| Peripheral Neuropathy and Disability Benefits |
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If you (or your loved one) suffer from disabling Peripheral Neuropathy or
other Nerve Disorder and can no longer work a full time work week, I would be
happy to help you obtain your rightful Disability Benefits. You may be eligible for
Social Security Disability benefits, even if you will eventually recover.
Start by filling out the FREE online Social Security Disability Claim Evaluation
Form (see Tab, on Left Hand Navigation), calling me at 201-317-0610 or emailing
SsiHelp@ptd.net or sojlaw@ptd.net.
other Nerve Disorder and can no longer work a full time work week, I would be
happy to help you obtain your rightful Disability Benefits. You may be eligible for
Social Security Disability benefits, even if you will eventually recover.
Start by filling out the FREE online Social Security Disability Claim Evaluation
Form (see Tab, on Left Hand Navigation), calling me at 201-317-0610 or emailing
SsiHelp@ptd.net or sojlaw@ptd.net.
| What is Peripheral Neuropathy? |
| MySsiCase.com |
| Brought to you by the Social Security Disability Law Office of Stephanie O. Joy, Esq. Helping clients, one-on-one, in all 50 U.S. States Ph: 201-317-0610 Email: SsiHelp@ptd.net Fax: 570-424-2384 |
Peripheral neuropathy describes damage to the peripheral nervous system, the
vast communications network that transmits information from the brain and spinal
cord (the central nervous system) to every other part of the body. Peripheral
nerves also send sensory information back to the brain and spinal cord, such as a
message that the feet are cold or a finger is burned. Damage to the peripheral
nervous system interferes with these vital connections. Like static on a telephone
line, peripheral neuropathy distorts and sometimes interrupts messages between
the brain and the rest of the body.
Because every peripheral nerve has a highly specialized function in a specific part
of the body, a wide array of symptoms can occur when nerves are damaged.
Some people may experience temporary numbness, tingling, and pricking
sensations (paresthesia), sensitivity to touch, or muscle weakness. Others may
suffer more extreme symptoms, including burning pain (especially at night),
muscle wasting, paralysis, or organ or gland dysfunction. People may become
unable to digest food easily, maintain safe levels of blood pressure, sweat
normally, or experience normal sexual function. In the most extreme cases,
breathing may become difficult or organ failure may occur.
Some forms of neuropathy involve damage to only one nerve and are called
mononeuropathies. More often though, multiple nerves affecting all limbs are
affected-called polyneuropathy. Occasionally, two or more isolated nerves in
separate areas of the body are affected-called mononeuritis multiplex.
In acute neuropathies, such as Guillain-Barré syndrome, symptoms appear
suddenly, progress rapidly, and resolve slowly as damaged nerves heal. In
chronic forms, symptoms begin subtly and progress slowly. Some people may
have periods of relief followed by relapse. Others may reach a plateau stage
where symptoms stay the same for many months or years. Some chronic
neuropathies worsen over time, but very few forms prove fatal unless complicated
by other diseases. Occasionally the neuropathy is a symptom of another disorder.
In the most common forms of polyneuropathy, the nerve fibers (individual cells
that make up the nerve) most distant from the brain and the spinal cord
malfunction first. Pain and other symptoms often appear symmetrically, for
example, in both feet followed by a gradual progression up both legs. Next, the
fingers, hands, and arms may become affected, and symptoms can progress into
the central part of the body. Many people with diabetic neuropathy experience this
pattern of ascending nerve damage.
How are the peripheral neuropathies classified?
More than 100 types of peripheral neuropathy have been identified, each with its
own characteristic set of symptoms, pattern of development, and prognosis.
Impaired function and symptoms depend on the type of nerves-motor, sensory, or
autonomic-that are damaged. Motor nerves control movements of all muscles
under conscious control, such as those used for walking, grasping things, or
talking. Sensory nerves transmit information about sensory experiences, such as
the feeling of a light touch or the pain resulting from a cut. Autonomic nerves
regulate biological activities that people do not control consciously, such as
breathing, digesting food, and heart and gland functions. Although some
neuropathies may affect all three types of nerves, others primarily affect one or
two types. Therefore, doctors may use terms such as predominantly motor
neuropathy, predominantly sensory neuropathy, sensory-motor neuropathy, or
autonomic neuropathy to describe a patient's condition.
What are the symptoms of peripheral nerve damage?
Symptoms are related to the type of affected nerve and may be seen over a
period of days, weeks, or years. Muscle weakness is the most common symptom
of motor nerve damage. Other symptoms may include painful cramps and
fasciculations (uncontrolled muscle twitching visible under the skin), muscle loss,
bone degeneration, and changes in the skin, hair, and nails. These more general
degenerative changes also can result from sensory or autonomic nerve fiber loss.
