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
excess glutamaate stimulation activates
NADPH oxidase - generating oxidative stress
26
mitochondrial calcium accumulation causes
membrane potential compromise generating free radicals
27
fluid percussion injury
* Intracranial hemorrhage, brain swelling, grey matter damage, skull fracture * Mixed focal/diffuse injury * Highly reproducible * Requires craniotomy * High mortality rate
28
controlled cortical impact
* 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
weight drop impact acceleration injury
* 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
Blast injury
* Mimics TBI amond military * Animal placed into as shock tube where a compression shock wave is generated * Creates brain edema, DAI and vasospasm
31
behavioral changes with TBI
headaches, attention deficits, cognition impairments, sensory processing deficiency, communication deficits, severe depression, anxiety, sleep disturbances, personality changes, aggression,
32
neuropathology - contusions
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
neuropathology - diffuse axonal injury
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
assessment of TBI - glasgow coma scale
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
chronic traumatic encephalopathy
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
clinical trials - hypothermia
mild to moderate, decreased mortality and improve rates of neurologic recovery
37
clinical trials - progesterone
no differential effects
38
clinical trials - bone marrow
mononuclear cells used in children and adults with severe TBI
39
clinical trials - deep brain stimulation
central thalamus stimulation for severe TBI, no results yet