Maria Leticia C.

Araullo, MD, FPNA

NEUROLOGICAL ASPECTS OF
SLEEP
Sleep Basics

 Sleep: a reversible physiological state of

decreased perception of and responsiveness
to external stimuli
 Function of Sleep (proposed theories)
1) Body repair
2) Brain restoration
3) Thermoregulation and energy conservation
4) Maintenance of immunocompetence
5) Memory consolidation and learning
Sleep basics
 Effects of age
 Duration of sleep  Pattern of sleep
 Newborn – 16-12 hours  Circadian rhythm appears
 Child – 10-12 hours after first few weeks post
partum
 10 years old – 9-10 hours  By the 4th-5th year, sleep is
 Adolescent – 7-7.5 hours consolidated into a single
 Adult – 6.5 hours nocturnal period
 Fragmentation of sleep
pattern begins in adult life
 Night awakenings tend to
increase in frequency;
daytime period tends to be
interrupted by episodic
sleep and longer naps
Sleep physiology

 Sleep-wakefulness control mechanisms are

exerted by specific neuronal groups of brainstem
ARAS
 Pedunculopontine nucleus (cholinergic)
 Laterodorsal tegmental nuclei (cholinergic)
 Locus ceruleus (noradrenergic)
 Raphe nuclei (serotonorgic)
 ARAS project to intralaminar thalamic nuclei,
posterior hypothalamus, basal forebrain
Sleep physiology

 Additional neurotransmitters involved in sleep-wake

regulation
 Histamine (tuberomamillary nucleus): promotes arousal
and wakefulness
 Dopamine (ventral tegmental area): promotes wakefulness
 Hypocretin (dorsolateral hypothalamus): promotes arousal
 Other sleep-promoting neurochemicals: GABA
(ventrolateral preoptic area), galanin, adenosine,
cytokines, prostagalndin D2, delta sleep-inducing peptide,
muramyl peptides, growth hormone-releasing factor,
cortistatin, opioid peptides
Sleep Physiology
EEG
Awake Posterior dominant 8-13 Hz alpha rhythm
Stage I Disappearance of alpha rhythm, occasional vertex waves and
positive occipital sharp transients (POSTs)
Stage II Sleep spindles, K complexes, vertex waves, POSTs
Stage III <2 Hz during 20-50% of each epoch; occasional sleep spindles,
K complexes, and vertex waves
Stage IV <2Hz during >50% of each epoch
REM Low amplitude (similar to waking) predominantly 4-13 Hz
activity; sawtooth (notched) theta waves over the central
head region
 Eye movements EMG Additional Features
Awake Rapid, saccadic tonic
Stage I Slow-roving lateral, may tonic 5% of nocturnal sleep
be present before loss of Low arousal threshold
alpha rhythm Sleep is not always perceived
Stage II None tonic 45-55% of nocturnal sleep;
increased arousal threshold
Stage III None tonic 3-8% of nocturnal sleep
 cerebral metabolic rate
High arousal threshold
Stage IV None Tonic 10-15% of nocturnal sleep
 cerebral metabolic rate
High arousal threshold
REM Rapid, abrupt, high Phasic, 20-25% of nocturnal sleep
amplitude, conjugate eye hypotonic, Mainly second half of night
movements or atonic High level of cerebral
(except metabolism
diaphragm Dreaming most prominent
and EOM) Penile tumescence
Irregular respiratory and heart
rate
Sleep physiology
 Normal sleep
 4-6 cycles of NREM followed by REM
 Cycle duration: 90 min
 NREM consists of stages I-IV
 NREM gets progressively deeper and
arousal threshold increased from stage I to
IV
 Stage I is typically followed sequentially by
stages II, III, and IV and again stage II
before REM
 Throughout the night:
 SWS periods shorten
 REM sleep periods lengthen
 Most NREM sleep occurs during the first
half and REM sleep in the second half of
the night
Sleep Physiology

