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Chika- SF2 > Physiology of Sleep: Allard > Flashcards

Physiology of Sleep: Allard Flashcards

1
Q

What is sleep?

A

a naturally occurring state of reduced or absent consciousness

a state of dramatically lowered sensory perception and absence of voluntary motor function that is easily reversed by sensory stimuli

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2
Q

What is the stage of sleep where you are pretty conscious?

A 
REM sleep 
(rapid eye movement) where you are aware of feelings and internal environment

lucid dreaming: you’re in your dream world, you know you are dreaming but you stay asleep because you know you can do things you will never doing real life; done in the younger brain

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3
Q

All mammals sleep. The amount of time they spend in sleep varies.

A

giraffe: 2 hours
brown: bat 20 hours
humans: 8-9 hours

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4
Q

What is sleep important for? What is the evidence of the importance of sleep?

A
  • all mammals do it
  • even the dolphin, which moves continuously, shows “unihemispheric sleep” where one hemipshere is asleep but the other one is active (they do not have REM sleep)
  • humans experience rebound sleep after a deprivation period (you body will make you sleep if you have deprived yourself of it by sleeping 2-3 hours a day even if you are driving)
  • if you deprive rats, flies, and cockroaches of sleep, they will actually die; prolonged sleep deprivation has been shown to kill rats, flies, and cockroaches
  • most psychiatric conditions are associated with sleep abnormalities
  • humans with genetic insomnia have increased mortality rate (fatal familial insomnia kills within 18 months of symptom onset); usually starts in middle age they can’t sleep and eventually die (hallucination, unregulated hormones)
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5
Q

What are the theories on sleep function?

A

growth and development:

  • newborns sleep 20 hours/day
  • during deep sleep, the pituitary gland releases growth hormone

restoration and repair (sleep is important for immune system):

  • sleep deprivation results in depressed immune system (you get a cold pretty quickly after studying for exams)
  • decreases insulin sensitivity
  • impairs thought and judgment
  • impairs motor performance

memory consolidation:
-sleep deprivation results in severe memory impairment (if you sleep you can remember stuff you already learned)

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6
Q

What are the areas of the brain that regulate sleep? What is arousal? What area in the brain is responsible for keeping us awake, conscious, alert, and aware of our environment?

A

neurons in the brainstem called the reticular formation (don’t confuse with the reticular nucleus of the thalamus)

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7
Q

The reticular formation is made up of what kind of projections? Where does it extend and where does it project to?

A
  • involves ascending and descending projections (somatosensory pathways, pathways to cerebellum for motor control, etc.)
  • extends from the rostral midbrain to the caudal medulla
  • projects to the thalamus, hypothalamus, limbic system, cerebellum, spinal cord and entire cerebral cortex
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8
Q

What are other functions of the reticular formation besides control of arousal and consciousness?

A

-control of arousal and consciousness through the reticular activating system
-control of movement through connections with spinal cord and cerebellum
and reticulospinal tracts
-modulates transmission of pain information
-filters sensory input
-modulates autonomic reflex activity

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9
Q

What type of neurons are found in the reticular formation?

A

substantia nigra: dopaminergic neurons (degenerate in PD)

  • cholinergic cells
  • lateral dorsal tegmental and peduncular pontine nucleus
  • locus coeruleus (the biggest source of norepinephrine in our body)
  • nuclei of raphe (bundle of different nuclei that go from pons to upper medulla)

all of these cells are grouped together and called the nucleus of the reticular formation

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10
Q

What do we call the group of ascending axons in the reticular formation?

A

reticular activating system

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11
Q

What neurons does the reticular activating system consist of? Describe the neurocircuitry of arousal.

A
  • cholinergic projections from the midbrain reticular formation (MRF)
  • noradrenergic projections from locus coeruleus (LC)
  • serotonergic projections from raphe nuclei (RN)
  • dopaminergic projections from the substantia nigra (SN)
  • cholinergic neurons from nucleus basalis (BN) of the basal forebrain (one of the first cells to degenerate in Alzheimer’s dz)
  • histaminergic neurons from the tuberomammilary nucleus (TMN) (in the posterior hypothalmus, histamine arouses us as anti-histamines make us sleepy)
  • orexinergic/hypocretin neurons from the lateral hypothalamus (LH)
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12
Q

The neurons just described, what happens to them when an individual goes to sleep and who performs the action?

