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Sleep physioloogy > sleep physiology > Flashcards

sleep physiology Flashcards

1
Q

Which of the following is correct
about recovery sleep following acute total sleep
deprivation?

A

On the first recovery night, large increase in NREM 3
sleep;
Rebound of REM sleep second night typical young;
little change in elders

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2
Q

Younger Subjects More Affected by

Sleep Deprivation than Elders

A

Normal older adults tolerate total sleep loss
better than young normal adults; older adults
tend to recover faster than younger;
Reaction times of young adults were significantly
slower after one recovery night compared with
older adults;
Young (not older) adults continued to have slow
reaction times on second recovery night.

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3
Q

Which of the following changes in plasma
levels are most likely after sleeping only 4 hours the
night before

A

Increased ghrelin, decreased leptin, increased evening

cortisol

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4
Q

Sleep deprivation and Ghrelin and Leptin

A

Ghrelin makes you Growl; Ghrelin stimulates hypocretin (“stay awake and get food”).

Leptin an adiokine released by fat cells signals satiety to brain, mediates appetite suppression (“stop eating, full”)

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5
Q

Leptin and sleep

A

Leptin-resistant: Some obese OSA patients have high leptin levels, but these do not suppress their appetite = leptin-resistant.
– CPAP treatment in such patients reduces elevated leptin levels, decreases abdominal visceral fat accumulation and improves glucose tolerance.

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6
Q

What are caffeine effects

A

caffeine = potent adenosine A1 receptor antagonist (combats rising homeostatic drive)

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7
Q

What is the effect Histamine on sleep

A

Histamine promotes wakefulness;
• Released by tuberomammillary nucleus (TMN) of posterior hypothalamus:
– Project widely to forebrain, brainstem and spinal cord;
• TMN neurons active when awake, increase their firing during W, decrease firing rates during drowsy states before sleep
• Destroy histaminergic TMN neurons in mice = can’t sleep

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8
Q

How do Histamine H1-Antagonists

Affect sleep

A

H1-receptor blockers increase sleepiness;
• First generation H1 antagonists (chlorpheniramine, diphenhydramine) are lipophilic so can readily cross blood brain barrier cause sedation & sleepiness;
• Second generation H-1 antagonists (certirizine, fexofenadine, loratadine) because hydrophilic do not cross BBB easily, less sedating stay awake

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9
Q

What is the role of Melanopsin and Glutamate

And neuropeptide Y in light entrainment

A
  • Retinal ganglion cells contain melanopsin;
  • Photic entrainment of circadian rhythms and pupillary responses to light especially 480 nm (blue/cyan range of visible light);
  • Retinal ganglion cells project via retinohypothalamic tract (RHT) to suprachiasmatic nucleus (SCN);
  • Release of glutamate from RHT stimulated by light, inhibits release of melatonin by pineal gland.
  • Secondary photic entrainment pathway (lateral geniculate to SCN; geniculohypothalamic tract = neurotransmitter = neuropeptide Y;
  • Glaucoma may selectively affect these photoreceptors in retina.
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10
Q

Hypocretin/Orexin Stabilize the Sleep and REM Switches = Excitatory

A

Stabilizes wakefulness;
• Produced by neurons in posterior lateral hypothalamus;
• Leptin and high glucose levels inhibits hypocretin (full, stop eating, go to sleep);
• Sleep deprivation increases hypocretin-1 transmission (stay awake and get some food).
• Ghrelin activates hypocretin (stay awake and get food);
• Human narcolepsy: deficiency of hypocretin-1;
– Canine narcolepsy = hypocretin-2 (dog is man’s best friend = #2).
Hypocretin neurons fire most vigorously during aroused awake state in which person actively exploring environment (e.g. walking – nice so you don’t fall);
• Hypocretin prevents transition from wake to REM sleep.

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11
Q

how is scoring central apneas in children performed

A

Score a central apnea which lasts 5 seconds in REM sleep if associated with a > 3 second EEG arousal and a 1 sec increase in chin EMG tone.

Central Apneas in Children Usually Require
Arousal or > 3% Desat to Score

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12
Q

When is Bradycardia in Central Apnea Scored in Infant < 1 year

A

New rule score a central apnea in children < 1 year if it lasts > 20 seconds or it is followed by significant bradycardia (HR <50/min > 5 sec or <60/min for > 15 sec);
• Why? Belief from neonatal apnea recordings that bradycardia throughout a central apnea makes it more pathological;
– One study of normal infants none had HR < 55/min for > 10 seconds related to CA.

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13
Q

What is the rule for scoring arousal

A

Score arousal after 20 seconds of stable sleep
Rule = score arousal during sleep if abrupt shift of EEG frequency including alpha, theta and/or frequencies > 16 Hz (but not sleep spindles) > 3 seconds, with > 10 seconds of stable sleep preceding the arousal:

– The 10 seconds of stable sleep required prior to scoring an arousal may begin in the preceding epoch, including a preceding epoch that is scored as stage W.

• To score an arousal in REM sleep additionally requires increase in chin EMG > 1 second.

