Basics of Sleep

Sleep Architecture and Sleep Stages

-

Non-REM sleep and REM sleep - both alternate and each cycle last about 90-100
90
minutes
Sleep is divided into 2 independent states:: Non
o Non-REM
REM Sleep (divided into 3 stages; used to be 4 stages until it was modified in 2007)
o N1

Diminishment in alpha rhythms (8-13
13 Hz), which are characteristics for wakefulness

Presence of slower theta rhythms appear (4-77 Hz) and beta waves (> 13 Hz)

EMG activity: slow, rolling eye movements

Vertex sharp waves noted toward the end of N1
o N2

Characteristic EEG findings: sleep spindles (12-18
18 Hz; most often 14 Hz) and K complexes

Also contains theta rhythms and fewer than 20% slow waves (0.5 - 2 Hz)

Lasts for about 30-60 minutes
o N3 (slow
(slow-wave sleep)

Now the slow waves will occupy > 20% up to 100%
o REM sleep

Noted 60 to 90 minutes after onset of sleep

Accounts for about 20-25%
25% of sleep time

Characterized by fast rhythms and theta activity

Believed that approximately 80% dreams occur during REM sleep (the other 20% occur during NREM)
Interesting trivia
trivia:: REM sleep dreams are highly emotionally charged, complex and bizarre; whereas NREM
dreams are more realistic and rational

Can be divided into 2 stages:
Tonic stage:: desynchronized EEG, hypotonia or atonia of major muscle gr
groups
oups and depression of monosynaptic
and polysynaptic reflexes
Phasic stage:: Characterized by rapid eye movements in all directions, phasic swings in blood pressure and heart
rate, irregular respiration, spontaneous middle
middle-ear
ear muscle activity and tongue movements.
m

Function of Sleep
I will not go over this too much as the function of sleep largely remains a mystery
Several theories
o Restorative theory:

sleep needed to restore cerebral function after periods of waking (evidence of increased anabolic hormones
hormo
and decreased
levels of catabolic hormones during sleep)

During NREM sleep: presence of slow wave sleep after sleep deprivation
o Memory consolidation

more recent studies have revealed that new memories can be strengthened by sleep (so remember to get a lot of sleep
before FND!)

synthesis of new RNA and proteins by neurons during sleep
o Maintenance of synaptic and neuronal network integrity
Some interesting associations: sleep deprivation leads to decreased levels of serum leptin and increased levels of ghrelin; which can possibly
explain the BMI observed with short sleep duration
Sleep Patterns with Age
Sleep requirements change dramatically from infancy to old age
o Newborns: poly-phasic
phasic sleep pattern with 16 hours of sleep per day

Sleep requirements
ents decrease to about 10 hours per day by ages 3 to 5 years
o Preschool children:: sleep assumes biphasic pattern (nap time!)
o Adult: mono-phasic
phasic sleep pattern (7.5 - 8 hours)
o Elderly:: changes back to biphasic pattern (nap time!)
Newborn spends 50% of the time in REM sleep; however, duration of the NREM
NREM-REM
REM cycle is shorter in infants -- lasting about 45-50 minutes
and increasing as they get older; by age 6, time in REM is decreased to about 25% but their NREM
NREM-REM
REM cycles are increased
increa

Approach to and Evaluation of Sleep Disorders

Sleep History
Provided by patient; but when possible, should be supplemented by bed partner, family member or roommate
Different Components of the sleep history
o Presenting sleep-related
related symptoms (onset, duration, frequency, severity, precipitating factors)
o Associated nocturnal symptoms (i.e. abnormal breathing, nocturnal behaviors, nocturnal awakenings)
o Time of symptoms
o Daytime functioning (sleepiness, concentration, mood ddisturbances)
o Sleep schedule and sleep hygiene
o Any use of sleep aids and/or stimulants?
Physical Examination (in addition to the routine things we check, i.e. vitals, weight, BMI)
Neck circumference
Detailed examination of the head/neck
o Facial morphology (looking for nasal symmetry, mandibular retrognathia)
o Oral cavity

There are different classifications including the modified Mallampati classification where it's an assessment of the oral
airway which was originally developed for tracheal intubation. I don't think this is important to know the details of this

