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Sanjeev V. Kothare, Rebecca Quattrucci Scott (Eds.) - Sleep Disorders in Adolescents - A Clinical Casebook-Springer International Publishing (2017)
Sanjeev V. Kothare, Rebecca Quattrucci Scott (Eds.) - Sleep Disorders in Adolescents - A Clinical Casebook-Springer International Publishing (2017)
Kothare
Rebecca Quattrucci Scott Editors
Sleep Disorders
in Adolescents
A Clinical Casebook
123
Sleep Disorders in Adolescents
Sanjeev V. Kothare
Rebecca Quattrucci Scott
Editors
Sleep Disorders
in Adolescents
A Clinical Casebook
Editors
Sanjeev V. Kothare Rebecca Quattrucci Scott
Department of Neurology NYU Comprehensive Epilepsy
Director, Pediatric Sleep Program Center-Sleep Center
NYU Comprehensive Sleep Department of Neurology
Disorders Center NYU Langone Medical Center
Professor, Department of New York, NY, USA
Neurology
NYU Langone Medical Center
and NYU School of Medicine
New York, NY, USA
We would like to dedicate this book to all the patients and their
families who taught us even more than our textbooks. We have
penned these experiences in this book to enrich your experience in
similar situations, and we hope that this will enable you to treat
your patients even more effectively. We would also like to
acknowledge all the fellows whom we have trained over the years
and who taught us to introspect on how we manage our patients to
their best satisfaction. Several of these trainees have contributed to
chapters in this book. Finally we would like to acknowledge our
families, for their understanding for being away from them as we
worked on this book.
v
Contents
1 Introduction .................................................................. 1
Sanjeev V. Kothare and Rebecca Quattrucci Scott
2 Delayed Sleep Phase Syndrome .................................. 7
Sasha D. Jaquez, Tushar P. Thakre,
and Jyoti Krishna
3 Restless Legs Syndrome............................................... 27
Mandana Mahmoudi and Sanjeev V. Kothare
4 Obstructive Sleep Apnea in Adolescence ................... 45
Stacey Gunn and Umakanth A. Khatwa
5 Narcolepsy in Adolescence .......................................... 61
Anne Marie Morse and Sanjeev V. Kothare
6 Parasomnias in Adolescents ........................................ 79
Joseph Kaleyias, Rebecca Quattrucci Scott,
and Sanjeev V. Kothare
7 Sleep in Adolescents with Psychiatric Disorders....... 95
Ujjwal Ramtekkar and Anna Ivanenko
8 Medical Disorders ........................................................ 119
Vicky Chiang and Alcibiades J. Rodriguez
9 Brain Tumors................................................................ 133
Danielle M. Graef and Valerie McLaughlin Crabtree
10 Insomnia........................................................................ 155
Mariya Narizhnaya and Matthew R. Ebben
vii
viii Contents
ix
x Contributors
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Delayed Sleep Phase
Syndrome 2
Sasha D. Jaquez, Tushar P. Thakre,
and Jyoti Krishna
Abbreviations
Case Presentation 1
Discussion
In the patient above, a thorough sleep history and sleep logs (see
Fig. 2.1) would be needed to properly diagnose her sleep con-
cerns. Lack of snoring and leg symptoms as well as a normal
physical examination make the diagnosis of sleep-related breath-
ing or movement disorder unlikely to explain her presentation.
Nor is she likely to have primary insomnia or hypersomnia disor-
der given her lack of symptoms on longer breaks from her school
when she is able to consistently delay her sleep schedule. Based
on her sleep logs, it is evident that the diagnosis that best fits
Hannah is DSWPD.
The International Classification of Sleep Disorders, Third
Edition (ICSD-3), lists DSWPD (formerly known as Delayed Sleep
Phase Syndrome) under the broad category of Circadian Rhythm
Sleep-Wake Disorders (CRSWD) [1]. In DSWPD, the problem lies
Fig. 2.1 Sample sleep logs. Sleep logs showing sleep-wake routines for
Hannah. Note the feeling of daytime tiredness on school days ceases during
winter break when a liberal sleep schedule is allowed
10 S.D. Jaquez et al.
Pitfalls
Learning Points
Case Presentation 2
Discussion
a 3
Advance
2
Phase Shift (h)
1
-1
Delay
-2
-3
-9 -6 -3 0 3 6 9 12 15
14 17 20 23 2 5 8 11
Average Clock Time (h)
b
2
Phase Shift (h)
1
0
-1
-2
-3
-4
6 9 12 15 18 21 0 3 6 9 12 15 18
Circadian Phase
(Melatonin midpoint = 22 h)
Fig. 2.3 (a) Melatonin phase response curve. The three pulse phase response
curve (PRC) to 3 mg of exogenous melatonin generated from subjects free-
running during an ultradian LD cycle. Phase shifts of the DLMO are plotted
against the time of administration of the melatonin pill relative to the base-
line DLMO (top x-axis). The average baseline DLMO is represented by the
upward arrow, the average DLMOff by the downward arrow, and the aver-
age assigned baseline sleep times from before the laboratory sessions are
enclosed by the vertical lines. Each dot represents the phase shift of an indi-
vidual subject, calculated by subtracting the phase shift during the placebo
session (free-run) from the phase shift during the melatonin session. The
curved line illustrates the dual harmonic curve fit. The average clock
time axis (bottom x-axis) corresponds to the average baseline sleep times.
This PRC can be applied to people with different sleep schedules by mov-
ing the average clock time axis until the vertical lines align with the individu-
al’s sleep schedule. Figure and legend reprinted with permission from [12].
2 Delayed Sleep Phase Syndrome 15
Fig. 2.3 (continued) (b) Light phase response curve The PRC to the bright
light stimulus using melatonin midpoints as the circadian phase marker. Phase
advances (positive values) and delays (negative values) are plotted against the
time of the center of the light exposure relative to the melatonin midpoint on
the pre-stimulus CR (defined to be 22 h), with the core body temperature mini-
mum assumed to occur 2 h later at 0 h. Data points from circadian phases 6–18
are double plotted. The filled circles represent data from salivary melatonin in
subject 1 8K8 from whom blood samples were not acquired. The solid curve
is a dual harmonic function fitted through all of the data points. The horizontal
dashed line represents the anticipated 0.54 h average delay drift of the pace-
maker between the pre- and post-stimulus phase assessments. Figure and
legend reprinted with permission from [13]
16 S.D. Jaquez et al.
Pitfalls
Exogenous
Bright light
melatonin
Clock time
Fig. 2.4 Phase advancement using melatonin and bright light therapy. Normal
sleep time is dependent on the circadian clock. In normal persons, endogenous
melatonin rises in the evening a little before natural sleep onset and falls to
low levels before natural awakening in phase with external time cues such as
sunlight (blue curve). In delayed sleep-wake phase disorder this rhythm is
shifted to a later clock time such that the person goes to sleep and rises later
relative to acceptable social norms (red curve). Therapy with low-dose exog-
enous melatonin early in the evening (blue arrow) and/or bright light in the
morning (red arrow) has been used to shift the circadian phase towards normal
(phase advancement)
Learning Points
Case Presentation 3
Discussion
Pitfalls
Learning Points
Case Presentation 4
Discussion
Pitfalls
Learning Points
Conclusion
Disclosure None of the authors has any financial support or conflicts of inter-
est to disclose.
