S8 L2 The reticular formation: control of consciousness Flashcards

1
Q

What is consciousness?

A
  • Related to awareness of external environment and internal states
    → Exteroreception- external world
    → Interoreception- internal world
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2
Q

What is aurosal?

A

Emotional state associated with some kind of goal or avoidance of something noxious

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3
Q

What are the basic component involved in consciousness?

A

Cerebral cortex and reticular formation
Connected to each other by reciprocal excitatory projections, forming a positive loop
Cerebral cortex- site where many conscious thoughts arise - receives many inputs
Reticular formation associated with keeping the cortex awake

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4
Q

What is the cerebral cortex?

A

Site where conscious thought arises

Receives many inputs, including from the reticular formation

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5
Q

What is the reticular formation?

A

The circuitry that keeps the cortex awake
Diffuse set of neurones throughout the brainstem
Receives many inputs→ sensory system and cortex
Widespread outputs
Large part devoted to arousal

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6
Q

What are the main outputs from the reticular formation?

A

3 main relay nuclei
Cholinergic (excitatory) projection to these relaya
1. Basal forebrain → excitatory cholinergic fibres to the cortex (think sedative side effects of anticholinergics)
2. The hypothalamus → excitatory histminergic fibres to the cortex (think sedative side effect of sedating antihistamines)
3. The thalamus → excitatory glutamatergic fibres to the cortex
Also projections down the spinal cord, responsible for maintaining muscle tone → rapid eye movement sleep- effectively paralysed by inhibitory inputs from the RF

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7
Q

How are the cortex and reticular formations connected?

A

Positive feedback loops are seen when there is a binary outcome
Sleep/awake, ovulating/not ovulating etc….
(binary outcome - only two possible outcomes)

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8
Q

How can you access consciousness?

A
Glasgow Coma Scale (GCS)
Three components 
→ Eye opening 
→ Motor response 
→ Verbal response 
Looking for the best response in all
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9
Q

What are the different levels of response in the eye opening pathway?

A
  1. Spontaneous = 4
    → Suggest normal cortical and brainstem function
  2. Speech response = 3
    → Slightly diminished cortical function but still functioning brainstem
    → e.g. sleeping
  3. To pain = 2
    → Subcortical reflex activity
    → Suggests impaired cortical function but brainstem preserved
  4. No response = 1
    → Suggests severe damage to brainstem +/- cortex
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10
Q

What are the different levels of response in the motor response pathway?

A
  1. Obeys command = 6
    → Normal function with working connections from the auditory to brainstem/spinal cord
    → Whole pathway intact
  2. Localises = 5
    → Able to bring hand up to the part of the body that you stimulate
    → Cortical activity but less
    → Connections from sensory to motor cortex still functioning
  3. Withdrawal = 4
    → Remove from painful stimuli
    → Physiological reflex response still working
    → Spinal reflex, brainstem mediated, doesn’t require cortical input
  4. Flexor response = 3
    → Flexion in response to painful stimuli
    → Physiological response
    → Decortical lesion above the level of the red nuclei
  5. Extensor response = 2
    → Lesion below red nuclei
    → Not a physiological response
  6. No response = 1
    → Nothing happens
    → Severe damage
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11
Q

What are the different levels of response in the verbal response pathway?

A
  1. Orientated = 5
    → Appropriate answer to question
    → Normal cortical function
  2. Confused conversation = 4
    → Understand question but don’t get the answer right
    → Suggest diminished higher cortical function
  3. Inappropriate word = 3
    → Still verbal
    → Suggests language centres have been damaged
  4. Incomprehensible sounds = 2
    → Cortical damage with brainstem mediated groans
  5. No response = 1
    → Severe damage to brainstem +/- cortex
    → Brainstem damage really bad, unable to activate muscles for phonation
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12
Q

What is the electroencephalogram?