Sensory nerve damage causes a more complex range of symptoms because
sensory nerves have a wider, more highly specialized range of functions. Larger
sensory fibers enclosed in myelin (a fatty protein that coats and insulates many
nerves) register vibration, light touch, and position sense. Damage to large
sensory fibers lessens the ability to feel vibrations and touch, resulting in a
general sense of numbness, especially in the hands and feet. People may feel as
if they are wearing gloves and stockings even when they are not. Many patients
cannot recognize by touch alone the shapes of small objects or distinguish
between different shapes. This damage to sensory fibers may contribute to the
loss of reflexes (as can motor nerve damage). Loss of position sense often makes
people unable to coordinate complex movements like walking or fastening
buttons, or to maintain their balance when their eyes are shut. Neuropathic pain is
difficult to control and can seriously affect emotional well-being and overall quality
of life. Neuropathic pain is often worse at night, seriously disrupting sleep and
adding to the emotional burden of sensory nerve damage.
Smaller sensory fibers without myelin sheaths transmit pain and temperature
sensations. Damage to these fibers can interfere with the ability to feel pain or
changes in temperature. People may fail to sense that they have been injured
from a cut or that a wound is becoming infected. Others may not detect pains that
warn of impending heart attack or other acute conditions. (Loss of pain sensation
is a particularly serious problem for people with diabetes, contributing to the high
rate of lower limb amputations among this population.) Pain receptors in the skin
can also become oversensitized, so that people may feel severe pain (allodynia)
from stimuli that are normally painless (for example, some may experience pain
from bed sheets draped lightly over the body).
Symptoms of autonomic nerve damage are diverse and depend upon which
organs or glands are affected. Autonomic nerve dysfunction can become life
threatening and may require emergency medical care in cases when breathing
becomes impaired or when the heart begins beating irregularly. Common
symptoms of autonomic nerve damage include an inability to sweat normally,
which may lead to heat intolerance; a loss of bladder control, which may cause
infection or incontinence; and an inability to control muscles that expand or
contract blood vessels to maintain safe blood pressure levels. A loss of control
over blood pressure can cause dizziness, lightheadedness, or even fainting when
a person moves suddenly from a seated to a standing position (a condition known
as postural or orthostatic hypotension).
Gastrointestinal symptoms frequently accompany autonomic neuropathy. Nerves
controlling intestinal muscle contractions often malfunction, leading to diarrhea,
constipation, or incontinence. Many people also have problems eating or
swallowing if certain autonomic nerves are affected.
What causes peripheral neuropathy?
Peripheral neuropathy may be either inherited or acquired. Causes of acquired
peripheral neuropathy include physical injury (trauma) to a nerve, tumors, toxins,
autoimmune responses, nutritional deficiencies, alcoholism, and vascular and
metabolic disorders. Acquired peripheral neuropathies are grouped into three
broad categories: those caused by systemic disease, those caused by trauma
from external agents, and those caused by infections or autoimmune disorders
affecting nerve tissue. One example of an acquired peripheral neuropathy is
trigeminal neuralgia (also known as tic douloureux), in which damage to the
trigeminal nerve (the large nerve of the head and face) causes episodic attacks of
excruciating, lightning-like pain on one side of the face. In some cases, the cause
is an earlier viral infection, pressure on the nerve from a tumor or swollen blood
vessel, or, infrequently, multiple sclerosis. In many cases, however, a specific
cause cannot be identified. Doctors usually refer to neuropathies with no known
cause as idiopathic neuropathies.
Physical injury (trauma) is the most common cause of injury to a nerve. Injury or
sudden trauma, such as from automobile accidents, falls, and sports-related
activities, can cause nerves to be partially or completely severed, crushed,
compressed, or stretched, sometimes so forcefully that they are partially or
completely detached from the spinal cord. Less dramatic traumas also can cause
serious nerve damage. Broken or dislocated bones can exert damaging pressure
on neighboring nerves, and slipped disks between vertebrae can compress nerve
fibers where they emerge from the spinal cord.
Systemic diseases — disorders that affect the entire body —often cause
peripheral neuropathy. These disorders may include: Metabolic and endocrine
disorders. Nerve tissues are highly vulnerable to damage from diseases that
impair the body's ability to transform nutrients into energy, process waste
products, or manufacture the substances that make up living tissue. Diabetes
mellitus, characterized by chronically high blood glucose levels, is a leading cause
of peripheral neuropathy in the United States. About 60 percent to 70 percent of
people with diabetes have mild to severe forms of nervous system damage.
Kidney disorders can lead to abnormally high amounts of toxic substances in the
blood that can severely damage nerve tissue. A majority of patients who require
dialysis because of kidney failure develop polyneuropathy. Some liver diseases
also lead to neuropathies as a result of chemical imbalances.
Hormonal imbalances can disturb normal metabolic processes and cause
neuropathies. For example, an underproduction of thyroid hormones slows
metabolism, leading to fluid retention and swollen tissues that can exert pressure
on peripheral nerves. Overproduction of growth hormone can lead to acromegaly,
a condition characterized by the abnormal enlargement of many parts of the
skeleton, including the joints. Nerves running through these affected joints often
become entrapped.
Vitamin deficiencies and alcoholism can cause widespread damage to nerve
tissue. Vitamins E, B1, B6, B12, and niacin are essential to healthy nerve function.
Thiamine deficiency, in particular, is common among people with alcoholism
because they often also have poor dietary habits. Thiamine deficiency can cause
a painful neuropathy of the extremities. Some researchers believe that excessive
alcohol consumption may, in itself, contribute directly to nerve damage, a
condition referred to as alcoholic neuropathy.