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Restless Legs Syndrome
3
Mandana Mahmoudi and Sanjeev V. Kothare
Abbreviations
Case 1
M. Mahmoudi, M.D.
Pulmonary, Critical Care, and Sleep Medicine, New York University
Langone Medical Center, New York, NY, USA
e-mail: mandana.mahmoudi@nyumc.org
S.V. Kothare, M.D. (*)
Department of Neurology, NYU Langone Medical Center
and NYU School of Medicine, 223 East 34th Street,
New York, NY, USA
e-mail: sanjeev.kothare@nyumc.org
Stephanie states that she has trouble falling asleep at night, as her
legs ache and occasionally cramp when lying in bed. She some-
times gets up and walks around, but that relieves her leg discomfort
only temporarily. Her parents describe her sleep as “restless,” and
she “tosses and turns” at least for an hour until she falls asleep.
Until 1 year ago, she would not awaken during the night, but now
she awakens 3–4 times at night, unless exhausted. Her symptoms
are worse when she is very tired, and occur at least 2–3 times a
week. The only other change is that she started menstruating about
18 months ago, at age 13. She has a normal developmental history,
as well as a normal general and neurologic examination. Her family
history is notable for RLS in her maternal aunt and cousin.
Biochemical investigations reveal a normal thyroid function, vita-
min B12 and folic acid levels, transferrin saturation, and complete
blood count. Her serum ferritin level was 22 ng/ml. Polysomnography
revealed delayed sleep onset due to leg movements, as well as 8
PLMS per hour of sleep, most of which occurred in stage 2 sleep,
with 72% being associated with arousals from sleep. RLS was con-
firmed, likely in the setting of relative iron deficiency, and Stephanie
was started on a trial of oral iron combined with vitamin C to
enhance absorption. At 3-month follow-up, her ferritin level was
97 ng/ml, and her symptoms of leg discomfort, restlessness, and
daytime irritability resolved almost entirely.
Discussion
Pitfalls
Learning Points
Case 2
Discussion
• Orthostatic tremor Fine leg tremor manifest by a sense of poor balance while Yes No No No
standing, but not while walking. Therefore, patients cannot
stand still but need to walk. Unlike RLS, there are no symptoms
while sitting or lying down and no circadian pattern
• Nocturnal cramps Leg cramps that come on at night and are relieved with No No No Yes
stretching or walking. Experienced as an unusually painful
muscular contraction, often involving the calf muscles. Unlike
RLS, sensations are sudden onset, short duration, usually
palpable contractions
• Arthritis, lower Discomfort centered mostly in joints, increased with movement No No No No
limb pain
• Positional Often comes on with prolonged sitting or lying in the same No No No No
discomfort position, but usually relieved by a simple change in position
(continued)
33
Table 3.1 (continued)
34
Pitfalls
Learning Points
Case 3
Discussion
Pitfalls
Learning Points
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70. Davis ID, Greenbaum LA, Gipson D, Wu LL, Sinha R, Matsuda-Abedini
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2012;27(3):451–9.
Obstructive Sleep Apnea
in Adolescence 4
Stacey Gunn and Umakanth A. Khatwa
Abbreviations
S. Gunn, M.D.
Division of Pulmonary, Critical Care and Sleep, Beth Israel Deaconess
Medical Center, Boston, MA, USA
U.A. Khatwa, M.D. (*)
Division of Respiratory Diseases, Department of Medicine,
Boston Children’s Hospital, 333 Longwood Ave, LO486,
Boston, MA 02115, USA
e-mail: umakanth.khatwa@childrens.harvard.edu
Clinical Case 1
Discussion
AHI > 5 events per hour) [5]. This decision depends on the clinical
context of the individual patient.
Patients with mild or moderate degrees of sleep apnea (less than
10 events per hour) may be at acceptable risk to undergo day sur-
gery. Patients with severe OSA, defined as AHI > 10 events per
hour, or severe gas exchange abnormalities (oxygen saturation
nadir <80 % or significant hypoventilation), are at higher risk for
postoperative complications and should be monitored at least over-
night in an inpatient setting. The most common complications
associated with adenotonsillectomy are pain and poor oral intake,
with more severe complications including hemorrhage, infection,
and respiratory decompensation. Risk factors for pulmonary
complications following adenotonsillectomy in the adolescent age
group include severe OSA (AHI > 10 events per hour, SpO2 nadir
<80 %, or significant hypoventilation), morbid obesity, neuromus-
cular disease, pulmonary hypertension, Down syndrome, craniofa-
cial abnormalities, asthma, sickle cell disease, congenital heart
disease, or a history of respiratory compromise. Respiratory
decompensation is associated with higher baseline AHI, higher
BMI z-score, and lower O2 saturation nadir [6].
Following adenotonsillectomy, all patients should be reassessed
clinically for residual symptoms. A follow-up PSG is indicated
when there was moderate-to-severe disease preoperatively, or fac-
tors associated with an increased risk of residual OSA, which are
outlined in Table 4.2. The ideal timing of a follow-up study is
2–3 months, to allow an appropriate postoperative recovery period,
but also protect the patient from prolonged periods of untreated
apnea in the event of residual disease.
Pitfalls
Table 4.2 Factors associated with high risk of residual OSA in adolescents
High preoperative AHI (AHI > 10/h)
Obesity (BMI > 30)
Underbite, overbite, crossbite
Severe allergic rhinitis (hypertrophic turbinates, regrown adenoids)
Neuromuscular weakness
Glossoptosis
Craniofacial syndromes
Lingual tonsillar hypertrophy
Occult laryngomalacia
Age-related increased upper airway collapsibility
Adenoid facies
Micrognathia
Age of adenotonsillectomy > 7 years
Learning Points
Clinical Case 2
sleep apnea with AHI of 40 events per hour, and O2 saturation nadir
87 %. He underwent adenotonsillectomy, tolerated the procedure
well, had an uneventful postoperative recovery, and was discharged
to home the following day.
