U.S. DEPARTMENT OF HEALTH

AND HUMAN SERVICES

Public Health Service

National Institutes of Health

Narcolepsy
 

Narcolepsy
 

What is narcolepsy? 

Narcolepsy is a chronic brain disorder that involves poor control of sleep-wake 

cycles. People with narcolepsy experience 

periods of extreme daytime sleepiness and 

sudden, irresistible bouts of sleep that can 

strike at any time. These “sleep attacks” 

usually last a few seconds to several minutes. 

Narcolepsy can greatly affect daily activities. 

People may unwillingly fall asleep while at 

work or at school, when having a conversation, 

playing a game, eating a meal, or, most 

dangerously, when driving or operating other 

types of machinery. In addition to daytime 

sleepiness, other major symptoms may include 

cataplexy (a sudden loss of voluntary muscle 

tone while awake that makes a person go limp 

or unable to move), vivid dream-like images or 

hallucinations, as well as total paralysis just 

before falling asleep or just after waking-up. 

Contrary to common beliefs, people with 

narcolepsy do not spend a substantially 

greater proportion of their time asleep 

during a 24-hour period than do normal 

sleepers. In addition to daytime drowsiness 

and uncontrollable sleep episodes, most 

individuals also experience poor sleep quality 

that can involve frequent waking during 

nighttime sleep, and other sleep disorders. 

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For most adults, a normal night’s sleep lasts 

about 8 hours and is composed of four to six 

separate sleep cycles. A sleep cycle is defined 

by a segment of non-rapid eye movement 

(NREM) sleep followed by a period of 

rapid eye movement (REM) sleep. The 

NREM segment can be further divided into 

increasingly deeper stages of sleep according 

to the size and frequency of brain waves. 

REM sleep is accompanied by bursts of rapid 

eye movement along with sharply heightened 

brain activity and temporary paralysis of 

the muscles that control posture and body 

movement. When subjects are awakened, 

they report that they were “having a dream” 

more often if they had been in REM sleep 

than if they had been in NREM sleep. 

Transitions from NREM to REM sleep are 

controlled by interactions among groups of 

neurons (nerve cells) located in different 

parts of the brain. 

For normal sleepers a typical sleep cycle 

is about 100 to 110 minutes long, beginning 

with NREM sleep and transitioning to REM 

sleep after 80 to 100 minutes. People with 

narcolepsy frequently enter REM sleep 

within a few minutes of falling asleep. 

Who gets narcolepsy? 

Narcolepsy affects both males and females equally and appears throughout 

the world. Symptoms often start in childhood 

or adolescence, but can occur later in life. 

The condition is life-long. Narcolepsy is 

not rare, but it is an underrecognized and 

underdiagnosed condition. Narcolepsy with 
cataplexy is estimated to affect about one in 

every 3,000 Americans. More cases without 

cataplexy are also likely to exist. 

What are the symptoms? 

People with narcolepsy experience 

various types of day- and nighttime sleep 

problems that are associated with REM sleep 

disturbances that tend to begin subtly and 

may change dramatically over time. The most 

common major symptom, other than excessive 

daytime sleepiness (EDS), is cataplexy, which 

occurs in about 70 percent of all people with 

narcolepsy. Sleep paralysis and hallucinations 

are somewhat less common. Only 10 to 25 

percent of affected individuals, however, 

display all four of these major symptoms 

during the course of their illness. 

Excessive daytime sleepiness (EDS) 

EDS, the symptom most consistently 

experienced by almost all individuals with 

narcolepsy, is usually the first to become 

clinically apparent. Generally, EDS interferes 

with normal activities on a daily basis, 

whether or not individuals had sufficient 

sleep at night. People with EDS describe it 

as a persistent sense of mental cloudiness, a 

lack of energy, a depressed mood, or extreme 

exhaustion. Some people experience memory 

lapses, and many have great difficulty 

maintaining their concentration while 

at school, work, or home. People tend to 

awaken from such unavoidable sleeps feeling 

refreshed and finding that their drowsiness 

and fatigue subsides for an hour or two. 