Tonsils should be classified by the degree of hypertrophy
4 different grades; the higher grades signify enlarged tonsils
Subjective Assessment
Most well-known and widely used is the Epworth Sleepiness Scale (subjective assessment of the patient's daytime sleep propensity)
o 4-point
point Likert scale (0, 1, 2, or 3) to indicate likelihood of dozing in eight distinct sedentary conditions
o If total score 10 (out of 24) suggests excessive da
daytime sleepiness.
o Scale can be used to follow the patient's self
self-assessment
assessment of sleepiness and also an indicator of treatment response

Objective Measures
Nocturnal Polysomnography (NPSG)
o Basic recording montage should include the following

EEG: central, frontal, and occipital (full 16 lead EEG is not needed unless nocturnal seizures are suspected)

Left/right eye electro-oculograms
oculograms

Mental/submental surface EMG (leg surface EMG can be used if history suggestive of motor behaviors during sleep)

EKG leads
o 4 basic types (keep in mind that there are several other portable types and usually attended nocturnal polysomnography is indicated if
the portable yields either negative or a technically inadequate result)
result):

Type 1: standard, attended, in
in-laboratory

Type 2: comprehensive, portable, unattended polysomnography

Type 3: modified portable sleep apnea testing

Type 4: continuous single or dual bioparameter recording (i.e. pulse oximetry)
Multiple sleep latency test (MSLT)
o Similar to NPSG but in addition,
on, can measure thoracic and abdominal effort, oxygen saturation
o Can used to objectively assess excessive daytime sleepiness
o Protocol for testing would be the following:

Five 20-minute
minute nap opportunities held at 22-hour intervals

If sleep is observed during these opportunities, patient is allowed to sleep and the sleep latency is measured as the time
from the start of the nap trial to the first epoch of sleep

Mean sleep latency is then calculated as the average sleep latency across all nap trials

Presence and
nd number of sleep
sleep-onset REM periods can be determined (SOREMPs)

Values to consider:
Mean sleep latency > 10 minutes
minutes: normal
Mean sleep latency between 88-10 minutes: physiologic gray zone
Mean sleep latency < 8 minutes: can be normal in about 30% of the population
o If comb
mbined with 2 or more SOREMPs - would meet part of the diagno
nostic criteria for narcolepsy

Maintenance of Wakefulness (MWT)

o Measures patient's ability to remain awake (rather than the tendency to fall asleep like MSLT)
o Protocol for testing would be the following:

Four 40 minute trials that begin at 2-hour intervals (the first should start about 1.5-3 hours after the patient wakes up)

Each trial is terminated after 40 minutes if no sleep occurs OR after sleep onset (measured by EEG evidence of stage N1)
o Limited amounts of normative data available unfortunately

Sleep Disord
Disorders
We will review the following common sleep disorders:
Insomnia
Narcolepsy and Idiopathic Hypersomnia
Sleep Apnea syndrome
Sleep-related Movement Disorders
Circadian Rhythm Sleep Disorders
Parasomnias
INSOMNIA
International Classification of Sleep Disorders: Diagnostic and Coding Manual, 2nd Edition: Diagnostic and Coding Manual (ICSD-2)
o Long list of criteria which I will not include here but essentially, it requires night-time and day-time elements

Night-time elements: difficulty falling asleep, staying asleep, awakening excessively or sense of sleep that is not refreshing

Day-time elements: fatigue, poor concentration, poor motivation, low energy, various physical symptoms, prone to making
mistakes, headaches, poor performance
o Acute: few days to weeks; typically associated with a stressful situation
o Chronic: persisting at least 1 month
Women and older adults at greater risk for insomnia
Can be described as either
o Primary insomnia (an independent disorder without concomitant disorders)
o Comorbid type of Insomnia
Primary Insomnia
Examples: psychophysiological, paradoxical, and idiopathic insomnias
Idiopathic insomnia
o Begins during childhood
o Generally have lifelong difficulty with initiating or maintaining sleep
o Diagnosis depends on exclusion of concomitant comorbid medical, neurological, psychiatric or psychological disturbances
o Typically continues into adulthood
Psychophysiological insomnia
o Begins during young adulthood
o Typically these patients are over-concerned and over-focused on sleep problems but typically do NOT have generalized anxiety
o Insomnia could have been initiated by a stressor but it persisted even after initial stress is gone
o Chronic insomnia with tension or agitation that results from learned sleep-preventing associations such as:

