Arousal, coma and unconsciousness: Implications for management of head trauma Flashcards

1
Q

What is consciousness?

A

At its least, normal human consciousness consists of a serially time-ordered, organized, restricted and reflective awareness of self and the environment. Moreover, it is an experience of graded complexity and quantity.

James, W. The physical basis of emotion. Psychol. Rev. 1, 516–529 (1894).

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2
Q

What is missing from the definition of consciousness?

A

Arousal level and the awareness of the contents of consciousness, which includes a range of specific functional types of attention, intention, memory, and mood–emotion.

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3
Q

What do disorders of consciousness affect?

A

They affect both arousal level and awareness of the contents of consciousness.

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4
Q

Where do we start in consciousness?

A

We start in the Brainstem Nuclei, specifically the Pedunculopontine Nucleus (part of the Ascending Reticular Activating System). From here, tracts go up to the hypothalamus and the basal forebrain, where arousal is driven from.

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5
Q

What are the key neurotransmitters in those pathways?

A

Orexin, Adrenergic, and Cholinergic are vital in sleep and consciousness.

If you have an antibody to orexin, you can get narcolepsy - rapid onset - cannot resist.

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6
Q

What are the neural substrates of consciousness?

A

Basal nuclei (RAS), Thalami-cortical circuits (Global workspace, Internal and external awareness), Striatum (stimulated by thalamus and frontal cortex, inhibits globus pallidus interna), and Globus pallidus interna (inhibits thalamus and brain stem nuclei).

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7
Q

Where is the second part of the circuit found?

A

In the thalamus, frontal and parietal cortex, and the striatum.

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8
Q

What is the thalamo-cortical circuit responsible for?

A

It is responsible for internal and external awareness.

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9
Q

What is the striatum stimulated by and what does it do?

A

The striatum is stimulated by the thalamus and frontal cortex and inhibits the Globus Pallidus Interna.

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10
Q

What does the globus pallidus interna do?

A

It inhibits the thalamus and brain stem nuclei.

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11
Q

Briefly describe how the mesocircuit model enables consciousness.

A
  1. RAS actively switches on the cortex and there is to and fro traffic between the two, activating consciousness. 2. Positive feedback in the frontal lobe stimulates the striatum to stay awake. 3. Striatum inhibits globus pallidus interna, maintaining a level of inhibition when we are conscious.
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12
Q

What happens in this mechanism when we start to become bored/tired?

A
  1. Stimulation from the cortex to the striatum reduces. 2. Inhibition to globus pallidus interna starts to be removed. 3. GPI becomes more active, inhibiting RAS. 4. RAS switches off, leading to sleepiness and fading consciousness.
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13
Q

What is this circuit called?

A

This circuit is known as the mesocircuit model, which includes more detail about the conscious network.

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14
Q

What step in this mechanism keeps you awake?

A

The inhibition of the striatum on the Globus Pallidus Interna keeps you awake.

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15
Q

What would happen if you have an injury that damages this connection?

A

Loss of inhibition in GPi will cause someone to slip into sleep/coma. Interestingly, the use of an inhibitory neurotransmitter can wake someone from a coma by inhibiting the Globus Pallidus Interna, allowing the brainstem nuclei (RAS) to switch back on and stimulate the cortex.

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16
Q

How does the mesocircuit model translate into clinical responsibilities?

A

The brainstem nuclei are the engine house of the conscious network of the meso circuit model, responsible for arousal. The cortex is responsible for awareness, including localized movement, language, thinking, and judgement.

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17
Q

Anatomically, how does internal awareness vary from external awareness?

A

Different parts of the brain are responsible for internal/self-awareness and other parts for external/sensory awareness.

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18
Q

What is brain injury?

A

It is primarily a disruption of networks, resulting in them not working properly. Some networks have other pathways, so injuries to the same degree in different locations can have different outcomes (neuroplasticity).

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19
Q

Define brain stem death.

A

It is when a person no longer has any brain stem functions, permanently losing the potential for consciousness and the capacity to breathe.

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20
Q

What are the diagnostic criteria for brain stem death?

A

The criteria include the absence of brain stem reflexes and the inability to breathe independently.

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21
Q

Define coma.

A

Coma is a complete failure of the arousal system, where the patient cannot have spontaneous eye opening or be awakened by vigorous sensory stimulation, equating to a Glasgow Coma Score of ≤8.

