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Physiology Exam 6 > 76 - Sleep > Flashcards

76 - Sleep Flashcards

1
Q

Alpha waves

A

(8 - 13 Hz)

a. associated with state of relaxed wakefulness in an adult with their eyes closed
b. prominent over occipital and parietal areas
c. EEG changes to beta rhythm if eyes open or in response to other sensory stimuli. Mental concentration such as that required to do arithmetic problems will also cause a change to the beta rhythm.

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2
Q

Beta waves

A

(13 - 30 Hz)

a. smaller amplitude than alpha waves
b. sometimes called desynchronized EEG
c. normally seen over frontal region
d. also found over other regions during intense mental activity

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3
Q

Theta waves

A

(4 - 7 Hz)

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4
Q

Delta waves

A

(0.5 - 3.5 Hz)

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5
Q

Which waves are associated with stages of sleep in a healthy adult?

A

Both theta and delta activity are associated with stages of sleep in a healthy adult

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6
Q

What are the stages of sleep?

A
  1. Stage 1 - transition awake – asleep; theta waves prominent
  2. Stage 2 - light sleep, K complexes and sleep spindles
  3. Stage 3 - moderately deep sleep some delta waves (more than 20% less than 50%)
  4. Stage 4 - deep sleep - delta waves more than 50% of period.

Note:

  • Stage 3 - 4 sleep sometimes grouped together as slow wave sleep or deep sleep or stage delta NREM sleep
  • Above 4 stages called Non - REM sleep.
  • REM or rapid eye movement sleep
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7
Q

Describe the awake to sleep transition

A
  1. Awake and alert with eyes open – beta waves
  2. Awake but relaxed with eyes shut – alpha waves
  3. Enter stage 1 sleep
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8
Q

Describe non-REM sleep

A
  1. Brain uses less oxygen than when awake or in REM sleep.
  2. decreased body temperature and metabolic rate
  3. decreased heart rate and blood pressure
  4. decreased respiratory rate
  5. Muscles relaxed but major postural adjustments made about every 20 minutes.
  6. Threshold for arousal increases as EEG wave frequency decreases. So it is harder to arouse sleeper in Stage 4 sleep than Stage 1.
  7. The pulsatile release of growth hormone (GH) is related to the sleep wake cycle with more than 70% of GH released during the first half (mainly slow wave sleep) of a person’s nightly sleep.
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9
Q

Describe REM sleep

A
  1. Also called paradoxical sleep since EEG similar to awake EEG. Other names active sleep and desynchronized sleep.
  2. PGO spikes (pontine - geniculate - occipital) associated with bursts of eye movements.
  3. Irregular heart beat and respiration. Penile erection in males, clitoral engorgement in women.
  4. Depressed muscle tone throughout body except for muscles moving eyes, and respiratory muscles. Intense postsynaptic inhibition of alpha motor neurons.
  5. REM dreams are longer, and more visual and emotional than the thought-like dreams of non-REM sleep.
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10
Q

How is REM sleep affected by alcohol?

A

REM rebound after suppression by alcohol, barbiturates or other REM suppressing drugs

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11
Q

How is REM affected during the onset of puberty in females?

A

At the start of puberty in females, there is pulsatile release of gonadotropin from the pituitary during REM sleep. At maturation pulses occur throughout the day.

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12
Q

Describe the normal sleep pattern in adults

A

Normal adult sleep pattern

a. Stage 4 sleep appears primarily in first half of sleep period
b. REM sleep does not usually occur until 90 minutes or more into sleep period.

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13
Q

What controls the sleep-wake cycle?

A

Circadian rhythmicity is under homeostatic regulation

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14
Q

Which nucleus of the hypothalamus is the “internal clock”?

A

Suprachiasmatic nucleus

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15
Q

Describe the role of the suprachiasmatic nucleus

A

• Circadian clocks help animals adjust their physiology and behavior to the 24 hour day-night cycle. Body rhythms are synchronized (or photoentrained) to the day/night cycle which changes with the seasons. There is a photopigment melanopsin in special retinal ganglion cells projecting to the SNC. These retinal ganglion cells depolarize in response to light and are probably responsible for setting the “master” biological clock in the SCN.

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16
Q

Where is melatonin synthesized and released?

A

Melatonin synthesis in the pineal gland is indirectly controlled by the suprachiasmatic nucleus.

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17
Q

What is the role of melatonin in sleep?

A

Melatonin is a sleep promoting neurohormone that is thought to help modulate the brainstem circuits that control the sleep-wake cycle.

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18
Q

What is epilepsy?

A

Epilepsy - disease characterized by tendency to have repeated seizures

19
Q

What are the classifications of epilepsy?

A

Several classification schemes for seizures and epilepsy

a. generalized seizure vs. partial (localized or focal) seizure
b. primarily generalized vs. secondary generalized

20
Q

What is grand mal epilepsy?

A

a. now called tonic - clonic seizures (new nomenclature)
b. patient losses consciousness during grand mal seizure
c. tonic period of increased muscle tone followed by
d. clonic period consisting of jerky movements
e. postictal state; period of confusion following the seizure that usually last ~ 5 to 30 minutes

21
Q

What is petit mal epilepsy?

