26; 95% confidence interval, − 0.60 to 1.13). There was no significant effect on the interaction between the treatment group and time point. Pain-related disability score improved, but other assessments showed no differences. No serious adverse events were observed. This study did not show significant pain relief; however, active rTMS tended to provide better results than sham. rTMS has the potential to improve pain-related disability in addition to pain relief.Clinical Trial Registration number: jRCTs052190110 (20/02/2020).

Spontaneous beta power, motor-related beta power and cortical thickness in major depressive disorder with psychomotor disturbance

IntroductionThe psychomotor disturbance is a common symptom in patients with major depressive disorder (MDD). The neurological mechanisms of psychomotor disturbance are intricate, involving alterations in the structure and function of motor-related regions. However, the relationship among changes in the spontaneous activity, motor-related activity, local cortical thickness, and psychomotor function remains unclear. MethodA total of 140 patients with MDD and 68 healthy controls performed a simple right-hand visuomotor task during magnetoencephalography (MEG) scanning. All patients were divided into two groups according to the presence of psychomotor slowing. Spontaneous beta power, movement-related beta desynchronization (MRBD), absolute beta power during movement and cortical characteristics in the bilateral primary motor cortex were compared using general linear models with the group as a fixed effect and age as a covariate. Finally, the moderated mediation model was tested to examine the relationship between brain metrics with group differences and psychomotor performance. ResultsThe patients with psychomotor slowing showed higher spontaneous beta power, movement-related beta desynchronization and absolute beta power during movement than patients without psychomotor slowing. Compared with the other two groups, significant decreases were found in cortical thickness of the left primary motor cortex in patients with psychomotor slowing. Our moderated mediation model showed that the increased spontaneous beta power indirectly affected impaired psychomotor performance by abnormal MRBD, and the indirect effects were moderated by cortical thickness. ConclusionThese results suggest that patients with MDD have aberrant cortical beta activity at rest and during movement, combined with abnormal cortical thickness, contributing to the psychomotor disturbance observed in this patient population.

Cortical phase-amplitude coupling is key to the occurrence and treatment of freezing of gait.

Freezing of gait is a debilitating symptom in advanced Parkinson’s disease and responds heterogeneously to treatments such as deep brain stimulation. Recent studies indicated that cortical dysfunction is involved in the development of freezing, while evidence depicting the specific role of the primary motor cortex in the multi-circuit pathology of freezing is lacking. Since abnormal beta-gamma phase-amplitude coupling recorded from the primary motor cortex in patients with Parkinson’s disease indicates parkinsonian state and responses to therapeutic deep brain stimulation, we hypothesized this metric might reveal unique information on understanding and improving therapy for freezing of gait.Here, we directly recorded potentials in the primary motor cortex using subdural electrocorticography and synchronously captured gait freezing using optoelectronic motion-tracking systems in 16 freely-walking patients with Parkinson’s disease who received subthalamic nucleus deep brain stimulation surgery. Overall, we recorded 451 timed up-and-go walking trials and quantified 7073 s of stable walking and 3384 s of gait freezing in conditions of on/off-stimulation and with/without dual-tasking.We found that (i) high beta-gamma phase-amplitude coupling in the primary motor cortex was detected in freezing trials (i.e. walking trials that contained freezing), but not non-freezing trials, and the high coupling in freezing trials was not caused by dual-tasking or the lack of movement; (ii) non-freezing episodes within freezing trials also demonstrated abnormally high couplings, which predicted freezing severity; (iii) deep brain stimulation of subthalamic nucleus reduced these abnormal couplings and simultaneously improved freezing; and (iv) in trials that were at similar coupling levels, stimulation trials still demonstrated lower freezing severity than no-stimulation trials.These findings suggest that elevated phase-amplitude coupling in the primary motor cortex indicates higher probabilities of freezing. Therapeutic deep brain stimulation alleviates freezing by both decoupling cortical oscillations and enhancing cortical resistance to abnormal coupling. We formalized these findings to a novel ‘bandwidth model,’ which specifies the role of cortical dysfunction, cognitive burden and therapeutic stimulation on the emergence of freezing. By targeting key elements in the model, we may develop next-generation deep brain stimulation approaches for freezing of gait.