Vascular damage and blood diseases can decrease oxygen supply to the
peripheral nerves and quickly lead to serious damage to or death of nerve
tissues, much as a sudden lack of oxygen to the brain can cause a stroke.
Diabetes frequently leads to blood vessel constriction. Various forms of vasculitis
(blood vessel inflammation) frequently cause vessel walls to harden, thicken, and
develop scar tissue, decreasing their diameter and impeding blood flow. This
category of nerve damage, in which isolated nerves in different areas are
damaged, is called mononeuropathy multiplex or multifocal mononeuropathy.
Connective tissue disorders and chronic inflammation can cause direct and
indirect nerve damage. When the multiple layers of protective tissue surrounding
nerves become inflamed, the inflammation can spread directly into nerve fibers.
Chronic inflammation also leads to the progressive destruction of connective
tissue, making nerve fibers more vulnerable to compression injuries and
infections. Joints can become inflamed and swollen and entrap nerves, causing
pain.
Cancers and benign tumors can infiltrate or exert damaging pressure on nerve
fibers. Tumors also can arise directly from nerve tissue cells. Widespread
polyneuropathy is often associated with the neurofibromatoses, genetic diseases
in which multiple benign tumors grow on nerve tissue. Neuromas, benign masses
of overgrown nerve tissue that can develop after any penetrating injury that
severs nerve fibers, generate very intense pain signals and sometimes engulf
neighboring nerves, leading to further damage and even greater pain. Neuroma
formation can be one element of a more widespread neuropathic pain condition
called complex regional pain syndrome or reflex sympathetic dystrophy syndrome,
which can be caused by traumatic injuries or surgical trauma. Paraneoplastic
syndromes, a group of rare degenerative disorders that are triggered by a
person's immune system response to a cancerous tumor, also can indirectly
cause widespread nerve damage.
Repetitive stress frequently leads to entrapment neuropathies, a special category
of compression injury. Cumulative damage can result from repetitive, forceful,
awkward activities that require flexing of any group of joints for prolonged periods.
The resulting irritation may cause ligaments, tendons, and muscles to become
inflamed and swollen, constricting the narrow passageways through which some
nerves pass. These injuries become more frequent during pregnancy, probably
because weight gain and fluid retention also constrict nerve passageways.
Toxins can also cause peripheral nerve damage. People who are exposed to
heavy metals (arsenic, lead, mercury, thallium), industrial drugs, or environmental
toxins frequently develop neuropathy. Certain anticancer drugs, anticonvulsants,
antiviral agents, and antibiotics have side effects that can include peripheral
nerve damage, thus limiting their long-term use.
Infections and autoimmune disorders can cause peripheral neuropathy. Viruses
and bacteria that can attack nerve tissues include herpes varicella-zoster
(shingles), Epstein-Barr virus, cytomegalovirus, and herpes simplex-members of
the large family of human herpes viruses. These viruses severely damage
sensory nerves, causing attacks of sharp, lightning-like pain. Postherpetic
neuralgia often occurs after an attack of shingles and can be particularly painful.
The human immunodeficiency virus (HIV), which causes AIDS, also causes
extensive damage to the central and peripheral nervous systems. The virus can
cause several different forms of neuropathy, each strongly associated with a
specific stage of active immunodeficiency disease. A rapidly progressive, painful
polyneuropathy affecting the feet and hands is often the first clinically apparent
sign of HIV infection.
Lyme disease, diphtheria, and leprosy are bacterial diseases characterized by
extensive peripheral nerve damage. Diphtheria and leprosy are now rare in the
United States, but Lyme disease is on the rise. It can cause a wide range of
neuropathic disorders, including a rapidly developing, painful polyneuropathy,
often within a few weeks after initial infection by a tick bite.
Viral and bacterial infections can also cause indirect nerve damage by provoking
conditions referred to as autoimmune disorders, in which specialized cells and
antibodies of the immune system attack the body's own tissues. These attacks
typically cause destruction of the nerve's myelin sheath or axon (the long fiber
that extends out from the main nerve cell body).
Some neuropathies are caused by inflammation resulting from immune system
activities rather than from direct damage by infectious organisms. Inflammatory
neuropathies can develop quickly or slowly, and chronic forms can exhibit a
pattern of alternating remission and relapse. Acute inflammatory demyelinating
neuropathy, better known as Guillain-Barré syndrome, can damage motor,
sensory, and autonomic nerve fibers. Most people recover from this syndrome
although severe cases can be life threatening. Chronic inflammatory
demyelinating polyneuropathy (CIDP), generally less dangerous, usually damages
sensory and motor nerves, leaving autonomic nerves intact. Multifocal motor
neuropathy is a form of inflammatory neuropathy that affects motor nerves
exclusively; it may be chronic or acute.
Inherited forms of peripheral neuropathy are caused by inborn mistakes in the
genetic code or by new genetic mutations. Some genetic errors lead to mild
neuropathies with symptoms that begin in early adulthood and result in little, if
any, significant impairment. More severe hereditary neuropathies often appear in
infancy or childhood.
The most common inherited neuropathies are a group of disorders collectively
referred to as Charcot-Marie-Tooth disease. These neuropathies result from flaws
in genes responsible for manufacturing neurons or the myelin sheath. Hallmarks
of typical Charcot-Marie-Tooth disease include extreme weakening and wasting of
muscles in the lower legs and feet, gait abnormalities, loss of tendon reflexes, and
numbness in the lower limbs.