A

they need to be turned off in order to sleep

neurons secreting GABA and galanin from the ventrolateral preoptic area/nucleus (VLPO) inhibit the RAS to initiate sleep

so they essentially inhibit all those arousal neurons of the reticular activating system

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13
Q

What is the role of adenosine?

A
  • has sleep inducing effects (drowsiness/sleepiness)
  • is thought to be an indication of energy consumption by the brain
  • adenosine is the A in ATP
  • tends to build up a lot in the basal forebrain
  • endogenous adenosine levels in the basal forebrain increase during wakefulness and decreases during recovery sleep
  • caffeine blocks the adenosine receptors
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14
Q

What is the role of nucleus of accumbens?

A

GABAergic neurons with a high density of adenosine receptors in the nucleus accumbens are activated by adenosine which will inhibit the arousal centers

caffeine blocks these adenosine receptors in the nucleus accumbens

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15
Q

What regulates the VLPO?

A

it gets activated and inhibits all of the arousal nuclei

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16
Q

Which nucleus regulates with the circadian rhythm of sleep? Where is it located?

A

suprachiasmatic nucleus

  • located in the anterior hypothalamus
  • cells have an endogenous rhythm (biological clock)

-it gets entrained by light (so when you go to other time zone you won’t be completely messed up)

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17
Q

How is the suprachiasmatic nucleus entrained?

A
  • suprachiasmatic nucleus is entrained by signals originating from light detected by the ganglion
  • ganglion cells of the retina contain the photopigment melanopsin which is most sensitive to blue light; these are not the same one associated with your visual pathway
  • it is also entrained by melatonin hormone
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18
Q

Sleep and wake patterns occur with what circadian periodicity in humans?

A

roughly 24 hours

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19
Q

What are the functions of the suprachiasmatic nucleus?

A

-function as a biological clock that governs many circadian rhythms of the body

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20
Q

What are input and output projections of the suprachiasmatic nucleus?

A
  • receives direct projections from the retina which entrains it to periods of daylight
  • contains ~20,000 neurons with genetically controlled molecular clocks (heterogeneous population of cells; wide variety of neurotransmitters)
  • projects to the locus coeruleus and ventrolateral preoptic nucleus (VLPO)
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21
Q

Suprachiasmatic nucleus contains numerous receptors for this?

A

melatonin receptors

-suprachiasmatic nucleus is tuned by melatonin

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22
Q

Where is melatonin secreted from?

A

pineal gland

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23
Q

What allows melatonin to diffuse easily through most cell membranes including the blood brain barrier?

A

its high lipid and water solubility

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24
Q

What are the levels of melatonin during the day and night time?

A

low levels of melatonin in the daytime (light periods)

high levels of melanting in the nighttime (dark periods)

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25
Q

Describe the pathway of axons from the suprachiasmatic nucleus to the pineal gland.

A

it is not a straightforward pathway

Retino-hypothalamo-pineal pathway
light comes into the retina; special ganglion cells project to the SCN
-melanopsin containing ganglion cells stimulate suprachiasmatic nucleus (SCN)
-SCN sends inhibitory projections to paraventricular nucleus (PVN)
-PVN axons descend to intermediolateral cell column with the neurons in the lateral horn (which is part of the preganglionic sympathetic neurons)
-preganglionic neurons project to superior cervical ganglion
-Superior cervical ganglion cells project to the pineal gland
-pineal gland secretes melatonin
-melatonin reaches SCN via blood

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26
Q

What inhibits the retino-hypothalamo-pineal pathway?

A

LIGHT

  • when there is light there is no synthesis of melatonin from the pineal gland as SCN sends inhibitory projections to paraventricular nucleus (PVN); once PVN is inhibited everything else behind it is inhibited
  • no stimulation of pineal gland and thus no production of melatonin
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27
Q

When you’re stressed your sympathetic system is overactive and you have a hard time falling asleep. Why is this?

A

there is opportunity for anything that impacts our cervical sympathetic system to impact the secretion and synthesis of melatonin

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28
Q

What are the functions of melatonin?

A
  • Melatonin generation by the pineal gland, which peaks during the nighttime hours, induces physiological changes that promote sleep, such as decreased body temperature and respiration rate. During the day, melatonin levels are low because large amounts of light are detected by the retina.
  • melatonin can help regulate the secretion of other hormones
  • it will also impact the SCN which also has a lot of receptors
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29
Q

What are some condition affecting circadian rhythm of sleep?