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Involuntary sleep episodes are sometimes 

very brief, lasting no more than seconds at a 

time. As many as 40 percent of people with 

narcolepsy are prone to automatic behavior 

during such “microsleeps.” Automatic 

behavior involves performing a task during 

a short period of sleep but without any 

apparent interruption. During these episodes, 

people are usually engaged in habitual, 

essentially “second nature” activities such 

as taking notes in class, typing, or driving. 

They cannot recall their actions, and their 

performance is almost always impaired. 

Their handwriting may, for example, 

degenerate into an illegible scrawl, or they 

may store items in bizarre locations and 

then forget where they placed them. If an 

episode occurs while driving, individuals 

may get lost or have an accident. 

EDS, the most common of all narcoleptic 

symptoms, can be the result of a wide range 

of medical conditions, including other sleep 

disorders such as sleep apnea, various viral 

or bacterial infections, mood disorders 

such as depression, and chronic illnesses 

such as anemia, congestive heart failure, 

and rheumatoid arthritis that disrupt 

normal sleep patterns. Some medications 

can also lead to EDS, as can consumption 

of caffeine, alcohol, and nicotine. Finally, 

sleep deprivation has become one of the most 

common causes of EDS among Americans. 

Cataplexy 

Cataplexy is a sudden loss of muscle tone 

while the person is awake that leads to 

feelings of weakness and a loss of voluntary 
muscle control. Attacks can occur at any time 

during the waking period, with individuals 

usually experiencing their first episodes 

several weeks or months after the onset of 

EDS. But in about 10 percent of all cases, 

cataplexy is the first symptom to appear and 

can be misdiagnosed as a seizure disorder. 

Cataplectic attacks vary in duration and 

severity. The loss of muscle tone can be 

barely perceptible, involving no more than 

a momentary sense of slight weakness in 

a limited number of muscles, such as mild 

drooping of the eyelids. The most severe 

attacks result in a complete loss of tone in 

all voluntary muscles, leading to physical 

collapse during which individuals are unable 

to move, speak, or keep their eyes open. But 

even during the most severe episodes, people 

remain fully conscious, a characteristic 

that distinguishes cataplexy from seizure 

disorders. Although cataplexy can occur 

spontaneously, it is more often triggered by 

sudden, strong emotions such as fear, anger, 

stress, excitement, or humor. Laughter is 

reportedly the most common trigger. 

The loss of muscle tone during a cataplectic 

episode resembles the interruption of muscle 

activity that naturally occurs during REM 

sleep. A group of neurons in the brain stem 

halts activity during REM sleep, inhibiting 

muscle movement. Using an animal model, 

scientists have learned that this same 

group of neurons becomes inactive during 

cataplectic attacks, a discovery that provides 

a clue to at least one of the neurological 

abnormalities contributing to human 

narcoleptic symptoms. 

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Sleep paralysis 

The temporary inability to move or speak while 

falling asleep or waking is similar to REM-induced 

inhibitions of voluntary muscle activity. This 

natural inhibition usually goes unnoticed by 

people who experience normal sleep because 

it occurs only when they are fully asleep and 

entering the REM stage at the appropriate 

time in the sleep cycle. The attacks usually last 

a few seconds or minutes. Experiencing sleep 

paralysis resembles undergoing a cataplectic 

attack affecting the entire body. As with 

cataplexy, people remain fully conscious. Even 

when severe, cataplexy and sleep paralysis do 

not result in permanent dysfunction—after 

episodes end, people rapidly recover their 

full capacity to move and speak. 

Hallucinations 

Hallucinations can accompany sleep paralysis 

and occur when people are falling asleep, 

waking, or during sleep. Referred to as 

hypnagogic hallucinations when occurring 

during sleep onset and as hypnopompic 

hallucinations when occurring during 

waking, these images are unusually vivid, 

seem real, and can be frightening. Most 

often, the content is primarily visual, but 

any of the other senses can be involved. 

Disrupted nocturnal sleep 

While individuals with narcolepsy have 

no difficulties falling asleep at night, most 

experience difficulties staying asleep. 

Sleep may be disrupted by insomnia, vivid 

dreaming, sleep talking, acting out while 

dreaming, and periodic leg movements. 
Obesity 

After developing narcolepsy, many 

individuals suddenly gain weight, a side 

effect that can be prevented by active 

treatment. 

When do symptoms appear? 

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n most cases, symptoms first appear when 

people are between the ages of 7 and 25. 

