Motor Neuron 

Diseases

U.S. DEPARTMENT OF HEALTH

AND HUMAN SERVICES

Public Health Service

National Institutes of Health

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Motor Neuron Diseases

What are motor neuron diseases?

The motor neuron diseases (MNDs) are a group of progressive neurological disorders 

that destroy motor neurons, the cells that 

control essential voluntary muscle activity 

such as speaking, walking, breathing, and 

swallowing. Normally, messages from nerve 

cells in the brain (called upper motor neurons) 

are transmitted to nerve cells in the brain 

stem and spinal cord (called lower motor 

neurons) and from them to particular muscles. 

Upper motor neurons direct the lower motor 

neurons to produce movements such as walking or chewing. Lower motor neurons control 

movement in the arms, legs, chest, face, 

throat, and tongue. Spinal motor neurons are 

also called anterior horn cells. Upper motor 

neurons are also called corticospinal neurons.

When there are disruptions in the signals 

between the lowest motor neurons and the 

muscle, the muscles do not work properly; 

the muscles gradually weaken and may begin 

to waste away and develop uncontrollable 

twitching (called fasciculations). When there 

are disruptions in the signals between the 

upper motor neurons and the lower motor 

neurons, the limb muscles develop stiffness 

(called spasticity), movements become slow 
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and effortful, and tendon reflexes such as 

knee and ankle jerks become overactive. 

Over time, the ability to control voluntary 

movement can be lost.

Who is at risk?

MNDs occur in adults and children. In children, particularly in inherited or 

familial forms of the disease, symptoms can 

be present at birth or appear before the child 

learns to walk. In adults, MNDs occur more 

commonly in men than in women, with 

symptoms appearing after age 40.

What causes motor neuron diseases?

Some MNDs are inherited, but the causes of most MNDs are not known. In sporadic 

or noninherited MNDs, environmental, toxic, 

viral, or genetic factors may be implicated. 

How are they classified?

MNDs are classified according to whether they are inherited or sporadic, and to 

whether degeneration affects upper motor 

neurons, lower motor neurons, or both. In 

adults, the most common MND is amyotrophic 

lateral sclerosis (ALS), which affects both upper 

and lower motor neurons. It has inherited and 

sporadic forms and can affect the arms, legs, 

or facial muscles. Primary lateral sclerosis is 

a disease of the upper motor neurons, while 

progressive muscular atrophy affects only lower 

motor neurons in the spinal cord. In progressive bulbar palsy, the lowest motor neurons 

of the brain stem are most affected, causing 

slurred speech and difficulty chewing and 
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swallowing. There are almost always mildly 

abnormal signs in the arms and legs.

If the MND is inherited, it is also classified 

according to the mode of inheritance. Autosomal dominant means that a person needs to 

inherit only one copy of the defective gene 

from one affected parent to be at risk of the 

disease. There is a 50 percent chance that each 

child of an affected person will be affected. 

Autosomal recessive means the individual must 

inherit a copy of the defective gene from both 

parents. These parents are likely to be asymptomatic (without symptoms of the disease). 

Autosomal recessive diseases often affect more 

than one person in the same generation (siblings 

or cousins). In X-linked inheritance, the mother 

carries the defective gene on one of her X 

chromosomes and passes the disorder along 

to her sons. Males inherit an X chromosome 

from their mother and a Y chromosome from 

their father, while females inherit an X chromosome from each parent. Daughters have a 

50 percent chance of inheriting their mother’s 

faulty X chromosome and a safe X chromosome from their father, which would make 

them asymptomatic carriers of the mutation.

What are the symptoms of motor 

neuron diseases?

A brief description of the symptoms of some of the more common MNDs follows.

Amyotrophic lateral sclerosis (ALS), also called 

Lou Gehrig’s disease or classical motor neuron 

disease, is a progressive, ultimately fatal disorder that disrupts signals to all voluntary 

muscles. Many doctors use the terms motor 
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neuron disease and ALS interchangeably. Both 

upper and lower motor neurons are affected. 

Symptoms are usually noticed first in the 

arms and hands, legs, or swallowing muscles. 

