Causes and Symptoms
Peripheral nerves, those nerves found outside the brain and spinal cord, function to carry information between the central
nervous system and the other portions of the body. These peripheral nerves consist of a bundle of nerve cells, also called neurons, which are wrapped in a protective sheath of connective tissue. A nerve consisting only of neurons that carry impulses toward the central nervous system is termed a sensory nerve. Nerves that contain only neurons that carry information from the central nervous system to the periphery of the body are called motor nerves, because they usually carry information telling a particular body part to move. Most nerves, however, consist of both sensory and motor neurons and are thus called mixed nerves.
The nerves of the peripheral nervous system can be divided into two different categories, cranial nerves and spinal nerves. Cranial nerves come directly out of the brain and supply information to and about the head and neck. There are twelve pairs of cranial nerves. Spinal nerves come directly out of the spinal cord and provide information to and from the arms, legs, chest, gut, and all other parts of the body not supplied by cranial nerves. In humans, there are usually thirty-one pairs of spinal nerves. Both cranial and spinal nerves can be affected by neuropathies.
Neurons (nerve cells) are highly specialized structures designed to convey information from one part of the body to another. This information is passed along in the form of electrical impulses. Neurons consist of three main parts: a cell body, which contains the nucleus and is the control center of the entire neuron; dendrites, which are slender, fingerlike extensions that convey electrical impulses toward the cell body; and an axon, which is a slender extension that carries electrical impulses away from the cell body.
Most of the dendrites and axons of peripheral nerves are covered with a white, fatty substance called myelin. Myelin acts to protect and insulate axons and dendrites. By insulating the axons and dendrites, myelin actually speeds up the rate at which an electrical impulse can be carried along these two structures. Damage to the myelin sheath surrounding axons and dendrites can greatly impair the function of a nerve.
Often, when a nerve becomes pinched, damaged, or inflamed, the result is excessive electrical stimulation of the nerve, which will be registered as pain. The pain associated with the damaged nerve is referred to as neuralgia. One of the most common forms of neuralgia occurs upon the striking of the “funny bone.” This area around the elbow is the spot where the ulnar nerve is easily accessible. The ulnar nerve runs from just under the shoulder to the little finger, and when the ulnar nerve is struck near the elbow it is compressed or pinched, leading to pain or a tingling sensation from the elbow down to the little finger.
Compression of nerves for prolonged periods can also lead to neuralgia. The most common example of compression neuralgia is
carpal tunnel syndrome. In this syndrome, the median nerve becomes compressed at the wrist, usually as a result of an inflammation of the sheaths of the tendons located on either side of the median nerve. The swelling of these tendon sheaths causes the compression of the median nerve, which may initially lead to neuralgia. As this condition progresses, it can lead to a loss of feeling along the palm side of the thumb and the index and middle fingers. This condition is most common in people who use their fingers for rigorous work over prolonged periods of time, such as typing.
Sciatica
is another common form of neuralgia, in which pain is associated with the sciatic nerve. The sciatic nerve is the longest nerve in the human body, running from the pelvis down the back of the thigh to the lower leg and then down to the soles of the feet. The symptoms of sciatica include sharp pains along the sciatic nerve. The pain may involve the buttocks, hip, back, posterior thigh, leg, ankle, and foot. Sciatica can result from many different causes, but the most common cause is from a ruptured intervertebral disk that puts pressure on, or causes a pinching of, the sciatic nerve.
Neuritis is defined as the inflammation of a nerve or of the connective tissue that surrounds the nerve. Many diseases can lead to the inflammation of peripheral nerves. Perhaps the most common disease leading to neuritis is shingles. Shingles are caused by the occurrence of
herpes zoster, a virus that attacks the dorsal root ganglion, a place near the spinal cord that houses the cell bodies of neurons. A rash, swelling, and pain progress from the dorsal root ganglion along one or more spinal nerves. The rash along the course of the spinal nerves usually disappears within a few days to a couple of weeks, but the pain along this path can persist for months.
Leprosy
is another disease that leads to the inflammation of nerves. Leprosy is a bacterial disease caused by Mycobacterium leprae. These bacteria invade the cells that make up the myelin sheath that surrounds the nerve. The result is a noticeable swelling of the nerves affected, primarily those that are close to the skin. Many times, this swelling will lead to neuralgia and, if left untreated, to muscle wasting.