A

jet lag

  • conflict between internal biological clock and time zone shift in light/dark phase
  • because the body finds it easier to delay sleep than to advance it, eastward travel is more problematic

shift work disorder “night owl”

  • conflict between internal clock and work hours
  • body never fully adjust to reverse cycle

delayed sleep phase syndrome

  • most common in adolescents and young adults
  • most alert, productive and creative at night
30
Q

What is nonREM sleep?

A

when we have the restful, the type of sleep . you associate with the body rejuvenating itself

31
Q

What are the 3 stages of nonREM sleep?

A

N1
N2
N3

32
Q

What is REM sleep?

A
  • stage of sleep we associate with dreams; sleep that resembles the awake state
  • also called rapid eye movement
33
Q

How do you determine the stage of sleep someone is in?

A

-perform a polysomnography
and see the dominant wave form to determine the stage of sleep

-encompases . the electroencephalograph (measuring brain activity), electromyograph (measuring muscle activity), and electrooculography (measuring eye movement)

34
Q

Low amplitude, high frequency waves in the awake person are what kind of waves?

A

beta waves

35
Q

Low amplitude, high frequency waves in the sleeping person are what kind of waves?

A

delta waves

36
Q

Describe the EEG, EMG, and EOG in awake state.

A

EEG: beta waves dominate

EMG has lots of muscle activity

EOG has eye movements

37
Q

Describe the EEG, EMG, and EOG in REM sleep.

A

EEG looks similar to the awake person with beta waves dominating

EMG not much muscle activity

EOG has eye movements

38
Q

Describe the EEG, EMG, and EOG in slow wave sleep (deep sleep).

A

EEG: delta waves dominate
EMG little muscle activity
EOG: no eye movement

39
Q

What is the differentiating study to use to differentiate REMS and awake state?

A

electromyograph

40
Q

Describe the different type of brain waves.

A

beta: 14-40 Hz, <20 uV; occurs during awake mental activity and REM sleep
alpha: 8-13 Hz, 25-100 uV; occur during quiet, inattentive wakefulness, eyes closed
theta: 4-7 Hz, 20 uV; occur during initial stages of slow wave sleep; occur during emotional stress, disappointment, frustration, degenerative brain states; getting into the N1 phase of sleep; more prominent when individuals are in a very high emotional charged state
delta: 0.5-3Hz; occurs during later stages of slow wave sleep (deep sleep); occurs with extensive brain disease, subcortical transection separating thalamuc from cerebral cortexl we’re n a real nice deep sleep; N3 phase of sleep

41
Q

What stage of sleep actually rejuvenates your body?

A

slow wave sleep dominates by delta waves

42
Q

What is a sleep histogram?

A

????46:52

43
Q

What is sleep latency?

A

how long it takes for you to fall asleep

-amount of time it takes to fallasleepafter lights off (norm=10-20 min).

44
Q

Normal sleep pattern contain how many sleep cycles?

A

4-5 cycles

45
Q

The 1st REM sleep occurs how many minutes after sleep onset?

A

between 90-120 minutes

46
Q

What happens to the duration of REM as time increases?

A

-it increases (why i be having weird dreams when i go back to sleep after a restful sleep)

47
Q

What happens to the duration of SWS (deep sleep) as time goes on?

A

decreases

48
Q

What is REM important for?

A
  • important for memory (making new connections and strengthening synapses)
  • important for emotional stability
49
Q

What is the condition called when an individual into REM sleep early on and don’t go into slow wave sleep?

A

narcolepsy

-sleep disorder characterized by excessive sleepiness, sleep paralysis, hallucinations, and in some cases episodes of cataplexy (partial or total loss of muscle control, often triggered by a strong emotion such as laughter)

50
Q

What is REM latency?

A
  • how long it takes you to go into REM sleep

- time from the sleep onset to the 1st REM epoch

51
Q

Describe stage I of sleep (N1): drowsy period.

A

predominance of theta waves with some alpha waves in the background

  • transition from alpha to theta waves on EEG (>50% theta frequencies)
  • light sleep (low arousal threshold), easily responsive to sounds
  • hypnic myoclonus may occur
  • decreased muscle tone
  • eyes make slow rolling movements
  • typically last from 1-7 minutes
52
Q

Describe the stage II sleep (N2): light sleep.

