Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label motor cortex. Show all posts
Showing posts with label motor cortex. Show all posts

Monday, January 8, 2024

Metabolic profile of motor cortex in stroke

 Profiling the cortex is useless, NOTHING HERE gets survivors recovered! You're fired! The idea is to solve stroke recovery, not just describe some aspect of it.

Metabolic profile of motor cortex in stroke

Motor and Premotor Cortices in Subcortical Stroke : Proton Magnetic Resonance Spectroscopy
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American Society of Neurorehabilitation
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Neurorehabilitation and Neural Repair
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What is This? - Jan 8, 2013OnlineFirst Version of Record - Jan 9, 2013OnlineFirst Version of Record >>
at UNIV OF KANSAS MEDICAL CENTER on January 16, 2013nnr.sagepub.comDownloaded from
 
Neurorehabilitation and Neural RepairXX(X) 1  –10© The Author(s) 2013Reprints and permission: http://www. sagepub.com/journalsPermissions.navDOI: 10.1177/1545968312469835http://nnr.sagepub.com
Introduction
Human imaging studies have revealed that early after subcortical stroke, restoration of paretic arm function is associated with a greater involvement of radiologically normal-appearing (or spared) motor (primary motor cortex or M1) and premotor (dorsal premotor cortex or PMd, supplementary motor area or SMA) areas in both injured (ipsilesional) and uninjured (contralesional) hemispheres.
1-3
 Later, successful recovery occurs in stroke survivors who exhibit relatively normal patterns of ipsilesional activation and less contralesional motor activation, whereas patients, who often show bilateral cortical activation, typically have less complete recovery.
4-6
 These results should be viewed in the context of the anatomic structures and pathways of these areas. Although M1 motor pathways are critical, the  premotor areas also contribute to motor control and might  be recruited during motor recovery after stroke. The  parallel nature of the direct (corticospinal) pathways from  premotor areas and M1 emphasizes that PMd and SMA are, in some respects, at a similar level of hierarchical
XXX10.1177/1545968312469835Neuroreailitation an Neural Repair XX(X)Craciunaset al2013© TheAuthor(s) 2010Reprintsand permission: http://www.sagepub.com/journalsPermissions.nav
1 University of Kansas Medical Center, Kansas City, KS, USA
Corresponding Author:
Carmen M. Cirstea, MD, PhD Hoglund Brain Imaging Center, University of Kansas Medical Center, 3901 Rainbow Boulevard, Mail Stop 1052, Kansas City, KS 66160, USA Email: ccirstea@kumc.edu
Motor and Premotor Cortices in Subcortical Stroke: Proton Magnetic Resonance Spectroscopy Measures and Arm Motor Impairment
Sorin C. Craciunas, MD, PhD 1, William M. Brooks, PhD 1, Randolph J. Nudo, PhD 1, Elena A. Popescu, PhD 1, In-Young Choi, PhD 1, Phil Lee, PhD 1, Hung-Wen Yeh, PhD 1, Cary R. Savage, PhD 1, and Carmen M. Cirstea, MD, PhD 1

Abstract

Background
. Although functional imaging and neurophysiological approaches reveal alterations in motor and premotor areas after stroke, insights into neurobiological events underlying these alterations are limited in human studies.
Objective
. We tested whether cerebral metabolites related to neuronal and glial compartments are altered in the hand representation in bilateral motor and premotor areas and correlated with distal and proximal arm motor impairment in hemiparetic persons.
 Methods
. In 20 participants at >6 months postonset of a subcortical ischemic stroke and 16 age- and sex-matched healthy controls, the concentrations of N-acetylaspartate and myo-inositol were quantified by proton magnetic resonance spectroscopy. Regions of interest identified by functional magnetic resonance imaging included primary (M1), dorsal premotor (PMd), and supplementary (SMA) motor areas. Relationships between metabolite concentrations and distal (hand) and proximal (shoulder/elbow) motor impairment using Fugl-Meyer Upper Extremity (FMUE) subscores were explored.
 