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14
Q

Sleep-related Respiratory Changes

During Pregnancy in a Nutshell

A

Engorgement, hyper secretion, mucosal edema in nose, oropharynx, larynx, trachea from increased estrogen, increased progesterone, increased blood and interstitial volumes increased nasal resistance more NEGATIVE airway pressure during inspiration;
• Expanding uterus decreased Functional Residual Capacity (20-25%), Expiratory Reserve Volume (33-40%), and Residual Volume (22%);
• Late pregnancy airway closure increased ventilation-perfusion mismatch and decreased gas exchange especially supine;
• Progesterone increases respiratory rate increased minute ventilation and increased tidal volume leading to hypocapnia and respiratory alkalosis causing respiratory instability with episodes of central apnea at sleep onset and during REM sleep.
• Frequent awakenings cause respiratory instability and periodic breathing;

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15
Q

What is the role of Progesterone on sleep

A

Progesterone targets GABA receptors  rises in progesterone has soporific and sedative effects;

Animal models progesterone decrease NREM latency, W and REM sleep;

Smooth-muscle relaxation leads to frequent urination, heartburn, rhinitis leading to nocturnal awakenings;

Raise body temperature (sleep better cooler than warmer)

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16
Q

What is the effect of Estrogen on sleep

A 
• Decrease REM sleep neurons in
VPLO area;
i• Cause vasodilation which
predisposes to nasal obstruction
and lower extremities edema
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17
Q

What Protects Pregnant Women From

Sleep Disordered Breathing?

A

• Progesterone increases tone of upper airway dilator genioglossus muscle activity and increases responsiveness to CO2 during sleep;
• R-shift oxyhemoglobin dissociation curve and increase HR,increase stroke volume, and increase cardiac output with increase peripheral vascular resistance improves O2 delivery to placenta and maternal tissues;
less time supine as pregnancy advances.

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18
Q

Describe changes in Infant sleep as they age

A

A. A dominant posterior rhythm when awake of 3-4 Hz first seen 3-4 months of age.
B. K-complexes first appear frontal regions 5-6 months of age;
C. Short REM sleep latencies in infants < 3 months post-term; (50% of TST spent REM sleep at term)
D. Sleep cycles in newborn term infants last 40-60 min;
E. Sleep spindles first appear over midline central region at 44-48 weeks conceptional age.

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19
Q

When Sleep spindles begin to appear in infant

A

First seen 43 weeks CA (3 weeks post-term, usually present age 2-3 months

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20
Q

When do K-complexes appear in infant

A

First appear age 5-6 months post-term maximal over the frontal regions.

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21
Q

NREM 3 Slow Wave Activity(0.5-2 Hz)

A

First seen age 2-3 months post-term, usually present age 4-4.5 months post-term, maximal over frontal regions.

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22
Q

When is REM first seen in Infants

A

First apparent by 30-32 weeks conceptional age (whereas full term in 38-42 weeks CA). Sleep in term neonate = 50% REM, 50% non-REM (quiet sleep)

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23
Q

at what age can we Distinguish sleep stages in infancy

A

As early as age 4 – 4.5 months and usually by age 5-6 months.

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24
Q

Dominant waking posterior rhythm (DPR):

A

– First appears, ages 3-4 months term, 3-4 Hz
– 5-6 Hz by 5-6 months, 70% have 6-8 Hz by 1 year;
– Most have 8 Hz by 3 years (range 7.5-9.5 Hz);
– Normal in young and older adults: > 8.5 Hz:
• Younger adults average 10.2 Hz; older adults 9.7 Hz;
• Normal for “healthy old” DPR >8.5 Hz.

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25
Q

Which of the following is the main

neurotransmitter regulating the pineal gland?

A

Correct answer = Norepinephrine

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26
Q

Describe the Regulation of melatonin

A

During daylight, the suprachiasmatic nucleus (SCN) inhibits paraventricular nucleus which inhibits melatonin secretion;
• Sun sets, inhibition of melatonin secretion diminishes, permitting melatonin to be secreted by pineal gland.
– Melatonin synthesized from tryptophan;
– Norepinephrine is the main neurotransmitter regulating pineal gland:
– Binds to melatonin receptors triggers cascade of secondary messengers which generate cyclic AMP which prompts
melatonin to be synthesized from tryptophan

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27
Q

GI effects of sleep

A

Unstimulated gastric acid secretion in normals has prominent circadian rhythm:
– Peaks 10 pm to 2 am; Lowest 5 am to 11 am.
– Vagal stimulation most likely to regulate this circadian rhythm, lost after vagotomy;
– Plasma gastrin levels do not have circadian rhythm.
• A solid meal before bedtime decreases sleep latency more than a liquid meal;
• Decreased gastric motility, salivation and swallowing during sleep;
• Decreased mucosal acid contact during sleep.

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28
Q

Wakefulness-promoting brain regions and respective neurotransmitters:

A 
– PPT/LDT: acetylcholine
– Posterior Lateral hypothalamic perifornical region:
hypocretin/orexin
– Locus coeruleus: norepinephrine
– Tuberomammillary nucleus: histamine
– Substantia nigra: dopamine
– Dorsal raphe nuclei: serotonin
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29
Q

What are the Respiratory changes occurring with sleep

A

Changes in Blood Gases Sleep Compared to Wakefulness
• During sleep (compared to wakefulness);
– PaCO2 increases 2-8 mm Hg;
– PaO2 decreases 3-10 mm Hg;
– SpO2 decresees 0-2%;
– Minute ventilation decreases0.5-1 L/min
• Periodic breathing especially NREM 1 sleep; if paCO2 drops below PaCO2 threshold, relative hypocapnia sensed at medullary chemoreceptor and induces hypoventilation/apnea until paCO2 rises. – Most apparent in people with Cheyne-Stokes respiration.