“Neuropathy” is a general term used to describe a decrease in the function of peripheral nerves, which may be caused by many factors. The first signs of a neuropathy are usually a tingling, prickling, or burning sensation in some part of the body. This is followed by a sensory loss; the inability to perceive touch, heat, cold, or pressure; and a weakness in the muscles in the area affected. This weakness may eventually lead to a loss of muscle termed muscular atrophy. Neuropathies may affect sensory neurons, motor neurons, or both and can occur in both spinal and cranial nerves. A neuropathy may develop over a few days or many years. Neuropathies can be caused by a number of factors, including toxic exposure to solvents, pesticides, or heavy metals; viral illness; certain medications; metabolic disturbances such as diabetes mellitus; excessive use of alcohol; vitamin deficiency; loss of blood to the nerve; or cold exposure.
Neuropathies can be categorized based on the number of nerves that they affect, whether it is the myelin sheath surrounding the axon that is affected or the axon itself is destroyed, and the amount of time before symptoms of the neuropathy occur and progress. Thus, neuropathies are usually broken down into four different types: polyneuropathy, in which more than one nerve is affected; mononeuropathy, in which only one nerve is affected; axonal neuropathy, in which the axon is affected and degenerates; and demyelinating neuropathy, in which the myelin sheath surrounding the nerve is destroyed. Each of the four categories can be further subdivided based on the time frame in which the symptoms occur. Those neuropathies that appear over days are termed acute, those that appear over weeks are termed subacute, and those neuropathies whose symptoms slowly appear over months or years are termed chronic.
Another type of neuropathy is autonomic neuropathy, a condition that affects the nerves of the autonomic nervous system. These are the peripheral nerves that go to the sweat glands, small blood vessels, gastrointestinal tract, urinary bladder, and genital organs. These nerves are referred to as autonomic since they automatically provide information between these organs and the central nervous system without the individual’s conscious effort. The symptoms associated with this form of neuropathy include loss of control over urination, difficulty swallowing food, occasional stomach upset, diarrhea, impotence, and excessive sweating.
The most common cause of neuropathies in the Western world is diabetes mellitus, while leprosy is the more common cause of neuropathies elsewhere. It is estimated that at least 70 percent of all diabetics have some degree of peripheral neuropathy. In most of these cases, the neuropathy is very slight and causes the patient no noticeable symptoms. In about 10 percent of those diabetics with a neuropathy, however, the symptoms will be serious.
Treatment and Therapy
Often, the first notable feature of a neuropathy that prompts a patient to seek medical attention is a tingling, prickling, or burning sensation in a particular area of the body. The occurrence of these sensations without any external stimuli is termed paresthesias. Since diabetes is the most common cause of neuropathy in the Western world, the sensations experienced by a diabetic patient can serve as an example of the symptoms that are associated with common neuropathies. These patients may first notice the above-mentioned symptoms in the balls of the feet or tips of the toes. As the neuropathy progresses, patients may lose feeling in their feet and experience a weakness in the muscles of the feet, leading to a difficulty in flexing the toes upward. This makes walking difficult, and many patients remark that they feel as if they are walking on stumps. This condition may lead to difficulties in maintaining balance. The neuropathy will begin to affect the legs above the ankles and then travel up the legs, eventually leading to atrophy of the leg muscles.
As the neuropathy worsens, it is critical that patients seek help because they can no longer feel pain. This situation is dangerous, as the patient may no longer sense the pain that can be caused by injuries from sharp objects or even a pebble in the shoe. If unnoticed, these injuries lead to ulcers that can easily become infected.
The first step in treating a neuropathy is to diagnose the type of neuropathy affecting the patient. A patient’s medical history is taken to identify any recent viral or bacterial illness, any exposure to toxic substances such as pesticides or heavy metals, the patient’s habits concerning alcohol use, or any other illness or injury that might have brought about a possible neuropathy. Next, a physical exam will be performed to determine if the patient’s sensations regarding touch, pain, pressure, or temperature have been affected, as well as the ability of the patient to react to these stimuli. The physician may also feel the affected area to determine if the nerve or nerves are inflamed and enlarged.
If the patient’s history and the physical examination point toward a neuropathy, further testing using electrodiagnostic tests will be performed. These tests measure the speed at which an electrical impulse travels down a nerve, which is called the nerve conduction velocity. Motor nerve conduction velocity is measured by stimulating the nerve with electrodes placed on the skin above the nerve. Stimulation of the nerve is typically done at two different sites. Using the arm as an example, one electrode would be placed on the inside of the arm at the elbow. The time that it takes for the impulse to reach a recording electrode on the thumb would be measured. A second site at the wrist would be tested to determine the time that it takes for the electrical impulse to reach the recording electrode on the thumb. The time that it took for the impulse to travel from the wrist to thumb would be subtracted from the amount of time that it took for the impulse to go from the inside of the arm at the elbow to the thumb. The resulting value would then be divided by the distance between the site at the wrist and the site at the elbow, giving a nerve conduction velocity value measured in meters per second.