Results. 
N-Acetylaspartate was lower in M1 (P = .04) and SMA (P = .004) and myo-inositol was higher in M1 (P = .003) and PMd (P = .03) in the injured (ipsilesional) hemisphere after stroke compared with the left hemisphere in controls.
N-Acetylaspartate in ipsilesional M1 was positively correlated with hand FMUE subscores (P = .04). Significant positive correlations were also found between N-acetylaspartate in ipsilesional M1, PMd, and SMA and in contralesional M1 and shoulder/elbow FMUE subscores (P = .02, .01,.02, and.02,respectively).
Conclusions
. Our preliminary results demonstrated that proton magnetic resonance spectroscopy is a sensitive method to quantify relevant neuronal changes in spared motor cortex after stroke and consequently increase our knowledge of the factors leading from these changes to arm motor impairment.
Keywords
subcortical stroke, motor and premotor cortices, proton magnetic resonance spectroscopy, distal and proximal arm motor impairment
 at UNIV OF KANSAS MEDICAL CENTER on January 16, 2013nnr.sagepub.comDownloaded from

Friday, October 13, 2023

Metabolic profile of motor cortex in stroke

I see nothing here that helps survivors recover.  Useless.

Metabolic profile of motor cortex in stroke

Abstract

Background
 
Although functional imaging and neurophysiological approaches reveal alterations in motor and premotor areas after stroke, insights into neurobiological events underlying these alterations are limited in human studies.  
 
Objective
 
We tested whether cerebral metabolites related to neuronal and glial compartments are altered in the hand representation in bilateral motor and premotor areas and correlated with distal and proximal arm motor impairment in hemiparetic persons. 
 
Methods. 
 
In 20 participants at >6 months postonset of a subcortical ischemic stroke and 16 age- and sex-matched healthy controls, the concentrations of N-acetylaspartate and myo-inositol were quantified by proton magnetic resonance spectroscopy. Regions of interest identified by functional magnetic resonance imaging included primary (M1), dorsal premotor (PMd), and supplementary (SMA) motor areas. Relationships between metabolite concentrations and distal (hand) and proximal (shoulder/elbow) motor impairment using Fugl-Meyer Upper Extremity (FMUE) subscores were explored.  
 
Results
 
N-Acetylaspartate was lower in M1 (P = .04) and SMA (P = .004) and myo-inositol was higher in M1 (P = .003) and PMd (P = .03) in the injured (ipsilesional) hemisphere after stroke compared with the left hemisphere in controls. N-Acetylaspartate in ipsilesional M1 was positively correlated with hand FMUE subscores (P = .04). Significant positive correlations were also found between N-acetylaspartate in ipsilesional M1, PMd, and SMA and in contralesional M1 and shoulder/elbow FMUE subscores (P = .02, .01, .02, and .02, respectively).  
 
Conclusions
Our preliminary results demonstrated that proton magnetic resonance spectroscopy is a sensitive method to quantify relevant neuronal changes in spared motor cortex after stroke and consequently increase our knowledge of the factors leading from these changes to arm motor impairment.
 
More at link.

Sunday, December 19, 2021

Clinically Significant Gains in Skillful Grasp Coordination by an Individual With Tetraplegia Using an Implanted Brain-Computer Interface With Forearm Transcutaneous Muscle Stimulation

But I would need to know where they are reading the brain signals from. From the forearm it seems, so not applicable to most stroke survivors unless they get the signals directly from the brain. Motor cortex? Pre-motor cortex? Executive control? Both my motor cortex and premotor cortex are heavily dead or damaged. Of course my doctor didn't tell me that, I got that from a research MRI scan.  But I bet with enough training I could use my good motor cortex to send those signals.

Clinically Significant Gains in Skillful Grasp Coordination by an Individual With Tetraplegia Using an Implanted Brain-Computer Interface With Forearm Transcutaneous Muscle Stimulation

Presented to the American Congress of Rehabilitation Medicine (November 2016; Chicago, IL); American Academy of Physical Medicine and Rehabilitation (October 2016, New Orleans, LA); Association of Academic Physiatrists (February 2018; Atlanta, GA; Society for Neuroscience (November 2017; Washington, DC); and Institute of Electrical and Electronics Engineers Engineering in Medicine and Biology (June 2018; Honolulu, HI).
https://doi.org/10.1016/j.apmr.2018.07.445Get rights and content
Under a Creative Commons license
open access

Highlights

A man with paralysis regained hand grasp through BCI-controlled arm muscle stimulation.