In rare cases, however, narcolepsy may 

appear at younger age or in older adults. 

If left undiagnosed and untreated, early 

onset narcolepsy can interfere with 

psychological, social, and cognitive function 

and development and can undermine 

academic and social activities. 

What causes narcolepsy? 

Narcolepsy may have several causes. Most people with narcolepsy have low levels 

of the neurotransmitter hypocretin, which 

promotes wakefulness. Neurotransmitters 

are chemicals that neurons produce to 

communicate with each other and to regulate 

biological processes. 

Most cases of narcolepsy are sporadic, 

meaning the disorder occurs in individuals 

with no known family history of the disorder. 

But clusters in families sometimes occur—up 

to 10 percent of individuals diagnosed with 

narcolepsy with cataplexy report having a 

close relative with the same symptoms. In 

extremely rare cases, narcolepsy is caused 

by a genetic defect that prevents normal 

production of hypocretin molecules. While 

close relatives of people with narcolepsy 

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have a statistically higher risk of developing 

the disorder than do members of the general 

population, that risk remains low when 

compared to diseases that are purely 

genetic in origin. 

When cataplexy is present, the cause is most 

often the discrete loss of brain cells that 

produce hypocretin. Although the reason for 

such cell loss remains unknown, it appears 

to be autoimmune in nature (an autoimmune 

disorder is when the body’s immune system 

mistakenly attacks healthy cells or tissue). 

That is, the body’s immune system selectively 

attacks hypocretin-containing brain cells. 

Other factors appear to play important roles 

in the development of narcolepsy. Some rare 

cases are known to result from traumatic 

injuries to parts of the brain involved in REM 

sleep or from tumor growth and other disease 

processes in the same regions. Infections, 

exposure to toxins, dietary factors, stress, 

hormonal changes such as those occurring 

during puberty or menopause, and alterations 

in a person’s sleep schedule are just a few 

of the many factors that may exert direct or 

indirect effects on the brain, thereby possibly 

contributing to disease development. 

How is narcolepsy diagnosed? 

clinical examination and exhaustive 

medical history are essential for diagnosis 

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nd treatment. Your doctor may ask you to 

keep a sleep journal noting the times of sleep 

and symptoms over a one-to-two-week period. 

Although none of the major symptoms is 

exclusive to narcolepsy, cataplexy is the 
most specific symptom and is rarely present 

outside of narcolepsy. 

A physical exam can rule out or identify a 

condition that may be causing the symptoms. 

A battery of specialized tests, which can 

be performed in a sleep disorders clinic, 

is usually required before a diagnosis can 

be confirmed. 

Two tests in particular are essential in 

confirming a diagnosis of narcolepsy: the 

polysomnogram (PSG) and the multiple 

sleep latency test (MSLT). The PSG is 

an overnight test that takes continuous 

multiple measurements while the individual 

is asleep to document abnormalities in the 

sleep cycle. It records heart and respiratory 

rates, electrical activity in the brain using 

electroencephalography, and nerve activity 

in muscles through electromyography. A PSG 

can help reveal whether REM sleep occurs 

at abnormal times in the sleep cycle and can 

rule out the possibility that an individual’s 

symptoms result from another condition. 

The MSLT is performed during the day to 

measure a person’s tendency to fall asleep 

and to determine whether isolated elements 

of REM sleep intrude at inappropriate times 

during the waking hours. The sleep latency 

test measures the amount of time it takes for 

a person to fall asleep. As part of the test, an 

individual is asked to take four or five short 

naps usually scheduled 2 hours apart over the 

course of a day. Because sleep latency periods 

are normally 12 minutes or longer, a latency 

period of 8 minutes or less suggests a disorder 

of excessive daytime sleepiness. However, a 

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sleep latency of 8 minutes or less can be due 

to many conditions other than narcolepsy. The 

MSLT also measures heart and respiratory 

rates, records nerve activity in muscles, and 

pinpoints the occurrence of abnormally timed 

REM episodes through EEG recordings. 

If a person enters REM sleep either at the 

beginning or within a few minutes of sleep 

onset during at least two of the scheduled naps, 

this is considered an indication of narcolepsy. 

