MODULE 1 Flashcards

1
Q

What are Sleep-Wake Disturbances (SWDs) and how prevalent are they in neurological and psychiatric disorders?

A

SWDs are disruptions in the sleep-wake cycle. They are extremely common in patients with neurological and psychiatric disorders.

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2
Q

How are SWDs linked to neurological and psychiatric functions?

A

SWDs are connected to the neurobiology of sleep and share overlapping neuronal networks and neurotransmitter systems.

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3
Q

What brain regions are involved in the control of sleep and wakefulness?

A

The hypothalamus, brainstem, thalamus, and basal forebrain are key brain regions involved.

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4
Q

Which brain structure serves as the master clock for circadian rhythms?

A

The suprachiasmatic nucleus (SCN) in the hypothalamus.

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5
Q

What neurotransmitters promote wakefulness and alertness?

A

Acetylcholine, norepinephrine, dopamine, histamine, and serotonin.

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6
Q

What is the role of the ascending reticular activating system (ARAS) in wakefulness?

A

The ARAS is a major pathway for maintaining wakefulness, sending projections to the thalamus and cortex.

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7
Q

Which brain region inhibits wake-promoting areas to promote sleep?

A

The ventrolateral preoptic nucleus (VLPO) in the hypothalamus.

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8
Q

What happens to neurotransmitters like serotonin and norepinephrine during sleep?

A

They are reduced during sleep.

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9
Q

What is the ‘depotentiation’ hypothesis in memory consolidation during sleep?

A

It suggests that local neuronal assemblies activated during learning are weakened or pruned during sleep to create space for new learning while preserving memory traces.

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10
Q

How does sleep contribute to memory integration and organization?

A

Sleep-induced reactivation and transfer of information across distributed cortical networks connect related pieces of memory into a more coherent and consolidated form.

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11
Q

When does neural network reactivation, promoting memory consolidation, occur during sleep?

A

During both rapid eye movement (REM) sleep and non-rapid eye movement (NREM) sleep.

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12
Q

What is an enduring memory trace?

A

It is the long-lasting memory representation that is preserved after depotentiation during sleep.

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13
Q

How is insomnia defined?

A

Insomnia is defined by subjective complaints of prolonged sleep latency, difficulties to maintain sleep, or early morning awakening, with negative daytime consequences.

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14
Q

What is the prevalence of chronic insomnia?

A

Chronic insomnia affects over 10% of the population and contributes to the risk or severity of various disorders.

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15
Q

How is the diagnosis of insomnia made?

A

The diagnosis is based on subjective complaints, but polysomnography (PSG) can be useful to rule out secondary forms and provide objective sleep measures.

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16
Q

What is the “master clock” in the circadian system?

A

The suprachiasmatic nuclei serve as the mammalian “master clock” that synchronizes cell-autonomous circadian clocks in various cells of the brain and body.

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17
Q

Why are disturbances of circadian functions common in neuropsychiatric disorders?

A

Circadian dysregulation is frequently observed in neuropsychiatric disorders like depressive disorders, stroke, Alzheimer’s disease, Parkinsonism, RLS, and traumatic brain injury.

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18
Q

How can specific interventions targeting the circadian system benefit neuropsychiatric disorders?

A

Interventions such as sleep deprivation and intensive light therapy have been shown to improve symptoms in mood disorders and Alzheimer’s disease, while behavioral circadian reinforcement can enhance well-being in elderly individuals.

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19
Q

How do polymorphic variations of clock genes contribute to psychopathology?

A

Polymorphic variations of clock genes may contribute to bipolar disorder, either through causative involvement or altered responses to external “zeitgebers” like light-dark cycles.

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20
Q

What detrimental effects can sleep loss and disturbances have on neuronal function?

A

Sleep loss may lead to diminished clearance of toxic substances in the brain and contribute to inflammation associated with these disorders.

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21
Q

What does SDB stand for, and what does it include?

A

SDB stands for sleep-disordered breathing, which includes various phenotypes like snoring, OSA, CSA, CSR, and hypoventilation syndromes.

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22
Q

What are the neuropsychiatric consequences of sleep-disordered breathing?

A

Neuropsychiatric consequences include excessive daytime sleepiness (EDS), fatigue, insomnia, and neuropsychiatric symptoms.

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23
Q

What are some potential treatments for OSA?

A

Continuous positive air pressure (CPAP) treatment can reduce blood pressure, improve EDS, and prevent the progression of mild OSA in obese patients.