In 2-month follow-up, his mother noted that he continued to
snore, and his symptoms of daytime sleepiness had not improved.
His weight had increased from prior, to BMI 32.5 kg/m2. On follow-
up PSG, he had a high residual AHI of 22 events per hour. CPAP
was titrated from 5–12 cm H2O, with 8 cm H2O appearing optimal
to relieve obstruction. He was started on therapy with CPAP 8 cm
H2O, recommended to sleep in non-supine positioning, and encour-
aged to focus on weight loss. He was also referred for otolaryngol-
ogy evaluation, and there were no clear sites of anatomic
obstruction observed on flexible nasolaryngoscopy in the clinic.
At his follow-up visit one month later, he had good compliance with
CPAP, with use on more than 80 % of nights, and reported improve-
ment in his daytime energy levels. A plan was made to continue CPAP
therapy, in conjunction with efforts at weight loss.
Discussion
Pitfalls
Learning Points
Clinical Case 3
He was scheduled for a repeat sleep study, with the baseline por-
tion notable for a high residual OAHI of 26 events per hour, again
with moderate desaturations and elevated CO2. On titration, 8 cm
H2O relieved obstruction in lateral NREM, although 13 cm H2O
could not completely eliminate obstruction in supine REM, and
the patient was unable to sleep at higher pressures. He was pre-
scribed AutoCPAP 8–13 cm H2O with a recommendation for non-
supine sleep.
In follow-up 6 weeks later, he reported ongoing difficulty toler-
ating CPAP, only able to tolerate therapy for 1–2 h per night. He
was scheduled for drug-induced sleep endoscopy (DISE), which
revealed significantly enlarged nasal turbinates blocking 90 % of
the nostrils, with a deviated nasal septum causing complete
obstruction of the right-sided nasal passage. There was adenoidal
regrowth, with more than 50 % obstruction. There was a signifi-
cant degree of tongue base obstruction with complete blockage,
and markedly enlarged 4+ lingual tonsils completely closing the
laryngeal inlet. The epiglottis was omega-shaped and retroflexed.
On jaw thrust maneuver, the airway opened nicely, and the vocal
cords were seen to have normal movement.
Based on the results of this procedure, the patient underwent
upper airway surgery, which included turbinectomy, nasal septo-
plasty, revision adenoidectomy, and lingual tonsillectomy. He tol-
erated the procedure well and was discharged to home with
AutoCPAP 5–10 cm H2O.
Repeat polysomnography 8 weeks later demonstrated good
reduction in the residual AHI to 4.8 events per hour, with O2 satu-
ration nadir 92 %. The patient reported less daytime sleepiness
and an improved attention span. He had lost 3 kg after enrolling in
a weight loss program. CPAP was able to be discontinued.
Discussion
There are multiple risk factors present that put this patient at a high
risk for perioperative complications (see previous discussion), and
he was appropriately admitted to the hospital for urgent initiation of
CPAP and adenotonsillectomy, then to the intensive care unit for
56 S. Gunn and U.A. Khatwa
Pitfalls
Learning Points
Conclusion
References
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et al. Diagnosis and management of childhood obstructive sleep apnea
syndrome. Pediatrics. 2012;130(3):e714–55.
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tomy. Arch Otolaryngol Head Neck Surg. 2011;137(1):15–8.
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of weight loss on sleep-disordered breathing in obese teenagers. Obesity.
2009;17(6):1178–83.
4 Obstructive Sleep Apnea in Adolescence 59
Abbreviations
Clinical Case 1
Discussion
Pitfalls
Learning Points
Clinical Case 2
Discussion
Pitfalls
Learning Points
Clinical Case 3
Results of Testing
Sleep logs prior to testing consistent with report of sleep time from
9 pm to 6 am and frequent intentional and unintentional napping
throughout the day.
PSG: AHI 0.7, lowest O2 95 %.
There was a reduced sleep latency during the study (2.5 min),
as well as a reduced REM latency of 4 min (SOREMP*). Sleep
efficiency was reduced (77 %).
MSLT: Mean Sleep Latency: 3.5 min, 5 SOREMPs.
HLA-DQB1*06:02 positive.
Discussion
The case demonstrates a clinical scenario that was seen after the
H1N1 pandemic in 2009. The history and clinical findings are diag-
nostic of narcolepsy with cataplexy. It is important to differentiate
delayed sleep phase disorder (DSPD) in this age group since MSLT
findings may falsely lead to a diagnosis of narcolepsy. Delayed
sleep phase disorders (DSPD) and insufficient sleep syndromes can
demonstrate reduced sleep latency as well as sleep onset REM peri-
ods. A careful history, use of a sleep log or actigraphy prior to PSG/
70 A.M. Morse and S.V. Kothare
MSLT, and thorough evaluation of the PSG for other primary sleep
disorders, such as sleep apnea, DSPD, insomnia, or periodic limb
movement disorders is critical to accurately diagnosing narcolepsy.
This is especially important in the diagnosis of narcolepsy type 2,
where there is an absence of cataplexy events to help in distinguish-
ing the diagnosis. A clue to DSPD is delayed sleep latency on the
sleep study and reduced sleep latency with possible sleep onset
REM in the first nap trial of her MSLT.
Narcolepsy has been seen associated with Pandemrix vaccina-
tion (an adjuvanted, influenza pandemic vaccine) and also with
infection by influenza virus during the 2009 A (H1N1) influenza
pandemic [18]. The vaccine safety surveillance system detected
this very rare adverse effect that occurred in less than one out of
10,000 vaccine recipients in subjects receiving AS03 adjuvanted A
(H1N1) pandemic vaccine made using the European inactivation/
purification protocol [19]. Individuals with HLA-DQB1*0602
allele(s) are considered to be genetically susceptible. In 2010, there
was a threefold increase in the number of 17–19 years old in Finland
that were affected with narcolepsy with this HLA subtype [20].
