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Chronic Problems of Spinal Cord Injury

Wise Young, MD, PhD

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 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 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.

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.

What happens to the bladder, bowel, and sexual function?

The spinal cord also carries "autonomic" signals that control blood pressure, blood flow, breathing, sweating, bowel, bladder, sexual, and other autonomic functions.

•  Bladder Paralysis and Spasticity. Spinal cord injury paralyzes the bladder. The bladder must be catheterized to drain urine. Indwelling catheters (such as a foley catheter inserted through the urethra) have a high risk of infections. Sterile intermittent catheterization is recommended but may be complicated by bladder spasticity or spontaneous contractions of the bladder. Bladder contractions can push urine into the kidney and this may lead to kidney damage. A drug called Ditropan suppresses bladder spasticity but have side effects such as dry mouth and eyes. Alternative approaches are available, including cutting the bladder sphincter so that urine drains freely into a condom catheter but this approach is not suitable for women. An approach that does not involve compromise of the urinary sphincter is placement of a suprapubic catheter or creation of a intestinal conduit from the abdominal wall to the bladder, i.e. a Mitrafanoff procedure.

•  Bowel constipation and incontinence.  The bowels usually operate without much voluntary control.  However, spinal cord injury slows bowel activity and transit time of food in the gut.  People use a variety of stimulants and suppositories to facilitate bowel activity. Bowel incontinence is a serious problem, often restricting social activity and employment options.  A common technique is to establish a bowel routine to empty the gut on a set schedule. Artificial sphincters are available but the success rates of such procedures are still limited.  Finally, alterations in secretion patterns can lead to indigestion, appetite changes, nausea, gallbladder stones, and other problems, especially in people with cervical spinal cord injury.

•  Erection and ejaculation. 
Most people assume that spinal cord injury eliminates the possibility of sexual function.  However, this is not true for a majority of people with spinal cord injury.  Penile erection is a reflex and many men are able to have erections after spinal cord injury unless the injury involves the lower spinal cord or roots that control erection.  Recent studies suggest that Viagra works for people with spinal cord injury.  Vibrators or electrical stimulation can be used to facilitate ejaculation.  Due to sphincter spasticity or poor coordination of the bladder sphincters, the ejaculate often goes into the bladder rather than outward.  However, with a combination of electroejaculation and semen collection, it is possible to collect ejaculates from nearly all males.  While spinal cord injury may interfere with menstrual cycles, a vast majority of young women with spinal cord injury remain fertile and can conceive.

How does spinal cord injury affect the skin?

Spinal cord injury reduces or eliminates skin sensation in dermatomes below the injury site. Because people cannot feel or move, they may sit or lie for long times on certain parts of their body.  Pressure impedes blood flow in the skin.  Due to muscle atrophy, the normal tissue padding that cushions the butt may be reduced. Absence of sensation, loss of muscle padding, and long periods of pressure can lead to skin breakdown and development of pressure sores or decubiti. Decubiti are potentially life threatening but preventable. 

Spinal cord injury impairs skin blood flow responses.  Normally, skin responds to pressure, mechanical stimulation, or inflammation with increased blood flow.  Loss of this response not only adds to the vulnerability of the skin to pressure sores but reduces the ability of the skin to repair decubiti.  Thus, great care must be taken to prevent decubiti by shifting sitting positions and frequent turning.  Special seats that distribute the pressure are used in wheelchairs to prevent sacral decubiti. Vulnerable areas such as the heels must be padded.  If a decubitus develops, all pressure must be removed or the decubitus can progress to loss of skin and tissues to the point of exposing bone.  The sores must be kept clean or they can become infected.  Plastic surgery may be necessary to repair the decubitus. 

Spinal cord injury also paralyzes sweating in dermatomes below the injury level. People with spinal cord injury must be very careful to maintain their body temperatures.  In contrast to loss of sweating below the injury site, many people with spinal cord injury may have abnormal increases of sweating above the injury site, often in their upper torso and face.  This is a form of autonomic hyperexcitability or spasticity.  It is not unusual for people to sweat profusely on one side of the face and not the other.  Such abnormal sweating responses may develop early or late after injury.

Spinal cord injury disables vascular responses that maintain blood pressure when a person sits or stands up.  Blood vessels in the guts and legs normally constrict when a person stands up, to keep blood from pooling.  When people with spinal cord injury sit up for the first time after injury, their blood pressure may drop sharply.  Such postural hypotension may prevent a person from sitting or standing during the first weeks after spinal cord injury.  The vascular responses recover over time but people must be be tilted gradually into the vertical position over the several weeks after spinal cord injury.  Loss of vascular responses in the legs leads to a tendency for fluid to accumulate in the legs when people sit for long times.  Such dependent edema can be prevented to some extent with stockings.

What is autonomic dysreflexia?

The autonomic nervous system often becomes hyperactive in people with spinal cord injury.  Autonomic dysreflexia manifests in large increases in blood pressure (hypertension) with systolic pressures exceeding 200 mm Hg, slow (bradycardia) or fast heart rate (tachycardia), headaches, facial flushing, exuberant sweating, hyperthermia, stuffy nose, goose pimples, nausea, and other signs of autonomic hyperactivity.  Called autonomic dysreflexia, these episodes may be spontaneously or may be instigated by infection, pain, or other conditions that stimulate the autonomic nervous system.  Severe autonomic dysreflexia may be life-threatening. 

Emergency treatments of autonomic dysreflexia should initially focus on identifying potential causes that can be relieved. If the episode occurred during manipulation of the body, such as rectal stimulation, that activity of course should be stopped.  The person should remain sitting and check for any blockage of bladder outflow.  If necessary, place a foley catheter to drain the bladder. If the cause cannot be identified and eliminated, drugs can be used to relieve the symptoms.  These include Procardia (a calcium channel blocker), nitroglycerin (a vasodilator), clonidine (alpha adrenergic agonist anti-hypertensive drug), or hydralazine (a vasodilator) to reduce blood pressure.  People with spinal cord injury should carry a card with instructions to inexperienced emergency personnel.

Causes of autonomic dysreflexia may sometimes be masked by the spinal cord injury.  For example, a bladder infection, kidney or bladder stones, bowel cramps, gallbladder stones, gastric ulcers, hemorrhoids, pressure sores, back pain, bone fractures, and many other potential causes may not be felt by an individual due to the spinal cord injury but may manifest in autonomic dysreflexia.  Autonomic dysreflexia may result from heterotopic ossification (a condition where abnormal and painful bone growth occurs on the hip and other bones).  Sometimes, back pain resulting from Harrington rods and other instrumentation may lead to autonomic dysreflexia that occur only when sitting up or lying down. 

Autonomic dysreflexia often occur during sexual activity, labor, and delivery.  Fortunately, the autonomic dysreflexia associated with orgasm and other sexual activity is usually mild and controllable with drugs but obstetricians should be aware and prepared to treat autonomic dysreflexia in women undergoing labor.  Some individuals who have uncomfortable autonomic dysreflexia during sexual activity should consult their doctors for the possibility of having medication on hand (such as nitroglycerin) to counter some of the symptoms before or after the activity.  Sometimes, a glass of wine can help reduce autonomic dysreflexia. 

To read more about spinal cord injury:

What is the Spinal Cord

What is Spinal Cord Injury

Spinal Cord Injury Levels and Classification

Acute Spinal Cord Injury

Chronic Problems of Spinal Cord Injury

Recovery and Treatment

Recovery from Spinal Cord Injury

Spinal Cord Injury and Family

Ten Frequently Asked Questions Concerning Cure of Spinal Cord Injury

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