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Neuro 210 > The Neurology of Sleep > Flashcards

The Neurology of Sleep Flashcards

1
Q

What are 4 theories of sleep function?

A
  • recuperative theories (sleep is used to maintain homeostasis and for recovery)
  • circadian theories: everyone sleeps due to internal circadian rhythm and it would not be efficient for humans to be awake at night
  • developmental theories: sleep changes form as we get older
  • learning theories: sleep changes when we learn something and sleep deprivation causes deficits in our ability to gain long term memory
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2
Q

What are 2 main characteristics on the organization of sleep?

A
  • sleep is a continuum

- EEG criteria artifically defines sleep stages (every stage of sleep occurs at once, but in different ratios)

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3
Q

What are sleep stages broken up into?

A

2 independant states (do not occur at the same time):

  • REM SLEEP
  • NON-REM SLEEP (NREM)

and
awake

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4
Q

what are the 4 divisions of nrem sleep?

A

N1, N2, N3

  • N3 = stages 3 and 4 which is the deepest stages of sleep/slow wave sleep (SWS)
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5
Q

At what times and how often do nrem and REM sleep alternate?

A
  • NREM and REM sleep alternate with each cycle lasting 90-100 mins with 4 to 6 cycles per night
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6
Q

What is the pattern of non-rem/sws sleep and Rem sleep

A

the first 2 cycles as we sleep are dominated by Slow wave sleep (SWS)

  • REM sleep increases from the first to the last cycle and towards the end of the night / longest end of the night
  • the first third of a normal sleep episode is dominated by SWS and the last third is dominated by REM sleep
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7
Q

How are EEG waves used to name sleep rhythms and define stages?

A

EEG rhythms are named according to the frequency of the activity going on at one second of record (# of waves/second)

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8
Q

what is one epoch?

A

during sleep, we define stages by what happens in one epoch which is 30 seconds of recording

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9
Q

What are the EEG frequencies of sleep rhythm?

A
  1. delta ( less than 4hz/s) –> deep sleep
  2. Theta (4-7 hz) –> somewhat going to deep sleep
  3. alpha (8-13hz) –> closed eyes resting state
  4. beta (greater than 14hz) –> awake
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10
Q

What is the most common clinical use for the sleep stages?

A

to identify and assess which stage people have problems by lookikng at scoring criteria and seeing what type of waves or activity was occuring during that stage of sleep

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11
Q

What is the EEG activity shown in awake state?

A

disorganized, low voltage, activity (low voltage/high freuqnecy)

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12
Q

what is the EEG activity shown in nREM sleep?

A

eeg becomes organized, in SWS we see high voltage, low frequency and slow activity

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13
Q

What is the EEG activity shown in REM sleep?

A

“awake” looking EEG except with no muscle tone and very rapid eye movements

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14
Q

When does dreaming occur and what kinds of dreams occur in NREM vs REM sleep?

A

dreaming occurs in both REM and NREM stages

  • In REM, dreams are really emotional and have narrative or a plot, vivid, bizarre
  • external stimuli can also be encorperated into dreams
  • dreams that we remember when we wake up in the morning are due to the long REM periods we have before we wake up which allow us to remember our dreams
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15
Q

How does sleep change during the course of development?

A
  1. time spent in REM sleep is greatest before birth and decreases with age
  2. SWS appears at 4-5 months of age and increases into adulthood, and then begins to decline w age (increases in teens)
  3. sleep requirements diminish throughout life
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16
Q

What happens to our brains when we are awake?

A

everything in our brain is firing and excitatory

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17
Q

What happens to our brains during NREM sleep?

A

EEG becomes organized, and looks more synchronized

  • everything starts to become inhibited
  • reduced firing
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18
Q

What happens to our brains during REM sleep?

A
  • a combination of excitatory connections in brain and inhibitory connections (mainly in the motor system and spinal cord)
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19
Q

What is hypocretin/Orexin?

A
  • it is produced by cells in hypothalamus
  • found to be decreased in patients with narcolepsy
  • increases during third embryonic trimester and is highest at 4 months of life and then they lower and stablize as we age
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20
Q

Where does hypocretin get distributed in the brain and what does it do?

