physiology of sleep Flashcards
Functions of REM, and NREM sleep
NREM: brain and body regeneration. REM: brain development and memory
Characteristics of REM and NREM sleep
NREM (N1, N2, N3 [SWS] sleep) = high amplitude slow brain waves, increased arousal threshold compared to wake, decreased muscle activity, slow rolling eye-movements, decreased heart rate, respirations and metabolism. REM: every 90 minutes in adults, EEG looks awake but arousal threshold is higher. Active brain in paralyzed body. Temp regulation suspended, brain temp rises, heart and respirations irregular
Disorders of arousal
•walking, terrors, confusional arousal, night eating syndrome- usually arise early out of N3, SWS.
basal forebrain function in sleep
Adenosine accumulates during wake, reduced during sleep, blocked by caffeine
Hypothalamus function in sleep
sleep wake switch
thalamus function in sleeps
gate to cortex, spindles, slow wave sleep
brainstem function in sleep
ascending cortical activation, REM/SWS switch. Activation of brain stem cholinergic neurons elicits wakefulness
Suprachiasmatic nucleus function in sleep
Conveys info from retina to sleep/wake switch in hypothalamus. Circadian clock modulates alertness, Core body temperature (CBT), cortisol and Melatonin secretion
Which area of brain is responsible for inhibiting the arousal systems during NREM and REM sleep
neurons of ventrolateral preoptic area
Neurotransmitters involved in REM sleep
REM sleep is driven by cholinergic pedunculo-pontine and laterodorsal tegmental (PPT/LDT) neurons. During wake and NREM sleep, these are inhibited by NE, 5HT, HA but during REM the aminergic neurons fall silent, thus disinhibiting the LDT/PPT REM-generating neurons. Also, dopaminergic neurons from ventral tegmental area and substantia nigra ar active
What neurotransmitters are involved in atonia of REM sleep
Cholingergic neurons - by activating the medial medulla, which inhibits motor neurons with glycine.
Neurotransmitters involved in NREM sleep
GABAergic neurons in ventral lateral pre-optic anterior hypothalamus
neurotransmitters involved in wake
Laterodorsal tegmental/ pedunculo-pontine cholinergic neurons, dorsal raphe serotoniergic neurons, locus coeruleus NE neurons, tubomammilary-posterior hypothalamus histaminergic neurons, adenosine in basal forebrain and hypocretin neurons in lateral hypothalamus
How do anti histamines cause sleepiness
lipophilic H1 blockers
Loss of what kind of cells is seen in narcolepsy with cataplexy
HCT secreting cells
function of hypocretin secreting neurons in lateral hypothalamus
arousal, wakefulness, appetite
Be able to describe the interaction of the circadian (process C) and homeostatic system (process S) and their effect on wake and on sleep.
Homeostatic drive S: The longer we are awake, the sleepier we get. Mediated by adenosine. Circadian system C: Sleepiness waxes and wanes under influence of circadian alerting system in the suprachiasmatic nuclei, and is linked to core body temperature.
Discuss the pathway of the circadian system
Light travels to suprachiasmatic nucleus (SCN) via the retinohypothalamic tract (RHT) > The SCN signals the pineal gland via the superior cervical ganglion & inhibits the production of melatonin. Melatonin normally reduces SCN activity and arousal, so in light SCN activity is increased and arousal occurs.
In absence of light, what happens
People “free run” and operate on a 24.2 hour day
Tool to measure sleepiness
Epworth sleepiness scale - asks how likely you are to fall asleep in certain situations to sort out sleepy from fatigued. 1-6: getting enough sleep. 7-8: average sleep deprived american. 9+: very sleepy and need follow up
Causes of high epworth rating
insufficient sleep, circadian rhythm disorder (shift work, jt lag), sleep apnea, narcolepsy, head injury, depression, drug use or withdrawal, medical illness
Causes of sleepiness with low epworth rating
fatigue: anxiety and depression, conditioned/learned insomnia
behavioral causes of insomnia or excessive daytime sleepiness
bedroom not dark or quiet, irregular sleep and wake times, big meals before bed, co-sleeping with pets, alcohol, caffeine, loud bed partner
Circadian alerting system is linked to what?
core body temp: People sleep best on the descending curve of their CBT and spontaneously awake about 2-3 hours after lowest CBT and CBT begins to rise.
core body temp: People sleep best on the descending curve of their CBT and spontaneously awake about 2-3 hours after lowest CBT and CBT begins to rise.
Delayed sleep phase syndrome
aka night owls- “insomnia” when trying to sleep at socially appropriate time or EDS when awakened for school or work before enough sleep & before alerting rhythms rise.
Advanced sleep phase syndrome
aka “larks”- “want” to sleep and wake early. If remain awake to watch news, they still wake early and EDS; their early morning awakening misinterpreted as insomnia due to depression.
Obstructive sleep apnea
increased work of breathing from snoring, to upper airway resistance syndrome, to respiratory effort related arousals, to hypopneas to apneas
Obstructive sleep apnea comorbid conditions
Increased stress leads to a pro-inflammatory response increasing risk of CVHD, stroke, HTN and pulmonary hypertension and can predict the development of depression. In kids may be one cause of attentional difficulties since tired kids get hyperactive and have decreased ability to concentrate and lead to wrong dx of ADHD
Categories of insomnia
- learned: hyper-arousal and learned, and not caused by other condition. 2. Co-morbid: due ot mediical, psychiatric, pain, restless legs, circadian problems, narcolepsy, meds
Insomnia treatment
sleep restriction and stimulus control
restless leg syndrome
•waking discomfort. Urge to move legs and/or arms, with onset or worsened by rest, usually at night, and somewhat relieved by movement. ? Associated with HTN
Restless leg syndrome treatment
iron replacement if serum ferritin is <55
What stage of sleep does sleep walking/night terrors occur
in first part of sleep period.
What is REM sleep behavior disorder
loss of muscle paralysis and acting out dreams in later part of nght when REM is more prevalent. Common in men <50
cause of narcolepsy
lesions in hypocretin system- loss of boundaries between sleep and wakefullness. Patients quickly enter REM sleep at any time, have loss of muscle tone while awake (cataplexy), sleep paralysis, and hypnagogic hallucinations
Narcolepsy treatment
naps, stimulants, sodium oxybutyrate
