Asymmetries in vestibular evoked myogenic potentials in chronic stroke survivors with spastic hypertonia: Evidence for a vestibulospinal role

Miller, Derek M.; Klein, Cliff S.; Suresh, Nina L.; Rymer, William Z.

doi:10.1016/j.clinph.2014.01.035

Cited by 52 publications

(46 citation statements)

References 62 publications

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“…There existed a strong positive relationship between the degree of asymmetry and the overall severity of spasticity from upper and lower limbs in spastic-paretic stroke survivors. The findings thus suggest a possible role of hyperexcitability of VST in poststroke spasticity (105). Yet, this level of acoustic stimuli is also likely to activate RS pathways via acoustic startle reflex (ASR) (106, 107).…”

Section: Rs Hyperexcitability As a Results Of Maladaptive Plastic Chanmentioning

confidence: 88%

“…With more extensive cordotomies that damaged the medial RST, spasticity was drastically reduced (103). Given unilateral nature of vestibulospinal projections (104), the role of VST in spasticity was recently tested in chronic stroke (105). Vestibular-evoked myogenic potentials in the sternocleidomastoid muscle in response to high-level acoustic stimuli (130 dB) to the ears of stroke survivors were greater on the impaired side than the non-impaired side.…”

Section: Rs Hyperexcitability As a Results Of Maladaptive Plastic Chanmentioning

confidence: 99%

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Spasticity, Motor Recovery, and Neural Plasticity after Stroke

2017

Front. Neurol.

210

161

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Spasticity and weakness (spastic paresis) are the primary motor impairments after stroke and impose significant challenges for treatment and patient care. Spasticity emerges and disappears in the course of complete motor recovery. Spasticity and motor recovery are both related to neural plasticity after stroke. However, the relation between the two remains poorly understood among clinicians and researchers. Recovery of strength and motor function is mainly attributed to cortical plastic reorganization in the early recovery phase, while reticulospinal (RS) hyperexcitability as a result of maladaptive plasticity, is the most plausible mechanism for poststroke spasticity. It is important to differentiate and understand that motor recovery and spasticity have different underlying mechanisms. Facilitation and modulation of neural plasticity through rehabilitative strategies, such as early interventions with repetitive goal-oriented intensive therapy, appropriate non-invasive brain stimulation, and pharmacological agents, are the keys to promote motor recovery. Individualized rehabilitation protocols could be developed to utilize or avoid the maladaptive plasticity, such as RS hyperexcitability, in the course of motor recovery. Aggressive and appropriate spasticity management with botulinum toxin therapy is an example of how to create a transient plastic state of the neuromotor system that allows motor re-learning and recovery in chronic stages.

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Section: Rs Hyperexcitability As a Results Of Maladaptive Plastic Chanmentioning

confidence: 88%

Section: Rs Hyperexcitability As a Results Of Maladaptive Plastic Chanmentioning

confidence: 99%

Spasticity, Motor Recovery, and Neural Plasticity after Stroke

2017

Front. Neurol.

210

161

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“…The absence, in the present study, of treatment-related changes in corticospinal excitability and on the monosynaptic component of the stretch reflex points to the involvement of other spinal and supraspinal mechanisms in the pathophysiology of MS spasticity. Among these are the oligosynaptic component of the stretch reflex [28] and non-reflex modulation of muscle tone through corticospinal, reticulospinal or vestibulospinal projections [29,30]. Possible effects of emotional stress or anxiety, acting as psychogenic triggers of spasticity [31], should also be taken into account.…”

