CASE CONFERENCES
Sleep Fragments
Section Editors: Bernie Sunwoo, M.D., and Mihaela Teodorescu, M.D.

A Case of Daytime Sleepiness after Motor Vehicle Collision
Yuki Iizuka1, Jason Cassidy2, and Omar A. Mesarwi2
1
School of Medicine, University of California, San Diego, and 2Division of Pulmonary, Critical Care, and Sleep Medicine, School of Medicine,
University of California, San Diego, San Diego, California

Case Vignette
A 26-year-old medical student presented to
the sleep center at the University of
California, San Diego, with excessive
daytime sleepiness occurring after a major
motor vehicle collision 18 months prior.

Injuries at that presentation included
intracranial hemorrhage and subdural
hematoma with cerebral edema and
severe deceleration shear injury; facial
fractures; and fractures of multiple long
bones. At the time of the clinic visit, the
patient reported 16 months of excessive

daytime sleepiness, with an Epworth
Sleepiness Scale score of 12; nightly sleep of
8–10 hours between 10:00 P.M. and 8:00 A.M.;
and one to three naps of 10–90 minutes
each per day. He drank two cups
of coffee daily; was not taking any
medications; and reported no recent weight

Figure 1. Aggregate data from the patient’s polysomnogram. Oxygen saturation as measured by pulse oximetry (SpO2), arousals, leg movements, respiratory
events, and hypnogram are shown (top to bottom). Respiratory events consisted almost exclusively of respiratory effort–related arousals; very few hypopneas or
apneas were seen. The hypnogram is notable for several spontaneous arousals from sleep, none of which led to prolonged periods of wakefulness.

(Received in original form June 9, 2018; accepted in final form October 12, 2018 )
Correspondence and requests for reprints should be addressed to Omar A. Mesarwi, M.D., Division of Pulmonary, Critical Care, and Sleep Medicine, School of
Medicine, University of California, San Diego, 9300 Campus Point Drive, Mail Code 7381, La Jolla, CA 92037. E-mail: omesarwi@ucsd.edu.
Ann Am Thorac Soc Vol 16, No 2, pp 265–267, Feb 2019
Copyright © 2019 by the American Thoracic Society
DOI: 10.1513/AnnalsATS.201806-383CC
Internet address: www.atsjournals.org

Case Conferences: Sleep Fragments

265

CASE CONFERENCES
Table 1. Sleep architecture and respiratory data from the patient’s polysomnogram
Sleep architecture
Time in bed
Total sleep time
Sleep efficiency
Sleep latency
Wake after sleep onset
REM latency
Respiratory data
Central apneas, n (index)
Obstructive apneas, n (index)
Hypopneas, n (index)
Respiratory effort related arousals, n (index)
Apneas 1 hypopneas, total (index)
Apneas 1 hypopneas 1 RERAs, total (index)

NREM
4 (0.7)
0 (0)
1 (0.2)
28 (4.6)
5 (0.8)
33 (5.5)

528 min
463 min
87.6%
39 min
27 min
54 min
REM
0 (0)
0 (0)
2 (1.2)
3 (1.8)
2 (1.2)
5 (3.0)

Total
4 (0.5)
0 (0)
3 (0.4)
31 (4.2)
7 (0.9)
38 (4.9)

Definition of abbreviations: NREM = non–rapid eye movement; REM = rapid eye movement; RERAs =
respiratory event–related arousals.

Figure 2. Representative 30-second epoch from nap 3 of the patient’s multiple sleep latency test, demonstrating rapid eye movement sleep.

change, hallucinations, sleep paralysis, or
cataplexy. The patient’s vital signs were
normal, and his body mass index was
24.6 kg/m2. Physical examination
demonstrated a neck circumference of
15.5 inches, Mallampati 4 airway, clear
breath sounds without stridor, and
various scars. Neurological examination was
unremarkable aside from a left homonymous
hemianopia.
A polysomnogram showed a sleep time
of 463 minutes with sleep efficiency of 88%.
Sleep latency was 39 minutes, and
266

rapid eye movement (REM) latency was
54 minutes. Sleep architecture was normal
aside from several spontaneous arousals
(Figure 1). Very mild periodic limb
movements (8.4/h) were observed.
The patient’s apnea–hypopnea index was
less than one event per hour with normal
oxyhemoglobin saturations (Table 1). A
multiple sleep latency test (MSLT) showed
sleep on five of five naps, mean sleep
latency of 7:32, and sleep-onset REM
periods (REM sleep occurring within
15 min of sleep onset) on four of five naps

(Figure 2). A diagnosis of narcolepsy type 2
was made.

Questions
1. What is the differential diagnosis for
excessive daytime sleepiness in this
presentation?
2. What other testing might be done to help
reinforce the diagnosis?
[Continue onto next page for answers]