What treatments are available?
No medical treatments now exist that can cure inherited peripheral neuropathy.
However, there are therapies for many other forms. Any underlying condition is
treated first, followed by symptomatic treatment. Peripheral nerves have the ability
to regenerate, as long as the nerve cell itself has not been killed. Symptoms often
can be controlled, and eliminating the causes of specific forms of neuropathy
often can prevent new damage.
In general, adopting healthy habits-such as maintaining optimal weight, avoiding
exposure to toxins, following a physician-supervised exercise program, eating a
balanced diet, correcting vitamin deficiencies, and limiting or avoiding alcohol
consumption-can reduce the physical and emotional effects of peripheral
neuropathy. Active and passive forms of exercise can reduce cramps, improve
muscle strength, and prevent muscle wasting in paralyzed limbs. Various dietary
strategies can improve gastrointestinal symptoms. Timely treatment of injury can
help prevent permanent damage. Quitting smoking is particularly important
because smoking constricts the blood vessels that supply nutrients to the
peripheral nerves and can worsen neuropathic symptoms. Self-care skills such as
meticulous foot care and careful wound treatment in people with diabetes and
others who have an impaired ability to feel pain can alleviate symptoms and
improve quality of life. Such changes often create conditions that encourage
nerve regeneration.
Systemic diseases frequently require more complex treatments. Strict control of
blood glucose levels has been shown to reduce neuropathic symptoms and help
people with diabetic neuropathy avoid further nerve damage. Inflammatory and
autoimmune conditions leading to neuropathy can be controlled in several ways.
Immunosuppressive drugs such as prednisone, cyclosporine, or azathioprine may
be beneficial. Plasmapheresis-a procedure in which blood is removed, cleansed
of immune system cells and antibodies, and then returned to the body-can limit
inflammation or suppress immune system activity. High doses of immunoglobulins,
proteins that function as antibodies, also can suppress abnormal immune system
activity.
Neuropathic pain is often difficult to control. Mild pain may sometimes be
alleviated by analgesics sold over the counter. Several classes of drugs have
recently proved helpful to many patients suffering from more severe forms of
chronic neuropathic pain. These include mexiletine, a drug developed to correct
irregular heart rhythms (sometimes associated with severe side effects); several
antiepileptic drugs, including gabapentin, phenytoin, and carbamazepine; and
some classes of antidepressants, including tricyclics such as amitriptyline.
Injections of local anesthetics such as lidocaine or topical patches containing
lidocaine may relieve more intractable pain. In the most severe cases, doctors can
surgically destroy nerves; however, the results are often temporary and the
procedure can lead to complications.
Mechanical aids can help reduce pain and lessen the impact of physical disability.
Hand or foot braces can compensate for muscle weakness or alleviate nerve
compression. Orthopedic shoes can improve gait disturbances and help prevent
foot injuries in people with a loss of pain sensation. If breathing becomes severely
impaired, mechanical ventilation can provide essential life support.
Surgical intervention often can provide immediate relief from mononeuropathies
caused by compression or entrapment injuries. Repair of a slipped disk can
reduce pressure on nerves where they emerge from the spinal cord; the removal
of benign or malignant tumors can also alleviate damaging pressure on nerves.
Nerve entrapment often can be corrected by the surgical release of ligaments or
tendons.
What research is being done?
The National Institute of Neurological Disorders and Stroke (NINDS), a component
of the Federal government's National Institutes of Health (NIH) within the U.S.
Department of Health and Human Services, has primary responsibility for
research on peripheral neuropathy. Current research projects funded by the
NINDS involve investigations of genetic factors associated with hereditary
neuropathies, studies of biological mechanisms involved in diabetes-associated
neuropathies, efforts to gain greater understanding of how the immune system
contributes to peripheral nerve damage, and efforts to develop new therapies for
neuropathic symptoms.
Because specific genetic defects have been identified for only a fraction of the
known hereditary neuropathies, the Institute sponsors studies to identify other
genetic defects that may cause these conditions. Presymptomatic diagnosis may
lead to therapies for preventing nerve damage before it occurs, and gene
replacement therapies could be developed to prevent or reduce cumulative nerve
damage.
Several NINDS-funded studies are investigating some of the possible biological
mechanisms responsible for the many forms of neuropathy, including the
autonomic neuropathies that affect people with diabetes. The Institute also is
funding studies to measure the frequency and progression rates of diabetic
neuropathies, examine the effects of these disorders on quality of life, and identify
factors that may put certain individuals at greater risk for developing diabetes-
associated neuropathies.
Scientists have found that the destructive effects of abnormal immune system
activity cause many neuropathies for which a cause could not previously be
identified. However, the exact biological mechanisms that lead to this nerve
damage are not yet well understood. Many NINDS-sponsored studies are studying
inflammatory neuropathies, both in research animals and in humans, to clarify
these mechanisms so that therapeutic interventions can be developed.
Neuropathic pain is a primary target of NINDS-sponsored studies aimed at
developing more effective therapies for symptoms of peripheral neuropathy.
