A Unifying Pathophysiological Account for Post-stroke Spasticity and Disordered Motor Control

Li, Sheng; Chen, Yen‐Ting; Francisco, Gerard E.; Zhou, Ping; Rymer, William Z.

doi:10.3389/fneur.2019.00468

Cited by 98 publications

(135 citation statements)

References 114 publications

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“…Instead, the results of the present study fit better within the recently proposed framework by Li et al . (2019) in which increased reliance on the ipsilateral SMA/PM cortico‐reticulospinal tract accounts for the movement impairments seen post‐stroke.…”

Section: Discussionmentioning

confidence: 99%

Limited capacity for ipsilateral secondary motor areas to support hand function post‐stroke

Wilkins

Yao

Owen

et al. 2020

The Journal of Physiology

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Key points Ipsilateral‐projecting corticobulbar pathways, originating primarily from secondary motor areas, innervate the proximal and even distal portions, although they branch more extensively at the spinal cord. It is currently unclear to what extent these ipsilateral secondary motor areas and subsequent cortical projections may contribute to hand function following stroke‐induced damage to one hemisphere. In the present study, we provide both structural and functional evidence indicating that individuals increasingly rely on ipsilateral secondary motor areas, although at the detriment of hand function. Increased activity in ipsilateral secondary motor areas was associated with increased involuntary coupling between shoulder abduction and finger flexion, most probably as a result of the low resolution of these pathways, making it increasingly difficult to open the hand. These findings suggest that, although ipsilateral secondary motor areas may support proximal movements, they do not have the capacity to support distal hand function, particularly for hand opening. Abstract Recent findings have shown connections of ipsilateral cortico‐reticulospinal tract (CRST), predominantly originating from secondary motor areas to not only proximal, but also distal muscles of the arm. Following a unilateral stroke, CRST from the ipsilateral side remains intact and thus has been proposed as a possible backup system for post‐stroke rehabilitation even for the hand. We argue that, although CRST from ipsilateral secondary motor areas can provide control for proximal joints, it is insufficient to control either hand or coordinated shoulder and hand movements as a result of its extensive spinal branching compared to contralateral corticospinal tract. To address this issue, we combined magnetic resonance imaging, high‐density EEG, and robotics in 17 individuals with severe chronic hemiparetic stroke and 12 age‐matched controls. We tested for changes in structural morphometry of the sensorimotor cortex and found that individuals with stroke demonstrated higher grey matter density in secondary motor areas ipsilateral to the paretic arm compared to controls. We then measured cortical activity when participants were attempting to generate hand opening either supported on a table or when lifting against a shoulder abduction load. The addition of shoulder abduction during hand opening increased reliance on ipsilateral secondary motor areas in stroke, but not controls. Crucially, the increased use of ipsilateral secondary motor areas was associated with decreased hand opening ability when lifting the arm as a result of involuntary coupling between the shoulder and wrist/finger flexors. Taken together, this evidence implicates a compensatory role for ipsilateral (i.e. contralesional) secondary motor areas post‐stroke, although with no apparent capacity to support hand function.

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Section: Discussionmentioning

confidence: 99%

Limited capacity for ipsilateral secondary motor areas to support hand function post‐stroke

Wilkins

Yao

Owen

et al. 2020

The Journal of Physiology

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“…However, EMG findings do not explain how or whether spastic muscles contribute to abnormal ankle and foot position or gait patterns. In the equinus deformity seen in Figure 2 , spontaneous motor unit firing was diffusely present, which is not uncommon [ 8 ]. However, history and physical exam suggested the gastrocnemius and soleus muscle spasticity was the primary contributor to the gait disorder.…”

Section: Discussionmentioning

confidence: 99%

“…Any isolated ankle movement is a net result of the combined activation of a group of target muscles, e.g., inversion occurs when dorsiflexors (primarily the tibialis anterior muscle) and plantarflexors (primarily the tibialis posterior muscle) co-activate. In the presence of spasticity, stroke survivors have less control and isolated activation; activation is more diffuse and divergent [ 7 , 8 ]. Therefore, a variety of ankle–foot deformities could be observed, depending on the severity of spasticity and weakness of individual muscles.…”

