Topic 18: Sleep and Sleep Disorder Flashcards
What types of clinicians are involved in treating sleep disorders?
family physicians
respirologists/pulmonologists (sleep apnea)
psychiatrists (psychological causes)
neurologists
What is the organization of sleep?
sleep is a continuum, no black and white distinction between some stages, blurring of continuum is the disease
there are changes observable at the scalp using EEG: used to define sleep stages
neurophysiology underlying some specific wave forms on EEG have been determined
certain sleep disorders occur during specific sleep stages
How does EEG measure sleep stages?
noninvasive measure neurophysiology
changes in voltage measured on the scalp
EEG rhythms named according to the frequency of the activity (number of waves in 1 second of recording)
What are delta waves?
0-3.99 Hz
slow waves: 0.5 - 2 Hz
critical stage
What are theta waves?
4-7.99 Hz
wakefulness
What are alpha waves?
8-13 Hz
quiet wakefulness (just before falling asleep)
decreased altertness
What are beta waves?
> 13 Hz
wakefulness
associated with medication like benzos
What are the three basic states of sleep?
awake
nREM sleep
REM sleep
How is being awake classified?
presence of alpha rhythm
What is nREM sleep?
N1: alpha “drop out”
N2: sleep spindles and K complexes
N3: slow wave sleep (SWS, previously 3 and 4)
What is REM sleep?
no muscle tone (chin electromyography - EMG) and rapid eye movements
loss of all movement except for eyes
What is the relationship between nREM and REM sleep in the sleep cycle?
NREM and REM sleep alternate during sleep, with each cycle lasting for approximately 90-100 minutes
4-6 cycles are noted during a normal sleep period
What is the N1 stage of sleep?
alpha drop out
What is the N2 stage of sleep?
sleep spindles –> increased seizure risk, in centro-temporal regions, hypersynchrony increases risk for seizure
EEG frequency of 11 to 16 Hz (usually 12 to 14 Hz)
fast end of alpha band
What are reticular neurons?
inhibitory input to relay nuclei via GABA-B receptors
What are relay neurons?
excitatory input to cortex
T-type calcium channels in relay neurons
unique because they possess capability for “low-threshold depolarization” which is depolarization from a hyperpolarized state
How are reticular and relay neurons involved in seizures in nREM sleep?
in non-REM sleep, there is an increase in reticular neuron activity, which hyperpolarizes relay neurons via GABA-B receptors
this hyperpolarization activates T-type calcium channels which allows low-threshold depolarization and BURST mode thalamo-cortical activation of relay neurons, this generates sleep spindles
this circuit is pathologically active in absence seizures: excessive and synchronous activity from reticular neurons, results in BURST mode thalamo-cortical activation by relay neurons
this generates 3 per second spike-wave seizure
ethosuximide acts as a T-type calcium channel antagonist, hence it’s clinical effect on absence seizures (only)
What are benzodiazepines associated with in relation to sleep?
increased stage N2 sleep
increased spindle activity
possibly due to increased GABA-ergic signalling
GABA agonist
What is rapid eye movement sleep?
rapid eye movements
lack of EMG muscle activity
“awake” looking EEG: absence of sleep morphologies or slow waves, considered a “lighter” phase of sleep