Fear and frustration about being unable to initiate and maintain sleep

Identification of the bedroom as an arousal sign
Paradoxical insomnia
o This is a sleep state misperception characterized by subjective complaints of sleeplessness without any objective evidence i.e. PSG
recording documents normal sleep patterns
Co-morbid type of Insomnia (I will not go into much detail about this as it is pretty extensive and some of them are pretty self-explanatory)
Examples: inadequate sleep hygiene, insomnia comorbid with psychiatric disorders, with general medical disorders, with neurological disorders,
or insomnia due to drug or other substance abuse
Evaluation of Insomnia
General advice: think very broadly about the etiology and expect multiple factors that can predispose someone to sleep difficulty
Typically, whatever triggered the sleep difficulty is NOT necessarily what is currently contributing to the persistent symptoms
As mentioned before under "Approach and Evaluation to Sleep Disorders," history should also be obtained from sleep partners if possible
Ask about daytime activities and functioning and sleep-wake schedule routines; is it the difficulty primarily sleep onset or sleep maintenance?
Have them keep a sleep log
Sleep laboratory testing (not routinely done) can be useful when suspicion that a concomitant sleep disorder is contributing to symptoms (i.e.
obstructive sleep apnea)
Treatment
For co-morbid type of insomnia, it is obvious that you would address the underlying cause
Educating on healthy sleep habits

Cognitive-behavioral
behavioral therapy for insomnia can help address factors that regulate sleep
sleep-wake
wake cycle, psychological processes that can affect
sleep and cognitive distortions that can be contributing to the perpetuation of insomnia
o Can also include relaxation therapy, biofeedback, "stimulus control therapy" - see below as an example

Pharmacologic approach
o As you already know, there are tons of over
over-the-counter
counter medications out there. I wanted to focus on the FDA approved medications
o Insomnia medications approved by US FDA include:

-amniobutyric
amniobutyric acid response modulators
There are several medications that can be used; I will not list all of them here but to name a few:
o Non-BZD:
BZD: Ambien, Zaleplon
o BZD: Flurazepam, Temazepam

melatonin receptor agonist (only one that has been approved: Ramelteon - activated melatonin type receptors that are
concentrated in the hypothalamic suprachiasmatic nuclei and by doing so, the SCN-driven
driven wake-promoting
wake
stimulus)
Use for insomnia characterized by difficulty with sleep onset; not beneficial for maintaining sleep

histamine H1 receptor antagonist
Low dose doxepin is approved for insomnia characterized by difficulty with sleep maintenance
should NOT be prescribed for patients w/ untreated narrow
narrow-angle
angle glaucoma or severe urinary retention or those
who are taking monoamine oxidase inhibitors
No abuse potential with doxepin
o Off-labeled Rx: many anti-depressants,
depressants, anti
anti-psychotics, and anti-epileptic
leptic have been used to treat insomnia;

these can be effective at times; but there is little evidence to guide treatment plan
To name a few that we use a lot: trazodone, amitriptyline, quetiapine,

NARCOLEPSY
Disorder of REM sleep; this is a classic hypersomnia
persomnia of central origin
Onset in most cases: adolescents and young adults with peak incidence between ages 15 and 30
Pathophysiology:
o association with HLA-DR
DR with narcolepsy and other HLA types

most closely linked being: HLA
HLA-DQB1*0602
o Hypocretin-11 has been implicated in human narcolepsy

hypocretin is a neurotransmitter that regulates arousal, wakefulness and appetite

hypocretin peptides bind to their own specific receptors (i.e. histaminergic tuberomamillary nucleus, ventrolateral preoptic
nucleus, cholinergic pedunculopontine nucleus)

patients with narcolepsy tend to have low or undetectable CSF hypocretin levels
Three types:
o Narcolepsy without Cataplexy
o Narcolepsy with Cataplexy
o Secondary Narcolepsy
Narcolepsy without Cataplexy (Criteria)

Narcolepsy with Cataplexy (Criteria)

