Postgraduate Medicine

ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20

What is causing excessive daytime sleepiness?

Mark W. Mahowald

To cite this article: Mark W. Mahowald (2000) What is causing excessive daytime sleepiness?,
Postgraduate Medicine, 107:3, 108-123, DOI: 10.3810/pgm.2000.03.932

To link to this article: http://dx.doi.org/10.3810/pgm.2000.03.932

Published online: 30 Jun 2015.

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 SYMPOSIUM: FIRST OF FOUR ARTICLES ON SLEEP DISORDERS

What is causing excessive daytime sleepiness?

Evaluation to distinguish sleep deprivation from sleep disorders

Mark W. Mahowald, MD

PREVIEW
Many people have a temporary spell, often in early afternoon, when they feel drowsy. This passing desire
for a quick nap is completely different from excessive daytime sleepiness, which is a much more significant
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problem. Considering the potentially dire personal and economic consequences of falling asleep uninten,
tionally or at inappropriate times, excessive daytime sleepiness must be taken very seriously. A thorough
evaluation, as described by Dr Mahowald, virtually always leads to a specific underlying cause, allowing
effective treatment recommendations.

T
he prevalence of excessive daytime sleepi-
ness, reported by up to 31% of the adult pop-
ulation, is extraordinary, 1 and consequences
of the complaint can be significant, including acci-
dents, negative economic and public health out-
comes, reduced work and school performance, and
impaired psychosocial functioning. For instance, ma-
jor industrial disasters, such as those at Chernobyl,
Three Mile Island, and Bhopal, and serious acci-
dents, such as those involving the Exxon Valdez and
Challenger, have been officially attributed to errors
in judgment caused by sleepiness in the workplace.
Each year in the United States, car crashes involving
drivers falling asleep at the wheel exceed 100,000 in
number and result in at least 1,500 deaths. This
death rate may surpass that of alcohol-related crashes
among young Americans. Given the number of people
with excessive daytime sleepiness and the potential
outcomes, it is important that physicians, educators,
and public policy makers approach this complaint
thoughtfully.
For a helpful guide to electronic and print resources on sleep dis-
orders for physicians and patients, see page 181.
True excessive daytime sleepiness is rarely, if ever
(contrary to popular opinion), due to a psychological
or psychiatric condition {eg, depression), laziness, or
boredom. In the absence of sleep deprivation, day-
time sleepiness is almost inevitably caused by an iden-
tifiable and treatable sleep disorder. Those discussed
in this article are sleep apnea, narcolepsy, and idio-
pathic central nervous system (CNS) hypersomnia.
Less common causes of excessive daytime sleepiness
are beyond the scope of this article but include
Kleine-Levin syndrome, menstrual-related hyper-
somnia, idiopathic recurrent stupor, and circadian
rhythm disturbances.
Volitional sleep deprivation
By far, the most common cause of excessive daytime
sleepiness in modern society is chronic sleep depriva-
tion. We sleep 25% less than our forebears did a cen-
tury ago. There is no evidence that they required
more sleep than we do or that we require less sleep.
than they did. Thus, our sleep deprivation is voli-
tional, often driven by social or economic factors.
For instance, about 20% of employees in industri-
alized countries are employed in shift work. It has

108 EXCESSIVE DAYTIME SLEEPINESS I VOL 107 I NO 3 I MARCH 2000 I POSTGRADUATE MEDICINE
Downloaded by [Ryerson University Library] at 21:55 25 September 2017
been shown that night-shift workers sleep an average
of 8 hours less each week than do day workers-an
amount equaling the loss of an entire night's sleep
every week. Nonstop availability of e-mail, shopping,
and stock market information on the Internet as well
as all-night television and 24-hour businesses are in-
creasingly encouraging sleep deprivation.
Sufficient sleep is not measured in absolute hours
VOL 107 I NO 31 MARCH 2000 I POSTGRADUATE MEDICINE I EXCESSIVE DAYTIME SLEEPINESS
Illustration:© 2000. Melissa Carden Bean
obtained but, rather, in terms of whether the patient
awakens rested and restored. The amount needed ap-
pears to be genetically determined. Although the av-
erage total sleep time nightly is 7.5 to 8 hours,
healthy adults can require anywhere from 4 to 10
hours of sleep. 2 Therefore, people who need 10 hours
of sleep a night but receive only 8 hours may become
severely sleep deprived and notably hypersomnolent.
continued
109
 EXCESSIVE DAYTIME SLEEPINESS, CONTINUED

