NEURO: Sleep Flashcards

1
Q

What is an EEG?

A

EEG stands for electroencephalogram.

An amplified recording of the waves of electrical activity generated by the brain. These waves are measured by non-invasive electrodes placed on the scalp-connected to amplifiers and a recording device.

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2
Q

How are the electrodes of an EEG labelled?

A

Right hemisphere
-labelled evenly

Left hemisphere
-labelled oddly

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3
Q

Requirements for EEG to measure brain activity

A

There needs to be:

  • the combined activity of a large number (1000s) of similarly orientated neurones
  • synchronous activity across groups of cells

*thousands of neurones must be firing synchronously to detect signals because EEG can’t measure the activity of individual neurones or small groups of neurones

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4
Q

What does the EEG measure?

A

the post-synaptic activity of a group (1000s) of synchronous neurones is summed to generate a large surface signal, which is then read on an EEG

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5
Q

Importance of synchronous firing for EEG measurement

A

If synchronous post-synaptic firing:
-summed response detected on EEG

If irregular post-synaptic firing:
-only a small summed signal detected on EEG

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6
Q

Describe EEG rhythms.

A

EEG rhythms correlate with states of behaviours. They are categorised by their frequency range.

High-frequency low-amplitude is associated with alertness and waking.
Low-frequency high amplitude is associated with non-dreaming sleep or coma.

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7
Q

List the different EEG rhythm during different functional states of the brain.

A

AWAKE WITH MENTAL ACTIVITY: β 14-30 Hz

AWAKE AND RESTING: α 8-13 Hz

SLEEPING: θ 4-7 Hz

DEEP SLEEP: <3.5 δ Hz

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8
Q

How is synchronous firing achieved?

A

1) Pacemaker:
>synchronous rhythms can be led by a central clock or pacemaker (e.g. thalamus)

2) Collective Behaviour of Cortical Neurones:
>cortical neurones can coordinate themselves and collectively generate synchronous brain rhythms (mutual excitation/inhibition)

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9
Q

Thalamic pacemaker

A

Synaptic connections in the thalamus between excitatory and inhibitory thalamic neurones force each individual neurone to conform to the rhythm of the group

Co-ordinated rhythms are then passed to the cortex by thalamocortical axons

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10
Q

Collective Behaviour of Cortical Neurones

A

Some rhythms don’t depend on the thalamic pacemaker but this:

  • excitatory and inhibitory interconnections of cortical neurones result in a co-ordinated synchronous pattern of activity
  • this can remain localised to a certain region in the cortex or can spread to encompass larger regions of the cortex, depending on the cortical network involved
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11
Q

What is the function of these brain rhythms?

A

The answer is, we don’t really know. However, there are hypotheses going around:

The hypothesis for slow-frequency high-amplitude rhythms during sleep: the thalamus acts as a gate-keeper for information transmission.
During wakefulness, information is transmitted. During sleep, there are synchronous rhythms that block information transmission.

The hypothesis for fast-frequency low-amplitude rhythms during wakefulness: the brain is ‘attention grabbing’ to ‘bind together’ regions needed for task execution.

Hypothesis:
-No direct function, by-products of strongly interconnected circuits.

However, even if brain rhythms don’t have a function, they provide us with a convenient therapeutic window on the functional states of the brain. For example, we can detect seizures in epilepsy patients by looking at EEGs.

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12
Q

What is sleep?

A

It is ‘a readily reversible state of reduced responsiveness to, and interaction with, the environment ’.

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13
Q

What are the different functional states of the brain?

A
  • Wakefulness
  • REM Sleep
  • Non-REM Sleep
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14
Q

Wakefulness (EEG activity)

A

AWAKE:

  • EEG: low-amplitude, high frequency
  • Sensation: vivid, externally generated
  • Thought: logical, progressive
  • Movement: continuous, voluntary
  • REM: often
  • alpha, beta and gamma rhythms
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15
Q

REM Sleep (EEG activity)

A
  • EEG: low-amplitude, high frequency
  • Sensation: vivid, internally generated
  • Thought: vivid, illogical, bizarre, detailed dreams
  • Movement: muscle paralysis, movement commanded by the brain but not carried out, body immobilised
  • REM: often
  • beta and gamma rhythms
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16
Q

Non-REM Sleep (EEG activity)

A
  • EEG: high-amplitude, low frequency
  • Sensation: dull or absent
  • Though: logical repetitive, rarely accompanied by vivid, detailed dreams
  • Movement: occasional, involuntary
  • REM: rare

· Stage 1: Theta Rhythms
· Stage 2: Spindle and K-complex Rhythms
· Stage 3: Delta Rhythms
· Stage 4: Delta Rhythms (deep sleep-higher in amplitude)

17
Q

Physiological changes in REM and non-REM sleep compared to when we are awake

A

Both have a decreased temperature, heart rate and breathing

However, brain energy consumption decreases in non-REM sleep, but increases in REM sleep.