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24
Q

What are central hypersomnias characterized by?

A

Central hypersomnias are characterized by excessive daytime sleepiness (EDS) and/or increased sleep (hypersomnia) not caused by disturbed nocturnal sleep or misaligned circadian rhythm.

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25
Q

WHAT IS cataplexy?

A

Cataplexy is a sudden and temporary loss of muscle tone or muscle weakness, typically triggered by strong emotions such as laughter, surprise, or excitement. It is a key symptom of narcolepsy, a neurological sleep disorder. Cataplexy occurs due to a lack of hypocretin (also known as orexin)

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26
Q

What treatments are effective for narcolepsy?

A

Effective treatments include lifestyle changes, antidepressants, stimulants, and sodium oxybate.

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26
Q

What treatments are effective for narcolepsy?

A

Effective treatments include lifestyle changes, antidepressants, stimulants, and sodium oxybate.

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27
Q

What is one reason why Restless Legs Syndrome (RLS) is under-diagnosed?

A

Lack of specific diagnostic markers and thresholds for symptom severity.

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28
Q

Which neurotransmitter is suggested to play a primary role in the pathophysiology of RLS?

A

Dopamine.

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29
Q

Approximately what percentage of adult RLS subjects present with Periodic Limb Movements in Sleep (PLMS)?

A

70% to 90%.

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30
Q

Name one neurological or psychiatric condition that is associated with higher rates of RLS.

A

Migraine, multiple sclerosis, spinal cord lesions, parkinsonism, and mood disorders.

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31
Q

What is a potential treatment option for chronic and clinically significant RLS?

A

Non-ergot dopamine agonists or a-2-d calcium channel ligands.

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32
Q

What is the prevalence of chronic fatigue in people seen in primary care?

A

Chronic fatigue is reported in more than 20% of people seen in primary care.

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33
Q

What are some examples of medical and neurological diseases in which chronic fatigue can be a part?

A

Chronic fatigue can be a part of medical and neurological diseases such as anaemia, multiple sclerosis, and poststroke.

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34
Q

What is the clinical definition of fatigue?

A

Fatigue is best defined as difficulty in initiation of or sustaining voluntary activities.

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35
Q

How can pathological fatigue be understood in neurological disorders?

A

Pathological fatigue is best understood as an amplified sense of normal (physiological) fatigue that can be induced by changes in one or more variables regulating work output.

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36
Q

What are some examples of fatigue being present in the disorders of the peripheral, autonomic, and central nervous system?

A

Fatigue is consistently seen with lesions in pathways associated with arousal and attention, reticular and limbic systems, and the basal ganglia.

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37
Q

How can peripheral fatigue be assessed clinically?

A

A distinctive topographic pattern of myopathic weakness is a strong clue for the peripheral origin of fatigue. Disorders of the neuromuscular junction are typical examples of muscle fatigability.

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38
Q

What is the Jolly test used for?

A

The Jolly test is a standard electrophysiological procedure for screening myasthenic disorders, involving repetitive electrical stimulation of selected motor nerves at low frequency (3 Hz).

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39
Q

What is Single Fiber Electromyography used for?

A

Single Fiber Electromyography is a special technique of recording single muscle fiber action potentials and is a sensitive test for neuromuscular junction transmission disorders.

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40
Q

What are some screening tests for mitochondrial myopathy?

A

Measurement of pre-exercise and postexercise oxygen saturation of venous blood during aerobic maximum forearm exercises can be used as screening tests for mitochondrial myopathy.

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41
Q

What is the typical exercise duration in the forearm ischaemic test for patients with disorders of glycogen metabolism?

A

Patients with disorders of glycogen metabolism are seldom able to exercise beyond 1 minute in the forearm ischaemic test.

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42
Q

What does failed lactate production during exercise suggest?

A

Failed lactate production during exercise suggests a metabolic block in the glycogenolytic or glycolytic pathway, as seen in McArdle’s disease.

43
Q

What happens to ammonia concentration in venous blood after ischaemic forearm exercise?

A

Ammonia concentration in venous blood rises after ischaemic forearm exercise.

44
Q

How is myoadenylate deaminase deficiency indicated in the forearm ischaemic test?

A

A typical lactate response without a postexercise rise in venous ammonia concentration indicates myoadenylate deaminase deficiency.

45
Q

What does a lack of change in venous oxygen saturation after aerobic maximum forearm exercises suggest?