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30
Q

Circadian-mediated decline in body temperature at night activates which neurons?

A

Correct answer = sleep-promoting GABA neurons

A. GABA

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31
Q

Sleep spindles generated where
in brain? What neurotransmitter
associated with them?

A

Thalamus (reticular nucleus) neurons contain GABA; Sleep spindles are hyperpolarized as sleep begins (reduces arousal). This produces a discharge of thalamic neurons which is transferred to a network of thalamo-cortical neurons.

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32
Q

Lesions where in the hypothalamus produce narcolepsy ?

A

lesion in posterior and lateral hypothalamus severe hypersomnia.

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33
Q

Lesions where in the hypothalamus produce insomnia?

A

Lesion preoptic area and basal forebrain severe insomnia;

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34
Q

Acetylcholine (cholinergic) neurons are located where in the brain

A

Pons and basal forebrain; early atrophy of these neurons predispose to sleep disorders in Alzheimer’s disease.

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35
Q

Which thalamic nucleus is preferentially affected in fatal familial insomnia?

A

Dorsomedial thalamus

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36
Q

Physiological mechanism underlying sleep drunkenness or sleep inertia?

A

VPLO abnormality

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37
Q

Injection of physostigmine et al. cholinergic agonists into LLD/PPT in humans would be expected to induce what sleep/wake state?

A

Cholinergic agents into dorsal pons LDT/PPT expected to induce REM sleep

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38
Q

Which neurotransmitter is contained in the projections from the ascending reticular activating system?

A

Norepinephrine/noradrenaline

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39
Q

VLPO (Ventral Lateral Preoptic) area important in regulation of which sleep/wake state?

A

VPLO promotes NREM sleep. Inhibitory GABAergic VPLO projections decrease ARAS neurons as NREM sleep begins and deepens. VPLO inhibit brainstem nuclei involved in EEG arousal, and inhibit histamine wakefulness promoting neurons in TMN

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40
Q

A secondary indirect pathway by which light reaches the SCN is via the lateral geniculate and geniculohypothalamic tract. What is the neurotransmitter for the geniculohypothalamic tract?

A

the lateral geniculate-SCN (geniculohypothalamic tract) neuropeptide Y as its neurotransmitter.

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41
Q

1-4 Hz delta activity (slow wave activity) of NREM 3 are generated by what mechanism?

A

Burst rhythmic discharges in thalamocortical neurons.

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42
Q

What are the wake-maintenance zones?

A

2 circadian peaks in alertness typically late morning and early evening. Difficult to fall asleep during these.

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43
Q

What are sleep-maintenance zones?

A

2 circadian troughs in alertness (increased sleep propensity) typically in early morning (e.g. 1-3 am) and early-mid afternoon; easier to fall asleep then

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44
Q

Sleep requirements in older adults compared to younger adults?

A

Sleep requirements do NOT decline with aging. However, aging associated with greater nocturnal sleep disturbance, EDS, daytime napping, greater prevalence of insomnia, OSA, CSA, PLMs, RLS, RBD, and advanced sleep phase type.

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45
Q

Which sleep disorders/medications are associated with ↑SOL, ↓ SE, ↓ TST and ↑WASO?

A

Disorders reporting insomnia and stimulant medication use.

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46
Q

Which sleep disorders/medications are associated with ↓SOL, ↑ SE, ↑ TST and ↓ WASO

A

Sleep deprivation, disorders presenting with EDS, sedating medications. ↑↓

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47
Q

What is the effect of oral melatonin on phase when taken in morning? In evening?

A

Melatonin synthesized and released by the pineal gland; secretion inhibited by light exposure. Melatonin when taken in morning DELAYS phase; taken in evening, ADVANCES phase.

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48
Q

What is the effect of oral melatonin on phase when taken in morning? In evening?

A

Melatonin synthesized and released by the pineal gland; secretion inhibited by light exposure. Melatonin when taken in morning DELAYS phase; taken in evening, ADVANCES phase.

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49
Q

What is the main neurotransmitter for REM

sleep?

A

Acetylcholine is the main neurotransmitter in

REM sleep

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50
Q

Which neurotransmitter responsible for REM sleep without atonia?

A

Glycine is the main inhibitory neurotransmitter in spinal cord and responsible for REM sleep without atonia (RSWA)

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51
Q

GABA-producing neurons in brain located

where?

A

GABA-producing neurons are located in VPLO = Ventrolateral pre-optic hypothalamus

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52
Q

Sleep pressure increases in relationship to prior wakefulness and correlates with a rise in CSF levels of what?

A

Homeostatic sleep pressure rises with increasing levels of CSF adenosine.

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53
Q

Production of which hormones increase during

sleep?

A

ADH (increased renal water reabsorption); GH and prolactin (during NREM 3) Renin (during NREM sleep) Testosterone (during REM sleep)

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54
Q

Production of which hormones decrease during

sleep?

A

Cortisol levels decrease during NREM 3 sleep; Insulin secretion

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55
Q

What is the effect of sleep on the cardiovascular,

A

CV system: decrease HR, CO and BP (NREM and tonic

REM sleep); decreased frequency of PVCs;

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56
Q

What is the effect of sleep on the GI,

A

GI system: ↓swallowing rate; ↓ salivary
production; ↓ esophageal and ↓ intestinal
motility

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57
Q

What is the effect of sleep on renal systems?

