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NEURO 411 > Chronic traumatic encephalopathy > Flashcards

Chronic traumatic encephalopathy Flashcards

1
Q

In literature; concussion = ___

A

sports

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2
Q

In literature; mTBI (mild traumatic brain injury) = ___

A

other causes

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3
Q

What is used to classify TBI?

A

Glasgow Coma scale; tells you about patients awareness

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4
Q

What is there a push for?

A

To classify concussion different from TBI based on bleeding/contusion

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5
Q

Define concussion

A

Acute neurophysiological event related to blunt impact applied to the head, body, neck, such as accelerations, declarations and rotational forces. Can be sustained from car crashed, sports, falls, etc

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6
Q

Which force is more likely to cause concussion? Direct or rotatory?

A

Rotatory

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7
Q

Direct vs rotatory force

A

Direct = one plane; rotatory = multiple planes

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8
Q

What are some long-term injuries with concussion?

A

Micro, axonal injuries, ex. shearing of white matter; oxidative stress; can affect deeper structures like brainstem, reticular activating sys.

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9
Q

Where is deformation maximized in the brain?

A

At depth of sulci and around blood vessels (areas of engineering weakness)(also areas of prototypical tau deposition)

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10
Q

What are some clinical features of acute concussion?

A
  • Amnesia (retre/antro) > loss of consciousness
  • May feel normal initially, symptoms develop later
    * Headache is most common symptom
  • Dizziness, nausea, irrtiliability, sensivitiy to light
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11
Q

Early concussions will have ____

A

symptoms at rest; over time symptoms only when exerting

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12
Q

Most people recover ____

A

quickly (days-weeks)

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13
Q

Roughly __ have prolonged recovery (beyond 3 months)

A

15%

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14
Q

What is clinical course dependent on ?

A

Thresholds, which are subjective. ex. lifestyle, personal activity etc; if you are a non-runner you obv wouldn’t be able to complete a 10k as well unlike a runner

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15
Q

What are the 5 classical domains of symptoms?

A

Headache, mental health (irritability, anxiety, ptsd), sleep, cognition, vestibular

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16
Q

What are risks that prolong recovery?

A
  • multiple concussions (esp. if they are closer together)
    * Concussion without full recovery –> biggest risk
  • Migraine history, psychiatric illness
  • Litigation, blame –> psychological trauma of blaming someone = increased symptoms

q

17
Q

Do severity of injury, loss of consciousness etc have a correlation to prolonged recovery?

A

NO

18
Q

What is prolonged recovery?

A

Beyond 3 months

Should be slow improvment/plateuing, however worsening is a red flag!

19
Q

Cognitive patterns w/ prolonged recovery?

A
  • Poor attention/concentrations
  • Easily lose focus
  • Short-term mem. loss, but respond to cues
  • Word-finding difficulty
20
Q

What are some issues patients encounter?

A
  • Lack of wareness in public, no empathy
  • Unsure of the science
  • Inabiity to gradually return to work
  • Screen sensitivity, headaches, balance can be barriers
  • Cognitive exertion, slower, easily irritable/anxious
21
Q

Who called CTE “punch drunk syndrome”

A

Martland 1928

22
Q

What did corsellis coin in 1973?

A

dementia pugilistica

23
Q

Who termed it CTE officially?

A

Omalu 2005 ; progressive neurodgeen disorder thought to arise from repeated concussive head injury; pathologic diagnosis

24
Q

Describe the axonal injury that occurs with repetitive trauma?

A
  • Mechanical deformation
  • Alters ion fluxes
  • Commonly seen in WM tracts (CC, internal capsule, brainstem, cerebellum)
  • Areas cololaclize with APP
25
Q

How is neurodegen. caused by neurovascular dysfunction during repetitive trauma?

A

Inflammation and impairment of perivasuclat glymphatic sys, specifically Aqp4 (aquaporin helps lymp sys clear abnormal proteins, thus leading to accumulation)

26
Q

Where is tau localized in CTE?

A

Around small vessels (perivascular regions) in an irregular pattern at the depths of cortical sulci

27
Q

Are CTE NFTs distinguishable from NFT in AD?

A

no

28
Q

What are the clinical features in order of frequency?

A
  1. Memory impariment
  2. Executive dysfunction
  3. Attention/conc.
  4. Depression
  5. Explositivity
  6. Languae
  7. Visuospatial
  8. Violent/suicidal
  9. Parkinson

i dont think u have to memorize this, just know parkinson less frequnet

29
Q

Can you diagnose CTE on living person?

A

nO

30
Q

What is traumatic encephalopathy sysndrome used for?

A

Identifying potetial CTE cases

31
Q

Could concussions bring out other NDDs?

A

Yes, could unmask other neurodegernative disorders (CTE plus pathologies)

32
Q

What was the flaw in the CNN article that found “99% of NFL players”

A

only studied players suspected of CTE

33
Q

Biomarkers of CTE:

A
  • Caved in septum pellucidum\
  • CSF –> normal amyloid beta, elevated p-tau/total tau
    *PET Imaging –> negative amyloid/positive tau
  • Cortical t hinning.atrophy
  • APOE4

NEURO 411 (12 decks)

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