A

A lack of change in venous oxygen saturation after aerobic maximum forearm exercises suggests mitochondrial myopathy, specifically failure to enhance oxygen extraction at the level of the respiratory chain.

46
Q

What are typical examples of peripheral neuromuscular fatigue disorders?

A

Myasthenic disorders and primary muscle diseases are typical examples of peripheral neuromuscular fatigue.

47
Q

What are the symptom triads of metabolic myopathies?

A

The symptom triads of metabolic myopathies are premature exertional muscle fatigability, exercise-induced cramps, and myalgia.

48
Q

What is the characteristic feature of central fatigue?

A

A feeling of constant exhaustion is a characteristic feature of central fatigue.

49
Q

What is an important clue to identify depressive fatigue?

A

Low motivation, loss of pleasure (anhedonia), early morning awakenings, self-imposed avoidance of social contacts, inappropriate guilt, and suicidal ideations are important clues to identify depressive fatigue.

50
Q

What could orthostatic symptoms indicate in patients with central fatigue?

A

Autonomic impairment, and formal autonomic and cardiac tilt-table tests might be needed to assess the condition.

51
Q

What type of diagnostic method is useful for narcolepsy?

A

The multiple sleep latency test is a useful diagnostic method for narcolepsy.

52
Q

What are some examples of neurological disorders associated with central fatigue?

A

Poststroke fatigue, basal ganglia disorders, brainstem fatigue generator model in postpoliomyelitis fatigue, posterior fossa lesions, Chiari malformations, hypothalamic-pituitary-diencephalic syndromes, and narcolepsy.

53
Q

How are hypocretins (orexins) related to narcolepsy?

A

Selective degeneration of neurons activated by hypocretin (orexin) in the perifornical area of the lateral hypothalamus can cause primary narcolepsy.

54
Q

What role does hypocretin play in the sleep-wake cycle?

A

Hypocretins regulate the sleep-wake cycle by promoting wakefulness and inhibiting rapid eye movement sleep.

55
Q

What is the suggested mechanism of fatigue in disorders associated with an underactive hypothalamic-pituitary-adrenal axis?

A

Fatigue in these disorders could be attributable to proinflammatory cytokines activated by reduced corticotropin-releasing factor and low cortisol concentrations.

56
Q

How is central fatigue different from muscle fatigability?

A

Central fatigue refers to a feeling of constant exhaustion, while muscle fatigability involves reduced muscle strength or endurance during exercise.

57
Q

What imaging methods have been used to study central fatigue?

A

1) Functional MRI

2) Proton magnetic resonance spectroscopy

3)Fludeoxyglucose-positron emission tomography brain scans

58
Q

What are some biological factors affecting central fatigue?

A

1) Cortisol concentrations

2) Rate of synaptic inactivation of norepinephrine

3) Synaptic monoamine levels

59
Q

What new class of drugs is being developed to target neuropeptide function in fatigue and anxiety?

A

1) Antagonists to substance P

2) Vasopressin

3) Melanocortin concentrating hormone

4) Corticotropin-releasing factors

60
Q

What are circadian rhythms, and how are they generated in mammals?

A

Circadian rhythms are self-sustained molecular core transcription-translation feedback loops that generate rhythms in cells, tissues, and organs in mammals.

61
Q

How has artificial bright light been used in clinical settings?

A

Artificial bright light has been used to treat mood and sleep disorders.

62
Q

What is the difference between daylight and electric light in terms of spectral power distribution?

A

Daylight has a broad continuous spectral power distribution that changes within and across days and with weather and sky conditions, while electric light sources have different spectral power distributions depending on the type (incandescent, fluorescent, or LED).

63
Q

How is daylight input to the eye and brain important for humans?

A

Daylight reaching the retina is crucial for both vision and non-visual input to the brain. Non-visual input is mediated by intrinsically photosensitive retinal ganglion cells (ipRGCs) expressing melanopsin and affects circadian rhythms, sleep, alertness, pupil size, and more physiological functions.

64
Q

What role do ipRGCs play in the entrainment of the circadian clock?

A

ipRGCs mediate entrainment of the circadian clock in the suprachiasmatic nuclei (SCN) to the 24-hour light-dark cycle.

65
Q

How does daylight impact circadian rhythms and sleep?

A

Daylight can synchronize and shift circadian rhythms, trigger seasonal responses, modify sleep, and increase alertness.

66
Q

How does daylight exposure affect the development of myopia in young individuals?

