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.

Saturday, June 15, 2024

Mapping of spastic muscle activity after stroke: difference between passive stretch and active contraction

 Survivors would like spasticity cured, not just mapped! GET THERE!

Mapping of spastic muscle activity after stroke: difference between passive stretch and active contraction

Abstract

Background

Investigating the spatial distribution of muscle activity would facilitate understanding the underlying mechanism of spasticity. The purpose of this study is to investigate the characteristics of spastic muscles during passive stretch and active contraction by high-density surface electromyography (HD-sEMG).

Methods

Fourteen spastic hemiparetic subjects and ten healthy subjects were recruited. The biceps brachii (BB) muscle activity of each subject was recorded by HD-sEMG during passive stretch at four stretch velocities (10, 60, 120, 180˚/s) and active contraction at three submaximal contraction levels (20, 50, 80%MVC). The intensity and spatial distribution of the BB activity were compared by the means of two-way analysis of variance, independent sample t-test, and paired sample t-test.

Results

Compared with healthy subjects, spastic hemiparetic subjects showed significantly higher intensity with velocity-dependent heterogeneous activation during passive stretch and more lateral and proximal activation distribution during active contraction. In addition, spastic hemiparetic subjects displayed almost non-overlapping activation areas during passive stretch and active contraction. The activation distribution of passive stretch was more distal when compared with the active contraction.

Conclusions

These alterations of the BB activity could be the consequence of deficits in the descending central control after stroke. The complementary spatial distribution of spastic BB activity reflected their opposite motor units (MUs) recruitment patterns between passive stretch and active contraction. This HD-sEMG study provides new neurophysiological evidence for the spatial relationship of spastic BB activity between passive stretch and active contraction, advancing our knowledge on the mechanism of spasticity.

Trial registration

ChiCTR2000032245.

Background

Spasticity is one of the disabling upper motor neuron syndromes following central nervous system (CNS) lesions, which is characterized by a velocity-dependent increase in muscle tone resulting from hyperexcitability of stretch reflex [1]. Studies have shown that the incidence of spasticity is as high as 40% after stroke [2, 3]. It can severely affect the activity of daily living (ADL) and quality of life (QoL) of stroke survivors through various secondary complications [4, 5]. A clear understanding of spasticity may facilitate the development of its interventions, which is important in preventing the onset of spasticity or slowing or limiting its progression [6]. The hyperexcitability of the alpha motoneuron pool is thought to play a critical role in the mechanism of spasticity [7,8,9].

Spasticity is involuntary muscle activity due to diminished regulation of inhibitory reflex pathways [10, 11]. In fact, the loss of descending corticospinal pathways to spinal motoneurons after stroke not only affects reflex excitability but also voluntary movement [12, 13]. The relationship of abnormal muscle activity between spasticity and voluntary movement disorders in stroke survivors still remains unclear [14, 15]. However, the characteristics of spastic muscles during voluntary movement have not been fully understood in the study of spasticity to date. Although different from traditional passive methods, it is essential to assess the response of spastic muscles during voluntary movement [16].

Despite the fact that clinical scales are widely used to evaluate spasticity, several studies have demonstrated their lack of validity and reliability in quantifying the involuntary muscle activity [17, 18]. To address this challenge, the surface electromyography (sEMG) technique was used to assess the reflex muscle response to passive stretch [19,20,21]. However, the conventional sEMG technique limits the sufficient and accurate recording of neuromuscular function [22, 23]. Not restricted to the number of electrodes, the high-density sEMG (HD-sEMG) technique has the potential to explore the spatial distribution of muscle activity through a closely spaced two-dimensional electrode grid, opening new possibilities for exploring the neuromuscular function [24, 25]. Recent studies based on HD-sEMG have demonstrated that muscle activity is spatially heterogeneous, which is associated with the non-uniform distribution and recruitment of motor units (MUs) within the muscle [26, 27]. Comprehensive knowledge of neuromuscular dysfunction associated with spasticity is necessary to further understand its underlying mechanism.

In this study, the HD-sEMG technique was applied to record the biceps brachii (BB) muscle activity of healthy subjects and spastic hemiparetic subjects during passive stretch and active contraction. We hypothesized that the spastic hemiparetic subjects would exhibit heterogeneous activation caused by an excessive response to muscle stretch. We further hypothesized there would be an association between the spatial heterogeneity of spastic BB activity during passive stretch and active contraction.

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