Other reasons for REM sleep on the MSLT 

must be ruled out, such as the effects of 

medication and disrupted sleep from sleep 

apnea or an irregular work-rest schedule. 

In some cases, human leukocyte antigen (HLA) 

typing (a marker of viral infection) may be 

helpful. Most HLA-associated disorders 

are autoimmune in nature. Certain alleles 

(genetic information found on a specific 

location on specific chromosomes) located 

on chromosome 6 are strongly associated 

with narcolepsy-cataplexy. To definitively 

identify a lack of hypocretin as the cause of 

narcolepsy, a sample of the cerebrospinal 

fluid (CSF) is removed by using a lumbar 

puncture and the level of hypocretin-1 is 

measured. When no other serious medical 

condition is present, low CSF hypocretin-1 

can establish hypocretin deficiency as the 

cause of narcolepsy. 

When cataplexy is not present, diagnosis 

must be made after excluding other possible 

causes of daytime sleepiness and fatigue, 

along with a positive MSLT. 
What treatments are available? 

Narcolepsy cannot yet be cured, but some of the symptoms can be treated 

with medicines and lifestyle changes. When 

cataplexy is present, the loss of hypocretin 

is believed to be irreversible and life-long. 

But EDS and cataplexy can be controlled 

in most individuals with drug treatment. 

Modafinil and sodium oxybate are two drugs 

that have been approved by the U.S. Food 

and Drug Administration for the treatment 

of narcolepsy. 

Doctors prescribe central nervous system 

alerting agents such as modafinil and 

amphetamine-like stimulants such as 

methylphenidate to alleviate EDS and reduce 

the incidence of sleep attacks. For most 

people these medications are generally quite 

effective at reducing daytime drowsiness 

and improving levels of alertness. However, 

use of these medications may be associated 

with several undesirable side effects and 

must be carefully monitored. Common side 

effects include irritability and nervousness, 

shakiness, disturbances in heart rhythm, 

stomach upset, nighttime sleep disruption, 

and anorexia. Individuals may also develop 

tolerance with long-term use, leading to 

the need for increased dosages to maintain 

effectiveness. In addition, doctors should 

be careful when prescribing these drugs 

and people should be careful using them 

because the potential for abuse is high 

with any amphetamine. 

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Two classes of antidepressant drugs have 

proved effective in controlling cataplexy 

in many individuals: tricyclics (including 

imipramine, desipramine, clomipramine, and 

protriptyline) and selective serotonin and 

noradrenergic reuptake inhibitors (including 

venlafaxine, fluoxetine, and atomoxetine). 

In general, antidepressants produce fewer 

adverse effects than do amphetamines. But 

troublesome side effects still occur in some 

individuals, including impotence, high blood 

pressure, and heart rhythm irregularities. 

In addition to central nervous system 

alerting agents and antidepressants, sodium 

oxybate or gamma hydroxybutyrate, also 

known as GHB or Xyrem®, can be used to 

treat narcolepsy. Sodium oxybate is a strong 

sedative that must be taken during the night. 

Sodium oxybate induces sleep and reduces 

the symptoms of daytime sleepiness and 

cataplexy. Due to safety concerns associated 

with the use of this drug, the distribution of 

sodium oxybate is tightly restricted. 

What behavioral strategies help people 

cope with symptoms? 

Currently available medications do not enable all people with narcolepsy to 

consistently maintain a fully normal state of 

alertness. Drug therapy should accompany 

various behavioral strategies according to 

the needs of the affected individual. 

Many individuals take short, regularly 

scheduled naps at times when they tend 

to feel sleepiest. 
Improving the quality of nighttime sleep 

can combat EDS and help relieve persistent 

feelings of fatigue. Among the most important 

common-sense measures people can take to 

enhance sleep quality are: 

•	 maintain a regular sleep schedule—go to 

bed and wake up at the same time every day 

•	 avoid alcohol and caffeine-containing 

beverages for several hours before bedtime 

•	 avoid large, heavy meals just before bedtime 

•	 avoid smoking, especially at night 

•	 maintain a comfortable, adequately 

warmed bedroom environment, and 

•	 engage in relaxing activities such as a 

warm bath before bedtime. 

Exercising for at least 20 minutes per day 

at least 4 or 5 hours before bedtime also 

improves sleep quality and can help people 

with narcolepsy avoid gaining excess weight. 