421 Coherence Between the Subthalamic Nucleus and the Primary Motor Cortex in Patients With Parkinson's Disease

INTRODUCTION: DBS is established as a safe and effective treatment for Parkinson’s Disease (PD). The development of second generation stimulators based on closed loop systems is dependent upon deeper understanding of the cortical control of motricity and its coupling with STN oscillations. METHODS: Experimental study on human subjects involving 10 patients with idiopathic PD with indication for deep brain stimulation implants into the STN. Primary motor area of the hands were identified preoperatively with fMRI. Corkscrew electrodes were implanted in the scalp to obtain C3-Cz and C4-Cz derivations of the EEG. Needle electrodes were implanted into the thenar and hypothenar muscles of both hands to record motor evoked potentials and voluntary myoelectric activity. At the time of implantation of the definitive macro-electrodes, the best contacts were connected to the electrophysiological monitoring device to record STN local field potentials (LFP) from 1 side at a time. During the next 3 minutes, the patient was asked to perform closing and opening movements of the hand contralateral to the implant. Simultaneously recordings of hand-EMG, EEG signals from M1, and STN field potentials were acquired for off line analysis. RESULTS: Our data indicate that during epochs of hand movements, theta and beta range components of the EEG related to M1 were significantly increased as compared with rest epochs. Additionally, we demonstrated that, during movement, the cross correlation between STN-LFP and M1 significantly increased (p < 0.001). CONCLUSION: Movement control is highly dependent upon theta and beta EEG components and upon a high coherence between STN and M1 specifically occurring during movement. The development of closed-loop stimulation devices should consider this physiology to reach better results.

Levodopa Changes Functional Connectivity Patterns in Subregions of the Primary Motor Cortex in Patients With Parkinson’s Disease

BackgroundThe primary motor cortex (M1) is a critical node in Parkinson’s disease (PD)-related motor circuitry; however, the functional roles of its subregions are poorly understood. In this study, we investigated changes in the functional connectivity patterns of M1 subregions and their relationships to improved clinical symptoms following levodopa administration.MethodsThirty-six PD patients and 37 healthy controls (HCs) were enrolled. A formal levodopa challenge test was conducted in the PD group, and the Unified Parkinson’s Disease Rating Scale motor section (UPDRS-III) was assessed before (off state) and 1 h after administration of levodopa (on state). The PD group underwent resting-state functional magnetic resonance imaging in both off and on states, whereas the HC group was scanned once. We used the Human Brainnetome Atlas template to subdivide M1 into twelve regions of interest (ROIs). Functional connectivity (FC) was compared between PD on and off states [paired t-test, voxel-level p < 0.001, cluster-level p < 0.05, Gaussian random field (GRF) correction] and between patients and HC (two-sample t-test voxel-level p < 0.001, cluster-level p < 0.05). Correlations between ΔFC (differences in FC between PD off and on states) and clinical symptom improvements were examined.ResultsThere was decreased FC between the right caudal dorsolateral area 6 and the anterior cingulate gyrus (ACC), the right upper limb region and the left medial dorsal thalamus (mdTHA), as well as increased FC between the left tongue and larynx region and the left medial frontal gyrus. ΔFC between the right caudal dorsolateral area 6 and ACC was positively correlated with improvements in UPDRS-III total scores as well as the rigidity (item 22) and bradykinesia (items 23–26 and 31) subscores. ΔFC between the right upper limb region and left thalamus was positively correlated with improvements in the left upper limb tremor (items 20c and 21b) and postural tremor (item 21b) subscores.ConclusionsOur results reveal novel information regarding the underlying mechanisms in the motor circuits in the M1 and a promising way to explore the internal function of the M1 in PD patients. Notably, M1 is a potential therapeutic target in PD, and the exploration of its subregions provides a basis and a source of new insights for clinical intervention and precise drug treatment.