Major clinical manifestations:

o Narcoleptic sleep attacks / excessive daytime sleepiness (100%)

heralding feature of narcolepsy

Irresistible urge to sleep w/o warning

Naps are often refreshing and often recommended as part of the treatment plan
o Disturbed night sleep (70-80%)

usually not considered as part of the classic tetrad; it is an essential symptom of narcolepsy

many experience sleep fragmentation due to multiple arousals, early morning awakenings, nocturnal eating and unun
refreshing nocturnal sleep
o Cataplexy (60-70%)

defined as a the sudden, involuntary loss or decrease of muscle tone

Most commonly precipitated by laughter or other intense positive emotions

These can either be profound with generalized atonia resulting in falls and injuries OR localized loss of muscle tone that can
ca
be misdiagnosed or not considered
Subtle weakness inclu
includes:
o slurring of speech | buckling of knees | jaw dropping | nodding of head
o Sleep paralysis (25%-50%)

Characterized by inability to move while being totally aware of one's surroundings

occur either at arousal or at sleep onset; rarely lass more than a few minutes

this is NOT pathognomonic of narcolepsy (can occur in those who are sleep deprived)

Hallucinations (20-40%)
Simple or complex visual hallucinations (auditory and tactile hallucinations can occur)

Can be either hypnagogic (transition from wakefulness to sleep) or hypnopompic (sleep to wakefulness)

Typically hypnagogic hallucination is commonly associated with narcolepsy

this is NOT pathognomonic of narcolepsy

Automatic behavior (20-40%)

described as act of pursuing purposeful behavior with no reminiscence of it

Patients either seem awake and alert or appear inattentive during the episode

Intrusion of microsleep into wakefulness is believed to be the cause of this symptom

Sleep deprivation can precipitate these symptoms

this is NOT pathognomonic of narcolepsy
Can be associated with:
o Periodic limb movements of sleep

characterized as cluster of limb movements occurring during sleep that resemble a triple flexion response

more prevalent as patient gets older

tend to occur during REM sleep
Evaluation:
o Can use the epworth sleepiness scale to assess subjective daytime sleepiness
o On polysomnogram, you would find:

decrease in total sleep time

a short sleep-onset latency

sleep fragmentation

REM without atonia

REM sleep occurring within 15 minutes of sleep onset
o Genetic testing to look for serum HLA-DQB1*0602 is available; typically do this for patients with narcolepsy with cataplexy
o Hypocretin level in CSF can be measured as well
Treatment:
o For the excessive daytime sleepiness:

Typically can use stimulants (i.e. d-amphetamines) or wake-promoting agents (i.e. modafinil)

encourage scheduled naps throughout the day
o For cataplexy

At the moment, nothing is FDA approved

Can try the following:
Tricyclic: imipramine
SSRI: fluoxetine
SNRI: Venlafaxine
o

IDIOPATHIC HYPERSOMNIA (I won't spend too much time on this; but wanted to make you aware of it)
Unknown etiology
Characterized by:
o Non-refreshing sleep with difficulty waking up (either in the morning or from a nap)
o Feel sleepy during the day
o Typically show a depressed mood
o Normal total sleep time
o Absence of sleep-disordered breathing
o Normal sleep architecture
Diagnosis of exclusion
Poorly understood so the precise prevalence of this disorder remains unknown
Treatment
o Behavioral interventions
o Pharmacologic approach is similar to narcolepsy
Recurrent Hypersomnia (under the umbrella term of hypersomnia)
Klein-Levin Syndrome
o Triad of: hyperphagia, hypersomnia, hypersexuality
o Clinical diagnosis; work-up is mainly to rule out other causes of hypersomnia
o Prevalence: 1 in 1 million so very rare
o Typically occur during second decade of life; but can really occur at any point
o Clinical presentation:

usually preceded by a precipitating factor; most common complaint is an infection or high fever

Patients report periods of excessive sleepiness that range from 2 days to 4 weeks with recurrence of these symptoms at
least 1x per year

Typically have normal cognitive function

Men tend to have more symptoms of hypersexuality than women

o
o

Work-up
up for these patients are typically normal including polysomnogram, imaging, etc)
Treatment:

Valproic acid, lithium, amantadine or lamotrigine have been tried and showed good responses in a few patients

Modafinil has been tried - shown to decrease the duration of the episodes but no effect on the recurrence rate

