From the Guidelines
Acute lower extremity spasticity is most commonly caused by stroke, which disrupts blood flow to the brain, as well as other conditions such as spinal cord injury, traumatic brain injury, multiple sclerosis, and cerebral palsy. The causes of acute lower extremity spasticity can be multifactorial, including:
- Damage to the upper motor neurons that control muscle movement
- Disruption of neural pathways between the brain and muscles
- Compression of neural pathways by brain or spinal tumors
- Central nervous system infections like meningitis or encephalitis
- Neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS)
- Metabolic disturbances including electrolyte imbalances, hypoglycemia, and certain medication side effects
According to the most recent and highest quality study, the prevalence of poststroke spasticity in any limb is in the range of 25% to 43% over the first year after stroke 1. This highlights the importance of early identification and management of spasticity in patients with stroke.
Treatment of acute lower extremity spasticity depends on identifying and addressing the underlying cause, with options including:
- Baclofen (starting at 5mg three times daily, gradually increasing to 20-25mg three times daily as needed)
- Tizanidine (2-4mg initially, increasing gradually to 8mg three times daily)
- Diazepam (2-10mg three times daily)
- Dantrolene (25mg daily, increasing to 100mg three to four times daily)
- Physical therapy to maintain range of motion and prevent contractures
- Botulinum toxin injections for focal spasticity
The use of Botulinum toxin–type A (BTX-A) for the focal treatment of spasticity in the lower extremity has been shown to be effective in improving gait speed and reducing spasticity 1. Additionally, range of motion exercises, stretching, and splinting can also be effective in preventing contractures and improving mobility 1.
It is essential to prioritize the treatment of spasticity to prevent complications such as contractures, pain, and activity limitations, which can significantly impact the patient's quality of life. Early intervention and a multidisciplinary approach to management are crucial in optimizing outcomes for patients with acute lower extremity spasticity.
From the FDA Drug Label
Tizanidine’s capacity to reduce increased muscle tone associated with spasticity was demonstrated in two adequate and well controlled studies in patients with multiple sclerosis or spinal cord injury.
The causes of acute lower extremity spasticity are not directly stated in the drug label, but it is mentioned that the studies were conducted in patients with multiple sclerosis or spinal cord injury, suggesting that these conditions may be associated with spasticity.
- Multiple sclerosis
- Spinal cord injury 2
From the Research
Causes of Acute Lower Extremity Spasticity
The causes of acute lower extremity spasticity can be attributed to various neurological conditions, including:
- Multiple sclerosis 3, 4, 5, 6, 7
- Stroke 3, 4, 5, 6, 7
- Cerebral palsy 3, 4, 5, 6, 7
- Traumatic brain injury 3, 4, 5, 6
- Spinal cord injuries 3, 4, 5, 6, 7
- Brain injury 4, 5, 6
- Cerebral paresis 5
Underlying Mechanisms
These conditions lead to upper motor neuron lesions, which can be located in the cerebrum or the spinal cord, resulting in spasticity 4, 5, 6, 7. The velocity-dependent increase in muscle tone and uncontrolled, repetitive, involuntary contractions of skeletal muscles are characteristic of spasticity 4, 7.
Clinical Presentation
Spasticity can present as upper motor neuron symptoms, causing significant pain and limited mobility, which can lead to decreased quality of life and difficulty maintaining personal care 4. The clinical assessment and management of spasticity are dependent on the underlying cause and the individual patient's condition 5.