Plasticity of the Primary Motor Cortex in Patients with Primary Brain Tumors.

There are two neuron-level mechanisms proposed to underlie neural plasticity: recruiting neurons nearby to support the lost function (ipsilesional plasticity) and uncovering latent pathways that can assume the function that was lost (contralesional plasticity). While both patterns have been demonstrated in patient groups following injury, the specific mechanisms underlying each mode of plasticity are poorly understood. In a retrospective case series of 13 patients, we utilize a novel paradigm that analyzes serial fMRI scans in patients harboring intrinsic brain tumors that vary in location and growth kinetics to better understand the mechanisms underlying these two modes of plasticity in the human primary motor cortex. Twelve patients in our series had some degree of primary motor cortex plasticity, an area previously thought to have limited plasticity. Patients harboring smaller lesions with slower growth kinetics and increasing distance from the primary motor region demonstrated recruitment of ipsilateral motor regions. Conversely, larger, faster-growing lesions in close proximity to the primary motor region were associated with activation of the contralesional primary motor cortex, along with increased activation of the supplementary motor area. These data increase our understanding of the adaptive abilities of the brain and may lead to improved treatment strategies for those suffering from motor loss secondary to brain injuries.

"Remind-to-Move" Treatment Enhanced Activation of the Primary Motor Cortex in Patients with Stroke.

"Remind-to-Move" (RTM) has been developed and used as a new treatment for rehabilitation of upper extremity functions in patients with hemiplegia. This study aimed to investigate the cortical activation patterns using functional near-infrared spectroscopic topography for patients with chronic stroke receiving RTM by comparing with their healthy counterparts. Twelve patients with right hemispheric stroke and 15 healthy adults participated in this study. All participants were instructed to completed three experimental conditions-RTM, Move without reminding (Sham), and Remind with No-move (RNoM). In patients with stroke, RTM elicited higher level of activation than the Sham in the contralateral somatosensory association cortex, primary motor cortex, primary somatosensory cortex and the dorsolateral prefrontal cortex, which has been found in healthy participants. However, effects of RTM were robust and more widely distributed in healthy participants, comparing to patients with stroke, comparatively RNoM showed no significant higher activation than the baseline in those areas in both populations. RTM enhances the recruitment of contralateral primary motor cortex and this effect appears to be associated with increased attention allocation towards moving hands upon tactile stimulation in the form of vibration. The RTM treatment is useful to patients with stroke.

Precentral degeneration and cerebellar compensation in amyotrophic lateral sclerosis: A multimodal MRI analysis.

Amyotrophic lateral sclerosis (ALS) is a progressive and intractable neurodegenerative disease of human motor system characterized by progressive muscular weakness and atrophy. A considerable body of research has demonstrated significant structural and functional abnormalities of the primary motor cortex in patients with ALS. In contrast, much less attention has been paid to the abnormalities of cerebellum in this disease. Using multimodal magnetic resonance imagining data of 60 patients with ALS and 60 healthy controls, we examined changes in gray matter volume (GMV), white matter (WM) fractional anisotropy (FA), and functional connectivity (FC) in patients with ALS. Compared with healthy controls, patients with ALS showed decreased GMV in the left precentral gyrus and increased GMV in bilateral cerebellum, decreased FA in the left corticospinal tract and body of corpus callosum, and decreased FC in multiple brain regions, involving bilateral postcentral gyrus, precentral gyrus and cerebellum anterior lobe, among others. Meanwhile, we found significant intermodal correlations among GMV of left precentral gyrus, FA of altered WM tracts, and FC of left precentral gyrus, and that WM microstructural alterations seem to play important roles in mediating the relationship between GMV and FC of the precentral gyrus, as well as the relationship between GMVs of the precentral gyrus and cerebellum. These findings provided evidence for the precentral degeneration and cerebellar compensation in ALS, and the involvement of WM alterations in mediating the relationship between pathologies of the primary motor cortex and cerebellum, which may contribute to a better understanding of the pathophysiology of ALS.

