What is paralysis?

Quick Answer
Pronounced weakness or the inability to produce movement in a part of the body resulting from a variety of causes.
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Nervous System Functions

To understand the causes of paralysis—weakness or the inability to move a part of the body—it is necessary to review briefly the motor nervous system and muscles. Following an action from initiation to completion through the motor nervous system may clarify this process. One may begin, for example, with a voluntary movement. An alarm clock rings early one morning. A sleeper hears the noise and decides to hit the snooze button. This decision is made in the cerebral cortex, which sends impulses to the nerves in the arm via the spinal cord.

The actual microscopic actions that result in a nerve impulse traveling from the motor cortex all the way to individual muscles will be briefly reviewed. An individual nerve cell, or neuron, comprises three parts: the dendrites, the cell body, and the axon. The cell body conducts the metabolism for the cell and otherwise keeps things in running order, but it has little direct involvement with the transmission of nerve impulses.

Dendrites are similar in appearance to the roots of plants. They are numerous and relatively short. Their function is to pick up impulses received either from sensory organs or from other cells. They do this when the receptors on their surface become activated by certain chemical signals released by neighboring nerve cells. Once these receptors are activated, they initiate a process known as depolarization.

In the most basic description, depolarization refers to the generation of a minute electrical charge on nerve cell membranes. It occurs through the motion of charged molecules, or ions, across the cell membrane. The specific ions involved include potassium, sodium, and calcium. Depolarization progresses down the length of the nerve cell. It passes through the dendrite to the cell body of the nerve cell and then to the axon. The axon is long and thin, some axons reaching lengths of three or more feet. Depending on its type and function, the axon may split into small filaments that go to several nerve or muscle cells, or it may remain single.

The sending axons do not touch the receiving cells when passing an impulse. Instead, they come close to the receiving cell’s dendrites but leave a small gap (the synapse). Once a nerve impulse reaches the end of an axon, the axon releases chemical compounds called neurotransmitters.

Synthesized by the nerve cell, the neurotransmitter is collected and stored in small packets resting at the end of the axon. In response to depolarization, the small packets of neurotransmitter are released into the synapse, and the original electrical nerve impulse is converted into a chemical impulse. When the neurotransmitter is released, it diffuses across the gap and contacts specific receptors on the dendrite of the receiving nerve cell. The receiving nerve cell’s receptors then depolarize the receiving nerve cell, converting the chemical impulse back into an electrical one.

The receiving nerve cell is forced to continue depolarizing until the neurotransmitter is no longer in contact with the receptor, or until the nerve cell itself becomes exhausted and cannot depolarize again. To allow the receiving nerve cell to stop firing and to prepare itself for another signal, the neurotransmitter must be removed rather quickly from the receptor. This can be done by the axon of the sending cell, which takes it back in, or by enzymes located within the synapse that actually destroy the neurotransmitter. The most common neurotransmitter is acetylcholine, and the most frequently encountered form of enzyme that destroys neurotransmitters is called acetylcholinesterase.

The transmission of the nerve impulses signaling the hand to press the alarm clock’s snooze button involves passing the impulses through several nerves. The impulses form synapses on nerve cells in the spinal cord before those cells pass the impulse down the spinal cord toward the arm to cause the desired action.

The spinal cord is protected inside the vertebral column, a hollow column of bone. This column is made up of a stack of vertebrae supported by solid bone in the front and a hollow ring of thinner bone in the back through which the spinal cord runs. The vertebrae are anchored to one another by bony connections; the facets and vertebral spines; fibrous ligaments to the front, back, and side; and the intervertebral disks. Disks are made up of soft, gelatinous material surrounded by fibrous tissue. The disks and joints in the vertebral column allow the spine to flex and turn, while the bony column surrounding the spinal cord provides protection.

When the nerve leaves the spinal cord, it travels in what is called the motor ramus, or “root.” The ramus passes through an opening in the vertebral column called a foramen. While passing through the foramen, the ramus passes near the intervertebral disk. The motor nerve fibers (and consequently the nerve impulses sent out to turn off the alarm clock) in the motor ramus join with the sensory nerve fibers in the sensory ramus just outside the vertebral column, and together they form the spinal nerves. These spinal nerves regroup to form peripheral nerves.

