Psychologic and psychiatric assessment

Tracy Jill Dotya, Michael R. Schoenbergb, Natalie S. Daileyc, and William D.S. Killgorea,c, a Walter Reed Army Institute of
Research, Silver Spring, MD, United States; b University of South Florida College of Medicine, Tampa, FL, United States; and
c
University of Arizona, Tucson, AZ, United States
© 2021 Elsevier Inc. All rights reserved.

Neuropsychological approach 1
Insomnia 2
Psychiatric symptoms 2
Anxiety 2
Depression 3
Suicide 3
Excessive daytime sleepiness 3
Sleep deprivation/restriction 3
Sleep apneas 4
Obstructive sleep apnea/obstructive sleep apnea–hypopnea syndrome 4
Central sleep apnea 5
Narcolepsy 5
Disclaimer 5
References 5

Glossary
Executive functions A term used to describe cognitive functions and behaviors that are frequently associated with frontal lobe
functional neuroanatomy and also involve/require function of other associated areas including basal ganglia and temporal/
parietal cortices. Example of executive functions include problem solving, reasoning, planning, behavioral inhibition, and
initiating and maintaining behaviors. Executive functions are measured in neuropsychology evaluations by a series of
standardized tests as well as behavioral observations.
Inhibition Restraining or suppressing a behavior. From a cognitive or behavioral standpoint, it is the ability to suppress one
(typically overlearned or primed) behavior for another behavior that is less automatic. Frequently tested by a person not
completing an overlearned behavior or cognitive task to instead engage in a less automatic or spontaneous behavior.
Psychomotor vigilance test (PVT) A computerized assessment metric that requires sustained attention and vigilance to a visual
display for a period of several minutes. A stimulus appears on the display at pseudorandom intervals and the participant is
required to respond as rapidly as possible.
Sleep hygiene Sleep habits; good sleep hygiene practices include setting standardized bedtime and awakening times, avoiding
reading or watching television in bed, avoiding naps, and remaining in bed only when sleepy.

Neuropsychological approach

Sleep disorders often prevent patients from obtaining sufficient nocturnal sleep, which can lead to a number of neurocognitive defi-
cits. From a functional neuroanatomic perspective, sleep deprivation has been associated with hypometabolism of glucose in the
thalamic, dorsolateral, ventrolateral/orbitofrontal, and medial/anterior cingulate regions. These areas are important for a variety of
cognitive abilities, including sustained attention, emotional processing, and some aspects of executive functioning.
A thorough neuropsychological evaluation of the patient with sleep complaints should endeavor to assess the patient’s cognitive
functioning, affective status, and sleep complaints. In addition to a review of sleep behaviors and sleep hygiene, the neuropsychol-
ogist should evaluate moderators that can potentially affect and be affected by sleep, including symptoms of depression and anxiety.
Assessment of patients with sleep disorders should also include measures of vigilance/sustained attention, executive functions, fine
manual dexterity, and visual ability (particularly visual motor/manual visuoconstructional skills). Less relevant to the assessment of
patients with sleep disorders is testing of general cognitive or language functioning. Neuropsychological assessment in the patient
with sleep complaints can be helpful to evaluate the extent and severity of cognitive dysfunction present for individuals with sleep
disorders and can provide a means for monitoring and documenting treatment efficacy over time.
Individuals with sleep problems can be roughly divided into two broad categories that may overlap: (1) the patient who has
trouble falling asleep at night, i.e., insomnia and (2) the patient who has trouble staying awake during the day, i.e., excessive
daytime sleepiness (EDS) (Pavlova and Latreille, 2019). The neuropsychological domains most relevant to each type of patient
are reviewed below.

Reference Module in Neuroscience and Biobehavioral Psychology https://doi.org/10.1016/B978-0-12-822963-7.00041-4 1

2 Psychologic and psychiatric assessment

Insomnia

Insomnia refers to difficulty initiating and/or maintaining sleep. Insomnia may present as a short-term problem or be a chronic
condition. Acute insomnia may be associated with a number of different psychological and medical conditions. Chronic insomnia
is generally associated with anxiety and self-conditioning that results in difficulty initiating or maintaining sleep (psychophysiolog-
ical etiology, rather than due to a neurological disorder). These sleep disturbances are often associated with anxiety, major depres-
sive disorders, and suicide (Pigeon et al., 2017).

