The National
Spinal Cord
Injury Association

SCI Life
Fall/Winter 1998

The Status of Research:
Effects of SCI

The following article, the second in a four-part series about spinal cord research, examines the different ways the spinal cord can be injured and the physical consequences of the injury.

How Paralysis Begins
SCI can result from damage to the vertebral column or to the spinal cord itself. Either can result in a displacement of the bones of the spine, which in turn can lead to SCI. Bone displacement can cause spinal cord bruising (contusion), pinching (com-pression), stretching (distraction), or some combination of these. In rare instances, injury to the vertebral column will result in an actual cutting or penetration of the spinal cord. Penetrating SCIs often are due to gunshot or stab wounds that may or may not damage surrounding vertebrae. SCI also can be caused by ischemia, a decrease or loss of blood flow to the cord. This results from injury, disease, or certain surgical procedures, particularly those involving clamping the aorta. Fortunately, SCI from surgery is rare.

Because the causes of SCI vary greatly, no two injuries are exactly alike. However, the basis of the resulting paralysis is the same: the death of neurons, and the disconnection and demyelination of axons. Thanks to research, scientists can describe the pathology (deviations from normal anatomy) and patho-physiology (abnormal biological and chemical processes) responsible for these changes, although they are still not completely understood.

At the time of injury, neurons, glia, and blood vessels in the injury zone experience an initial mechanical damage. Following this "primary" injury, several mechanisms become operative. This leads to further damage, called "secondary" injury, which often is responsible for more of the funtional deficit people with SCI experience than is the initial trauma itself.

Typicallly, after a moderately severe trauma, secondary injury begins within 30 minutes with hemorrhage or bleeding in the central gray matter of the spinal cord. Over the course of several hours, this hemorrhage radiates outward to include surrounding white matter. Within six hours, edema (swelling) is visible in the area. The edema, hemorrhage, and ischemia all result in decreased oxygen supply (hypoxia) in that region of the spinal cord, which leads to the death (necrosis) of local tissue.

Also about two hours after injury, inflammatory cells begin their invasion. These immune-system cells protect us from disease and infection by killing harmful bacteria in our body and clearing away waste and debris. By the forth hour, some of these inflammatory cells begin killing the damaged nerves in the spinal cord.

All of the events described above ultimately lead to further nerve damage in the spinal cord. If the initial trauma is severe, the secondary injury process may begin immediately, and the entire injury zone can become filled with dead or necrotic tissue within 48 hours. However, immune-system cells eventually clean up the area by removing all the dead tissue. Several weeks after the initial trauma, only a cavity and/or scar tissue remain at the injury site. However, even in the most severe injuries, surviving neurons cross the injury zone along the perimeter of the spinal cord. Although these neurons are intact, they are damaged, demyelinated, and nonfunctioning.

Injury Classification
In general, "complete" means no voluntary movement or sensation exists below the injury level. Some feeling or voluntary movement remains in an "incomplete" injury.

A British neurologist, Dr. Frankel, developed a more detailed system of classification of neurological function. The American Spinal Injury Association (ASIA) subsequently refined this scale, which grade injuries from "A" (a complete injury) to "E" (recovery). The International Medical Society of Paraplegia (IMSOP) adopted the refined ASIA Impairment Scale, which in now the international standard for classification of neurological function.

ASIA and IMSOP also have developed standardized classifications for levels of SCI. According to these standards, the neurologic level of injury is defined as "the most caudal (lowest) segment of the spinal cord with nonnal sensory and motor function on both sides of the body." The generic way that level of injury is described is by the classifications "quadriplegic" or tetraplegia" referring to injures of the cervical regions, and "paraplegia," referring to injures of the thoracic, lumbar or sacral regions.

Consequently, the parts of the body innervated by the nerves below the level of injury, don't function the way they used to. In fact, some parts no longer may operate at all.

in addition to affecting a person's ability to move and feel, SCI can affect skin, breathing, bladder, bowel, sexual function, and subconsciously controlled phenomena like blood pressure and sweating.

Part 1 of this series explained that spinal-cord nerves that control movement are called upper motor-neurons (UMNs); nerves that leave the spinal cord to connect with muscles are lower motor-neurons (LMNs). More specifically, axons from nerve-cell bodies in the brain run inside the white matter of the spinal cord to connect with specific nerve-cell bodies (motor neurons) in the gray matter. The axons from these motor neurons then leave the cord to make connection with the muscles in the body. UMNs, which originate in the brain, regulate and control the movement stimulated by LMNs, the nerves that originate in the spinal cord.

