This document discusses sleep physiology and sleep disorders. It begins by defining sleep and outlining the three basic physiological processes of wakefulness, non-rapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep. It then describes sleep architecture and the stages of NREM and REM sleep in detail. Key aspects of sleep such as circadian rhythms, sleep requirements, neurobiology, and disorders like insomnia are also summarized. The document provides an overview of normal sleep patterns and processes as well as common sleep disorders.

1. Sleep
physiology and
Sleep disorders
Dr Amruta Rajamanya
DNB Neurology Trainee
1st year
KMC Mangalore

2. Sleep
Lucretius postulated that sleep is an absence of
wakefulness.
Macnish in 1830 -“suspension of sensorial power
in which the voluntary functions are absent but the involuntary
functions, such as circulation, respiration, and other functions
controlled by the autonomic nervous system, remain
intact.”
Sleep, however, is not simply an absence of wakefulness,
nor is it just suspension of sensorial power; it results from a
combination of passive withdrawal of afferent stimuli
to the brain and activation of certain neurons in selective brain
areas.

3. Definition
 Behavioral criteria include lack of mobility or slight
mobility, closed eyes, a characteristic species-specific
sleeping posture, reduced response to external
stimulation, quiescence, increased reaction time,
elevated arousal threshold, impaired cognitive function,
and a reversible unconscious state.
 Physiological criteria are based on EEG, electro-
oculography (EOG), and electromyography (EMG)
findings as well as other physiological changes in
ventilation and circulation.

4. Three basic physiological processes of
life consist of
Wakefulness,
 Nonrapid eye movement (NREM) sleep,
 Rapid eye movement (REM) sleep,
with independent functions and controls.

5. Sleep Architecture and Sleep
Stages
 Based on the physiological criteria, sleep is
divided into two independent states:
NREM and REM sleep
 NREM and REM sleep alternate, with each
cycle lasting for approximately 90 to 100
minutes.
 Four to six such cycles are noted during a
normal sleep period.

7. Conversely, the duration of the REM sleep cycle increases
from the first to the last cycle, and toward the end of the
night, the longest REM cycle may last as long as 1 hour.
Thus the first third of a normal sleep episode is dominated
by slow-wave sleep, and REM sleep dominates the last
third.

9. NREM sleep
Rechtschaffen and Kales (RK) [1968 ]divided
NREM sleep into stages 1, 2, 3, and 4.
In 2007, American Academy of Sleep Medicine
(AASM) Task Force NREM sleep is now divided into
three stages: N1, N2, and N3 (slow-wave sleep).
NREM sleep accounts for 75% to 80% of sleep time in
adult humans.

10. Stage N1
 3% to 8% of sleep time,
 the alpha rhythms (8–13 Hz) characteristic of wakefulness
diminish to less than 50% in an epoch
 a mixture of slower theta rhythms (4–7 Hz) and beta
waves (>13 Hz) appears
 EMG activity decreases slightly, and slow, rolling eye
movements may be recorded
 positive myoclonus, hypnagogic hallucinations

11. Stage N2 sleep
 begins after approximately 10 to 12 minutes of stage N1
 lasts for approximately 30 to 60 minutes.
 EEG-
 Sleep spindles (12–18 Hz, most often 14 Hz) and
 K complexes intermixed with vertex sharp waves
 theta activity and fewer than 20% slow waves (0.5–2 Hz)

12. Stage N3
the slow waves occupy 20% to 100% of the epoch
20% delta waves ranging from 0.5–2 Hz
parasomnias such as night terrors, nocturnal enuresis,
somnabulism and somniloquy occur

13. NREM SLEEP
 Most sleep during each night is of the NREM
variety ; this is the deep, restful sleep that the
person experiences during the 1st hour of
sleep after having been awake for many hours.
 "dreamless sleep“, realistic and rational
 There are 10 to 30 per cent decrease in blood
pressure, respiratory rate and basal metabolic
rate

14. REM sleep(Paradoxical
Sleep, Desynchronized Sleep)
episode is noted 60 to 90 minutes after the
onset of sleep
accounts for 20% to 25% of sleep time
Based on EEG, EMG, and EOG characteristics,
REM sleep can be subdivided into two stages:
 tonic
 phasic.

