Neurological Aspects of Sleep

8/7/2019 Neurological Aspects of Sleep

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NEUROLOGICAL ASPECTS OF

SLEEP

Maria Leticia C. Araullo, MD, FPNA


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Sleep Basics

Sleep: a reversible physiological state of

decreased perception of and responsiveness

to external stimuli Function ofSleep (proposed theories)

1) Body repair

2) Brain restoration

3) Thermoregulation and energy conservation

4) Maintenance of immunocompetence

5) Memory consolidation and learning


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Sleep basics

Effects of age Duration of sleep

Newborn 16-12 hours

Child 10-12 hours

10 years old 9-10 hours Adolescent 7-7.5 hours

Adult 6.5 hours

Pattern of sleep Circadian rhythm appears

after first few weeks postpartum

By the 4th-5th year, sleep isconsolidated into a singlenocturnal period

Fragmentation of sleeppattern begins in adult life

Night awakenings tend toincrease in frequency;daytime period tends to beinterrupted by episodicsleep and longer naps


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Sleep physiology

Sleep-wakefulness control mechanisms areexerted 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


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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-inducingpeptide, muramyl peptides, growth hormone-releasing factor, cortistatin, opioid peptides

Sleep physiology


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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 (POS

Ts)Stage II Sleep spindles, K complexes, vertex waves, POSTs

Stage III


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Eye movements EMG Additional Features

Awake Rapid, saccadic tonic

Stage I Slow-roving lateral, may

be present before loss ofalpha rhythm

tonic 5% of nocturnal sleep

Low arousal thresholdSleep 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

q cerebral metabolic rateHigh arousal threshold

Stage IV None Tonic 10-15% of nocturnal sleep

q cerebral metabolic rateHigh arousal threshold

REM Rapid, abrupt, high

amplitude, conjugate eyemovements

Phasic,

hypotonic,or atonic(except

diaphragmand EOM)

20-25% of nocturnal sleep

Mainly second half of nightHigh level of cerebralmetabolism

Dreaming most prominentPenile tumescence

Irregular respiratory and heart

rate


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Normal sleep

4-6 cycles of NREM followed by REM

Cycle duration: 90 min

NREM consists of stages I-IV

NREM gets progressively deeper andarousal threshold increased from stage I to

IV

Stage I is typically followed sequentially by

stages II, III, and IV and again stage IIbefore REM

Throughout the night:

SWSperiods shorten

REM sleep periods lengthen

Most NREM sleep occurs during the firsthalf and REM sleep in the second half ofthe night

Sleep physiology


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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


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Circadian rhythms

Biological rhythms that repeat q24 hours Suprachiasmatic nucleus in the ventral anterior

hypothalamus ( circadian pacemaker) projects toareas of the brain involved in sleep-wake regulation:

basal forebrain, thalamus, hypothalamus, pineal gland Regulating factors

Circadian clock genes determine internal circadianrhythmicity

Light is the most effective stimulus for the internalclock via the retinohypothalamic tract

Other stimuli: food, exercise, activity, hormones,social cues


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Approach to Diagnosis

History

Complaints of

I cannot get enough sleep Im sleepy during the day or I fall asleep all the

time

There is some unusual sleep behavior

An observer should be encouraged to attend theinitial interview


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Questions to ask: sleep habits usual hours of sleep

sleep problems current medications

other medical problems Weight gain

Alcohol intake

Conditions under whichsleep occur Dietary stimulants

Activities other than thosepertaining to sleep or sexthat take place while inbed (eating, writing)

Occurrence or history ofvarious abnormal sleepbehaviors (enuresis, sleepwalking)

Occurrence of other

relevant symptoms (sleepparalysis, cataplexy,hypnagogic hallucinations,early morning headache,loud snoring, difficultybreathing at night)


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Physical exam:

Weight

Vital signs Neurological examination

Auscultaion of the heart

Inspection of nasal and oral airways

Presence of redundant tissue, tonsillarhypertrophy, micrognathia, malocclusion,erythema of soft palate and posterior pharynx


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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


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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 sleeponset REM periods during 4-5 daytime nap opportunities at 2hour intervals

Maintenance of wakefulness testing 4 nap studies at 2 hour intervals lasting 20 minutes, terminated

with sleep onset

Actigraphy

Estimates a persons circadian rhythm


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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 tobe related to difficulties with partial arousal

