Traumatic Brain Injury (TBI) and Chronic Traumatic Encephalopathy (CTE) Flashcards

1
Q

traumatic brain injury (TBI)

A
  • occurs when a force to the head causes neuropathological damage and impairement of brain function
    • mild vs. moderate/severe
    • mild TBI (mTBI) is often used interchangeably with concussion
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2
Q

chronic traumatic encephalopathy (CTE)

A

progressive neurodegenerative disorder usually caused by repetitive head trauma

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3
Q

TBI - primary injury

A

stage of closed head injury

occurs at the time of impact

focal
- contusions/brusing

diffuse
- diffuse axonal injury

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4
Q

TBI - secondary injury

A

stage of closed head injury

occurs after impact

several pathologies, mostly leading to increased intracranial pressure, bleeds, and cell death

can lead to:
- edema
- ischema
- hemorrage
- seizures

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5
Q

open head injury

A

aka penetrating head injury
- penetration from outside resulting in focal damage (e.g. gunshot wound, stabbing)

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6
Q

closed head injury

A

no open wound with damage resulting in diffuse damage (e.g. fall or car accident)

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7
Q

edema

A

swelling resulting in increased intracranial pressure

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8
Q

ischema

A

disruption of cerebral blood flow

leads to hypoxia/anoxia

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9
Q

hemorrhage

A

bleeding or development of blood clots

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10
Q

moderate/severe TBI & memory (Rigon et al., 2020)

A

spatial reconstruction/relational memory task

WORSE IN:
- accuracy
- misplacement

-compared to healthy comparison participants, individuals with a history of moderate-severe TBI performed significantly worse on a relational memory task

-more individuals were identified as memory impaired on the spatial reconstruction task than the standard neuropsychological measure of episodic memory (CVLT)

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11
Q

mild TBI and memory (Monti et al., 2013)

A
  • compared to matched controls, individuals who had an mTBI decades ago were less accurate on a face-scene relational memory task (middle aged groups)

-c ompared to matched controls, individuals who had an mTBI decades ago had smaller hippocampi bilaterally

  • compared to matched controls, there was no impairment evident in memory or neuroimaging in individuals with recent mTBI (young groups)
  • these findings implicate the combination of aging and a history of mTBI as the source of the deficit observed in the MI group, rather than mTBI alone
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12
Q

TBI and aging

A
  • moderate to severe TBI raises risk of developing AD later in life
    * whether these cases are actually CTE masquerading as AD remains to be seen
  • CTE seems to be due to repeated mTBIs/concussions and sub-concussive blows to the head
    • not just the big hits
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13
Q

CTE and aging

A
  • symptoms typically appear in middle-age
  • approx in 40’s but can be earlier or later
  • usually symptoms onset after retirement
  • symptoms can occur while still playing (generally more mild)
  • diseases gets worse with progressing age
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14
Q

emergence of CTE?

A

many NFL players commit suicide in a way to preserve brain

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15
Q

brain changes after one season of football (Hivard et al., 2019)

A
  • 38 football players wore accelometers on helmet all season and had MRIs pre and post season

FINDINGS:
- decrease in integrity of corticospinal tract in right midbrain
- the biggest changes that were happening in brain were individuals who had highest # of rotational hits

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16
Q

CTE time course

A
  • symptoms typically appear in middle-age
    • approx in 40s, but can appear earlier or later
      ** usually symptoms onset after retirement
      ** symptoms can occur while still playing (generally more mild)
17
Q

CTE cognitive changes

A
  • main complaints seem to be of memory loss and later, executive dysfunction
  • memory loss seems to be greatest for recent events
    *difficulty forming new memories
  • also have difficulty with planning, judgement
18
Q

CTE psychological changes

A
  • major affective/emotional component present in all stages of disease
    * depression
    * rage/anger
    * lack of inhibition leading to outbursts
  • motor dysfunction also common
    * gait disturbances (e.g. some difficulty walking smoothly)
19
Q

tau depositions

A

earliest accumulation of deposition occurs in:
* depths of cortical sulci
* near blood vessels (perivascular regions)

in moderate stages tau is found in hippocampus and MTL

20
Q

axon damage

A

in addition to NFT formation, axon damage is seen in all four stages of CTE

** possible that this damage is accounting for any clinical symptoms observed in the early stages, as NFT formation is not that dense

21
Q

differentiating CTE and AD – patient history

A

former football player with multiple TBIs more likely to have CTE than a librarian

22
Q

differentiating CTE and AD – age of onset of symptoms

A

CTE affects people younger than AD
- CTE onset approx 40s w more variability
- AD onset typically above age 65, with risk increasing greatly into 70s and 80s

23
Q

differentiating CTE and AD – memory deficit

A

in the early stages of CTE research, it seems memory probs may be somewhat similar to those of AD
- initial symptoms of difficulty for recent, declarative memories

24
Q

differentiating CTE and AD – emotional/affective symptoms

A
  • both can have depression, but seems more common in CTE
  • explosive anger, rage, and impulsivity more common in CTE
25
Q

differentiating CTE and AD – more symptoms

A

gait disturbances and movement problems more common in CTE, though not unheard of in AD

26
Q

differentiating CTE and AD – pattern of tau deposition

A

AD-earliest deposition in hippocampus and entorhinal cortex, then spreading to cortical areas

CTE-earliest deposition in depths of cortical sulci and around blood vessels, then spreading to hippocampal region and other cortical areas

27
Q

differentiating CTE and AD – amyloid deposition

A

much more common in AD

CTE patients seems to have little amyloid in brain