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Neuroscience Unit 2 > Traumatic Brain Injury > Flashcards

Traumatic Brain Injury Flashcards

1
Q

What are the three types of brain injuries?

A
  1. Traumatic
  2. Acquired (i.e. stroke, tumor, disease)
  3. Congenital
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2
Q

What are the two primary causes of TBI?

A
  1. Firearms

2. Vehicle accidents

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3
Q

What is the biggest cause of TBI in the elderly?

A

Falls

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4
Q

What is an important TBI differential diagnosis for soldiers?

A

mild TBI vs PTSD

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5
Q

What age group has the highest incidence of TBI?

A

Children and young adults -> 5-20 years old

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6
Q

What is meant by penetrating vs perforating versus closed? What is most common?

A

Perforating - object has entrance and exit wound
Penetrating - object pierces dura but remains in skull
Closed - most common, brain not exposed

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7
Q

What is diffuse versus focal TBI?

A

Diffuse - affects several areas of brain

Focal - injury restricted to a specific region of brain

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8
Q

What is a contusion-type injury?

A

An injury which leaves a bruise at the point of impact, produces an area of edema, and may have hemorrhagic progression

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9
Q

What is coup and countercoup injury?

A

Coup - contusion at site of impact

Countercoup - contusion at opposite side of impact, due to recoil of brain in cranial cavity

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10
Q

What causes diffuse axonal injury (DAI)?

A

The result of acceleration / deceleration injury that causes a shearing injury / stretch of axons. These axons will swell and axonal transport will be disrupted.

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11
Q

How are damaged axons revealed in DAI?

A

Immunostaining for beta amyloid precursor protein (Beta-APP)

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12
Q

How often does DAI occur and where is it found?

A

About 50% of brain trauma, found in cerebral cortex, especially white matter like corpus callosum, SCP. Also basal ganglia, thalamus, and rostral brainstem

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13
Q

What are two common causes of DAI? What will be seen on the skin?

A
  1. IED (improvised explosive device) exposure
  2. Shaken baby syndrome

On the skin: petechial hemorrhages

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14
Q

What are the clinical signs of shaken baby syndrome? What will cause death?

A
  1. Encephalopathy
  2. Subdural hematomas
  3. Retinal hemorrhages

Death causes
HIE - hypoxic ischemic encephalopathy
Increased ICP

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15
Q

What is the normal cause of epidural hemorrhage? What symptoms are associated?

A

Tearing of middle meningeal artery, associated with skull fracture.

Biconvex (lens-shaped) hemorrhage as the bleeding is contained by suture lines in the skulll, and “talk-and-die” -> lucid period before getting worse

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16
Q

What increases risk for subdural hemorrhage?

A

Brain atrophy, as emissary / bridging veins are already stretched

17
Q

What type of hemorrhage is associated with terrible headache?

A

Subarachnoid hemorrhage -> blood can be found in CSF

18
Q

What causes intraparenchymal hemorrhage? why is this a problem?

A

Usually from hemorrhagic stroke or penetrating injuries. Can increase ICP but also BLOOD IS VERY TOXIC TO BRAIN

19
Q

What are two diagnostic signs of basilar skull fracture?

A
  1. Battle’s sign -> bruising near mastoid process

2. Raccoon eyes

20
Q

What does PTA stand for?

A

Post-traumatic amnesia

21
Q

What are the three measures tested by the glasgow coma scale? What are the score ranges?

A
  1. Eye opening
  2. Verbal response
  3. Motor response

3-15

22
Q

What are the GCS numbers which define mild, moderate, and severe TBI?

A

Mild: 13-15 -> represents 75% of all TBI
Moderate: 9-12
Severe: 3-8

23
Q

What is chronic traumatic encephalopathy?

A

Brain injury caused by repeated mild TBI which become additive. Prominent in football players / soccer players

Prominent defects in memory and executive function as well as tau-immunoreactive neurofibrillary tangles

24
Q

What is Dementia pugilistica?

A

Condition of boxers where goal of sport is to produce concussion, produces chronic encephalopathy

25
Q

What is primary vs secondary injury?

A

Primary - result of direct forces on brain that affect axons / dendrites / blood vessels and cause immediate cell death

Secondary - The sequellae -> breakdown of BBB, cerebral edema, ischemia, hypoxia, free radical production, Ca+2 influx, increased ICP, glutamate excitotoxicity

26
Q

What is glutamate excitotoxicity?

A

One of the secondary results of TBI, it is general depolarization from ATP depletion from constantly activated glutamate neurotransmitter. The Ca+2 which leaks through NMDA / AMPA channels will cause activation of proteases which degrade the cytoskeleton

27
Q

Where is cytotoxic cerebral edema most common?

A

In astrocytes, which Na/K/Ca pumps are disrupted and water enters through aquaporins

28
Q

What are cerebrovascular alterations?

A

Loss of autoregulatory capacity of cerebral microvessels due to chronic hypoperfusion and chronic vasoconstriction. Will lead to ischemia and loss of metabolites in brain tissue

29
Q

What is Cushing’s triad and what is it diagnostic of?

A

Slow heart rate, high blood pressure, and irregular breathing. Diagnostic of high ICP

30
Q

What are the mild treatments of high ICP?

A

Drainage of CSF, and osmotherapy with mannitol or hypertonic saline

31
Q

What are the extreme measures to treat high ICP?

A
  1. Barbiturate coma
  2. Hypothermia
  3. Decompressive craniotomy
32
Q

How is cerebral perfusion pressure calculated? What is normal?

A

CPP = MAP - ICP

Normal is between 50 and 150 mmHg

33
Q

How are MAP and ICP found?

A

MAP = 1/3 systolic + 2/3 diastolic

ICP = measured using barometer

34
Q

What are some reasons why TBI clinical trials failed?

A
  1. Clinical heterogeneity - TBI’s are different from person to person
  2. Poor animal models
  3. Lack of sensitive biomarkers
  4. Difficult to know when to apply therapies based on animal models alone
  5. Insufficient preclinical studies

Neuroscience Unit 2 (19 decks)

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