Section: Discussionmentioning

confidence: 99%

Sativex® and clinical–neurophysiological measures of spasticity in progressive multiple sclerosis

et al. 2015

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Despite the proven efficacy of Sativex(®) (9-delta-tetrahydrocannabinol plus cannabidiol) oromucosal spray in reducing spasticity symptoms in multiple sclerosis (MS), little is known about the neurophysiological correlates of such effects. The aim of the study was to investigate the effects of Sativex on neurophysiological measures of spasticity (H/M ratio) and corticospinal excitability in patients with progressive MS. This was a randomized, double-blind, placebo-controlled, crossover study. Consecutive subjects with progressive MS and lower limb spasticity referred to our center were randomized to 4 weeks' treatment (including 2 weeks' titration) with Sativex or placebo, with crossover after a 2-week washout. Clinical and neurophysiological measures (H/M ratio and cortical excitability) of spasticity were assessed. The H/M ratio was the primary outcome, with sample size calculation of 40 patients. Of 44 recruited patients, 34 were analyzed due to 6 drop-outs and 4 exclusions, which lowered the power of the study to show differences between treatments. Neurophysiological measures did not differ significantly according to treatment and did not correlate significantly with clinical response. Response on the modified Ashworth scale (at least 20 % improvement) was significantly more frequent after Sativex than placebo (50 vs 23.5 %; p = 0.041; McNemar). Side effects did not differ significantly according to treatment. Our findings confirm the clinical benefit of Sativex on MS spasticity. The lack of corresponding changes in corticospinal excitability and on the monosynaptic component, of the stretch reflex, although in a limited sample size, points to the involvement of other spinal and supraspinal mechanisms in the physiopathology of spasticity in progressive MS.

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“…Responses of neck muscles to vestibular stimulation (cervical vestibular-evoked myogenic potentials) were compared on the intact and lesioned sides in stroke survivors with spasticity. The differences on the two sides were proportional to the severity of the spasticity (248); the responses on the lesioned side were amplified, as illustrated in Figure 4. In combination with data from animals discussed previously, these data support the notion that supratentorial regions of the brain regulate the excitability of vestibulospinal neurons.…”

Section: Transformation Of Vestibular Reflexes By Descending Pathwaysmentioning

confidence: 97%

Descending Influences on Vestibulospinal and Vestibulosympathetic Reflexes

2017

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This review considers the integration of vestibular and other signals by the central nervous system pathways that participate in balance control and blood pressure regulation, with an emphasis on how this integration may modify posture-related responses in accordance with behavioral context. Two pathways convey vestibular signals to limb motoneurons: the lateral vestibulospinal tract and reticulospinal projections. Both pathways receive direct inputs from the cerebral cortex and cerebellum, and also integrate vestibular, spinal, and other inputs. Decerebration in animals or strokes that interrupt corticobulbar projections in humans alter the gain of vestibulospinal reflexes and the responses of vestibular nucleus neurons to particular stimuli. This evidence shows that supratentorial regions modify the activity of the vestibular system, but the functional importance of descending influences on vestibulospinal reflexes acting on the limbs is currently unknown. It is often overlooked that the vestibulospinal and reticulospinal systems mainly terminate on spinal interneurons, and not directly on motoneurons, yet little is known about the transformation of vestibular signals that occurs in the spinal cord. Unexpected changes in body position that elicit vestibulospinal reflexes can also produce vestibulosympathetic responses that serve to maintain stable blood pressure. Vestibulosympathetic reflexes are mediated, at least in part, through a specialized group of reticulospinal neurons in the rostral ventrolateral medulla that project to sympathetic preganglionic neurons in the spinal cord. However, other pathways may also contribute to these responses, including those that dually participate in motor control and regulation of sympathetic nervous system activity. Vestibulosympathetic reflexes differ in conscious and decerebrate animals, indicating that supratentorial regions alter these responses. However, as with vestibular reflexes acting on the limbs, little is known about the physiological significance of descending control of vestibulosympathetic pathways.

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Asymmetries in vestibular evoked myogenic potentials in chronic stroke survivors with spastic hypertonia: Evidence for a vestibulospinal role

Cited by 52 publications

References 62 publications

Spasticity, Motor Recovery, and Neural Plasticity after Stroke

Spasticity, Motor Recovery, and Neural Plasticity after Stroke

Sativex® and clinical–neurophysiological measures of spasticity in progressive multiple sclerosis

Descending Influences on Vestibulospinal and Vestibulosympathetic Reflexes

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