15. TONIC REM SLEEP:
A desynchronized EEG, hypotonia, or atonia of the major muscle
groups and depression of monosynaptic and polysynaptic reflexes
Phasic REM sleep
rapid eye movements in all directions, as well as phasic swings in
blood pressure and heart rate, irregular respiration, spontaneous
middle-ear muscle activity, and tongue movements.

16. REM SLEEP
 The person is even more difficult to arouse by sensory
stimuli than during deep slow wave sleep, and yet
people usually awaken spontaneously in the morning
during an episode of REM sleep
 Muscle tone throughout the body is exceedingly
depressed, indicating strong inhibition of the spinal
muscle control areas
 Heart rate and respiratory rate usually become
irregular, which is characteristic of the dream state

19. Sleep Microstructure
In 1992, a Task Force of the American Sleep Disorders Association
(ASDA),

20. Arousals
an arousal is a shift in EEG frequency lasting for 3 to 14 seconds and
includes alpha, beta, or theta activities but not spindles or delta
waves.
The subject must be asleep for 10 consecutive seconds
before an arousal can be scored.
An arousal index
the number of arousals per hour of sleep;
up to 10 can be considered a normal arousal index.

21. Cyclic alternating pattern
the CAP indicates sleep instability
a repetitive EEG pattern that is noted mainly during
NREM sleep and lasts for 2 to 60 seconds.
increased EEG potentials, with contributions from both synchronous
high-amplitude slow and desynchronized fast rhythms in the EEG
recording.
A CAP cycle consists of an unstable phase (phase A) and a relatively stable
phase (phase B)

22. During phase A, heart rate, respiration, blood pressure, and muscle tone
increase.
The rates of CAP cycles and arousals increase in both older individuals
and a variety of sleep disorders.
The CAP sequence, confined between the two black arrows, shows three
phase As and two phase Bs, which illustrate the minimal requirements for the
definition of a CAP sequence (at least three phase As in succession).

23. Ontogeny of Sleep Patterns with Age
Sleep spindles begin to appear at about 3
months of age; K complexes are seen by
about 6 months.

24. Sleep Habits
 evening types and morning types
 Evening types(“owls”)
 have difficulty getting up early and feel tired in the morning;
however, they feel fresh and energetic toward the end of the day.
 These people perform best in the evening; they go to sleep late
and wake up late.
 Morning types (“larks”)
 wake up early, rested and refreshed, and work efficiently in the
morning.
 Katzenberg and colleagues (1998)- CLOCK gene polymorphism

25. Sleep Requirements and
Quantity of Sleep
 optimal amount of sleep required to remain
alert and fully awake and to function
adequately throughout the day
approximately 7.5 to 8 hours

26. Neurobiology of Sleep and
Wakefulness
 Wakefulness is controlled by the ascending reticular
activating system (ARAS) containing glutamatergic,
cholinergic, aminergic, and hypocretinergic neurons
Wakefulness promoting
i. Aminergic neurons include noradrenergic
neurons in the locus coeruleus,
ii. Serotonergic neurons in the dorsal raphe of
the brainstem,
iii. Histaminergic neurons in the
tuberomammillary nucleus of the
hypothalamus
Cortical arousal is generated through two
systems:
dorsal route through the thalamus
ventral route through the hypothalamus and
basal forebrain (BF).

27. Neuroanatomical Substrates
for REM Sleep
McCarley-Hobson reciprocal
interaction model
LDT-PPT cholinergic
neurons promote REM
sleep through pontine
reticular formation (PRF)
effector neurons, which in
turn send feedback loops
to LDT-PPT neurons.