Neurophysiological correlates of bradykinesia in Parkinson's disease.

Many neurophysiological abnormalities have been described in the primary motor cortex of patients with Parkinson's disease. However, it is unclear whether there is any relationship between them and bradykinesia, one of the cardinal motor features of the condition. In the present study we aimed to investigate whether objective measures of bradykinesia in Parkinson's disease have any relationship with neurophysiological measures in primary motor cortex as assessed by means of transcranial magnetic stimulation techniques. Twenty-two patients with Parkinson's disease and 18 healthy subjects were enrolled. Objective measurements of repetitive finger tapping (amplitude, speed and decrement) were obtained using a motion analysis system. The excitability of primary motor cortex was assessed by recording the input/output curve of the motor-evoked potentials and using a conditioning-test paradigm for the assessment of short-interval intracortical inhibition and facilitation. Plasticity-like mechanisms in primary motor cortex were indexed according to the amplitude changes in motor-evoked potentials after the paired associative stimulation protocol. Patients were assessed in two sessions, i.e. OFF and ON medication. A canonical correlation analysis was used to test for relationships between the kinematic and neurophysiological variables. Patients with Parkinson's disease tapped more slowly and with smaller amplitude than normal, and displayed decrement as tapping progressed. They also had steeper input/output curves, reduced short-interval intracortical inhibition and a reduced response to the paired associative stimulation protocol. Within the patient group, bradykinesia features correlated with the slope of the input/output curve and the after-effects of the paired associative stimulation protocol. Although dopaminergic therapy improved movement kinematics as well as neurophysiological measures, there was no relationship between them. In conclusion, neurophysiological changes in primary motor cortex relate to bradykinesia in patients with Parkinson's disease, although other mechanisms sensitive to dopamine levels must also play a role.

Semiautomated Evaluation of the Primary Motor Cortex in Patients with Amyotrophic Lateral Sclerosis at 3T.

Amyotrophic lateral sclerosis is a neurodegenerative disease involving the upper and lower motor neurons. In amyotrophic lateral sclerosis, pathologic changes in the primary motor cortex include Betz cell depletion and the presence of reactive iron-loaded microglia, detectable on 7T MR images as atrophy and T2*-hypointensity. Our purposes were the following: 1) to investigate the signal hypointensity-to-thickness ratio of the primary motor cortex as a radiologic marker of upper motor neuron involvement in amyotrophic lateral sclerosis with a semiautomated method at 3T, 2) to compare 3T and 7T results, and 3) to evaluate whether semiautomated measurement outperforms visual image assessment. We investigated 27 patients and 13 healthy subjects at 3T, and 19 patients and 18 healthy subjects at 7T, performing a high-resolution 3D multiecho T2*-weighted sequence targeting the primary motor cortex. The signal hypointensity-to-thickness ratio of the primary motor cortex was calculated with a semiautomated method depicting signal intensity profiles of the cortex. Images were also visually classified as "pathologic" or "nonpathologic" based on the primary motor cortex signal intensity and thickness. The signal hypointensity-to-thickness ratio of the primary motor cortex was greater in patients than in controls (P < .001), and it correlated with upper motor neuron impairment in patients (ρ = 0.57, P < .001). The diagnostic accuracy of the signal hypointensity-to-thickness ratio was high at 3T (area under the curve = 0.89) and even higher at 7T (area under the curve = 0.94). The sensitivity of the semiautomated method (0.81) outperformed the sensitivity of the visual assessment (0.56-0.63) at 3T. The signal hypointensity-to-thickness ratio of the primary motor cortex calculated with a semiautomated method is suggested as a radiologic marker of upper motor neuron burden in patients with amyotrophic lateral sclerosis. This semiautomated method may be useful for improving the subjective radiologic evaluation of upper motor neuron pathology in patients suspected of having amyotrophic lateral sclerosis.

Reversal of long term potentiation-like plasticity in primary motor cortex in patients with progressive supranuclear palsy.

