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Neuro Rehab 2 > TBI - 1a Mild TBI > Flashcards

TBI - 1a Mild TBI Flashcards

1
Q

what is a traumatic brain injury

A

insult to brain (not degenerative or congenital) by external physical force that can produce a diminished or altered state of consciousness which leads to impaired cognitive abilities and physical functioning

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2
Q

what are 3 modes of injury

A
  1. impact loading
  2. impulsive loading
  3. static or quasi-static loading
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3
Q

what is impact loading

A

head hits an object in environment or an object hits the head
- impact causes trauma to brain or skull

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4
Q

what is impulsive loading

A

rapid acceleration/deceleration of head so that brain hits inside of skull

head set into motion by indirect impact
- whiplash
- blow to thorax
- shaken baby syndrome
- blast injuries

can be repetitive in nature from multiple small injuries

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5
Q

what is static or quasi-static loading

A

effects of speed aren’t significant (ie slowly moving object traps the head)

ex: some kind of vice
- workplace working w machinery
- head run over by car

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6
Q

what are coup and contra coup injuries and when is this seen

A

impact and impulsive loading
- brain bounces back and forth against skull

coup = original blow
contra coup = injury where brain bounced off other side of skull, counter blow injury

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7
Q

what is the most common location for a coup injury

A

frontal lobe

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8
Q

what is the most common location for a contra coup injury

A

occipital lobe

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9
Q

mild TBI/concussion vs mod/severe TBI

A

mild/concussion:
- functional damage
- contusion
- nothing visible on imaging

mod/severe TBI
- structural damage
- hematoma
- visible on imaging

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10
Q

structural vs functional damage and when are they each seen

A

structural = damage can be seen on imaging
- mod/severe TBI

functional = no structural changes, nothing visible on imaging, evident by behavior/sx
- mild TBI/concussion

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11
Q

hematoma vs contusion and when are they seen

A

HEMATOMA: bleeding w accumulation of blood
- d/t lacerations or rupture of vessels from impact or from bony ridges of skull
- mod/severe TBI

CONTUSION: bruising of brain
- blood escaped from ruptured capillaries/small vessels and is interspersed between tissue
- mild TBI/concussion

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12
Q

how would a diffuse axonal injury (DAI) present differently in mild TBI/concussion vs mod/severe TBI

A

mild TBI/concussion
- mild DAI, axonal dysfunction (distortion or stretching)
- mimic DAI but won’t have structural damage

mod/severe TBI
- DAI - axonal shearing w diffuse damage

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13
Q

what intracranial sites can hematomas form in mod/severe TBIs

A

intra-cerebral
epidural
subdural
subarachnoid (hemorrhage)

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14
Q

what is a diffuse axonal injury (DAI)

A

axonal shearing across brain w diffuse damage
- see tissue tearing, shearing

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15
Q

what are the mechanics of why DAIs happen

A

brain tissues differ in structure and weight experience unequal acceleration, deceleration, or rotation during rapid head movement or impact

heavy front part of brain and back part of brain (brainstem and cerebellum) anchored by tentorium in the posterior fossa
- contributes to shearing when brain violently oscillates

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16
Q

what is a common MOI for a DAI

A

high speed MVA

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17
Q

what locations in the brain are DAI commonly found in

A

high density of tracts (ascending and descending tracts):
- white matter
- pontine-mesencephalic junction
- corpus callosum

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18
Q

what is the result of a DAI on brain trauma

A

whole diffuse group of axons throughout brain have gotten stretched, sheared and broken
- if cell survives, signals and impulses sent won’t go anywhere

if motor tract doesn’t survive, cell death occurs at later time
- presents as deterioration few days after injury
- continue to see functional degeneration over time

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19
Q

what is the physiology behind a concussion

A

concussions happen in brain’s white matter -> force transmitted strain nerve cells and axons
- disrupts function of brain cells more than their structure

nerve cell and axon distortion/strain/stretching causes a neurophysiological cascade effect

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20
Q

what causes a neurophysiological cascade effect

A

nerve cell and axon distortion/strain/stretching

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21
Q

what happens physiologically if the concussion is caused by a rotational force

A

stretches and twists axons
- strains nerve cells more than linear/angular

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22
Q

what type of force to head is most common to cause concussion

A

rotational forces

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23
Q

why don’t helmets prevent concussions

A

it’s the whipping motion of the head that causes the brain to jostle around in skull
- helmet can’t prevent this

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24
Q

why can’t you see concussions on imaging

A

axonal dysfunction disrupts physiology of brain cells rather than anatomy
- no structural damage

25
Q

why can you see a LOC from concussions

A

rotational forces centered on midbrain and thalamus which causes transient and disruptive components of the reticular activating system (RAS)