A

Renal system↓ glomerular filtration but ↑ADH production (increased renal water reabsorption).

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58
Q

What is the effect of sleep deprivation on autonomic nervous system activity? Cortisol, ghrelin and insulin resistance?

A

Sleep deprivation increases SNS activity, cortisol

secretion, insulin resistance and ghrelin

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59
Q

Criteria for terminating a nap in MWT?

A

Nap trial in MWT is terminated if: 1) 3 consecutive epochs of N1 sleep; 2) 1 epoch of any other sleep stage; 3) No sleep after 40 minutes

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60
Q

To score an arousal on a PSG what is

needed?

A

During NREM arousals – require changes in EEG only REM arousals – require changes in EEG and EMG EEG changes – abrupt EEG frequency shift (alpha, theta or > 16 Hz, but not spindles)  3 seconds and preceded by  10 seconds of stable sleep EMG changes – increase in chin EMG  1 second

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61
Q

What are the clinical correlates of phasic activity of REM sleep

A

Rapid eye movements, twitching of distal muscles, middle ear activity, and PGO (ponto-geniculo-occipital) waves;

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62
Q

What percentage of arousals from REM sleep do subjects report vivid dream recall?

A

80%

63
Q

sleep in young adult

A

NREM; N1 2-5%; N2 45-55%; N3 = 13-23%;

NREM 75-80%; REM 20-25%; 4-6 NREM-REM sleep cycles;

64
Q

How is Slow Wave Sleep (NREM 3)

different in children than adults?

A

Almost impossible to arouse child from NREM 3 to 123 dB tone age 10 years; children more often Skip their first REM sleep episode of night; SWS decreases by 40% during adolescence during 2nd decade; might parallel loss of cortical synaptic density; By mid-adolescence sleep resembles that of young adults.

65
Q

What are distinctive changes in normal sleep architecture seen in older adults?

A

Arousals increase, extended wake episodes, brief unremembered arousals, PLMs, sleep-related respiratory irregularities, but MOST notable finding = marked increase in inter-individual variability (so can’t generalize about what is normal sleep architecture in elder vs. young adult). Loss of SWS particularly

66
Q

What it the effect of chronic restriction of nocturnal sleep, an irregular sleep/wake schedule or frequent disturbance of nocturnal sleep on sleep architecture?

A

Most commonly characterized by SOREMPs and these may be associated with hypnagogic hallucinations, sleep paralysis, or an increased incidence of hypnic myoclonia in persons with no organic sleep disorder

67
Q

Effects of sleep deprivation on EEG?

A

Large reduction in alpha activity in waking EEG with an increase in theta and delta

68
Q

Gender differences in sleep architecture among adults

A

1) Objective findings on PSG in adult women = shorter sleep latencies, higher sleep efficiency, and maybe even greater %NREM 3 than adult men; 2) Adult men have normal awakenings and NREM 1 than women; 3) Adult women have more subjective complaints about insomnia, non-restorative sleep, and difficulty falling asleep than men)

69
Q

Neurotransmitter crucial in generation of

respiratory rhythm is?

A

Glutumate (and interacts primarily with NMDA receptors).

70
Q

Benzodiazepine hypnotics (traizolam, flurazepam, temazepam) have what effects on sleep EEG and sleep architecture?

A

Increase N1, N2, decrease in NREM 3 and REM sleep. Increased sleep spindles, decrease NREM 3 delta power, and increase REM sleep latency.

71
Q

RBD in animal models best induced by lesion in what part of brain?

A

Brainstem ventral to locus coeruleus

72
Q

Where in the brain are
REM –onset cells
(neurons) located?

A 
Laterodorsal pontine tegmentum (LPT) and reduculopontine tegmentum (PPT); these have highest discharge rates during REM sleep; BUT 2nd highest firing during W.
Tuberomammillary nucleus (TMN) neurons fire wake-onset and promote W;
Ventrolateral preoptic area (VPLO) neurons fire W to N, NREM-on, and discharge during N and R sleep compared to W)
Dorsal raphe nucleus neurons have highest discharge rate in W, decrease in N and R sleep.
73
Q

Effect of benzodiazepines on sleep architecture?

A

Suppress NREM 3, no effect on REM; acute w/d from BZPs = increase NREM 3;

74
Q

Effect of antidepressants on sleep architecture?

A

TCAs, MOAI, and certain SSHIs tend to suppress REM sleep. REM sleep without atonia may occur with these (esp venlafaxine/Effexor) and fluoxetine with REMs all stages of sleep. Acute w/d from TCS or MOAI REM sleep rebound, some SOREMPs may be seen.

75
Q

Acute presleep alcohol

A

Increase in NREM 3 + suppression of REM sleep early night followed by REM sleep rebound latter portion of night as alcohol metabolized; low doses of alcohol have minimal effects on sleep stages but can cause sleepiness.

76
Q

Acute and chronic marijuana use

A

Slight reduction in REM sleep; chronic ingestion of THC  long-term suppression of SWS. Recent interesting studies show SOREMPs and shorter MSL on MSLT but unlikely to be on test.

77
Q

Effect of benzodiazepines on sleep architecture?