Some scientists hope to identify substances that will block the brain chemicals that
generate pain signals, while others are investigating the pathways by which pain
signals reach the brain.
Studies of neurotrophic factors represent one of the most promising areas of
research aimed at finding new, more effective treatments for peripheral
neuropathies. These substances, produced naturally by the body, protect
neurons from injury and encourage their survival. Neurotrophic factors also help
maintain normal function in mature nerve cells, and some stimulate axon
regeneration. Several NINDS-sponsored studies seek to learn more about the
effects of these powerful chemicals on the peripheral nervous system and may
eventually lead to treatments that can reverse nerve damage and cure peripheral
nerve disorders.
National Institutes of Health
vast communications network that transmits information from the brain and spinal
cord (the central nervous system) to every other part of the body. Peripheral
nerves also send sensory information back to the brain and spinal cord, such as a
message that the feet are cold or a finger is burned. Damage to the peripheral
nervous system interferes with these vital connections. Like static on a telephone
line, peripheral neuropathy distorts and sometimes interrupts messages between
the brain and the rest of the body.
Because every peripheral nerve has a highly specialized function in a specific part
of the body, a wide array of symptoms can occur when nerves are damaged.
Some people may experience temporary numbness, tingling, and pricking
sensations (paresthesia), sensitivity to touch, or muscle weakness. Others may
suffer more extreme symptoms, including burning pain (especially at night),
muscle wasting, paralysis, or organ or gland dysfunction. People may become
unable to digest food easily, maintain safe levels of blood pressure, sweat
normally, or experience normal sexual function. In the most extreme cases,
breathing may become difficult or organ failure may occur.
Some forms of neuropathy involve damage to only one nerve and are called
mononeuropathies. More often though, multiple nerves affecting all limbs are
affected-called polyneuropathy. Occasionally, two or more isolated nerves in
separate areas of the body are affected-called mononeuritis multiplex.
In acute neuropathies, such as Guillain-Barré syndrome, symptoms appear
suddenly, progress rapidly, and resolve slowly as damaged nerves heal. In
chronic forms, symptoms begin subtly and progress slowly. Some people may
have periods of relief followed by relapse. Others may reach a plateau stage
where symptoms stay the same for many months or years. Some chronic
neuropathies worsen over time, but very few forms prove fatal unless complicated
by other diseases. Occasionally the neuropathy is a symptom of another disorder.
In the most common forms of polyneuropathy, the nerve fibers (individual cells
that make up the nerve) most distant from the brain and the spinal cord
malfunction first. Pain and other symptoms often appear symmetrically, for
example, in both feet followed by a gradual progression up both legs. Next, the
fingers, hands, and arms may become affected, and symptoms can progress into
the central part of the body. Many people with diabetic neuropathy experience this
pattern of ascending nerve damage.
How are the peripheral neuropathies classified?
More than 100 types of peripheral neuropathy have been identified, each with its
own characteristic set of symptoms, pattern of development, and prognosis.
Impaired function and symptoms depend on the type of nerves-motor, sensory, or
autonomic-that are damaged. Motor nerves control movements of all muscles
under conscious control, such as those used for walking, grasping things, or
talking. Sensory nerves transmit information about sensory experiences, such as
the feeling of a light touch or the pain resulting from a cut. Autonomic nerves
regulate biological activities that people do not control consciously, such as
breathing, digesting food, and heart and gland functions. Although some
neuropathies may affect all three types of nerves, others primarily affect one or
two types. Therefore, doctors may use terms such as predominantly motor
neuropathy, predominantly sensory neuropathy, sensory-motor neuropathy, or
autonomic neuropathy to describe a patient's condition.
What are the symptoms of peripheral nerve damage?
Symptoms are related to the type of affected nerve and may be seen over a
period of days, weeks, or years. Muscle weakness is the most common symptom
of motor nerve damage. Other symptoms may include painful cramps and
fasciculations (uncontrolled muscle twitching visible under the skin), muscle loss,
bone degeneration, and changes in the skin, hair, and nails. These more general
degenerative changes also can result from sensory or autonomic nerve fiber loss.
Sensory nerve damage causes a more complex range of symptoms because
sensory nerves have a wider, more highly specialized range of functions. Larger
sensory fibers enclosed in myelin (a fatty protein that coats and insulates many
nerves) register vibration, light touch, and position sense. Damage to large
sensory fibers lessens the ability to feel vibrations and touch, resulting in a
general sense of numbness, especially in the hands and feet. People may feel as
if they are wearing gloves and stockings even when they are not. Many patients
cannot recognize by touch alone the shapes of small objects or distinguish
between different shapes. This damage to sensory fibers may contribute to the
loss of reflexes (as can motor nerve damage). Loss of position sense often makes
people unable to coordinate complex movements like walking or fastening
buttons, or to maintain their balance when their eyes are shut. Neuropathic pain is
difficult to control and can seriously affect emotional well-being and overall quality
of life. Neuropathic pain is often worse at night, seriously disrupting sleep and
adding to the emotional burden of sensory nerve damage.