The device enabled the patient to twist and pour using lateral, palmar, and tip-to-tip grips.

Grips for training objects carried over successfully to novel objects and tasks.

The patient’s functional motor level improved when using the BCI from C5-6 to C7-T1.

Translation to home use could decrease dependence for activities of daily living.

Abstract

Objective

To demonstrate naturalistic motor control speed, coordinated grasp, and carryover from trained to novel objects by an individual with tetraplegia using a brain-computer interface (BCI)-controlled neuroprosthetic.

Design

Phase I trial for an intracortical BCI integrated with forearm functional electrical stimulation (FES). Data reported span postimplant days 137 to 1478.

Setting

Tertiary care outpatient rehabilitation center.

Participant

A 27-year-old man with C5 class A (on the American Spinal Injury Association Impairment Scale) traumatic spinal cord injury

Interventions

After array implantation in his left (dominant) motor cortex, the participant trained with BCI-FES to control dynamic, coordinated forearm, wrist, and hand movements.

Main Outcome Measures

Performance on standardized tests of arm motor ability (Graded Redefined Assessment of Strength, Sensibility, and Prehension [GRASSP], Action Research Arm Test [ARAT], Grasp and Release Test [GRT], Box and Block Test), grip myometry, and functional activity measures (Capabilities of Upper Extremity Test [CUE-T], Quadriplegia Index of Function-Short Form [QIF-SF], Spinal Cord Independence Measure–Self-Report [SCIM-SR]) with and without the BCI-FES.

Results

With BCI-FES, scores improved from baseline on the following: Grip force (2.9 kg); ARAT cup, cylinders, ball, bar, and blocks; GRT can, fork, peg, weight, and tape; GRASSP strength and prehension (unscrewing lids, pouring from a bottle, transferring pegs); and CUE-T wrist and hand skills. QIF-SF and SCIM-SR eating, grooming, and toileting activities were expected to improve with home use of BCI-FES. Pincer grips and mobility were unaffected. BCI-FES grip skills enabled the participant to play an adapted “Battleship” game and manipulate household objects.

Conclusions

Using BCI-FES, the participant performed skillful and coordinated grasps and made clinically significant gains in tests of upper limb function. Practice generalized from training objects to household items and leisure activities. Motor ability improved for palmar, lateral, and tip-to-tip grips. The expects eventual home use to confer greater independence for activities of daily living, consistent with observed neurologic level gains from C5-6 to C7-T1. This marks a critical translational step toward clinical viability for BCI neuroprosthetics.

Keywords

Activities of daily living
Brain-computer interfaces
Hand strength
Quadriplegia
Rehabilitation
Transcutaneous electric nerve stimulation

List of abbreviations

ARAT
Action Research Arm Test
BBT
Box and Block Test
BCI
brain-computer interface
CUE-T
Capabilities of Upper Extremity Test
FES
functional electrical stimulation
GAIN
Generalizability, Ability, Independence, Neurologic Level
GRASSP
Graded Redefined Assessment of Strength, Sensibility, and Prehension
GRT
Grasp and Release Test
MEA
microelectrode array
MMT
manual muscle training
QIF-SF
Quadriplegia Index of Function-Short Form
SCI
spinal cord injury
SCIM-SR
Spinal Cord Independence Measure–Self-Report
SRD
smallest real difference

Individuals with tetraplegia prioritize recovery of upper limb strength and dexterity to facilitate their independence.1, 2, 3, 4, 5 Voluntary control of hand grasp has been restored to paralyzed limbs using noninvasive6, 7, 8, 9, 10, 11 and cortical microelectrode array (MEA)-based12, 13, 14, 15, 16 brain-computer interfaces (BCIs) that translate brain activity to hand movements evoked through implanted10, 11, 12 or transcutaneous6, 7, 8, 9, 13, 14, 15, 16 functional electrical stimulation (FES).6, 7, 8, 9, 12, 13 However, clinically significant gains on tests of upper limb function have not been demonstrated using BCI-FES. The critical translational path for BCI neuroprosthetics requires demonstration of clinically meaningful gains in speed, dexterity, and smooth integration of grip with other arm movements to perform complex tasks.