SLEEP APNEA SYNDROME

Broadly divided into two types:
o Upper airway obstructive sleep apnea syndrome
o Central sleep apnea syndrome
Obstructive Sleep Apnea Syndrome (I will only highlight the importance features)
Obesity is associated with 70% of the cases; so that also means 30% of the cases it's not so it's important to not miss these cases
Upper airway anatomical abnormalities that can cause reduction of the upper airway space
o Low-hanging soft palate
o Large edematous uvula
o Large tonsils and adenoids (typically seen in children)
Consequences of untreated OSA:
o Increased morbidity and mortality due to both short term consequences (falling asleep behind the wheel) and long term consequences
consequ
o Associated with systemic HTN
o Pulmonary hypertension (can occur 15
15-20% of the cases)
o Cardiac arrhythmias
o Heart failure (mostly systolic heart failure) -- tend to occur more in central sleep apneas
o Stroke, TIA
o Cognitive dysfunction
o Depression
o Insomnia
Treatment: positive airway pressure (CPAP or BiPAP), surgery (i.e. adenoidectomy, tonsillectomy, etc)
o Can typically use the AHI score to determine the effectiveness of the treatment

AHI: apnea-hypopnea
hypopnea index score; measures the number of apnea and hypopn
hypopnea
ea episodes occur per hour of sleep
Hypopneas: defined as a reduction in the airflow sensor signal by 30% or more of the baseline amplitude for at
least 10 seconds accompanied by oxygen desaturation of 4% or more from the pre-event
pre
baseline
Typically AHII > 10 is considered significant
Central Sleep Apnea
second period of loss of airflow with the absence of respiratory effort indicative of brief loss of ventilatory drive
Defined as at least a 10-second
Normal physiology:
o During sleep: respiration is primarilyy driven by partial pressure of arterial CO2
o Normally, there is a level of PaCO2 below which a pause in breathing will occur (this is called the apneic threshold)
o Apneic threshold is higher during wake than sleep; so can be normal to have brief central ap
apnea
nea during transition to sleep
Cheyne-Stokes
Stokes breathing is noted in patients with congestive heart failure
o Characterized by cyclical changes in breathing with a crescendo
crescendo-decrescendo
decrescendo sequence separated by apneas or hypopneas
o In heart failure, CSA can develop because of chronic hypocapnia related to changes in the hemodynamics in the left heart -- an as a
result of these changes, peripheral and central chemosensitivity are augmented

This hypersensitivity of the receptors can llead
ead to an exaggerated response to the fall in partial pressure of arterial oxygen
(PaO2) and rise in PaCO2 seen during a single apnea --> leading to hyperventilation -->> which will again decrease the
PaCO2 below the apneic threshold --> leading to hypoventilation

SLEEP-RELATED MOVEMENT DISORDERS

Restless Leg Syndrome
MC movement disorder but uncommonly recognized and treated
No single diagnostic test for RLS
Lifelong sensory-motor
motor neurological disorder that begins at a very young age but doesn't get diag
diagnosed
nosed until middle or later years
o the sensory manifestations are described as: creeping, crawling, tingling, burning, aching, cramping, knifelike, or itching sensations
s
In order to make the diagnosis; you need all four essential diagnostic criteria (see below)

Most of movements (early stages) are noted to in the evening while the patient is resting in bed
o in severe cases, can occur during the day (at least 80% of RLS patients have periodic
periodic-limb
limb movement syndrome as well)
Pathophysiology
o likely related to abnormalities in the body's use and storage of iron and dopamine dysfunction
o Iron is an important cofactor for tyrosine hydroxylase (rate
(rate-limiting
limiting enzyme in dopamine synthesis); therefore, in an iron deficiency,
there may be a decrease number
umber of dopamine D2 receptor binding sites
o So remember to check your ferritin in suspected RLS
Investigation/Management of RLS
o Check iron panel; particularly ferritin as it is the most sensitive measure of iron stores

remember, ferritin is also an acute phase reactant so it may be falsely elevated in acute infections
in these cases, also check the total iron
iron-binding
binding capacity and percent saturation
o Polysomnography is not routinely indicated
o Treatment

If ferritin is low, iron therapy can be considered (add vitamin C to each dose to enhance absorption)

Dopaminergic agents (i.e. pramipexole, ropinirole) - approved by FDA for treatment of RLS
Maximum dose for RLS
o Pramipexole 0.75 mg (should start out with 0.125 mg and titrate up slowly)
o Ropinirole
pinirole 4 mg (should start out at 0.5 mg and titrate up)
Important: long term use of these agents can lead to augmentation (worsening of the restless leg
syndrome earlier in the day)
day),, impulse control disorder and daytime sleepiness
o Augmentation: in one study, at least 42% of patients treated with pramipexole developed
augmentation; in order to treat this is to discontinue the medication
o Excessive daytime sleepiness
sleepiness:: can develop in about 50% of patients
o Impulse control disorder: typically includes pathologic
ologic gambling and compulsive shopping (occur in 6
to 17%)

