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Neuro > TBI > Flashcards

TBI Flashcards

1
Q

traumatic brain injury TBI

A

occurs when an insult to the brain from an external mechanical force causes the brain to move rapidly within the skull, leading to damage

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2
Q

TBI can be an impact event

A

head makes direct contact with an object

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3
Q

TBI can be a nonimpact event

A

head encounters a force such as blast waves or rapid acceleration/deceleration

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4
Q

is TBI higher in men or women?

A

men

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5
Q

leading cause of TBI?

A

falls

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6
Q

more than 2/3 of TBI cases are

A

milk (aka concussions)

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7
Q

the brain is naturally protected from injury - the skull

A

a natural helmet that absorbed impacts & protects

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8
Q

Severity of TBI can be divided into 4 categories

A

subclinical, mild, moderate, severe

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9
Q

TBI can lead to - changes in

A

molecular signaling

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10
Q

TBI can lead to - alteration in cellular

A

structure/function

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11
Q

TBI can lead to what type of injury

A

primary tissue injury

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12
Q

TBI can lead to BBB

A

dysfunction

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13
Q

2 phases of TBI

A

acute primary injury

delayed, secondary injury

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14
Q

1st phase - acute primary injury

A

mechanical forces disrupting the integrity of cels

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15
Q

2nd phase - delayed, secondary injury

A

days to months after trauma, stretching of membrane, unregulated flux of ions, increased glutamate release, cytoskeletal degradation, inflammation, mitochronrial dysfunction, increased oxidative stress, edema, ischemia

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16
Q

neuroinflammation based therapies - minocycline

A

anti-inflammatory properites, crosses BBB. Conflicting effects in animal models

17
Q

neuroinflammation based therapies - melatonin

A

neuroprotective properties, lipophilic. Varying results in animals

18
Q

neuroinflammation based therapies - statins

A

neuroprotective and anti-inflammatory properties in mouse model. Suppression of glial activity

19
Q

neuroinflammation based therapies - stem cells

A

regenerative therapy. Suppression of inflammation

20
Q

neuroinflammation based therapies - granulocyte colony stimulating factor

A

FDA approved, recruits endogenous stem cells to injury site for neuroprotection

21
Q

changes in excitation and inhibition with TBI are associated with

A

glutamate and GABA

22
Q

ionic flux modifications - glutamate induces

A

depolarization

23
Q

metabolic crisis with TBI

A

energy failure by trying to restore ionic homeostasis through ATP pumps activity

24
Q

Excitoxicity with TBI causes creation of

A

free radicals and mitochondrial impairments leading to cell death

25
Q

excess glutamaate stimulation activates

A

NADPH oxidase - generating oxidative stress

26
Q

mitochondrial calcium accumulation causes

A

membrane potential compromise generating free radicals

27
Q

fluid percussion injury

A
  • Intracranial hemorrhage, brain swelling, grey matter damage, skull fracture
  • Mixed focal/diffuse injury
  • Highly reproducible
  • Requires craniotomy
  • High mortality rate
28
Q

controlled cortical impact

A
  • Impact is created using a pneumatic/electromagnetic devise to drive an impactor onto the intact dura
  • Creates focal cortical tissue damage, subdural hemtomas, DAI and disrupts the BBB
  • High reproducible
  • Low mortality rate
  • Requires craniotomy
29
Q

weight drop impact acceleration injury

A
  • Feeney’s model – dropping weight on intact dura, focal cortical injury, requires craniotomy, resembles human focal TBI but has high mortality rate
  • Shohami’s method – close injury model, weight dropped on skull resulting in a fracture. Creates BBB dysfunction, behavioral deficits and inflammation. Easy to execute but not highly reproducible
  • Marmarou’s model – skull is surgically exposed and a steel disc is glued to skull and brass weight is dropped. Produces DAI and resembles human injury but as poor reproducibility and high mortality rate
  • Maryland Model – like that ^^ but with force applied to the anterior portion of the cranium. Prouces DAI but no skull fracture/contusion
30
Q

Blast injury

A
  • Mimics TBI amond military
  • Animal placed into as shock tube where a compression shock wave is generated
  • Creates brain edema, DAI and vasospasm
31
Q

behavioral changes with TBI

A

headaches, attention deficits, cognition impairments, sensory processing deficiency, communication deficits, severe depression, anxiety, sleep disturbances, personality changes, aggression,

32
Q

neuropathology - contusions

A

areas of cerebral bruising particularly involving gray matter, whereby blood leaks into the extravascular space and it results in cell death and local loss of tissue

33
Q

neuropathology - diffuse axonal injury

A

affects white matter throughout the cerebrum and brain stem. Followed by generalized atrophy with ventricular enlargement; takes a few weeks/month to develop
• Usually responsible for slurred speech

34
Q

assessment of TBI - glasgow coma scale

A

used soon after injury
• Most common scoring system
• Used to gauge severity of acute injury
• Limitations: drug use, shock or low blood oxygen can lead to inaccurate score

35
Q

chronic traumatic encephalopathy

A

o Neurodegenerative syndrome that has been linked to serious psychiatric symptoms including depression and suicidal behavior
o Found in individual with a history of repeated TBI

36
Q

clinical trials - hypothermia

A

mild to moderate, decreased mortality and improve rates of neurologic recovery

37
Q

clinical trials - progesterone

A

no differential effects

38
Q

clinical trials - bone marrow

A

mononuclear cells used in children and adults with severe TBI

39
Q

clinical trials - deep brain stimulation

A

central thalamus stimulation for severe TBI, no results yet

Neuro (15 decks)

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