[ARTICLE] Post-stroke Spasticity: A Review of Epidemiology, Pathophysiology, and Treatments – Full Text

Summary

Spasticity is a common condition in stroke survivors, and may be associated with pain and joint contracture, leading to poor quality of life and increased caregiver burden. Although the underlying mechanisms are not well-understood, it may be due to disruption of the balance of supra-spinal inhibitory and excitatory sensory inputs directed to the spinal cord, leading to a state of disinhibition of the stretch reflex. The treatment options include physical therapy, modality and pharmacological treatments, neurolysis with phenol and botulinum toxin, and surgical treatment. A successful treatment of spasticity depends on a clear comprehension of the underlying pathophysiology, natural history, and impact on patient’s performances. This review focuses on the epidemiology, presumed mechanism, clinical manifestation, and recent evidences of management.

Keywords

• stroke,
• muscle spasticity,
• mechanism,
• symptom management

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1. Introduction

Stroke is one of the leading causes of mortality and morbidity in adults in most countries.^{1; 2 ;  3} Spasticity is a common, but not an inevitable condition, in patients with stroke. Spasticity following stroke is often associated with pain, soft tissue stiffness, and joint contracture, and may lead to abnormal limb posture, decreased quality of life, increased treatment cost, and increased caregiver burden.⁴ Early detection and management of post-stroke spasticity may not only reduce these complications, but may also improve function and increase independency in patients with spasticity.

Spasticity was first described by Lance⁵ in 1980 as a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes (muscle tone), with exaggerated tendon jerks, resulting from hyper-excitability of the neurons involved in stretch reflex, as a component of the upper motor neuron syndrome. This definition is useful in clinical practice, because the guideline “velocity-dependent increase in tonic stretch reflexes,” can distinguish spasticity from other similar movement disorders such as hypertonia, rigidity, and hyperreflexia. However, this definition ignores the important aspect of sensory input in the experience of spasticity. Some studies have found that abnormal processing of sensory inputs from muscle spindles leads to excessive reflex activation of alpha-motoneurons, and increases spasticity. The new definition from the Support Program for Assembly of a Database for Spasticity Measurement (SPASM) project defines spasticity as “disordered sensory-motor control, resulting from an upper motor neuron lesion, presenting as intermittent or sustained involuntary activation of muscles”.⁶This definition takes into account the contribution of viscoelastic properties of soft tissue to joint stiffness, and the roles of proprioceptive and cutaneous sensory pathways.[…]

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