Section: Introductionmentioning

confidence: 99%

Ankle and Foot Spasticity Patterns in Chronic Stroke Survivors with Abnormal Gait

2020

Toxins

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Chronic stroke survivors with spastic hemiplegia have various clinical presentations of ankle and foot muscle spasticity patterns. They are mechanical consequences of interactions between spasticity and weakness of surrounding muscles during walking. Four common ankle and foot spasticity patterns are described and discussed through sample cases. The patterns discussed are equinus, varus, equinovarus, and striatal toe deformities. Spasticity of the primary muscle(s) for each deformity is identified. However, it is emphasized that clinical presentation depends on the severity of spasticity and weakness of these muscles and their interactions. Careful and thorough clinical assessment of the ankle and foot deformities is needed to determine the primary cause of each deformity. An understanding of common ankle and foot spasticity patterns can help guide clinical assessment and selection of target spastic muscles for botulinum toxin injection or nerve block.

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“…This may relate to the fact that the trained task was designed to produce voluntary control over the extensors (not the flexors), and/or because wrist extensors may receive a greater proportion of monosynaptic corticospinal projections compared with the wrist flexor muscles [78,79]. Because changes in reticulospinal pathways may ultimately cause pathological synergistic muscle activation after stroke [80][81][82], it may be that there is a greater contribution of reticulospinal drive to wrist flexion compared with extension movements [83]. Accordingly, if one aim of our training task was to reduce unintended flexor activation, then the reinforced neural activity might have been a reduction of brainstem or reticulospinal output to the flexors.…”

Section: Neuromuscular Controlmentioning

confidence: 99%

A Virtual Reality Muscle–Computer Interface for Neurorehabilitation in Chronic Stroke: A Pilot Study

Marin-Pardo

Laine

Rennie

et al. 2020

Sensors

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Severe impairment of limb movement after stroke can be challenging to address in the chronic stage of stroke (e.g., greater than 6 months post stroke). Recent evidence suggests that physical therapy can still promote meaningful recovery after this stage, but the required high amount of therapy is difficult to deliver within the scope of standard clinical practice. Digital gaming technologies are now being combined with brain–computer interfaces to motivate engaging and frequent exercise and promote neural recovery. However, the complexity and expense of acquiring brain signals has held back widespread utilization of these rehabilitation systems. Furthermore, for people that have residual muscle activity, electromyography (EMG) might be a simpler and equally effective alternative. In this pilot study, we evaluate the feasibility and efficacy of an EMG-based variant of our REINVENT virtual reality (VR) neurofeedback rehabilitation system to increase volitional muscle activity while reducing unintended co-contractions. We recruited four participants in the chronic stage of stroke recovery, all with severely restricted active wrist movement. They completed seven 1-hour training sessions during which our head-mounted VR system reinforced activation of the wrist extensor muscles without flexor activation. Before and after training, participants underwent a battery of clinical and neuromuscular assessments. We found that training improved scores on standardized clinical assessments, equivalent to those previously reported for brain–computer interfaces. Additionally, training may have induced changes in corticospinal communication, as indexed by an increase in 12–30 Hz corticomuscular coherence and by an improved ability to maintain a constant level of wrist muscle activity. Our data support the feasibility of using muscle–computer interfaces in severe chronic stroke, as well as their potential to promote functional recovery and trigger neural plasticity.

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A Unifying Pathophysiological Account for Post-stroke Spasticity and Disordered Motor Control

Cited by 98 publications

References 114 publications

Limited capacity for ipsilateral secondary motor areas to support hand function post‐stroke

Limited capacity for ipsilateral secondary motor areas to support hand function post‐stroke

Ankle and Foot Spasticity Patterns in Chronic Stroke Survivors with Abnormal Gait

A Virtual Reality Muscle–Computer Interface for Neurorehabilitation in Chronic Stroke: A Pilot Study

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