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BB2 > Sleep and Arousal > Flashcards

Sleep and Arousal Flashcards

1
Q

What is consciousness or arousal from a medical point of view?
How is it assessed?

A

The ability of an individual to react appropriately to stimuli in the outside world.
Glasgow Coma Score

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2
Q

What are the six stages on the scale of consciousness?

A

Coma = unarousable unresponsiveness (with or without reflexes present)
Unconsciousness =arousable (but perhaps only temporarily by intense stimuli)
Sleep= arousable by normal stimuli
Drowsy wakefulness= responding in a non-reflex way
Normal wakefulness= responding to spoken or written stimuli
High arousal= hyper alert and fast reactivity

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3
Q

What does EEG stand for?

A

Electroencephalograph

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4
Q

What are the best uses for EEG?

A

Detecting seizure activity (large groups of neurones firing synchronously) or sleep/coma.

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5
Q

What produces large amplitude waves on the EEG?

A

Large group of neurons all firing action potentials at the same time

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6
Q

On an EEG, are the waves of high amplitude during wakefulness or sleep?

A

Sleep - they are high amplitude, but no frequency

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7
Q

Why during wakefulness does an EEG show low amplitude and high frequency?

A

If individual neurones are firing out of phase with each other, the EEG shows a low amplitude ‘desynchronised’ appearance. E.g. in stage 4 sleep.
If they are firing in phase, the EEG shows high amplitude ‘slow wave’ appearance.

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8
Q

The EEG represents activity of the neurons mainly in which part of the brain?
What does this make you think about which part mediates consciousness? Why is this wrong?

A

Cerebral cortex - for both answers
However, in certain stages of sleep the cortical electrical activity is identical with that in the waking alert brain, so clearly there are problems with defining consciousness in terms of electrical activity in the neocortex.

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9
Q

If someone is in a coma, what does the EEG look like?

A

No electrical activity

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10
Q

What occurs during ‘normal’ (slow wave) sleep?

Comment on metabolism, the cardiovascular system, and hormone levels.

A

Heightened anabolic state
Increased growth and rejuvenation (immune, nervous, skeletal and muscular systems)
Decreased heart rate, blood pressure (nocturnal dipping), and sympathetic nervous activity
Growth hormone AND leptin secreted
Wound repair and regrowth of injured tissue
Decreased cortisol levels

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11
Q

What diseases are associated with diminished/absence of nocturnal dipping?

A 
Secondary causes of hypertension, and resistant hypertension
CKD
Diabetes
Older age
Obstructive sleep apnoea
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12
Q

What is considered normal in terms of nocturnal dipping?

A

A decrease of 10-20% in mean nocturnal BP compared with mean daytime BP

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13
Q

What is diminished nocturnal dipping a strong predictor of?

A

Cardiovascular disease - each 5% deficiency in the normal decline in nocturnal BP is associated with 20% greater risk in cardiovascular mortality

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14
Q

How is sleep linked to obesity?

A

During slow wave sleep, leptin is released from fat cells. When you don’t get enough sleep, you end up with lower than normal levels of leptin in your body, which can result in a constant feeling of hunger and overeating leading to obesity.

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15
Q

How many stages of sleep are there?

A

Four stages of normal sleep and one stage of REM sleep

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16
Q

Stages 1-4 of the sleep cycle repeats in cycles through the night. How long are these cycles?

A

90 minutes

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17
Q

Which phase of sleep has an EEG appearance similar to wakefulness?

A

REM

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18
Q

What does the synchronisation of cortical activity say about the consciousness of the person?
What does this say about consciousness?

A

The more synchronisation, the less conscious
Consciousness seems to be a function of the pattern of firing or ‘neuronal programs’ that the cortical cells are running.

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19
Q

Can some people be more conscious than others?

A

Yes - by training our brains to solve puzzles/working out solutions, we may be improving our neuronal programming and increasing our levels of consciousness.

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20
Q

Where are the key control centres that control sleep and wakefulness located?

A

The RETICULAR FORMATION of the PONS

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21
Q

Explain how the pontine neurons control sleep? What are these centres modulated by?

A

There are certain systems of neurons in the pons whose activity keeps us awake and alert (when these are switched off we sleep). These project diffusely to the cerebral cortex.
The centres are modulated by signals from the hypothalamus.

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22
Q

What are the two major types of stimuli for sleep?

A

Chemicals in the blood

Diurnal rhythms

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23
Q

What do the medial and ventrolateral preoptic nuclei in the hypothalamus detect?
What is special about the blood-brain barrier here?

A

They detect blood levels of various molecules, such as ghrelin and adenosine, and these levels can initiate or inhibit sleep.
It is ‘leaky’.

