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Clinical neuroscience > Lecture 12- The brainstem, arousal, sleep and consciousness > Flashcards

Lecture 12- The brainstem, arousal, sleep and consciousness Flashcards

1
Q

definine consciouness (arousal and consciousness)

A
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2
Q

Two basic ingredients are required for consciousness

A
  • Cerebral cortex
  • Reticular formation
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3
Q

Reticular formation​

A
  • Diffuse set of neurones sitting throughout the full length of the brainstem (midbrain, pons, medulla)
    • Many inputs from the sensory system and the cerebral cortex
    • Also projects back up to the cortex (excitatory- cholinergic) – monoamine neurones (green)
  • Keeps us awake
  • Positive feedback loop
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4
Q

what is the reticular formation made up of

A
  • A population of specialise interneurons in the brainstem
  • Numerous inputs regulate the level of arousal
    • Sensory system
    • Cortex
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5
Q

how does the reticular formation control consciousness

A

​Occurs via three major relay nuclei- reticular formation sends cholinergic (excitatory) projections to these relays

  • Basal forebrain nuclei send excitatory cholinergic fibres to cortex (think sedative side effects of anticholinergics)
  • The hypothalamus sends excitatory histaminergic fibres to the cortex (think sedative side-effects of sedating antihistamines)
  • The thalamus sends excitatory glutamatergic fibres to the cortex

The reticular formation also sends projections down the cord, responsible formaintaining muscle tone

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6
Q

how can we assess consciousness

A

glasgow coma scale

electroenecephalogram (EEG)

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7
Q

The Electroencephalogram (EEG)

A
  • Measures the combined activity of thousands of neurones in a particular region of cortex
  • High temporal resolution, low spatial resolution
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8
Q

Deprived of sensory input, neurones in the brain tend to fire

A

synchronously

  • EEG good for detecting neuronal synchrony (a phenomenon which occurs commonly in the brain during both physiological and pathological processes such as sleep and epilepsy), and evidence of normal cerebral function
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9
Q

hypongram shows

A

6 stages of sleep

  • Awake
  • Stage 1
  • Stage 2
  • Stage 3
  • Stage 4 (deepest level of sleep)
  • REM
  • Cycle moving from stage 1 to 4 up to REM sleep
  • Rapid Eye Movement sleep
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10
Q

EEG can be used to during sleep to show how the neural pattern changes throughout the different stages of sleep

A

reduced activity of the thalamus as we go down the stages

  • less sneosry info and motor info having to pass through the thalamus
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11
Q

eyes closed EEG

A
  • EEG pattern becomes more ordered and amplitude increases (10hz)
    • Closing eyes causes sensory input deprivation – allows neurones to become more synchronous- therefore amplitude can increase
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12
Q

Stage 1 sleep (5hz) EEG

A
  • Similar to eyes closed
  • Slow and synchronous theta waves
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13
Q

Stage 2/3 EEG

A
  • Background of theta activity
  • Also sleep spindle (spikes of activity arising from the thalamus) and K complex (prelude to delta waves seen in stage 4 sleep)
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14
Q

Stage 4 (1hz) EEG

A
  • High amplitude delta waves
  • Slow waves
  • Very synchronous cortical neurone= intrinsic rhythm of cerebral cortex (inactivated hypothalamus)
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15
Q

REM EEG

A
  • Looks identical to EEG when we are awake
  • When we dream
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16
Q

Neural mechanism of sleep

A
  • Complex
  • Basically about ‘deactivating’ the reticular activating system (and hence cortex) and inhibiting the thalamus
  • Positive feedback loop between RAS and cortex is inhibited leading to decreased cortical inhibition
  • Inhibition of positive feedback loop is assisted by removal of sensory inputs
17
Q

where is REM sleep initiated

A

by neurones in the pons

18
Q

the paradox of REM sleep

A
  • EEG activity is similar to that seen during arousal (beta waves), however the person is difficult to rouse due to strong inhibition of the thalamus
  • Muscle tone in most of the body is lost due to descending inhibition of LMNs by glycinergic fibres arising from the reticular formation and running down the reticulospinal tracts
    • To stop us acting out our dreams e.g. sleep walking
  • Eye movements and some other cranial nerve functions are preserved (e.g. nocturnal bruxism)
  • Autonomic effects are seen including penile erection and loss of thermoregulation (how people die if they sleep without adequate shelter)
19
Q

REM sleep is essential for life

A

– animals deprived of it die

20
Q

Functions of sleep

A
  • not fully understood
  • Energy conservation and bodily repair?
  • Memory consolidation?
  • Clearance of extracellular debris?
  • ‘Resetting’ of the CNS?
21
Q

some disorders of sleep

A

insomnia

narcolepsy

sleep apnoea

22
Q

Narcolepsy (chronic sleep)

