Useless, describes a problem but offers NO SOLUTION. So you are allowing 3 million survivors every year to suffer from spasticity with not even a suggestion of a cure. Good to know how helpful stroke research is for survivors. And researchers will never solve stroke until stroke survivors are in charge of stroke(hospitals, stroke associations, research).
Stretch reflex excitability in contralateral limbs of stroke survivors is higher than in matched controls
Abstract
Background
Spasticity, characterized by hyperreflexia, is a motor impairment that can arise(30% get spasticity
) following a hemispheric stroke. While the neural mechanisms underlying spasticity in chronic stroke survivors are unknown, one probable cause of hyperreflexia is increased motoneuron (MN) excitability. Potential sources of increased spinal MN excitability after a stroke include increased vestibulospinal (VS) and/or reticulospinal (RS) drive. Spasticity, as clinically assessed in stroke survivors, is highly lateralized, thus RS contributions to stroke-induced spasticity are more difficult to reconcile, as RS nuclei routinely project bilaterally to the spinal cord. Yet studies in stroke survivors suggest that there may also be changes in neuromodulation at the spinal level, indicative of RS tract influence. We hypothesize that after hemispheric stroke, alterations in the excitability of the RS nuclei affect both sides of the spinal cord, and thereby contribute to increased MN excitability on both paretic/spastic and contralateral sides of stroke survivors, as compared to neurologically intact subjects.Methods
We estimated stretch reflex thresholds of the biceps brachii (BB) muscle using a position-feedback controlled linear motor to progressively indent the BB distal tendon in both spastic and contralateral limbs of hemispheric stroke survivors and in age-matched intact subjects.Results
Our previously reported results show a significant difference between reflex thresholds of spastic and contralateral limbs of stroke survivors recorded from BB-medial (p < 0.005) and BB-lateral (p < 0.001). For this study, we report that there is also a significant difference between the reflex thresholds in the contralateral limb of stroke subjects and the dominant arm of intact subjects, again measured from both BB-medial (p < 0.05) and BB-lateral (p < 0.05).Conclusion
The reduction in stretch reflex thresholds in the contralateral limb of stroke survivors, based here on comparisons with thresholds of intact subjects, suggests an increased MN excitability on contralateral sides of stroke survivors as compared to intact subjects. This in turn supports our contention that RS tract activation, which has bilateral descending influences, is at least partially responsible for increased stretch reflex excitability, post-stroke, as both contralateral and affected sides show increased MN excitability as compared to intact subjects. Still, spasticity, presently diagnosed only on the affected side, with increased MN excitability on the affected side as compared to the contralateral side (our previous study), may be due to a different strongly lateralized pathway, such as the VS tract, which has not been directly tested here. Currently available clinical methods of spasticity assessment, such as the Modified Ashworth Scale, lack the resolution to quantify this phenomenon of a bilateral increase in MN excitability.Background
Spasticity
is a frequent consequence of hemispheric stroke, in which
contralesional muscles demonstrate exaggerated stretch reflex responses.
About one-third of stroke survivors develop this physical sign [1].
We now believe that spasticity is a manifestation of increased
motoneuron (MN) excitability, and that this increased excitability is
due primarily to a sustained depolarization of the membrane potential of
MNs innervating spastic muscles. This means that there is a reduction
in necessary muscle afferent driven synaptic input required to reach the
motoneuron excitation threshold [2].
Thus, a reduction in the stretch reflex threshold is a key finding in
examining the sources of increased motoneuron excitability. In addition
to reduced membrane potentials, suppression of presynaptic inhibitory
mechanisms has also been proposed as a cause of spasticity [3, 4].
To establish an association between MN excitability and spasticity, it is essential to address the role of the descending pathways in modulating the stretch reflex. It is well established that excitatory and inhibitory signals of supraspinal origin are responsible for the regulation of excitability of the stretch reflex pathway [3, 5, 6]. Evidence from invasive animal lesion studies indicates that among the major descending tracts i.e., corticospinal, reticulospinal (RS), vestibulospinal (VS), rubrospinal, and tectospinal, only RS and VS tracts, originating in the brainstem, are substantially involved in the regulation of spinal stretch reflex circuitry [3]. Similar findings have been reported in humans with no neurological disorder. Corticospinal and rubrospinal tracts have limited influence on stretch reflex excitability [3], and the tectospinal tract appears not to exist in humans [7]. Thus, potential sources of increased spinal MN excitability after a stroke include increased VS and/or RS drive, potentially due to disruption of cortico-bulbar inhibitory pathways projecting to these brainstem nuclei. While animal studies have provided evidence of brainstem participation in spasticity, analogous direct approaches in humans to assess brainstem activity have not been possible [8]. The role of the RS tract in the pathophysiology of spasticity in humans has been examined with the acoustic startle reflex (ASR) studies in stroke survivors. ASR is a brainstem-mediated reflex that has been utilized as a non-invasive tool to examine the RS activity in humans [9,10,11]. In these studies, an exaggerated ASR response has been observed in spastic muscles of chronic stroke survivors as compared to the contralateral limbs of stroke survivors and control subjects [10, 12]. Specifically, RS tract contributions have been thoroughly studied in fast hand extension movements [13], ballistic movements [14] and two-dimensional reaching tasks [15] in stroke subjects.