A

it gets distributed to alot of nuclei in the brain and helps stabilize their functions

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21
Q

what are 4 functions of hypocretin?

A
  1. promotes wakefulness
  2. helps maintain sleep/wake episodes (HcrtR1)
  3. involved in maintenance of skeletal tone during wakefulness (HcrtR2) –> makes sure u dont collapse or go into REM sleep when u are awake
  4. potential role in the process of sleep and wakefulness consolidation that occurs during early infancy
22
Q

What is Adenosine and its role in sleep?

A
  • adenosine is a mediator of sleepiness after prolonged wakefulness
  • thought to promote the transition to SWS by inhibiting basal forebrain neurons (which are imp for maintaining wakefulness)
  • caffeine and theophylline are adenosine receptor antagonists and reduce the effects of sleepiness by adenosine
23
Q

What is the role of melatonin in sleep?

A
  • melatonin is released from the pineal gland during times of darkness
  • it has a role in maintaining our circadian rhythm
24
Q

What is the brain processes involved in melatonin secretion?

A
  • when our retinas detect light, theres a signal that goes to the suprachaismatic nuclei and the paraventricular nucleus in the hypothaloamus and stops the pineal gland from producing melatonin

in the dark its reversed

25
Q

What are the 7 symptoms of abnormal sleep?

A
  1. excessive daytime sleepiness
  2. insomnia
  3. abnormal movements during sleep
  4. awwakenings
  5. abnormal breathing during sleep
  6. sleep paralysis
  7. hallucinations (hypnogogic and hypnopompic)
26
Q

What are 5 things to go over when asking about patient’s sleep history?

A
  1. symptoms
  2. talk to bed partner about what happens
  3. medications and habits
  4. other medical illnesses
  5. family history
27
Q

What are the characteristics of insufficient sleep syndrome?

A
  • most common cause of sleepiness

- not getting enough sleep every night (less than 7 hours typically)

28
Q

what are some negative consequences associated with insufficient sleep syndrome? (2)

A
  • chronic sleep deprivation can lead to weight gain, HBP and diabetes
  • one night of sleep deprivation impairs hippocampal function and result in a deficit in the ability to commit new experiences to memory
29
Q

How does insufficient sleep syndrome affect obesity rates in children?

A
  • obese children have been found to get less sleep than normal weight children
  • sleep is one of the most powerful predictors of obesity in prepubertal children
  • suspected mechanisms include altered activity of various hormones like leptin, ghrelin and cortisol
30
Q

What are the 4 symptoms of narcolepsy?

A
  1. excessive daytime sleepiness with sleep attacks (overwhelming urge to sleep despite all efforts)
  2. cataplexy (sudden temporary loss of muscle tone with no loss of awareness as if it occurred in REM)
  3. sleep paralysis (waking up and being paralyzed still from REM inhibitors)
  4. hallucinations (can be hypnogogic –> upon falling asleep or hypnopompic —> upon waking up)
31
Q

How does hypocretin/orexin levels effect narcolepsy?

A
  • through frequent and innapropriate transitions between sleep and wakefulness
  • intrusion of REM phenomena into wakefulness
  • loss of sleep/wake episode maintenance
  • loss of skeletal tone maintenance during wakefulness
32
Q

What is obstructive sleep apnea syndrome?

A
  • second most common cause of sleepiness
  • temporary pauses in breathing while sleeping that wakes the person up
  • occurs usually because of loss in muscle tone during sleep and airway collapsing
  • associated with obesity and snoring
  • neck tissue falls on pathways and blocks airways
33
Q

What is a negative consequences of sleep apnea syndrome? how is sleep apnea treated?

A

increased risk of heart attack and stroke

  • treated using CPAP machine
34
Q

What are two types of conditions where theres abnormal movements during sleep?

A
  1. restless legs syndrome

2. parasomnias (like sleep terrors and REM sleep behavior disorder)

35
Q

What is restless Legs syndrome? when does it occur and why?

A
  • it is uncomfortable sensations in legs with an urge to move legs
  • gets worse in the evening
  • family history in many patients
  • can be associated with iron deficiency anemia and pregnancy
  • periodic leg movements of sleep is seen in patients
  • can be treatable but depends on symtomps
36
Q

What are parasomnias?

