Abstract
Objective: To assess the short-term effects of strenuous dynamic stretching of the elbow joint using an intelligent stretching device in chronic spastic stroke survivors.Methods: The intelligent stretching device was utilized to provide a single session of intensive stretching to the spastic elbow joint in the sagittal plane (i.e., elbow flexion and extension). The stretching was provided to the extreme range, safely, with control of the stretching velocity and torque to increase the joint range of motion (ROM) and reduce spasticity and joint stiffness. Eight chronic stroke survivors (age: 52.6 ± 8.2 years, post-stroke duration: 9.5 ± 3.6 years) completed a single 40-min stretching intervention session. Elbow passive and active ROM, strength, passive stiffness (quantifying the non-reflex component of spasticity), and instrumented tendon reflex test of the biceps tendon (quantifying the reflex component of the spasticity) were measured before and after stretching.Results: After stretching, there was a significant increase in passive ROM of elbow flexion (p = 0.021, r = 0.59) and extension (p = 0.026, r = 0.59). Also, elbow active ROM and the spastic elbow flexors showed a trend of increase in their strength.Conclusion: The intelligent stretching had a short-term positive influence on the passive movement ROM. Hence, intelligent stretching can potentially be used to repeatedly and regularly stretch spastic elbow joints, which subsequently helps to reduce upper limb impairments post-stroke.
Highlights
Stroke is one of the leading causes of long-term motor disability in adults, with ∼795,000 people experiencing a new or recurrent episode of stroke every year in the United States [1]
The passive extension range of motion (ROM) showed a significant change after the session of strong stretching; it improved from 11◦ ± 9.6◦ to 4.6◦ ± 7.8◦ (p = 0.026, r = 0.59). (A full elbow extension corresponds to 0◦ elbow flexion and the values provided here denote the decrease in this flexion towards 0◦)
The elbow passive flexion ROM improved from 125.0◦ ± 4.7◦ to 130.5◦ ± 6.3◦ (p = 0.021, r = 0.59) (Figure 5)
Summary
Stroke is one of the leading causes of long-term motor disability in adults, with ∼795,000 people experiencing a new or recurrent episode of stroke every year in the United States [1]. Spastic hemiplegia is a common motor impairment post-stroke. Spasticity and muscle weakness often occur together and contribute to the disordered motor control [2]. Spasticity has been defined as “a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome” [3]. To better reflect the underlying pathophysiology, the characterization of spasticity has been extended beyond the velocity dependence. Li et al extended velocity dependence to velocity as well as muscle lengthdependent increase in resistance [5]. It results from hyperexcitable descending excitatory brainstem pathways and the resultant exaggerated stretch reflex responses. Other related motor impairments, including abnormal synergies, inappropriate muscle activation, and anomalous muscle coactivation, coexist with spasticity and share similar pathophysiological origins [5, 6]
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