 Structures needed for NREM sleep

 Basal forebrain
 Anterior hypothalamus-preoptic region
 Midline brainstem
 Dorsolateral medullary reticular formation
 Structures needed for REM sleep
 Dorsolateral pons
Circadian rhythms
 Biological rhythms that repeat q24 hours
 Suprachiasmatic nucleus in the ventral anterior
hypothalamus ( circadian pacemaker) projects to areas
of the brain involved in sleep-wake regulation: basal
forebrain, thalamus, hypothalamus, pineal gland
 Regulating factors
 Circadian clock genes determine internal circadian
rhythmicity
 Light is the most effective stimulus for the internal clock
via the retinohypothalamic tract
 Other stimuli: food, exercise, activity, hormones, social
cues
Approach to Diagnosis

 History
 Complaints of
 “I cannot get enough sleep”
 “I’m sleepy during the day” or “I fall asleep all the
time”
 “There is some unusual sleep behavior”
 An observer should be encouraged to attend the
initial interview
Approach to Diagnosis

 Questions to ask:  Activities other than those

 sleep habits pertaining to sleep or sex that
 usual hours of sleep take place while in bed (eating,
writing)
 sleep problems
 Occurrence or history of
 current medications various abnormal sleep
 other medical problems behaviors (enuresis, sleep
 Weight gain walking)
 Occurrence of other relevant
 Alcohol intake
symptoms (sleep paralysis,
 Conditions under which cataplexy, hypnagogic
sleep occur hallucinations, early morning
 Dietary stimulants headache, loud snoring,
difficulty breathing at night)
Approach to Diagnosis

 Physical exam:
 Weight
 Vital signs
 Neurological examination
 Auscultaion of the heart
 Inspection of nasal and oral airways
 Presence of redundant tissue, tonsillar
hypertrophy, micrognathia, malocclusion,
erythema of soft palate and posterior pharynx
Approach to Diagnosis

 Laboratory exam
 Plasma electrolytes
 Renal and hepatic function
 Complete blood count
 Endocrine function
 Thyroid function texts should be obtained in all
patients with sleep apnea
 Rheumatological disease
 Infectious disease
Approach to Diagnosis

 Sleep laboratory testing

 Polysomnography
 evaluates sleep characteristics and disorders
 Incorporates EEG, surface EMG, and respiratory parameters
 Multiple sleep latency testing
 Performed after PSG to detect mean sleep latency and sleep onset
REM periods during 4-5 daytime nap opportunities at 2 hour
intervals
 Maintenance of wakefulness testing
 4 nap studies at 2 hour intervals lasting 20 minutes, terminated
with sleep onset
 Actigraphy
 Estimates a person’s circadian rhythm
 Diagnosis and Classification
 Dyssomnias
 disorders which cause either excessive sleepiness or an
inability to initiate or maintain sleep
 narcolepsy, OSA, restless legs syndrome,
psychophysiological insomnia

 Parasomanias
 disorders intruding into the sleep process that appear to
be related to difficulties with partial arousal
 Sleepwalking, sleep terrors, REM sleep behavior disorder,
sleep paralysis
Diagnosis and Classification

 Medical/Psychiatric Sleep Disorders

 Associated with mental disorders, associated with
neurological disorders (parkinsonism, sleep related
epilepsy) or with other medical disorders (sleep
related asthma, sleep related gastroesophageal reflux)

 Proposed Sleep Disorders

 Sleep related laryngospasm, short sleeper, long
sleeper
SLEEP DISORDERS

 Sleep-related breathing disorders

 Hypersomnias of central origin
 Insomnia
 Sleep related movement disorder
 Circadian rhythm disorder
 Parasomnias
 Sleep disorders associated with neurological
conditions
Sleep-related breathing disorders

 Sleep apnea syndromes

 Obstructive Sleep apnea
 Recurrent partial or complete upper airway
obstruction resulting in decreased (hypopnea) or
absent (apnea) airflow in setting of increased
respiratory effort
 Ass’d w/ desaturation, repeated arousals, sleep
fragmentation
 Risk factors: Obesity, narrow upper airway,
retrognathia, macroglossia, enlarged tonsils,
craniofacial malformations
Sleep-related breathing disorders