Abnormal primary motor cortex plasticity might be involved in the pathophysiology of progressive supranuclear palsy. In the present study we aimed to investigate possible abnormalities of depotentiation, a mechanism involved in plasticity regulation, in this condition. Primary motor cortex excitability, investigated with single and paired-pulse transcranial magnetic stimulation, as well as long-term potentiation-like plasticity and its reversibility, were studied using theta burst stimulation in 15 patients with progressive supranuclear palsy and 11 healthy controls. Participants underwent two sessions using (1) the intermittent theta-burst stimulation (potentiation protocol) and (2) intermittent theta-burst stimulation combined with a depotentiation protocol (a short continuous theta-burst stimulation). Patients with PSP had higher corticospinal excitability and lower intracortical inhibition than healthy controls. Intermittent theta-burst stimulation elicited an abnormally increased long term potentiation-like effect in patients in comparison to healthy subjects. However, the depotentiation protocol was able to reverse the effects intermittent theta-burst stimulation on motor cortex excitability both in patients and in healthy controls. Altered primary motor cortex plasticity in patients with PSP does not reflect an abnormality of depotentiation. This study provides information for a deeper understanding of the possible pathophysiological mechanisms underlying the altered M1 plasticity in PSP.

Effects of cerebellar theta-burst stimulation on arm and neck movement kinematics in patients with focal dystonia.

To investigate the cerebellar inhibitory influence on the primary motor cortex in patients with focal dystonia using a cerebellar continuous theta-burst stimulation protocol (cTBS) and to evaluate any relationship with movement abnormalities. Thirteen patients with focal hand dystonia, 13 patients with cervical dystonia and 13 healthy subjects underwent two sessions: (i) cTBS over the cerebellar hemisphere (real cTBS) and (ii) cTBS over the neck muscles (sham cTBS). The effects of cerebellar cTBS were quantified as excitability changes in the contralateral primary motor cortex, as well as possible changes in arm and neck movements in patients. Real cerebellar cTBS reduced the excitability in the contralateral primary motor cortex in healthy subjects and in patients with cervical dystonia, though not in patients with focal hand dystonia. There was no correlation between changes in primary motor cortex excitability and arm and neck movement kinematics in patients. There were no changes in clinical scores or in kinematic measures, after either real or sham cerebellar cTBS in patients. The reduced cerebellar inhibitory modulation of primary motor cortex excitability in focal dystonia may be related to the body areas affected by dystonia as opposed to being a widespread pathophysiological abnormality. The present study yields information on the differential role played by the cerebellum in the pathophysiology of different focal dystonias.

Increased cerebellar activation after repetitive transcranial magnetic stimulation over the primary motor cortex in patients with multiple system atrophy.

Previous review reported that the high-frequency repetitive transcranial magnetic stimulation (rTMS) over the primary motor area (M1) of Parkinson's disease (PD) patients could alleviate their symptoms. This study aimed to investigate the effect of rTMS over the left M1 of patients with multiple system atrophy (MSA). Fifteen MSA patients were randomly assigned to receive a 10-session real (EP: group of experimental patients; n=7) or sham (CP: group of control patients; n=8) rTMS stimulation over two weeks. The overall experimental procedure consisted of two functional magnetic resonance imaging (fMRI) sessions, before and after a 10-session rTMS treatment. A complex self-paced sequential tapping task was performed during fMRI scanning. In addition, 18 age and gender matched healthy controls (HC) were enrolled. Subjects from the HC group did not receive any rTMS treatment and they underwent fMRI examination only once. The primary end point was the motor score change of the Unified Multiple System Atrophy Rating Scale (UMSARS-II) measured before and after the 5th and 10th session. Task-related activation was also compared among groups. After active rTMS treatment, only patients of EP group significant improvement in UMSARS-II score. Compared to HC, MSA patients showed significant activation over similar brain areas except for the cerebellum. Increased activation was obtained in the bilateral cerebellum after rTMS treatment in the EP group. On the contrary, no increased activation was identified in the CP group. Our results highlight rTMS over M1 induced motor improvement in MSA patients that may be associated with increased activation in the cerebellum.

