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PHRM 100 – APPP > APPP 06: Gross Anatomy of the CNS – Consciousness and Sleep > Flashcards

APPP 06: Gross Anatomy of the CNS – Consciousness and Sleep Flashcards

1
Q

What are the 2 types of waking (awake/conscious)?

A
  • active waking (aW)
  • quiet waking (qW)
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2
Q

What are the 2 types of sleep?

A
  • slow wave sleep (SWS) / non-REM sleep (NREM)
  • paradoxical sleep / rapid eye movement (REM) sleep
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3
Q

While waking and sleep, in general, are readily distinguishable, they are each split into subtypes that are best quantified by what?

A

muscle and brain activity, described as waves

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4
Q

What do electromyograms (EMG) and electroencephalograms (EEG) do?

A

help discern the current state of a person

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5
Q

What do EMGs measure?

A

muscle tension

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6
Q

What do EEGs measure?

A

brain activity

  • electrodes placed on scalp record electrical activity of the brain (mostly from the cortex)
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7
Q

How do EMGs and EEGs both measure activity?

A

using amplitude and frequency measurements

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8
Q

What does an increase in amplitude mean in EMGs and EGGs?

A

more voltage

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9
Q

What does an increase in frequency mean in EMGs and EGGs?

A

spikes happen more often

  • hertz (Hz) = cycles per second
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10
Q

What is sleep?

A

behaviourally quiescent state

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11
Q

What is slow-wave sleep characterized by?

A
  • decreased motor tone – still some tone, entering sleep
  • loss of awareness to surroundings
  • staged from light sleep to deep sleep by the pattern of rhythmic slow waves, indicating marked synchronization of neuronal firing
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12
Q

What is REM sleep characterized by?

A
  • motor atonia – tone in antigravity muscles disappears during this stage of sleep
  • dreaming
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13
Q

What are the stages of sleep?

A

4 stages of slow-wave sleep followed by an REM sleep stage

  • states of active inhibition of different arousal circuits in the brain
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14
Q

What are the 4 stages of slow-wave sleep?

A

stage 1: light sleep

  • eye movement slow
  • loss of awareness
  • easily awakened

stage 2: light sleep

  • heart rate slows
  • occasional high amplitude slow waves (delta)

stage 3: deep sleep

  • breathing slows, muscles relax
  • more delta waves

stage 4: very deep sleep

  • very deep, dreamless sleep
  • mostly delta waves

(sleepwalking occurs in slow wave sleep)

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15
Q

What is paradoxical sleep typified by?

A

rapid eye movement (REM)

  • phasic periods include REM
  • tonic periods do not
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16
Q

What is paradoxical sleep more accurately defined by?

A
  • behavioural sleep (quiescence)
  • complete muscle atonia, and paradoxically, cortical activity typical of waking
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17
Q

What does motor atonia during REM do?

A

prevents movement during dreaming

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18
Q

What is idiopathic rapid eye movement sleep behaviour disorder?

A
  • nocturnal dream enactment behaviour that occurs in REM and occurs every night – punching, kicking, falling out of bed, talking, screaming
  • some medications may promote this (antidepressants, beta blockers)
19
Q

What is the cause of idiopathic rapid eye movement sleep behaviour disorder?

A

loss of motor atonia – dysfunction in the lower brainstem nuclei that control REM sleep

20
Q

What happens to patients with idiopathic rapid eye movement sleep behaviour disorder?

A
  • overtime, they develop motor and cognitive dysfunction
  • associated with development of Parkinsons and Dementia and some forms of Narcolepsy
21
Q

What are the treatment options for idiopathic rapid eye movement sleep behaviour disorder?

A
  • melatonin
  • benzodiazepine – enhances activity of GABA
22
Q

What is the average sleep structure?

A
  • 16 hours awake, 8 hours of sleep
  • sleep progresses from slow wave sleep (4 stages) into REM – each forms a sleep cycle
  • each REM episode becomes longer towards the end of the sleep period
23
Q

Describe the sleep structure of infants.

A
  • 16 hours sleeping
  • most time in REM
  • can transition rapidly from wake into REM
24
Q

Describe how sleep changes with age.

A
  • slow-wave sleep is maximal in young children and declines with age
  • as we age, we spend less time sleeping, in particular slow wave sleep is progressively decreased
  • arousal from sleep is difficult in a young child in slow wave sleep or REM, but considerably easier in an elderly individual
25
Q

Describe the structure of the arousal system.

A
  • largely originates from a series of well-defined cell groups with identified neurotransmitters
  • includes a set of interconnected nuclei that are located throughout the brainstem
  • divided into two major pathways
26
Q

What does the arousal system stimulate?

