EEG and the Sleep Wake Cycle Flashcards

1
Q

What does an EEG measure?

A

It measure electrical signals ont he scalp coming from the pyramidal cells of the cortex

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2
Q

Why is the scale of the EEG smaller than the electrical activity of actual action potentials?

A

the voltage from the APs is attenuated by passage thorugh the skull and because all the electrical activity going on tends to cancel each other out and you get smaller signals on the surface

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3
Q

Why is the reading from a particular electrode not exactly what’s coming out from that region?

A

because it’s actually a relative measurement - compares it to the neighboring electrode or to a reference electrode placed on the ear lobe.

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4
Q

WHat sort of EEG waves do you see when a patient is awake with open eyes? High or low frequency? High or low amplitude?

A

you see beta waves

high frequency, low amplitude

this is because the patient is experiencing all sorts of inputs and outputs and the signals cancel each other out, leading to high frequency, low frequency waves

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5
Q

What sort of EEG waves do you see with a patient who is awake with eyes closed?

A

alpha waves

these are sliely lower frequency and hihger amplitude than the beta waves with eyes open.

this is because they have slightly fewer signals with the eyes closed, so they cancel eachother out less

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6
Q

WHat sort of EEG waves do you see when someone is awake, but very drowsy? or meditating?

A

theta waves

low freqnecy, high amplitude

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7
Q

What sort of EEG waves do you see in slow wave sleep?

A

delta wavves - these are really big and slow

low frequency, high amplitude

you don’t have tons of activity and the cortex is more synchrnized, so you have a decrease in cancellation and additive characteristics leading to slow, big waves

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8
Q

Besides slow-wave sleep, when can synchronicity of the cortex occur?

A

in seizures

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9
Q

What sort of EEG pattern characterizes abscence seizures?

A

spikes and waves

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10
Q

What are the sleep stages?

A

Non-REM sleep: Stage 1-4 (gradual increase in amplitude and decrease in frequency)

REM sleep

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11
Q

What type of EEG waves do you see in REM sleep?

A

beta waves - look very similar to wha tyou have when the patient is awake with open eyes

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12
Q

During sleep, what is the general progression of sleep stages?

A

awake, stage 1, stage 2, stage 3, stage 4 (deep, restorative sleep), then back up..

stage 3, stage 2, REM (briefest)

then back down to stage 2, REM (slightly longer)

back down to 2, then 3, then 2, then REM

then back down to 2, then REM

etc.

overal, the periods of time you spend in REM get increasingly long as you spend more time asleep

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13
Q

What happens to sleep in sleep apnea?

A

the soft palate collapses over the airway in stage 2 sleep, so the body wakes itself up so the patient can breath

this means they never get down to stage 4 sleep or REM sleep - don’t get quality sleep ever

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14
Q

What system is really what promotes wakefulness?

A

the Ascending Reticular Activating System (ARAS)

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15
Q

What makes up the ARAS? WHat NTs?

A

Monoaminergic nuclei:
Substantia nigra/VTA (DA), locus ceruleus (NE), Raphe (5HT), and Tuberomammillary nucleus (HA)

Choinergic Nuclei: laterodorsal tegmental nucleus and pedunculopontine tegmental nucleus

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16
Q

What role does the lateral hypothalamus play in sleep?

A

It has two sets of neurons that secretes peptides necessary for sleep and wakefullness:

orexin (arousal)

melanin-concentrating hormone (promotes REM)

17
Q

How does Orexin stimulate wakefulness?

A

It is excitatory to all the nuclei involved in the ARAS

18
Q

What disorder occurs if you lose the orexin-secretin neurons in the lateral hypothalamus?

A

narcolepsy

(also seems to be a target in TBI and Parkinsons)

19
Q

The preoptic promotes sleep through what neurotransmitters? What do they act on?

A

the ventrolateral preoptic nucleus and median preoptic nucleus secrete GABA and galanin that act to inhibit the ARAS nuclei

20
Q

What is the only part of the thalamus that inhibits the rest of the thalamus? Does this promote arousal or sleep?

A

the thalamuc reticular nucleus - surrounds the thalamus and inhibits it

this promtoes sleep

21
Q

What is the awake affect of the ARAS on the reticular thalamic nuclei?

A

the ARAS (specifically the LDT and PPT) inhibit the reticular nucleus of the thalamus

this means tthere is no inhibition onthe thalamus, so it’s free to activate the cortex

22
Q

Specifically, how does the thalamocortical circuit contribute to sleep spindles and slow waves of non-REM sleep?

A
  1. the LDT and PPT of the ARAS is no longer active, so you don’t get inhibition of the reticular nucleus of the thalamus
  2. the reticular nucleus inhibits the rest of the thalamus
  3. inhibition does NOT mean turn off here though
  4. It promotes bursting patterns in the entire thalamus
  5. the bursts in the thalamus promote synchronized bursts in the cortex
  6. feedback from the cortex will turn off the burst in the thalamus, but re-activate the reticular cell
  7. the re-activated reticular cell then causes a second burst pattern int he thalamus, which stimulates a second burst in the cortex
    etc. …

because of the synchronicity, you get high amplitude, low frequency slow waves

23
Q

During what stage of sleep does the cortex start becoming synchronized? WHat pattern will you see on the EEG here?

A

stage 2 - you’ll see sleep spikes as it starts to synch

24
Q

Describe what’s going on in the thalamocortical circuit during REM sleep?

A

it’s actually similar to what’s going on when you’re awake…

  1. a subset of the LDT and PPT neurons are active during REM sleep
  2. they activate the thalamus and inhibit the thalamic reticular nucleus
  3. the thalamus is free to send “sensory” information to the cortex

so you get more of the cancellation of signals from all the activity, leading to beta waves with high frequency, low amplitude waves

25
Q

How do you get motor suppression during REM sleep?

A

melanin concentrating hormone from the lateral hypothalamus (in the REM-on system) will go to activate the ventromedial medulla

this then secretes glycine onto motoneurons, inhibiting motor function

26
Q

How are the locus ceruleus and raphe nucleu part of the REM-off?

A

they will inhibit the neurons of the LDT/PPT that are active during REM sleep, so that the entire LDT/PPT will be turned off, thus allowing the reticular nucleus of the thalamus to inhibit the rest of the thalamus

27
Q

What are the short term conseqences of lack of sleep?

A

mostly cognitive

reaction time and judgement decrease

28
Q

What are long term consequences of lack of sleep?

A

problems with homeostasis (metabolism and temperature)

infections

hallucinations, seizures

death

29
Q

Is REM sleep necessary for life?

A

It’s not necessary for life in general, but it is needed for aspects of cognition like brain plasticity, consolidation/association/pruning of memories

learning consolidation

30
Q

What does sleep potentially do for brain metabolism?

A

It reduces the energy expenditure to replinish brain glycogen

31
Q

Describe the metabolite clearance theory for sleep?

A

the theory suggests that “somnogen” are buildups of brain metabolism waste products that can’t be cleared while you’re awake because active neurons swell and block CSF outflow.

When you sleep, the neurons shrink and increase the interstitial space, thus allowing the wasteproducts (like adenosine) to leave

32
Q
A