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)
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
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
4
Q
What do electromyograms (EMG) and electroencephalograms (EEG) do?
A
help discern the current state of a person
5
Q
What do EMGs measure?
A
muscle tension
6
Q
What do EEGs measure?
A
brain activity
- electrodes placed on scalp record electrical activity of the brain (mostly from the cortex)
7
Q
How do EMGs and EEGs both measure activity?
A
using amplitude and frequency measurements
8
Q
What does an increase in amplitude mean in EMGs and EGGs?
A
more voltage
9
Q
What does an increase in frequency mean in EMGs and EGGs?
A
spikes happen more often
- hertz (Hz) = cycles per second
10
Q
What is sleep?
A
behaviourally quiescent state
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
12
Q
What is REM sleep characterized by?
A
- motor atonia – tone in antigravity muscles disappears during this stage of sleep
- dreaming
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
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)
15
Q
What is paradoxical sleep typified by?
A
rapid eye movement (REM)
- phasic periods include REM
- tonic periods do not
16
Q
What is paradoxical sleep more accurately defined by?
A
- behavioural sleep (quiescence)
- complete muscle atonia, and paradoxically, cortical activity typical of waking
17
Q
What does motor atonia during REM do?
A
prevents movement during dreaming
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
Describe the structure of the arousal system.
- 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
What does the arousal system stimulate?
frontal/cortical activation, maintaining wakefulness
27
What is major pathway 1 of the arousal system?
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
What is major pathway 2 of the arousal system?
- 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
How is major pathway 2 augmented?
- 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
When are orexin neurons most active?
during wakefulness
31
When are MCH neurons most active?
during REM sleep
32
When are basal forebrain (BF) neurons (including most cholinergic neurons) active?
during both wake and REM sleep
33
What is orexin also responsible for? How does it work?
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
What is a loss of orexin responsible for?
narcolepsy
35
How does sleep occur?
by active inhibition
- ventrolateral preoptic nucleus (VLPO) sends inhibitory signals to the ascending, arousal-promoting regions
- mainly GABAergic neurons
36
What is the flip-flop switch theory?
proposes that the nuclei of major pathway 2 (LC, Raphe, TMN) and VLPO inhibit each other to achieve sleep or waking
37
How does circadian control work?
- 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
Describe the homeostatic control that occurs.
as the energy carrier adenosine triphosphate (ATP) breaks down, adenosine builds up and triggers neuron activity in the ventrolateral preoptic nucleus (VLPO)
39
What is obstructive sleep apnea?
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
What are the symptoms of obstructive sleep apnea? (5)
- 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
What conditions can you develop as a result of obstructive sleep apnea? (6)
- hypertension
- diabetes
- cardiac arrhythmias
- strokes
- myocardial infarction development
- congestive heart failure
42
What is narcolepsy?
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
What molecule has low levels in narcoleptics and why?
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
What is the treatment for narcolepsy?
use of stimulants to prevent daytime sleepiness (such as histamine agonists)