Benzodiazepines (clonazepam, zolpidem)

Opioids - good for severely refractory cases; though these are addictive and exacerbate sleep apnea

Periodic Limb Movement of Sleep Disorder

Characterizedd by periodically recurring stereotyped limb movements , particularly dorsiflexion of the ankles and sometimes flexion of the knees
and hips at the average interval of 20 to 40 seconds
o For adults: has to occur more than 15 per hour
o For children: occur more than 5 per hour
Appear most commonly in RLS
On PSG: findings of PLMS without associated
ed RLS causing repeated awakenings and sleep fragmentations

Significance of this diagnosis has been debated

o typically occur in 80 to 88% of patients with RLS; however, there are still up to 20% of the cases where it is not associated with RLS
o No definite relationship has been detected between the presence of PLMS and symptoms of insomnia or hypersomnia
o Other studies have shown no association between PLMS and PSG measures i.e. total sleep time, wake time after sleep onset,
arousal index and sleep deficiency

Treatment
o Levodopa eliminates the movements; but arousals may still persist during sleep
o Optimal treatment for PLMD is uncertain; at this time dopaminergic agonists may be the drug of choice but there has been no
controlled trials of any agents for pure PLMD

CIRCADIAN RHYTHM SLEEP DISORDERS

Result from mismatch between body's internal clock and geophysical environment either from malfunction of biological clock or a shift in
environment causing this to be out phase
Some of the more obvious ones: i.e. jet lag or shift-work sleep disorders (this one we know all too well) - I won't talk about this - instead I'll
focus more of the disorders where the biological clock is malfunctioning
Delayed Sleep-Phase Disorder
Characterized by chronic or recurrent inability to fall asleep and wake up at socially acceptable times
o by definition: there is more than 2 hour delay in the major sleep period
o typically when these patients are allowed to sleep at their biologically preferred time, they function well
o Typically sleep between 1 AM - 6 AM and wake up late morning or early afternoon
Prevalence: 0.2 to 10% severe cases; milder cases are more prevalent, typically among adolescents and young adults
Pathogenesis: several mechanisms have been postulated
o Decreased response to the phase-advancing effect of light in the morning
o Increased sensitivity to the phase delay response of the evening light
o Longer than normal time to complete one circadian cycle
Diagnosis:
o careful history and sleep diary for at least 7 days
o more of a clinical diagnosis
Treatment:
o Recommend appropriately timed morning light exposure and evening exogenous melatonin either alone or in combination

Bright light in the morning for 2 hours help advance the circadian rhythms in these patients

Melatonin given 5 to 6.5 hours before sleep can help advance sleep and rise times

Effectiveness can lasts up to 1 year with daily melatonin intake but relapses can occur in up to 90% if they stop
Advanced Sleep-Phase Disorder
Characterized by an advance in phase of the major sleep episode in relation to the desired or required sleep and wake-up times
o Typically these patients are sleepy and struggle to stay awake between 6 PM and 9 PM and wake-up earlier than desired between 2
AM and 5 AM
Prevalence: less common than DSPD (about 1%); occur during middle age
Pathogenesis:
o shortened circadian period has been postulated
o 2 gene mutations have been identified: gene hPer2 and the casein kinase I delta gene -- these mutations result in a shortened
circadian period
Diagnosis:
o Again, based on clinical history and a sleep diary
Treatment:
o Timed light exposure in the evening and avoiding light in early morning hours
o Melatonin may be beneficial for sleep maintenance
o Bright light administered before the nadir of body core temperature is potent stimulus for delaying circadian phase