Our goal was to evaluate whether an individual with tetraplegia could make clinically significant gains in skillful grasp coordination17, 18 using an investigational MEA-BCI-FES. We formulated a framework19 called Generalizability, Ability, Independence, Neurologic Level (GAIN) that reflects design goals for BCI neuroprosthetics to assist in this assessment. GAIN was inspired by end-user perspectives,4, 20, 21 challenges to translation,22, 23 and clinical evaluations developed for surgical interventions for tetraplegia.24 We anticipate it being useful for comparing performance across neuroprosthetic technologies and justifying (eg, to regulatory or payer sources) that a device measurably improves function on the International Classification of Functioning, Disability, and Health domains recognized by the World Health Organization.25

Devices meeting the GAIN standard include the following: (1) demonstrate generalizability, defined as performing well without retraining for objects with similar grip features (e.g., lateral, tip-to-tip, palmar, pincer grasps); (2) confer clinically significant gains in motor ability on standardized, psychometrically validated, and expert-endorsed24, 26, 27, 28, 29, 30, 31, 32, 33 tests of upper limb function; (3) affect daily life by facilitating functional independence for activities of daily living (ADLs) on psychometrically validated assessments24, 26, 27, 28, 29, 30, 31, 32, 33; and (4) improve the user’s neurologic level of function on validated measures normed to the International Standards for the Neurological Classification of Spinal Cord Injury standards.34

Methods

This was a Phase I trial of a MEA-BCI interfaced with the Neurolifea transcutaneous, forearm FES. Like similar intracortical BCI studies,12, 13, 14, 15, 16, 17, 18, 35, 36 this report was limited to 1 participant, the first to use the system, due to the invasive nature of the investigational brain implant and time required for training and assessment. Technical BCI-FES features13, 37 (fig 1), the Utah Arrayb MEA implantation procedures, and machine learning algorithms used to generate decoders were described previously. The participant provided written informed consent as approved by our local institutional review board.

More at link.
 

Wednesday, February 26, 2020

Brain stimulation device could improve motor function after stroke

But did they recover function? Brain activity is not a valid measurement for stroke rehab.  'Could' is not enough, does improve is the only acceptable answer, go back to the drawing board and do your research right to get stroke protocols out of it.  Without an objective damage diagnosis you have no clue whom this might work on.  Eg. me, with a massive dead area in the motor cortex and premotor cortex.  If only stroke survivors were in charge we wouldn't waste all this stroke research.

Brain stimulation device could improve motor function after stroke

y



A non-invasive magnetic stimulation headset could improve motor function in stroke patients, a new study has found.
In a clinical trial of 30 patients who had survived chronic ischemic strokes, the transcranial rotating permanent magnet stimulator (TRPMS) produced significant increases in physiological brain activity in areas near the stroke site. Brain activity was measured using functional magnetic resonance imaging (fMRI).
Houston Methodist Hospital Eddy Scurlock Stroke Center director Dr David Chiu said: “The robustness of the increase in physiological brain activity was surprising. With only 30 subjects, a statistically significant change was seen in brain activity.”
The participants in the study were all stroke survivors who experienced weakness on one side of their body at least three months post-stroke.(So absolutely no objective damage diagnosis. What the hell were you thinking?)
Half of them were treated with brain stimulation, administered in 20 40-minute sessions over four weeks. The rest received a sham treatment.
Researchers analysed brain activity before, immediately after and one month after the therapy was administered and found that active treatment produced nine times greater increases in brain activity than the sham treatment.
Alongside this, the patients who underwent the TRPMS treatment demonstrated numerical improvements in five of six clinical scales of motor function. The scales measured gait velocity, grip strength, pinch strength and other motor functions of the arm.

Tuesday, July 30, 2019

Consensus: Motor cortex plasticity protocols

Your doctor can read the 18 pages and apply this to your recovery.  I, however could find no objective starting point for using this. 