A

Exposure to natural light, particularly being outdoors for 2-3 hours daily, has been shown to be protective against the development of myopia in young individuals.

67
Q

What are some health risks associated with increased screen time and reduced natural daylight exposure in children?

A

Physiological disorders (sleep, obesity), psychological problems (depression, anxiety), and cognitive impairment.

68
Q

What role does Vitamin D play in bone development and health?

A

Vitamin D is essential for bone development and health, and it is synthesized by ultraviolet-B in daylight reaching the skin.

69
Q

What role does Vitamin D play in bone development and health?

A

Vitamin D is essential for bone development and health, and it is synthesized by ultraviolet-B in daylight reaching the skin.

70
Q

How is Vitamin D linked to the circadian system and the sleep-wake cycle?
Answer:

A
71
Q

How is Vitamin D linked to the circadian system and the sleep-wake cycle?

A

Vitamin D is linked to the circadian system and the sleep-wake cycle, possibly through the immune system or the newly discovered melanopsin-photosensitive system in human skin.

72
Q

How is bright light used as an antidepressant for seasonal and other depressions?

A

Bright light is an established antidepressant for seasonal and other types of depressions.

73
Q

What is excessive daytime sleepiness (EDS), and what is its key symptom?

A

EDS is an increased tendency or need to fall asleep. Its key symptom is an increased need for sleep during the daytime.

74
Q

How is impaired vigilance quantified in narcolepsy?

A

Using the sustained attention to response task (SART), which involves pressing a key when a number appears on a screen, except when that number is 3.

75
Q

What does the SART error score measure?

A

The SART error score measures both commission errors (key presses when no key should be pressed) and omission errors (absent presses when a key should have been pressed).

76
Q

How do the SART error scores compare between patients with narcolepsy and healthy controls?

A

In a previous study, SART error scores showed excellent sensitivity (87%) and specificity (100%) in a comparison of patients with narcolepsy and healthy controls.

77
Q

What does the multiple sleep latency test (MSLT) measure, and how does it differ from the SART?

A

The MSLT measures the propensity to fall asleep quickly, while the SART, requiring prolonged attention, likely reflects impaired vigilance.

78
Q

What could be the possible mechanism for impaired SART parameters in sleep disorders?

A

Impaired SART parameters in sleep disorders may be associated with changes in frontal brain regions responsible for decision-making and arousal.

79
Q

What are the five stages of vigilance scored in polysomnography?
Answer:

A

The five stages of vigilance scored in polysomnography are:

1) Wake (W)

2) Light sleep stage 1 (N1)

3) Light sleep stage 2 (N2)

4) Slow-wave sleep (N3) (N1 + N2 + N3 = non-rapid eye movement (NREM) sleep)

5) Rapid eye movement sleep (R)

80
Q

How is a stage assigned to each 30-seconds epoch of a polysomnography recording?

A

A stage (the main stage) is assigned to each 30-seconds epoch of a polysomnography recording based on EEG, chin EMG, and EOG criteria.

81
Q

What are the criteria for determining each stage based on EEG frequencies?

A

The criteria for determining each stage based on EEG frequencies are as follows:

–> Slow-wave activity: [0.5 ; 2 Hz[, > 75µV amplitude from peak to peak in frontal derivations

–> Delta: [0,5 ; 4 Hz[

–> Theta: [4 ; 8 Hz[

–> Alpha: [8 ; 13 Hz[

–> Beta: > 13 Hz

82
Q

What does NREM sleep stand for, and how is it calculated in polysomnography?

A

NREM sleep stands for non-rapid eye movement sleep.

It is calculated by combining the durations of:

  • light sleep stage 1 (N1)
  • light sleep stage 2 (N2)
  • slow-wave sleep (N3)
83
Q

What are some of the events that are scored during polysomnography?

A
  • Arousals
  • Cardiac events
  • Motor events
  • Respiratory events.
84
Q

What is the EEG frequency range for slow-wave activity, and what is its amplitude criterion for frontal derivations?

A

The EEG frequency range for slow-wave activity is [0.5 ; 2 Hz[, and its amplitude criterion for frontal derivations is > 75µV from peak to peak.

85
Q

What EEG frequency range is associated with the delta wave?

A

The delta wave is associated with the EEG frequency range of [0.5 ; 4 Hz[

86
Q

Which stage of vigilance is characterized by EEG frequencies in the theta range?

A

The light sleep stage 1 (N1) is characterized by EEG frequencies in the theta range ([4 ; 8 Hz[).