A

frontal/cortical activation, maintaining wakefulness

27
Q

What is major pathway 1 of the arousal system?

A

arousal is promoted by acetylcholine-producing cell groups in two brainstem nuclei – pednuculepontine (PPT) and laterodorsal tegmental (LDT)

  • cholinergic neurons stimulate thalamocortical relay neurons (sensory information to the cortex)
  • neurons the PPT/LDT fire most rapidly during wakefulness and rapid eye movement (REM) sleep
28
Q

What is major pathway 2 of the arousal system?

A
  • originates from neurons in the upper brainstem and caudal hypothalamus
  • locus ceruleus (LC) norepinephrine system innervates prefrontal cortex and exerts a potent modulatory influence on executive functions
  • tuberomammillary nucelus (TMN) containing histamine (His) releasing neurons
  • raphe nuclei release histamine and serotonin – increase the excitability of cortical neurons and contribute to arousal
  • nuclei of major pathway 2 have the property of firing fastest during wakefulness, slowing down during SWS/NREM sleep, and stopping altogether during REM sleep
29
Q

How is major pathway 2 augmented?

A
  • basal forebrain (BF) projections to the forebrain are largely cholinergic (acetylcholine) with the minority being GABAergic
  • lateral hypothalamic (LH) neurons release melanin-concentrating hormone (MCH) or orexin
30
Q

When are orexin neurons most active?

A

during wakefulness

31
Q

When are MCH neurons most active?

A

during REM sleep

32
Q

When are basal forebrain (BF) neurons (including most cholinergic neurons) active?

A

during both wake and REM sleep

33
Q

What is orexin also responsible for? How does it work?

A

arousal – (in addition to norepinephrine, acetylcholine, histamine, and serotonin)

  • located in hypothalamus
  • sends excitatory projections to the entire CNS
  • innervates the LC, raphe, LDT, and PPT
34
Q

What is a loss of orexin responsible for?

A

narcolepsy

35
Q

How does sleep occur?

A

by active inhibition

  • ventrolateral preoptic nucleus (VLPO) sends inhibitory signals to the ascending, arousal-promoting regions
  • mainly GABAergic neurons
36
Q

What is the flip-flop switch theory?

A

proposes that the nuclei of major pathway 2 (LC, Raphe, TMN) and VLPO inhibit each other to achieve sleep or waking

37
Q

How does circadian control work?

A
  • superchiasmatic nucleus (SCN) receives information from the retina
  • signals to the pineal gland to control the secretion of melatonin which promotes sleep
  • this contributes to the change in the flip-flop switch by increasing the activity of the VLPO
38
Q

Describe the homeostatic control that occurs.

A

as the energy carrier adenosine triphosphate (ATP) breaks down, adenosine builds up and triggers neuron activity in the ventrolateral preoptic nucleus (VLPO)

39
Q

What is obstructive sleep apnea?

A

fragmented sleep at night due to partial (hypopnea) or complete (apnea) cessation of breathing for periods of 10 seconds or more

  • common cause of daytime sleepiness
  • due to reduced muscle tone in the pharynx and altered respiratory during sleep
  • apnea causes brief arousals from sleep in order to re-establish upper airway tone
  • about half of patients are obese
  • obstruction can be caused by large tonsils, treated with oral glucocorticoids or surgery
40
Q

What are the symptoms of obstructive sleep apnea? (5)

A
  • snore soon after falling asleep
  • snoring gets progressively louder until interrupted by an episode of apnea
  • followed by a loud snort and gasp to re-establish breathing
  • results in a much greater time in stage 1 sleep and marked reduction in slow-wave sleep
  • daytime sleepiness, reduced attention, increased automobile and industrial accidents, and generally decreased quality of life
41
Q

What conditions can you develop as a result of obstructive sleep apnea? (6)

A
  • hypertension
  • diabetes
  • cardiac arrhythmias
  • strokes
  • myocardial infarction development
  • congestive heart failure
42
Q

What is narcolepsy?

A

excessive daytime sleepiness

  • characterized by unwanted, sudden, and intrusive attacks of daytime sleep that can last from seconds to minutes
  • dream during these short naps
  • caused by intrusions of REM sleep while awake
  • hypnogogic hallucinations – usually visual, can be bizarre
43
Q

What molecule has low levels in narcoleptics and why?

A

orexin

  • primarily due to loss of orexin neurons
  • proposed that an autoimmune response that destroys orexin neurons underlies narcolepsy
  • also runs in families, suggesting a genetic predisposition
44
Q

What is the treatment for narcolepsy?

A

use of stimulants to prevent daytime sleepiness (such as histamine agonists)

PHRM 100 – APPP (23 decks)

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