Early-evening light therapy between 7 PM and 9 PM

This has been shown to improve sleep duration and sleep maintenance
Irregular Sleep-Wake Rhythm Disorder
Characterized by temporally disorganized sleep and wake pattern such that multiple sleep and wake periods occur throughout the 24 hr period
Prevalence: MC among institutionalized older adults particularly those with Alzheimer disease; been described in patients with head trauma,
children with developmental delay, and patients with schizophrenia
Pathogenesis:
o Most likely include central degeneration of SCN neurons and decreased exposure or input of external synchronizing agents such as
light and activity that result in a weakened central circadian oscillation and temporal disorganization of circadian rhythm
o This problem is perpetuated by a variety of factors inherent in the lifestyle of older adults in nursing homes, etc.
Clinical presentation:
o sleep bouts occur in 3+ short intervals of approximately 1 to 4 hours each spread over 24 hours
o typically the overall amount of sleep per 24-hour period is relatively normal for the patient's age

Diagnosis
o Clinical history and history of a minimum of 3 irregular sleep-wake cycles in a 24 hour period for 14 days evident by sleep diary

Treatment:
o Creating a cognitively enriched environment with structured social and physical activity during the day is probably the best treatment
modality to help these patients

i.e. minimizing noise and light during the scheduled sleep period and addressing issues such as nocturia and enuresis to
reduce sleep disturbances

exposure to bright lights for 2 hours every morning to improve daytime alertness, decrease napping and consolidate
nighttime sleep and reduce nocturnal agitation

PARASOMNIAS
defined as abnormal movements or behaviors that occur in sleep or during arousals from sleep
Can be broken down into 3 broad categories
o Disorders of arousal (from NREM sleep)

confusional arousals, sleepwalking (somnambulism), sleep terrors
o Parasomnias associated with REM sleep

sleep paralysis, RBD (REM sleep behavior disorder)
o Other parasomnias including sleep-related dissociative disorders, sleep enuresis, sleep-related groaning
Disorders of Arousal from Non-REM Sleep
these parasomnias typically arise from slow-wave sleep in the 1st half of the nocturnal sleep
Confusional arousals:
o episodes of mental confusion or confusional behavior during an arousal or awakening from nocturnal sleep or daytime nap
o responsiveness to environmental stimuli is reduced
o speech is generally slow and devoid of content
o affected individuals typically appear bewildered and have little to no memory of the event
Sleepwalking
o characterized by sequence of complex behaviors in sleep, including ambulation that is more elaborate and seemingly goal-directed
o ambulation is typically slow and quiet with eyes open
o Occur more often in children than adults; peak between ages 8 and 12
Sleep terrors
o sudden arousal and sitting up in bed associated with a cry or vocalization and intense autonomic system activation
o affected individuals appear frightened and confused and are inconsolable; no recollection of the events the following AM
Parasomnias associated with REM sleep
REM sleep behavior disorder
o REM sleep parasomnia that presents with complex nocturnal behaviors
o Presenting complaint: recurrent dream-enacting behaviors including vocalization and motor activity in relation to altered dream
mentation
o sleep-related injuries to affected person or bed partner occur about 1/3 of the cases
o different from those that occur during non-REM sleep is that the patients typically wake-up abruptly at the end of an episode and are
alert and able to recount a coherent dream of being confronted, chased or attacked
o important to know that this is the ONLY parasomnia that REQUIRES polysomnographic confirmation

PSG: shows that patient is in REM sleep without atonia in the chin or limb EMG
o Occur later in life (typically after age 50)
o More common in men than women (9x)
o Pathophysiology: requires bilateral pontine tegmental lesions resulting in loss of REM atonia and disinhibition of locomotor pathways;
thereby facilitating dream enactment
o several drugs/medications have been shown to exacerbate or cause RBD

anti-depressants i.e. SSRI, SNRI (venlafaxine) and trcyclics
o Treatment:

modifying sleep environment to protect the patient and bed partner

Clonazepam is remarkably effective in treating RBD
Sleep-Related Dissociative Disorders
emerge at the transition from wake to sleep or shortly following awakening
most patients have psychiatric co-morbidities including mood disorders, PTSD, history sexual abuse
Episodes are non-stereotyped and feature screaming, running and even self-mutilating, violent behaviors that may represent re-enactment of
prior traumatic events
psychogenic non-epileptic seizures occurring in relation to sleep may be considered a form of sleep-related dissociative disorder
o difficult to differentiate from frontal lobe seizures
o Characterized by waxing and waning patterns and long durations
o Motor manifestations include: asynchronous movements, side-to-side head movements, pelvic thrusting, opisthotonic posturing and
prolonged body flaccidity and preserved awareness during bilateral motor activity