The underlying pathophysiology related to the sudden increase in
incidence was not well understood until recently. Melen et al. evalu-
ated for risk of H1N1 virus infection contributing to the sudden
increase in the incidence of childhood narcolepsy observed in Finland
in 2010 and found it to be unlikely [21]. In 2015, Ahmed et al. pro-
vided evidence of the relationship of the Pandemrix vaccine to the
development of narcolepsy [19]. They demonstrated that a signifi-
cant proportion of sera from HLA-DQB1*0602 haplotype-positive
narcoleptic Finnish patients with a history of Pandemrix vaccination
(vaccine-associated narcolepsy) contained antibodies to hypocretin
receptor 2 compared to sera from nonnarcoleptic individuals with
either 2009 A (H1N1) pandemic influenza infection or history of
receiving the Focetria vaccination given in Italy [18]. Influenza vac-
cines containing the A (H1N1) pdm09 virus strain used in the United
States were not associated with an increased risk of narcolepsy [22].
Therefore, Pandremix is no longer available, but other vaccinations
appear to be safe even for genetically susceptible patients. Effect of
the vaccine on patients with an established diagnosis of narcolepsy is
unknown.
5 Narcolepsy in Adolescence 71
Pitfalls
Learning Points
Clinical Case 4
Discussion
Pitfalls
Learning Points
Conclusions
References
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78 A.M. Morse and S.V. Kothare
Abbreviations
PSG Polysomnography
REM Rapid eye movement
RDB REM behavior disorder
RLS Restless legs syndrome
SRED Sleep-related eating disorder
SSRI Selective serotonin reuptake inhibitor
ST Sleep terrors
SW Sleep-walking
SWS Slow wave sleep
Clinical Case 1
Two brothers aged 13 and 16 years old were brought to the emer-
gency room accompanied by their parents due to a violent incident
which occurred around 3 am in the children’s bedroom. The
younger boy reported that his brother punched him violently in
sleep, pushed him away, and finally attempted to chock him while
screaming loudly. The clinical examination of the younger boy
revealed several bruises and lacerations consistent with his allega-
tions. The elder boy reported that, when his parents woke him up
during that incident, he was dreaming that he was in a space craft
and was fighting with an alien. Several months ago, he began spo-
radically to have episodes in which he would sit up in bed while
sleeping, with his eyes closed, speak loudly and clearly for several
minutes, and then fall back to sleep. Other behaviors included run-
ning out of his room. The frequency of these episodes gradually
increased and in the last month he had at least three episodes every
week. The adolescent was difficult to wake up during these events;
on awakening, he had partial dream recall of a violent scene,
appeared confused, and was unaware of the motor activity. The
adolescent suffers from depression and is under anti-depressant
treatment for the last 9 months. The patient denied smoking or
consuming alcohol. The physical examination was unremarkable.
Overnight polysomnographic monitoring showed a total sleep
time of 8.1 h, poor sleep continuity, decreased sleep efficiency, and
a lack of normal muscle paralysis (atonia) during REM sleep. The
patient was diagnosed as having REM sleep behavior disorder
(RBD). The selective serotonin reuptake inhibitor (SSRI) was
6 Parasomnias in Adolescents 81
Discussion
Pitfalls
Learning points
Clinical Case 2
Discussion
weight gain from eating high calorie foods and causing various
injuries due to consumption of inedible or toxic items [1]. Level of
consciousness during SRED episodes ranges from partial con-
sciousness to dense unawareness typical of somnambulistic epi-
sodes [16]. This disorder typically involves eating peculiar forms
or combinations of food, or possibly dangerous or toxic sub-
stances. Like disorders of arousal, most patients do not have full
recall of the event. Eating can occur multiple times in one night,
typically with high caloric foods.
SRED can be idiopathic or commonly associated with other
primary sleep disorders such as sleepwalking, restless legs syn-
drome (RLS), obstructive sleep apnea syndrome (OSAS), other
clinical conditions, or use of sedative-hypnotic medications
[16–21].
SRED should be distinguished from night eating syndrome
(NES), which is characterized by full recall of the eating and
absence of bizarre or toxic ingestion [22]. Night eating syndrome
(NES) is another important condition in the disordered night-time
eating spectrum, showing hyperphagia episodes just before noc-
turnal sleep without accompanying amnesia. NES could be con-
sidered an abnormality in the circadian rhythm of meal timing
with accompanying anxiety disorder. The two conditions often
overlap and possibly share a common pathophysiology [16].
The sleep-related eating episodes are not linked to daytime eat-
ing disturbances such as bulimia nervosa, binge-eating disorder, or
anorexia nervosa [1]. The average age of onset is approximately
from 22–27 years. This condition affects females (65 %) more than
males, and 80 % of patients describe a diminished level of con-
sciousness during eating episodes, with a varying degree of amne-
sia for the events [23]. The main feature that distinguishes these
two conditions is the level of awareness during the food intake,
which is not impaired in NES. Furthermore, consumption of at
least 25 % of intake after the evening meal and morning anorexia
are typical features of NES. Studies have suggested that SSRIs
may be an effective treatment of NES, while the anti-seizure medi-
cation topiramate may be an effective SRED treatment [24, 25].
SSRIs can worsen SRED [25].
6 Parasomnias in Adolescents 85
Pitfalls
Learning Points
Clinical Case 3
Discussion
1. Confusional arousals
Confusional arousals (CA) are characterized by disoriented
behavior or slow mentation during or after an arousal from
NREM sleep [1]. They occur most often out of stage N3 sleep
and during the first third of the night. Therefore, most of the
episodes tend to occur at the same time every night and can be
predictable. The patient often displays vocalizations with occa-
sional complex behaviors and typically has a poor recall of
events the following day. Attempts to awaken the person are
often unsuccessful and may be met with vigorous resistance;
occasionally, the patient can become aggressive and violent.
Prevalence rate in children 3–13 years of age is 17.3 %, while in
children older than 15 years and in adults, prevalence is as high
as 6.9 % [33]. In most cases, patients outgrow the problem.
88 J. Kaleyias et al.
Sleep walking
Risk assessment
(frequency, violence, consequences)
NO
DisablingSW YES
Safety precautions
Sleep hygiene
No treatment Avoid alcohol PSG
Reassure family Avoid medication inducing SW
Pitfalls
Learning Points
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Sleep in Adolescents
with Psychiatric Disorders 7
Ujjwal Ramtekkar and Anna Ivanenko
Discussion
Learning Points
asked about the content, she reveals that she was sexually assaulted
by two boys at age 14 during the out of town tennis camp that she
disclosed only to close friends in the camp. However, during the
most recent tournament, she saw one of the boys and suddenly
started having anxiety, nightmares about the assault, and irritabil-
ity during the day due to intrusive thoughts. She reports feeling
emotionally drained and very guilty when thinking about the inci-
dent and always worries about the reaction of her parents and
friends if they were to find out. Jane reports that her decision to
quit sports is based on avoiding any chances to confront the boy
again. She also endorses significant anxiety interfering with her
ability to focus on school and family.
