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NEURO 210 > Topic 18: Sleep and Sleep Disorder > Flashcards

Topic 18: Sleep and Sleep Disorder Flashcards

1
Q

What types of clinicians are involved in treating sleep disorders?

A

family physicians

respirologists/pulmonologists (sleep apnea)

psychiatrists (psychological causes)

neurologists

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2
Q

What is the organization of sleep?

A

sleep is a continuum, no black and white distinction between some stages, blurring of continuum is the disease

there are changes observable at the scalp using EEG: used to define sleep stages

neurophysiology underlying some specific wave forms on EEG have been determined

certain sleep disorders occur during specific sleep stages

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3
Q

How does EEG measure sleep stages?

A

noninvasive measure neurophysiology

changes in voltage measured on the scalp

EEG rhythms named according to the frequency of the activity (number of waves in 1 second of recording)

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4
Q

What are delta waves?

A

0-3.99 Hz

slow waves: 0.5 - 2 Hz

critical stage

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5
Q

What are theta waves?

A

4-7.99 Hz

wakefulness

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6
Q

What are alpha waves?

A

8-13 Hz

quiet wakefulness (just before falling asleep)

decreased altertness

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7
Q

What are beta waves?

A

> 13 Hz

wakefulness

associated with medication like benzos

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8
Q

What are the three basic states of sleep?

A

awake

nREM sleep

REM sleep

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9
Q

How is being awake classified?

A

presence of alpha rhythm

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10
Q

What is nREM sleep?

A

N1: alpha “drop out”

N2: sleep spindles and K complexes

N3: slow wave sleep (SWS, previously 3 and 4)

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11
Q

What is REM sleep?

A

no muscle tone (chin electromyography - EMG) and rapid eye movements

loss of all movement except for eyes

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12
Q

What is the relationship between nREM and REM sleep in the sleep cycle?

A

NREM and REM sleep alternate during sleep, with each cycle lasting for approximately 90-100 minutes

4-6 cycles are noted during a normal sleep period

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13
Q

What is the N1 stage of sleep?

A

alpha drop out

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14
Q

What is the N2 stage of sleep?

A

sleep spindles –> increased seizure risk, in centro-temporal regions, hypersynchrony increases risk for seizure

EEG frequency of 11 to 16 Hz (usually 12 to 14 Hz)

fast end of alpha band

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15
Q

What are reticular neurons?

A

inhibitory input to relay nuclei via GABA-B receptors

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16
Q

What are relay neurons?

A

excitatory input to cortex

T-type calcium channels in relay neurons

unique because they possess capability for “low-threshold depolarization” which is depolarization from a hyperpolarized state

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17
Q

How are reticular and relay neurons involved in seizures in nREM sleep?

A

in non-REM sleep, there is an increase in reticular neuron activity, which hyperpolarizes relay neurons via GABA-B receptors

this hyperpolarization activates T-type calcium channels which allows low-threshold depolarization and BURST mode thalamo-cortical activation of relay neurons, this generates sleep spindles

this circuit is pathologically active in absence seizures: excessive and synchronous activity from reticular neurons, results in BURST mode thalamo-cortical activation by relay neurons

this generates 3 per second spike-wave seizure

ethosuximide acts as a T-type calcium channel antagonist, hence it’s clinical effect on absence seizures (only)

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18
Q

What are benzodiazepines associated with in relation to sleep?

A

increased stage N2 sleep

increased spindle activity

possibly due to increased GABA-ergic signalling

GABA agonist

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19
Q

What is rapid eye movement sleep?

A

rapid eye movements

lack of EMG muscle activity

“awake” looking EEG: absence of sleep morphologies or slow waves, considered a “lighter” phase of sleep

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20
Q

What are general characteristics of the sleep stages?

A

REM sleep increases throughout the night

slow wave sleep is predominately in U1 and U2, but is gone as the night progresses

N2 seizures can occur at any time

21
Q

What neurotransmitters promote wakefulness and sleep?

A

excite: glutamate –> promote wakefulness

inhibit: GABA –> promotes sleep

22
Q

What structures secrete glutamate?

A

parabrachial/precoeruleus nuclei (pons)

supramammillary nuclei (midbrain) –> to a lesser extent

23
Q

Where does excitatory transmission from the brainstem nuclei travel to?

A

caudally to motor neurons in the spinal cord

rostrally to neurons throughout the cortex

thalamo-cortical transmission primarily supported via a “dorsal pathway” using acetylcholine is also required to maintain consciousness

24
Q

What does neurotransmitter activity look like in non-REM sleep?

A

we have inhibitory synaptic transmission from the VLPO (ventro-latera preoptic nucleus) to all of the brainstem nuclei important for wakefulness