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22
Q

What is Unresponsive Wakefulness (Vegetative State) characterized by?

A

It is characterized by the complete absence of behavioral evidence for self or environmental awareness, with preserved capacity for spontaneous or stimulus-induced arousal, evidenced by sleep-wake cycles.

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23
Q

What is minimal conscious state (MCS)?

A

MCS is when cognitively mediated behavior occurs inconsistently but is reproducible or sustained long enough to be differentiated from reflexive behavior.

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24
Q

What does MCS look like in a patient?

A

Patients may follow simple commands, provide gestural or verbal yes/no responses, and exhibit purposeful behavior, including appropriate emotional responses and reaching for objects.

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25
What can MCS be sub-stratified into?
MCS can be sub-stratified into MCS without language (MCS–) and MCS with language (MCS+), which may have prognostic significance.
26
How can you define emergence from a MCS?
Emergence is characterized by functional communication with accurate yes/no responses and functional object use, such as bringing a comb to the head.
27
What is Akinetic Mutism?
Akinetic mutism (AM) is a subtype of MCS, characterized by reduced goal-directed behavior due to severely diminished drive.
28
How does Akinetic mutism present?
Speech, movement, thought, and emotional expression are uniformly reduced, but responses may be facilitated by high-intensity sensory stimuli.
29
What is Akinetic mutism?
Reduced goal-directed behaviour due to severely diminished drive, rather than decreased arousal or direct damage to neural systems.
30
How does Akinetic mutism present?
Speech, movement, thought, and emotional expression are uniformly reduced. These responses may be facilitated following exposure to high-intensity sensory or personally salient stimuli. ## Footnote E.g. 'telephone effect’ - Pt has profound lack of responsiveness to stimuli, then put a telephone to their ear and get someone meaningful to talk to them and they start to speak.
31
What is post-traumatic confusional state/delirium?
Patient slowly recovers and moves through the different stages of disorders of consciousness and eventually reaches a state of post-traumatic confusion or delirium.
32
What are the characteristics of post-traumatic confusional state/delirium?
Prolonged periods of consciousness with both arousal and a degree of awareness, disorientation, functional object use, expressive language, perseveration, and cognitive impairments. ## Footnote Cognitive impairments include loss of reading ability and lack of curiosity.
33
What is locked-in syndrome?
A de-efferented state characterized by quadriplegia and paralysis of the lower cranial nerves, with retained consciousness, arousal, and awareness but blocked outflow of information.
34
How would locked-in syndrome present in a patient?
Can classically communicate by vertical eye movements and eye blinking.
35
Outline the subtypes of locked-in syndrome.
1. Classical LIS: preserved midbrain function with up-gaze and blinking only. 2. Incomplete LIS: minimal movement in other limbs noted. 3. Complete LIS: no limb or eye movements but preserved consciousness.
36
What is Cognitive Motor Dissociation (CMD)?
Volitional brain activity detected in a patient whose bedside behavioural diagnosis suggests coma, VS/UWS, or MCS, characterized by unconscious awareness.
37
How is covert cognition assessed?
Covert cognition is seen in patients with MCS-, VS/UWS, or coma, where tests show awareness despite lack of consciousness.
38
Outline the stages of recovery of disorders of consciousness.
A patient may enter a coma after a cardiac arrest due to diffuse brain injury, potentially progressing to brain death or recovering to VS, MCS, and emergence from disorder of consciousness.
39
What are the stages of recovery if a patient had acute brain injury and entered a coma?
Stages include coma, potential progression to VS, MCS, and eventual recovery.
40
What is the summary of disorders of consciousness?
| | **arousal** | **awareness** | **extra info** | | --- | --- | --- | --- | | brain stem death | ❌ | ? | legally dead - looks like a coma but there's loss of brainstem reflexes & there’s apnea | | coma | ❌ | ❌ | unconscious - can't feel pain | | vegetative state (UW) | ✅ | ❌ | all reflexive, not voluntary | | minimal conscious state | ✅ | ~✅ | intermittent cognitive behaviour | | locked-in syndrome | ✅ | ✅ | outflow of information is blocked | | cognitive motor dissociation (covert consciousness) | ❌ | ~✅ | looks like coma but there's brain activity on MRI |
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42