A peripheral nerve is the part of the nervous system that finally contacts the muscles that turn off the alarm clock. Peripheral nerves carry both sensory and motor information in the same nerve. They are the only locations in which sensory and motor nerve fibers are so completely joined. Peripheral nerves must sometimes pass through relatively tight or exposed locations. An example of an exposed nerve is the “funny bone,” the ulnar nerve, which causes an unpleasant sensation when struck. Nerves that pass through tight spaces may suffer entrapment syndromes. A common nerve entrapment syndrome is carpal tunnel syndrome, in which the median nerve is squeezed in the fibrous band around the wrist.

Finally, the arm muscles themselves become involved in the process of turning off the alarm. The muscles are made up of numerous muscle fibers, and each muscle fiber is made up of numerous muscle cells. Inside each muscle cell are two active protein filaments, actin and myosin, which pull together when activated, causing the muscle cell to shorten. When the majority of muscle cells “fire” at once, the whole muscle contracts. The signal from nerve to muscle cell is transmitted across a synapse. The snooze button is pushed, and the alarm ends. Finally, the signals to the arm end, and the filaments slide back to their initial positions, relaxing the muscle cells.

For actin and myosin to move well, there must be adequate blood flow and adequate concentrations of substances such as oxygen, glucose, potassium, sodium, and calcium. Many other substances are needed indirectly to keep muscle cells functioning optimally, including thyroid hormone and cortisone.

Types of Paralysis

True paralysis is the inability to produce movement of a part of the body. Paralysis may result from problems at many locations in the body, such as the motor cortex of the brain, the spinal cord, the nerves in the arms or legs, the blood, or the muscle cells themselves. Doctors must determine the specific cause of paralysis or weakness since the treatment of each disease is different. The first task is to determine whether the weakness or paralysis is caused by a disease of the nervous system, the muscle cells, or one of the substances that interferes with nerve conduction or muscular contraction. Some characteristics of specific problems are helpful in this diagnosis.

Disease of the nervous system is most often associated with complete paralysis. Diseases affecting the muscle cells or the factors controlling them are usually associated with a partial rather than complete paralysis—there is weakness rather than a lack of movement. When weakness is severe, however, it may be mistaken for complete paralysis. The fact that diseases of the nervous system cause paralysis of one side of the body (hemiplegia) or one part of the body is helpful in diagnosis. Paralyzing conditions that affect muscle cells tend to result in whole-body weakness, although some muscles may be more severely affected than others. Another aid in differentiation is that neurologic diseases are almost always associated with some degree of impairment in sensation, while muscular causes are never associated with sensory loss.

Damage to the central nervous system and to the peripheral nervous system can be differentiated by features of the dysfunction. Central nervous system problems affect either half of the body or one region of the body, while peripheral damage affects only the muscles controlled by the damaged nerve or nerves. Central nervous system damage leaves pronounced reflexes, while damage to peripheral nerves results in an affected area without any reflexes. There is some muscle wasting with either type of paralysis, but the wasting seen after a peripheral nerve disease appears more quickly and more severely. When central nervous system damage occurs, the muscles involved are generally tight (spastic paralysis). Conversely, in patients with peripheral nervous system damage, muscles are usually loose. Through attention to these differentiating features, the source of paralysis can usually be discovered.

In adults, the most common cause of paralysis is stroke. A stroke results from interruption of the blood supply to a part of the brain. After being cut off from blood flow, the affected area dies. Brain tumors may also cause paralysis. Unlike strokes, however, which cause most of their damage as soon as the blood supply is interrupted, the damage produced by tumors tends to increase slowly as the tumor grows. An interesting feature of brain tumors is that they are surrounded by an area of swelling called edema. The edema, not the tumor itself, causes most of the neurologic changes. This distinction is important because edema is usually responsive to medical treatment.

Subdural hematomas are collections of blood that are outside the brain but inside the skull. They are seen most frequently in older people and alcoholics. To form a subdural hematoma, a small blood vessel becomes injured in such a way that blood slowly oozes from it, accumulates, and clots. Interestingly, the trauma may be so slight as to not be remembered by the patient. This clot may cause pressure on the motor cortex that results in paralysis. Generally, subdural hematomas are slow in onset.