Psychiatric symptoms
The association between complaints of poor sleep and psychiatric disorders has been known for centuries. Epidemiological studies
have confirmed this association, with the risk of developing depression 39.8 times greater for individuals with complaints of
insomnia than for those without sleep complaints (Ford and Kamerow, 1989). In contrast, the likelihood an individual met criteria
for a depressive disorder at 1-year follow-up was not significant in those individuals reporting normal sleep at the 1-year follow-up
visit (OR 1.9, CI 0.5–5.3).
Insomnia may be divided into initial, middle, or terminal insomnia. Initial insomnia refers to difficulty falling asleep, as evi-
denced by increased sleep latency. The most frequent cause of initial insomnia is an anxiety disorder. Middle insomnia describes
a difficulty maintaining sleep after initial sleep onset. For these individuals, sleep is fragmented with frequent awakenings at night.
Middle insomnia is commonly associated with neurological syndromes (e.g., restless leg syndrome, RLS), pain syndromes, or
depression. Terminal insomnia describes a pattern of frequent early morning awakenings that usually occur several hours before
the desired rise time. Terminal insomnia is most frequently associated with depressive disorders. We now turn to evaluating the
features of insomnia and (neuro)psychological assessment related to anxiety and depressive disorders as well as suicide.

Anxiety
Sleep disturbances are frequently a feature of anxiety disorders (Mellman, 2006), in which insomnia is most commonly associated
with generalized anxiety disorder, panic disorder, and posttraumatic stress disorders. Indeed, insomnia is a core diagnostic feature of
generalized anxiety disorder and posttraumatic stress disorder. Posttraumatic stress disorder includes a core feature of recurring
nightmares, often with difficulty initiating and maintaining sleep. Panic disorders have also been associated with complaints of
insomnia, and patients sometimes experience some symptoms of panic attacks during sleep. Insomnia can exacerbate anxiety
and psychological distress, and anxiety causes sleeping problems. In fact, one to two nights of sleep deprivation can lead to signif-
icant increases in subjectively rated symptoms of psychopathology, including somatic complaints, anxiety, depression, and para-
noid thinking (Kahn-Greene et al., 2007). In particular, after two nights of sleep deprivation, 25% of subjects in one study
showed clinically significant increases in depressive symptoms (Kahn-Greene et al., 2007). Sleep deprivation has also been shown
to reduce coping capacities and emotional problem-solving abilities (Killgore et al., 2007).
Neuropsychological/psychological assessment for patients with insomnia should always include an evaluation of psychiatric/
psychological problems, particularly anxiety and depression. Patients with anxiety disorders frequently complain of difficulty
initiating sleep, which is often subjectively communicated as “my brain won’t turn off,” and may be objectively expressed as
perseverative thoughts, recurrent worries, and/or obsessions/compulsions. These patients may have recurrent intrusive thoughts
and ruminations when falling asleep. Furthermore, these patients may experience increased distress with their difficulty in initiating
sleep, further exacerbating their insomnia. Similarly, patients with anxiety may also experience difficulty maintaining sleep, with
awakenings related to recurrent nightmares in the case of posttraumatic stress disorders or to stress/anxiety related to monitoring
their sleep and concern over hypnagogic myoclonus, snoring, or fears of death/dying in sleep.
From a neuropsychological standpoint, patients with anxiety and depression often complain of cognitive problems in addition
to insomnia. Frequently, memory problems reflect difficulties in maintaining attention and/or task engagement. Patients will often
“give up” on questions, responding with “I don’t know” responses.
Treatment for insomnia related to anxiety disorders generally involves behavioral interventions to improve sleep hygiene and
working with the patient to develop cognitive and behavioral strategies to reduce anxiety/worry. Some basic intervention techniques
include the following:
1. Maintain a regular light exposure schedule. Bright light exposure for a few minutes in the morning helps to reset the brain’s
sleep–wake clock. Avoid bright light (especially blue light) in the evenings.
2. Avoid afternoon caffeine, especially within 6 h prior to bedtime.
3. Identify 7–9 h per night for uninterrupted sleep. Set the same time to fall asleep and wake-up each day every day.
4. Establish a relaxing presleep routine about an hour before bedtime. Meditate, listen to relaxing music, read a book, etc. Avoid
stimulants before bed (e.g., no coffee or chocolate before bed) and reduce ambient lighting.
5. The bedroom is for sleeping. Individuals should never watch TV or use the computer in bed. Avoid anxious/- nervous tasks
before bed (do not pay bills before bed). If you do not fall asleep after being in bed for 15 min, get up and go to another room
and do something relaxing for about 20–30 min before going to bed again.
 Psychologic and psychiatric assessment 3