What is normal consciousness?
Full awareness and full arousal with full cortex and brainstem function
43
What is coma?
No awareness and no arousal; brainstem switched off, leading to loss of awareness.
44
What is vegetative unresponsive wakefulness?
Full arousal but no awareness; brainstem is active but cortex is damaged and disconnected.
45
What is minimally responsive state?
Full arousal with some patchy awareness; awareness increases towards minimally conscious state.
46
What is locked-in syndrome?
Brainstem function allows for arousal and full awareness, but damage prevents any action.
47
What is cognitive motor dissociation?
No arousal due to non-functioning brainstem nuclei; awareness exists in cortex but patient cannot move.
48
What is the Glasgow Coma Score?
A scale used to measure coma based on eye opening, verbal response, and motor response.
49
What are the physical signs assessed in acute assessment?
Pupils, motor responses, and breathing/autonomic responses.
50
What is the aim of hyperacute assessment?
To assess changes in structural pathology rapidly to prevent deterioration.
51
What is brain herniation?
A condition where increased intracranial pressure causes brain to shift and push out of its compartment.
52
What are the clinical implications of brain herniation?
Can cause critical focal compression of brainstem and spinal cord, leading to rapid decline and death.
53
What is the Monro-Kellie doctrine?
The principle that the skull contains brain, blood, CSF, and ISF, and changes in one component affect the others.
54
What happens if a pathological mass develops in the skull?
CSF and ISF are expelled to accommodate increased volume without pressure increase until a critical volume is reached.
55
What is coning?
A rapid increase in intracranial pressure that pushes brain contents down into the tentorium cerebelli or foramen magnum.
56
What is Cushing's triad?
A set of symptoms indicating increased ICP: hypertension, bradycardia, and respiratory irregularity.
57
What is brainstem death?
A condition where a person has permanently lost all brainstem functions and the potential for consciousness.
58
What spinal reflexes are preserved in brainstem death?
Extension-pronation, plantar responses, muscle stretch reflexes, abdominal reflexes, and the 'Lazarus sign'.
59
What scales are used for assessing consciousness outcomes?
Coma Recovery Scale – R, SMART, and WHIM.
60
What are some pitfalls in ABI consciousness assessment?
Presence of drugs, epilepsia partialis continuans, critical illness neuromyopathy, late hydrocephalus, and hypothermia.
61
What factors affect prognosis in ABI?
Underlying diagnosis and trajectory of the brain injury.
62
What can result in profound switching down of cerebro-cortical activity?
Coma ## Footnote Reversible if hypothermia is treated.
63
What occurs along with Acquired Brain Injury (ABI)?
Occult Spinal Injury ## Footnote Reduced motor responses may result from this.
64
What factors affect prognosis in ABI?
Underlying diagnosis and trajectory.
65
What types of brain injury are considered in ABI prognosis?
Traumatic Brain Injury, Hypoxic Ischaemic Brain Injury, and Other brain injuries (e.g., infection, vascular).
66
Why is a patient's trajectory in ABI important?
It provides clues as to what might happen in the future based on the patient's clinical course to date.
67
What are the survival rates across various ABI aetiologies?
Non-traumatic, non-anoxic injuries show steady attrition with mortality, while non-traumatic anoxic injuries show steeper attrition.
68
How does the length of vegetative and minimally conscious states indicate trajectory/survival rate?
Patients in vegetative state for one month due to traumatic brain injury have a small but significant chance of regaining consciousness over the next 11 months, whereas those with hypoxic injury have very few emerge after 11 months.
69
What is the prognosis of Persistent Vegetative State (PVS) at one month for traumatic injury?
52% of patients will have regained consciousness compared to only 15% for non-traumatic (hypoxic injury) at 12 months.
70
What are the traumatic brain injury outcomes following persistent vegetative state at one month?
Outcomes vary and are illustrated in provided data.
71
What are the outcomes of hypoxic-ischemic brain injury following Out of Hospital Cardiac Arrest with Therapeutic Hypothermia?
Outcomes vary and are illustrated in provided data.
72
How can futility be assessed across different brain injury types?
Futility can be reasonably predicted in Hypoxic Injury – Diffuse Injuries, especially if still in VS at 1 month.
73
When might futility be hard to define?
With traumatic brain injury (TBI) – focal injuries, where declaring futility may lead to a self-fulfilling prophecy.