AnnalsATS Volume 16 Number 2 | February 2019

CASE CONFERENCES
Discussion
Narcolepsy is a disorder characterized
by excessive daytime sleepiness. Most
individuals with narcolepsy also have
cataplexy, a sudden loss of muscle tone
during wakefulness that is evoked by strong
emotional stimuli such as laughter. Patients
with narcolepsy may experience a host of
other symptoms, including nocturnal
hallucinations, sleep paralysis, vivid dreams,
or sleep disturbance. Patients are
categorized as having narcolepsy type 1
(NT1, with cataplexy or low cerebrospinal
fluid [CSF] hypocretin levels), or narcolepsy
type 2 (NT2, without these features).
Although NT1 is believed to arise from
a lack of hypocretin signaling in the
lateroposterior hypothalamus, perhaps by
an autoimmune mechanism, the pathologic
insult leading to NT2 is less clear (1).
NT1 is diagnosed by clinical presentation
(cataplexy and at least 3 mo of daily periods
of irrepressible need for sleep) and MSLT
demonstrating a mean sleep latency less
than or equal to 8 minutes and two or
more sleep-onset REM periods. Patients
without cataplexy may also be diagnosed
with NT1 if their CSF hypocretin level is less
than or equal to 110 pg/ml, but this test is
uncommonly performed in clinical practice.
Patients with NT2 have at least 3 months
of daily periods of irrepressible need for
sleep, but there is no cataplexy, and CSF
hypocretin levels are normal. MSLT in NT2
is similarly abnormal to MSLT in those with
NT1 (2). Patients in whom narcolepsy is
suspected should generally be free of REMsuppressing medications, such as certain
classes of antidepressants, before their
polysomnogram/MSLT, and adequate sleep
times should usually be documented with
actigraphy or sleep diaries (1).
Several reports and case series have
described the apparent association between
narcolepsy and traumatic or other brain
insult. As far back as 1936, Hall and LeRoy

reported that a sharp increase in narcolepsy
cases had been reported since World War I
(3). Although polysomnography was
nonexistent at that time, they presented
several cases that seem clinically consistent
with NT1 and in each case described a
history of head injury antecedent to the
development of symptoms. Lankford
and colleagues reported a case series of
post-traumatic narcolepsy and suggested
that “narcolepsy may be ‘dormant’ and that,
in cases genetically at risk, even a minor
injury to the central nervous system can
cause that person to become symptomatic”
(4). In this series, several patients had
human leukocyte antigen markers
associated with narcolepsy. Narcolepsy
associated with brain injury may be
underdiagnosed: In a well-characterized
cohort of 87 patients with traumatic brain
injury (TBI), 6% were identified to have
narcolepsy using criteria slightly more strict
than those published in the International
Classification of Sleep Disorders, Third
Edition (2, 5, 6). Intriguingly, there have been
reports of TBI specifically affecting the
hypothalamus, giving rise to post-traumatic
narcolepsy (7). However, no studies
have correlated the severity of TBI with
narcolepsy incidence. Given that there are
approximately 1.5 million TBI cases per
year in the United States (8), the true
prevalence of post-traumatic narcolepsy may
be quite high. Thus, this clinical entity is
likely underrecognized, and therefore it is
important for clinicians evaluating patients
with TBI to query for symptoms of
narcolepsy among other sleep disorders.

Answers
1. What is the differential diagnosis for
excessive daytime sleepiness in this
presentation?
With examination evidence of a crowded
upper airway and history of TBI, both

References
1 Scammell TE. Narcolepsy. N Engl J Med 2015;373:2654–2662.
2 American Academy of Sleep Medicine. International Classification of
Sleep Disorders. 3rd ed. Darien, IL: American Academy of Sleep
Medicine; 2014.
3 Hall GW, LeRoy GB. Post-traumatic narcolepsy. JAMA 1936;106:
431–434.
4 Lankford DA, Wellman JJ, O’Hara C. Posttraumatic narcolepsy in
mild to moderate closed head injury. Sleep 1994;17(8, Suppl):
S25–S28.

Case Conferences: Sleep Fragments

obstructive and central sleep apnea
are possible; other issues related to the
patient’s prior injuries may include
nocturnal seizures, pain and associated
a-wave intrusion, and post-traumatic
hypersomnolence.
2. What other testing might be done to help
reinforce the diagnosis?
In general, patients undergoing
polysomnography with MSLT should have
sleep time documented by use of either
sleep diaries or actigraphy for 1–2 weeks
before the test date, because insufficient
sleep may cause an abnormally reduced
mean sleep latency. This was not done in the
present case, owing to family members
adamantly substantiating the patient’s
sleep time, although in general this history
may be subjective. Insufficient sleep
should not cause sleep-onset REM periods
during the majority of naps, however. In
addition, once the diagnosis of narcolepsy is
made, CSF may be sampled to check the
hypocretin level. If low (<110 pg/ml), this
would reclassify the patient as NT1.
However, this reclassification would not
likely impact treatment decisions.

Follow-Up
The patient was started on 200 mg of
modafinil with significant improvement
in his daytime sleepiness. He did note
a persistent sense of daytime fatigue
and said that he takes a nap if his
schedule permits. Owing to the patient’s
reluctance to try other stimulant agents,
he was instead encouraged to take an
additional dose of modafinil before
evening shifts or during long hospital
shifts. This has been tolerated to good
effect. He continues to have no difficulty
falling asleep. n
Author disclosures are available with the text
of this article at www.atsjournals.org.

5 Castriotta RJ, Wilde MC, Lai JM, Atanasov S, Masel BE, Kuna ST.
Prevalence and consequences of sleep disorders in traumatic brain
injury. J Clin Sleep Med 2007;3:349–356.
6 Ruoff C, Rye D. The ICSD-3 and DSM-5 guidelines for diagnosing
narcolepsy: clinical relevance and practicality. Curr Med Res Opin
2016;32:1611–1622.
7 Yi K, Chung S, Park B, Kim JS. Post-traumatic narcolepsy associated
with thalamic/hypothalamic injury. Sleep Med Res 2015;6:81–83.
8 Taylor CA, Bell JM, Breiding MJ, Xu L. Traumatic brain injury–related
emergency department visits, hospitalizations, and deaths — United
States, 2007 and 2013. MMWR Surveill Summ 2017;66:1–16.

267