28. Neuroanatomical Substrates of
NREM Sleep
Sleep-promoting neurons are thought to reside in
the
 ventrolateral preoptic (VLPO)
 median preoptic neurons (MnPn) of the anterior
hypothalamus
 in the region of the NTS in the medulla.
VLPO neurons consist of two subgroups,
Clustered -project to the tuberomammillary nuclei and
promote NREM sleep
Diffuse-project tothe aminergic nuclei in the locus
coeruleus and the dorsal raphe region of the brainstem,
participating in REM sleep

29. Circadian Rhythm and
Chronobiology of Sleep
 French astronomer de Mairan (1731)
 circadian rhythm originates from the Latin
circa, meaning “about,” and dies, meaning
“day.”
 Biological clock- paired SCN of the
hypothalamus above the optic chiasm

30. The master circadian clock in
the SCN receives photic information
from the retinohypothalamic tract
Through a polysynaptic projection, the
SCN inhibits the activity of the superior
cervical ganglia (SCG),which supply
the pineal gland with an excitatory,
noradrenaline (NA)-containing input
This mechanism allows light
to suppress the production and
release of melatonin from the
pineal gland and, subsequently,
melatonin secretion is enhanced in
the dark period
maximum level of melatonin
between 3:00AM and 5:00AM

31. 1. Homeostatic factor refers to
a prior period of wakefulness
and sleep debt. After a
prolonged period of
wakefulness, there is an
increasing tendency to sleep.
2. The circadian
factor
determines the body’s
propensity to maximal
sleepiness between 3:00AM
and 5:00AM
Physiological sleepiness depends on two processes:

39. Insomnia

40. Insomnia
 Insomnia - an inability to initiate or maintain
sleep, early awakening, inadequate sleep
time, or poor sleep quality associated with a
lack of feeling restored and refreshed in the
morning, leading to a general sleep
dissatisfaction and poor daytime functioning

42. Short-Term Insomnia Disorder
(Acute Insomnia)
short-term difficulty in initiating or maintaining sleep that results in general sleep
dissatisfaction and is accompanied by daytime distress about the poor sleep
quality or impairment in social, family, occupational, academic, or other important
areas of functioning.
The disorder and its associated symptoms occur despite having adequate
time and circumstances to obtain necessary sufficient sleep

43. Chronic Insomnia
The clinically significant consequences (both short-term and long-term)
of insomnia most typically develop when sleep difficulties occur at least
three times per week and persist for at least 3 months.

44. Idiopathic Insomnia
 Onset- early childhood
 lifelong difficulty with initiating or maintaining sleep, or both,
resulting in poor daytime functioning
Psychophysiological insomnia-
 young adulthood
 chronic insomnia with increased tension or agitation that results
from learned sleep-preventing associations
 The development of conditioned responses incompatible with
sleep is the predominant feature
 PET imaging- overall cortical hyperarousal

45. Paradoxical Insomnia
 Sleep state misperception characterized by
subjective complaints of sleeplessness
without objective evidence
 Actigraphy (an accelerometer which
measures sleep/ wake activities) or PSG
recording documents normal sleep patterns in
such patients

50. Narcolepsy
 French physician Gelineau
 The prevalence of narcolepsy
1 in 2000 individuals in the United States
, 1 in 600 people in Japan, and
1 in 500,000 individuals in Israel

51. Genetics of Narcolepsy
 10 to 40 times greater prevalence of
narcolepsy in families
 HLA-DQB1*0602 is a marker for narcolepsy
on chromosome 6

52. Pathogenesis of Narcolepsy-
Cataplexy Syndrome
depletion (degeneration or
autoimmune disorder) of the
hypocretin neurons in the lateral
and perifornical region of the
hypothalamus

53. Clinical Manifestations of
Narcolepsy
The onset-peak incidence between ages 15 and 30
two types
 narcolepsy type 1 (with cataplexy,or low hypocretin levels),
 narcolepsy type 2 (without cataplexy, and with normal hypocretin levels)

55. Narcoleptic sleep attack
 is an irresistible desire to fall asleep in inappropriate
circumstances and at inappropriate places
 last from a few minutes to as long as 20 to 30 minutes
 Attacks generally persist throughout the patient’s
lifetime, although fluctuations and rare temporary
remissions may occur
 decline in performance at school and work and
encounter psychosocial and socioeconomic difficulties