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24
Q

How do ghrelin and low blood glucose affect sleep?

A

Inhibitory action (hunger)

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25
Q

How does cholecytokinin affect sleep?

A

Increased sleepiness (satiated)

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26
Q

How does caffeine keep us awake in relation to adenosine?

A

Antagonist at A1 adenosine receptors

High adenosine levels induce sleepiness

27
Q

What do the preoptic nuclei project to? Explain how they regulate sleep.
What does this area contain?

A

Tuberomamillary nucleus of the hypothalamus - they may regulate sleep by modulating the activity of the histaminergic neurones at the TMN. These neurons are active during waking and silent sleep. They project diffusely to all areas of neocortex.

28
Q

Why do antihistamines cause drowsiess?

A

Because they block the histaminergic neurons at the TMN - these neurons are active during waking, so blocking them promotes sleep.

29
Q

How is the suprachiasmatic nucleus involved in regulating the diurnal rhythm of sleep? Mention the retina and the TMN.

A

The suprachiasmatic nucleus receives an input from fibres from special photoreceptor cells in the retina. These cells fire continuously during daylight and the SCN integrates this to compute the hours of daylight.
The SCN projects to the tuberomamillary nucleus.

30
Q

What is seen in animals with lesions in the suprachiasmatic nucleus?

A

Destroyed diurnal sleep rhythm (sleep in irregular patterns)

31
Q

What is narcolepsy?

What certain peptide is lost in this condition?

A

A disorder characterised by abnormal sleep tendencies, including excessive daytime sleepiness, disturbed nocturnal sleep and pathological REM sleep.
Massive loss of orexins

32
Q

What is thought to be the cause of narcolepsy?

A

The loss of orexin-containing neurones by an autoimmune attack from T-cell lymphocytes

33
Q

What are orexin neurons important for? Where are the cell bodies found? Where do they project to?

A

Maintaining wakefulness
Posterior hypothalamus, with diffusue projections to the cerebral cortex (in particular the association cortex)
They innervate the brainstem, especially the locus coeruleus and raphe nuclei.

34
Q

Do orexins act as transmitter molecules?

How do they promote and maintain wakefulness?

A

No - they are too large (28-33 amino acids long)

They project to nuclei in the brainstem to stimulate release of Ach, NA, serotonin and dopamine.

35
Q

Where are the orexins?

A

The posterior area of the hypothalamus, close to the tuberomamillary nucleus.

36
Q

There are two systems of the hypothalamus necessary for wakefulness. What are these and where do they project/stimulate?

A

The TMN and posterior hypothalamus (histamine and orexins) stimulate the pontine reticular formation – an excitatory drive to the monoamine neurons in the pontine RF which are necessary for arousal (the RF has diffuse projections to the cerebral cortex).
They also project diffusely to the cerebral cortex directly.

37
Q

Where are the monoamine transmitters found in the brainstem?

What do lesions to this area result in?

A

Cell groups in the upper brainstem (midbrain and pons).

Coma, which may be permanent.

38
Q

Orexins project to nuclei in the brainstem to stimulate release of acetylcholine, noradrenaline, serotonin and dopamine.
Where are these nuclei located and what are they called? (4)

A

Pedunculopontine nucleus – cholinergic cells (pons)
Locus coeruleus – noradrenergic cells (pons)
Raphe nuclei – serotoninergic cells (pons)
Ventral tegmental area – dopaminergic cells (midbrain)

39
Q

Apart from the pedunculopontine nuclei, where else are cholinergic neurons found?

A

Basal forebrain nucleus (nucleus basalis), adjacent to the accumbens nucleus

40
Q

Where does the nucleus basalis project to?

In what disease is this nucleus damaged?

A

All parts of the cerebral cortex/neocortex

Alzheimer’s

41
Q

How many % of Alzheimer’s patients have sleep disorders?

A

70%

42
Q

Where do cholinergic neurons of the pedunculopontine nuclei project to?

A

Thalamus

43
Q

What is special about the release of acetylcholine during wakefulness/sleep?

A

Acetylcholine, noradrenaline, and serotonin neurons are all active during wakefulness and all decreased during non-REM sleep.
Noradrenaline and serotonin neurons are INACTIVE during REM sleep, however Ach neurons are active to near waking levels.
Ach is released during REM sleep.

44
Q

If Ach neurons are active during REM to near waking levels, what is it reasonable to suggest that Ach enables?

A

Thalamic and cortical programs (motor and sensory) to run during normal alert waking and also during REM sleep.
We can say that ACETYLCHOLINE ACTIVATES THE THALAMUS (pedunculopontine nuclei) AND CORTEX (nuclei basalis) during both waking and dreaming.

45
Q

Why do we normally forget dreams?