Sleepwalking, sleep terrors, REM sleep behavior disorder,

sleep paralysis


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Diagnosis and Classification

Medical/PsychiatricSleep Disorders

Associated with mental disorders, associated withneurological disorders (parkinsonism, sleep relatedepilepsy) or with other medical disorders (sleeprelated asthma, sleep related gastroesophageal reflux)

P

roposedS

leep Disorders Sleep related laryngospasm, short sleeper, long

sleeper


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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


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Sleep apnea syndromes

ObstructiveSleep apnea

Recurrent partial or complete upper airwayobstruction resulting in decreased (hypopnea) orabsent (apnea) airflow in setting of increased

respiratory effort

Assd w/ desaturation, repeated arousals, sleep

fragmentation

Risk factors: Obesity, narrow upper airway,

retrognathia, macroglossia, enlarged tonsils,craniofacial malformations


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Obstructive sleep apnea

Associated features: hypertension, arrhythmias,cardiovascular disease, CHF, possible stroke, type II

DM

Treatment: weight loss, avoidance of alcohol &sedatives, CPAP, surgery



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Central sleep apnea Primary

recurrent episodes of diminished airflow without upper airwayobstruction

Absence of respiratory effort during apnea/hypopnea

Etiology is unknown

Pathophysiology:

heightened ventilatory response to CO2 leads to instability ofrespiratory control during wake-sleep transition and may persist intoNREM sleep; typically ceases in REM

CO2 levels tend to be lower, thus a small increase in ventilation leads toapnea

May be seen in neurologic disorders with associated ANSdysfunction (MSA, Parkinson)

Treatment: oxygen, positive airway pressure therapy



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Mixed apnea

initial cessation of both airflow and effort (centralapnea), followed several seconds later by the

appearance of effort without airflow (obstructiveapnea)



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Other disorders1) 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 assd with morbid obesity,neuromuscular disorders, chest wall restriction, highspinal cord or brainstem lesions, lower airwayobstruction, pulmonary parenchymal or vascularidiopathic disorders



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Disorders of excessive sleepiness

Medications

Acute medical illness of themononucleosis type

Post surgical andpostantesthetic states

Chronic neurologicdiseases: MS, dementia

Depression

Metabolic derangements:hypothyroidism, Addisondisease

Encephalitic desases:following viral encephalitis,trypanosomiasis,encephalitis lethargica

Lesions of thehypothalamus KleineLevin syndrome,hypothalamic tumor or

granuloma Sleep apnea syndromes

Narcolepsy-cataplexy

Idopathic hypersomnia


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Narcolepsy Gradual onset between 15-35

Classic tetrad:

excessive daytime sleepiness usually 1st symptom

Cataplexy most specific symptom

hypnogogic/hypnopompic hallucinations

sleep paralysis

Proposed 5th symptoms: disturbed nocturnal sleep

Proposed disease mechanism: destruction ofhypocretin secreting cells in posterolateralthalamus



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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 REMsleep)



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Idiopathic hypersomnia

Severe excessive daytime sleepiness w/ or without

long nocturnal sleep episodes without evidence ofcataplexy lasting more than 6 months with notother causes of sleepiness by history or PSG

Naps typically not refreshing

Onset in adolescence, early adulthood

Pathophysiology unknown



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Recurrent hypersomnia (Kline LevinSyndrome)

Recurrent episodes of hypersomolence with transientcognitive, mood, or behavioral disturbance ;

hyperphagia; hypersexuality

Each episode lasts 1-2 weeks, followed by return tonormal cognitive and psychosocial function for severalweeks or months

Usually affects teenage boys Pathophysiology: unclear; likely involves

hypothalamic dysfunction, autoimmune

No proven therapy; lithium may prevent recurrence



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Insomnia

Chronic inability to sleep despite adequate

opportunity to do so

Used popularly to indicate any impairment inthe duration, depth or restorative propertiesof sleep

Divided in 3 categories

Sleep onset insomnia

Sleep maintenance insomnia

Early morning awakening without return to sleep


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Insomnia

Insomniacs tend to underestimate actual time theyspend 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

Assd features: often influenced by environmental factorsand/or psychological disturbance esp stress, anxiety,depression, drug dependence, or other mental illness


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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 patientmisperceives the amount of time spent asleep