ID 99 – Functional connectivity study on repetitive transcranial magnetic stimulation for central post-stroke pain

Objective Central post-stroke pain (CPSP) is one of the most refractory chronic pain syndromes. We and others have reported that repetitive transcranial magnetic stimulation (rTMS) of the primary motor cortex relieves pain in patients with CPSP. However, the mechanism underlying the pain relief remains unclear. This study aimed to investigate functional connectivity specific to CPSP and functional connectivity alteration associated with pain relief by rTMS. Methods Subjects were 12 patients with CPSP and 12 age-matched healthy controls. Resting-state function MRI (rs-fMRI) was taken before and after 5 Hz-rTMS of the ipsilesional primary motor cortex in patients, meanwhile rs-fMRI was taken once in controls without the rTMS intervention. rs-fMRI data was preprocessed, and second-level analyses of seed-to-voxel connectivity were implemented. Results The functional connectivity related to the ipsilesional primary motor cortex (FC-M1) was larger in patients than in controls. The alteration of FC-M1 after rTMS negatively correlated with pain relief. Conclusions Our findings suggested that alteration of the functional connectivity might be one of the mechanisms underlying pain relief by rTMS in CPSP. Key message rTMS might affect the functional connectivity related to the stimulation site in patients with CPSP.

Reduced functional connectivity within the primary motor cortex of patients with brachial plexus injury.

This study aims at the effects of traumatic brachial plexus lesion with root avulsions (BPA) upon the organization of the primary motor cortex (M1). Nine right-handed patients with a right BPA in whom an intercostal to musculocutaneous (ICN-MC) nerve transfer was performed had post-operative resting state fMRI scanning. The analysis of empirical functional correlations between neighboring voxels revealed faster correlation decay as a function of distance in the M1 region corresponding to the arm in BPA patients as compared to the control group. No differences between the two groups were found in the face area. We also investigated whether such larger decay in patients could be attributed to a gray matter diminution in M1. Structural imaging analysis showed no difference in gray matter density between groups. Our findings suggest that the faster decay in neighboring functional correlations without significant gray matter diminution in BPA patients could be related to a reduced activity in intrinsic horizontal connections in M1 responsible for upper limb motor synergies.

Homeostatic plasticity in the primary motor cortex of patients with non-specific chronic low back pain