A

The part of our brain that enables experiences in immediate memory (consciousness) to long term memory (noradrenaline activates these circuits) is switched off during REM sleep.

46
Q

The locus coeruleus (noradrenaline) is a control centre for the sympathetic nervous system, but what else does it project to/activate?

A

It also projects rostrally to the cerebral cortex and activates a form of ‘central sympathetic system’.
This activates our ALERTNESS AND ATTENTION, as well as activating the motor system (so our reflexes are faster). Introspection and contemplation are suppressed.

47
Q

When might we remember a dream?

A 
If we are woken during the dream (the noradrenaline system switches on)
Frightening dreams (they activate the noradrenaline system)
48
Q

What does the nigrostriatal dopamine system do during waking?
What about the mesolimbic and mesocortical dopamine systems?

A

It ‘activates’ the basal ganglia so that we can move fluently and smoothly.
Activate the frontal cortex and limbic system (for alertness, focus, planning etc)

49
Q

Why are our motor systems paralysed during REM sleep?

A

The dopamine systems are switched off

50
Q

How does amphetamine and cocaine prevent sleep?

A

By continually releasing dopamine and noradrenaline from nerve terminals despite the amine cell bodies in the brainstem being inactive.

51
Q

What is the suggested activity of serotonin?

How does this relate to dreaming?

A

It keeps a ‘sensory gate’ open. If serotonin activity stops, the thalamus becomes unable to transmit messages from sensory receptors to the cortex. The cortex then generates images/perceptions from its internal memories instead of from reality. These are our dreams.

52
Q

How do SSRIs affect sleep?

A

They suppress REM sleep (as do serotonin-noradrenaline reuptake inhibitors):

Increased sleep onset latency
Increased number of awakenings
Decrease in sleep efficiency
Change in frequency, intensity and content of dreams

53
Q

What are the most troubling side effects of SSRIs? (3)

A

Sexual dysfunction
Weight gain
Sleep disturbance

54
Q

Give an example of a tricyclic antidepressant.

In what way do they affect sleep and how?

A

Amitriptyline (also there is doxepin/silenor)

They promote sleep by blocking histamine H1 receptors and noradrenaline re-uptake.

55
Q

What type of drugs are tranylcypromine and phenelzine?

How do they affect REM sleep?

A

Monoamine oxidase inhibitors
They suppress it (first one associated with insomnia, second one is more typically sedating and less associated with insomnia).

56
Q

What are the two main functions of REM sleep?

A 
Memory consolidation (transfer from short-term to long-term memory)
Removing junk and defragmenting memories
57
Q

Do SSRIs contribute to short-term memory loss?

A

If antidepressants, especially SSRIs inhibit REM sleep, and REM sleep is used by the brain to help consolidate memory, then we might expect some memory problems in patients taking SSRIs. There is limited clinical evidence that chronic use of SSRIs do indeed contribute to short-term memory loss.

58
Q

How is insomnia treated? (5)

A

Lifestyle changes (fixed times for bed, relaxing bedtime routine, comfortable sleeping environment, avoiding caffeine)
Cognitive behavioural therapy
Antihistamines (e.g. Nytol)
Benzodiazepines (for short term insomnia)
Zopiclone, zolpidem, and zaleplon (sedatives that increase GABA release)

59
Q

What is sleepwalking a failure of?

A

During dreams the motor cortex is active and sends motor commands down the corticospinal tract. However the lower motor neurons are functionally disconnected from the corticospinal tract by a powerful descending inhibitory system, so the body’s muscles don’t contract.
Sleepwalking is a failure of this motor disconnection.

60
Q

What is sleep apnoea?

A

This disconnection of motor neurons from the corticospinal tract during REM must AVOID the respiratory system. This isn’t the case in these patients, so they stop breathing when they are dreaming.
The muscles of the throat relax too much and obstruct the airway. If the diaphragm is paralysed, the person wakes up after a minute or so, agitated due to a build up of CO2 (Ondine’s curse).

61
Q

Why do the muscles shut down during sleep/are disconnected from the corticospinal tract?

A

Serotonin and dopamine systems project down the spinal cord, and up to the forebrain.
The ascending systems allow sensory information in, and the descending systems may allow motor commands out to the muscles.
These two systems shut down during REM sleep, so input and output channels are disconnected.

62
Q

How much sleep do we need?

A

Lowest mortality was seen in individuals who slept between 6.5-7.5 hours per night.
Even sleeping 4.5 hours per night is associated with very little increase in mortality.

63
Q

Is insomnia related to depression?

A

Chronic insomnia is a major risk factor for clinical depression.
Once the depression is established, the insomnia may get worse or paradoxically disappear, with the patient now sleeping excessively.

BB2 (32 decks)

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