56. Cataplexy
 sudden loss of tone in all voluntary muscles with the
exception of the respiratory and ocular muscles
 universally preceded by a prodromal of emotion leading to a
transient episode of muscle weakness
 triggers - laughter and excitement, rage, or anger more than
95% of the time
 Complete or partial
 head nodding, sagging of the jaw, buckling of the knees,
dropping of objects from the hands, dysarthria, or loss of
voice, but sometimes they may slump or fall forward to the
ground for a few seconds
 Flaccidity
 H reflex and F responses are decreased or absent
 EEG recording- wakefulness during brief cataplectic spells,
but if the attack lasts longer than 1 to 2 minutes, the EEG
shows REM sleep

57. Sleep paralysis:
 25% to 50%
 sudden apparent paralysis of one or both
sides of the body
 hypnagogic or hypnopompic
 attacks last from a few minutes to 15 to 20
minutes
 retains consciousness

58. Hypnagogic hallucinations:
 20% to 40%
 at sleep onset or on awakening
 Hallucinations are most commonly vivid and visu
Disturbed Night Sleep and Automatic
Behavioral:
 70% to 80%
 repeated performance of a single function

61. Idiopathic Hypersomnia
 Greater than 3-month duration of EDS and an irrepressible
need to sleep or daytime lapses into sleep in the absence,
and after correction, of sleep deprivation
 15 to 30 years
 Total 24-hour sleep time is 660 minutes or more (typically
12–14 hours) on 24-hour polysomnographic monitoring or
wrist actigraphic recording
 profound sleep inertia k/a sleep drunkenness
 mental fatigability
 long (> 1 hour) unrefreshing naps
 no abnormal neurological findings

62. Kleine–Levin Syndrome (KLS) (aka Recurrent
Hypersomnia, Periodic Hypersomnolence)
 form of recurrent hypersomnia associated with symptoms of
hyperphagia , megaphagia, cognitive impairment, and
hypersexuality
 adolescent patients (males > females)
 sleeps for 16 to 18 hours a day
 upon awakening eats voraciously
 hyperorality, memory impairment, confusion, hallucinations,
and polydipsia
 at least two episodes of excessive sleepiness lasting between
2 days and 5 weeks in duration, more frequent than once a
year and once every 18 months, with periods of normalcy
between episodes
 normal sleep cycling and MSLTs show pathological sleepiness
without sleep-onset REM
 lithium treatment

65.  Parasomnias can be defined as abnormal
movements or behaviors that occur in sleep
or during arousals from sleep; they may be
intermittent or episodic, and sleep architecture
may not be disturbed

66. Somnambulism (Sleepwalking)

67. Sleep Terrors (Pavor Nocturnus)

68. Confusional Arousals
 Mostly before age 5
 episodes arise out of slow-wave sleep but
occasionally may occur out of stage N2
NREM sleep
 some automatic and inappropriate behavior,
including abnormal sexual behavior
(“sexsomnia” or sleep sex) when this occurs
in adults

69. Rapid Eye Movement Sleep
Behavior Disorder

70. Nightmares (Dream Anxiety
Attacks)
 fearful, vivid, often frightening dreams, mostly visual but
sometimes auditory, and seen during REM sleep
 occur during the middle to late part of sleep at night
 Causes
 Antiparkinsonian drugs (pergolide, levodopa), anticholinergics,
and antihypertensive drugs, particularly beta-blockers
 alcohol ingestion or
 sudden withdrawal from barbiturates
 schizophreniform psychosis
 Treatment
 combined behavioral or psychotherapy and
 REM sleep-suppressant medications

71. Sleep Talking (Somniloquy)
 utterances of speech or sounds that occur
during the sleep episode without awareness
of the event
 episodes are generally brief, infrequent, and
devoid of signs of emotional stress.
 Self-limited and benign

72. Catathrenia (Expiratory
Groaning)
 recurrent episodes of expiratory
groaning(high-pitched, loud humming, or
roaring sounds)
 occurs in clusters,
 predominantly during REM sleep, but it may
also occur during NREM sleep
 PSG findings resemble central apnea with
protracted expiratory bradypnea without
oxygen desaturation

