Spasticity, Motor Recovery, and Neural Plasticity after Stroke

Abstract

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 poststroke 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 keys 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.

Music Restores Propriospinal Excitation During Stroke Locomotion

“…Therefore, we assume that the enhanced propriospinal CPQ reflex during post-stroke walking likely results from modification of the subcortical influence on spinal circuitries likely of reticular origin. In line with this, connections from the cerebral cortex to the reticular formation in the brainstem allow motor commands to be sent over the reticulospinal tract to spinal networks, and after stroke, these pathways are likely particularly involved in the functional recovery (Baker et al, 2015;Li, 2017).…”

“…On the contrary, in stroke patients, the CPQ reflex was depressed by music, reaching normal values as those observed in controls. This might be related to the neuromodulation in the cortico-reticulospinal system following stroke, used for motor commands and functional recovery (Baker et al, 2015;Li, 2017). On the other hand, it is not clear whether the reticulospinal hyperexcitability and associated spasticity is a good or maladaptive plasticity (Li, 2017).…”

Measuring muscle tone with isokinetic dynamometer technique in stroke patients

“…Increased stretch reflex gain is the mechanism underlying spasticity. Cumulative evidence from animal and human studies supports the supraspinal origin of stretch reflex hyperexcitability [19]. More specifically, the loss of balanced inhibitory and excitatory descending reticulospinal projections after a stroke is the most plausible mechanism for post-stroke spasticity [20].…”

Can rehabilitation exercise alter the oxidative profile in stroke patients?

“…Plastic reorganization occurs immediately after stroke. Following focal damage to the motor cortex and its descending pathways, the surviving portions of the brain usually undergo substantial structural and functional reorganization [4]. Because of the difficulties in measuring the stress biomarkers in stroke rehabilitation research is crucial to better understand the pathophysiology.…”