What is spasticity and neuropathic pain?
Spinal cord injury disconnects the brain from the spinal cord below the injury site. The spinal cord below the injury site does not die unless it has been damaged by loss of blood flow (ischemia). The lower spinal cord becomes hyperactive because spinal cord injury interrupts not only excitatory but also inhibitory connections to the cord. The spinal cord above the injury site also may become hyperactive, producing abnormal sensations.
- Spasticity and spasms. Reflexes may be hyperexcitable in the lower spinal cord isolated from the brain by injury. Such reflex hyperexcitability is called spasticity, including neurons that mediate muscle reflexes for feedback control, more complex reflexes such as the withdrawal reflex, anti-gravity reflexes for standing and postural control, and locomotor programs that mediate walking and running. Hyperactive reflexes may be present even when there is voluntary control of the muscle. Spasms are spontaneous or evoked movements of multiple muscles. Spasms can occur in limbs that a person has little or no control of and can be violent enough to throw a person out of a wheelchair. Pain, bladder infection, and irritation of the spinal cord can aggravate spasticity and spasms. A drug called baclofen is often used to control spasticity. Baclofen usually does not prevent spasms unless very high doses are used and causes weakness or flaccidity. Baclofen can be given directly to the spinal cord (intrathecally) to treat severe spasticity when oral doses of 100-120 mg per day are insufficient. Several other drugs also suppress spasticity, including clonidine and tizanidine.
For Friends and Family of the Newly Injured Topic List
Here is what I say to families
Some frequently asked questions
How is acute spinal cord injury treated?
What is spasticity and neuropathic pain?
What happens to the bladder, bowel, and sexual function?
How does spinal cord injury affect the skin?
What is autonomic dysreflexia?
- Dysesthesia and pain. Abnormal sensations (dysesthesia) and neuropathic pain are the flip side of the coin to spasticity and spasms. When the spinal cord loses sensory input, sensory neurons above the injury site become hyperexcitable and can generate abnormal sensations and pain. This is akin to “phantom pain” after limb amputations and peripheral nerve injuries. Neuropathic pain is often described as “burning” or pressure involving areas that have little or no sensation. It can also occur in deeper organs. Neuropathic pain may be associated with spasticity and spasms. For many years, doctors did not recognize neuropathic pain and treated it as psychogenic pain. Several therapies are available for reducing neuropathic pain. For example, the tricyclic antidepressant amitriptyline (Elavil) may reduce dysesthesia. Some of the most promising therapies, interestingly, are drugs that are anti-epileptic. For example, gabapentin (Neurontin) is an anti-epileptic drug that has been reported to reduce neuropathic pain when given in very high doses. Some recent studies suggest that glutamate receptor blockers such as dextromethorphan and oral ketamine may be useful for refractory neuropathic pain.