Ask the Experts - What Is the Cause of Muscle Spasms in Paraplegic...
Ask the Experts - What Is the Cause of Muscle Spasms in Paraplegic...
What is the cause of flexor and extensor spasms seen in patients with paraplegia? What is the prognosis in such patients? How do we manage such a problem?
In a spinal cord injury resulting in paraplegia, there is significant remodeling of the central nervous system control of motor output. Normally descending cortical inputs (upper motor neuron) exert an inhibitory effect on local spinal circuits that control motor output. Such spinal elements include the spinal motor neuron (lower motor neuron) connection to the muscle as well as the afferent connections of sensory fibers originating from the muscle (motor unit), which synapse onto the lower motor neuron and ascend upward in the spinal cord to higher motor control centers. In general, control of the muscle at the spinal level is of a predominantly excitatory nature. Descending influences from the cortex via upper motor neuron pathways on spinal motor neurons provide an inhibitory influence on local spinal motor circuits. With the loss of this inhibitory input on the spinal cord (as occurs in spinal cord injury), local spinal reflex nerve networks lose inhibitory influences. The loss of this cortical inhibition gives way to hyperactivity of local reflex circuits leading to hyperactive motor output manifested as extensor and flexor spasms.
Treatment of flexor and extensor spasms involves the use of antispasticity agents. Included in this group of agents are baclofen (both via oral route and intrathecal via implanted pump), tizanidine, clonazepam, and gabapentin. At the muscle level local injections of botulinum toxin in extremely spastic, hyperactive muscle groups can be highly effective in controlling spasms and the pain associated with them. With the use of the agents mentioned above (both alone and in combinations) improved control of movement can be obtained. Reduction of spasticity may allow an individual to perform simple movement patterns (transfers, weight bearing) that might have been interfered with because of the hyperactive motor output.
What is the cause of flexor and extensor spasms seen in patients with paraplegia? What is the prognosis in such patients? How do we manage such a problem?
In a spinal cord injury resulting in paraplegia, there is significant remodeling of the central nervous system control of motor output. Normally descending cortical inputs (upper motor neuron) exert an inhibitory effect on local spinal circuits that control motor output. Such spinal elements include the spinal motor neuron (lower motor neuron) connection to the muscle as well as the afferent connections of sensory fibers originating from the muscle (motor unit), which synapse onto the lower motor neuron and ascend upward in the spinal cord to higher motor control centers. In general, control of the muscle at the spinal level is of a predominantly excitatory nature. Descending influences from the cortex via upper motor neuron pathways on spinal motor neurons provide an inhibitory influence on local spinal motor circuits. With the loss of this inhibitory input on the spinal cord (as occurs in spinal cord injury), local spinal reflex nerve networks lose inhibitory influences. The loss of this cortical inhibition gives way to hyperactivity of local reflex circuits leading to hyperactive motor output manifested as extensor and flexor spasms.
Treatment of flexor and extensor spasms involves the use of antispasticity agents. Included in this group of agents are baclofen (both via oral route and intrathecal via implanted pump), tizanidine, clonazepam, and gabapentin. At the muscle level local injections of botulinum toxin in extremely spastic, hyperactive muscle groups can be highly effective in controlling spasms and the pain associated with them. With the use of the agents mentioned above (both alone and in combinations) improved control of movement can be obtained. Reduction of spasticity may allow an individual to perform simple movement patterns (transfers, weight bearing) that might have been interfered with because of the hyperactive motor output.
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