thus, there is inhibition of the normal pathway for wakefulness

25
What does neurotransmitter activity look like in REM sleep?
during REM sleep, REM-on neurons in the PendunculoPontine Tegmentum (PPT) and Lateral Dorsal Tegmentum (LDT) have: excitatory connection to the thalamus, resulting in an "awake" looking EEG (absence of slow waves, sleep spindles, or other sleep morphologies), dream, recollect excitatory connection to glycinergic neurons in the medial medulla which inhibit motor neurons in the spinal cord so that the muscles of the body don't move in response to all this activity (muscle atonia), inhibit skeletal muscles
26
What are some other neurotransmitters involved in sleep?
hypocretin (orexin) adenosine melatonin
27
What is hypocretin (orexin)?
produced by cells in the hypothalamus thought to provide inputs to various nuclei important in sleep to support these and "stabilize" sleep states
28
What are the functions of hypocretin (orexin)?
promotes wakefulness help "stabilize" sleep/wake episodes involved in maintenance of skeletal tone during wakefulness
29
What is adenosone?
mediator of sleepiness after prolonged wakefulness thought to promote the transition to SWS by inhibiting basal forebrain neurons (important in the maintenance of wakefulness) caffeine is an adenosine receptor antagonist
30
What is melatonin?
light stimulates SCN in hypothalamus and thereby inhibits melatonin release from pineal darkness releases the pineal from SCN inhibition, resulting in melatonin release thereby linking our circadian rhythm to the light and dark cycles of day of light
31
What are symptoms of abnormal sleep?
excessive daytime sleepiness: falling asleep when they should be wakeful insomnia: having difficulty falling asleep or getting up to early abnormal movements during sleep awakenings: children it's parasomnias, adults it's dementia abnormal breathing during sleep sleep paralysis: first symptom of narcolepsy hallucinations (hypnogogic [while falling asleep] and hypnopompic [upon awakening])
32
What things are looked at when examining sleep history?
symptoms talk to bed-partner medications and habits (caffeine use, alcohol and tobacco use) other medical illnesses family history
33
What is insufficient sleep syndrome?
most common cause of sleepiness daily sleep requirements range from person to person, and over lifetime one study found 19.5% reported having moderate excessive sleepiness and 11% reported severe excessive sleepiness; majority associated with insufficient sleep adults in the US average less than seven hours of sleep per night (nearly 2 hours less than in 1980); 1/3rd get less than six hours per night
34
What is the relationship between insufficient sleep and your body?
chronic sleep deprivation can lead to weight gain, high blood pressure, and diabetes shift work is also associated with weight gain obese children have been found to get less sleep than normal weight children
35
What is the relationship between obese children and sleep?
sleep is one of the most powerful predictors of obesity in prepubertal children suspected mechanisms include altered activity of various hormones, such as leptin, ghrelin, and cortisol
36
What is the relationship between sleep and your brain?
sleep deprivation is one of the most potent triggers for breakthrough seizures in patients with epilepsy one night of sleep deprivation impairs hippocampal functions; results in a deficit in the ability to commit new experiences to memory restricting sleep by just one hour per night for 6 nights results in statistically decline in performance in tests of working memory in University students, insufficient sleep is strongly associated with mental health disorders
37
Why do we sleep less?
spending more hours per day on electronic devices associated with shorter sleep duration at all ages may be what drives association between screen time and obesity still true when accounting for levels of physical activity
38
What is obstructive sleep apnea syndrome?
second most common cause of sleepiness temporary pause in breathing while sleeping occurs as muscle tone diminishes during sleep and airway collapses person tries to make breathing efforts against closed airway and eventually awakens with effort associated with obesity and smoking increased risk of heart attack and stroke due to high blood pressure best treated with CPAP machine
39
What is the practical approach to improving sleep?
increasing exercise and resulting weight loss (effect on obstructive sleep apnea) no caffeine use after noon smoking cessation sleep hygiene (not using electronics in bed)
40
What are the symptoms of narcolepsy?
excessive daytime sleepiness with sleep attacks cataplexy (sudden temporary loss of muscle tone with no loss of awareness) sleep paralysis hallucinations hypnogogic: upon falling asleep hypnopompic: upon awakening
41
What are the causes of narcolepsy?
associated with low levels of hypocretin (orexin), the neurotransmitter important for stabilizing sleep-wake transitions as a result, there are frequent and inappropriate transitions between sleep and wakefulness intrusion of REM phenomena into wakefulness in narcolepsy, the REM-on neurons (in dorsal pathway) turn on inappropriately (due to loss of hypocretin) and cause the paralysis of REM sleep during wakefulness; resulting in cataplexy
42
What are abnormal movements during sleep?
timing of events during sleep can be used to classify and characterize by history and polysomnography sleep-wake transition movements disorders of arousal REM sleep behavior disorder, nightmares, and sleep paralysis
43
What is restless leg syndrome?
earliest period - when attempting to fall asleep uncomfortable sensations in legs with an urge to move legs, relief from sensations when they move their legs family history in many patients can be associated with iron-deficiency anemia and pregnancy treatable depending on severity of symptoms: iron supplementation, GABApentin, dopamine agonists
44
What are parasomnias?
defined as abnormal movements or behaviors intruding into sleep classified based on what stage of sleep they originate from
45
What are disorders of arousal from non-REM sleep?
confusional arousals: confused, think they are in unfamiliar surroundings, is it a seizure? sleep terrors and sleepwalking: slow wave sleep, starts in childhood
46
What are REM parasomnias?
REM sleep behavior disorder
47
What are sleep terrors?
arise out of slow-wave sleep more common in kids can be brought on by stress, sleep deprivation, alcohol and fever associated with sleep-walking and confusional arousals strong family history different from nightmares (REM sleep)
48
What is REM Sleep Behavior Disorder?
loss of REM atonia occurs early in the morning act out dreams; kick and yell in sleep more common in elderly associated with Parkinson's disease and dementia with Lewy bodies
49
What are the neuronal causes of REM sleep behavior disorder?
there is degeneration of glycinergic neurons in the medulla resulting in loss of REM atonia and dream enactment behavior

NEURO 210 (23 decks)

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