A

defined as abnormal movements or behaviors intruding into sleep
- they are clssified based on what stage of sleep they originate from

37
Q

What is a parasomnia that occurs during REM sleep?

A

REM Sleep Behavior Disorder

38
Q

what is a parasomnia that occurs during SWS sleep? (3)

A
  1. sleep terrors
  2. sleep walking
  3. confusional arousals
39
Q

What occurs during REM sleep behavior disorder?

A
  • loss of REM atonia (loss of paralysis during REM)
  • acts out dreams and kicks and yells in sleep during REM
  • more common in eldery with dementia and parkingson’s disease
  • individuals who are more vulnerable to those diseases often show these signs before they are diagnosed years later
40
Q

What are sleep terrors?

A
  • arises out of SWS
  • more common in kids and normal in kids
  • can be due to stress, sleep deprivation, alcohol and fever
  • associated with sleep walking, and confusional arousals (getting up to get food while still in SWS)
  • strong fam history
  • different from nightmares (bc nightmares occur in REM sleep)
41
Q

What are the symptoms caused by post concussion syndrome?

A

headaches, decreased attention, mood disturbance and sleep disturbance

42
Q

What are 3 ways to characterize sleep disturbances in mild traumatic brain injury?

A
  1. reduce sleep efficiency (get to bed at the right time but amount actually sleeping is low)
  2. increased sleep onset latency
  3. increased time awake after sleep onset
43
Q

What are sleep disturbances associated with in mild traumatic brain injury?

A
  1. anxiety/depression
  2. pain
  3. slowed information processing
  4. need for increased effort in performing tasks
44
Q

What is the association between melatonin in patients with mild traumatic brain injury?

A

have reduced evening melatonin production and may indicate disruption to circadian regulations of melatonin synthesis

45
Q

What kind of association is it between sleep and headache disorders?

A

associations between sleep and migranes and cluster headaches

46
Q

How does sleep effect headaches?

A

in migrane patients, sleep disturbances are commonly reported to trigger attacks and has been associated with disease chronification and is used as abortive mechanism (people with migranes like to sleep alot to get rid of it)

47
Q

How does headache affect sleep?

A

results in imbalance in sleep-wake regulations (people wake up more when they have headaches

48
Q

What are brain regions that are shared between headaches and sleep?

A

shared neural pathways:

  • trigemnial pain signalling networks converge at multiple levels with the neural netowrks regulating arousal and sleep
  • presence of fatigue as common pemonitory symptom in migrane suggests that theres a disruption of hypothalamic networks (since its connected with sleep)
  • the TCC has connections to the dura and blood vessels in the brain and gives out inflammatory mediators on blood vessels and affects all areas of the brain
  • the sleep centers and headache areas are controlled by top-down processing (cortex controls it)
  • the same key brainstem nuclei play a role in headache and arousal
  • hypothalamus is the master circadian pacemaker which is implicated in headache disorders
49
Q

How is migrane related to light and melatonin?

A

migrane is light sensitive

- connections from retina goes to parametric nucleus in melatonin secretions and neurons fire excessively in migranes

50
Q

What is the role of adenosine in headaches and sleep?

A
  • caffeine can be analgesic (make headaches better) or precipitate (make it worse) for migranes
  • A1 agnoists (excitatory) can inhibit trigeminovascular nociceptive afferents in experimental models
  • genetic polymorphism of A2 receptor (inhibitory) linked to migrane and auras
  • increase plasma adenosine levels during migrane attacks make individual feel sleepy
  • adenosine demonstrated to trigger migrane in susceptible individuals
51
Q

How does meltaonin play a role in both headache and sleep?

A
  • altered melatonin secretion seen in cluster headaches
  • melanonin alterations also seen in migrane
  • melatonin plays a benefit in both cluster and migrane headaches
52
Q

How does orexin/hypocretin play a role in both headaches and sleep?

A
  • mainly in narcoleptics, it increases the risk of a migrane 2-4 folds (having low hypocretin/orexin)
  • orexin neurons intrinsically linked to key brainstem and diencephalic areas activated udring eadache attacks

Neuro 210 (12 decks)

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