Hyperexcitability of RS tract provides increased neuromodulatory input to the spinal cord. A well-studied source of neuromodulation to MNs is the raphe pathway descending from the raphe nuclei in the brainstem and that releases the key monoamine, serotonin. Anatomical studies have consistently shown near symmetrical bilateral projections of these RS pathways [16, 17]. Furthermore, hyperexcitability of the RS tract could lead to increased motor overflow i.e., unilateral voluntary activation could elicit activation of the contralateral limb [8], indicating the bilateral influence of the RS tract. Thus, a change in excitability of brainstem RS centers is likely to impact both sides of the body.
The pivotal issue in addressing the effects of the RS tract in humans is the sharp lateralization of clinical spasticity in stroke survivors. Accordingly, the objective of our study is to quantitatively assess whether there is also an increased MN excitability on the contralateral side of stroke survivors, in comparison to matched neurologically intact subjects. If so, this would help us evaluate the contributing role of the RS tract towards spasticity, and help us quantify its putative magnitude. Our goal is to utilize precision reflex measurement techniques to characterize and compare changes in (deep tendon) reflex behavior in both the spastic and contralateral muscles of stroke survivors and neurologically intact subjects. We propose that reflex threshold measures could be used as a surrogate estimate of MN excitability and thereby enable the characterization of the impact of the bilaterally distributed systems such as the RS tract and other brainstem monoaminergic pathways.
To establish an association between MN excitability and spasticity, it is essential to address the role of the descending pathways in modulating the stretch reflex. It is well established that excitatory and inhibitory signals of supraspinal origin are responsible for the regulation of excitability of the stretch reflex pathway [3, 5, 6]. Evidence from invasive animal lesion studies indicates that among the major descending tracts i.e., corticospinal, reticulospinal (RS), vestibulospinal (VS), rubrospinal, and tectospinal, only RS and VS tracts, originating in the brainstem, are substantially involved in the regulation of spinal stretch reflex circuitry [3]. Similar findings have been reported in humans with no neurological disorder. Corticospinal and rubrospinal tracts have limited influence on stretch reflex excitability [3], and the tectospinal tract appears not to exist in humans [7]. Thus, potential sources of increased spinal MN excitability after a stroke include increased VS and/or RS drive, potentially due to disruption of cortico-bulbar inhibitory pathways projecting to these brainstem nuclei. While animal studies have provided evidence of brainstem participation in spasticity, analogous direct approaches in humans to assess brainstem activity have not been possible [8]. The role of the RS tract in the pathophysiology of spasticity in humans has been examined with the acoustic startle reflex (ASR) studies in stroke survivors. ASR is a brainstem-mediated reflex that has been utilized as a non-invasive tool to examine the RS activity in humans [9,10,11]. In these studies, an exaggerated ASR response has been observed in spastic muscles of chronic stroke survivors as compared to the contralateral limbs of stroke survivors and control subjects [10, 12]. Specifically, RS tract contributions have been thoroughly studied in fast hand extension movements [13], ballistic movements [14] and two-dimensional reaching tasks [15] in stroke subjects.
Hyperexcitability of RS tract provides increased neuromodulatory input to the spinal cord. A well-studied source of neuromodulation to MNs is the raphe pathway descending from the raphe nuclei in the brainstem and that releases the key monoamine, serotonin. Anatomical studies have consistently shown near symmetrical bilateral projections of these RS pathways [16, 17]. Furthermore, hyperexcitability of the RS tract could lead to increased motor overflow i.e., unilateral voluntary activation could elicit activation of the contralateral limb [8], indicating the bilateral influence of the RS tract. Thus, a change in excitability of brainstem RS centers is likely to impact both sides of the body.
The pivotal issue in addressing the effects of the RS tract in humans is the sharp lateralization of clinical spasticity in stroke survivors. Accordingly, the objective of our study is to quantitatively assess whether there is also an increased MN excitability on the contralateral side of stroke survivors, in comparison to matched neurologically intact subjects. If so, this would help us evaluate the contributing role of the RS tract towards spasticity, and help us quantify its putative magnitude. Our goal is to utilize precision reflex measurement techniques to characterize and compare changes in (deep tendon) reflex behavior in both the spastic and contralateral muscles of stroke survivors and neurologically intact subjects. We propose that reflex threshold measures could be used as a surrogate estimate of MN excitability and thereby enable the characterization of the impact of the bilaterally distributed systems such as the RS tract and other brainstem monoaminergic pathways.
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