A
  • Measure combined activity of thousands of neurones in a particular region of the cortex
  • High temporal resolution → electrical changes in the brain per ms
  • Low spatial resolution → unable to localise lesion as it looks at the summed activity of thousands of neurones
  • Detects neuronal synchrony, sign of normal cerebral function
    → occurs in the brain during physiological and pathological process such as sleep and epilepsy
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13
Q

What is the normal EEG look like during sleep?

A

Awake with eyes open → beta waves - irregular 50 Hz
Awake with eyes closed → alpha waves - regular 10 Hz
4 stages and REM stage
Cycles through about 6 times per night
Stage 1 sleep → Back ground alpha + interspersed theta waves (theta at around 5 Hz, regular)
Stage 2/3 sleep → Background of theta + interspersed sleep spindles and k-complexes
Stage 4 sleep → delta waves - regular 1Hz, related to k-complexes seen in stages 2/3
REM sleep → EEG similar to beta waves, dreaming occurs in this stage, so similar to the EEG in a conscious patient

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14
Q

What are the functions of sleep?

A
Generally unknown - enigmatic 
Energy conservation/repair 
Memory consolidation 
Clearance of extracellular debris 
Resetting of the CNS
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15
Q

What is the neural mechanism of sleep?

A
  • Complex
  • Basically about deactivating the reticular activating system (and hence the cortex) and inhibiting the thalamus
  • Facilitated by the removal of sensory inputs (fewer positive influences on positive feedback loops) → from the reticular formation
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16
Q

What is REM sleep?

A
  • Initiated by groups of neurones in the pons → appears to be an active process
  • EEG activity is similar to that seen during arousal (beta waves), person difficult to rouse due to strong inhibition of the thalamus
  • ↓muscle tone due to glycinergic inhibitor of lower motor neurones
  • Autonomic effects are seen e.g. penile erection, loss of thermoregulation
  • Essential for life- long term deprivation leads to death
17
Q

What are some sleep disorders?

A

Insomnia → commonly caused by underlying psychiatric disorder as opposed to primary insomnia
Narcolepsy → rare disorders, some cases are caused by mutation in the orexin gene, orexin is a peptide transmitter involved in sleep
Sleep apnoea → common condition, often caused by excess neck fat leading to compression of airways during sleep and frequent waking, causes excessive daytime sleepiness

18
Q

What are some disorders of consciousness?

A

Brain death
Coma
PVS (persistent vegetative state)
Locked in syndrome

19
Q

What happens in brainstem death?

A

Widespread cortical and brainstem damage, flat EEG

20
Q

What happens in a coma?

A
  • Widespread brainstem and cortical damage
  • With various (disordered) EEG patterns detectable
  • Unarousable and unresponsive to psychologically meaningful stimuli
  • No sleep-wake cycle detectable
21
Q

What happens in PVS?

A
  • Widespread cortical damage
  • With various (disordered) EEG patterns detectable
  • Some spontaneous eye opening
  • Localise to stimuli via brainstem reflex
  • Sleep-wake cycle detectable
22
Q

What happens in locked in syndrome?

A
  • Basilar/pontine artery occlusion
  • Eye movements can be preserved
  • All other somatic motor functions are lost from the pons down
  • Can still hear but can’t speak
23
Q

What neurotransmitters are used in wakefulness?

A
  • All excitatory projections
  • All projections from the RF to the subcortical structures use ACh
  • Inputs
    → Cortex sends excitatory projections down into the reticular formation
    → Sensory neurones ascend through spinal cord and synapse on the RF
  • Outputs
    → From RF projects to thalamus then the cortex (thalamus- glutaminergic (+vs))
    → From RF- projects to the hypothalamus and then to the cortex (hypothalamus- histaminergic (+ve))
    → From RF- basal forebrain nuclei which projects to the cortex (uses ACh at both synpases)
24
Q

What is the clinical important of knowing the neurotransmitters involved?

A
  1. Antihistamines → drowsiness
    → Antagonise histamine at cortex, removed excitatory inputs from hypothalamus causing +ve feedback loop to round slower- less wakefulness
  2. Cholinergic agents → drowsiness
    → Inhibit ACh to cortex