Sleep deprivation is also cumula- the disorder. Commonly used sub-

tive. A person does not come to
require less sleep or get used to
being sleep-deprived.
Obstructive sleep apnea
The prevalence of clinically sig-
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Sleep deprivation is
cumulative. Aperson does
not come to require
less sleep or get used to
being sleep-deprived.
jective sleepiness questionnaires
(eg, the Epworth Sleepiness
Scale) may have poor correlation
with the presence or severity of
obstructive sleep apnea and with
the degree of objective sleepi-
ness.5 For this reason, formal sleep

nificant obstructive sleep apnea studies (discussed later) are

in the general population is high.
It is found in at least 2% of women and 4% of men,
making it about as prevalent as asthma or diabetes. 3
Although it is most common in adults, men, snorers,
postmenopausal women, the elderly, and overweight
people, obstructive sleep apnea is also seen often in
children, young women, and asthenic people. The
erroneous impression that sleep apnea is confined to
middle-aged, overweight men has resulted in under-
4
diagnosis in women and children. In addition, about
one third of patients with sleep apnea are not obese.
In fact, most obese men and the overwhelming ma-
jority of obese women do not have sleep apnea.
Consequences of obstructive sleep apnea fall into
two major categories: excessive daytime sleepiness
caused by sleep fragmentation, and physiologic after-
effects of sleep-related desaturation ( eg, systemic or
pulmonary hypertension, right-sided heart failure,
polycythemia). Morning headaches are a less reliable
symptom of sleep apnea than previously thought.
Clinical diagnosis of sleep apnea may be difficult.
Numerous studies have repeatedly shown marked
discrepancies between the clinically suspected and
the laboratory-documented presence or severity of
Mark W. Mahowald, MD
Dr Mahowald is director, Minnesota Regional Sleep Disorders Center,
Hennepin County Medical Center, and professor, department of neurology,
University of Minnesota Medical School, Minneapolis.
Correspondence: Mark W. Mahowald, MD, Minnesota Regional Sleep
Disorders Center, Hennepin County Medical Center, 701 Park Ave S,
Minneapolis, MN 55415-1829. E-mail: mahow002@tc.umn.edu.
mandatory in suspected cases.
Indications for formal sleep studies are well accepted,
and numerous clinical-practice guidelines exist for
both adults 6·9 and children. 10
There is substantial evidence that in many pa-
tients with obstructive sleep apnea, the upper airway
is smaller and more narrow laterally than in people
without the disorder. 11 Techniques developed to eval-
uate the structure of the upper airway include
cephalometric roentgenography, somnofluoroscopy,
acoustic-reflection studies, flow-volume curves, and
Muller's and Valsalva's maneuvers. Such studies have
been proposed as selective and predictive for success
of upper airway surgical procedures (particularly
uvulopalatopharyngoplasty). Regrettably, the predic-
tive value, with few anecdotal exceptions, has been
disappointing.
Efforts to develop ambulatory or screening studies
are ongoing. Practice parameters for use of portable
recordings in assessment of obstructive sleep apnea
have recently been developed. 12 '13 However, before
these techniques are widely adopted, they must be
thoroughly evaluated.
Currently, the treatment of choice for obstructive
sleep apnea is nasal continuous positive airway pres-
sure.14 Another option is one of the various surgical
procedures, including permanent tracheostomy, uvu-
lopalatopharyngoplasty, mandibular-advancement
measures, and hyoid suspension. 11 The variable and
often disappointing results of upper airway surgery for
apnea are likely related to the fact that craniofacial
abnormalities in these patients may involve multiple
continued on page 115