A

Suppress NREM 3, no effect on REM; acute w/d

from BZPs = increase NREM 3;

78
Q

What is the sleep of a cat with Diencephalon removed

A

Behavioral wakening with persistent local Mersin orientation to oratory stimuli a quiet sleep like state. In summary at least in the cat neocortex in Stratham are not required for behaviorally define sleep wake States and not Rim state occurs in the absence of sleep spindles and small waves

79
Q

What are the REM off arousal systems

A

Serotonin from the raphe nucleus Norepinephrine from the locus ceruleas and histamine from the tuberomamillary nucleus orexin From the middle lateral hypothalamus

80
Q

What are the wake on REM on arousal systems

A

Acetylcholine from the pedicular Pontine tegmental region and lateral dorsal tegmental nuclei in the basal forebrain
Dopamine containing neurons in the substantial nigra and ventral tegmental area of the midbrain and the basal and medial hypothalamus

81
Q

How does the flip-flop switch work

A

The median preoptic nucleus and the Ventral lateral preoptic nucleus release GABA which inhibits Locus ceruleas Tuberomandibular nucleus preforical lateral hypothalamic nucleus
The TMN PFLH and DR (dorsal raphe) are wake active NREM diminishing and REM off

82
Q

Where do MnPN VLPO neurons project

A

Basal forebrain PFLH, tuberomammilary, pontomesencephalic ACH, DR, and LC

83
Q

What inhibits MnPN

A

Norepinephrine

84
Q

What inhibits VPLO

A

Acetylcholine serotonin And norepinephrine

85
Q

What is theRole of the thalmocortical Projections in sleep

A

Single tonic firing during a week and burst firing during NREM sleep
tonic firing when stimulated from a resting depolarized state and Burst firing from a hyperpolarized resting state

86
Q

What is the effect of POA warming

A

POA warming suppresses the discharge of arousal related neurons

87
Q

What is the key structure in the generation of REM sleep

A

The brainstem

88
Q

What transmitters do the REM on cells use

A

GABA ACH

89
Q

What Transmitters do the REM off cells use

A

Norepinephrine and epinephrine serotonin histamine or GABA

90
Q

Where do the REM sleep on cholinergic sells project

A

Acetylcholine responsive region of the subcoeruleus area

91
Q

What is the role of monamine containing cells in REM sleep

A

The cells reduce in non-REM sleep and turn off during REM sleep

92
Q

How does cataplexy differ from normal REM sleep

A

Histamine neurons remain active

93
Q

It what two ways and loss of atonia occur during REM sleep

A

Extensive transient muscle activity (basic activity) and sustained muscle activity (tonic activity). To evaluate basic activity, divide a single 30 second epoch into 10 3 seconds epochs. If greater than 5 of these epochs contain muscle activity burst phasic activity is present

94
Q

Described propriospinal myoclonus

A

The patient states that when she tries to sleep, her whole body seems to jerk, arousing her. The jerks affect her abdomen initially. Sometimes her arms and legs are also affected. The jerks do not occur when she has fallen sleep

95
Q

What are the dynamics of the clock and per genes

A

During the day, body temperature, cortisol, and blood pressure increase. They decrease at night.
During the day melatonin growth hormone testosterone and prolactin decrease. They increase at night.
As might be expected, the mammalian per genes, clock, and bmal are all expressed in the suprachiasmatic nuclei, but whereas the genes encoding Clock and Bmal are turned on permanently, expression of the per gene is rhythmic, being highest in the middle of the day and suppressed at later stages of the cycle. The assumption is that the inactivation reflects the negative feedback of Per (and possibly Tim) proteins antagonising the positive drive from Clock and Bmal, just as it does in drosophila.

96
Q

What are sleep requirements

A

Newborns (0 to 3 months): 14 to 17 hours each day
Infants (4 to 11 months): 12 to 15 hours
Toddlers (1 to 2 years): 11 to 14 hours
Preschoolers (3 to 5 years): 10 to 13 hours
School-age children (6 to 13 years): 9 to 11 hours
Teenagers (14 to 17 years): 8 to 10 hours
Adults (18 to 64 years): 7 to 9 hours
Older adults (over 65 years): 7 to 8 hours

97
Q

What are sleep times by age

A

Newborn 14-17

Infants 12–15

Toddlers 11–14

Preschool 10–13

School-age 9–11

Teenage 8–10

Young adults 7–9

Older adults 7–8

98
Q

What are glutaminergic in the parabrachial nucleus

A

Wake Promoting neurons

99
Q

What generates slow wave sleep

A

GABA and gallanin Containing neurons in the VPLO and Activation of cortically projecting inhibitory neurons

100
Q

What is the function of parabrachial neurons

A

Trigger NREM and slow wave activity

101
Q

What is the effect of the decline in body temperature in the evening

A

Activation of sleep active GABA neurons thus promoting sleep be a change in the position of the sleep wake switch

102
Q

What is the REM Generating region.