87
Q

What is sinus tachycardia during sleep, and what is the heart rate threshold for adults?

A

Sustained sinus heart rate of > 90 bpm (beats per minute) in adults.

88
Q

What is sinus bradycardia during sleep, and what is the heart rate threshold for ages > 6 years through adulthood?

A

Sustained sinus heart rate of < 40 bpm (beats per minute) for ages > 6 years through adulthood.

89
Q

Define asystole during sleep and the duration criteria for ages > 6 years through adulthood.

A

Cessation of cardiac electrical activity lasting > 3 seconds for ages > 6 years through adulthood.

90
Q

What is the definition of wide complex tachycardia during sleep, and what are the criteria for heart rate and QRS duration?

A

At least 3 consecutive beats with a frequency > 100 bpm (beats per minute) and a QRS duration ≥ 120 ms (milliseconds).

91
Q

What is narrow complex tachycardia during sleep, and what are the criteria for heart rate and QRS duration?

A

At least 3 consecutive beats with a frequency > 100 bpm (beats per minute) and a QRS duration < 120 ms (milliseconds).

92
Q

Describe atrial fibrillation during sleep based on the changes in QRS complexes and P waves.

A

Atrial fibrillation during sleep is characterized by irregular QRS complexes associated with the replacement of consistent P waves by rapid oscillations varying in size, shape, and duration.

93
Q

What are the heart rate thresholds for sinus tachycardia and sinus bradycardia during sleep?

A

Sinus tachycardia: > 90 bpm
Sinus bradycardia: < 40 bpm

for ages > 6 years through adulthood.

94
Q

What are the non-visual responses to light and why are they important?

A

known as “non-image-forming” responses, refer to the physiological and behavioural effects of light exposure that go beyond supporting visual perception.

These responses include:

  • circadian rhythm regulation
  • melatonin secretion
  • sleep
  • alertness
  • pupil constriction
  • other neurobehavioral functions.

They are important determinants of health, well-being, and performance and can have clinical relevance in conditions such as circadian rhythm sleep disorders and depression.

95
Q

What are intrinsically photosensitive retinal ganglion cells (ipRGCs), and what is their role in non-visual responses to light?

A

Intrinsically photosensitive retinal ganglion cells (ipRGCs) are a specialized class of retinal neurons that are responsible for non-visual responses to light.

They play a crucial role in transmitting light information to the brain, influencing circadian rhythms, melatonin secretion, sleep, and other physiological responses.

The light-sensing photopigment within ipRGCs is called melanopsin, which is most sensitive to light in a distinct portion of the visible spectrum.

96
Q

How do melanopic EDI and other metrics help in understanding the impact of light on non-visual responses?

A

By quantifying the effective rates of photon capture for each human retinal opsin under a given light condition.

They provide a more accurate representation of the spectral sensitivity of melanopsin-dependent responses to light compared to traditional photometric quantities. This allows researchers to better assess how different light exposures affect non-visual responses, such as circadian entrainment/resetting, sleep/arousal, hormone secretion, and mood.

97
Q

What are the recommended minimum melanopic EDI levels for indoor environments during the daytime?

A

It is 250 lux at the eye. This measurement is taken in the vertical plane at approximately 1.2 meters height, which represents the vertical illuminance at eye level when seated.

98
Q

What are the recommended maximum melanopic EDI levels for indoor environments during the evening?

A

Starting at least 3 hours before bedtime, the recommendation is maximum 10 lux at the eye. This measurement is also taken in the vertical plane at approximately 1.2 meters height.

99
Q

What are the recommended maximum melanopic EDI levels for the sleep environment at night?

A

The sleep environment should be as dark as possible, and the recommended maximum is 1 lux at the eye.

100
Q

False or True?

Stage N1 increases predominantly in male as they age.

A

True

101
Q

False or True?

Sleep spindles are known for being very important for the learning process and intelligence level

A

True

102
Q

What does CAP and NCAP stands for?

A

(non) Cyclic alternating Pattern

It is the EEG marker of unstable sleep. Sleep restorative = stable sleep

103
Q

Where are the glutamatergic neurons that trigger the muscle atony of REM sleep located?

A

The sublaterodorsal tegmental nucleus

104
Q

Excessive daytime sleepiness (EDS) and fatigue reflect different dimensions of sleepiness. Which of the following statements is correct (only one answer)?

A

Currently there is no test for objectively assessing fatigue.

105
Q
A