Event Abstract Back to Event Homeostatic plasticity in the primary motor cortex of patients with non-specific chronic low back pain Tribikram Thapa1*, Lucinda Chipchase1*, Thomas Graven-Nielsen2* and Siobhan Schabrun1 1 Western Sydney University, School of Science and Health, Australia 2 Aalborg University, Health Science and Technology, Denmark Aims Homeostatic Plasticity (HP) mechanisms are known to regulate and stabilise use-dependent cortical plasticity. Previous studies suggest use-dependent cortical plasticity is altered in individuals with non-specific chronic Low Back Pain (cLBP). However, no study has investigated the effects of cLBP on HP. Here, we investigated HP in individuals with non-specific cLBP compared with pain-free controls. Methods Fifty individuals participated with non-specific cLBP experiencing low [n=25; Visual Analogue Scores (VAS): 1.6  1.1] and moderate (n=25; VAS: 5.7  1.4) pain, as well as 25 age- and sex-matched healthy controls. Participants received a single block of excitatory transcranial direct current stimulation (tDCS) for 7-minutes in one session to confirm the existence of an excitatory response to tDCS. In a separate session, participants were exposed to two excitatory blocks of tDCS (7-min and 5-min separated by a 3 min rest period), to evaluate homeostatic responses to cortical over-excitation. Sessions were randomised and conducted one week apart. Transcranial magnetic stimulation induced motor evoked potentials (MEPs) were recorded from the First Dorsal Interosseous muscle before and after excitatory tDCS at baseline, and at 0, 10, 20 and 30-minutes follow-up. Results MEP amplitudes reflecting corticomotor excitability were increased at all time-points in all three groups (p<0.001) following 7-min of tDCS, confirming the existence of an excitatory response to this protocol. However, only healthy controls demonstrated reduced MEP amplitudes (p<0.05) as a homeostatic response. MEP amplitudes in the two pain groups either increased over time (low pain group; p<0.049), or remained static (moderate pain group; p=0.996) indicating homeostatic impairment. Conclusions These results demonstrate failure to stabilize excessive corticomotor excitability in the primary motor cortex of individuals with cLBP. This suggests impaired homeostatic mechanisms could contribute to maladaptive use-dependent plasticity in cLBP. Further research is required to determine the relationship between homeostatic plasticity and symptoms in cLBP. Keywords: homeostatic plasticity, Primary motor cortex (M1), non-invasive brain stimulation, Corticomotor Excitability, motor evoked potential (MEP) Conference: ASP2016 - The 26th Annual Meeting of the Australasian Society for Psychophysiology, Adelaide Australia, Adelaide,SA, Australia, 12 Dec - 14 Dec, 2016. Presentation Type: Oral Presentation Topic: Abstract (student award) Citation: Thapa T, Chipchase L, Graven-Nielsen T and Schabrun S (2016). Homeostatic plasticity in the primary motor cortex of patients with non-specific chronic low back pain. Conference Abstract: ASP2016 - The 26th Annual Meeting of the Australasian Society for Psychophysiology, Adelaide Australia. doi: 10.3389/conf.fnhum.2016.221.00028 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 10 Oct 2016; Published Online: 05 Dec 2016. * Correspondence: Mr. Tribikram Thapa, Western Sydney University, School of Science and Health, Sydney, Australia, t.thapa@westernsydney.edu.au Dr. Lucinda Chipchase, Western Sydney University, School of Science and Health, Sydney, Australia, l.chipchase@westernsydney.edu.au Dr. Thomas Graven-Nielsen, Aalborg University, Health Science and Technology, Aalborg,, Denmark, tgn@hst.aau.dk Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Tribikram Thapa Lucinda Chipchase Thomas Graven-Nielsen Siobhan Schabrun Google Tribikram Thapa Lucinda Chipchase Thomas Graven-Nielsen Siobhan Schabrun Google Scholar Tribikram Thapa Lucinda Chipchase Thomas Graven-Nielsen Siobhan Schabrun PubMed Tribikram Thapa Lucinda Chipchase Thomas Graven-Nielsen Siobhan Schabrun Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

High-Resolution 7T MR Imaging of the Motor Cortex in Amyotrophic Lateral Sclerosis.

Amyotrophic lateral sclerosis is a progressive motor neuron disorder that involves degeneration of both upper and lower motor neurons. In patients with amyotrophic lateral sclerosis, pathologic studies and ex vivo high-resolution MR imaging at ultra-high field strength revealed the co-localization of iron and activated microglia distributed in the deep layers of the primary motor cortex. The aims of the study were to measure the cortical thickness and evaluate the distribution of iron-related signal changes in the primary motor cortex of patients with amyotrophic lateral sclerosis as possible in vivo biomarkers of upper motor neuron impairment. Twenty-two patients with definite amyotrophic lateral sclerosis and 14 healthy subjects underwent a high-resolution 2D multiecho gradient-recalled sequence targeted on the primary motor cortex by using a 7T scanner. Image analysis consisted of the visual evaluation and quantitative measurement of signal intensity and cortical thickness of the primary motor cortex in patients and controls. Qualitative and quantitative MR imaging parameters were correlated with electrophysiologic and laboratory data and with clinical scores. Ultra-high field MR imaging revealed atrophy and signal hypointensity in the deep layers of the primary motor cortex of patients with amyotrophic lateral sclerosis with a diagnostic accuracy of 71%. Signal hypointensity of the deep layers of the primary motor cortex correlated with upper motor neuron impairment (r = -0.47; P < .001) and with disease progression rate (r = -0.60; P = .009). The combined high spatial resolution and sensitivity to paramagnetic substances of 7T MR imaging demonstrate in vivo signal changes of the cerebral motor cortex that resemble the distribution of activated microglia within the cortex of patients with amyotrophic lateral sclerosis. Cortical thinning and signal hypointensity of the deep layers of the primary motor cortex could constitute a marker of upper motor neuron impairment in patients with amyotrophic lateral sclerosis.