 Obstructive sleep apnea

 Associated features: hypertension, arrhythmias,
cardiovascular disease, CHF, possible stroke, type II
DM
 Treatment: weight loss, avoidance of alcohol &
sedatives, CPAP, surgery
Sleep-related breathing disorders

 Central sleep apnea

 Primary
 recurrent episodes of diminished airflow without upper airway
obstruction
 Absence of respiratory effort during apnea/hypopnea
 Etiology is unknown
 Pathophysiology:
 heightened ventilatory response to CO2 leads to instability of respiratory
control during wake-sleep transition and may persist into NREM sleep;
typically ceases in REM
 CO2 levels tend to be lower, thus a small increase in ventilation leads to
apnea
 May be seen in neurologic disorders with associated ANS dysfunction
(MSA, Parkinson)
 Treatment: oxygen, positive airway pressure therapy
Sleep-related breathing disorders

 Mixed apnea
 initial cessation of both airflow and effort (central
apnea), followed several seconds later by the
appearance of effort without airflow (obstructive
apnea)
Sleep-related breathing disorders

 Other disorders
1) Cheyne Stokes respiration
2) High altitude periodic breathing
3) CSA due to drug/substance (opioids)
4) Sleep related hypoventilation/hypoxemic syndromes
 Sleep related non obstructive alveolar hypoventilation
 Congenital central alveolar hypoventilation
 Secondary forms ass’d with morbid obesity,
neuromuscular disorders, chest wall restriction, high spinal
cord or brainstem lesions, lower airway obstruction,
pulmonary parenchymal or vascular idiopathic disorders
Disorders of excessive sleepiness

 Medications  Encephalitic desases:

 Acute medical illness of the following viral encephalitis,
mononucleosis type trypanosomiasis,
encephalitis lethargica
 Post surgical and
 Lesions of the hypothalamus
postantesthetic states
– Kleine Levin syndrome,
 Chronic neurologic
hypothalamic tumor or
diseases: MS, dementia granuloma
 Depression  Sleep apnea syndromes
 Metabolic derangements:  Narcolepsy-cataplexy
hypothyroidism, Addison
 Idopathic hypersomnia
disease
Hypersomnias of central origin

 Narcolepsy
 Gradual onset between 15-35
 Classic tetrad:
 excessive daytime sleepiness usually 1 st symptom
 Cataplexy most specific symptom
 hypnogogic/hypnopompic hallucinations
 sleep paralysis
 Proposed 5th symptoms: disturbed nocturnal sleep
 Proposed disease mechanism: destruction of
hypocretin secreting cells in posterolateral thalamus
Hypersomnias of central origin

 Narcolepsy
 Symptomatic narcolepsy – occurs with HPA
abnormalities: tumors, vascular malformations,
sarcoidosis, head injury, after cranial irradiation
 Treatment:
 Regular sleep wake schedule
 Scheduled naps
 Avoidance of sleep deprivation
 Avoid sedentary work environment
 Stimulants, modafinil to improve alertness
 TCA/SSRI for cataplexy, sleep paralysis (suppress REM
sleep)
Hypersomnias of central origin

 Idiopathic hypersomnia
 Severe excessive daytime sleepiness w/ or without
long nocturnal sleep episodes without evidence of
cataplexy lasting more than 6 months with not
other causes of sleepiness by history or PSG
 Naps typically not refreshing
 Onset in adolescence, early adulthood
 Pathophysiology unknown
Hypersomnias of central origin

 Recurrent hypersomnia (Kline Levin Syndrome)

 Recurrent episodes of hypersomolence with transient
cognitive, mood, or behavioral disturbance ;
hyperphagia; hypersexuality
 Each episode lasts 1-2 weeks, followed by return to
normal cognitive and psychosocial function for several
weeks or months
 Usually affects teenage boys
 Pathophysiology: unclear; likely involves
hypothalamic dysfunction, autoimmune
 No proven therapy; lithium may prevent recurrence
Insomnia