6. The bedroom should be dark, cool (but not cold), and quiet. A fan can help to drown out other ambient noises. Mattress and
pillows should be comfortable.
7. Avoid looking at a clock when in bed. Turn clock away so you cannot see it.
8. Implement a regular exercise routine either in the morning or in the afternoons (not in evening).

Depression
A common symptom of depressive disorders, including major depressive disorder and bipolar disorder or cyclothymia is disruption
of sleep. Sleep may be characterized as either significant insomnia, with problems initiating and maintaining sleep, or, conversely,
hypersomnia, with excessive sleep. Most commonly, patients with depression experience difficulty maintaining sleep, with early
wakening and difficulty falling back asleep. Alternatively, patients may also have difficulty maintaining sleep in the middle of
the night (middle insomnia). It is also common for individuals with major depressive disorder to experience hypersomnia
(complaints of EDS). Rather than exhibiting clear problems in maintaining alertness, patients with major depression often
complain of feeling tired/fatigued and frequently exhibit apathy. Patients with major depression often also complain of concentra-
tion and memory problems. Chronic insomnia may weaken the capacity to cope with life stressors, further exacerbating depressive
symptoms.

Suicide
Suicide is a leading cause of death across the world. Recent research suggests that insomnia is an independent risk factor for suicide,
(Liu et al., 2020). In fact, the risk of suicide attempts in insomnia patients is 18-fold that of patients without insomnia, and this
relationship persists even after controlling for psychiatric illness. This striking relationship necessitates that a suicide risk assessment
be conducted on any patient endorsing insomnia, regardless of psychiatric history. Insomnia’s link to two aspects of impulsive
behavior may underlie the relationship: urgency (i.e., engaging in impulsive behaviors to lessen negative emotions) and lack of
perseverance (i.e., being unable to suppress irrelevant thoughts or memories) (Woznica et al., 2015).

Excessive daytime sleepiness

EDS is a term to describe individuals who experience excessive drowsiness during the day with difficulty maintaining alertness
(wakefulness) and unintentionally falling asleep. Individuals with EDS may fall asleep in dangerous situations (driving a car) or
at inappropriate times (during a business meeting). Sleepiness refers to the biological drive or propensity to fall asleep and can
be distinguished from fatigue, tiredness, and boredom. Common causes of EDS include insufficient nocturnal sleep due to self-
imposed sleep deprivation, sleep disorders, hypercalcemia, hypothyroidism (Grave’s disease), hyponatremia, medications (tran-
quilizers, antihistamines, and sleep aides), diabetes, chronic pain, etc. Additionally, specific sleep disorders that contribute to
daytime sleepiness can include breathing-related sleep disorders, such as obstructive sleep apnea (OSA) or restless leg syndrome
(RLS), which is characterized by unpleasant sensations in the legs with an associated strong urge to move.
Self-imposed sleep deprivation is a common cause of mild to moderate EDS. Indeed, studies have found self-imposed sleep
deprivation may begin as early as late childhood or adolescence. While physiological studies suggest adolescents require about
9 h of sleep per night, studies have shown adolescents and older children routinely limiting their sleep to 6–7 h per night due
to the demands of school, extracurricular activities, social activities, and electronic media. The neuropsychological effects of chronic
sleep restriction among healthy children and adolescents have recently received considerable attention. General neuropsychological
deficits found among patients with EDS include impairments in psychomotor speed/motor coordination, vigilance/sustained atten-
tion, and executive functions (e.g., working memory, mental flexibility, sequencing, fluency/mental flexibility, and planning/
problem solving) as well as mood/affect (e.g., Belenky et al., 2003; Dinges et al., 1997; Killgore et al., 2006, 2007).