Approximately 75 percent of people with classic ALS will develop weakness and wasting 

of the bulbar muscles (muscles that control 

speech, swallowing, and chewing). Muscle 

weakness and atrophy occur on both sides of 

the body. Affected individuals lose strength 

and the ability to move their arms and legs, 

and to hold the body upright. Other symptoms 

include spasticity, spasms, muscle cramps, 

and fasciculations. Speech can become slurred 

or nasal. When muscles of the diaphragm 

and chest wall fail to function properly, individuals lose the ability to breathe without 

mechanical support. Although the disease 

does not usually impair a person’s mind or 

personality, several recent studies suggest that 

some people with ALS may develop cognitive 

problems involving word fluency, decisionmaking, and memory. Most individuals with 

ALS die from respiratory failure, usually 

within 3 to 5 years from the onset of symptoms. However, about 10 percent of affected 

individuals survive for 10 or more years.

ALS most commonly strikes people between 

40 and 60 years of age, but younger and older 

individuals also can develop the disease. Men 

are affected more often than women. Most 

cases of ALS occur sporadically, and family 

members of those individuals are not considered to be at increased risk for developing 

the disease. Familial forms of ALS account 

for 10 percent or less of cases of ALS, with 
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more than 10 genes identified to date. However, most of the gene mutations discovered 

account for a very small number of cases. The 

most common familial forms of ALS in adults 

are caused by mutations of the superoxide 

dismutase gene, or SOD1, located on chromosome 21. There are also rare juvenile-onset 

forms of familial ALS. 

Progressive bulbar palsy, also called progressive bulbar atrophy, involves the brain stem—

the bulb-shaped region containing lower 

motor neurons needed for swallowing, 

speaking, chewing, and other functions. 

Symptoms include pharyngeal muscle weakness (involved with swallowing), weak jaw 

and facial muscles, progressive loss of speech, 

and tongue muscle atrophy. Limb weakness 

with both lower and upper motor neuron signs 

is almost always evident but less prominent. 

Individuals are at increased risk of choking 

and aspiration pneumonia, which is caused 

by the passage of liquids and food through 

the vocal folds and into the lower airways 

and lungs. Affected persons have outbursts of 

laughing or crying (called emotional lability). 

Stroke and myasthenia gravis may have 

certain symptoms that are similar to those 

of progressive bulbar palsy and must be ruled 

out prior to diagnosing this disorder. In about 

25 percent of individuals with ALS, early 

symptoms begin with bulbar involvement. 

Some 75 percent of individuals with classic 

ALS eventually show some bulbar involvement. 

Many clinicians believe that progressive bulbar 

palsy by itself, without evidence of abnormalities in the arms or legs, is extremely rare.
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Pseudobulbar palsy, which shares many 

symptoms of progressive bulbar palsy, is 

characterized by degeneration of upper motor 

neurons that transmit signals to the lower 

motor neurons in the brain stem. Affected 

individuals have progressive loss of the 

ability to speak, chew, and swallow. Progressive weakness in facial muscles leads to an 

expressionless face. Individuals may develop 

a gravelly voice and an increased gag reflex. 

The tongue may become immobile and unable 

to protrude from the mouth. Individuals may 

have outbursts of laughing or crying.

Primary lateral sclerosis (PLS) affects the 

upper motor neurons of the arms, legs, and 

face. It occurs when specific nerve cells in 

the motor regions of the cerebral cortex (the 

thin layer of cells covering the brain which 

is responsible for most high-level brain functions) gradually degenerate, causing the 

movements to be slow and effortful. The 

disorder often affects the legs first, followed 

by the body trunk, arms and hands, and, 

finally, the bulbar muscles. Speech may 

become slowed and slurred. When affected, 

the legs and arms become stiff, clumsy, slow, 

and weak, leading to an inability to walk or 

carry out tasks requiring fine hand coordination. Difficulty with balance may lead to 

falls. Speech may become slow and slurred. 

Affected individuals commonly experience 

pseudobulbar affect and an overactive startle 

response. PLS is more common in men than 

in women, with a very gradual onset that 

generally occurs between ages 40 and 60. The 

cause is unknown. The symptoms progress 
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gradually over years, leading to progressive 

stiffness and clumsiness of the affected 

muscles. PLS is sometimes considered a variant of ALS, but the major difference is the 

sparing of lower motor neurons, the slow rate 

of disease progression, and normal lifespan. 

PLS may be mistaken for spastic paraplegia, 

a hereditary disorder of the upper motor neurons that causes spasticity in the legs and usually starts in adolescence. Most neurologists 

follow the affected individual’s clinical course 

for at least 3 to 4 years before making a diagnosis of PLS. The disorder is not fatal but may 

affect quality of life. 

