Traumatic Brain Injuries - Hammeke Flashcards

1
Q

Give the definition of a Traumatic Brain Injury.

A

TBI is defined as an alteration in brain function, or other evidence of brain pathology, caused by an external force.

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2
Q

What is the mechanism by which function is impaired in TBI?

Describe the staging of this process.

A

Difuse Axonal Injury (DAI).

Stage I (\<5% stretch) - Nodal ionic disturbances
Stage II (5-10%) - Reversible cytoskeletal damage (disrupts transport)
Stage III (15-20%) - Secondary axotomy (disrupts homeostasis)
Stage IV (\>20%) - Primary axotomy
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3
Q

Describe four molecular processes by which TBI pathology is mediated.

A
  1. Mechanoporation (causes calcium influx, potassium efflux, and excitotoxicity)
  2. Receptor dysfunction
  3. Free radical damage
  4. Inflammation
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4
Q

Describe some of the metabolic changes seen immediately following a traumatic brain injury.

What about cerebral blood flow?

A

Calcium influx is elevated (and remains high for days). Many other solutes (2DG, lactate, potassium, glutamate) increase “activity”.

Cerebral blood flow actually attenuates (recovers in days).

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5
Q

Review

Where do hemorrhagic contusions appear?

How would you describe these hemorrhages?

What is the difference between a subdural and epidural hematoma?

A

Review

Hemorrhagic contusions appear mostly on the inferior frontal and temporal lobes (overlying rough bony surfaces).

Contusions display petechial hemorrhaging.

Epidural hematomas accumulate blood between the dura and bone (lens-shaped), subdural is exactly that–subdural (crescent-shaped).

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6
Q

Describe the range of amnesia experienced following a traumatic brain injury.

How does this compare to the duration of loss of consciousness?

A

Amnesia may be both retrograde (can’t remember the moments immediately leading to the injury) and anterograde (difficult making memories for up to days after).

Consciousness recovers before the amnesia state ends (otherwise, we couldn’t really call it an amnestic state!)

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7
Q

Recall the components of the Glasgow Coma Scale.

What corresponds to mild, moderate, or severe scores?

A

Eye opening (1-4) + Verbal response (1-5) + Motor response (1-6)

Highest possible score is 15, lowest is 3. Mild impairment is 13-15, moderate is 9-12, and severe is 3-8.

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8
Q

What marker can we use following TBI to estimate duration and fullness of recovery?

A

Measure the duration of post-traumatic amnesia–anything longer than a week more strongly portends residual defect.

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9
Q

Describe some of the residual deficits experienced by those who suffer moderate to severe TBIs.

A

Impaired attention/concentration, speed of information processing.

Impaired mental flexibility, memory & learning.

Diminished impulse control, irritability, depression, & anxiety.

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10
Q

What are the criteria needed to satisfy a diagnosis of mild traumatic brain injury?

A
  1. Loss of consciousness (generally not longer than 30min)
  2. Loss of memory for events immediately before or after the accident (PTA < 24hrs)
  3. Alteration in mental state at time of accident
  4. Focal neurological deficits

*GCS usually only mild 30min after injury.

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11
Q

Try to describe a few of the many symptoms experienced by those suffering postconcussion syndromes.

A

Cognitive: Memory impairment, confusion, poor concentration, “slowing down”

Physical: Headache, blurred vision, N/V, sensory sensitivity, poor balance or dizziness, low energy

Emotional: Irritability, lability, sadness, anxiety

Sleep Disturbances: Disturbed rhythm (sleepiness, difficulty falling asleep)

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12
Q

Explain the concept of the window of vulnerability.

A

Most mild TBIs take 7-10 days to achieve full recovery. However, most repeat concussions (when they occur) also happen during this period. Repetitive injury has bad outcomes…

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13
Q

Contrast between the acute and post-acute phases of TBI recovery.

A

Acute: Patient exhibits symptoms and functional impairment. Clinical recovery marks the end of this phase.

Post-acute: Patient seems normal, but subclinical physiological dysfunction persists. Physiological recovery takes longer, but many resume things like contact sports during this time.

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14
Q

Try to recall 5-6 factors that portend a slower or less complete recovery from a TBI.

A

Severe injury (more symptoms for longer, with complications on imaging), prior history of TBI, psychiatric illness, other systemic injury, older age, and some genetic factors (eg APOE4).

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15
Q

How should mild TBIs be treated?

A
  1. Education: What symptoms to watch out for, how to stay rested
  2. Early monitoring and intervention: Watch for red flags like headache, sleep disturbance, vertigo and depression
  3. Medication (mostly for symptomatic treatment)
  4. Gradual return to work
  5. Follow-up
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16
Q

What are the complications of repetitive acute injury?

In what context do they generally occur?

A

Long-term impairment eg Dementia. Example: Second impact syndrome, which bears poor outcomes.

Contact sports.

17
Q

What is Dementia Pugilistica now known as?

What are its histopathologic markers?

Describe the classic disease history.

A

Chronic traumatic encephalopathy.

Accumulation of tau protein following repetitive mild brain injury. Beta-amyloid plaques may be present.

An athlete with a history of concussive injuries seems to recover fully from his injuries and retires. However, 15-30 years later he experiences onset of mood, behavior, & cognitive changes.