18
Q

Describe the sleep cycle.

A

The EEG stages can be sub-divided to
indicate the depth of sleep (Stages 1-4).

Each night begins with a period of
non-REM sleep, and as the night progresses, there is a shift from
non-REM to REM sleep.

Sleep stages are then cycled throughout the night, repeating ~90 minutes.

19
Q

Why do we sleep?

A

We don’t really know.

Is it to:
>Restoration: to rest and recover and to prepare to be awake again
>Adaptation: to protect ourselves (e.g. hide from predators) and to conserve energy

20
Q

Brainstem activity during wakefulness

A

Increase brainstem activity:

> several sets of neurones increase the rate of firing in anticipation of wakening to enhance the waking state (e.g. ACh, 5-HT, NE and histamine)

> synapse directly with regions e.g. thalamus and cerebral cortex
increasing excitatory activity in the thalamic pacemaker, which suppresses the rhythmic/synchronous form of firing in the thalamus and cortex present during sleep

21
Q

Brainstem activity during sleep

A

decrease in brainstem activity
>several sets of neurones decrease rate of firing during sleep (e.g. ACh, 5-HT and NE).

We get thalamic driven θ and δ waves.

22
Q

Theory of dreaming

A

Cholinergic neurones in the pons have been shown to increase the rate of firing to induce REM sleep. There is a theory of this increased firing and why we dream:

> there is semi-random firing in the pons during REM sleep that activates regions of our brain associated with memories and emotion, translating into vivid dreams

23
Q

Why are dreams often bizarre, vivid and sometimes delusional?

A

> because the pattern of cholinergic firing from pons isn’t particularly synchronised and is happening in various regions of the brain randomly

24
Q

What are some sleep-promoting factors?

A
  • Adenosine
  • Nitric Oxide (NO)
  • Inflammatory Factors
  • Melatonin
25
Q

Adenosine

A

-receptor activation causes decreased heart rate, respiratory rate and smooth muscle tone (decreasing blood pressure)

26
Q

Adenosine antagonists

A

Caffeine

-promote wakefulness

27
Q

Nitric Oxide

A

potent vasodilator which decreases smooth muscle tone (decreasing blood pressure)
-stimulates adenosine release, therefore promoting sleep

28
Q

Inflammatory Factors

A

cytokines (e.g. interleukin-1) released during infection (e.g. cold, flue) have been shown to promote non-REM sleep
>linked to adaptation theory-sleeping to protect ourselves

29
Q

Melatonin

A

a hormone secreted by pineal gland at night, shown to initiate and maintain sleep

30
Q

Circadian rhythm?

A

A physiological cycle of about 24 hours is present in all eukaryotic organisms and that persists even in the absence of external cues (e.g. daylight/darkness) due to us having biological/brain clocks for circadian rhythms.

31
Q

What is a zeitgeber?

A

Environmental cues (e.g. light-dark cycle, temperature, humidity) that entrain circadian rhythms

32
Q

Where are isolation circadian studies best performed?

A

in deep caves, where there are no environmental cues that affect the circadian rhythm:

If humans are separated from all possible zeitgebers, they are said to be in a “free-running” state- internal biological clock of approximately 24.5-25.5 hours.

> Length of the circadian cycle remains constant compared to the natural situation

> But, there are fluctuations in the time of the circadian rhythms, due to the absence of environmental cues (free-running)

> If we were to reintroduce the natural situation, we can become entrained again to display the initial natural situation circadian cycle

33
Q

What is our biological clock?

A

suprachiasmatic nucleus

34
Q

Suprachiasmatic Nucleus

A

small nucleus of hypothalamus directly above optic chiasm that receives retinal innervation and synchronises circadian rhythms with the daily light-dark cycle

35
Q

What are the retinal cells synchronising the SCN?

A

not rods or cones, but speciaised photoreceptor cells expressing the photopigment melanopsin

36
Q

SCN mechanism in circadian rhythms

A

· Photoreceptors expressing melanopsin are slowly excited by light and can detect changes in luminosity.
· Melanopsin receptors project directly to the SCN, inhibiting the production of melatonin by the pineal gland
· Therefore, in a light environment, we stay awake

37
Q

Importance of SCN in circadian rhythms

A

In a control environment, animals were kept in a constant light environment. The animals showed a normal circadian clock around 24-25 hours, with temperature dropping during sleep.

If we were to abolish or inhibit the SCN in these animals, this rhythm is completely disrupted. There are fluctuations in the sleep/wake cycle and body temperature. Therefore, it seems that the SCN is important in the absence of environmental cues.