Safety precautions, particularly when driving, 

are particularly important for all persons 

with narcolepsy. EDS and cataplexy can lead 

to serious injury or death if left uncontrolled. 

Suddenly falling asleep or losing muscle 

control can transform actions that are 

ordinarily safe, such as walking down a 

long flight of stairs, into hazards. People 

with untreated narcoleptic symptoms are 

involved in automobile accidents roughly 

10 times more frequently than the general 

population. However, accident rates are 

normal among individuals who have 

received appropriate medication. 

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Support groups frequently prove extremely 

beneficial because people with narcolepsy 

may become socially isolated due to 

embarrassment about or misunderstandings 

related to their symptoms. Many people also 

try to avoid strong emotions, since humor, 

excitement, and other intense feelings can 

trigger cataplectic attacks. Support groups 

also provide individuals with a network of 

social contacts who can offer practical help 

and emotional support. 

The Americans with Disabilities Act 

requires employers to provide reasonable 

accommodations for all employees with 

disabilities. Adults can often negotiate with 

employers to modify their work schedules 

so they can take naps when necessary and 

perform their most demanding tasks when 

they are most alert. Similarly, children 

and adolescents with narcolepsy may be 

able to work with school administrators 

regarding special needs, including medication 

requirements during the school day, and to 

modify class schedules. 

What is the state of the science 

involving narcolepsy? 

During the past decade, scientists have made considerable progress 

in understanding narcolepsy-cataplexy 

pathogenesis and in identifying genes 

strongly associated with the disorder. 

The majority of people diagnosed with 

narcolepsy and cataplexy are known to 

have a specific HLA gene variant called 

DQB1*0602. They also frequently have 

specific alleles at a gene called the T- cell 
receptor alpha (TCRA), a protein on T cells 

that recognize HLA proteins. However, 

some people with narcolepsy-cataplexy do 

not have the variant genes, while many 

people in the general population without 

narcolepsy do possess these variant genes. 

Specific variations in HLA and TCRA genes 

increase an individual’s predisposition to 

develop the disorders—possibly through a 

yet-undiscovered route involving changes 

in immune-system function—when other 

causative factors are present. 

Many other genes besides those making up 

the HLA complex and the T-cell receptor 

may contribute to the development of 

narcolepsy. Groups of neurons in several 

parts of the brain stem and the central brain, 

including the thalamus and hypothalamus, 

interact to control sleep. Large numbers 

of genes on different chromosomes control 

these neurons’ activities, any of which could 

contribute to the development of the disease. 

Scientists studying narcolepsy in dogs have 

identified a mutation that appears to cause 

the disorder in Dobermans, Labradors, and 

Dachshunds. This mutated gene disrupts the 

ability to receive the signal from hypocretins 

(also known as orexins) that are produced 

by neurons located in the hypothalamus. 

The neurons that produce hypocretins are 

active during wakefulness, and research 

suggests that they keep the brain systems 

needed for wakefulness from shutting 

down unexpectedly. Mice born without 

functioning hypocretin genes develop 

symptoms of narcolepsy. 

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Except in rare cases, narcolepsy in humans 

is not associated with mutations of the 

hypocretin gene. However, scientists 

have found that brains from humans with 

narcolepsy often contain greatly reduced 

numbers of hypocretin-producing neurons. 

It is believed that certain HLA and TCRA 

subtypes increase susceptibility to an 

immune attack on hypocretin neurons in 

the hypothalamus, leading to degeneration 

of these important cells. Other factors also 

may interfere with proper functioning 

of this system. The hypocretins regulate 

appetite and feeding behavior in addition 

to controlling sleep. Therefore, the loss of 

hypocretin-producing neurons may explain 

not only how narcolepsy develops in some 

people, but also why people with narcolepsy 

have higher rates of obesity compared to 

the general population. 

Narcolepsy onset follows a seasonal pattern 

of higher rates in spring and early summer, 

following winter upper airway infection 

season. When studied close to disease 

onset, individuals with narcolepsy have 

high levels of antibodies to a marker 

called ASO, indicating response to a recent 

bacterial infection such as strep throat. 