110 EXCESSIVE DAYTIME SLEEPINESS I VOL107 I NO 3 I MARCH 2000 I POSTGRADUATE MEDICINE

 EXCESSIVE DAYTIME SLEEPINESS, CONTINUED

levels of the upper airway. Me- reduced environmental stimula-

chanical devices designed to ad- tion ( eg, reading, watching tele-
vance the mandible may be ef- Formal sleep studies are vision, riding in or driving a mo-
fective in certain (usually mild) mandatory in suspected cases tor vehicle, during classes or
cases. 16 of obstructive sleep apnea. meetings).
Ancillary symptoms may in-
Narcolepsy clude cataplexy, sleep paralysis,
and hypnagogic (at sleep onset) and hypnopompic
Narcolepsy is a relatively common disorder (preva- (upon awakening) hallucinations. Notably, fewer
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lence, 0.09%) that affects at least 250,000 people in
the United States. The prevalence approximates that
of Parkinson's disease and multiple sclerosis. More
than 90% of patients carry the HLA-DR2/DQ1 (un-
der current nomenclature, HLA-DR15 and HLA-
DQ6) gene, which is found in less than 30% of the
17
general population. This association is present to
varying degrees in different ethnic populations and
represents the highest disease-HLA linkage known
in medicine. Clearly, there is a genetic component in
narcolepsy, and it is of intense scientific interest and ness is complete, resulting in falling down or being
research value. However, the variability in the pres-
ence of HLA associations in the general public and
in patients with narcolepsy precludes the genetic
component's utility as a diagnostic test. The associ-
ated HLA type is neither necessary nor sufficient for
the appearance of narcolepsy.
Age at onset of narcolepsy is usually adolescence
or early adulthood, although it ranges from early
childhood to senescence (3 to 72 years of age). Onset
appears to peak about age 15, with a secondary peak
about age 36. After a relatively brief period of pro-
gression as the disease declares itself, narcolepsy
tends to stabilize. However, it rarely, if ever, com-
pletely disappears.
Manifestations
Psychosocial and socioeconomic consequences of
narcolepsy are significant. 18 Excessive daytime sleepi- rapidly oscillating occurrence of wakefulness and
ness is the primary symptom. Unwanted or unantici-
pated sleep episodes last seconds to minutes and occur
at inappropriate times, particularly during periods of
than half (14% to 42%) of patients with narcolepsy
report all three of these ancillary symptoms along
with sleep attacks. In many patients, sleep attacks
precede the appearance of ancillary symptoms, often
by decades.
Cataplexy is sudden loss of muscle tone, typically
triggered by emotion (eg, laughter, anger, excitement,
delight, surprise). About 65% to 70% of patients with
narcolepsy have cataplexy, and about 30% never ex-
perience it. Although occasionally the muscle weak-
forced to sit, more commonly it is mild and more fo-
cal, taking the form of facial sagging, slurred speech,
localized weakness of an extremity, or a feeling of the
knees giving way. The absence of a history of cata-
plexy does not rule out the diagnosis of narcolepsy.
Sleep paralysis is experienced by up to 60% of pa-
tients with narcolepsy and is often very frightening.
It consists of total-body paralysis, with sparing of res-
piration and eye movements, lasting from seconds to
minutes. Hallucinations consisting of extremely vivid,
often frightening dreams that occur during the tran-
sition between wakefulness and sleep are reported by
12% to 50% of patients. Both sleep paralysis and hal-
lucinatory phenomena are also found quite often
among people who do not have narcolepsy.
Automatism occurs in as many as 80% of patients
with narcolepsy and represents the simultaneous or
sleep. During such spells, the patient appears to be
awake but does not have full awareness and may ex-
hibit extremely inappropriate behavior. As a result,
continued

VOL 107 I NO 3 I MARCH 2000 I POSTGRADUATE MEDICINE I EXCESSIVE DAYTIME SLEEPINESS 115
 EXCESSIVE DAYTIME SLEEPINESS, CONTINUED

r----------------------------------------------------------------------------------------------------------------------------------------------.,
''
INFORMATION FOR PATIENTS ''
''
''
''
What to expect during sleep studies '
i
''
''
Sleep studies are used to evaluate The Multiple Sleep Latency Test What happens after the MSL T? i '
excessive sleepiness during the day (MSLT) The electrodes will be removed '
J,

