Spasticity mechanisms - for the clinician

Area of Science:

• Neuroscience
• Clinical Neurology
• Physiology

Background:

• Spasticity is a hallmark of upper motor neuron lesions, characterized by velocity-dependent increases in muscle tone.
• Clinically, it presents as resistance to passive stretching, often accompanied by phenomena like clonus and spasms.
• The underlying mechanism involves increased muscle stretch reflex excitability, linked to muscle spindle activity and spinal circuitry influenced by supraspinal pathways.

Purpose of the Study:

• To elucidate the complex mechanisms contributing to human spasticity.
• To understand the role of spinal and supraspinal pathways in the development of spasticity.
• To explore the neuroplastic changes underlying spasticity following central nervous system lesions.

Main Methods:

• Review of traditional and physiological definitions of spasticity.
• Analysis of clinical manifestations and associated phenomena.
• Investigation of the role of muscle spindles, spinal circuits, and supraspinal control.
• Consideration of central nervous system adaptations and neuroplasticity.

Main Results:

• Spasticity arises from increased muscle stretch reflex excitability, influenced by supraspinal pathways.
• Adaptations in spinal neuronal circuitry, including reduced inhibitory mechanisms, are implicated.
• Delayed onset and eventual reduction in reflex excitability suggest plastic changes in the central nervous system.
• Multiple, not fully elucidated, mechanisms likely contribute to human spasticity.

Conclusions:

• Human spasticity results from a complex interplay of factors, including altered supraspinal control and spinal adaptations.
• Neuroplastic changes in the central nervous system play a significant role in the development and progression of spasticity.
• Further research is needed to fully understand the mechanisms of spasticity and guide the development of effective treatments.