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 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.

• 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 amitryptaline (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.

Atrophy and Learned Non-Use

Due to loss of activity, muscle, bone, and skin atrophy occur after spinal cord injury. In addition, parts of the neural circuitry in the brain and spinal cord may turn off.

• Atrophy. When parts of the body are not used, they undergo atrophy. For example, muscles shrink, bones lose calcium and strength, and skin gets thinner. Activity of muscles, stress on bones, and contact with skin prevent atrophy. Even passive movement will help prevent muscle atrophy and fibrosis. Spasticity and spasms prevent atrophy and maintain muscle bulk. It is not a good idea to take so much anti-spasticity medication that the legs become flaccid (i.e. show no movement). Electrical stimulation (functional electrical stimulation) can be used to activate muscles to drive legs to pedal bicycles and prevent muscle atrophy. Weight bearing may prevent bone loss or osteoporosis while ambulation training on treadmills may reverse osteoporosis. Many drugs are available for increasing calcium in bones. Without exercise or stress on the bones, such drugs may increase the brittleness of bone without increasing ability of the bones to support weight.

• Learned non-use. Neural circuits in the spinal cord may also turn off when they are not used. Spinal cord injury causes a prolonged period of inactivity in people. For example, a person may not walk for many months after a spinal cord injury and this may turn off neuronal circuits needed for walking. In the early 1990’s, several groups reported that intensive ambulation training can restore independent locomotion to 50% or more of people who have some residual sensory or motor function but have never walked after spinal cord injury. Suspending a person over a treadmill and manually moving the legs until they start stepping on their own is one approach to ambulation training. Many rehabilitation centers around the world are studying these effects of weight-supported treadmill walking.

Preventing atrophy and reversing “learned non-use” are important goals of rehabilitation. Learned non-use may prevent recovery of function despite regenerative and remyelinative therapies. Some rehabilitation programs offer intensive motor training programs that can prevent or reverse learned non-use. Unfortunately, intensive and prolonged ambulation programs are very labor-intensive and consequently costly. Various clinical trials are being conducted to determine the optimal parameters for weight-supported ambulation, biofeedback, and other forms of motor training. Many rehabilitation centers in the United States have biofeedback, weight-supported ambulation, and functional electrical stimulation (FES) programs.