lecture 12 sleep disorders Flashcards
What is sleep paralysis
What is it associated with
temporary period of paralysis (hypnogogic or hypnopompic)
associated with hallucinations
associated with REM at sleep onset
able to hear and open their eyes but unable to move
associated wit hnarcolepsy and familial inheritance, isolated or substance-induced
higher incidence when sleeping supine
3 types of sleep paralysis and their characteristics
intruder - threatening presence with other hallucinations
incubus - difficulty breathing, suffocation, pressure, pain, feeling of impending death
- correlaiton between intruder and incubus - both correlated with fear
vestibular-motor - acceleration, floating, flying, autoscopy (outof body experience)
- less correlated with the other two
link betwen sleep paralysis and fear and anxiety
Experience is typically scary
trauma, porr sleep quality, stress linked to higher incidence of sleep paralysis
fear can arise due to suppression of respiratory movement (unable to increase respiratory rate when woken up)
involvement of amygdala - brain attempts to resolve fear by creating athreat
Epidimeology of sleep paralysis
varying prevalence rate reported - 3-62%
occurs mostly in adolescent period
occurence deceases with age
more prevenlent in shift-work population
thought to be due to disturbances in sleep-wake system
symptoms of narcolepsy
mandatory - excessive daytime sleepiness (EDS)
typically present
- cataplexy
- hypnagogic or hypnopompic halluciations
- sleep paralysis
what is cataplexy
sudden loss of muscle tone in response to emotional stimuli
knee jerk reflex reduced
link betwen REM and narcolepsy
REM sleep component intruding into wake
- cataplexy - REM atonia
- sleep paralysis - again atonia
- hallucination - intrusion of dreams
- REM appears at sleep onset and MSLT (NANI THE FUCK IS MSLT)
prevalence of narcolepsy
adolescnet onset
equally in males and females
lowest in israel and highest in japan
what possibly causes narcolepsy
low orexin in most cases, receptor abnormality
what is the mechanism behind cataplexy
normally orexin excites vlPAG and NE, 5HT which inhibit SLD
(SLD excites MM and spinal interneuron who inhibites motor neuron, thus SLD inhibit motor neuron = REM atonia)
in cataplexy AMYGDALA takes over inhibiting vlPAG - allowing SLD to produce atonia
amygdala alos directly excites SLD
How is the sleep of someone with narcolepsy different from sleep of a normal person
- early REM intrusion
- less SWS (to be confirmed? i dont remember)
- more awakening
- REM looks funny
- JUST CHECK LETURE CAPTURE
- why does low level of orexin affect sleep???
How to diagnosis narcolepsy
narcolepsy emerges in teens - 20s, often following illness/vaccination - involvement of autimmune system
diagnosis
- abormal immune function - HLA subtyping
- sleep study (short sleep onset latency, short REM latency, increases awakening)
- multiple sleep latency test (rapid sleep onset, REM onset)
treatment ofr narcolepsy
1.Excessive daytime sleepiness - planned naps, CNS stimulants, sodium oxybate
cataplexy - antidepressants, sodium oxybate - why does antidepressants work???
orexin agonists - but orexin can’t cross BBB - no luck yet
what is REM behaviour disorder
loss of atonia in REM - act out dreams
link between REM behaviour disorder and degenerative diseases?
Often precedes degenerative disease by many years (Parkinson’s, Lewy body dementia, multiple systems atrophy).
Diagnosis may provide an opportunity for early intervention for such disorders.
What is the mechanism of REM muscle atonia
Lesion of sublateral dorsal (SLD) region resulted in REM sleep without atonia in rats.
Injected tracer into this region and found projections through the pons and medulla to the spinal ventral horn (contain thealpha-motor neurons).
Why do you still even get REM sleep with lesion of the SLD?
Two populations of SLD neurons: one part of flip flop switch and other responsible for atonia.
Human RBD: PPT/LDT involved too.
signs and symptoms of somnambulism/sleepwalking
Signs and Symptoms:
Performing complex behaviours while asleep
Walking
Talking
Driving
Hard to awaken while experiencing and episode
Little or no memory of the event after waking
Confusion and distress when aroused during episode
Sleepwalking onset and prevalence
Paradoxically occurs during NREM (SWS) sleep
Most sufferers experience it chronically
Seems to have familial/genetic component
Onset usually in childhood and frequency of episodes is greater in childhood than adulthood
Prevalence ~1-15%
sleepwalking pathology
Speculation that it is incomplete arousals from deep sleep or brain attempting to directly transition from deep sleep to wake
The result is most likely activation of isolated neuronal networks permitting movement
risk factors underlying sleepwalking
Associated with depression, alcoholism, OCD, anti-depressant and sedative medication
Triggers: sleep deprivation, illness, excessive deep sleep (SSRIs or sleeping pills) can predispose to an episode
treatment of sleepwalking
Improve sleep hygeine
Avoiding triggers – sleep dep, alcohol, drugs
Create safe space or put measures in place to protect them and others
To wake or not to wake?
