[WEB SITE] Managing spasticity with a focus on rehabilitation

Introduction

Spasticity as a motor disorder is a result of injury to the brain and/or the spinal cord. Its gradual development is caused by a group of neurophysiologic mechanisms emerging after central nervous system (CNS) injury.

Loss of descending inhibitory (reticulospinal) influences leads to exaggerated excitability of dynamic gamma neurons and alpha motor neurons. Other spinal tracts such as the vestibulospinal and rubrospinal tracts become more active. Essentially, spasticity can result from injury to the cortex, basal ganglia, thalamus, brainstem, cerebellum, central white matter, or spinal cord.

It affects patients with cerebrovascular episodes, traumatic brain injury, spinal cord injury, multiple sclerosis (MS), and others. (1)

In order to study “spasticity” and provide the right treatment at the right time, we must first analyze all aspects of the phenomenon, such as:

a) The nature of spasticity, b) its differentiation from other clinical syndromes of muscle tone disorders, c) its different development according to the site and degree of the injury, d) the modification it shows in time, e) its changes throughout the day and during sleep, f) its coexistence with other symptoms such as pain, and g) its changes in intensity due to external and internal sensory stimuli.

Definition and clinical particularities of spasticity

In the traditional sense of the term, James Lance, MD, described spasticity in 1980 as “a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyperexitability of the stretch reflex as one component of the upper motor neurone syndrome.” (2)

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