Smaller sensory fibers without myelin sheaths transmit pain and temperature
sensations. Damage to these fibers can interfere with the ability to feel pain or
changes in temperature. People may fail to sense that they have been injured
from a cut or that a wound is becoming infected. Others may not detect pains that
warn of impending heart attack or other acute conditions. (Loss of pain sensation
is a particularly serious problem for people with diabetes, contributing to the high
rate of lower limb amputations among this population.) Pain receptors in the skin
can also become oversensitized, so that people may feel severe pain (allodynia)
from stimuli that are normally painless (for example, some may experience pain
from bed sheets draped lightly over the body).
Symptoms of autonomic nerve damage are diverse and depend upon which
organs or glands are affected. Autonomic nerve dysfunction can become life
threatening and may require emergency medical care in cases when breathing
becomes impaired or when the heart begins beating irregularly. Common
symptoms of autonomic nerve damage include an inability to sweat normally,
which may lead to heat intolerance; a loss of bladder control, which may cause
infection or incontinence; and an inability to control muscles that expand or
contract blood vessels to maintain safe blood pressure levels. A loss of control
over blood pressure can cause dizziness, lightheadedness, or even fainting when
a person moves suddenly from a seated to a standing position (a condition known
as postural or orthostatic hypotension).
Gastrointestinal symptoms frequently accompany autonomic neuropathy. Nerves
controlling intestinal muscle contractions often malfunction, leading to diarrhea,
constipation, or incontinence. Many people also have problems eating or
swallowing if certain autonomic nerves are affected.
What causes peripheral neuropathy?
Peripheral neuropathy may be either inherited or acquired. Causes of acquired
peripheral neuropathy include physical injury (trauma) to a nerve, tumors, toxins,
autoimmune responses, nutritional deficiencies, alcoholism, and vascular and
metabolic disorders. Acquired peripheral neuropathies are grouped into three
broad categories: those caused by systemic disease, those caused by trauma
from external agents, and those caused by infections or autoimmune disorders
affecting nerve tissue. One example of an acquired peripheral neuropathy is
trigeminal neuralgia (also known as tic douloureux), in which damage to the
trigeminal nerve (the large nerve of the head and face) causes episodic attacks of
excruciating, lightning-like pain on one side of the face. In some cases, the cause
is an earlier viral infection, pressure on the nerve from a tumor or swollen blood
vessel, or, infrequently, multiple sclerosis. In many cases, however, a specific
cause cannot be identified. Doctors usually refer to neuropathies with no known
cause as idiopathic neuropathies.
Physical injury (trauma) is the most common cause of injury to a nerve. Injury or
sudden trauma, such as from automobile accidents, falls, and sports-related
activities, can cause nerves to be partially or completely severed, crushed,
compressed, or stretched, sometimes so forcefully that they are partially or
completely detached from the spinal cord. Less dramatic traumas also can cause
serious nerve damage. Broken or dislocated bones can exert damaging pressure
on neighboring nerves, and slipped disks between vertebrae can compress nerve
fibers where they emerge from the spinal cord.
Systemic diseases — disorders that affect the entire body —often cause
peripheral neuropathy. These disorders may include: Metabolic and endocrine
disorders. Nerve tissues are highly vulnerable to damage from diseases that
impair the body's ability to transform nutrients into energy, process waste
products, or manufacture the substances that make up living tissue. Diabetes
mellitus, characterized by chronically high blood glucose levels, is a leading cause
of peripheral neuropathy in the United States. About 60 percent to 70 percent of
people with diabetes have mild to severe forms of nervous system damage.
Kidney disorders can lead to abnormally high amounts of toxic substances in the
blood that can severely damage nerve tissue. A majority of patients who require
dialysis because of kidney failure develop polyneuropathy. Some liver diseases
also lead to neuropathies as a result of chemical imbalances.
Hormonal imbalances can disturb normal metabolic processes and cause
neuropathies. For example, an underproduction of thyroid hormones slows
metabolism, leading to fluid retention and swollen tissues that can exert pressure
on peripheral nerves. Overproduction of growth hormone can lead to acromegaly,
a condition characterized by the abnormal enlargement of many parts of the
skeleton, including the joints. Nerves running through these affected joints often
become entrapped.
Vitamin deficiencies and alcoholism can cause widespread damage to nerve
tissue. Vitamins E, B1, B6, B12, and niacin are essential to healthy nerve function.
Thiamine deficiency, in particular, is common among people with alcoholism
because they often also have poor dietary habits. Thiamine deficiency can cause
a painful neuropathy of the extremities. Some researchers believe that excessive
alcohol consumption may, in itself, contribute directly to nerve damage, a
condition referred to as alcoholic neuropathy.
Vascular damage and blood diseases can decrease oxygen supply to the
peripheral nerves and quickly lead to serious damage to or death of nerve
tissues, much as a sudden lack of oxygen to the brain can cause a stroke.
Diabetes frequently leads to blood vessel constriction. Various forms of vasculitis
(blood vessel inflammation) frequently cause vessel walls to harden, thicken, and
develop scar tissue, decreasing their diameter and impeding blood flow. This
category of nerve damage, in which isolated nerves in different areas are
damaged, is called mononeuropathy multiplex or multifocal mononeuropathy.
Connective tissue disorders and chronic inflammation can cause direct and
indirect nerve damage. When the multiple layers of protective tissue surrounding
nerves become inflamed, the inflammation can spread directly into nerve fibers.