Multiple sclerosis, a disease affecting the nervous system, causes scattered, multiple small areas of destruction virtually anywhere in the brain or spinal cord. The extent of paralysis depends on the sites and extent of the damaged areas. Patients often have impairments in vision, speaking, sensation, and coordination.

If the spinal cord is the cause, the extent and location of the paralysis and numbness depend on the size, location, and level of the lesion. Spinal cord paralysis may result from trauma, tumors, interruption of blood flow, blood clots, or infections such as abscesses. These disorders are similar, except for location, in most respects to the previously described conditions in the brain. One of the conditions, however—trauma of the spinal cord—is very different from trauma of the brain.

Significant trauma may result in fracture of the vertebral column. Spinal fractures may be classified as stable or unstable. Unstable fractures, unlike stable ones, are often associated with paralysis because unstable fractures allow subluxation to occur. Subluxation is a dislocation of the vertebral column that compresses the spinal cord. If it occurs in the neck, quadriplegia (paralysis of all four limbs) results. If it occurs lower down the spine, paraplegia (paralysis of both lower limbs) is seen. On occasion, through inadvertent or excessive movement, overenthusiastic rescuers cause permanent paralysis by converting a nonsubluxated fracture to a subluxated one during rescue attempts.

Another unique type of spinal cord trauma is the rupture of an intervertebral disk, which allows the gelatinous material to press on the spinal cord or on the rami leaving the spinal cord. In addition to causing severe pain, an intervertebral disk rupture may cause weakness or paralysis. It usually affects only one or two rami and spares the spinal cord itself. Trauma to the spinal cord is particularly dangerous to individuals with conditions that weaken the bony spine. These conditions include osteoporosis of all types and rheumatoid arthritis.

Peripheral nerve damage can occur through a number of conditions that may result in nerve degeneration, including diabetes mellitus, vitamin deficiencies, use or abuse of certain medications, and poisoning by toxins such as alcohol and lead. Sometimes, a temporary nerve degeneration called Guillain-Barré syndrome follows upper respiratory tract infections and may be quite serious if the respiratory muscles are affected. A peripheral nerves may also be damaged by direct trauma, or by pressure as it passes through a narrow compartment, as happens in carpal tunnel syndrome. Peripheral nerve conditions are accompanied by numbness, tingling, and weakness or paralysis of only the area served by the affected nerve.

Paralysis may complicate diseases affecting muscles, although in these cases the patients usually demonstrate weakness rather than paralysis. In muscular diseases, the paralysis (or weakness) tends to affect all the muscles of the body, although some may be more affected than others. The most frequent causes of paralysis in children are inherited diseases such as muscular dystrophy. In adults, muscular diseases are mainly attributable to hormonal imbalances caused by problems such as an underactive thyroid gland or an overactive adrenal gland.

Paralysis may result if the concentration of certain substances in the body is significantly altered, although weakness is a much more common occurrence. The concentration of potassium, sodium, calcium, glucose, and specific hormones may dramatically affect muscle strength. A specific, though uncommon, disease of this type is periodic hypokalemic paralysis, a condition that runs in families. In this disorder, the amount of potassium in the blood can be dramatically reduced for short periods of time, resulting in brief periods of severe weakness or paralysis. These episodes rarely have serious consequences.

Weakness or paralysis may result if the body is unable to produce adequate amounts of acetylcholine, or if this neurotransmitter is destroyed in the synapse before it can pass on its message. Myasthenia gravis is the most common example of this type of disorder. Affected patients initially have adequate strength, but they develop weakness and paralysis in muscles during periods of use because acetylcholine stores become depleted. The weakness in this condition tends to become more prominent as the day wears on. The most frequently used muscles are the most affected. This type of paralysis temporarily improves after rest or medication.

Another unique type of paralysis, called Todd’s paralysis, may follow a generalized epileptic seizure. It happens only when the seizure has been so extensive and prolonged that the nerve cells in the brain are literally exhausted and no longer able to initiate the nerve impulses needed to generate movements. This paralysis is temporary.