Progressive muscular atrophy is marked by 

slow but progressive degeneration of only the 

lower motor neurons. It largely affects men, 

with onset earlier than in other MNDs. Weakness is typically seen first in the hands and 

then spreads into the lower body, where it 

can be severe. Other symptoms may include 

muscle wasting, clumsy hand movements, 

fasciculations, and muscle cramps. The trunk 

muscles and respiration may become affected. 

Exposure to cold can worsen symptoms. The 

disease develops into ALS in many instances.

Spinal muscular atrophy (SMA) is a hereditary 

disease affecting the lower motor neurons. 

It is an autosomal recessive disorder caused 

by defects in the gene SMN1, which makes 

a protein that is important for the survival 

of motor neurons (SMN protein). In SMA, 

insufficient levels of the SMN protein lead to 

degeneration of the lower motor neurons, producing weakness and wasting of the skeletal 

muscles. This weakness is often more severe 
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in the trunk and upper leg and arm muscles 

than in muscles of the hands and feet. SMA in 

children is classified into three types, based 

on ages of onset, severity, and progression 

of symptoms. All three types are caused by 

defects in the SMN1 gene.

SMA type I, also called Werdnig-Hoffmann 

disease, is evident by the time a child is 6 

months old. Symptoms may include hypotonia 

(severely reduced muscle tone), diminished 

limb movements, lack of tendon reflexes, fasciculations, tremors, swallowing and feeding 

difficulties, and impaired breathing. Some 

children also develop scoliosis (curvature of 

the spine) or other skeletal abnormalities. 

Affected children never sit or stand and the 

vast majority usually die of respiratory failure before the age of 2. However, the survival 

in individuals with SMA type I has increased 

in recent years, in relation to the growing 

trend toward more proactive clinical care.

Symptoms of SMA type II, the intermediate 

form, usually begin between 6 and 18 months 

of age. Children may be able to sit but are 

unable to stand or walk unaided, and may 

have respiratory difficulties. The progression 

of disease is variable. Life expectancy is 

reduced but some individuals live into 

adolescence or young adulthood.

Symptoms of SMA type III (Kugelberg-Welander 

disease) appear between 2 and 17 years of age 

and include abnormal gait; difficulty running, 

climbing steps, or rising from a chair; and a 

fine tremor of the fingers. The lower extremities are most often affected. Complications 

include scoliosis and joint contractures—
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chronic shortening of muscles or tendons 

around joints, caused by abnormal muscle 

tone and weakness, which prevents the joints 

from moving freely. Individuals with SMA 

type III may be prone to respiratory infections, 

but with care may have a normal lifespan.

Congenital SMA with arthrogryposis (persistent 

contracture of joints with fixed abnormal 

posture of the limb) is a rare disorder. 

Manifestations include severe contractures, 

scoliosis, chest deformity, respiratory problems, 

unusually small jaws, and drooping of the 

upper eyelids.

Kennedy’s disease, also known as progressive 

spinobulbar muscular atrophy, is an X-linked 

recessive disease caused by mutations in the 

gene for the androgen receptor. Daughters of 

individuals with Kennedy’s disease are carriers and have a 50 percent chance of having 

a son affected with the disease. The onset of 

symptoms is variable and the disease may 

first be recognized between 15 and 60 years 

of age. Symptoms include weakness and 

atrophy of the facial, jaw, and tongue muscles, 

leading to problems with chewing, swallowing, and changes in speech. Early symptoms 

may include muscle pain and fatigue. Weakness in arm and leg muscles closest to the 

trunk of the body develops over time, with 

muscle atrophy and fasciculations. Individuals with Kennedy’s disease also develop 

sensory loss in the feet and hands. Nerve conduction studies confirm that nearly all individuals have a sensory neuropathy (pain from 

sensory nerve inflammation or degeneration). 
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Affected individuals may have enlargement 

of the male breasts or develop noninsulindependent diabetes mellitus.

The course of the disorder varies but is 

generally slowly progressive. Individuals 

tend to remain ambulatory until late in the 

disease. The life expectancy for individuals 

with Kennedy disease is usually normal. 

Post-polio syndrome (PPS) is a condition that 

can strike polio survivors decades after their 

recovery from poliomyelitis. Polio is an acute 

viral disease that destroys motor neurons. 

Many people who are affected early in life 

recover and develop new symptoms many 

decades later. After acute polio, the surviving 

motor neurons expand the amount of muscle 

that each controls. PPS and Post-Polio Muscular 

Atrophy (PPMA) are thought to occur when 

the surviving motor neurons are lost in the 

aging process or through injury or illness. 