 Chronic inability to sleep despite adequate

opportunity to do so
 Used popularly to indicate any impairment in
the duration, depth or restorative properties
of sleep
 Divided in 3 categories
 Sleep onset insomnia
 Sleep maintenance insomnia
 Early morning awakening without return to sleep
Insomnia

 Insomniacs tend to underestimate actual time they

spend asleep
 In addition to difficulty initiating/maintaining sleep:
 Nonrestorative sleep, light sleep, short sleep
 Impaired cognition, attention, mood, daytime functioning
 Fatigue and reduced motivation
 Excessive daytime sleepiness
 Social dysfunction
 Headaches, GI distress, anxiety over sleep loss
 Ass’d features: often influenced by environmental factors
and/or psychological disturbance esp stress, anxiety,
depression, drug dependence, or other mental illness
Insomnia
 Primary insomnias (states of hyperarousal)
 Idiopathic
 with onset in early childhood
 lifelong condition
 Pathophysiology: abnormal sleep-wake regulation,
organic hyperarousal state

 Paradoxical insomnia (sleep-state misperception)

 Subjective complaint of insomnia in which patient
misperceives the amount of time spent asleep
 No PSG evidence of sleep disturbance; objectively
normal sleep duration
Insomnia

 Pyschophysiologic
 Patient does not associate bedroom/bedtime with sleep usually as a
learned behavior that prevent sleep from occurring. Frustration and
anxiety develop from inability to sleep leading to states of increased
arousal and tension that prevent sleep, thereby perpetuating the
insomnia
 Can develop from transient or chr0nic insomnia of any cause
 Patient usually sleep better in a different environment than their
own bedroom
 Treatment:
 sleep hygiene
 behavioral therapy – relaxation therapy, sleep restriction, stimulus
control therapy
 hypnotics
Insomnia

 Behavioral insomnia - due to learned behaviors or

voluntary actions inconsistent with sleep
 Sleep onset association disorder
 Child falls asleep only under certain conditions – rocking chair, in
parents’ bed
 Limit setting sleep disorder
 Child refuses to go to bed when asked to
 Inadequate sleep hygiene
 Caffeine intake, exercise, TV in bed, frequent daytime naps
INSOMNIA

 Secondary insomnia
 Environmental factors
 Psychological factors
 Abnormal shift schedule
 Circadian rhythm disorders
 Medications
 Medical conditions
 Psychiatric disorders
 Primary neurologic diseases: fatal familial insomnia,
Morvan’s fibrillary chorea
INSOMNIA
 Fatal Familial insomnia
 Begins with difficulty initiating sleep and leads to severe complete
insomnia within months
 Progression to coma/death within 2 years
 Other symptoms: ataxia, tremor, myoclonus, dystonic posturing,
pyramidal signs, cognitive changes, sympathetic nervous system
hyperactivity, episodic stupor
 Epidemiology:
 prion disease
 Autosomal dominant
 Onset 5th-6th decade
 PSG: no SWS, decreased stage II NREM sleep, dissociated REM sleep
without muscle atonia
 Autopsy: anterior and dorsomedial thalamic nuclei atrophy with
neuronal loss and reactive gliosis
 Treatment: barbiturates, benzodizepines may induce EEG sleep pattern
INSOMNIA
 Morvan’s fibrillary chorea
 Severe insomnia, fluctuating encephalopathy, peripheral nerve
hyperexcitability, weakness, cramping, neuromyotonia,
dysautonomia
 Pathophysiology: unknown, possible autoimmune mechanism or
paraneoplastic phenomenon (ass’d w/ myasthenia, malignancy;
positive antibodies to voltage gated potassium channels_
 PSG: no NREM sleep features (K complexes, spindle waves, delta
waves)’ “subwakefulness” state characterized by EEG theta activity
associated with behavioral sleep, brief REM sleep periods without
atonia
 EMG: spontaneous repetitive discharge (doublets, triplets,
multiplets, myokymia)
 Labs: increased plasma norepinephrine level
 Treatment:
 plasma exchange, immunemodulating agents, thymectomy
 opioids
INSOMNIA

