Velocity-Dependent Spasticity is Brought on by Movement
Spasticity that is brought on by movement is velocity-dependent spasticity, characterized by abnormal velocity-dependent increases in muscle tone and exaggerated reflexes that worsen with faster movements. 1
Understanding Velocity-Dependent Spasticity
Velocity-dependent spasticity is the most common form of spasticity and has specific characteristics:
- It manifests as increased muscle resistance that becomes more pronounced with faster movement of the affected limb
- It results from hyperactivity of tonic stretch reflexes 2
- It occurs in approximately 35% of stroke survivors 1
- It is a component of the upper motor neuron syndrome following central nervous system damage 3
Pathophysiology
The mechanism behind velocity-dependent spasticity involves:
- Interruption of neural circuitry regulating muscles 4
- Loss of descending inhibitory signals from the brain to the spinal cord
- Increased excitability at the segmental spinal level 2
- Hypersensitivity of the stretch reflex arc 3
Clinical Presentation
Velocity-dependent spasticity presents with:
- Resistance that increases proportionally to the speed of passive movement
- Minimal resistance with slow movements, significant resistance with rapid movements
- Can affect both upper and lower limbs
- May interfere with function and cause pain 1
- Can lead to contractures if left untreated 1
Distinguishing Features
Velocity-dependent spasticity should be distinguished from other types of spasticity-associated movements that may co-exist:
- Tonic spasms (sustained muscle contractions)
- Spontaneous clonus (rhythmic contractions)
- Myoclonus (brief, shock-like contractions)
- Focal dystonia (sustained abnormal postures) 5
Clinical Implications
If left untreated, velocity-dependent spasticity can lead to:
- Contractures limiting joint movement
- Pain and discomfort
- Impaired mobility and activities of daily living
- Decreased quality of life
- Difficulties with personal care 6
Management Approaches
Treatment should target the velocity-dependent nature of the spasticity:
Physical interventions:
- Antispastic positioning
- Range of motion exercises
- Stretching
- Splinting
- Serial casting 1
Pharmacological options:
Procedural interventions for refractory cases:
- Phenol/alcohol injections
- Selective dorsal rhizotomy
- Dorsal root entry zone lesions 1
Important Clinical Considerations
- Botulinum toxin is particularly effective for focal spasticity affecting gait function 1, 7
- Oral medications may cause sedation and other side effects that limit their utility 1
- Benzodiazepines should be avoided during stroke recovery due to potential negative effects on recovery 1
- Combining treatments (e.g., botulinum toxin with physical therapy) typically yields better outcomes 7
Monitoring and Follow-up
Regular assessment of spasticity using standardized scales (e.g., Modified Ashworth Scale) is essential to track treatment response and adjust management accordingly. Treatment effectiveness should be evaluated based on improvement in function, pain reduction, and prevention of contractures.