Sleep Flashcards
Light has what impact on retinal ganglion cells?
What impact does this have on each subsequent system that regulates sleep/awake cycles? i.e. from RGCs to pineal gland.
Light inhibits firing of retinal ganglion cells that would otherwise tell you to sleep. Thus, absence of light disinhibits retinal ganglion cells, which tell the suprachiasmatic nucleus—> paraventricular nucleus—> intermediolateral gray of spinal cord—> superior cervical ganglion—> pineal gland release of melatonin
Describe the EEG frequency and voltage progression through the various stages of sleep (N1-N3).
EEG frequency v through stages of sleep N1-3
EEG voltage ^ through stages of sleep N1-3
REM sleep has voltage similar to N1 w/ mixed frequency
~90mins from stage N1-REM
Describe the lightness vs heaviness of the various stages of sleep (N1-REM). Also describe the waveforms used to distinguish the three stages.
N1 Lightest high freq, low amplitude waves
N2 Heavier (start to see K complexes and sleep spindles)
N3 Heaviest (lots of K complexes)
REM Light- (sawtooth waves of low amp, mixed freq)
Which stage of sleep is associated w/ muscle paralysis?
REM
Which stage of sleep is associated most with vivid dreaming?
REM
Which stage of sleep is associated with sleep walking?
N3
Which stage of sleep is associated w/ hypnotic jerks?
W (drifting off) and N1
What stage of sleep is lost in age-related sleep loss?
REM
“morning wood” is found during this stage of sleep
REM- due to partial arousal
Which brain centers are more/less active during REM sleep that explain vividness or bizarre nature of dreams during this time?
^ activity of amygdala, parahippocampal gyrus, ant. cingulate gyrus accounts for emotion, vividness of dreams
v activity of Frontal cortex + posterior cingulate gyrus accounts for bizarre nature of dreams due to irrational thought
Ach, Orexin/hypocretin, DA, serotonin, histamine, and NE are most active when you are awake, N1, N2, N3, or REM?
Awake.
Some activity in NREM
No activity in REM (except for Ach, activity in REM accounts for beta wave activity and inactivity in NREM accounts for slow wave activity)
Name the nucleus where this Neurotx is released:
Ach
PPT + LDT
Name the nucleus where this Neurotx is released:
DA
Substancia nigra
Name the nucleus where this Neurotx is released:
Serotonin
Raphe nuclei
Name the nucleus where this Neurotx is released:
Histamine
Tuberomamillary nucleus
Name the nucleus where this Neurotx is released:
NE
Locus ceruleus
Name the nucleus where this Neurotx is released:
Orexin/hypocretin
Lateral hypothalamus
What is the VLPO and what stages of sleep does its activity induce and why?
VentroLateral PreOptic nucleus (VLPO), found in hypothalamus is responsible for inducing NREM sleep by inhibiting all the other arousal nuclei.
Its inhibition causes unbalanced wakefullness—> insomnia
Nacrolepsy is attributed to decreased levels of this neurotx and a decreased number of neurons that secrete it.
Orexin
This sleep disorder can cause daytime symptoms of fatigue, heartburn, memory loss and poor cognitive performance, headache, and impotence. It can cause nighttime symptoms of snoring, reflux, nightmares, and tonsil hypertrophy.
Obstructive Sleep Apnea (OSA)
This sleep disorder is characterized by Sleep attack/intrusions, Cataplexy (wakeful loss of muscle tone), Sleep paralysis (wake up and experience brief paralysis), and hypnagogic hallucinations (very vivid day dreams)
Narcolepsy
How can we tx narcolepsy and cataplexy?
Daytime narco: methylphenidate (CNS stimulant also used for ADHD), modafinil (DA reuptake inhibitor), gamma-hydroxybutyrate (date rape drug)
Cataplexy: TCAs/SSRIs
What causes REM sleep behavior disorder, characterized by loss of REM atonia and possible acting out of dreams during sleep?
What demographic is this most often seen in?
::Primary component: alpha-synucleopathies (Parkinson’s, Progressive Supranuclear Palsy, Multiple System Atrophy, Lewy Bodies)
::Secondarily from EtOH withdrawl or overdose of TCAs/SSRIs
Most often seen in males over 50yo