Consensus: Motor cortex plasticity protocols

 

Tuesday, September 12, 2017

Innovative brain implant helps paralyzed people to text

Well, not much help as currently designed for those like me who have a mostly dead motor cortex. 
 http://www.digitaljournal.com/tech-and-science/science/innovative-brain-implant-helps-paralyzed-people-to-text/article/501515#ixzz4sRDfaULN
Neurosurgeons, teaming up with engineers, have created a device that allows paralyzed patients to communicate their thoughts into speech. The brain controlled device has come out of a research center at Stanford University.

Although the device is still at the experimental stage, the success reported for three patients means that the research towards a commercial product is moving closer to realization. The development of the device was led by Jaimie Henderson and Krishna Shenoy and it takes the form of a brain-computer interface. Most brain-computer interface research has focused on neuroprosthetics applications that aim at restoring damaged hearing, sight and movement. The device has been tested out in a clinical trial. The device itself is small, resembling the size of a tablet, and it has taken some fifteen years of research. The device, once implanted into the brain of a person, functions to record signals from the motor cortex. The motor cortex is the region of the cerebral cortex involved in the planning, control, and execution of voluntary movements. This region is the main contributor to generating neural impulses that pass down to the spinal cord and control the execution of movement. Once recorded by the implant, the signals are transported to a computer. The signals are interpreted by algorithms and used to move a cursor to characters on a keyboard. The final result is the production of text: in other words, the paralyzed patient can compose a text messages based on their thoughts. The text message can then either be displayed on a screen, or ‘sent’ like any other conventional message. The following video explains more about the tehcnology: In an interview with Stanford, one of the researchers, Dr. Krishna Shenoy explains his motivation with the project: “My mother’s father suffered from multiple sclerosis for around 40 years. He was wheelchair-bound. It was not like I ever had a conscious epiphany, ‘I want to help him,’ but I think it subconsciously influenced me greatly. With the trials, QMed reports, each patient was able to master the technique relatively quickly with messages composed fairly rapidly and the messages were intelligible by the recipients. Long-term it is hoped that the device will be able to control both tablets and smartphones. Further development is required before the implant can be made available to the medical sector. Once it is ready it should change how paralysis and nervous system disorders are cared for. The research is described in the journal eLife under the heading “High performance communication by people with paralysis using an intracortical brain-computer interface.”

Friday, July 21, 2017

Behaviorally Selective Engagement of Short-Latency Effector Pathways by Motor Cortex

What about humans?  If the motor cortex is not needed for walking in mice then why is my walking still screwed up?  Of course my pre-motor cortex is mostly dead also, no idea how much white matter damage there is underlying those cortex areas. Because I never got any objective damage diagnosis I have no idea what needs fixing.
http://www.cell.com/neuron/fulltext/S0896-6273(17)30594-9
Publication stage: In Press Corrected Proof

Highlights

  • In mice, motor cortex is required for a trained forelimb task, but not walking
  • Motor cortex activates short-latency effector pathways only during the trained task
  • Distinct weighted sums of motor cortical firing patterns vary strongly in each task
  • This change could permit motor cortex to engage short-latency pathways differentially

Summary

Blocking motor cortical output with lesions or pharmacological inactivation has identified movements that require motor cortex. Yet, when and how motor cortex influences muscle activity during movement execution remains unresolved. We addressed this ambiguity using measurement and perturbation of motor cortical activity together with electromyography in mice during two forelimb movements that differ in their requirement for cortical involvement. Rapid optogenetic silencing and electrical stimulation indicated that short-latency pathways linking motor cortex with spinal motor neurons are selectively activated during one behavior. Analysis of motor cortical activity revealed a dramatic change between behaviors in the coordination of firing patterns across neurons that could account for this differential influence. Thus, our results suggest that changes in motor cortical output patterns enable a behaviorally selective engagement of short-latency effector pathways. The model of motor cortical influence implied by our findings helps reconcile previous observations on the function of motor cortex.

Wednesday, December 14, 2016

Robotic Arm Can Be Controlled With The Mind

Probably not that useful for stroke survivors. At least if you have some dead area in that motor cortex. My motor cortex is about half dead, this wouldn't work at all for me, unless you allow the good side to control it.
http://www.rdmag.com/article/2016/12/robotic-arm-can-be-controlled-mind?