A
  • Orexin gene mutation
  • this gene encodes a hypothalamic neuropeptide precursor protein that gives rise to two mature neuropeptides, orexin A and orexin B, by proteolytic processing.
  • Orexin A and orexin B, which bind to orphan G-protein coupled receptors HCRTR1 and HCRTR2, function in the regulation of sleep and arousal.
23
Q

Sleep apnoea

A
  • Extra fatty tissue around the neck can occlude the airway multiple times during the night
  • Therefore people keep waking up to breathe
  • Wont feel refreshed after sleep
24
Q

disorders of consciousness

A
  • brain death
  • comae
  • persistent vegetative state (PVS)
  • locked in syndrome
25
Q

brain death

A
  • Widespread cortical and brainstem damage.
    • Flat EEG
26
Q

Coma

A

Widespread brainstem and cortical damage

  • Various (disordered) EEG patterns detectable.
  • Unarousable and unresponsive to psychologically meaningful stimuli(may have reflexes).
  • No sleep-wake cycle detectable
27
Q

Persistent Vegetative State (PVS)

A

Widespread cortical damage, with various (disordered) EEG patterns detectable.

  • Like coma but with some spontaneous eye opening. Can even localise to stimuli via brainstem reflexes.
  • Sleep-wake cycle detectable
28
Q

Locked in syndrome

A

​can be caused by basilar/pontine artery occlusion.

  • Eye movements can be preserved, but all other somatic motor functions lost from the pons down.
  • brain functioning other than this
29
Q

Consciousness depends on the integrity of and connection between the

A
  • Cerebral cortex
  • Reticular formation
30
Q

Cortex excites the RF and the RF excites the cortex

A
  • Positive feedback loop
  • To sleep this loop must be disrupted
  • Cortical and brainstem (diffuse structure of the RF can be found) lesions can affect consciousnes
31
Q

Important structures for the maintenance of consciousness

A
  1. Inputs to the RF which keeps us conscious
    1. Excitatory (cholinergic) input from the cerebral cortex to the reticular formation in the brainstem
    2. Also constant sensory input (e.g. first/2nd order sensory neurones from the body) to the RF
  2. Outputs from the RF to the cortex to keep us conscious
    1. RF provides outputs which have to pass the thalamus (cholinergic synapse) and project up to the cortex
      1. Glutaminergic projections up to the cortex
    2. Other outputs of the RF include those via the hypothalamus (cholinergic synapse) which project up to the cortex
      1. Histinermergic projections up to the cortex
    3. RF sends outputs to the basal forebrain (cholinergic synapse) nuclei which also project up to the cortex
      1. Cholinergic projections up to the cortex
  3. Both input and output projections are excitatory- positive feedback loop (cholinergic – ACh transmitter)
  4. Transmitters released in the cortex maintain awake fullness
32
Q

why do antihistamines and anticholinergics make you drowsy

A

Both antihistamines (antagonising histamine at the level of the cortex- removing excitatory input at the level of the cortex) and anticholinergic agents (e.g. drugs) can make us more drowsy due to slowing down the positive feedback loop

33
Q

glasgow coma scale

A
  • Prognostic tool
  • Lesion localisation tool
34
Q

Eye opening and GCS

A
  • Spontaneous eye opening (4) suggests normal cortical and brainstem function
  • Response to speech (3) suggests slightly diminished cortical function but still functioning brainstem
  • Response to pain (2) suggests impaired cortical function but brainstem preserved so that reflex opening can occur e.g. facial nerve mediates reflex
  • No response (1) suggests severe damage to brainstem +/- cortex
35
Q

Motor response

A
  • Obeys commands (6) suggests normal function with working connections from auditory system to brainstem/cord
  • Localises to stimuli (5) suggests diminished higher cortical function but still connections working from sensory to motor cortex
  • Withdraws to pain (4) suggests that there is still a ‘physiological’ reflex response to stimuli
    • Brainstem and spinal cord reflex
  • Flexor response to pain (3) suggests a lesion above the level of the red nuclei. This response is still ‘semi- physiological’
  • Extensor response to pain (2) suggests a lesion below the red nuclei. This response is not physiological at all o No response to pain (1) suggests severe damage to brainstem +/- cortex
36
Q

Verbal response

A
  • Oriented in time/place (5) suggests normal cortical function
  • Confused conversation (4) suggests diminished higher cortical function but language centres are still functioning adequately
  • Inappropriate words(3)suggests language centres have been damaged
  • Incomprehensible sounds (2) suggests cortical damage with brainstem mediated groans
  • No response (1) suggests severe damage to brainstem +/- cortex
37
Q
A

Clinical neuroscience (30 decks)

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