Discussion
Learning Points
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7 Sleep in Adolescents with Psychiatric Disorders 117
Abbreviations
V. Chiang, B.S.
Department of Neurology, New York University Medical School,
16019 Crestline Dr., La Mirada, CA 90638, USA
e-mail: vc936@nyumc.org
A.J. Rodriguez, M.D. (*)
Department of Neurology, New York University Medical School,
724 Second Avenue, New York, NY 10016, USA
e-mail: alcibiades.rodriguez@nyumc.org
Clinical Case 1
Discussion
Pitfalls
Learning Points
Clinical Case 2
Discussion
Table 8.2 Obstructive sleep apnea (OSA) and hypothyroidism clinical features
Clinical OSA Hypothyroidism
Obestiy Yes Yes
Sleepiness Variable in children, Mostly fatigue
hyperactive
Snoring Most of the time Variable, present if OSA
Thyroid levels Normal Abnormal
Enlarged thyroid No Variable
Systemic None usually Constipation, slow reflexes, brittle
manifestations hair, sensitivity to cold increased
Depression At times if severe Frequent
Cognition Decreased attention, Impaired memory if severe,
hyperactive, irritable irritable
Pitfalls
Learning Points
Clinical Case 3
Sixteen year-old girl who presents with his mother due to exacerba-
tion of migraine headaches for the last two months. She has had
headaches since age 11. These headaches are throbbing, unilateral
126 V. Chiang and A.J. Rodriguez
(either left or right side), associated with nausea and, at times, vomit.
She mentions phonophobia and photophobia associated with them.
The typical headaches occur, at least, once a week and last from
4–12 h if untreated, but she also has chronic daily headaches, which
may last the whole day if untreated. In the past, the headaches
occurred once or twice a year. She has tried acetaminophen and ibu-
profen for these headaches with no success. She has been given
butalbital/acetaminophen/caffeine tablets with resolution of her
headaches, but these return quickly after the effect wears off. She
takes this medication several times a day. She was recommended to
take valproic acid for headache prevention, but she did not like the
side effects profile and she did not take it.
Her mother and paternal aunt have a history of migraines. Her
past medical history is significant for having heavy menstrual peri-
ods since 1 year ago and significant weight gain. She sleeps from
10–11 PM and she does not have any problems to fall or stay asleep.
She wakes up at 7:00 AM with help of an alarm clock. She snores
loudly every night and she is very restless sleeper. She has noted
being more tired lately. Her Epworth Sleepiness Scale (ESS) is
10/24. There has been a minor decrease in grades at school and she
seems irritable at times.
Her physical exam is normal, except for her weight at 95 kg;
height is 152.4 cm. This accounts for a BMI of 40.9. Upon more
questioning, she also admits feeling a “crawly” feeling in legs at
night or when sitting quietly. She feels better moving the legs.
Discussion
The intimate connection between sleep and headaches has been rec-
ognized for centuries. Pain stimuli and pain disorders may affect
sleep quality and quantity. One of the most common triggers for
headaches is sleep deprivation [18, 19], and it is well-known that
sleep can terminate migraine attacks [18].
There are different ways a headaches and sleep interact
(Table 8.3). First, sleep deprivation may be the cause of headaches.
This headache is usually dull and localized in the frontal head
regions [20]. A sleep disorder, such as, OSA can produce morning
8 Medical Disorders 127
Headaches
Migraine
Tension type
Others
Fig. 8.1 Relationship between headaches, disrupted sleep, and medical conditions
Pitfalls
Learning Points
Conclusions
As we can see, medical disorders can impair sleep and sleep affect
disease entities in different ways. Asthma and related conditions,
such as, allergic rhinitis may produce sleep disturbances that can
affect daytime functioning. We also have hypothyroidism, which
may be overlooked since all symptoms may be attributed to
OSA. Hypothyroidism may cause OSA due to weight gain and
macroglossia. Persistent symptoms after treated OSA or clinical
characteristics not typical of the condition may require further
evaluation (including the possibility of another sleep disorder), in
which hypothyroidism must not be forgotten. Headaches and sleep
interaction could be complex. The treatment of one disturbance
certainly will help control the other one.
A detailed evaluation of the above disorders requires sleep as
part of the clinical history and, sometimes, physical exam. A good
sleep evaluation takes into account medical comorbidities.
References
1. Meltzer LJ, Ullrich M, Szefler SJ. Sleep duration, sleep hygiene, and
insomnia in adolescents with asthma. J Allergy Clin Immunol Pract.
2014;2(5):562–9.
2. van Maanen A, Wijga AH, Gehring U, Postma DS, Smit HA, Oort FJ,
et al. Sleep in children with asthma: results of the PIAMA study. Eur
Respir J. 2013;41(4):832–7.
3. Stores G, Ellis AJ, Wiggs L, Crawford C, Thompson A. Sleep and psycho-
logical disturbance in nocturnal asthma. Arch Dis Child. 1998;78(5):
413–9.
8 Medical Disorders 131
Clinical Case
History
Diagnostic Studies
Cognitive Testing
Behavioral Observations
During his research-based cognitive assessment prior to proton
therapy (month 2), Henry was described as exhibiting some lapses
in attention and motivation as well as frequent fidgeting, but he
otherwise appeared to be adequately engaged throughout testing.
He put forth strong effort throughout his cognitive testing in month
12, and he did not exhibit outward signs of inattention, distractibil-
ity, or impulsive behaviors. There were also no observable signs of
sleepiness (e.g., dozing off, “zoning out”). Henry displayed poor
speech articulation, and he frequently exhibited difficulties with
word finding and expressive language (i.e., poor coherence of sen-
tence construction and often talking around the point he was mak-
ing). He did not demonstrate difficulties following directions (i.e.,
receptive language). The results were thought to reflect valid esti-
mates of his functioning at the time of administration.
Intellectual Functioning
Henry was administered the Wechsler Intelligence Scale for
Children, 4th edition (WISC-IV) in month 2 during his baseline
research-based cognitive assessment. In month 12, given the
recent WISC-IV administration, Henry was administered the
Wechsler Abbreviated Scale of Intelligence, 2nd Edition
(WASI-II), as a brief re-assessment of cognitive functioning as
part of his clinical assessment. The results in months 2 and 12
indicated variable and generally underdeveloped cognitive abili-
ties. His performance fell 1.33 to 2.75 standard deviations (SDs)
below age-based norms across domains, including verbal reason-
ing, nonverbal reasoning, and working memory. Henry exhibited
a significant personal strength in his Average range processing
speed skills. During his month-15 research-based follow-up
assessment, Henry continued to exhibit impairments on verbal
reasoning and working memory tasks. He exhibited a significant
improvement in his performance on nonverbal reasoning tasks
(i.e., nearly 2 SD increase), which fell within expected age limits.
