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 joint control. Show all posts
Showing posts with label joint control. Show all posts

Sunday, August 24, 2025

Durable, Breathable, and Sweat-Resistant Nanocrack-Based Fiber Strain Sensors for Joint Monitoring in Elderly Stroke Rehabilitation

I can really see no use for this, monitoring stroke rehab DOES NOTHING FOR RECOVERY! 

Unless this monitoring leads to EXACT PROTOCOLS to recover from the deficits in your joint movements, I can't see much use for this.

Durable, Breathable, and Sweat-Resistant Nanocrack-Based Fiber Strain Sensors for Joint Monitoring in Elderly Stroke Rehabilitation

 Joint Monitoring in Elderly Stroke Rehabilitation

  • Xinxin Zhang
  • Dongxing Lu
  • Huihui Xu
  • Zhengtong Song
  • Xiuming Cao
  • Yanhong Cao
  • Yong Xu
  • Qufu Wei
  • Qingqing Wang*
Other Access OptionsSupporting Information (3)

Abstract

Abstract Image

Flexible fiber-based strain sensors show great promise for joint motion monitoring in stroke rehabilitation and elderly care. However, the rational design of low-cost sensors that simultaneously offer high sensitivity, excellent stability, and practical applicability is still a great challenge. In this study, multiwalled carbon nanotubes were incorporated into thermoplastic polyurethane to fabricate a coaxial fiber structure with crack effects via wet spinning. By adjusting the extrusion speed ratio between the core and sheath layers, the thickness of the fiber shell was optimized and a fine crack network was formed, enhancing both sensitivity and mechanical properties. Experimental results show that the fabricated fiber sensor exhibits a high sensitivity (strain range: 70–175%, gauge factor = 3.154), with a wide detection range (250% strain), an ultralow detection limit (<0.1%), and excellent cyclic durability (>2000 cycles). The sensor can be effectively applied to monitor human joint movements. Meanwhile, the nanocrack-based fiber sensor (NFS) exhibits excellent photothermal characteristics, strong resistance to sweat and washing, and good breathability (981.9 mm/s). Notably, the NFS enables real-time monitoring of physiological movements with Bluetooth data transmission. Furthermore, its localized photothermal effect can promote blood circulation, providing additional therapeutic value in stroke rehabilitation. These features highlight the great potential of NFS sensors in smart healthcare and wearable health technologies.

© 2025 American Chemical Society

Thursday, July 19, 2018

The Increase in Overlap of Cortical Activity Preceding Static Elbow/Shoulder Motor Tasks Is Associated With Limb Synergies in Severe Stroke

Fucking useless, no attempt to even try any intervention. Survivors don't care about descriptions of their problems, they want solutions. Have you never talked to a stroke survivor?
http://journals.sagepub.com/doi/abs/10.1177/1545968318781028
First Published June 11, 2018 Research Article



The loss of independent joint control, clinically referred to as limb synergies, is prevalent in the paretic upper limb of individuals with chronic hemiparetic stroke. To understand the underlying neural mechanisms, we previously reported that an increased overlap of cortical representations of shoulder/elbow could contribute to the abnormal poststroke synergies. However, these previous results were limited to a fixed time window just before the onset of motor tasks. Questions such as (1) how this overlap develops during motor preparation and (2) whether such development is also linked to upper limb synergies, remain unclear. To answer these questions, we investigated cortical overlap during motor preparation of isometric shoulder and elbow torque generation tasks in healthy individuals (n = 8), and individuals with moderate to severe chronic hemiparesis following a subcortical stroke (n = 12). We found a significant group difference in how the cortical overlap developed. In the healthy control and moderately impaired stroke groups, cortical overlap between shoulder and elbow motor tasks decreased during the motor preparation; however, this overlap increased in individuals with severe stroke. Furthermore, the rate of cortical overlap decrease/increase was linked to the upper limb Fugl-Meyer scores and limb synergies. These results demonstrate, for the first time, that the increase in overlap of the cortical activity during motor preparation is associated with the expression of synergies in the paretic upper limb of severely impaired poststroke individuals.

Thursday, June 28, 2018

Neuromodulatory Inputs to Motoneurons Contribute to the Loss of Independent Joint Control in Chronic Moderate to Severe Hemiparetic Stroke

So fucking what? You've described a problem but offered NO solution. 

Neuromodulatory Inputs to Motoneurons Contribute to the Loss of Independent Joint Control in Chronic Moderate to Severe Hemiparetic Stroke

  • 1Department of Physical Therapy and Human Movement Sciences, Northwestern University Feinberg School of Medicine, Chicago, IL, United States
  • 2Department of Biomedical Engineering, Florida International University, Miami, FL, United States
  • 3Department of Physiology, Northwestern University Feinberg School of Medicine, Chicago, IL, United States
  • 4Department of Physical Medicine and Rehabilitation, Northwestern University Feinberg School of Medicine, Chicago, IL, United States
  • 5Department of Biomedical Engineering, Northwestern University, Evanston, IL, United States
In chronic hemiparetic stroke, increased shoulder abductor activity causes involuntary increases in elbow, wrist, and finger flexor activation, an abnormal muscle coactivation pattern known as the flexion synergy. Recent evidence suggests that flexion synergy expression may reflect recruitment of contralesional cortico-reticulospinal motor pathways following damage to the ipsilesional corticospinal tract. However, because reticulospinal motor pathways produce relatively weak post-synaptic potentials in motoneurons, it is unknown how preferential use of these pathways could lead to robust muscle activation. Here, we hypothesize that the descending neuromodulatory component of the ponto-medullary reticular formation, which uses the monoaminergic neurotransmitters norepinephrine and serotonin, serves as a gain control mechanism to facilitate motoneuron responses to reticulospinal motor commands. Thus, inhibition of the neuromodulatory component would reduce flexion synergy expression by disfacilitating spinal motoneurons. To test this hypothesis, we conducted a pre-clinical study utilizing two targeted neuropharmacological probes and inert placebo in a cohort of 16 individuals with chronic hemiparetic stroke. Test compounds included Tizanidine (TIZ), a noradrenergic α2 agonist and imidazoline ligand selected for its ability to reduce descending noradrenergic drive, and Isradipine, a dihyropyridine calcium-channel antagonist selected for its ability to post-synaptically mitigate a portion of the excitatory effects of monoamines on motoneurons. We used a previously validated robotic measure to quantify flexion synergy expression. We found that Tizanidine significantly reduced expression of the flexion synergy. A predominantly spinal action for this effect is unlikely because Tizanidine is an agonist acting on a baseline of spinal noradrenergic drive that is likely to be pathologically enhanced post-stroke due to increased reliance on cortico-reticulospinal motor pathways. Although spinal actions of TIZ cannot be excluded, particularly from Group II pathways, our finding is consistent with a supraspinal action of Tizanidine to reduce descending noradrenergic drive and disfacilitate motoneurons. The effects of Isradipine were not different from placebo, likely related to poor central bioavailability. These results support the hypothesis that the descending monoaminergic component of the ponto-medullary reticular formation plays a key role in flexion synergy expression in chronic hemiparetic stroke. These results may provide the basis for new therapeutic strategies to complement physical rehabilitation.
More at link.