73. Sleep Starts
 sudden brief myoclonic movement of the
limbs or the whole body lasting for a few
seconds
 physiological phenomena without any
pathological significance
 triggered by stress, fatigue, or sleep
deprivation

74. Hypnagogic Foot Tremor
 rhythmic movement of feet or toes
 occurring at the transition between wake and
sleep or during stages 1 and 2 NREM sleep
 PSG findings :
 typically of trains of 1- to 2-Hz (range, 0.3–4 Hz)
 EMG potentials or movement in one or both feet,
with the burst duration longer than 250 to 1000
microseconds; the minimum number needed to
make a train is four bursts

75. Alternating Leg Muscle Activation
 brief activation of the tibialis anterior muscle in
one leg alternating with similar activation in the
other leg during sleep or arousals from sleep
 PSG finding,
 with a frequency of 0.5 to 3Hz with an individual
activation duration between 100 and 500msec;
 A minimum of four alternating activations with less
than 2 seconds between the activations is required
for diagnosis, and each sequence may last up to 30
seconds

76. Excessive Fragmentary
Myoclonus
 small muscle jerks without visible movements of
the fingers, toes, or corners of the mouth or small
muscle twitches resembling fasciculations that do
not cause gross movement across the joint space
 PSG finding
 brief myoclonic bursts (75–150 msec) of more than 5
potentials per minute, sustained for at least 20
minutes during NREM sleep

78. Sleep Apnea Syndrome
 upper airway OSAS
 central sleep apnea syndrome (CSAS)

79.  An arousal is defined
as either a transient return of alpha activities (8–13 Hz) or
beta rhythms (>13 Hz) or a change from delta to theta
activities in the EEG lasting from 3 to 14 seconds.
 Paradoxical breathing
movements of the thorax and abdomen in opposite
directions, indicating increased upper airway resistance
and upper airway obstruction

80.  Cheyne-Stokes breathing
is a type of periodic breathing characterized by cyclical
changes in breathing with a crescendo-decrescendo
sequence separated by central apneas or hypopneas
 Dysrhythmic breathing is
Nonrhythmical respiration of irregular rate, rhythm, and
amplitude that becomes worse during sleep
 Apneustic breathing is
prolonged inspiration with an increase in the ratio of
inspiratory to expiratory time
Lesion -caudal pons disconnecting the apneustic center in
the lower pons from the pneumotaxic center in the upper
pons

81.  Inspiratory gasp is characterized by
short inspiratory time and a relatively prolonged expiration and
has been noted in association with a lesion in the medulla
 Ataxic breathing is characterized by
clusters of cyclic breathing followed by recurrent periods of apnea
(the apnea length is greater than the ventilatory phase). Lesion-
medulla
 Biot breathing
is a variant of ataxic breathing characterized by two to three
breaths of nearly equal volume separated by long periods of
apnea

84.  hypertension, heart
failure, myocardial
infarction,
 cardiac arrhythmias,
stroke due to both
supratentorial
 and infratentorial
infarctions, and transient
ischemic attacks
 as well as cognitive
dysfunction, depression,
and insomnia

85. Upper Airway Resistance
Syndrome
 Guilleminault and colleagues in 1993
 Nasal pressure monitoring with a nasal
cannula is more sensitive
 Intraesophageal balloon recording, however,
is the standard method
 CPAP titration is widely used as the first line
of therapy

86. Central Sleep Apnea Syndrome
 primary CSA,
 CSA with Cheyne-Stokes breathing,
 CSA due to high altitude periodic breathing,
 CSA due to a medical disorder without Cheyne-
Stokes breathing,
 CSA due to drug or substance abuse (e.g., use of
opiates) ,
 Primary CSA of infancy,
 primary CSA of prematurity, and
 Treatment emergent CSA

88. Restless Legs Syndrome

90.  RLS is a lifelong sensory-motor neurological disorder
 often begins at a very young
 autosomal dominant
 Pathophysiology
 Iron is a necessary cofactor for tyrosine hydroxylase, the
rate-limiting enzyme in dopamine synthesis, and iron
deficiency may decrease the number of dopamine D2
receptor binding sites, so the most exciting and current
research focus is centered on iron-dopamine dysfunction.
 CSF analysis, special MRI, and neuropathological studies
demonstrate reduction in CNS iron or ferritin or both

92. Periodic Limb Movements in
Sleep

93. Rhythmic Movement Disorder
 before age 18 months
 benign condition
 It is a sleep-wake transition disorder with
three characteristic movements:
 head banging,
 head rolling,
 body rocking.