Sleep deprivation/restriction

Studies have found initial neuropsychological deficits in vigilance/sustained attention and reaction times after even one night of
acute sleep deprivation. In fact, reduced attention and psychomotor vigilance appear to be the hallmark cognitive deficits of sleep
deprivation. Some studies have shown deficits on various other cognitive abilities during sleep deprivation, including complex
higher-order executive functions such as divergent thinking and decision making, but these are not consistently observed across
studies and may depend on the extent to which sustained vigilance is required. Sleep loss need not be continuous in order to
produce attentional lapses and slowing of psychomotor vigilance. For instance, in one study, when sleep was reduced to just
6 h per night for 2 weeks, performance declined precipitously to the same level of impairment as that of someone acutely sleep
deprived for 48 h (Van Dongen et al., 2003). Fig. 1 summarizes the combined findings from two companion studies examining
the effects of chronic sleep restriction on the number of attentional lapses (i.e., momentary periods of nonresponsiveness lasting
at least 500 ms) that were observed during a psychomotor vigilance task (Belenky et al., 2003; Van Dongen et al., 2003).
4 Psychologic and psychiatric assessment

20

3h TIB

PVT Performance Lapses

15 4h TIB

6h TIB
10
5h TIB

5
7h TIB 8h TIB

9h TIB
0
BL 1 2 3 4 5 6 7 8 9 10 11 12 13 14
Days of Sleep Restriction
Fig. 1 Summary data extracted from two similar studies of sleep restriction. One study examined psychomotor vigilance test (PVT) performance for
7 nights restricted to either 3, 5, 7 or 9 hours of sleep, while the other study examined PVT performance across 14 nights restricted to 4, 6, or 8
hours of sleep per night. Lapses on a psychomotor vigilance test (PVT) demonstrate clearly increasing levels of impairment as the duration of time in
bed (TIB) is reduced. Modified from Belenky, G., Wesensten, N.J., Thorne, D.R. et al., 2003. Patterns of performance degradation and restoration
during sleep restriction and subsequent recovery: A dose-response study. Journal of Sleep Research 12 (1), 1–12, and Van Dongen, H.P.A., Maislin,
G., Mullington, J.M., Dinges, D.F., 2003. The cumulative cost of additional wakefulness: Dose-response effects on neurobehavioral functions and
sleep physiology from chronic sleep restriction and total sleep deprivation. Sleep 26 (2), 117–126.

As evident in the figure, one study examined performance during 7 days of sleep that was restricted to 3, 5, 7, or 9 h per night,
while the other study examined performance for 2 weeks when sleep was restricted to 4, 6, or 8 h per night. Overall, consistently
obtaining 7 or more hours of sleep per night was associated with relatively sustained cognitive performance, but with 6 or less
hours per night, performance declined over time, with severe deficits emerging rapidly for durations less than 5 h per night.
Notably, even up to three full nights of recovery sleep were insufficient at restoring performance to baseline levels following
a week of sleep restriction. This stands in stark contrast to findings from studies of total sleep deprivation, which typically
show restoration of baseline performance after a single night of recovery sleep. Apparently, chronic sleep restriction may
adversely affect the brain’s short-term capacity to benefit fully from recovery sleep. Finally, a study employing a simple but
elegant model for sleep deprivation that was implemented in subjects’ own home found sleep restriction of 6 h per night in
adolescents and young adults resulted in significant declines in reaction times for working memory tasks in adolescents
(but not adults) without self-perceived EDS (Jiang et al., 2011). This suggests that sleep loss may impair performance without
subjective awareness of the extent of such deficits.