For the first time ever researchers at the University of Minnesota developed a robotic arm that can be controlled through the mind.
Bin He, a University of Minnesota biomedical engineering professor and lead researcher on the study, explained this is a breakthrough that could help millions of people who are paralyzed or have neurodegenerative diseases.
“This is the first time in the world that people can operate a robotic arm to reach and grasp objects in a complex 3D environment using only their thoughts without a brain implant,” he said in a statement. “Just by imagining moving their arms, they were able to move the robotic arm.”
The arm is controlled using a noninvasive technique called electroencephalography (EEG), which is based on brain-computer interfaces. It records weak electrical activity of the subjects’ brain through a specialized, high-tech EEG cap fitted with 64 electrodes and converts the “thoughts” into action by advanced signal processing and machine learning.
The researchers tested the invention on eight healthy human subjects.
The participants gradually learned to imagine moving their own arm without actually moving them to control a robotic appendage in 3D space.
The subjects improved from initially being able to control a virtual cursor on a computer screen to being able to control a robotic arm to reach and grasp objects in fixed locations on a table to a three-layer shelf by only thinking about the movements.
Average success rates for the eight subjects in controlling the robotic arm and picking up objects in fixed locations was above 80 percent and the success rate in moving objects from the table onto the shelf was above 70 percent.
“This is exciting as all subjects accomplished the tasks using a completely non-invasive technique,” He said. “We see a big potential for this research to help people who are paralyzed or have neurodegenerative diseases to become more independent without a need for surgical implants.”
The brain-computer interface is able to work due to the geography of the motor cortex—the area of the cerebrum that governs movement.
Neurons in the motor cortex produce tiny electric currents when humans move or think about a movement. When a human thinks about a different movement it activates a new assortment of neurons, a phenomenon confirmed by cross-validation using functional MRI in He’s previous study.
According to He, sorting out these assortments using advanced signal processing laid the groundwork for the brain-computer interface used by University of Minnesota.
The robotic arm is seen as an advancement of his previous research.
“Three years ago, we weren’t sure moving a more complex robotic arm to grasp and move objects using this brain-computer interface technology could even be achieved,” He said. “We’re happily surprised that it worked with a high success rate and in a group of people.”
He said the next step would be to further develop the brain-computer interface technology realizing a brain-controlled robotic prosthetic limb attached to a person’s body or examine how the technology could work with someone who has had a stroke or is paralyzed.
In addition to He, who also serves as director of the University of Minnesota Institute for Engineering in Medicine, the research team includes biomedical engineering postdoctoral researcher Jianjun Meng (first author); biomedical engineering graduate student Bryan Baxter; Institute for Engineering in Medicine staff member Angeliki Bekyo; and biomedical engineering undergraduate students Shuying Zhang and Jaron Olsoe. The researchers are affiliated with the University of Minnesota College of Science and Engineering and the Medical School.
The study was published in Scientific Reports.

Tuesday, May 31, 2016

Neural Substrates of Motor Recovery in Severely Impaired Stroke Patients With Hand Paralysis

Do these fucking idiots not even comprehend that there has to be different interventions for dead brain vs. damaged brain. They talk but never tell us anything useful. They excluded primary motor cortex damage, cherry picking at its' worst.
http://nnr.sagepub.com/content/30/4/328.full

  1. Michelle L. Harris-Love, PhD1,2
  2. Evan Chan, MS2
  3. Alexander W. Dromerick, MD1,2,3
  4. Leonardo G. Cohen, MD4
  1. 1Georgetown University Medical Center, Washington, DC, USA
  2. 2MedStar National Rehabilitation Hospital, Washington, DC, USA
  3. 3District of Columbia VA Medical Center, Washington, DC, USA
  4. 4Human Cortical Physiology and Neurorehabilitation Section, NINDS, NIH, Bethesda, MD, USA
  1. Michelle L. Harris-Love, PhD, 102 Irving Street NW, Room 1058, Washington, DC 20010, USA. Email: Mh672@georgetown.edu

