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 post-stroke 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 key 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.

Walking dysfunction occurs at a very high prevalence in stroke survivors. Human walking is a phenomenon often taken for granted, but it is mediated by complicated neural control mechanisms. The automatic process includes the brainstem descending pathways (RST and VST) and the intraspinal locomotor network. It is known that leg muscles are organized into modules to serve subtasks for body support, posture and locomotion. Major kinematic mechanisms are recognized to minimize the center of gravity (COG) displacement. Stroke leads to damage to motor cortices and their descending corticospinal tracts and subsequent muscle weakness. On the other hand, brainstem descending pathways and the intraspinal motor network are disinhibited and become hyperexcitable. Recent advances suggest that they mediate post-stroke spasticity and diffuse spastic synergistic activation. As a result of such changes, existing modules are simplified and merged, thus leading to poor body support and walking performance. The wide range and hierarchy of post-stroke hemiplegic gait impairments is a reflection of mechanical consequences of muscle weakness, spasticity, abnormal synergistic activation and their interactions. Given the role of brainstem descending pathways in body support and locomotion and post-stroke spasticity, a new perspective of understanding post-stroke hemiplegic gait is proposed. Its clinical implications for management of hemiplegic gait are discussed. Two cases are presented as clinical application examples.

Spasticity is one of many consequences after stroke. It is characterized by a velocity-dependent increase in resistance during passive stretch, resulting from hyperexcitability of the stretch reflex. The underlying mechanism of the hyperexcitable stretch reflex, however, remains poorly understood. Accumulated experimental evidence has supported supraspinal origins of spasticity, likely from an imbalance between descending inhibitory and facilitatory regulation of spinal stretch reflexes secondary to cortical disinhibition after stroke. The excitability of reticulospinal and vestibulospinal tracts has been assessed in stroke survivors with spasticity using non-invasive indirect measures. There are strong experimental findings that support the reticulospinal hyperexcitability as a prominent underlying mechanism of post-stroke spasticity. This mechanism can at least partly account for clinical features associated with spasticity and provide insightful guidance for clinical assessment and management of spasticity. However, the possible role of VST hyperexcitability can not be ruled out from indirect measures. In vivo measure of individual brainstem nuclei in stroke survivors with spasticity using advanced fMRI techniques in the future is probably able to provide direct evidence of pathogenesis of post-stroke spasticity.

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.