NB12-2 - Sleep and DLA Flashcards

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1
Q

List the different methods for examining brain activity during sleep.

A
  • Electroencephalogram (EEG) - records electrical potentials created by neuronal activity
  • Positron emiision tomography (PET)
  • fMRI - detects changes in cerebral blood flow
  • Magnetoencephalogram (MEG) - detects magnetic signals generated by neural activity
  • Electromyography (EMG) together with nerve conduction velocity (NCV)
  • Polysomnogram (PSG) sleep study - EEG, electrooculogram (EOG), EMG, ECG, and pulse oximetry
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2
Q

Describe how an EEG detects brain activity. Describe the basics of reading an EEG.

A

Using more than 20 electrodes placed on the scalp, an EEG can detect voltage differences generated between electrodes by the electrical activity of neuron APs. The firing of a signal neuron is extremely low so the EEG can only detect the summed electrical activity of thousands of neurons and has to use an amplifier to do so.

Two basic things can be learned from an EEG strip: the height (amplitude) of a wave corresponds to the voltage generated and the frequency of waves correspons to the rythmic frequency of that area of the brain.

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3
Q

How can you determine a persons state of consciousness from an EEG?

A

When someone is awake, cortical activity causes low amplitude, desynchronized EEG wave patterns

When someone is sleeping, cortical activity causes high amplitude, synchronized EEG wave patterns

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4
Q

List the EEG brain rhythms we need to know. Why is it important to know these?

A
  • Beta waves are low amplitude and at 12-40 Hz
  • Alpha waves are low amplitude and at 9-12 Hz
  • Theta waves are medium amplitude and at 4-8 Hz
  • Delta waves are high amplitude and at 0-4 Hz

Being able to recognize the different brain waves will enable you to identify the different stages of sleep.

Refer to image

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5
Q

Which EEG rhythms are present when awake and what causes them?

A

Alpha Rhythms - present when eyes are closed

Beta Rhythms - present when eyes are open

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6
Q

List the stages of sleep and describe the EEG rhythms seen in each stage. List other names these stages go by.

A
  • Stage 1 (non-REM) - theta rhythms
  • Stage 2 (non-REM) - spindle (very high frequency & low amplitude) and K complex (large amplitude low frequency blips) rhythms.
  • Stage 3 (non-REM) - delta rhythm
  • Stage 4 (non-REM) - larger amplitude delta rhythm
  • REM Sleep - mostly beta rhythms

Each stage can also be denoted by N1, N2, N3, & N4. Stages 3 & 4 are often grouped together and called slow-wave sleep (SWS) or just N3.

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7
Q

Describe the typical sleep cycle, providing timeframes. About how much of a normal night’s sleep is non-REM (NREM)?

A

A normal sleep cycle progresses from stage 1 to stage 2 to stage 3/4 back to stage 2 and then REM sleep. This whole process from the beginning of stage 1 to the end of REM sleep takes about 90minutes and it repeats until we awaken. REM sleep becomes a little longer with each cycle.

About 80% of sleep is NREM

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8
Q

Describe what sleep pressure is and what is thought to cause it. How does sleep drive correlate with the circadian sleep rhythm?

A

Sleep pressure is a homeostatic pressure that keeps track of how long we have been awake. The longer we are awake the greater sleep pressure becomes. It is believed to be caused by increasing adenosine levels.

As sleep pressure increases, the circadian drive for arousal diminishes. When the difference between the two increases enough, you fall asleep.

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9
Q

List the nuclei that drive wakefullness, the type of neurotransmitters they release, and where they synapse.

A

Arousal systems are all either cholinergic or monoaminergic (except for lateral hypothalamus) pathways and are all part of either the Ascending Reticular Activating System (ARAS), basal forebrain, or hypothalamus:

  • Cholinergic projection from pedunculopontine and laterodorsal tegmental nuclei which project to the thalamus and cerebral cortex. Also, from basal forebrain to the cortex
  • Serotonergic projections from raphe nuclei to the cortex
  • Noradrenergic projections from locus coeruleus to the cortex
  • Dopaminergic projections from ventral tegmentum to the cortex
  • Histaminergic projections from tuberomamillary nuclei to cortex
  • Orexinergic projections from lateral hypothalamus to everywhere
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10
Q

Which arousal center is responsible for activating all the other arousal centers?

A

Lateral hypothalamus

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11
Q

List the nuclei that drive sleep, the type of neurotransmitters they release, and where they synapse.

A

Sleep is controlled by prjections from the ventrolateral preoptic region in the hypothalamus (VLPO) and they release GABA or galanin on all of the arousal systems, inhibiting their activity, which causes sleepiness.

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12
Q
A
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13
Q

Describe how the sleep-wake cycle affects the thalamic relay neurons?

A

During the waking state, cholinergic input to the thalamus from the arousal centers allow the thalamic neurons to be more responsive to sensory information. They’re said to be in a “transmission mode” which is seen as alpha waves on an EEG

During the sleeping state, the absence of cholinergic input to the thalamus causes the thalamic relay neurons to be unresponsive to sensory information. As a result, the neurons are mostly hyperpolarized until enough Ca++ accumulates in them to trigger one synchronized AP. This is said to be “burst mode” and is observable on an EEG as delta rhythms during SWS.

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14
Q
A

F

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15
Q

Describe how the presence of sunlight influences the sleep/wake switch.

A

The SCN strongly innervates the subparaventricular zone (SPZ) of the thalamus and the dorsomedial hypothalamic nuclei (DMH).

The DMH will integrate feeding, temperature, and light information from the SPZ and SCN before having its projections release GABA on the VLPO, inhibiting it, and excitatory NTs on the LH, stimulating it and causing arousal.

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16
Q

What does the EEG patern of REM sleep appear so similar to the waking state EEG?

A

During NREM, the VLPO is inhibiting all of the arousal centers. During REM, the VLPO stops inhibiting the cholinergic arousal centers which allows the thalamus to behave how it would during the waking state.

17
Q

How is cerebral blood flow different in the waking state, NREM sleep, and REM sleep?

A

REM sleep has increased blood flow, relative to NREM sleep, in the pons, midbrain, basal ganglia, thalamus, basal forebrain, paralimbic regions, and some association cortices.

The waking brain also has increased blood flow to the dorsolateral PFC and more association cortices. It has slightly decreased blood flow to the paralimbic regions.

18
Q

Describe what REM associated atonia is and what is believed to cause it.

A

It is the active inhibition of motor systems, except for respiratory and ocular, during REM sleep.

It is believed to be caused by the supraolivary nucleus, in the ventromedial medulla, releasing glutamate on the spinal cord ventral horn interneurons which then release GABA/Gly on motor neurons

19
Q
A

D

20
Q
A

C

21
Q

What are the neurological signs of sleep deprivation?

A
  • Mild inconstant nystagmus
  • Impaired saccadic eye movements
  • Ptosis of eyelids
  • Slight hand tremor
  • Flat speech
  • Anomia (trouble finding words to say)
  • Reduced seizure threshold
  • Perceptual distortions
22
Q

List the major health effects of sleep deprivation.

A
  • Increased risk for heart disease, high BP, stroke, and heart attack
  • Increased chance for weight gain and diabetes
  • Immune system depression
23
Q

Why is sleep important for memory consolidation?

A

Synpases grow quite a bit during the waking state which can cause signals to get noisey. Synaptic pruning occurs during sleep and enhances the primary memory signal.

There also appear to be memory replay during sleep.