Chronic inflammation also leads to the progressive destruction of connective
tissue, making nerve fibers more vulnerable to compression injuries and
infections. Joints can become inflamed and swollen and entrap nerves, causing
pain.
Cancers and benign tumors can infiltrate or exert damaging pressure on nerve
fibers. Tumors also can arise directly from nerve tissue cells. Widespread
polyneuropathy is often associated with the neurofibromatoses, genetic diseases
in which multiple benign tumors grow on nerve tissue. Neuromas, benign masses
of overgrown nerve tissue that can develop after any penetrating injury that
severs nerve fibers, generate very intense pain signals and sometimes engulf
neighboring nerves, leading to further damage and even greater pain. Neuroma
formation can be one element of a more widespread neuropathic pain condition
called complex regional pain syndrome or reflex sympathetic dystrophy syndrome,
which can be caused by traumatic injuries or surgical trauma. Paraneoplastic
syndromes, a group of rare degenerative disorders that are triggered by a
person's immune system response to a cancerous tumor, also can indirectly
cause widespread nerve damage.
Repetitive stress frequently leads to entrapment neuropathies, a special category
of compression injury. Cumulative damage can result from repetitive, forceful,
awkward activities that require flexing of any group of joints for prolonged periods.
The resulting irritation may cause ligaments, tendons, and muscles to become
inflamed and swollen, constricting the narrow passageways through which some
nerves pass. These injuries become more frequent during pregnancy, probably
because weight gain and fluid retention also constrict nerve passageways.
Toxins can also cause peripheral nerve damage. People who are exposed to
heavy metals (arsenic, lead, mercury, thallium), industrial drugs, or environmental
toxins frequently develop neuropathy. Certain anticancer drugs, anticonvulsants,
antiviral agents, and antibiotics have side effects that can include peripheral
nerve damage, thus limiting their long-term use.
Infections and autoimmune disorders can cause peripheral neuropathy. Viruses
and bacteria that can attack nerve tissues include herpes varicella-zoster
(shingles), Epstein-Barr virus, cytomegalovirus, and herpes simplex-members of
the large family of human herpes viruses. These viruses severely damage
sensory nerves, causing attacks of sharp, lightning-like pain. Postherpetic
neuralgia often occurs after an attack of shingles and can be particularly painful.
The human immunodeficiency virus (HIV), which causes AIDS, also causes
extensive damage to the central and peripheral nervous systems. The virus can
cause several different forms of neuropathy, each strongly associated with a
specific stage of active immunodeficiency disease. A rapidly progressive, painful
polyneuropathy affecting the feet and hands is often the first clinically apparent
sign of HIV infection.
Lyme disease, diphtheria, and leprosy are bacterial diseases characterized by
extensive peripheral nerve damage. Diphtheria and leprosy are now rare in the
United States, but Lyme disease is on the rise. It can cause a wide range of
neuropathic disorders, including a rapidly developing, painful polyneuropathy,
often within a few weeks after initial infection by a tick bite.
Viral and bacterial infections can also cause indirect nerve damage by provoking
conditions referred to as autoimmune disorders, in which specialized cells and
antibodies of the immune system attack the body's own tissues. These attacks
typically cause destruction of the nerve's myelin sheath or axon (the long fiber
that extends out from the main nerve cell body).
Some neuropathies are caused by inflammation resulting from immune system
activities rather than from direct damage by infectious organisms. Inflammatory
neuropathies can develop quickly or slowly, and chronic forms can exhibit a
pattern of alternating remission and relapse. Acute inflammatory demyelinating
neuropathy, better known as Guillain-Barré syndrome, can damage motor,
sensory, and autonomic nerve fibers. Most people recover from this syndrome
although severe cases can be life threatening. Chronic inflammatory
demyelinating polyneuropathy (CIDP), generally less dangerous, usually damages
sensory and motor nerves, leaving autonomic nerves intact. Multifocal motor
neuropathy is a form of inflammatory neuropathy that affects motor nerves
exclusively; it may be chronic or acute.
Inherited forms of peripheral neuropathy are caused by inborn mistakes in the
genetic code or by new genetic mutations. Some genetic errors lead to mild
neuropathies with symptoms that begin in early adulthood and result in little, if
any, significant impairment. More severe hereditary neuropathies often appear in
infancy or childhood.
The most common inherited neuropathies are a group of disorders collectively
referred to as Charcot-Marie-Tooth disease. These neuropathies result from flaws
in genes responsible for manufacturing neurons or the myelin sheath. Hallmarks
of typical Charcot-Marie-Tooth disease include extreme weakening and wasting of
muscles in the lower legs and feet, gait abnormalities, loss of tendon reflexes, and
numbness in the lower limbs.
What treatments are available?
No medical treatments now exist that can cure inherited peripheral neuropathy.
However, there are therapies for many other forms. Any underlying condition is
treated first, followed by symptomatic treatment. Peripheral nerves have the ability
to regenerate, as long as the nerve cell itself has not been killed. Symptoms often
can be controlled, and eliminating the causes of specific forms of neuropathy
often can prevent new damage.