A

a. now called absence seizures since transient loss of consciousness (usually just 5-10 seconds)
b. 3 per second spike and dome (or spike and wave) pattern seen on EEG during seizure
c. seizures begin in childhood and rarely persist through adolescence (Usually just in childhood for patients with normal intelligence and normal background activity on EEG)
d. Muscle tone is maintained so patient rarely falls.
e. Subtle motor manifestations such as eye blinking are common during the seizure.
f. no postictal state since full orientation found immediately after the seizure

22
Q

Grand mal and petit mal epilepsy are examples of which type of epilepsy?

A

Genealized epilepsy

23
Q

What are the two types of focal or partial epilepsy?

A

Simple partial or complex partial

24
Q

Describe a simple partial seizure

A

Simple partial seizures do not affect general consciousness.

• Example - Jacksonian motor seizures

25
Q

Describe a complex partial seizure

A

a. affect consciousness
b. usually in temporal lobe or frontal lobe
c. formerly called temporal lobe seizures or psychomotor seizures.
d. Verbal and/or motor automatisms can occur. Motor automatisms may be simple oral behaviors (such as lip smacking, chewing) or manual automatisms (patting, picking at clothing). Complex motor automatisms such as cycling movements of the legs may also occur.

26
Q

What are the symptoms of narcolepsy?

A

a. Sleep attacks - principal symptom; associated with excessive daytime sleepiness
b. Cataplexy - abrupt attack of muscle weakness and hypotonia triggered by an emotional stimulus
c. Sleep paralysis
d. Hypnagogic hallucinations - hallucinations at transitions between wakefulness and sleep
e. Sleep - onset REM
f. Decreased voluntary sleep latency

27
Q

What is the cause of narcolepsy?

A

Cause in humans – reduction or absence of hypothalamic cells that produce and secrete orexin (hypocretin). The loss of these cells is probably due to an autoimmune attack on the cells. There is probably a genetic susceptibility to narcolepsy which increases chance that certain infections will result in autoimmune attack on orexin/hypocretin cells.

28
Q

What is a parasomnia?

A

Parasomnias are a category of sleep disorders that involve abnormal movements, behaviors, emotions, perceptions, and dreams that occur while falling asleep, sleeping, between sleep stages, or during arousal from sleep.

29
Q

What are some examples of parasomnias?

A
  • Bed wetting or nocturnal enuresis
  • Sleep walking or somnambulism
  • Sleep terrors
  • REM sleep behavior disorder
  • Sleep apnea
30
Q

Describe sleep terrors

A

sleep terrors: occur during non-REM sleep, different from nightmares which are bad dreams in REM sleep

31
Q

Describe REM sleep behavior disorder

A

REM sleep behavior disorder is REM sleep without atonia or hypotonia

32
Q

Describe sleep apnea

A

Sleep apnea – at least 10 sec. pause in breathing during sleep

a. central sleep apnea
b. obstructive sleep apnea
c. mixed apnea

33
Q

Why do we sleep?

A

Several different hypotheses have been proposed. Recent research shows that sleep can increase interstitial space in the brain and contribute to the removal of potentially neurotoxic waste products.

34
Q

What is another theory of why we sleep?

A

Another hypothesis is that sleep has an important role in learning and memory. Recent research showed that sleep has a key role in promoting learning-dependent synapse formation

35
Q

Which brain areas and neurotransmitters are closely associated with wakefulness?

A
  • Cholinergic neurons of the pons-midbrain junction
  • Norepinephrine in the locus coeruleus
  • Serotonin in the pontine raphe neuron
36
Q

Describe the cholinergic neurons of wakefulness

A

Cholinergic neurons (of the pons-midbrain junction) are part of the reticular activating system. These neurons fire at high rates during waking and REM sleep but are quiet during non-REM sleep.

37
Q

Describe the locus coeruleus and pontine nuclei of wakefulness

A

The locus coeruleus and pontine nuclei are also active during wakefulness but they are not active during REM sleep.

38
Q

Describe histaminergic neurons in relation to sleep and wakefulness

A

Histaminergic neurons of the posterior hypothalamus (in the tuberomammillary nucleus (TMN)) are selectively active in the awake state. Antihistamine drugs which can cross the blood-brain barrier might promote sleep by blocking central histamine receptors responsible for arousal.

39
Q

Describe the role of orexin in promoting wakefulness

A

Certain neurons in the lateral hypothalamus which release orexin (also called hypocretin) excite the monoaminergic neurons in the locus coeruleus and raphe. These orexin neurons also promote wakefulness via their excitation of the histamine-containing neurons in the tuberomammillary nucleus.

40
Q

Describe the neurotransmitters that are active during the onset of sleep (NREM)

A
  • Sleep onset is caused by decreased firing of the cholinergic, monoaminergic and histamine-containing neurons above.
  • Neurons in the VPLO (ventrolateral preoptic nucleus of the hypothalamus) periodically inhibit the above neurons and thus are involved in non-REM sleep onset.
41
Q

What generalization can we make regarding monoaminergic and cholinergic systems?

A

Both monoaminergic and cholinergic systems are active during the waking state and suppressed during non-REM sleep.

42
Q

What are sensory evoked potentials?

A

Potentials extracted from an EEG by use of computer averaging techniques - this requires repeated sensory stimuli

43
Q

What types of sensory evoked potentials can be tested?

A
  • Brainstem auditory evoked potentials
  • Visual evoked potentials
  • Somatosensory evoked potentials (stimuli electrical stimulation of peripheral nerve - used during some spinal surgery)
44
Q

How are sensory evoked potentials clinically relevant?

A

Useful for evaluating demyelinating diseases such as multiple sclerosis.

Physiology Exam 6 (16 decks)

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