38% of stroke survivors experience post-stroke spasticity within one year after a first stroke, while the overall prevalence of post-stroke spasticity is approximately 0.2% (taken from the WHO MONICA project)
Spasticity is diagnosed if the patient shows an increased resistance to passive movements that increases with speed and typical positioning of the limbs, due to increased muscle tone. The diagnosis is not complicated for rehabilitation specialists but unfortunately a lot of other specialists/HCP are not trained and thus don’t recognized the symptoms or when they do so, don’t see the potential benefit of an adapted treatment.
38% of stroke survivors experience post-stroke spasticity within one year after a first stroke.
Spasticity is one of several clinical features/motor behaviors that may result following damage to the part of the brain or spinal cord involved in controlling voluntary movement. Collectively, these features are known as the upper motor neuron (UMN) syndrome. Spasticity is associated with a pathologically increased muscle tone. This creates stiffness and resistance to passive movement (the word ‘spasm’ originates from the Greek word, ‘spasmos’, which means to drag or pull). This change in muscle tone may increase the disability related to the disease at the origin of spasticity.
Post-stroke spasticity is usually diagnosed and treated at rehabilitation centers, where many experts, such as, rehabilitation specialists, occupational therapists, physical therapists, speech therapists, psychologists, social workers, nurses…, work together to provide patients with different treatment options.
Botulinum toxin type A (BoNT/A) is recommended as a first-line therapy in national and international guidelines as part of an integrated treatment approach for post-stroke spasticity.
Botulinum toxin creates a ‘window of opportunity’ for improving motor and activity performance3 and should always be followed by physical therapy.
Physical therapy is the mainstay of treatment for spasticity, and is designed to reduce muscle tone, maintain or improve range of motion and mobility, increase strength and coordination, and improve care and comfort.
When not controllable by physical therapy, oral or intrathecal medications and/or botulinum toxin injections, spasticity symptoms can be treated with selective ablative procedures. In most cases, complementary neurosurgical and functional orthopedic approaches are used.
With surgical interventions, muscles can be denervated or tendons and muscles can be released, lengthened, or transferred to relieve the symptoms of spasticity. In practice, only 5% of spasticity patients undergo a surgical intervention.
By orthopedic surgery, muscles can be denervated, and tendons and muscles can be released, lengthened, or transferred. In order to release contractures, the contracted tendon is partially or completely split surgically and then the joint is repositioned at a more normal angle. A cast stabilizes the joint over a period of several weeks while the tendon regrows. After removing the cast, physical therapy is necessary to strengthen the muscles and improve the patient’s range of motion.
Surgical intervention that is used for the treatment of spasticity is called functional or selective dorsal rhizotomy (SDR). In this procedure, the neurosurgeon cuts nerve roots (rhizotomy) – the nerve fibers lying just outside the back bone (spinal column) that send sensory messages from the muscles to the spinal cord. ‘Selective’ indicates that only certain nerve roots are cut, and ‘dorsal’ refers to the target nerves that are located at the back of the spinal cord (the upper surface when a person is lying on his or her stomach).
Spasticity can occur in the upper and lower limbs. The body region and the extent to which it is affected depend on the area of the brain or spinal cord that has been damaged.