Botox Reduces Spasticity And Tone, Improves Function
Published in UAB Insight, Winter 2007
Self-care, self-esteem, and caregiver burden benefit
The same neurotoxin used to diminish the appearance of wrinkles may now help smooth the frustration of patients with upper motor neuron syndrome-related spasticity following stroke, spinal cord injury, traumatic brain injury, cerebral palsy, or multiple sclerosis.
“Spasticity is characterized by a velocity-dependent increase in tonic stretch reflexes, or muscle tone, with exaggerated tendon jerks. It may lead to chronically flexed elbows or wrists, clenched fists, thumb-in-palm, adducted and internally rotated shoulders, or pronated forearms, all of which dramatically diminish quality of life and the ability of patients and caregivers to perform daily routines of hygiene, dressing, and eating,” says UAB physiatrist Robert C. Brunner, MD, medical director of the Spain Rehabilitation Center. “Lower-limb positions, such as flexed hips or knees, adducted thighs, striatal toes, or equinus foot, may interfere with seating, gait, or patient transfer or transport. Botox relaxes affected muscles, reducing spasticity and pain and improving function.”
All botulinum toxins (A-G) are powerful neurotoxins that temporarily weaken muscles by inhibiting acetylcholine release, which signals muscles to contract. In clinical trials, potential side effects of prepared Botox A doses (5 ng per 100 units) have ranged from injection-site pain to headache, dry mouth, muscle weakness, and dysphagia.
“Spasticity can affect mood, mobility, fatigue, sexuality, self-esteem, and self-care,” Brunner says. “Contractures can develop and may lead to pain, poor orthotic fit, disfigurement, and increased risk of falls. Our strategy when injecting Botox is to relieve tone and improve function, position, posture, and personal care, as well as to reduce pain, pressure sores, and caregiver burden. We look at individual limitations and identify functional goals; for example, loosening fingers enough to grasp an object, such as a spoon, or improve gait by ‘Botoxing’ toe-curl flexors in patients with focal foot dystonias.”
Brunner emphasizes treatments take 2 to 3 days to become effective, with efficacy peaking at 2 weeks and lasting for up to 3 months. He introduces physical or occupational therapy 1 week post-injection and, when necessary, offers serial casting every 3 to 5 days until contractures resolve.
The longer a patient lives with spasticity, the greater the risk of increased hospital costs, skin problems due to pressure sores, and physical and emotional burdens of pain and limited function. Brunner encourages early intervention, when spastic joints are most amenable to treatment. He evaluates tone; assesses clonus, spasms, gait, and disfigurement; reviews comorbidities; and studies optimal treatment options, including drugs, such as oral or intrathecal baclofen, surgical referral, or chemodenervation, such as Botox. He notes Botox benefits focal spastic joints, not diffuse spasticity, which responds better to other options.
“Botox is excellent for focal spasticity and muscle overactivity in patients with upper motor neuron syndrome. It avoids central side effects of systemic oral medication, can engineer a targeted response when aimed at specific muscles, does not cause sedation, requires no recovery period or activity restrictions, and significantly improves quality of life.”