 Treatment of insomnia
 Depends on underlying cause
 Cognitive behavioral therapy, relaxation
techniques, stimulus control, sleep restriction
 Good sleep hygiene
 Short term pharmacologic therapy with hypnotics
 reassurance
Rules of sleep hygiene for
patients
 Sleep only as long as needed to feel refreshed the next
day. Avoid excessively long times in bed
 Maintain a regular arousal time in the morning in order
to establish a constant circadian sleep pattern
 Maintain a steady daily amount of exercise
 Eliminate noise in the bedroom environment
 Keep the bedroom temperature comfortable. Avoid a
sleeping environment that is too warm
 Use the bedroom for sleep only. Do not perform other
activities in the bed, such as writing letters or eating
Rules of sleep hygiene for
patients
 Do not go to bed hungry
 Avoid the frequent use of sleeping pills
 Avoid caffeine in the evening, even if you think it does
not disturb sleep
 Do not use alcohol as a sedative. It facilitates the onset of
sleep but later acts as a stimulant
 Avoid the frequent use of tobacco
 If you feel upset because you cannot sleep, get up, turn
on the light and do something else
Sleep Related Movement Disorder

 Restless Legs Syndrome

 Complaints of unusual and severe leg sensations; relief
gained by walking, rubbing legs, applying heat; most
prominent in evening and nightime, resulting in sleep
onset and sleep maintenance insomnia
 Hallmark is the irresistible urge to move the legs to
relieve discomfort
 Arms may be involved
 Pathophysiology: cerebral iron and dopamine
pathways have been implicated
Sleep Related Movement Disorder
 Primary restless leg syndrome
 Positive family history of similar symptoms, including adolescent
“growing pains”
 Autosomal dominant inheritance
 Onset: childhood, adolescence
 Secondary restless leg syndrome
 Ass’d w/ pregnancy, peripheral neuropathy, chronic renal failure,
iron deficiency anemia, latent iron deficiency, folate deficiency
 Linked to several medications: antidepressants, neuroleptics,
dopamine agonists, sedating antihistamines
 Treatment: dopaminergic agonists, gabapentin,
benzodiazepines, low potency opioids, iron replacement
therapy if serum ferritin <50g/L
Sleep Related Movement Disorder
 Periodic Leg Movement Disorder
 Repetitive stereotyped movements that cause
repeated arousals from sleep, each resembling a
Babinski reflex response usually during NREM sleep
 Clinical significance is debated
 Often seen with restless leg syndrome, RBD,
narcolepsy
 Pathophysiology
 Decreased brain iron and dopaminergic pathways have been
implicated
 Low serum ferritin level
 Treatment: dopamine agonists
Sleep Related Movement Disorder

 Rhythmic movement disorder

 Stereotyped, repetitive, rhythmic movements of body
parts, usually of head, neck, trunk that occur before sleep
onset and persist into light sleep or occur only during sleep
 Movements include head banging, head rolling, body
rocking
 Considered a disorder only if it interferes with sleep,
results in daytime sleepiness, or leads to injury
 Seen mostly in infants and young children, also mentally
handicapped children; typically resolves by 2-3 years but
may persist into adulthood
 Treatment: benzodiazepines, antidepressants if necessary
Sleep Related Movement Disorder

 Bruxism
 Stereotyped,intermittent rhythmic al teeth
grinding and clenching during any sleep stage
 May have sore jaw muscles in the morning,
headache, facial pain, abnormal dental wear
 Pathophysiology: unknown, may be worsened by
stress
 Treatment: dental appliance, relaxation
technique, stress management
Circadian rhythm disorders

 Persistent inability to sleep at desired or

expected time and/or excessive sleepiness
during the wake period as defined by
environmental/societal factors
 Types
 Delayed sleep phase disorder
 Advanced sleep phase disorder
 Circadian rhythm sleep disorder, nonentrained
type
Circadian rhythm disorders
 Delayed sleep phase disorder
 Delayed sleep onset and wake times in relation to societal norms
 When allowed to sleep at own schedule, total sleep duration and alertness during
the wake period are normal
 Most common in adolescents and young adults in whom a delayed sleep phase
tendency is physiologic
 Genetic predisposition, familial occurrence
 Pathophysiology:
 delayed circadian rhythm including body temperature and melatonin secretion
 Bright light exposure in evening delays internal circadian rhythm
 Caffeine and other stimulant use in the day
 Treatment
 Chronotherapy
 Light therapy (early morning bright light)
 Melatonin 1-3 hours before bedtime
 Strict adherence to sleep wake schedule
Circadian rhythm disorders