No PSG evidence of sleep disturbance; objectivelynormal sleep duration

Insomnia


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Pyschophysiologic Patient does not associate bedroom/bedtime with sleep

usually as a learned behavior that prevent sleep fromoccurring. Frustration and anxiety develop from inability to

sleep leading to states of increased arousal and tensionthat prevent sleep, thereby perpetuating the insomnia

Can develop from transient or chr0nic insomnia of anycause

Patient usually sleep better in a different environment thantheir own bedroom

Treatment: sleep hygiene behavioral therapy relaxation therapy, sleep restriction,

stimulus control therapy hypnotics

Insomnia


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Insomnia

Behavioral insomnia - due to learned behaviors orvoluntary actions inconsistent with sleep

Sleep onset association disorder

Child falls asleep only under certain conditions rocking chair, inparents 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


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INSOMNIA

Secondary insomnia

Environmental factors

Psychological factors Abnormal shift schedule

Circadian rhythm disorders

Medications

Medical conditions Psychiatric disorders

Primary neurologic diseases: fatal familial insomnia,Morvans fibrillary chorea


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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 systemhyperactivity, episodic stupor

Epidemiology: prion disease Autosomal dominant

Onset 5th

-6th

decade PSG: noSWS, 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


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INSOMNIA

Morvans fibrillary chorea Severe insomnia, fluctuating encephalopathy, peripheral

nerve hyperexcitability, weakness, cramping,neuromyotonia, dysautonomia

Pathophysiology: unknown, possible autoimmunemechanism or paraneoplastic phenomenon (assd w/myasthenia, malignancy; positive antibodies to voltagegated potassium channels_

PSG: no NREM sleep features (K complexes, spindle waves,delta waves) subwakefulness state characterized by EEGtheta activity associated with behavioral sleep, brief REMsleep periods without atonia

EMG: spontaneous repetitive discharge (doublets, triplets,multiplets, myokymia)

Labs: increased plasma norepinephrine level

Treatment: plasma exchange, immunemodulating agents, thymectomy

opioids


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Rules of sleep hygiene for

patients

Sleep only as long as needed to feel refreshed thenext 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 oreating


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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 doesnot disturb sleep

Do not use alcohol as a sedative. It facilitates the onset ofsleep but later acts as a stimulant

Avoid the frequent use of tobacco

If you feel upset because you cannot sleep, get up, turnon the light and do something else


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Restless Legs Syndrome

Complaints of unusual and severe leg sensations; reliefgained by walking, rubbing legs, applying heat; most

prominent in evening and nightime, resulting in sleeponset and sleep maintenance insomnia

Hallmark is the irresistible urge to move the legs torelieve discomfort

Arms may be involved Pathophysiology: cerebral iron and dopamine

pathways have been implicated

Sleep Related Movement Disorder


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Primary restless leg syndrome Positive family history of similar symptoms, including

adolescent growing pains Autosomaldominant inheritance

Onset: childhood, adolescence Secondary restless leg syndrome

Assd w/ pregnancy, peripheral neuropathy, chronic renalfailure, iron deficiency anemia, latent iron deficiency, folatedeficiency

Linked to several medications: antidepressants, neuroleptics,

dopamine agonists, sedating antihistamines Treatment: dopaminergic agonists, gabapentin,

benzodiazepines, low potency opioids, ironreplacement therapy if serum ferritin


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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 beenimplicated

Low serum ferritin level

Treatment: dopamine agonists


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Rhythmic movement disorder Stereotyped, repetitive, rhythmic movements of body

parts, usually of head, neck, trunk that occur before sleeponset and persist into light sleep or occur only during sleep

Movements include head banging, head rolling, bodyrocking

Considered a disorder only if it interferes with sleep, resultsin daytime sleepiness, or leads to injury

Seen mostly in infants and young children, also mentallyhandicapped children; typically resolves by 2-3 years butmay persist into adulthood

Treatment: benzodiazepines, antidepressants if necessary



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Bruxism

Stereotyped,intermittent rhythmic al teethgrinding 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



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Persistent inability to sleep at desired or

expected time and/or excessive sleepiness

during the wake period as defined byenvironmental/societal factors

Types

Delayed sleep phase disorder

Advanced sleep phase disorder

Circadian rhythm sleep disorder, nonentrainedtype


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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 melatoninsecretion