A

theta waves predominate in the EEG

sleep spindles

  • (10-15 Hz, 0.5-2 sec)
  • brief bursts of high frequency activity
  • rapidly increase in amplitude and then rapidly decays

K complexes:

  • sharp high voltage waves
  • triggered by sensory stimulus

Lasts 10-25 minutes in first cycle
-5-15 in following cycles

Eye and body movements are minimal

53
Q

Describe stage III and IV (N3): SWS/deep sleep.

A
  • fewer sleep spindles and K complexes
  • high voltage DELTA waves account for ≥ 20% of EEG
  • high stimulus threshold for arousal
  • no eye or body movements
  • respiratory rate, heart rate, blood pressure and temperature are all reduced and rhythmic
  • theoretically the restorative phase of sleep
  • about 20% of total sleep time
  • lasts 20-40 minutes in the 1st and 2nd cycles
54
Q

Describe REM/paradoxical sleep.

A
  • EEG shows mixed pattern including beta waves
  • rapid eye movements
  • loss of muscle tone (atonia); paralysis of large skeletal muscle groups (with exception of eye, middle ear, and respiratory muscle)
  • vivid, emotional dreams
  • penile and clitoral erection (clinically important for impotence)
  • increases in body temperature and metabolic rate (compared to NREM)
  • irregular and increased BP, HRm respiration
  • each episode lasts 5-50 min
  • constitutes 20-25% of total sleeping time
55
Q

What are ponto-geniculo-occipital (PGO) waves in REM sleep?

A
  • PGO waves propagate from the pons into the lateral geniculate nucleus of the thalamus (LGN) and then into the primary visual cortex
  • appearances of PGO waves are most prominent right before onset of REM and continue throughout REM sleep

may be intricately involved with eye movement

may account for visual imagery observed during REM sleep

56
Q

How do we transition from nonREM to REM sleep?

A

VLPO inhibition of cholinergic cells is released

during awake you have all these activating nuclei (cholinergic cells, locus coeruleus, raphe, histamine, orexin)

but cholinergic cells in midbrain and nucleus basalis are inhibited during slow wave sleep but are turned on again during REM sleep

57
Q

How is inhibition from preoptic area altered during REM sleep?

A

Inhibition of midbrain reticular formation (MRF) cells is decreased.

Inhibition of Lateral Hypothalamus
(LH), Tuberomammillary N.
(TMN), Locus Coeruleus
(LC) and Raphe Nuclei
(RN) is increased.

midbrain reticular formation (MRF)

58
Q

What is sleep efficacy?

A

percentage of total time in bed actually spent in sleep (norm=>85%)

59
Q

Describe the developmental distribution of sleep stage (NREM and REM) for the following:

  • in utero
  • newborn
  • adult
A

remember NREM= N1, N2, N3

in utero: NREM (0%); REM (100%)

newborn: NREM (50%); REM (50%)
adult: NREM (75%); REM (25%)

60
Q

What is the sleep need by age?

A

Newborns (0-2 months): 15-18 hours

Infants (3 months to 1 year): 14-15 hours

Toddlers (1 to 3 years): 12-14

Preschoolers (3 to 5 years): 11-13 hours

School-aged children (5 to 12 years): 10-11 hours

Teens and preteens (12 to 18 years): 8.5-9.25 hours

Adults (18 and older): 7-9 hours

61
Q

What are sleep changes with normal aging?

A
  • fragmented sleep
  • reduced REM sleep
  • increased N1 and N2 sleep
  • decreased N3 sleep
  • decreased circadian rhythm (sleep is not consolidated in the night time so they tend to take naps during the day)
62
Q

What are some sleep disorders?

A
  • insomnia
  • hypersomnia
  • sleep apnea
  • narcolepsy
  • REM sleep behavioral disorder
  • restless leg syndrome
  • night terrors
  • somnambulism (sleepwalking)
63
Q

What is insomnia? What are its symptoms, causes, and treatments?

A
  • the inability to fall asleep or stay asleep
  • Fatigue and daytime sleepiness
  • Moodiness, Irritability or anger
  • Lack of concentration and poor memory
  • Frequent mistakes/accidents at work or while driving

Incidence: 30-50% general, 10% chronic

Causes:

  • Major depression, stress, illness
  • Caffeine and other stimulants
  • Altered circadian rhythm (jet lag, night shift)

Treatments:

  • Melatonin receptor stimulant (Rozerem)
  • Benzodiazepines (Valium, GABA enhancer), Zolpidem
  • Antihistamines (Benadryl)
64
Q

What is sleep apnea? Incidence?