 Advanced sleep phase disorder

 Sleep onset and wake times are several hours earlier
than societal norms
 Sleep duration is normal per 24 hours and sleep
schedule is normal but advanced
 More common in elderly
 Genetic predisposition, familial occurrence
 Chronic course
 Treatment:
 Light therapy in early evening
 Can try melatonin in morning
Circadian rhythm disorders

 Circadian rhythm sleep disorder, nonentrained type

 Circadian rhythm either lacks chronization with 24 hour
environmental rhythms or is free running at a non-24 hour
rhythm (typically >24 hours)
 Observed most often in visually impaired patients, mental
retardation
 Occasionally due to behavioral patterns, environmental
factors in sighted people
 Pathophysiology: lack of light stimulus to the
suprachiasmatic nucleus in blind persons leading to lack of
entrainment of circadian rhythm to environmental rhythm
 Treatment: melatonin before bedtime, light therapy
Circadian rhythm disorders

 Irregular sleep-wake rhythm

 Sleep is fragmented into several naps throughout the
24 hour period ; total 24 hour sleep duration is normal
 Occurs mostly in patients with cerebral dysfunction or
those who choose an inconsistent sleep-wake
schedule but are capable of entrainment
 Pathophysiology: abnormal circadian clock function
 Treatment: light therapy, melatonin, strict adherence
to schedules
Circadian rhythm disorders

 Others
 Jet lag syndrome
 Eastward travel requires a phase advance
 Westward travel requires a phase delay of circadian rhythms
 On average, one day per time zone is required to adjust to local
time
 Shift work sleep disorder
 Insomnia in the setting of a work schedule that requires late
night, early morning, or rotating shifts
 Reduced 24 hour sleep time, sleep may be fragment, duration of
symptoms for at least a month
 Due to general medical condition – blindness,
encephalopathies, dementias
Parasomnias

 NREM parasomnias
 Abnormal behavior occur with sudden partial arousal from NREM
sleep, usually SWS, typically in the first 1/3 of the night
 Patients are not responsive to external stimuli and appear
confused when awakened; often no recall in AM
 Triggered by sleep deprivation, stress, environmental (loud
noises), medical conditions leading to increased arousals, CNS
depressant medications which prevent arousal from sleep and
increase SWS/arousal threshold (hypnotics, alcohol)
 Types
 Sleep walking
 Sleep terrors
 Confusional arousals
Parasomnias

 Sleepwalking (somnambulism)
 Walking and other complex behavior occurring in stage III or IV
 Behaviors often inappropriate (urinating in a closet, moving
objects randomly)
 May become violent when attempting to awaken
 Most common in children
 Treatment
 Reassurance
 Secure sleeping environment
 Eliminate precipitants
 Benzodiazepines or tricyclic antidepressants can be prescribed
 Hypnosis, psychotherapy, relaxation techniques, stress management
strategies
Parasomnias

 Sleep terrors (night terrors or parvor nocturnus)

 Sudden partial arousal from slow-wave sleep
 subsequent attack heralded by a piercing scream or cry with behavioral
and autonomic manifestations of intense fear
 Unlike nightmares, these tend to occur during the first 1/3 of the night
when slow wave sleep predominates; no recollection of dream content
 Benign condition
 More common in children
 Treatment
 Reassurance
 Avoidance of precipitants
 Behavioral therapy – scheduled awakenings
 Benzodiazepines, antidepressants if severe
Parasomnias

 Confusional arousals
 Least dramatic form of arousal disorder
 Patient awakens temporarily and shows confusion,
disorientation; poor response to external stimuli
 No associated prominent vocalization, motor activity,
or fear
 No memory of the event
 No treatment required
Parasomnias