94. Sleep-Related Leg Cramps
 intensely painful sensations accompanied by
muscle tightness that occur during sleep
 spasms usually last for a few seconds but
sometimes persist for several minutes

95. Bruxism (Tooth Grinding)
 between age 10 and 20
 stereotypical tooth grinding and is often
precipitated by anxiety, stress, and dental disease.
 associated with various movement and
degenerative disorders such as oromandibular
dystonia and Huntington disease
 Nocturnal bruxism is noted most prominently
during stages N1 and N2 sleep and REM sleep

96. Benign Sleep Myoclonus of
Infancy
 first few weeks of life
 seen in NREM sleep but sometimes during
REM sleep
 Episodes often occur in clusters
 jerky flexion, extension, abduction, and
adduction
 benign,
 No treatment required

97. Propriospinal Myoclonus at Sleep
Onset
 occurs between wakefulness and the moment
of sleep onset (predormitum)
 transient sudden muscle jerks predominantly
involving the axial muscles
 special type of spinal myoclonus originating
from a myoclonic generator in the midthoracic
region with propagation up and down the
spinal cord at a very slow speed (3 to 16
m/sec)

99. Circadian Rhythm Sleep
Disorders
 result from a mismatch between the body’s
internal clock and the geophysical
environment

100. Jet Lag
 The experience of jet lag follows eastward or
westward jet travel that crosses several time
zones, disrupting synchronization between the
body’s inner clock and external cues;
 north-south travel does not evoke this disorder
 difficulty maintaining sleep, frequent arousals, and
EDS, typically resolving within a few days to 2
weeks.

101. Shift-Work Sleep Disorder
 may affect up to 5 million workers in the
United States
 Features
 sleep disruption,
 fatigue,
 gastrointestinal symptoms, increasing chances
of
 being involved in traffic accidents,
 and making errors on the job

102. Delayed Sleep Phase State
 patient’s major sleep episode is delayed in relation to
desired clock time, causing sleep-onset insomnia or
difficulty awakening at the desired time
 A typical schedule consists of going to sleep late
between 2:00AM and 6:00AM, and waking up during the
late morning between 10:00AM and 2:00PM.
 Familial ASPS has been ascribed to mutation in the
HPER2 gene

103. Advanced Sleep Phase State
 Patients go to sleep early in the evening and wake
up early in the morning.
 The patient experiences sleep disruption and
daytime sleepiness when not going to sleep at
early hours.
 The condition is often seen in patients with
depression and in normal elderly individuals.
 Familial ASPS has been ascribed to mutation in
the HPER2 gene

104. Free-Running Circadian Rhythm
Disorder
 Characterized by a patient’s inability to
maintain a regular bedtime sleep onset that
occurs at irregular hours (ICSD-III)
 The patient displays increasing delay of sleep
onset by approximately 1 hour during each
24-hour sleep-wake cycle, causing an
eventual progression of sleep onset through
the daytime hours into the evening.
 Blind people

105. Irregular Sleep/Wake Circadian
Rhythm Disorder
 Irregular Sleep/Wake Circadian Rhythm
Disorder
 napping throughout the 24-hour period, but
total sleep time is normal
 degenerative neurological disorders such as
dementia and children with mental retardation

106. Neurological Disorders and
Sleep Disturbance
 Sleep and Epilepsy
 Degenerative Dementia and Sleep Dysfunction
 Sleep Disorders Associated with Neuromuscular
Disorders
 Sleep and Spinal Cord Diseases
 Sleep and Headache Syndromes
 Stroke and Sleep/Wake Disturbance
 Sleep and Multiple Sclerosis
 Sleep Disorders in Autonomic Failure: Multisystem
Atrophy (Shy-Drager Syndrome)