In a UMN injury, control by the brain no longer exists because messages from the brain are cut off at the point of SCI. Therefore, LMNs react without limit or inhibition, causing uncontrolled muscle contractions. This is called spacticity, and an UMN injury is said to result in "spastic" paralysis. On the other hand, LMN injuries cause a "flacid" paralysis because muscles of the limbs get cut off from nerves that supply them. This lack of innervation causes muscles to become limp or flaccid. Muscle spasms can either be "alternating" (producing twitching or shaking) or "sustained" (causing rigidity in the limbs). All spacticity represents the activity of uncontrolled reflexes of the LMNs and is the result of the brain's loss of control over the somatic nervous system.

Another example of uncontrolled reflexes is autonomic dysreflexia (AD). This is the lack of the brain's control over the autonomic nervous system. AD is a serious condition that may occur in individuals with SCI at T-6 or above. Before SCI, a stimulus below the level of injury would have signaled pain or discomfort from such things as a full bladder, sunburn, or labor contractions. After SCI, these conditions can cause AD, which if not treated promptly, can lead to stroke and is potentially life threatening.

Pain After SCI
Whether people with SCI experience spasticity or AD depends on the level of injury. In the initial period after injury, pain comes as a result of fractured bones or damaged tissues such as ligaments, muscles, and skin. As injured tissue heals, most of the pain associated with the initial trauma goes away. However, many people develop a chronic pain syndrome that can be severe and further disabling. This may begin at the time of injury but more commonly develops months or many years later.

One condition known to cause pain is "syringomyelia." This condition occurs when a tubular cavity (syrinx) in the central area of the spinal cord gradually expands and fills with fluid. In severe and untreated cases, this cavity can extend up and down several levels of the spinal cord and cause further neurological damage. Oddly enough, when the syrinx is in the cervical region of the cord, it can actually produce a loss of pain awareness in the hands.

Other Effects
Prolonged pressure from the body's weight in the same position, such as when sitting in a wheelchair or lying, presses the bones against the skin. This blocks the blood vessels in that area and cuts off the oxygen flow to the surrounding skin. If pressure continues, the skin begins to die. This death appears as a skin breakdown (ulceration). Since a decrease or absence of sensation follows injury, signals that normally warn people they have been in one position too long do not work and consequently, ulcers may develop. Certain skin changes develop after SCI and seem to predispose to pressure ulcers.

Breathing is a largely involuntary action made possible by three sets of muscles: diaphragm, intercostals, and abdominals. Breathing out (exhilation) is generally a passive action requiring no effort or energy. Consequently, SCI does not affect it much as it does breathing-in (inspiration), which is an active process. Nerves from the C3-5 levels innervate the diaphragm, the main muscle of inspiration. Injury above C4 usually results in people not being able to breathe on their own. Typically, these individuals will rely on ventiators to fill their lungs with air. Injuries at or below C4 spare most of the diaphragm muscle's function, but because the other breathing muscles may be impaired, people may still have some difficulties breathing normally and coughing to clear fluid buildup in the lungs.

People are no longer able to sense the need to empty their bladders or prevent involuntary bladder leakage. This inference in function is known as "neurogenic bladder."

There are two types of neurogenic bladders, depending on the type of injury. A UMN bladder tends to hold smaller volumes of urine than before injury. Just as a limb muscle may have spasms and contract on its own, so can the bladder muscle. The result may be frequent small urination.

An LMN bladder, however, loses its ability to contract and can be easily stretched. Consequently, this type can hold larger than normal volumes of urine. Because the muscle cannot contract, urine eventually leaks out when the bladder reaches capacity, like water spilling out of an overfilled glass. Initially after injury, this system is in a state of shock and unable to function properly. However, within days most of the digestive system, with the exception of the bowel, returns to normal.

The bowel consists of the small intestines, large intestines, and rectum and is the channel through which food passes from the stomach for elimination. Wave-like contractions (peristalsis) automatically move food's waste products through the intestines to the lower bowel, where the waste is stored until a person is ready to have a bowel movement. After SCI, as is the case with the bladder, people no longer are able to sense the need to empty the bowel or prevent involuntary bowel movements.

Erections in men and lubrication in women can be either "psychogenic" caused by thinking, such as a response to an attractive person, or "reflexogenic," which occurs in response to physical stimulation. If an injury is incomplete and T-12 or below, psychogenic erections and lubrication may still occur. However, even if the injury is at a higher level, an injured person can have reflexogenic erections or lubrication. In men, proper ejaculation is a more complex, highly coordinated action than is erection, and it may or not be possible after SCI.

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GLOSSARY
Anatomy
The normal structural makeup of the body, organs and tissues.