Many scientists believe PPS is latent weakness among muscles previously affected by 

poliomyelitis and not a new MND. Symptoms 

include fatigue, slowly progressive muscle 

weakness, muscle atrophy, fasciculations, 

cold intolerance, and muscle and joint pain. 

These symptoms appear most often among 

muscle groups affected by the initial disease, 

and may consist of difficulty breathing, swallowing, or sleeping. Other symptoms of PPS 

may be caused by skeletal deformities such 

as long-standing scoliosis that led to chronic 

changes in the biomechanics of the joints and 

spine. Symptoms are more frequent among 

older people and those individuals most 

severely affected by the earlier disease. 
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Some individuals experience only minor 

symptoms, while others develop muscle 

atrophy that may be mistaken for ALS. PPS is 

not usually life threatening. Doctors estimate 

that 25 to 50 percent of survivors of paralytic 

poliomyelitis usually develop PPS.

How are motor neuron diseases diagnosed?

T here are no specific tests to diagnose most MNDs although there are now gene 

tests for SMA. Symptoms may vary among 

individuals and, in the early stages of the 

disease, may be similar to those of other 

diseases, making diagnosis difficult. A physical exam should be followed by a thorough 

neurological exam. The neurological exam 

will assess motor and sensory skills, nerve 

function, hearing and speech, vision, coordination and balance, mental status, and 

changes in mood or behavior.

Tests to rule out other diseases or to measure 

muscle involvement may include the following:

Electromyography (EMG) is used to diagnose 

disorders of lower motor neurons, as well as 

disorders of muscle and peripheral nerves. 

In an EMG, a physician inserts a thin needle 

electrode, attached to a recording instrument, 

into a muscle to assess the electrical activity 

during a voluntary contraction and at rest. The 

electrical activity in the muscle is caused by 

the lower motor neurons. When motor neurons 

degenerate, characteristic abnormal electrical 

signals occur in the muscle. Testing usually 

lasts about an hour or more, depending on 

the number of muscles and nerves tested. 
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EMG is usually done in conjunction with a 

nerve conduction velocity study. Nerve conduction studies measure the speed and size 

of the impulses in the nerves from small electrodes taped to the skin. A small pulse of electricity (similar to a jolt from static electricity) 

is applied to the skin to stimulate the nerve 

that directs a particular muscle. The second 

set of electrodes transmits the responding 

electrical signal to a recording machine. 

Nerve conduction studies help to differentiate 

lower motor neuron diseases from peripheral 

neuropathy and can detect abnormalities in 

sensory nerves.

Laboratory tests of blood, urine, or other 

substances can rule out muscle diseases 

and other disorders that may have symptoms 

similar to those of MND. For example, analysis of the fluid that surrounds the brain and 

spinal cord can detect infections or inflammation that can also cause muscle stiffness. 

Blood tests may be ordered to measure levels 

of the protein creatine kinase (which is needed 

for the chemical reactions that produce energy 

for muscle contractions); high levels may 

help diagnose muscle diseases such as 

muscular dystrophy.

Magnetic resonance imaging (MRI) uses a 

powerful magnetic field to produce detailed 

images of tissues, organs, bones, nerves, and 

other body structures. MRI is often used to 

rule out diseases that affect the head, neck, 

and spinal cord. MRI images can help diagnose 

brain and spinal cord tumors, eye disease, 

inflammation, infection, and vascular 

irregularities that may lead to stroke. 
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MRI can also detect and monitor inflammatory 

disorders such as multiple sclerosis and can 

document brain injury from trauma. Magnetic 

resonance spectroscopy is a type of MRI scan 

that measures chemicals in the brain and may 

be used to evaluate the integrity of the upper 

motor neurons.

Muscle or nerve biopsy can help confirm nerve 

disease and nerve regeneration. A small sample 

of the muscle or nerve is removed under local 

anesthetic and studied under a microscope. 

The sample may be removed either surgically, 

through a slit made in the skin, or by needle 

biopsy, in which a thin hollow needle is inserted 

through the skin and into the muscle. A small 

piece of muscle remains in the hollow needle 

when it is removed from the body. Although 

this test can provide valuable information 

about the degree of damage, it is an invasive 

procedure and many experts do not believe 

that a biopsy is always needed for diagnosis.

Transcranial magnetic stimulation was first 

developed as a diagnostic tool to study areas 

of the brain related to motor activity. It is 

also used as a treatment for certain disorders. 