107. Sleep and Epilepsy
 Sleep increases interictal epileptiform discharges,
causing repeated arousals and sleep fragmentation
resulting in EDS, which again triggers seizures and
epileptiform discharges, thus repeating the cycle.
 Most of the time, seizures are triggered during stages N1
and N2 sleep; occasionally, however, they are triggered
during slow wave sleep.
 In epileptic patients, NREM sleep acts as a convulsant,
causing excessive synchronization and activation of
seizures in an already hyperexcitable cortex.
Nocturnal
Diurnal
Diffuse epilepsy

109. Effect of Sleep on Epilepsy
 Lennox-Gastaut syndrome:
 more frequent during NREM sleep than during wakefulness, and
are never seen during REM sleep
 EEG-trains of fast spikes intermixed with slow spike-and-wave
discharges at 2 to 2.5 Hz
 Benign focal epilepsy of childhood with rolandic spikes:
 focal clonic facial twitchings, often preceded by perioral
numbness, seen most frequently during drowsiness and sleep.
 The EEG shows centrotemporal or rolandic spikes or sharp
waves.
 These discharges are present throughout the night in all stages
of sleep

110.  Continuous spike-and-wave
 generalized continuous slow spike-and-wave discharges
 seen during at least 85% of NREM sleep and suppressed
during REM sleep
 Juvenile myoclonic epilepsy
 massive bilaterally synchronous myoclonic jerks which are
most frequently noted on awakening.
 It commonly occurs in young adults aged 13 to 19 years.
 A typical EEG shows synchronous and symmetrical multiple
spikes and spike-and-wave discharges

111.  Nocturnal frontal lobe epilepsy
 Includes nocturnal paroxysmal dystonia, paroxysmal
arousals and awakenings, episodic nocturnal wanderings,
and autosomal dominant nocturnal frontal lobe epilepsy

112. Degenerative Dementia and
Sleep Dysfunction

113. Fatal familial insomnia
 rare and rapidly progressive autosomal dominant prion disease
 missense mutation at codon 178 of the prion protein gene (PrP)
 Clinical manifestion :
 impaired control of the sleep/wake cycle, including circadian rhythms;
 autonomic and neuroendocrine dysfunction;
 somatic neurological, cognitive, and behavioral manifestations
 PSG
 almost total absence of sleep pattern and only short
 episodes of REM sleep, lasting for a few seconds or minutes,
 without muscle atonia.
 This abnormal sleep pattern is associated with dream-enacting behavior in the form of
complex gestures and motions and myoclonus. The terminal stage of
 the illness is characterized by progressive slowing on the EEG,
 with the patient drifting into coma.
 neuropathological hallmark of FFI is severe atrophy of the thalamus,

114. Sleep Disorders Associated with
Neuromuscular Disorders
 transient nocturnal hypoxemia and
hypoventilation- repeated arousals and sleep
fragmentation

115. Sleep and Spinal Cord Diseases
 Poliomyelitis and Postpolio Syndrome:
 Respiratory disturbances, sleep-related apnea or
hypoventilationnz
 Amyotrophic Lateral Sclerosis
 repeated arousals and sleep fragmentation due to nocturnal
hypoventilation, recurrent episodes of sleep apnea,
hypopnea, hypoxemia, and hypercapnia

116. Sleep and Headache Syndromes
 cluster headaches show a strong relationship
between REM sleep and attacks of headache
 Migraine headaches may occur during the day
and both slow-wave and REM sleep.
 Chronic paroxysmal hemicrania, which is probably
a variant of cluster headache, is most commonly
associated with REM sleep.
 Hypnic headache tends to occur during REM
sleep but also has been reported to occur in
Stage N3

117. Stroke and Sleep/Wake
Disturbance
 Sleep apnea, snoring, and stroke are
intimately related; sleep apnea may
predispose to stroke, and stroke may
predispose to sleep apnea.

118. Sleep and Multiple Sclerosis