 REM Sleep Parasomnias

 REM Sleep Behavior Disorder
 Loss of atonia during REM sleep, with elaborate motor activity and dream
mentation
 Mostly in men in 6th to 7th decade
 Distinctly unpleasant dreams of intruders or attackers and are recalled
immediately after the event
 Frequent injury to self or partner
 Chronic form usually associated with neurologic disorders, especially
neurodegenerative disorders associated with  synuclein – positive
intracellular inclusions (Parkinson’s, Lewy body, MSA)
 Pathophysiology: unclear, possibly lesions in the pontomedullary pathways
promoting REM sleep atonia in combination with increased activity in
locomotor generators
 Treatment: bedroom safety, clonazepam, melatonin
Parasomnias

 Nightmares
 Frightening dreams resulting in awakening
 No prominent vocalization, motor activity
 Usually, full alertness and dream recall
immediately after awakening
 More frequent in children and patients with
psychiatric disorders (substance abuse, PTSD)
 Treatment
 Treat underlying disorder
 Psychotherapy, hypnosis, behavioral therapy
Parasomnias

 Sleep paralysis
 Partial or complete muscle paralysis at sleep
onset or awakening with preserved consciousness
 Spared muscles: extraocular muscles, diaphragm
 May be accompanied by hallucinations
 Attacks can be aborted by sensory stimuli (calling
or touching the patient)
Sleep disorders associated
with Neurologic Conditions
 Parkinsonism
 At risk for disrupted sleep due to the following
 Degeneration of neural systems that regulate sleep, resulting in
sleep fragmentation and reduced REM and slow wave sleep
 Bradykinesia and rigidity and a reduction in the normal number
of body shifts during sleep
 Periodic lg movmenets, termors, or medication induced
movement disorders
 Abnormal muscle tone which facilitates breathing abnormalities
 Disorders of circadian rhythm and sleep-wakefulness schedule
 Treat underlying disorder
Sleep disorders associated
with Neurologic Conditions
 Multiple system atrophy
 Nocturnal stridor from vocal cord
dystonia/paralysis, paradoxical vocal cord
adduction with inspiration
 May cause sudden death in sleep
 Treatment: tracheostomy, nasal CPAP
Sleep disorders associated
with Neurologic Conditions
 Alzheimer’s disease
 Cognitive decline is paralleled by a decline in slow wave
sleep and REM sleep and an increase in the number of
nocturnal awakenings and amount of time spent
awake during normal sleep time (due to degeneration
of brainstem and basal forebrain pathways)
 “sundowning” – evening attacks of delirium in which
patients experiences emotional and perceptual
disturbances with irrational thinking, disorganized
speech, and agitation (from suprachiasmatic nucleus
degeneration?)
Sleep disorders associated
with Neurologic Conditions
 Epilepsy
 Convulsive seizures often occur in sleep
 Mainly in stage III and IV of NREM
 Epileptiform discharges are suppressed in REM sleep and
become more focal
 Certain seizure types are more closely related to sleep
 Frontal lobe epilepsy
 Temporal lobe epilepsy
 Juvenile myoclonic epilepsy
 Benign childhood epilepsy with centrotemporal spikes
 Epilepsy with generalized tonic clonic seizures on awakening
Sleep disorders associated
with Neurologic Conditions
 Effects of nocturnal seizures on sleep
 Increased nocturnal awakening and sleep fragmentation
 Increased percentage of lighter sleep stages
 Decreased REM sleep
 May cause excessive daytime sleepiness
 Effect of sleep on seizures: deprivation
 Lowers seizure threshold
 Increases frequency of interictal discharge
 Used to enhance detection of epileptiform discharges on EEG

 Anticonvulsants tend to consolidate sleep, may cause

excessive daytime sleepiness
SLEEP DISORDERS

 Sleep-related breathing disorders

 Hypersomnias of central origin
 Insomnia
 Sleep related movement disorder
 Circadian rhythm disorder
 Parasomnias
 Sleep disorders associated with neurological
conditions