This noninvasive procedure creates a magnetic 

pulse inside the brain that evokes motor activity 

in an area of the body. Electrodes taped to 

different areas of the body pick up and record 

the electrical activity in the muscles. Measures 

of the evoked activity may help in diagnosing 

upper motor neural dysfunction in MND or 

monitoring disease progression.
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How are motor neuron diseases treated?

There is no cure or standard treatment for the MNDs. Symptomatic and supportive 

treatment can help people be more comfortable 

while maintaining their quality of life. Multidisciplinary clinics, with specialists from neurology, physical therapy, respiratory therapy, 

and social work are particularly important in 

the care of individuals with MNDs.

The drug riluzole (Rilutek®), the only prescribed drug approved by the U.S. Food and 

Drug Administration to treat ALS, prolongs 

life by 2-3 months but does not relieve symptoms. The drug reduces the body’s natural 

production of the neurotransmitter glutamate, which carries signals to the motor 

neurons. Scientists believe that too much 

glutamate can harm motor neurons and 

inhibit nerve signaling.

Other medicines may help with symptoms. 

Muscle relaxants such as baclofen, tizanidine, 

and the benzodiazepines may reduce spasticity. Botulinum toxin may be used to treat 

jaw spasms or drooling. Excessive saliva can 

be treated with amitriptyline, glycopyolate, 

and atropine or by botulinum injections into 

the salivary glands. Combinations of dextromethorphan and quinidine have been shown 

to reduce pseudobulbar affect. Anticonvulsants and nonsteroidal anti-inflammatory 

drugs may help relieve pain, and antidepressants may be helpful in treating depression. 

Panic attacks can be treated with benzodiazepines. Some individuals may eventually 

require stronger medicines such as morphine 

to cope with musculoskeletal abnormalities or 
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pain, and opiates are used to provide comfort 

care in terminal stages of the disease.

Physical therapy, occupational therapy, and 

rehabilitation may help to improve posture, 

prevent joint immobility, and slow muscle 

weakness and atrophy. Stretching and strengthening exercises may help reduce spasticity, 

increase range of motion, and keep circulation 

flowing. Some individuals require additional 

therapy for speech, chewing, and swallowing 

difficulties. Applying heat may relieve muscle 

pain. Assistive devices such as supports or braces, 

orthotics, speech synthesizers, and wheelchairs 

may help some people retain independence.

Proper nutrition and a balanced diet are 

essential to maintaining weight and strength. 

People who cannot chew or swallow may 

require insertion of a feeding tube. In ALS, 

insertion of a percutaneous gastronomy tube 

(to help with feeding) is frequently carried 

out even before it is needed, when the individual is strong enough to undergo this minor 

surgery. Non-invasive ventilation at night can 

prevent apnea in sleep, and some individuals 

may also require assisted ventilation due to 

muscle weakness in the neck, throat, and 

chest during daytime.

What is the prognosis?

Prognosis varies depending on the type of MND and the age of onset. Some MNDs, 

such as PLS or Kennedy’s disease, are not fatal 

and progress slowly. People with SMA may 

appear to be stable for long periods, but improvement should not be expected. Some MNDs, 

such as ALS and some forms of SMA, are fatal.
What research is being done?

T he NINDS supports a broad range of research aimed at discovering the 

cause of MNDs, finding better treatments, 

and, ultimately, preventing and curing 

the disorders. Various MND animal models 

(animals that have been manipulated to 

mimic the disease in humans) are being 

used to study disease pathology and identify 

chemical and molecular processes involved 

in cellular degeneration. 

Research options fall largely into three categories: drugs, gene therapy, and stem cells.

Clinical trials are testing whether different 

drugs or interventions are safe and effective 

in slowing the progression of MNDs in 

patient volunteers. 

•	 The antibiotic ceftriaxone has been shown 

to protect nerves by reducing glutamate 

toxicity—believed by many scientists to play 

a critical role in the development of ALS—

in a mouse model of the disease. One study 

found that cellular ability to manage glutamate can alter the course of ALS. The drug 

is currently being tested in a NINDS-sponsored multi-center human clinical trial.

•	 The novel compound dexpramipexole 

has shown neuroprotective properties in 

multiple preclinical studies of ALS, and 

may work by increasing the efficiency 

of mitochondria—the energy-producing 

portion of the body’s cells. Mitochondria 

in the motor neurons undergo significant 

stress in ALS patients. The compound 

is currently being tested in an industrysponsored multi-center clinical trial.
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•	 Several early-stage clinical trials are 

testing the safety and feasibility of novel 

treatment strategies for ALS. These include 

cell-based approaches such as the transplantation of neural precursor cells into 

the spinal cord of ALS patients, and the 

infusion of so-called “anti-sense” compounds into the fluid that surrounds the 

spinal cord and brain to block production 

of toxic SOD1 protein in ALS patients who 

carry SOD1 mutations. 

