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

Abstract

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.

Comprehensive Assessment of the Time Course of Biomechanical, Electrophysiological and Neuro-Motor Effects after Botulinum Toxin Injections in Elbow Flexors of Chronic Stroke Survivors with Spastic Hemiplegia: A Cross Sectional Observation Study

“…Secondary to damage to the motor cortex and/or to the corticobulbar pathways after stroke, excitability of the contralateral medial cortico-reticulo-spinal pathways becomes unopposed and gradually upregulated, thus resulting in un-opposed excitatory inputs to spinal reflex circuits [5][6][7]. In the presence of externally imposed muscle stretch, the phenomenon of velocity-dependent stretch reflex responses, i.e., spasticity, is manifested [8,9]. On the other hand, this pathophysiological process of hyperexcitable descending brainstem pathways is shared by other motor impairments, e.g., inappropriate muscle activation [7,9].…”

“…In the presence of externally imposed muscle stretch, the phenomenon of velocity-dependent stretch reflex responses, i.e., spasticity, is manifested [8,9]. On the other hand, this pathophysiological process of hyperexcitable descending brainstem pathways is shared by other motor impairments, e.g., inappropriate muscle activation [7,9]. During sustained voluntary elbow flexion on the spastic-paretic side of stroke survivors, Rymer and colleagues have reported that spinal motor neurons are hyperexcitable and even spontaneously firing.…”

Early Use of Phenol Neurolysis Likely Reduces the Total Amount of Botulinum Toxin in Management of Post-Stroke Spasticity

“…Spasticity and muscle weakness on the affected side (i.e., hemiparesis) are two hallmark motor impairments after stroke. Recent advances have shown that these two motor impairments are mediated by distinctly different pathophysiological mechanisms (1)(2)(3)(4). Hemiparesis, as a result of damage of motor cortex and/or its descending corticospinal tracts, occurs immediately after stroke.…”

Effect of Stretching of Spastic Elbow Under Intelligent Control in Chronic Stroke Survivors—A Pilot Study

“…Wu et al extended velocity dependence to position as well as velocity dependence ( 4 ). Li et al extended velocity dependence to velocity as well as muscle length-dependent increase in resistance ( 5 ). It results from hyperexcitable descending excitatory brainstem pathways and the resultant exaggerated stretch reflex responses.…”

“…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 ).…”