Botulinum toxin A modifies nociceptive withdrawal reflex in subacute stroke patients

Alvisi, Elena; Serrao, Mariano; Conte, Carmela; Alfonsi, Enrico; Tassorelli, Cristina; Prunetti, Paolo; Cristina, Silvano; Perrotta, Armando; Pierelli, Francesco; Sandrini, Giorgio

doi:10.1002/brb3.1069

Cited by 10 publications

(6 citation statements)

References 36 publications

(48 reference statements)

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“…There was a lack of significant correlation between the max RsE value and the MAS values for all tested subjects. A decrement of the MAS values after BT injection has been reported earlier by other research groups and attributed to the unavailability of the fibers with active NMJ innervation [30,31]. Despite the fact that primary actions of BT are centered around the NMJ of the injected muscle, the recovery of motor outflow (measured by RsE values during the voluntary contraction) lags the recovery of MAS, which is likely an issue due to the lack of resolution of the MAS.…”

Section: The Difference In Clinical Scores (Mas and Fms) And Rsementioning

confidence: 52%

“…Reduction of contractile force and of the RsE after the intramuscular injection is assumed to be primarily attributable to the reduced active muscle fiber population, which can be explained by the BT induced presynaptic blockade of the cholinergic transmission [ 6 , 36 ]. Faster recovery of force may be due to altered load sharing activity from synergistic muscles during flexion [ 31 , 37 ], thus our force measurement is potentially impacted by actions of other synergistic flexors. Whereas, the RsE values reflect injected muscle characteristics.…”

Section: Discussionmentioning

confidence: 99%

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Precise quantification of the time course of voluntary activation capacity following Botulinum toxin injections in the biceps brachii muscles of chronic stroke survivors

Chandra

Afsharipour

Rymer

et al. 2020

J NeuroEngineering Rehabil

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Background: Spasticity is a key motor impairment that affects many hemispheric stroke survivors. Intramuscular botulinum toxin (BT) injections are used widely to clinically manage spasticity-related symptoms in stroke survivors by chemically denervating muscle fibers from their associated motor neurons. In this study, we sought to understand how BT affects muscle activation, motor unit composition and voluntary force generating capacity over a time period of 3 months. Our purpose was to characterize the time course of functional changes in voluntary muscle activity in stroke survivors who are undergoing BT therapy as part of their physician-prescribed clinical plan. Method: Our assessment of the effects of BT was based on the quantification of surface electromyogram (sEMG) recordings in the biceps brachii (BB), an upper arm muscle and of voluntary contraction force. We report here on voluntary force and sEMG responses during isometric elbow contractions across consecutive recording sessions, spread over 12 weeks in three segments, starting with a preliminary session performed just prior to the BT injection. At predetermined time points, we conducted additional clinical assessments and we also recorded from the contralateral limbs of our stroke cohort. Eight subjects were studied for approximately 86 experimental recording sessions on both stroke-affected and contralateral sides. Results: We recorded an initial reduction in force and sEMG in all subjects, followed by a trajectory with a progressive return to baseline over a maximum of 12 weeks, although the minimum sEMG and minimum force were not always recorded at the same time point. Three participants were able to complete only one to two segments. Slope values of the sEMG-force relations were also found to vary across the different time segments. While sEMG-force slopes provide assessments of force generation capacity of the BT injected muscle, amplitude histograms from novel sEMG recordings during the voluntary tasks provide additional insights about differential actions of BT on the overall motor unit (MU) population over time.

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Section: The Difference In Clinical Scores (Mas and Fms) And Rsementioning

confidence: 52%

Section: Discussionmentioning

confidence: 99%

Precise quantification of the time course of voluntary activation capacity following Botulinum toxin injections in the biceps brachii muscles of chronic stroke survivors

Chandra

Afsharipour

Rymer

et al. 2020

J NeuroEngineering Rehabil

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“…Only a few studies have investigated changes in NWR excitability in post-stroke hemiparetic patients with limb motor deficits ( Spaich et al , 2006 ; Serrao et al , 2012 ; Rueterbories et al , 2013 ; Spaich et al , 2014 ). The NWR-related EMG kinematic responses were increased and NWR modulation impaired in stroke patients with hemiparesis ( Serrao et al , 2012 ; Alvisi et al , 2018 ). The NWR-based functional electrical therapy was found to be useful in the rehabilitation of gait in severely impaired hemiparetic patients by improving post-treatment walking velocity and gait symmetry ( Spaich et al , 2014 ; Gervasio et al , 2018 ).…”

Section: Introductionmentioning

confidence: 99%

Hindlimb motor responses to unilateral brain injury: spinal cord encoding and left-right asymmetry