In addition, there is growing evidence that 

exposure to H1N1 virus (also called swine 

flu), or a special form of H1N1 vaccine 

(administered in Europe) can act as a 

rare trigger for the disease. It is not yet 

known if these infectious agents are direct 

triggers for the disease, or whether they 

increase likelihood of disease indirectly. 
What research is being done? 

Within the Federal government, the National Institute of Neurological 

Disorders and Stroke (NINDS), a component 

of the National Institutes of Health (NIH), 

has primary responsibility for sponsoring 

research on neurological disorders. As part 

of its mission, the NINDS supports research 

on narcolepsy and other sleep disorders 

through grants to medical institutions 

across the country. 

Within the National Heart, Lung, and 

Blood Institute, also a component of the 

NIH, the National Center on Sleep Disorders 

Research (NCSDR) coordinates Federal 

government sleep research activities, 

promotes doctoral and postdoctoral training 

programs, and educates the public and 

health care professionals about sleep 

disorders. For more information, visit 

the NCSDR website at www.nhlbi.nih.gov/ 

about/ncsdr/index.htm. 

NINDS-sponsored researchers are 

conducting studies devoted to further 

clarifying the wide range of genetic factors— 

both HLA genes and non-HLA genes—that 

may cause narcolepsy. Other scientists are 

conducting investigations using animal 

models to identify neurotransmitters other 

than the hypocretins that may contribute to 

disease development. A greater understanding 

of the complex genetic and biochemical 

bases of narcolepsy will eventually lead 

to the formulation of new therapies to 

control symptoms and may lead to a cure. 

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Researchers are also investigating the 

modes of action of wake-promoting 

compounds to widen the range of available 

therapeutic options. 

Abnormal immunological processes may 

be an important element in the cause of 

narcolepsy. NINDS-sponsored scientists 

have demonstrated the presence of unusual, 

possibly pathological, forms of immunological 

activity in narcolepsy. Further, strep throat 

is now suggested to be involved as a trigger 

in some predisposed individuals. These 

researchers are now investigating whether 

drugs that suppress immunological 

processes may interrupt the development 

of narcolepsy. 

Finally, the NINDS continues to support 

investigations into the basic biology of 

sleep, including the brain mechanisms 

involved in generating and regulating 

REM sleep. A more comprehensive 

understanding of the complex biology 

of sleep will undoubtedly further clarify 

the pathological processes that underlie 

narcolepsy and other sleep disorders. 

How can I help research? 

The NINDS contributes to the support of the Human Brain and Spinal Fluid 

Resource Center in Los Angeles. This 

bank supplies investigators around the 

world with tissue from individuals with 

neurological and other disorders. Tissue 
from individuals with narcolepsy is needed 

to enable scientists to study this disorder 

more intensely. Prospective donors 

may contact: 

Human Brain and Spinal Fluid 

Resource Center 

Building 212 

West Los Angeles Healthcare Center 

11301 Wilshire Blvd. (127A) 

Los Angeles, CA 90073 

310-268-3536 

24-hour pager: 310-636-5199 

www.loni.ucla.edu/uclabrainbank 

The NINDS supports genetic and 

immunological research in narcolepsy at 

Stanford University. This research involves 

the study of blood samples. Blood samples 

from individuals with narcolepsy can be sent 

by mail and are needed to enable scientists 

to study this disorder more intensely. 

Prospective donors may contact: 

Stanford University Center For Narcolepsy 

450 Broadway Street 

M/C 5704 

Redwood City, CA 94063 

650-721-7550 

www.med.stanford.edu/school/psychiatry/ 

narcolepsy 

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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, 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 

Information also is available from the 

following organizations: 

Narcolepsy Network, Inc. 

129 Waterwheel Lane 

North Kingstown, RI 02852 

401-667-2523 

888-292-6522 

www.narcolepsynetwork.org 

National Sleep Foundation 

1010 N. Glebe Road, Suite 310 

Arlington, VA 22201 

703-243-1697 

www.sleepfoundation.org 

National Heart, Lung, and Blood 

Institute (NHLBI) 

Health Information Center 

National Institutes of Health, DHHS 

P.O. Box 30105 

Bethesda, MD 20892-0105 

301-592-8573 

240-629-3255 (TTY) 

www.nhlbi.nih.gov 

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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 2540 

NIH Publication No. 13 1637 July 2013