A

It is located in the Dorsal PONS and the activation of this region produces defining signs including low-voltage fast way EEG activity and muscle atonia In the subcoeruleus sublaterodorsal tegmental nucleus lead to REM through glutaminergic means

103
Q

What drives REM

A

Glutamate cells in the subcereleus nucleus project to And excite GABA and glycine cells in the ventral medial medulla which in turn project to somatic motor neurons to cause REM sleep paralysis. The same cells also participate in controlling the timing of REM sleep itself. They do this, in part by projecting to the basal forebrain which causes the cortical activation that defines the brain arousal asleep during REM sleep. Cholinergic cells in the PPT and LDT also communicate with the subcoeruleus to impact REM sleep time and control. Importantly, REM Sleep is suppressed by GABA cells in the ventrolateral periaqueductal gray That project to and inhibit the glutaminergic cells in the subC that promote REM sleep

104
Q

Is there a difference in aging when women are compared to men

A

Age-related findings included an increase of sleep latency, increased percent Stage 1 and Stage 2 sleep, and in adults, REM sleep decreased. The data demonstrated that the associations between sleep variables and aging were generally the same for both sexes;
However, larger effect sizes were observed in women for total sleep time (TST), sleep efficiency, percentage of Stage 1 sleep, and REM latency. In other words, age is a more important factor in women. Women had longer TST and sleep latency than men. They also have less Stage 2 sleep and more slow wave sleep than age-matched men.

105
Q

Is there A difference in slow wave sleep between men and women

A

Age-related changes of the overall architecture of sleep are similar between men and women, though some subtle differences exist. Percent slow wave sleep (SWS) declines more slowly with age in women.1-4 Women also tend to have an increased percentage of slow wave sleep & higher power delta sleep in spectral analysis.5 Recent EEG analysis in older men and women show similar patterns but more delta waves in REM in women.

106
Q

What is the difference in sleep efficiency between men and women

A

Young women have shorter sleep latency and higher sleep efficiency compared to young men

A trend was found for older women to have a higher sleep efficiency Elderly men spend more time in bed Women wake more often, longer latency & more symptoms of disturbed sleep

107
Q

How does the menstrual cycle affects sleep

A

. In general, sleep appears better (fewer arousals) in the early luteal phase when hormones are increasing. As those hormones recede, the numbers of arousals increases, leading to worse sleep. When comparing the luteal and follicular phase, there is a higher percentage of NREM sleep in the luteal phase (decreasing REM percentage).1 In perimenopausal women, worst sleep efficiency and lowest TST in 4th week of menstrual cycle (week prior to onset on menses).2
Subjective lower sleep quality is reported during the 3 pre-menstrual days and 4 menstruating days, compared with the mid-follicular and early to mid luteal phases. 3 Actigraphy studies indicate gradual decline in sleep efficiency across the menstrual cycle, which is most pronounced in the pre-menstrual week.4 The rate of rise in progesterone levels from the follicular phase through the mid-luteal phase is associated with greater sleep fragmentation in the luteal phase of the menstrual cycle.

108
Q

What is the effect of progesterone on sleep

A

Sex-related steroid hormones have effects on sleep. Progesterone acts as a sedating agent, acting in an agonistic manner on the same receptors (GABAA) as benzodiazepines and barbiturates, though it may act in a unique binding site. Similar to these medications, this hormone also affects REM sleep, prolonged the latency to REM sleep and reducing the amount of REM sleep. It appears to act via progesterone metabolites (5-alpha-pregnanolone and 5-beta-pregnanolone), apparently increasing the frequency and duration of chloride channel openings. Exogenous administration of progesterone in humans has been shown a sedating effect on both men and women, and in one placebo-controlled study of 9 men, it increased NREM sleep.

109
Q

What is the affective estrogen on REM sleep

A

Increases REM sleep

110
Q

What is the affective exogenous estrogen during perimenopausal time

A

Women who are perimenopausal and are treated with estrogen tend to report decreased sleep latency, decreased nocturnal waking, and increased total sleep time. When comparing humans who are receiving estrogen exogenously, they appear to increase REM sleep time and decreased REM sleep latency.

111
Q

What is the affective pregnancy and sleep

A

Pregnant women report having significant sleep disturbances. 40% have snoring, apneas and restless legs syndrome.

112
Q

How much her pregnant women with during the night

A

Pregnant women were most likely to be awake a lot during the night (74%) and/or wake up too early and be unable to get back to sleep (46%).

113
Q

How much time he pregnant women spend in bed

A

When compared to women in general, pregnant women were the only group to average more than 8 hours in bed on both workdays (8 hours 14 minutes) and non-workdays (8 hours 52 minutes).

114
Q

how does sleep ,progress during pregnancy

A

The first trimester of pregnancy is notable for increasing progesterone levels, which may increase the woman’s sleepiness level. In addition, nocturnal sleep may be disrupted due to the physiological changes in a woman’s body and the resultant effects. Sleep usually improves in the second trimester, followed by a return of sleep difficulties in the third trimester.

115
Q

Sleep in the second trimester

A

Many report improved sleep and daytime alertness
Hormones usually stablize during this trimester
Decreased nausea
Less fatigue, more energy
Vivid dreams
Nasal congestion
Onset of snoring, restless leg symptomatology, irregular uterine contractions, back pain and joint pain

116
Q

Sleep in the first trimester

A

Daytime sleepiness and fatigue resulting in more frequent naps as early as 10th week of pregnancy
Slow wave sleep decreases
Prolonged wake after sleep onset can occur
Urinary frequency increases
Discomfort: back pain, breast tenderness
Nausea and vomiting

117
Q

Sleep in the third trimester

A 
Decreased total sleep time
Increased insomnia / nocturnal awakenings
Increased daytime sleepiness
Increase in naps
Increased N1 sleep
Decreased REM sleep
Increased urinary frequency, shortness of breath and heartburn
Fatigue and drowsiness reappear
118
Q

What are sleep changes in pregnancy

A

There was a significant decline in SWS in the first trimester as compared to pre-pregnancy. There was a significant increase in SWS postpartum as compared to the last trimester. There was no significant change in REM sleep before, during and post partum.