Zhang

Watanabe

Sarkisyan

et al. 2020

Brain Communications

131

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Mechanisms of motor deficits (e.g. hemiparesis and hemiplegia) secondary to stroke and traumatic brain injury remain poorly understood. In early animal studies, a unilateral lesion to the cerebellum produced postural asymmetry with ipsilateral hindlimb flexion that was retained after complete spinal cord transection. Here we demonstrate that hindlimb postural asymmetry in rats is induced by a unilateral injury of the hindlimb sensorimotor cortex, and characterize this phenomenon as a model of spinal neuroplasticity underlying asymmetric motor deficits. After cortical lesion, the asymmetry was developed due to the contralesional hindlimb flexion and persisted after decerebration and complete spinal cord transection. The asymmetry induced by the left-side brain injury was eliminated by bilateral lumbar dorsal rhizotomy, but surprisingly, the asymmetry after the right-side brain lesion was resistant to deafferentation. Pancuronium, a curare-mimetic muscle relaxant, abolished the asymmetry after the right-side lesion suggesting its dependence on the efferent drive. The contra- and ipsilesional hindlimbs displayed different musculo-articular resistance to stretch after the left but not right-side injury. The nociceptive withdrawal reflexes evoked by electrical stimulation and recorded with EMG technique were different between the left and right hindlimbs in the spinalized decerebrate rats. On this asymmetric background, a brain injury resulted in greater reflex activation on the contra- versus ipsilesional side; the difference between the limbs was higher after the right-side brain lesion. The unilateral brain injury modified expression of neuroplasticity genes analysed as readout of plastic changes, as well as robustly impaired coordination of their expression within and between the ipsi- and contralesional halves of lumbar spinal cord; the effects were more pronounced after the left side compared to the right-side injury. Our data suggest that changes in the hindlimb posture, resistance to stretch and nociceptive withdrawal reflexes are encoded by neuroplastic processes in lumbar spinal circuits induced by a unilateral brain injury. Two mechanisms, one dependent on and one independent of afferent input may mediate asymmetric hindlimb motor responses. The latter, deafferentation resistant mechanism may be based on sustained muscle contractions which often occur in patients with central lesions and which are not evoked by afferent stimulation. The unusual feature of these mechanisms is their lateralization in the spinal cord.

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“…In a recent study, we demonstrated that, in subjects with upper limb spasticity, the BoNT-A injection reduced in parallel the degree of spasticity and the size of the nociceptive withdrawal reflex (NWR) response of the upper limb, irrespective of the site of injection [20]. The NWR is an objective nociceptive reflex response mediated by a central circuitry sustained by WDR neurons [21], so these data support an intrinsic antinociceptive effect of the BoNT-A, encouraging further studies.…”

Section: Introductionmentioning

confidence: 99%

OnabotulinumtoxinA Reduces Temporal Pain Processing at Spinal Level in Patients with Lower Limb Spasticity

Icco

Perrotta

Berra³

et al. 2019

Toxins

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Spasticity is a muscle tone disorder associated with different neurological conditions. Spasticity could be associated with pain, high disability, poor functional recovery, and reduced quality of life. Botulinum neurotoxin type A (BoNT-A) is considered a first-line treatment for spasticity and, more recently, it also represents a therapeutic option for various chronic pain conditions. In this open label study, we aim to evaluate the effect of the BoNT-A on the spinal nociception in patients affected by spasticity of the lower limbs with associated pain with predominantly neuropathic features. Ten patients with stroke, 10 with multiple sclerosis and 5 with spinal cord injury were enrolled in the study. They were tested with clinical scales (neuropathic pain scale inventory (NPSI), numerical rating scale (NRS), modified Ashworth scale (MAS) and with the nociceptive withdrawal reflex at lower limbs to explore the spinal temporal summation threshold at baseline and 30 day after BoNT-A injection. OnabotulinumtoxinA (50 to 200 units per site) was injected in the lower limb muscles according to the distribution of spasticity. No significant differences were found at baseline for neurophysiological features across groups. After the BoNT-A injection, we recorded a significant reduction in MAS and NRS scores. Regarding the neurophysiological parameters, we described a significant increase in the temporal summation threshold after the BoNT-A injection. Our data supports the hypothesis that peripherally injected OnabotulinumtoxinA modulates the excitability of spinal cord nociceptive pathways. This activity may take place irrespective of the effect of the drug on spasticity.

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Botulinum toxin A modifies nociceptive withdrawal reflex in subacute stroke patients

Cited by 10 publications

References 36 publications

Precise quantification of the time course of voluntary activation capacity following Botulinum toxin injections in the biceps brachii muscles of chronic stroke survivors

Precise quantification of the time course of voluntary activation capacity following Botulinum toxin injections in the biceps brachii muscles of chronic stroke survivors

Hindlimb motor responses to unilateral brain injury: spinal cord encoding and left-right asymmetry

OnabotulinumtoxinA Reduces Temporal Pain Processing at Spinal Level in Patients with Lower Limb Spasticity

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