Sleep apneas
Obstructive sleep apnea/obstructive sleep apnea–hypopnea syndrome
OSA is well recognized as being associated with daytime sleepiness and can lead to occupational deficits and increases the risk
of motor vehicle accidents (Lloberes et al., 2000). Adverse effects on objectively measured neuropsychological domains have
also been well recognized, including psychomotor speed/coordination, vigilance/sustained attention, executive functions
(mental flexibility, planning, and working memory/mental manipulation of information), and visual ability (motor visuocon-
structional skills) (Aloia et al., 2004; Beebe et al., 2003; Olaithe et al., 2018). Less consistent findings have been reported for
memory (Beebe et al., 2003; Olaithe et al., 2018). Visual memory deficits have particularly been reported for patients with
OSA. While verbal memory is not typically considered to be impaired, some studies report that deficits in executive functions
reduce verbal memory through difficulty in developing encoding strategies (organization) and retrieval strategies but do not
adversely affect memory storage or forgetting. General intelligence and language ability are not affected for most patients with
even severe OSA.
The largest adverse effects of OSA on neuropsychological functioning are in domains of attention/vigilance (sustained atten-
tion for extended periods of time), executive functions, and psychomotor speed (Aloia et al., 2004; Beebe et al., 2003;
Olaithe et al., 2018). Attention/vigilance measures most sensitive to the effects of EDS associated with OSA include the Digit
Vigilance test (Lewis, 1995) and continuous performance tasks or measures (e.g., psychomotor vigilance test [e.g., Thorne
et al., 2005]) requiring maintaining attention/vigilance for sustained periods of time. Executive functions are typically operation-
alized as tasks involving mental flexibility, working memory, behavioral inhibition, and problem solving. The adverse effects of
OSA on motor speed/dexterity have not been consistent but can be quite large. Motor speed has typically been measured using
the grooved pegboard or finger oscillation (finger tapping) test.
 Psychologic and psychiatric assessment 5

Visual ability deficits tend to be most pronounced for drawing tasks that require fine motor skill (Aloia et al., 2004; Beebe et al.,
2003; Olaithe et al., 2018). Interestingly, severity of OSA as measured by polysomnography measures (e.g., apnea–hypopnea index)
has not been consistently related to neuropsychological functions in a linear fashion, beyond having polysomnography findings
sufficient to meet diagnostic criteria for OSA that requires treatment with continuous positive airway pressure (CPAP) or surgery.
Treatment of OSA/obstructive sleep apnea–hypopnea syndrome (OSAHS) can include a variety of methods, including loss of
weight, CPAP or bilevel positive airway pressure, or surgery (e.g., uvulopalatopharyngoplasty). Treatment of OSA/OSAHS using
CPAP has produced improvements in attention/vigilance, executive functions, and memory functions in some patients.
Interestingly, compared to baseline measures, individuals with OSAHS treated with CPAP demonstrated an improvement in general
cognitive function, or intelligence quotient (IQ) with CPAP, although no gross deficit in general cognitive function is typically
identified among patients with OSAHS. Psychomotor speed and visuoconstructional functions tend not to improve with CPAP
treatment. More sophisticated studies employing placebo control for CPAP have failed to replicate general improvement in
neuropsychological functioning with CPAP over 1–2 weeks, establishing instead modest gains in information processing speed,
sustained attention, and alertness using the Digit Vigilance test (Lewis, 1995), which is a speeded measure involving rapid visual
tracking to accurately select target stimuli (e.g., Bardwell et al., 2001; Lim et al., 2007). Studies of surgical outcome have found
patients with successful surgery resulting in increased oxygen desaturation index were associated with improved vigilance/attention,
executive and verbal learning/memory, and to a lesser extent, general cognitive functioning (e.g., Dahlof et al., 2002; Klonoff
et al., 1987).

Central sleep apnea

Detailed neuropsychological studies of central sleep apnea are few, but available data suggest similar neuropsychological domains
to those impaired in OSA are likely affected. Similarly, with treatment, improvement in vigilance/sustained attention and psycho-
motor speed/coordination has also been reported (e.g., Larner and Ghadiali, 2008).

Narcolepsy

Neuropsychological evaluation of patients with narcolepsy have identified deficits in vigilance/sustained attention, executive
(verbal fluency, inhibition, and initiation), and verbal memory (list learning, story memory) but not visual memory functions
(Daum, 2003; Nauman et al., 2006; Zamarian et al., 2015). Performance on brief and more difficult tasks is generally normal.
Subjective attentional and memory complaints are common for patients with narcolepsy, but these complaints may not be asso-
ciated directly with objective deficits but rather may be associated with mood variables and high rates of depression observed
for these individuals.

Disclaimer

Material has been reviewed by the Walter Reed Army Institute of Research. There is no objection to its presentation and/or publication. The opinions
or assertions contained herein are the private views of the authors, and are not to be construed as official, or as reflecting true views of the Department
of the Army or the Department of Defense.

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