Narcolepsy
General
Symptoms
Objective Findings
Patho-physiology
Epidemiology
Interventions
Sleep-wake
control disorder
Excessive daytime
sleepiness
PSG, MSLT: very short
sleep latencies
Prevalence - 0.05%
(uncommon, but not rare)
Symptomatic therapy
Cataplexy
Sleep-onset REM
Selective loss of
hypocretin neurons in
the lateral
hypothalamus
Hallucinations
Daytime naps with REM
activity
Reactive gliosis
Remains stable
Genetics?
Familial aggreggation
sleep paralysis
Onset – 2nd decade
Sleepiness: stimulants (methylphenidate,
dextroamphetamine, modafinil); scheduled
naps
Cataplexy: Antidepressants, gammahydroxybutyrate (GHB)
Paralysis, hallucinations: 5-HT
antidepressants, GHB
Insomnia
Sleep
difficulties
despite
adequate
opportunities
Prolonged sleep
latency and
awakenings, frequent
awakenings, impaired
daytime performance
PSG not routinely
indicated (10-15% of
insomniacs show normal
PSGs)
Prolonged sleep latency
Poor sleep continuity
Circadian
rhythm
sleep
disorders
(CRSD)
Mismatch
between
desired slepewake times and
circadian
rhythm phases
Specific time patterns
of insomnia and
sleepiness
Hyperarousal
Maintained coscience
perception into EEG
defined sleep stages
Reduced homeostatic
drive?
Increased high frequency
EEG activity during
sleep
Increased corticolimbic system activity
No specific PSG findings
Mismatch of
endogenous pacemaker
and desired sleep-wake
hours
Endogenous circadian
rhythms are abnormal
DSPS – difficulty
falling asleep and
waking up
Prevalence of symptoms: 3040%
Prevalence of disorder: 5-10%
Onset – early adulthood;
increases with age
Women > men
Regularizing sleep-wake schedule
Benzo-receptor agonists (BzRA), melatonin
receptor agonist, low dose sedating
antidepressants, natural remedies
(melatonin, valerian)
Chronic in 85% of insomnia
cases
Prevalence is unknown
DPSP peaks in adolescence
DSPS – early morning exposure to bright
light; melatonin in early evening hours
ASPS – evening light exposure; morning
melatonin
Voluntary behavior
Behavioral chronotherapy – having DSPS
patients go to bed at successively later times
until they arrive at “normal” sleep times
Abnormal timing of
exposure to zeitgebers
(light)
ASPS – early evening
sleepiness and early
morning awakening
Reducing time in bed
Absence of
photoreception
(enucleated blind pts)
Genetics?
OSAS
(obstructiv
e sleep
apnea
syndrome)
Repeated
airway closures
during sleep
Excessive daytime
sleepiness
Loud snoring,
rescucitative
snort/gasp
Repeated episodes of
airflow cessation (apnea)
or limitation (hypopnea)
lasting >10 seconds
Oxygen desaturation
Obesity, hypertension
Repeated arousals
Upper airway
“crowding”
Continued efforts to
breath during apneic
period
Occlusion of upper
airway (velopharynx
or hypopharynx)
Mechanical factors (
Neurological (impaired
hypoglossal reflex,
secondary cerebral
damage?)
Loss of hypoxic drive
Prevalence: 4-10% males, 25% females
Onset: middle age; stable or
progressive
Mechanical: Continuous positive airway
pressure (CPAP); oral appliances to protrude
mandible
Surgical: bariatric surgery,
uvulopalatopharyngoplasty, maxillomandibular advancement
REM sleep
behavior
disorder
(RBD)
General
Symptoms
Objective Findings
Patho-physiology
Epidemiology
Interventions
Violent
behavior during
REM sleep
Awaken fully at time
of episode
Increased muscle activity
during REM sleep
Brainstem lesion
Prevalence – unknown
BzRA
Lewy body disease
Onset – middle age
Gabapentin, dopamine agonists
Idiopathic
Men>Women
Exacerbated by certain antidepressants!
Vivid recall of storylike drems
Stable, mildly progressive
Usually occur during
2nd half of night
Sleep
walking
Sleep
terrors
Abnormal
behavior during
deep NREM
sleep
Partial arousal from
deep sleep
Higher than normal stage
3/4 NREM sleep
Limited recall
Episodes occur during
synchronous delta EEG
activity
Walking, eating, etc.
Usually occur during
first half of night
PLMD
(periodic
limb
movement
disorder)
Unpleasant
sensations in
legs that
prevent sleep
onset
PLMD –
periodic jerking
movements
during sleep
Urge to move limbs,
accompanied by
dysesthesias (creepy
crawly)
Almost always affects
lower legs (Babinskilike response)
Immediately but
temporarily relieved
by movement
Diurnal variation –
worsens at night
Prevalence – 25% during
middle childhood; 1% of adults
Usually stops by early
adolescence
BzRA
Preemptive awakenings before usual time of
sleep terrors
Avoiding precipitating factors
Precipitated by stress,
sleep deprivation,
alcohol, medications,
physical movement
Difficult to awaken
RLS
(Restless
Leg
Syndrome)
Incomplete state
transition disorders
(partial arousal, but not
complete awakening
from NREM sleep)
PLMD movements
continue into light
NREM stages
Twitches observed every
20-90 seconds;
associated with transient
EEG arousals
Mild Fe deficiency
Secondary form
associated with irondeficiency anemia,
kidney failure,
pregnancy (up to
27%), medications
(antidepressant,
antipsychotic)
Reduction of DA
activity in basal
ganglia
Abnormal Fe
metabolism in CNS
(need Fe as cofactor
for DA synthesis)
Genetics?
Increased familial aggregation
(50%); possible linkage to
chromosome 12q
DA agonists
RLS prevalence: 5-10%
Benzodiazapines, opiates
Onset - 2nd decade of life;
chronic
L-dopa