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

Li, Sheng

doi:10.3390/toxins12100646

Cited by 39 publications

(31 citation statements)

References 20 publications

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“…Passive ankle ROM was not different between low and high spasticity groups. A previous study has reported that a higher spasticity was associated with higher limitations in the passive ROM ( Li, 2020 ). In this study, both the low and high spasticity group had significant restricted ankle passive ROM.…”

Section: Discussionmentioning

confidence: 97%

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Role of Spasticity Severity in the Balance of Post-stroke Patients

Mahmoudzadeh

Ansari

Naghdi

et al. 2021

Front. Hum. Neurosci.

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Background: Lower limb spasticity after stroke is common that can affect the balance, increase the risk of falling, and reduces the quality of life.Objective: First, evaluate the effects of spasticity severity of ankle plantar flexors on balance of patients after stroke. Second, to determine the relationship between the spasticity severity with ankle proprioception, passive ankle dorsiflexion range of motion (ROM), and balance confidence.Methods: Twenty-eight patients with stroke based on the Modified Modified Ashworth Scale (MMAS) were divided into two groups: High Spasticity Group (HSG) (MMAS > 2) (n = 14) or a Low Spasticity Group (LSG) (MMAS ≤ 2) (n = 14). The MMAS scores, Activities-Specific Balance Confidence Questionnaire, postural sway of both affected and non-affected limbs under the eyes open and eyes closed conditions, timed up and go (TUG) test, passive ankle dorsiflexion ROM, and ankle joint proprioception were measured.Results: The ankle joint proprioception was significantly better in the LSG compared to the HSG (p = 0.01). No significant differences were found between the LSG and HSG on all other outcome measures. There were no significant relationships between the spasticity severity and passive ankle dorsiflexion ROM, and balance confidence.Conclusion: The severity of ankle plantar flexor spasticity had no effects on balance of patients with stroke. However, the ankle joint proprioception was better in patients with low spasticity. Our findings suggest that the balance is affected regardless of the severity of the ankle plantar flexor spasticity in this group of participants with stroke.

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Section: Discussionmentioning

confidence: 97%

“…This suggests that the ankle passive ROM is influenced by ankle muscle spasticity regardless of spasticity intensity. Spasticity, weakness of ankle muscles, and muscle contracture may explain the limited ankle passive ROM in both groups ( Mecagni et al, 2000 ; Li, 2020 ).…”

Section: Discussionmentioning

confidence: 98%

Role of Spasticity Severity in the Balance of Post-stroke Patients

Mahmoudzadeh

Ansari

Naghdi

et al. 2021

Front. Hum. Neurosci.

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“…The sample size was small and only the gastrocnemius muscle was injected. So, we have no information about the other muscles involved in the spastic equinus/equinovarus pattern, such as the soleus, tibialis posterior, flexor digitorum (longus and brevis), flexor hallucis (longus and brevis), extensor hallucis longus and tibialis anterior [ 14 ]. The study did not include a long-term timeline of serial (clinical and ultrasonographic) evaluations after the onset of stroke or BoNT-A treatment, except for follow-up evaluation at 1 month after BoNT-A injection.…”

Section: Discussionmentioning

confidence: 99%

Does Botulinum Toxin Treatment Affect the Ultrasonographic Characteristics of Post-Stroke Spastic Equinus? A Retrospective Pilot Study

Picelli

Filippetti

Melotti

et al. 2020

Toxins

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Equinovarus/equinus foot is a pattern most commonly treated with botulinum toxin type A in patients with post-stroke spasticity involving the lower limbs; the gastrocnemius is the muscle most frequently injected. Spastic equinovarus/equinus can present a mixture of conditions, including spasticity, muscle/tendon shortening, muscle weakness and imbalance. In this study, we wanted to determine whether botulinum toxin treatment affects the ultrasonographic characteristics of post-stroke spastic equinus. The same dose of AbobotulinumtoxinA was injected into the gastrocnemius medialis and lateralis of 21 chronic stroke patients with spastic equinus. Clinical (Ashworth scale and ankle range of motion) and ultrasound (conventional and sonoelastography) evaluation of the treated leg was carried out before and 4 weeks after injection. No significant effects of botulinum toxin treatment on the ultrasonographic characteristics of spastic equinus were observed. As expected, there were significant improvements in ankle passive dorsiflexion range of motion and calf muscle spasticity at 1 month after treatment. There was a direct association between Achilles tendon elasticity and calf muscle spasticity at baseline evaluation. Larger studies with a long-term timeline of serial evaluations are needed to further investigate the possible effects of botulinum toxin injection on spastic muscle characteristics in patients with post-stroke spasticity.

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“…69 However, clinical presentation of poststroke gait varies depending on severity of spasticity, involvement, and distribution of spastic muscles. 69,73,74 Another example is shown in Figure 2A. Spastic equinovarus of the ankle and foot localizes weight-bearing on the lateral foot, undoubtedly causing calluses and pressure sores over time.…”

Section: Neuromechanical Consequencesmentioning

confidence: 99%

A New Definition of Poststroke Spasticity and the Interference of Spasticity With Motor Recovery From Acute to Chronic Stages

Francisco

Rymer

2021

Neurorehabil Neural Repair

Self Cite

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The relationship of poststroke spasticity and motor recovery can be confusing. “True” motor recovery refers to return of motor behaviors to prestroke state with the same end-effectors and temporo-spatial pattern. This requires neural recovery and repair, and presumably occurs mainly in the acute and subacute stages. However, according to the International Classification of Functioning, Disability and Health, motor recovery after stroke is also defined as “improvement in performance of functional tasks,” i.e., functional recovery, which is mainly mediated by compensatory mechanisms. Therefore, stroke survivors can execute motor tasks in spite of disordered motor control and the presence of spasticity. Spasticity interferes with execution of normal motor behaviors (“true” motor recovery), throughout the evolution of stroke from acute to chronic stages. Spasticity reduction does not affect functional recovery in the acute and subacute stages; however, appropriate management of spasticity could lead to improvement of motor function, that is, functional recovery, during the chronic stage of stroke. We assert that spasticity results from upregulation of medial cortico-reticulo-spinal pathways that are disinhibited due to damage of the motor cortex or corticobulbar pathways. Spasticity emerges as a manifestation of maladaptive plasticity in the early stages of recovery and can persist into the chronic stage. It coexists and shares similar pathophysiological processes with related motor impairments, such as abnormal force control, muscle coactivation and motor synergies, and diffuse interlimb muscle activation. Accordingly, we propose a new definition of spasticity to better account for its pathophysiology and the complex nuances of different definitions of motor recovery.

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

Cited by 39 publications

References 20 publications

Role of Spasticity Severity in the Balance of Post-stroke Patients

Role of Spasticity Severity in the Balance of Post-stroke Patients

Does Botulinum Toxin Treatment Affect the Ultrasonographic Characteristics of Post-Stroke Spastic Equinus? A Retrospective Pilot Study

A New Definition of Poststroke Spasticity and the Interference of Spasticity With Motor Recovery From Acute to Chronic Stages

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