Other compounds, including minocycline, 

coenzyme Q10, and lithium, have been tested 

and found ineffective in treating motor 

neuron diseases.

Cellular and molecular studies seek to 

understand the mechanisms that trigger 

motor neurons to degenerate. Examples 

include the following:

•	 Scientists are developing a broad range 

of model systems in animals and cells 

to investigate disease processes and 

expedite the testing of potential therapies. 

Among these efforts, a NINDS-sponsored 

consortium of scientists is deriving a type 

of stem cell from ALS patients and using 

these stem cells to form motor neurons 

and surrounding support cells. 

•	 Scientists have used gene therapy to 

halt motor neuron destruction and slow 

disease progression in mouse models of 

SMA and inherited ALS. The NINDS 

supports research to further explore this 

method and to provide a path toward 

clinical tests in patients.
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•	 Scientists have found that a specific class of 

compounds referred to as anti-sense oligonucleotides can either block or correct the 

processing of RNA molecules, which are the 

intermediates between genes and proteins. 

These compounds have shown therapeutic 

promise in model systems of ALS and SMA, 

and early-stage clinical testing is underway 

in ALS patients who carry SOD1 mutations.

•	 Scientists are using advance sequencing 

technologies to identify new gene mutations 

that are associated with MNDs. These gene 

discoveries have provided new insights into 

the cellular disease processed and identified 

possible intervention points for therapy.

•	 The excessive accumulation of free radicals, which has been implicated in ALS 

and a number of other neurodegenerative 

diseases, is being closely studied. Free 

radicals are highly reactive molecules 

that bind with other body chemicals and 

are believed to contribute to cell degeneration, disease development, and aging.

Where can I get more information? 

For more information on neurological disorders or research programs funded 

by the National Institute of Neurological 

Disorders and Stroke (NINDS), contact the 

Institute’s Brain Resources and Information 

Network (BRAIN) at: 

BRAIN

P.O. Box 5801

Bethesda, MD 20824

800-352-9424

www.ninds.nih.gov
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For general information about MNDs, contact: 

The ALS Association

1275 K Street, N.W., Suite 1040

Washington, DC 20005

202-407-8580

800-782-4747

www.alsa.org

ALS Therapy Development Institute

215 First Street, Second Floor

Cambridge, MA 02142

617-441-7200

www.als.net

Les Turner ALS Foundation

5550 W. Touhy Avenue, Suite 302

Skokie, IL 60077-3254

847-679-3311

888-ALS-1107

www.lesturnerals.org

Muscular Dystrophy Association

3300 East Sunrise Drive

Tucson, AZ 85718-3208

520-529-2000

800-344-4863

www.mda.org

Project ALS

3960 Broadway, Suite 420

New York City, NY 10032

212-420-7382

800-603-0270

www.projectals.org

Spastic Paraplegia Foundation

7700 Leesburg Pike, Suite 123

Falls Church, VA 22043

877-773-4483

www.sp-foundation.org
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For information primarily about SMA, contact:

Families of Spinal Muscular Atrophy

925 Busse Road

Elk Grove Village, IL 60007

847-367-7620

800-886-1762

www.fsma.org

Fight SMA/Andrew’s Buddies

1807 Libbie Avenue, Suite 104

Richmond, VA 23226

804-515-0080

www.fightsma.org

Kennedy’s Disease Foundation

P.O. Box 1105 

Coarsegold, CA 93614-1105

559-658-5950

www.kennedysdisease.org

Spinal Muscular Atrophy Foundation

888 Seventh Avenue, Suite 400

New York City, NY 10019

646-253-7100

877-386-3762

www.smafoundation.org

For information primarily about PPS, contact:

Post-Polio Health International, Including 

Ventilator Users Network

4207 Lindell Boulevard, Suite 110

St. Louis, MO 63108-2930

314-534-0475

www.post-polio.org

NIH . . . Turning Discovery Into Health

Prepared by:

Office of Communications and Public Liaison

National Institute of Neurological 

Disorders and Stroke

National Institutes of Health

Department of Health and Human Services

Bethesda, Maryland 20892

NIH Publication No. 12-5371 March 2012