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



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Circadian rhythm sleep disorder, nonentrained type Circadian rhythm either lacks chronization with 24 hour

environmental rhythms or is free running at a non-24 hourrhythm (typically >24 hours)

Observed most often in visually impaired patients, mentalretardation

Occasionally due to behavioral patterns, environmentalfactors in sighted people

Pathophysiology: lack of light stimulus to thesuprachiasmatic nucleus in blind persons leading to lack ofentrainment of circadian rhythm to environmental rhythm

Treatment: melatonin before bedtime, light therapy



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Irregular sleep-wake rhythm

Sleep is fragmented into several naps throughout the24 hour period ; total 24 hour sleep duration is normal

Occurs mostly in patients with cerebral dysfunction orthose who choose an inconsistent sleep-wakeschedule but are capable of entrainment

Pathophysiology: abnormal circadian clock function

Treatment: light therapy, melatonin, strict adherenceto schedules



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Others Jet lag syndrome

Eastward travel requires a phase advance

W

estward travel requires a phase delay of circadianrhythms

On average, one day per time zone is required to adjustto 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



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NREM parasomnias Abnormal behavior occur with sudden partial arousal from

NREM sleep, usually SWS, typically in the first 1/3 of thenight

Patients are not responsive to external stimuli and appearconfused when awakened; often no recall in AM

Triggered by sleep deprivation, stress, environmental (loudnoises), medical conditions leading to increased arousals,CNS depressant medications which prevent arousal fromsleep and increase SWS/arousal threshold (hypnotics,

alcohol) Types

Sleep walking Sleep terrors Confusional arousals

Parasomnias


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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

ReassuranceSecure sleeping environment

Eliminate precipitants Benzodiazepines or tricyclic antidepressants can be prescribed Hypnosis, psychotherapy, relaxation techniques, stress

management strategies


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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 thenight when slow wave sleep predominates; no recollection ofdream content

Benign condition More common in children Treatment

Reassurance Avoidance of precipitants Behavioral therapy scheduled awakenings Benzodiazepines, antidepressants if severe

Parasomnias


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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


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Parasomnias

REMSleep Parasomnias REMSleep Behavior Disorder

Loss of atonia during REM sleep, with elaborate motor activity anddream 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 Esynuclein positive intracellular inclusions (Parkinsons, Lewy

body, MSA) Pathophysiology: unclear, possibly lesions in the pontomedullary

pathways promoting REM sleep atonia in combination withincreased activity in locomotor generators

Treatment: bedroom safety, clonazepam, melatonin


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Nightmares Frightening dreams resulting in awakening

No prominent vocalization, motor activity

Usually, full alertness and dream recallimmediately after awakening

More frequent in children and patients withpsychiatric disorders (substance abuse, PTSD)

Treatment Treat underlying disorder

Psychotherapy, hypnosis, behavioral therapy

Parasomnias


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Sleep paralysis

Partial or complete muscle paralysis at sleeponset 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)

Parasomnias


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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 inducedmovement disorders

Abnormal muscle tone which facilitates breathingabnormalities

Disorders of circadian rhythm and sleep-wakefulnessschedule

Treat underlying disorder

Sleep disorders associated

with Neurologic Conditions


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with Neurologic Conditions Multiple system atrophy

Nocturnal stridor from vocal corddystonia/paralysis, paradoxical vocal cordadduction with inspiration

May cause sudden death in sleep

Treatment: tracheostomy, nasal CPAP


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with Neurologic Conditions Alzheimers disease

Cognitive decline is paralleled by a decline in slowwave sleep and REM sleep and an increase in the

number of nocturnal awakenings and amount of timespent awake during normal sleep time (due todegeneration of brainstem and basal forebrainpathways)

sundowning evening attacks of delirium in which

patients experiences emotional and perceptualdisturbances with irrational thinking, disorganizedspeech, and agitation (from suprachiasmatic nucleusdegeneration?)


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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 andbecome 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 onawakening


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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 onEEG

Anticonvulsants tend to consolidate sleep, maycause excessive daytime sleepiness


with Neurologic Conditions


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SLEEP DISORDERS



Insomnia Sleep related movement disorder

Circadian rhythm disorder

Parasomnias Sleep disorders associated with neurological

conditions

Neurological Aspects of Sleep

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