and the possibility of obstructive This test is also a series of record- with a liquid that dissolves the glue
sleep apnea, narcolepsy, or other ings that monitor your sleep pat- without hurting your hair or skin. !'
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sleep disorder. The tests cause no
pain or discomfort.
The polysomnogram
A polysomnogram is a series of
recordings of measurements taken
while you sleep. The measurements
help show your doctor what is hap-
pening during the various stages of
sleep. Yau may be asked to remain
in the sleep laboratory for the en-
tire night to complete this study.
A technologist will glue elec-
trodes to your scalp, face, chest,
and legs. He or she will then attach
a wire (called a lead) to each
electrode, which is connected to
equipment that will measure such
functions as your eye and leg move-
ments and the electrical activity of
your heart and brain. In addition,
elastic bands may be put around
your chest and abdomen to mea-
sure your breathing. You will be
able to read or watch television un-
til you are ready to fall asleep. The
leads are long, so you can turn over
and sleep in any position you wish.
terns by measuring your eye move-
ments, muscle-tone changes, and
brain electrical activity. It takes 8
to 10 hours and is performed during
the day.
How is the MSLT performed?
• A technologist will glue record-
ing electrodes to your scalp and
face and then check with a meter
to ensure that all electrodes are
functioning properly.
• Yau will be taken into a "sleeping"
room, the lights will be turned off,
and you will be asked to take a 15- to
20-minute nap. Recordings will be
taken while you sleep. Even if you
cannot sleep during the test, the in-
formation gained will still be useful.
• After each testing (nap) period,
the technologist will awaken you
and disconnect all the wires. Yau
may leave the area but will be
asked to return in 2 hours for an-
other testing period. There will be
at least four testing periods, some-
times five depending on results,
spaced 2 hours apart.
''
Unless given other instructions, ''
''
you will be ready to go home. Yau ''
''
may wash your hair as you wish. '
Test results should be available i
''
from your doctor in about a week. ''
''
''
:
How should I prepare for the
MSLT?
• If you are taking stimulant drugs
for narcolepsy, you should discon-
tinue them (under the direction of
your doctor) about 2 to 3 weeks be-
fore the test. Continue taking any
other prescribed medications un-
less your doctor gives you special
instructions.
• Wash any sprays, gels, or other
products out of your hair before
coming for the test.
• Bring reading material or some-
thing else to keep you occupied
during the 2-hour intervals be-
tween testing periods. Yau may
want to bring a family member or
friend along to help keep you
awake during these intervals.