Paralysis may be caused by a variety of psychiatric disorders, including hysteria, catatonic psychosis, conversion disorder, factitious disorder, and somatization disorder. In psychological paralysis, the patient’s inability to move parts of the body is psychological. This paralysis is particularly common during periods of high stress such as combat. Psychological paralysis should be differentiated from malingering. In a psychological paralysis, the patients genuinely believe that they are paralyzed, whereas malingerers, though they deny it, know that they are not paralyzed. Malingering is usually seen when some benefit resulting from the paralysis is anticipated.

Perspective and Prospects

Once a nerve cell has been destroyed, it cannot be repaired. This is the main reason that the outlook is quite poor when most types of paralysis occur. The only thing that doctors can do is to try to limit the extent of the paralysis. Improvements can be made only by training the neighboring cells to take over the functions of the lost cells.

After suffering a paralyzing event, a patient begins rehabilitation using a number of exercises. These activities are usually carried out with the help of physical therapists, occupational therapists, or kinesiotherapists. Unfortunately, progress is rather limited, and most patients are not able to resume their old lifestyle after suffering extensive paralysis.

It is very important to take seriously paralysis or weakness that is localized to a single muscle or single group of muscles. Doctors need to find out the cause of this weakness as soon as possible and take steps to minimize or reverse the damage prior to complete destruction of the nerve cells. Initial and subsequent stroke prevention, tumor treatments, hematoma evacuation, spinal alignment and stabilization, intervertebral disk surgery, toxin removal, hormonal manipulation, and ion correction are all currently available methods of dealing with paralysis.

Because of the poor prognosis for overcoming paralysis, research has focused on understanding how nerve cells grow. Some lower animals possess an ability to regenerate nerve cells when they are damaged. It is well known that a lobster which has lost one of its claws can regenerate that claw, as well as the nerves that control the claw’s functioning. A lower animal nerve growth factor has been identified and is being examined by a number of researchers. It is likely that drugs which could aid regeneration of damaged nerve cells in higher animals will be discovered. Once available, these drugs will improve the outlook for recovery of patients with paralysis. These medications may also help with other conditions associated with nerve cell damage, such as Alzheimer’s disease and Parkinson’s disease.

Progress in medical treatment and an increased health awareness by the public will reduce the incidence of diseases such as diabetes mellitus and the intake of toxins, such as alcohol, that may cause paralysis. Seat belt laws and motorcycle helmet laws may reduce the incidence of paralysis by reducing the severity of injuries in motor vehicle accidents.

Progress in neurosurgery should also improve a patient’s hope for recovery in trauma cases. Although dead nerve cells cannot regenerate, cut nerve filaments may be able to regenerate and reattach, which is why surgeons have been able to reattach severed limbs. With progressively finer techniques and equipment, the success rate should improve further. Future progress in neurosurgery may also benefit patients whose paralysis is attributable to causes other than trauma. Progress in genetic research may allow scientists to isolate the genes responsible for diseases causing paralysis. Diseases such as myasthenia gravis and muscular dystrophy could respond to treatment if genetic therapies are found.

Bibliography

Bear, Mark F., Barry W. Connors, and Michael A. Paradiso. Neuroscience: Exploring the Brain. 3rd ed. Philadelphia: Lippincott, 2009. Print.

Christopher and Dana Reeve Foundation, Paralysis Resource Center. http://www.christopherreeve.org.

Cure Paralysis Now. http://www.cureparalysisnow.org.

Goroll, Allan H., and Albert G. Mulley, eds. Primary Care Medicine. 5th ed. Philadelphia: Lippincott, 2006. Print.

Kandel, Eric R., James H. Schwartz, and Thomas M. Jessell. Principles of Neural Science. 5th ed. New York: McGraw, 2013. Print.

Lukas, Rimas. "Quadriplegia and Paraplegia." Health Library, 15 Mar. 2013. Web.

MedlinePlus. "Paralysis." MedlinePlus, 9 Aug. 2013. Web.

Nicholls, John G., A. Robert Martin, and Bruce G. Wallace. From Neuron to Brain. 5th ed. Sunderland: Sinauer, 2012. Print.

"Progress for the Paralyzed." MedlinePlus Magazine 8.1 (2013): 10. Print.

Tortora, Gerard J. Principles of Anatomy and Physiology. 14th ed. [S.I.]: Wiley, 2013. Print.

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