The variability between domains and across time points called
into question the stability of his cognitive functioning. See
Table 9.3 for results.
9 Brain Tumors 141
Academic Achievement
Henry was administered selected subtests of the Woodcock-
Johnson III Tests of Achievement to obtain an assessment of his
academic achievement in the domains of reading and mathematics.
His performance consistently fell below expected age and grade
limits across measures of reading and mathematics overall, with a
particular weakness in his calculation and applied math skills. His
performance was consistent across assessments (i.e., <1 SD differ-
ence), with the exception of his significantly increased perfor-
mance for reading fluency (i.e., 1 SD; see Table 9.3).
142 D.M. Graef and V.M. Crabtree
Verbal Fluency
On the Woodcock-Johnson Tests of Cognitive Abilities, 3rd Edition
(WJ-III Cognitive; see Table 9.3), Henry’s performance in month 2
fell within the low end of the Borderline range and below expected
age limits on a task assessing speeded retrieval of categorical and
verbal information. His performance was nearly 1 SD higher and
falling within the Low Average range during his month-15 follow-up
assessment.
Adaptive Functioning
The Adaptive Behavioral Assessment System, 2nd Edition
(ABAS-II), was completed by Henry’s mother in month 2 as a
measure of his adaptive functioning. Her responses indicated that
9 Brain Tumors 145
Henry’s functioning was below expected age limits across the con-
ceptual, social, and global adaptive functioning composites
(Standard Score Range = 70–75). The exception to this was the
practical skills composite that fell within the Low Average range
(Standard Score = 85). Parent ratings indicated a relative strength
in health and safety skills (Scaled Score = 10) and relative weak-
nesses in social and self-direction skills (Scaled Scores = 3).
Subscale ratings otherwise ranged from Low Average (i.e., func-
tional academics, home living, self-care skills) to Borderline (i.e.,
communication, leisure, community use skills).
Diagnostic Impressions
Management Chosen
Discussion
Clinical Pearls/Pitfalls
Learning Points
References
1. Kukal K, Dobrovoljac M, Boltshauser E, Ammann RA, Grotzer MA. Does
diagnostic delay result in decreased survival in paediatric brain tumours?
Eur J Pediatr. 2009;168(3):303–10.
2. Garre ML, Cama A. Craniopharyngioma: modern concepts in pathogene-
sis and treatment. Curr Opin Pediatr. 2007;19(4):471–9.
152 D.M. Graef and V.M. Crabtree
18. Walker MP, van der Helm E. Overnight therapy? The role of sleep in
emotional brain processing. Psychol Bull. 2009;135(5):731–48.
19. Weissman DH, Roberts KC, Visscher KM, Woldorff MG. The neural
bases of momentary lapses in attention. Nat Neurosci. 2006;9(7):971–8.
20. Anderson B, Storfer-Isser A, Taylor HG, Rosen CL, Redline S.
Associations of executive function with sleepiness and sleep duration in
adolescents. Pediatrics. 2009;123(4):e701–7.
21. Daly BP, Brown RT. Scholarly literature review: management of neuro-
cognitive late effects with stimulant medication. J Pediatr Psychol.
2007;32(9):1111–26.
22. Moore 3rd BD. Neurocognitive outcomes in survivors of childhood
cancer. J Pediatr Psychol. 2005;30(1):51–63.
23. Spencer J. The role of cognitive remediation in childhood cancer survivors
experiencing neurocognitive late effects. J Pediatr Oncol Nurs. 2006;
23(6):321–5.
24. Mong S, Pomeroy SL, Cecchin F, Juraszek A, Alexander ME. Cardiac risk
after craniopharyngioma therapy. Pediatr Neurol. 2008;38(4):256–60.
Insomnia
10
Mariya Narizhnaya and Matthew R. Ebben
Clinical Case
Physical Exam
The young woman was oriented to person, place, and time and is
of average height and weight. No abnormal movements were pres-
ent, and her posture and gait appeared normal. She is not suicidal,
homicidal, and did not display evidence of a thought disorder, or
serious psychopathology. She denies any substance abuse, medical
illnesses, history of trauma, or previous hospitalizations.
The patient’s general physical evaluation showed that she was
healthy. She did not appear to be in acute distress. Her vital signs
were within normal limits for her age. However, she yawned fre-
quently during the intake session and reported that she was suffer-
ing from excessive sleepiness and lack of energy. An evaluation of
her current lifestyle and daily habits, which was designed to iden-
tify behaviors and thought patterns that might contribute to her
sleep problems, indicated that she experiences situational distress
and does not possess coping skills to deal with this stress appropri-
ately. She stated that she thought that sleep was stressful and ter-
rible because of the pressure she experienced to fall asleep. She
also worried about not being able to sleep enough or not falling
asleep quickly at bedtime and negative effects of lack of sleep on
her daily functioning and performance in class.
Diagnostic Interview
During her first session, the patient was asked open-ended questions
about her presenting sleep problem. She began having trouble
sleeping at 17 years old. She remembers lying in bed and experienc-
ing worrisome thoughts about her performance on a math test. She
felt overwhelmed with her school work and lay in bed for hours, not
feeling tired. At the time of the initial consultation, the patient con-
tinued to experience worrisome thoughts at bedtime about the next
day and the effects of her insufficient sleep on her school work. She
frequently used her smartphone in bed to text her friends and peruse
social media websites. She experienced difficulty falling asleep
every night. She denied previous treatment for her sleep problems.
Often, she felt that she would never find relief from her sleep trou-
ble and needed to learn to function on limited sleep quantity.
10 Insomnia 157
Management Chosen
she felt tired and explained that the bed should only be used for
sleep or physical intimacy. If she did not feel sleepy while lying in
bed, she was recommended to get out of bed and perform relaxing
activities. The patient identified drawing and reading as calming.
Therefore, she was encouraged to perform those activities at her
desk instead of lying in bed and forcing herself to go to sleep. This
was recommended to help her form a positive association between
her bed and sleep.