116 EXCESSIVE DAYTIME SLEEPINESS I VOL 107 I NO 3 I MARCH 2000 I POSTGRADUATE MEDICINE
 EXCESSIVE DAYTIME SLEEPINESS, CONTINUED
partial complex seizures or a psychogenic dissociative
(fugue) state may be erroneously diagnosed.
The underlying pathophysiology of narcolepsy re-
sults in impaired control of the boundaries that nor-
mally separate the state of wakefulness from rapid eye
movement (REM) or non-REM sleep. Total sleep
time per 24-hour period in people with narcolepsy is
similar to that in people without the disorder. 19 How-
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ever, control of onset and offset of both REM and
non-REM sleep is impaired. Moreover, there is a clear
dissociation of various components of the individual
wake and sleep states. Cataplexy and sleep paralysis
simply represent the isolated and inappropriate in-
trusion or persistence of REM sleep-related atonia
(paralysis) into wakefulness. The hypnagogic or
hypnopompic hallucinations are REM sleep-related
dreams occurring during wakefulness.
Diagnostic approach
The diagnosis of narcolepsy may be suspected on the
basis of the patient's history. Some investigators be-
lieve that a report of cataplexy is pathognomonic of
narcolepsy, but that is not necessarily the case. A his-
tory of "classic" narcolepsy with cataplexy may be
the manifestation of a somatoform disorder. 20 In view
of the nature and duration of narcolepsy treatment
with stimulant medications, objective sleep labora-
tory diagnosis is imperative.
In narcolepsy, formal sleep studies should consist
of polysomnography and a multiple sleep latency test
(MSLT). (See box on page 116.) All-night polysom-
nography must be performed the night before the
MSLT to determine the quality and quantity of the
preceding night's sleep. The MSLT is a well-validated
measurement of the tendency to fall asleep during nor-
mal waking hours. It consists of four or five opportuni-
ties, at 2-hour intervals throughout the day, to take a
15- to 20-minute nap. Patients with narcolepsy typi-
cally fall asleep in 5 minutes or less and usually display
REM sleep on at least two of the daytime naps, an
occurrence rarely seen in people without the disorder.
VOL 107 I NO 3 I MARCH 2000 I POSTGRADUATE MEDICINE I EXCESSIVE DAYTIME SLEEPINESS
The MSLT is particularly valuable in differentiating
between true sleepiness and fatigue or lack of energy.
False-negative MSLTs do occur. 21 Therefore,
MSLT results must be interpreted in light of the pa-
tient's clinical symptoms and results of the preceding
night's polysomnogram. Telling a patient that he or
she does not have narcolepsy on the basis of negative
MSLT results is analogous to discharging a patient
with chest pain from the emergency department on
the basis of normal electrocardiography results.
The occurrence of symptomatic narcolepsy caused
by identifiable CNS abnormalities is extremely rare.
Further neurologic studies are indicated only in cases
in which history taking or neurologic examination
strongly suggests structural CNS abnormality.
Treatment
Stimulant medications, such as mazindol (Mazanor,
Sanorex), methylphenidate hydrochloride (Methylin,
Ritalin), methamphetamine hydrochloride (Desoxyn),
dextroamphetamine sulfate, and modafinil (Pro-
vigil), are used to control hypersomnia. (Use of pe-
moline [Cylert] is discouraged because it has been as-
sociated with fatal hepatic necrosis.) Only modafinil
(200 mg once daily) has been studied and approved
for use in narcolepsy, rendering recommended maxi-
mum doses for the other agents arbitrary and without
scientific basis. Many practitioners gradually increase
the dosage until symptoms are controlledY The
abuse potential of such agents in patients for whom
they are therapeutic has been greatly overrated, as
have cardiovascular and psychiatric consequences. 22 •26
Treatment of ancillary symptoms includes use of
tricyclic antidepressants, selective serotonin reup-
take inhibitors, and gamma-hydroxybutyrate (cur-
rently not available in the United States). 21
Idiopathic CNS hypersomnia
Idiopathic CNS hypersomnia may represent one of
several conditions that present as unexplained exces-
continued
117
 EXCESSIVE DAYTIME SLEEPINESS, CONTINUED
Locations of sleep-disorder centers and
laboratories
US clinics accredited by the American Sleep
Disorders Association, listed by state, are available
at http://www.asda.org/centers.htm.
Canadian clinics, listed by province, are available
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at http:/ /www.geocities.com/HotSprings/183 7/
can-labs2.html.
sive daytime sleepiness in the absence of sleep depri-
vation or other identifiable abnormality.Z 8 Chronic
sleep deprivation must be aggressively ruled out. As
with narcolepsy, the implications of indefinite treat-
ment with stimulant medications require objective
diagnosis with formal studies to confirm the subjec-
tive complaint of excessive daytime sleepiness and to
rule out unsuspected sleep-related disorder.
In idiopathic CNS hypersomnia, results of the all-
night polysomnogram are unremarkable, and the
MSLT reveals objective hypersomnia without the oc-
currence of REM sleep during the naps. HLA studies
are not indicated, nor are neuroimaging studies in
the absence of clinical or neurologic examination
findings suggestive of structural CNS abnormality.
Medication-induced hypersomnia
Certain agents may cause true hypersomnia. The
best studied are the conventional sedative-hypnotic
agents, such as barbiturates, benzodiazepines, and the
newer nonbenzodiazepine sedative-hypnotic drugs
(eg, zolpidem tartrate [Ambien], zaleplon [Sonata],
zopiclone [which is not available in the United
States]). Many medications that are occasionally
118
prescribed for insomnia, such as tricyclic antidepres-
sants and antihistaminic agents, may cause drowsi-
ness, but their ability to improve the quality or quan-
tity of sleep has been poorly studied.
Although it is common to attribute excessive day-
time sleepiness to a wide variety of medications, few
objective studies are available to document that
non-sedative-hypnotic drugs truly cause hypersom-
nia. Obermeyer and Benca29 have published a review
of this topic.
Conclusion
In the absence of obvious sleep deprivation, formal
sleep studies are usually indicated in cases of hyper-
somnia that is severe enough to interfere with work,
driving, or enjoyment of family activities or hobbies.
An MSLT should be performed whenever any identi-
fied abnormality on the all-night polysomnogram is
not clearly sufficient to explain the extent of daytime
symptoms. Obstructive sleep apnea and periodic ex-
tremity movements during sleep are very common in
asymptomatic patients, so their presence during
polysomnography must be interpreted in the entire
clinical context. Notably, although a given patient
may have depression, depression is not an explana-
tion for true excessive daytime sleepiness. Sleep dis-
orders and depression certainly may coexist, how-
ever, and sleepiness may masquerade as or exacerbate
depression. Use of sleep diaries and actigraphy (see
the article by Dr Attarian in this symposium, page
12 7) may be invaluable in the setting of recurrent
hypersomnia or circadian dysrhythmias. IUt'l
Earn CME credit on the Web.
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continued on page 123
EXCESSIVE DAYTIME SLEEPINESS I VOL 107 I NO 3 I MARCH 2000 I POSTGRADUATE MEDICINE
 EXCESSIVE DAYTIME SLEEPINESS, CONTINUED
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