The typical nerve conduction velocity for the motor and sensory peripheral nerves of adults is approximately 40 to 80 meters per second. If a neuropathy is the result of demyelination, the affected nerve will have a much slower nerve conduction velocity. If the neuropathy is a result of axonal damage, then the nerve conduction velocity is usually not altered from normal. Thus, electrodiagnostic testing helps to determine if the neuropathy is a demyelination neuropathy or an axonal neuropathy. Such a determination is important because the different neuropathies are caused by different diseases and are thus treated differently. Electrodiagnostic tests can also provide useful information regarding the site of the neuropathy and whether the neuropathy is affecting sensory neurons, motor neurons, or both.
The last diagnostic test to be performed, if other methods are inconclusive, is a biopsy of the affected nerve. This procedure involves the surgical removal of a portion of the afflicted nerve. The small sample of nerve will be placed under a microscope and examined for specific changes in the nerve. The nerve sample may also be subjected to various biochemical studies to determine if metabolic disturbances have occurred. Nerve biopsies are rarely performed, however, and are usually not recommended.
Once the type of neuropathy afflicting the patient has been determined, treatment can begin. Unlike axons in the central nervous system, axons in the peripheral nervous system are capable of regenerating under certain conditions. If the neuropathy is the result of exposure to toxic substances such as pesticides or heavy metals, removal of the patient from the exposure to such substances is the simple cure. If the neuropathy is the result of viral or bacterial infections, the treatment and recovery from these infections will also usually correct the neuropathy. The same principle applies to neuropathies caused by metabolic diseases and vitamin deficiencies: corrections of these problems will lead to the correction of the neuropathy.
Should the neuropathy be of the mononeuropathy type and caused by trauma, anti-inflammatory drugs such as corticosteroids may be used or surgery may be performed to repair the nerve. If the mononeuropathy is caused by compression, as in carpal tunnel syndrome, surgery may also be needed to increase the space around the nerve and thus relieve the compression. Surgery is also used to remove tumors on the nerve that might be causing a neuropathy.
The time required to recover from a neuropathy is dependent on the severity and type of neuropathy. Recovery from demyelination is typically quicker than recovery from axonal neuropathies. If only the myelin surrounding the axon is damaged, and not the axon itself, the axon can quickly replace the damaged myelin. Demyelinating neuropathies usually require three to four weeks for recovery. In contrast, recovery from axonal neuropathies may take from two months to more than a year, depending on the severity of the neuropathy.
Perspective and Prospects
Perhaps the earliest documentation of peripheral neuropathies occurred during biblical times, when the term “leprosy” was coined. It is likely, however, that this term was employed rather loosely, as it was used to describe not only the disease leprosy but also a number of skin diseases not involving neuropathies, such as psoriasis.
The actual diagnosis of neuropathies and their subsequent categorization did not occur until the advent of electrical diagnostic testing. The earliest use of electricity to study nerve function occurred in 1876 when German neurologist Wilhelm Erb noted that the electrical stimulation of a damaged peripheral nerve below the site of injury resulted in muscular contraction. In contrast, electrical stimulation at a site above the injured nerve brought about no activity in the muscle. Erb concluded that the injury blocked the flow of electrical impulses down the nerve.
The actual use of electrical diagnostic testing did not take place until the late 1940s, when electrodes and an oscilloscope, an instrument that measures electrical activity, were used to measure the rate at which an electrical impulse could travel down a nerve. This discovery allowed the testing of nerve function and would become useful in the discrimination between axonal and demyelinating neuropathies. During this period, the invention of the electron microscope and the discovery of better nerve-staining techniques enhanced the ability of scientists to study the physiological and anatomical changes that occur in nerves with the onset of neuropathies.
Neuropathies received considerable attention in 1976 when approximately five hundred cases of the neuropathy called
Guillain-Barré syndrome occurred in the United States following a national vaccination program for swine flu. The reason that the swine flu vaccine caused this neuropathy has never been discovered, but this syndrome often occurs after an upper respiratory tract or gastrointestinal infection.
Those suffering from neuropathies that result from exposure to toxic substances, viral or bacterial infections, or metabolic diseases have a good prognosis of recovery if the underlying cause of the neuropathy is treated. The prognosis of recovery is not as good for those who suffer neuropathies as a result of hereditary diseases. Advances made in genetic research and continued research in gene therapy may someday greatly increase the prognosis of recovery for those suffering from hereditary neuropathies.
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