119
Q

What menopausal changes affect sleep

A

more then 35% of midlife or older women are considered obese
weight gain
change in distribution of adipose tissue
After menopause, there is also a preferential increase in intra-abdominal or visceral deposition of fat relative to other areas of the body
genioglossus muscle activity was lowest in a group of postmenopausal women

120
Q

How satisfied are women with her sleep after menopause

A

dissatisfaction with sleep typical during menopause transition
major factor: hot flashes
epidemiologic studies shows subjective increase in trouble sleeping during the menopause transition and early postmenopause
objective findings from PSG studies have been mixed
Wisconsin Sleep Cohort Study of 589 midlife women showed that postmenopausal women had more SWS and lower WASO despite reporting less sleep satisfaction compared with premenopausal women
Campbell et al: quantitative analysis to the sleep EEG in women and found no differences were found in PSG measures

121
Q

What is the effect of menopause and sleep apnea

A

narrowing of gender gap with prevalence of SDB

partial upper airway obstruction more common than sleep apnea in postmenopausal women

122
Q

How do women compar to men in obstructive sleep apnea

A

OSA (AHI ≥ 15) found in 4% of middle aged women and about 9% of middle-aged men (ratio 2:1)
if define AHI ≥ 5: Men 26%, Women 13% (ratio 2:1)
If define AHI ≥15 & ESS > 10: Men 3.9% & 1.2% of women (ratio of 3.3 : 1)

A retrospective review of 830 consecutively diagnosed OSAH patients evaluated the male : female ratio
The ratio was 2.2 : 1 amongst mild cases (AHI 5-25/h)
The ratio increased to 7.9 : 1 for severe cases (AHI>50)

123
Q

Do symptoms of apnea differ between men and women

A

Men are much more likely to present with snoring and witnessed apneas; women may suffer more from morning headaches and have depressive symptoms. Women appear to have more hypopneas and fewer overt apneas.
Classical symptoms not as prominent in women
Women are 50% less likely to describe snoring and apneic spells when compared to men with similar respiratory disturbance indices (AHI >15)

Sleepiness is considered a primary symptom of OSA
majority of symptoms described in women are fatigue / tiredness / lack of energy Therefore OSA may be under-diagnosed in women Symptoms attributed to depression rather than evaluated for OSA

124
Q

What causes the difference between men and women when it comes to sleep apnea

A

conclude that the most likely cause of the gender difference in obstructive sleep apnea syndrome is hormones, and the most likely effect of the hormones is to change the collapsibility of the upper airway. Postmenopausal women have nearly twice as much obstructive apnea as premenopausal women.

125
Q

Comorbidities associated with obstructive sleep apnea and man and women

A

OSA an independent predictor of CHD in:
Men < 70 years of age but NOT women

OSA an independent predictor of heart failure in: Men NOT women

OSA had significant positive association with stroke in: en (stroke increases with increasing OAHI) Women only at an OAHI > 25

126
Q

What are criteria for RLS

A

1) Desire to move the limbs usually associated with paresthesias/ dysesthesias
2) Motor restlessness
3) Worsening of symptoms at rest with at least partial and temporary relief by activity
4) Worsening of symptoms in the evening or night

127
Q

What lesion causes issues with arousal

A

Due to concentration of multiple ascending pathways, damage to posterior hypothalamus or rostral reticular formation in the midbrain can result in prolonged and severe hypersomnolence.

128
Q

Describe cholinergic activation

A

The lateral dorsal tegmentum nuclei are a major group of cholinergic neurons which are active in wakefulness and REM sleep. The adjacent group of neurons in the peduncopontine tegmental nuclei also contain another group of cholinergic neurons.

129
Q

What sleep processes arise from the medial medulla

A

The medial medulla contains GABA and glycine and is thought to be atonia-promoting during REM sleep.

130
Q

What is Pontus Oralia

A

The pontis oralis is GABAergic and cholinergic system, responsible for generation of wakefulness and REM sleep but lesion here is not thought to produce severe deficit due to redundant systems.

131
Q

What is ventrolateral preoptic area

A

The ventrolateral preoptic area promotes sleep as these nuclei are GABAergic (inhibitory) and innervate wake-promoting regions, although this region is also redundant.

132
Q

Describe changes in posterior dominant rhythm

A

The posterior dominant rhythm (or “alpha”) increases with age. In children less than 3 months of age it ranges from 3.5 to 4.5?Hz. During infancy and early childhood it increases in frequency, reaching 5–6?Hz by 5–6 months of age, and 7–9?Hz by 3 years of age.

133
Q

What occurs during heart rhythm decelerations in REM

A

Heart rhythm decelerations occur during tonic REM sleep.

these decelerations occurred 3 seconds prior to a burst in eye movement (phasic )

This phenomenon is truly due to an increase in vagus nerve tone rather than a decrease in sympathetic nerve activity.