Abstract

In well-recovered stroke patients with preserved hand movement, motor dysfunction relates to interhemispheric and intracortical inhibition in affected hand muscles. In less fully recovered patients unable to move their hand, the neural substrates of recovered arm movements, crucial for performance of daily living tasks, are not well understood. Here, we evaluated interhemispheric and intracortical inhibition in paretic arm muscles of patients with no recovery of hand movement (n = 16, upper extremity Fugl-Meyer Assessment = 27.0 ± 8.6). We recorded silent periods (contralateral and ipsilateral) induced by transcranial magnetic stimulation during voluntary isometric contraction of the paretic biceps and triceps brachii muscles (correlates of intracortical and interhemispheric inhibition, respectively) and investigated links between the silent periods and motor recovery, an issue that has not been previously explored. We report that interhemispheric inhibition, stronger in the paretic triceps than biceps brachii muscles, significantly correlated with the magnitude of residual impairment (lower Fugl-Meyer scores). In contrast, intracortical inhibition in the paretic biceps brachii, but not in the triceps, correlated positively with motor recovery (Fugl-Meyer scores) and negatively with spasticity (lower Modified Ashworth scores). Our results suggest that interhemispheric inhibition and intracortical inhibition of paretic upper arm muscles relate to motor recovery in different ways. While interhemispheric inhibition may contribute to poorer recovery, muscle-specific intracortical inhibition may relate to successful motor recovery and lesser spasticity.


Introduction


Over the past nearly 2 decades, there has been a great deal of investigation into mechanisms of impairment and recovery of hand movement after human stroke.(But no protocols) This work has demonstrated that limitations in recovery of functional hand movements poststroke are often linked to abnormalities in intracortical and interhemispheric inhibition. These findings have provided insight into the mechanisms of behavioral rehabilitation approaches, such as constraint-induced movement therapy,1-5 and have informed the development of cortical stimulation paradigms to improve hand recovery.6-9

Previous studies have used transcranial magnetic stimulation (TMS) to investigate intracortical inhibition of primary motor cortex (M1) hand representations in well-recovered stroke patients with at least partial recovery of hand function. Paired-pulse measurements of short-interval intracortical inhibition (SICI),10 associated with GABAA-mediated intracortical inhibition,11 have shown abnormally decreased levels of intracortical inhibition targeting the paretic hand.1,2,12-15 In contrast, intracortical inhibition reflected by the contralateral silent period (cSP), associated with GABAB receptor–mediated inhibition,11 is reported to be abnormally increased in the paretic hand1,15-19 and to decrease with recovery.16 Thus, it appears that SICI, reflecting GABAA-mediated intracortical inhibition, is abnormally decreased while cSP, reflecting GABAB receptor–mediated inhibition, is abnormally increased in the paretic hand post-stroke.

In addition to intracortical inhibition, interhemispheric inhibition between M1 hand representations in stroke patients with hand recovery has also been widely studied, and like intracortical inhibition, it has been studied using both paired-pulse and silent period TMS techniques. Paired-pulse measurements have shown that interhemispheric inhibition targeting the affected hemisphere (ie, paretic hand) is stronger than that targeting the unaffected hemisphere20-22 and abnormally persistent during paretic finger movement preparation,23,24 particularly in those with poorer hand recovery. Ipsilateral silent period measurements have provided further support for the notion that interhemispheric inhibition targeting the paretic hand is stronger than that targeting the nonparetic hand15,25 and that measured in controls.26

Mechanisms of upper arm motor recovery in stroke patients unable to use their hands, however, are not well understood. To examine interhemispheric and intracortical inhibition in paretic elbow flexors and extensors, we evaluated silent periods during voluntary isometric contractions of paretic arm biceps (flexor) or triceps (extensor) brachii and measured the correlation between these measures and clinical and behavioral tests of motor ability, reaching performance, and spasticity. Recognizing that specific electrophysiological measurements, such as silent periods, reflect only a portion of the larger processes of intracortical and interhemispheric inhibition, we emphasize that when we refer to intracortical and interhemispheric inhibition we are referring only to that reflected by the contralateral and ipsilateral silent periods, respectively.

Given that many patients have particular difficulty deactivating elbow flexors, we postulated that inhibition targeting an elbow flexor muscle (biceps brachii) would be less than that targeting an elbow extensor (triceps brachii) and that biceps inhibition would correlate negatively with motor impairment. We report that interhemispheric inhibition and intracortical inhibition of these paretic upper arm muscles relate to paretic arm motor recovery differently in this population. 

More at link.