A

cessation of breathing during sleep lasting for more than 10 seconds at a time

Affects about 4% of population

65
Q

What are the two types of sleep apnea? What is the difference?

A

obstructive vs. central

obstructive: more common
- Palate or airway shape that causes narrower /more collapsible airway
- Large tonsils and adenoids in children that can block the airway
- Large tongue, which may fall back and block the airway
- Obesity

central:

  • high CO2 and low O2 and O2 and CO2 chemoreceptor insensitivity which do not trigger respiratory centers
  • Neurodegenerative disorders
  • Cervical spine injury
66
Q

What is the treatment for sleep apnea?

A
  • weight loss
  • continuous positive airway pressure(CPAP): pushing high pressure air into your nose to keep the airway open; uncomfortable
  • respiratory stimulants for purely central apnea
67
Q

What is narcolepsy? What are symptoms and treatments?

A

Presentation of symptoms:

  • Excessive daytime sleepiness
  • Cataplexy: complete loss of muscle tone while they’re conscious; triggered by emotion; usually limited to the muscles of the face, arms, and legs
  • –Atonia w/o loss of consciousness
  • –Triggered by excitement, stress
  • Hypnagogic hallucinations: right before you’re about to fall asleep you start seeing things that are not there
  • Sleep paralysis (characteristics of REM sleep intruding when you’re awake)
  • when these individuals go to sleep they go right into REM sleep

Incidence is 1 in 2000

  • Causes:
  • –Autoimmune destruction of orexinergic cells: no orexin cells as your immune cells are degenerating these cells; orexin plays a role in your feeding patterns (cells will decrease they’re firing when you’re full); is part of the arousal system and so will cause sleepiness when not there
  • –Genetic mutation of HLA complex (immune function)

Treatment:

  • CNS stimulants (Ritalin, Modafinil, amphetamines)
  • Gamma-hydroxybutyrate/ sodium oxybate: for cataplexy ( increases SWS)
68
Q

What is REM sleep behavior disorder?

A

Presentation:

  • Sleep talking, yelling, limb movements during sleep
  • Dream enactment behavior

Incidence

  • 0.38-0.5% of general population
  • 87-90% men
  • Onset > 50 yrs.

Causes

  • Associated with Parkinson’s, MSA & Lewy body dementia; associated with dopamine and iron deficiency
  • Muscle atonia not concurrent with REM sleep
  • Narcolepsy or brainstem tumors
  • Antidepressants, pesticide exposure

Treatment:

  • Injury proof bedroom environment
  • clonazepam- controls motor behaviors and unpleasant dreams in 90%
  • Melatonin and pramipexole
69
Q

What is resting leg syndrome and what are symptoms?

A

Presentation:

  • Unpleasant prickling or tingling in the legs (Paraesthesias)
  • Triggered by rest, relaxation or sleep
  • Relieved by movements (85%)
  • Periodic limb movement disorder (PLMD)

some somatosensory dysfunction here

Incidence:

  • 5–15 % of Americans
  • Increases with age

Causes:

  • 60% are Familial
  • Pregnancy, kidney failure
  • Dopamine dysfunction and iron deficiency in brain

Treatment:

  • Iron supplements and dopamine agonists
  • Benzodiazepine
70
Q

What are night terrors?

A

more common in males
Presentation of Symptoms:
-Awaken with extreme anxiety and panic
-Marked tachycardia and deep, rapid respirations
-Within first 2 hrs. of sleep during SWS
-Lasts 1-10 min. and not recalled on waking
-sleep walking (somnambulism)

Incidence:

  • Affects 6% of Children 3-12 yrs.
  • <1% of adults
  • Runs in families

Causes: stress, fever, medication, sleep deprivation

Treatment: Diazepam suppresses deep sleep

ask them about it later they will have no recollection (what are you talking about?)

71
Q

What are healthy sleep habits?

A
  • 7-8 hrs each night.
  • Keep a regular sleep/wake pattern.
  • Develop a 30 min. relaxing pre-bedtime routine.
  • Decrease exposure to bright light in the evening.
  • Avoid electronic device screen time ≥ 1 hr. before bedtime.
  • Avoid heavy meals at ≥3 hrs. before bedtime.
  • Avoid caffeine, alcohol & nicotine ≥3 hrs. before bedtime.
  • Exercise in morning or early afternoon.

Chika- SF2 (63 decks)

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