A part of her nighttime regiment was getting into bed with her
smartphone. While in bed, she spent several hours texting, talking
on the phone, and visiting social media sites. Due to the stimulat-
ing social content as well as the potential effect of short wave blue
light emitting from this device on her melatonin levels and circa-
dian rhythms these activities prolonged her bedtime. Because
communicating with her friends was exciting and physically
arousing, she would not feel tired for several hours after the con-
versations were done. Therefore, she was advised to refrain from
going to bed with her smartphone. Removing the arousing and
emotionally and physiologically engaging stimulus from her bed-
time routine was recommended to help her relax.
Because the negative thoughts associated with sleep caused her
frustration at bedtime, cognitive restructuring was introduced. This
patient’s negative beliefs were identified with open-ended ques-
tions about her thoughts and feelings about sleep. Clinicians may
also utilize the Dysfunctional Beliefs and Attitudes about Sleep
(DBAS-16) [1] questionnaire, which is a tool that is often used to
assess dysfunctional beliefs about sleep. The patient was encour-
aged to begin to recognizing her negative thoughts associated with
sleep and bedtime. Some of the thoughts that she reported included,
“falling asleep is stressful and I’m not good at it,” “I will lie in bed
for hours,” “I will not be able to study for my test tomorrow because
I cannot sleep long enough.” Once the thoughts were identified, she
was taught the connection between her thoughts and their impact
on emotional and physiological arousal. Because her negative
thoughts about sleep contribute to emotional arousal and produce
anxiety at bedtime, she was encouraged to change her beliefs about
sleep from thoughts that induced feelings of stress, such as “I am
going to sleep right now,” to thoughts that would help her relax,
such as “I am going to lie in my bed and rest.” She was also taught
10 Insomnia 161
breathing exercises (Table 10.1). She was also reminded that cog-
nitive restructuring and visual imagery have worked for her in the
past and that she should try to rely on these techniques even more
during stressful time periods.
The patient reported that using cognitive restructuring
(Table 10.2) aided her in gaining control over her stressful thoughts
at bedtime. She was successful at sleep restriction during the
school week, being able to sleep 6 h on most nights, with one or
two short awakenings. It was more challenging for the patient to
follow her sleep schedule during the weekends. She was engaged
in social activities with her friends and did not go to bed until
4:00 am. She reported being unable to wake up at 6:00 am because
she would not be able to study on this limited amount of sleep. She
also expressed that she could not get out of bed when her alarm
clock rang. She kept falling asleep and pressing the snooze bottom
until 8:00 am. However, showing her the impact her weekend sleep
schedule (e.g., bedtime of 4:00 am and morning awakening of
10:00 am) (see sleep log 3, week 5 (Fig. 10.3)) had on her daytime
functioning on Monday, motivated her to adhere to her designed
bedtime schedule. Despite her attempts, she has not been able to
164 M. Narizhnaya and M.R. Ebben
Discussion
[2]. Patients often report feeling tired during the day and can have
difficulty concentrating in class. Common complaints include
stress associated with bedtime, difficulty initiating sleep, frequent
and prolonged arousals during the night, and early morning awak-
enings, with the inability to go back to sleep. The individual dis-
cussed in this case study suffered from an irregular sleep schedule
marked by sporadic napping and a lack of a consistent bedtime,
inability to fall asleep at bedtime or following an early morning
arousal as well as frequent and long awakenings during the night.
She often worried that her daytime functioning would be nega-
tively impacted by her lack of sleep.
Undiagnosed and untreated insomnia can result in excessive
daytime sleepiness, irritability, difficulty concentrating, and poor
academic performance. Fatigue and inability to focus on school
work may not warrant concerns for adolescents. They may not be
aware that they are struggling with a sleep disorder. Therefore,
practitioners are encouraged to enquire about the adolescent’s sleep
when clinically indicated. Once insomnia has been diagnosed, an
individualized treatment plan should be designed, taking into
account the patient’s sleep schedule.
In order to formulate an appropriate treatment plan for an
insomniac, it is essential to properly diagnose the disorder. Sleep
problems can be associated with several factors, including sleep
hygiene problems (e.g., varied sleep schedule, frequent napping,
and emotionally and physically stimulating activities close to bed-
time). It should be noted that there are several sleep disorders, such
as delayed sleep phase (e.g., sleep disturbance due to changes to
the circadian rhythm), sleep disordered breathing, and movement
disorders, (e.g., restless legs or REM behavior disorder) as well as
psychiatric disorders (e.g., anxiety, depression, and attention defi-
cit hyperactivity disorder) that may cause individuals to have
symptoms that are similar to insomnia. In addition, family or
school pressure, and acute infection disease, or chronic disease
may also have a negative effect on sleep [3, 4]. Therefore, a practi-
tioner is advised to carefully evaluate the patient’s presenting prob-
lem. After thorough assessment, which includes open-ended
questions about sleep problems, bedtime and daytime regiment,
caffeine and medication use, and origin of the presenting problem,
a patient may be diagnosed with insomnia. Using a sleep log to
166 M. Narizhnaya and M.R. Ebben
Clinical Pearls/Pitfalls
Learning Points
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Epilepsy and Sleep
in Adolescents 11
Sejal V. Jain and Sanjeev V. Kothare
Clinical Case 1
Discussion
the night, and the patient being partially aware of the events.
However, these features do not rule out the possibility of parasom-
nia, especially in the presence of a positive family history.
Parasomnia
Pitfalls
Learning Points
Clinical Case 2
Discussion
This case describes a teenager with JME who has recently transi-
tioned to college. He starts having breakthrough seizures, which
could be caused by sleep deprivation. In order to ensure adequate
treatment of both his sleep and epilepsy, it is important to deter-
mine the existence of behavioral factors (staying up late and “par-
tying”) and/or circadian factors (delayed sleep phase/irregular
sleep schedule) that could interfere with successful management.
Pitfalls
Learning Points
Clinical Case 3
Discussion
The case describes a young woman with the diagnosis of JME and
sleepiness. The sleepiness in patients with epilepsy can be multi-
factorial, caused by changes in antiepileptic drugs, poor quality
sleep that is associated with epilepsy, and poor behavior/psychiat-
ric disorders that are associated with epilepsy. In this case how-
ever, additional symptoms are very suggestive of narcolepsy. It is
important to get a proper history, as sleep paralysis and cataplexy
may be missed as symptoms of seizures.
