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Medical Studies 2A > 1.11 Acute Insults to the CNS: Traumatic Brain Injury > Flashcards

1.11 Acute Insults to the CNS: Traumatic Brain Injury Flashcards

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USMLE® Step 1 flashcards
1
Q

What is the biggest cause of death and disability (combined) in adults under 45?

A

Traumatic brain injury

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2
Q

What GCS corresponds to mild, moderate, and severe brain injury?

A

13-15: Mild
9-12: Moderate
3-8: Severe

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3
Q

What periods of unconsciousness correspond to what severity of TBI?

A

Mild: <30mins
Moderate: 30mins-24hrs
Severe: Over 24hrs

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4
Q

What periods of post-traumatic amnesia correspond to what severity of TBI?

A

Mild: Less than a day
Moderate: Days to a week
Severe: More than a week

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5
Q

Chronically, what pathologies is TBI associated with?

A
  • Seizures
  • Sleep disorders
  • Neurodegenerative diseases
  • Psychiatric disorders
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6
Q

Differentiate between focal vs diffuse TBI

A

Focal: one area of the brain
Diffuse: more than one area of the brain

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7
Q

Are primary/secondary TBI pathologies treatable?

A
  • Primary can only be prevented by preventing the trauma in the first place
  • Secondary can be treated, since it is occurring after the initial insult itself
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8
Q

What are some potential secondary consequences of traumatic brain injury?

A
  • Neuroinflammation
  • Cerebral oedema
  • Oxidative stress
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9
Q

Summarise the pathology of penetrating TBIs

A

Laceration of brain tissue, crushing of brain tissue, intracerebral haematoma and ischaemia secondary to clotting.

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10
Q

Summarise the pathology of blast TBIs

A

Blast wave induces sudden increase in intracranial pressure, particularly at interfaces between CSF and brain. Results in penetration/cavitation of brain tissue, damage to blood vessels, and disruption of axonal pathways.

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11
Q

What causes focal brain injuries?

A

Object striking the head, or brain coming into contact with skull

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12
Q

Coup vs contrecoup injuries

A

Coup: At site of impact
Contrecopu: directly opposite

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13
Q

What are some downstream pathologies of focal TBI?

A
  • Cranial fracture
  • Intracranial haemorrhage
  • Bruising
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14
Q

What is unique about TBIs at the base of the skull?

A
  • Can cause tearing of meninges and leaking of CSF
  • Can damage foramen of blood vessels/nerves
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15
Q

Describe the appearance of extradural haemorrhage on CT imaging

A
  • Biconvex in shape (curve away from the skull)
  • Limited by cranial sutures
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16
Q

Where is the most common site of an extradural haemorrhage?

A
  • Pterion (pteron; Hermes)
  • Point at which temporal, parietal, frontal, and sphenoid bones meet
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17
Q

Which of a subdural vs extradural haemorrhage worsens faster? Why?

A
  • Extradural worsens faster
  • Subdural is usually venous, so progresses slower than extradural, which is usually arterial
18
Q

Which veins are commonly torn in subdural haemorrhage?

A

Bridging veins

19
Q

Describe the imaging presentation of a subdural haemorrhage

A

Run with curvature of the brain.

20
Q

Which has worse prognosis: subdural haemorrhage or extradural haemorrhage?

A

Subdural; associated with more brain injury

21
Q

Cerebral contusions mech

A
  • Brain comes into contact with irregular bony protuberances of skull
  • Damages small blood vessels and other components of brain parenchyma
  • Causes bruising (“contusions”); creating toxic environment that damages surrounding tissue
22
Q

True or false: diffuse brain injury requires the brain to come into contact with the skull

A

False. It’s more likely to be axonal/vascular damage in response to acceleration/deceleration

23
Q

Why is the brain particularly vulnerable to traumatic injury?

A
  • Large weight relative to body
    -High white:grey ratio (white is more vulnerable to damage)
  • Large size
24
Q

What is the biggest cause of widespread axonal damage?

A

Secondary injury processes. Axotomy is actually quite rare.

25
Q

What are the two main component proteins of the axonal structure (and their functions)?

A
  • Neurofilaments: main structural protein
  • Microtubules: highways for transport to and from soma
26
Q

Describe secondary axonal injury (specific mechanism)

A
  • Microtubules tear apart in response to inflammation
  • Calcium leaks into axons, triggering enzymatic cascade that worsens damage to cytoskeleton and microtubules
  • Triggers apoptosis
27
Q

Describe the pathology of hypoxia/ischaemia secondary to TBI

A
  • Damage to blood vessels leads to hypoperfusion, hypoxia, and ischaemia
  • Can contribute to oedema, and occurs alongside increased glucose demand (extra harmful)
28
Q

Physical symptoms of concussion

A
  • Headaches
  • Nausea
  • Dizziness
  • Sensitive to light and noise
29
Q

Mental symptoms of concussion

A
  • Fogginess
  • Difficulty concentrating and remembering
30
Q

Sleep-based concussion symptoms

A
  • Sleeping more/less
  • Difficulty falling/staying asleep
31
Q

Emotional and behavioural concussion symptoms

A
  • Sadness
  • Anger
  • Frustration
  • Irritable
32
Q

True or false: concussion, particularly repeated concussion, may be linked to later development of neurodegenerative disease

A

True

33
Q

Why is concussion difficult to diagnose?

A
  • No imaging abnormalities
  • No biomarkers/routine tests
  • Other things (e.g. hangover) show up as false positives
  • Subjectivity of symptoms
34
Q

List important history points in a suspected concussion

A
  • Details of event (eye witnesses?)
  • Loss of consciousness, amnesia, seizures?
  • Previous concussions? Psychiatric illnesses? Migraines? Seizures?
  • Improvement/deterioration (bleeds)?
35
Q

Describe how a person should re-enter life post-concussion

A
  • Wait 1-2 days
  • Do something (not sport etc.), and see if it causes symptoms. If so, rest for longer.
  • When re-entering sport, start with lowest risk activity, and move from there
36
Q

Describe the pathophys of chronic traumatic encephalopathy

A
  • Tau protein leaves microtubules, destabilising axons and leading to axonal damage
37
Q

Describe the pathophys of concussion

A
  • Initial trauma sets of secondary injurious processes, leading to axonal death
  • Indiscriminate neurotransmitter release causes increase in ion pump activity
  • Increased glucose demand, yet decreased blood supply
38
Q

Describe the shape of the increase in ICP. Why does this happen?

A
  • As the pressure rises, autoregulatory mechanisms fail.
  • This leads to decompensation, causing a sharp upward increase in ICP.
39
Q

Describe the acute management of traumatic brain injury

A
  • DR ABCDE
  • Protect airway, ventilate, administer oxygen
  • Maintain systolic >90
  • Record GCS
  • Check pupil size
  • Be careful of cervical spine

This is all with the idea of preventing 2° injury

40
Q
A

Medical Studies 2A (110 decks)

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