134
Q

What affect does chronic sleep deprivation have on hormones

A

chronic sleep deprivation (SD) alters the hormonal homeostasis, causing an increase in catabolic hormones cortisol and TSH levels, catecholamines,

to lesser extent, a decrease in testosterone concentrations and in growth hormone (GH) release. This situation occurs both in rats and in humans exposed

135
Q

What lesion causes reduction in arousal

A

However, one region in which a lesion results in significant reduction in arousal is the rostral reticular formation in the midbrain and posterior hypothalamus. It is believed to be the result of damage to the ascending monoaminergic and cholinergic pathway

136
Q

What Elise doe locus ceruleas play in sleep

A

The locus coeruleus (LC), an area where norepinephrine is synthesized sends projections to the cortex and hippocampus and subcortical areas such as the thalamus and hypothalamus. The LC neurons are active in the wakefulness state.

137
Q

Describe GABA pathways in sleep

A

GABAergic pathway can be both sleep promoting (slow firing; in the preoptic hypothalamus, lateral hypothalamus and brainstem) and wakefulness promoting (fast firing; brainstem, ventral tegmental area in the midbrain, and basal forebrain).

138
Q

When does Hypnogogic hypersynchrony occur

A

Hypnogogic hypersynchrony is found commonly in the infant age with almost all children in the 6-8 month old age range demonstrating this finding. It decreases in prevalence with age and only about 10% of otherwise healthy 10-year-olds will demonstrate this finding.

139
Q

How Foy you score tachycardia

A
  1. Score sinus tachycardia during sleep for a sustained sinus heart rate of greater than 90 beats per minute for adults.
140
Q

How do you score bradycardia

A
  1. Score bradycardia during sleep for a sustained heart rate of less than 40/minute for ages 6 years through adult.
141
Q

Hose do you score narrow tachycardia

A
  1. Score narrow complex tachycardia for a rhythm lasting a minimum of 3 consecutive beats at a rate of greater than 100 per minute with QRS duration of less than 120 msec.
142
Q

How do you score a fib

A
  1. Score atrial fibrillation if there is an irregularly irregular ventricular rhythm associated with replacement of consistent P waves by rapid oscillations that vary in size, shape, and timin
143
Q

How do you score daytime

A
  1. Score asystole for cardiac pauses greater than 3 seconds for ages 6 years through adult.
144
Q

how do you Score wide complex tachycardia

A
  1. Score wide complex tachycardia for a rhythm lasting a minimum hof 3 consecutive beats at a rate greater than 100 per minute with QRS duration of greater than or equal to 120 msec.
145
Q

How Foy you score arousal

A

An arousal out of any stage of sleep requires a sudden change in EEG frequency (increase) that lasts at least 3 seconds. Stable sleep lasting 10 seconds or longer needs to precede this shift. For an arousal out of stage R sleep an increase in chin EMG for at least one second is concurrently required.

146
Q

When do spindles occur

A

Sleep spindles initially appear between 4 - 6 weeks post-term but are well developed by 8 weeks. These are the first sleep specific waveforms to appear. The other N2 sleep waveforms, K complexes, don’t appear until 5-6 months post-term.

147
Q

What is the function of ore in neurons

A

Neurons containing orexin are most active during the waking state. They activate monoaminergic neurons of the arousal system and they activate the REM-off neurons. They function in wakefulness promotion and the stability of behavioral states, and also are active in certain behavioral states to maintain postural tone.

148
Q

Describe EEG maturation

A

Posterior dominant rhythm of 5-6 Hz should be evident by 5-6 months. Sleep spindles appear around two months of age, although they may appear longer than in adults. K complexes should be evident by 4-6 months and slow-wave activity by 2-5 months. With these sleep stage defining waveforms present, N1, N2, and N3 sleep stages should be stageable by 5-6 months.

149
Q

Describe sleep in HIV

A

When compared to the normative mean data, HIV infected individuals were noted to have increased arousal index (6.2 vs 3.5), decrease in stage 2 (44.9 vs 52.8), increase in total REM periods (6.1 vs 4.5) and increased in SWS (21.4% vs 15%). They were also noted to have decreased sleep latency (4.7 vs 10).

150
Q

What is the role of lepton

A

Leptin an adiokine released by fat cells signals satiety to brain, mediates appetite suppression (“stop eating, full”) Leptin inhibits hypocretin /orexin (so you can fast across a night of sleep)hunger, food intake, and appetite especially for foods rich in complex carbohydrates. insulin sensitivity, slows rate of glucose clearance on glucose tolerance test, profile similar to 80 year old; predisposes to insulin resistance.

151
Q

What is effect of narcolepsy on lepton

A

Narcoleptics with cataplexy: >50% reduction in leptin levels in serum (but not CSF) narcolepsy patients compared to controls.

152
Q

What is effect of lepton on ventilatory drive

A

Leptin: Stimulates hypercapnic ventilatory drive; correlates with severity of hypoxemia in OSA.

153
Q

What is the role of adenosine

A

Adenosine secreted by neurons in basal forebrain:

Rise with prolonged W; fall with recovery sleep;
• Promotes NREM 3 sleep; responsible for homeostatic drive;
• Adenosine A1 receptors are inhibited by caffeine;
• Adenosine A1 Rc inhibit wake neurotransmitters (histaminergic neurons in tuberomammilary nuclei (TMN);
• Adenosine A2A receptors: activate VLPO  promote sleep

Sleep physioloogy (1 decks)

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