JME
Narcolepsy
The Interaction
Pitfalls
Learning Points
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Traumatic Brain Injury
12
Kanwaljit Singh and Sanjeev V. Kothare
K. Singh, M.D.
Department of Pediatrics (Neurology), University of Massachusetts
Medical School, Worcester, MA, USA
e-mail: kanwaljit.singh@umassmed.edu
S.V. Kothare, M.D. (*)
Department of Neurology, NYU Langone Medical Center and NYU
School of Medicine, 223 East 34th Street, New York, NY 10016, USA
e-mail: sanjeev.kothare@nyumc.org
(mean of the time to sleep onset during the 5 naps), and rapid eye
movement sleep latency (time from sleep onset to rapid eye move-
ment sleep onset), during the MSLT were shortened at 2, 3, and
10 min, respectively), while the sleep study showed mild periodic
limb movements of sleep (8/h) fragmented sleep characterized by
an arousal index of 30/h (normal < 10/h) and sleep efficiency at
58 % (normal > 85 and an early sleep onset REM latency of 8 min.
Twenty-four-hour electroencephalography and repeat magnetic
resonance imaging of the brain were normal. The serum chemistries
were normal as well.
Initially he was put on a course of daytime caffeine combined
with a sleep hygiene program, which failed to make any significant
impact on his symptoms. He was then started on a course of
modafinil 100 mg twice a day; one dose in the morning upon
awakening and a second dose at midday. He was also given a trial
with oral amantadine 100 mg three times a day for improving his
alertness. Within a month of starting this regimen, his cataplexy
and excessive daytime sleepiness started to improve without any
further dose titration. He reported no significant adverse effects
from modafinil. Three months later, his amantadine was discontin-
ued. Six months after the initiation of modafinil therapy, the patient
is completely asymptomatic. The plan would be to stop his
modafinil to assess for a spontaneous remission of his symptoms.
Learning Points
Pitfalls
Learning Points
Pitfalls
• The “brain rest” period also has the potential to actually worsen
sleep problems if handled incorrectly. For example, the person
who is on brain rest spending their evenings watching TV can
quickly exacerbate their sleep problems. It is very important to
spend the “rest period” by actually giving complete cognitive
rest to the brain, especially in the evenings.
Learning Points
Pitfalls
Discussion
limb movements of sleep are amongst the most common sleep dis-
orders diagnosed after TBI [13]. Excessive daytime sleepiness
(EDS) in conjunction with nighttime difficulty initiating or main-
taining sleep is also common after TBI, especially in patients
recently discharged from hospital after TBI [14] with various stud-
ies indicating a prevalence ranging from 25–52 % [15–18].
Symptoms of cognitive impairment have also been associated with
TBI and are correlated with increasing severity of injury [19].
Interestingly, patients with TBI and sleep disordered breathing
have a higher likelihood of impaired cognitive impairment, such as
problems with memory and sustained attention [16].
The prevalence of periodic limb movement of sleep (PLMS) in
institutionalized TBI patients was reported to be as high as 25.4 %
[17] while in another multicentered study, 17 % of both institution-
alized and ambulatory TBI patients had PLMS [15]. Another study
found the prevalence of parasomnias (most often REM behavior
disorder) in 25 % of patients with TBI [18].
reduced rapid eye movement (REM) sleep [34], yet another found
increased REM sleep in the second half of the night [35], one found
decreased REM onset latency [33], and another found increased N3
sleep [36] in patients with TBI. Another study found no differences
whatsoever in TBI patients as compared to healthy controls [33].
Therefore, sleep studies, such as polysomnography, and other
modalities such as maintenance of wakefulness tests and multiple
sleep latency tests (MSLT) may have limited utility in TBI. As a first
step, suspected insomnia cases can be evaluated using standard
insomnia questionnaires and sleep logs. If expected progress is not
achieved, objective tests should be considered to determine other dis-
orders, such as sleep-related breathing (obstructive sleep apnea, sleep
disruptive snoring), movement disorders such as PLMS, atypical
EEG arousal bursts and conditions such as narcolepsy, hypersomnia,
and parasomnias complicating the sleep problems in this population.
Due to PTSD
SSRIs, psychology counsel, pain management
Due to pain counsel, CBT, sleep hygiene, +/− melatonin
Due to depression
Hypersomnia Stimulant medications (i.e., methylphenidate,
dextroamphetamine, modafinil, armodafinil)
[38]
Obstructive sleep apnea CPAP, surgical interventions, mandibular
devices, weight loss
Periodic limb movements Iron supplementation, dopamine agonists,
of sleep/restless leg gabapentin
syndrome
Circadian rhythm disorder Melatonin supplementation, +/− stimulant
[39] medication in daytimeb, +/− hypnotic
medication in eveningb, bright light therapy in
Delayed sleep phase AM/reduced light exposure in PM, prescribed
sleep/wake scheduling, sleep hygiene
education
Advanced sleep phase Advance chronotherapy (bright light therapy
in PM/reduced light exposure in AM),
+/− melatoninb, sleep hygiene education,
prescribed sleep/wake scheduling
Narcolepsy Stimulant medications (i.e., methylphenidate,
dextroamphetamine, modafinil, armodafinil),
sodium oxybate
a
All patients should be educated on future TBI prevention and consequence of
recurrent TBI
b
There is insufficient evidence to support the efficacy or safety of these medi-
cations in these disorders
198 K. Singh and S.V. Kothare
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Index
A B
Adaptive Behavioral Assessment Body mass index (BMI), 120
System, 2nd Edition Brain tumor, 4, 139–145
(ABAS-II), 144 cognitive testing
Adenotonsillectomy, 46, 48–52, 54, academic achievement and
56, 57 functioning, 141
ADs. See Arousal disorders (ADs) adaptive functioning,
AHI. See Apnea/hypopnea index 144–145
(AHI) behavioral observations, 140
American Academy of executive functioning and
Otolaryngology-Head attention, 142–144
and Neck Surgery intellectual functioning,
(AAO-HNSF), 48 140–141
American Academy of Pediatrics learning and memory,
(AAP), 48 142, 143
American Academy of Sleep verbal fluency, 141, 142
Medicine (AASM), 13, 48 craniopharyngioma
Anemia, 37 (see Craniopharyngioma)
Anti-glutamic acid decarboxylase EDS, 135, 138
(GAD) antibody follow-up sleep study and
syndrome, 195 subjective sleep
Apnea/hypopnea (AHI) index, ratings, 139
128, 136 MRI, 136, 146
Arousal disorders (ADs), 91 obstructive hydrocephalus, 133
Arousal parasomnias, 173, 176 PSG, 136
Asthma sleep and fatigue, 135
sleep complaints, 121 Bright light therapy, 14, 16, 18
Attention-deficit hyperactivity
disorder (ADHD), 8,
62, 64 C
Autosomal dominant nocturnal CA. See Confusional arousals (CA)
frontal lobe epilepsy, 174 Caffeine, 12, 18–20