In general, adopting healthy habits-such as maintaining optimal weight, avoiding
exposure to toxins, following a physician-supervised exercise program, eating a
balanced diet, correcting vitamin deficiencies, and limiting or avoiding alcohol
consumption-can reduce the physical and emotional effects of peripheral
neuropathy. Active and passive forms of exercise can reduce cramps, improve
muscle strength, and prevent muscle wasting in paralyzed limbs. Various dietary
strategies can improve gastrointestinal symptoms. Timely treatment of injury can
help prevent permanent damage. Quitting smoking is particularly important
because smoking constricts the blood vessels that supply nutrients to the
peripheral nerves and can worsen neuropathic symptoms. Self-care skills such as
meticulous foot care and careful wound treatment in people with diabetes and
others who have an impaired ability to feel pain can alleviate symptoms and
improve quality of life. Such changes often create conditions that encourage
nerve regeneration.
Systemic diseases frequently require more complex treatments. Strict control of
blood glucose levels has been shown to reduce neuropathic symptoms and help
people with diabetic neuropathy avoid further nerve damage. Inflammatory and
autoimmune conditions leading to neuropathy can be controlled in several ways.
Immunosuppressive drugs such as prednisone, cyclosporine, or azathioprine may
be beneficial. Plasmapheresis-a procedure in which blood is removed, cleansed
of immune system cells and antibodies, and then returned to the body-can limit
inflammation or suppress immune system activity. High doses of immunoglobulins,
proteins that function as antibodies, also can suppress abnormal immune system
activity.
Neuropathic pain is often difficult to control. Mild pain may sometimes be
alleviated by analgesics sold over the counter. Several classes of drugs have
recently proved helpful to many patients suffering from more severe forms of
chronic neuropathic pain. These include mexiletine, a drug developed to correct
irregular heart rhythms (sometimes associated with severe side effects); several
antiepileptic drugs, including gabapentin, phenytoin, and carbamazepine; and
some classes of antidepressants, including tricyclics such as amitriptyline.
Injections of local anesthetics such as lidocaine or topical patches containing
lidocaine may relieve more intractable pain. In the most severe cases, doctors can
surgically destroy nerves; however, the results are often temporary and the
procedure can lead to complications.
Mechanical aids can help reduce pain and lessen the impact of physical disability.
Hand or foot braces can compensate for muscle weakness or alleviate nerve
compression. Orthopedic shoes can improve gait disturbances and help prevent
foot injuries in people with a loss of pain sensation. If breathing becomes severely
impaired, mechanical ventilation can provide essential life support.
Surgical intervention often can provide immediate relief from mononeuropathies
caused by compression or entrapment injuries. Repair of a slipped disk can
reduce pressure on nerves where they emerge from the spinal cord; the removal
of benign or malignant tumors can also alleviate damaging pressure on nerves.
Nerve entrapment often can be corrected by the surgical release of ligaments or
tendons.
What research is being done?
The National Institute of Neurological Disorders and Stroke (NINDS), a component
of the Federal government's National Institutes of Health (NIH) within the U.S.
Department of Health and Human Services, has primary responsibility for
research on peripheral neuropathy. Current research projects funded by the
NINDS involve investigations of genetic factors associated with hereditary
neuropathies, studies of biological mechanisms involved in diabetes-associated
neuropathies, efforts to gain greater understanding of how the immune system
contributes to peripheral nerve damage, and efforts to develop new therapies for
neuropathic symptoms.
Because specific genetic defects have been identified for only a fraction of the
known hereditary neuropathies, the Institute sponsors studies to identify other
genetic defects that may cause these conditions. Presymptomatic diagnosis may
lead to therapies for preventing nerve damage before it occurs, and gene
replacement therapies could be developed to prevent or reduce cumulative nerve
damage.
Several NINDS-funded studies are investigating some of the possible biological
mechanisms responsible for the many forms of neuropathy, including the
autonomic neuropathies that affect people with diabetes. The Institute also is
funding studies to measure the frequency and progression rates of diabetic
neuropathies, examine the effects of these disorders on quality of life, and identify
factors that may put certain individuals at greater risk for developing diabetes-
associated neuropathies.
Scientists have found that the destructive effects of abnormal immune system
activity cause many neuropathies for which a cause could not previously be
identified. However, the exact biological mechanisms that lead to this nerve
damage are not yet well understood. Many NINDS-sponsored studies are studying
inflammatory neuropathies, both in research animals and in humans, to clarify
these mechanisms so that therapeutic interventions can be developed.
Neuropathic pain is a primary target of NINDS-sponsored studies aimed at
developing more effective therapies for symptoms of peripheral neuropathy.
Some scientists hope to identify substances that will block the brain chemicals that
generate pain signals, while others are investigating the pathways by which pain
signals reach the brain.
Studies of neurotrophic factors represent one of the most promising areas of
research aimed at finding new, more effective treatments for peripheral
neuropathies. These substances, produced naturally by the body, protect
neurons from injury and encourage their survival. Neurotrophic factors also help
maintain normal function in mature nerve cells, and some stimulate axon
regeneration. Several NINDS-sponsored studies seek to learn more about the
effects of these powerful chemicals on the peripheral nervous system and may
eventually lead to treatments that can reverse nerve damage and cure peripheral
nerve disorders.
National Institutes of Health
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