Normalization of sensorimotor integration by repetitive transcranial magnetic stimulation in cervical dystonia.

Previous studies indicated that sensorimotor integration and plasticity of the sensorimotor system are impaired in dystonia patients. We investigated motor evoked potential amplitudes and short latency afferent inhibition to examine corticospinal excitability and cortical sensorimotor integration, before and after inhibitory 1Hz repetitive transcranial magnetic stimulation over primary sensory and primary motor cortex in patients with cervical dystonia (n=12). Motor evoked potentials were recorded from the right first dorsal interosseous muscle after application of unconditioned transcranial magnetic test stimuli and after previous conditioning electrical stimulation of the right index finger at short interstimulus intervals of 25, 30 and 40ms. Results were compared to a group of healthy age-matched controls. At baseline, motor evoked potential amplitudes did not differ between groups. Short latency afferent inhibition was reduced in cervical dystonia patients compared to healthy controls. Inhibitory 1Hz sensory cortex repetitive transcranial magnetic stimulation but not motor cortex repetitive transcranial magnetic stimulation increased motor evoked potential amplitudes in cervical dystonia patients. Additionally, both 1Hz repetitive transcranial magnetic stimulation over primary sensory and primary motor cortex normalized short latency afferent inhibition in these patients. In healthy subjects, sensory repetitive transcranial magnetic stimulation had no influence on motor evoked potential amplitudes and short latency afferent inhibition. Plasticity of sensorimotor circuits is altered in cervical dystonia patients.

Effects of High-Frequency Repetitive Transcranial Magnetic Stimulation on Motor Functions in Patients with Subcortical Stroke

Article type: Original Article Background: Motor function impairment occurs in approximately two-thirds of patients with subcortical stroke. Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive technique for modulating cortical excitability. Objectives: The present study was designed for assessing the efficacy of highfrequency rTMS (5 Hz) on ipsilesional primary motor cortex in patients with subcortical stroke. Materials and Methods: Thirty participants who had subcortical stroke in the previous four weeks to four months were enrolled in this randomized double blinded clinical trial. Participants were divided into experimental and control groups and their motor ability of both upper and lower extremities were assessed using Fugl-Meyer assessment of motor recovery after stroke (FMA) before and after intervention. The study intervention rTMS (5 Hz) was administered in six 10-minute sessions on the ipsilesional primary motor cortex in the experimental group and on the vertex in the control group. Results: Mean change in FMA score after rTMS sessions was significantly higher in the experimental group than in the control group (p = 0.00). Mean time interval between the stroke and rTMS intervention had a weak and insignificant (ρ = 0.097; p = 0.61) correlation with changes of FMA score. Conclusions: High-frequency (5 Hz) rTMS effectively improved motor function in patients with subcortical stroke.

Histological-MRI correlation in the primary motor cortex of patients with amyotrophic lateral sclerosis.

To establish the relationship between ALS histopathology and quantitative MRI metrics. ALS patients (N = 8) in advanced stages of the disease were enrolled and, immediately after death, the brain of each patient was removed. Freshly excised ALS tissue was imaged at 3.0 Tesla with T1 and T2 mapping protocols and subsequently stained with astrocyte, myelin, and neuronal markers. Measures of ALS histological stains were compared with the internal control (primary visual cortex) and longitudinal parametric maps. Post-mortem T1 -weighted images demonstrate diminished contrast between gray and white matter and alterations in T1 relaxation within the primary motor cortex. An increase in astrocyte number and reactivity as well as evident neuronal loss, a decrease in axonal density, and unraveling of the myelin sheaths in subcortical white matter were found in the ALS primary motor cortex exhibiting significant T1 relaxation and contrast changes. This study provides a histopathological basis for differences in MR T1 contrast and relaxation seen in the ALS brain.