26
Q

is a concussion more: coup/contra coup injury or a stretch/shear

A

stretch and shear
- white matter axon injury and not bruising to outer cortex like gray matter cell bodies

27
Q

what are the 2 main phases in the neurophysiological cascade

A

excitatory phase
depressive phase

28
Q

what happens during the excitatory phase of the neurophysiological cascade

A

concussion
1. axons undergo stretch/shear
2. cell membrane/ion channels pulled apart creating a gap which changes the concentration gradients (K floods out, Na and Ca in)
3. ion exchange causes action potential and nerve fires
4. this happens millions of times, electrical storm in brain as neurons stim and fire passing signal from cell to cell

29
Q

what is a super simplified way to think of the neurophysiological cascade

A

excitatory phase where cells are firing millions of times and then depressed phase where don’t have enough energy and there is a cellular energy crisis

30
Q

what happens during the depressive phase of the neurophysiological cascade

A
  1. Ca in cell disrupts mitochondria’s ETC in making ATP
  2. massive drop in energy, ATP and energy stores plummet
  3. ATP getting used to reset ion balance, energy stores continue to plummet
  4. blood flow to brain restricted d/t edema -> not getting glucose to brain; causing disparity b/w glucose supply and demand = cellular energy crisis
31
Q

what mechanisms are impaired that prevent the neurophysiological cascade from leading to a cellular energy crisis and what does this lead to which perpetuates it

A

mechanisms that regulate consistency of blood flow in response to changes in SBP are impaired
- results in high sympathetic drive and low parasympathetic drive
-> brain shunts blood around to where it is most impaired after concussion

32
Q

what are sx of insufficient blood flow to brain

A

brain activity slows
- foggy cognition, dizziness, compromised balance

33
Q

what is the significance of the neurophysiological cascade in terms of rehab

A

it can happen over days to weeks
- people might get worse before better

34
Q

what is the significance of DAI recovery in the inner vs outer shell of brain cells

A

inner shell of healthy cells that were sheared from axons but survived will need to sprout new axons and neuronal connections

outer shell of brain cells which was concussed will have to recover
- might not die as do w mod/severe TBIs
- but will have impaired cell and axonal function until recover

35
Q

what are the 3 GCS TBI classifications

A
  1. mild = concussion (13-15)
  2. moderate (9-12)
  3. severe (3-8)
36
Q

what are characteristics of a mild TBI per the GCS classification

A

dazed & confused
may or may not LOC
no change in imaging

37
Q

what are characteristics of a moderate TBI per the GCS classification

A

LOC for min-hrs
confused for days - wks
physical, cog, behavioral issues may or may not be permanent

38
Q

what are characteristics of a severe TBI per the GCS classification

A

prolonged LOC or coma
physical, cognitive, and/or behavioral issues w permanent damage

39
Q

what are the 3 categories that the GCS looks at

A

eye opening response
verbal response
motor response

40
Q

what is a mild TBI

A

no universal definition or standard dx criteria

neuropathological disturbances are functional and not structural
- neuroimaging is normal

41
Q

what are the 4 criteria to dx a mild TBI or concussion

A
  1. LOC <30min
  2. initial GCS >13/15
  3. PTA is <24hrs
  4. normal imaging
42
Q

for a mild TBI what is the significance of the force of impact

A

not necessarily related to the severity of the TBI

43
Q

what are prognostic factors for a mild TBI/concussion (4)

A

body’s ability to heal
whether you rest after
report sx accurately
amt of ms support in neck (stability)

44
Q

what is PTA and what is the significance of this sx

A

post traumatic amnesia
- can’t form new memories after injury
- indication of severity
- mod/severe TBI >24hrs

45
Q

how do deficits present after a mild TBI/concussion

A

physical, emotional, cognitive deficits, and frequently changes in sleep patterns that usually resolve spontaneously

46
Q

what was a concussion label (as opposed to a mild TBI label) significantly associated w

A

early hospital dc
early return to school
(independent of GCS score)

47
Q

what does the label concussion (as opposed to mild TBI) imply

A

transient injury w no long-term effects

48
Q

mild TBI vs concussion

A

same thing
different vibes from the label tho
- used to be treated as 2 separate diagnostic categories

recent move to start calling concussions mild TBIs instead

49
Q

why do individuals who have a concussion have a vulnerability to a second injury

A

physiological changes inc brain’s vulnerability to further injury

50
Q

how long does it take to recover from a concussion

A

22-30days

51
Q

why do the physiological changes after a concussion inc vulnerability to a second injury

A

if residual dec in blood flow when get another hit, the cascade starts on cells that weren’t normal or back to baseline
- energy levels were in a low state and will only get lower after another hit
-> cells can’t maintain process and not enough energy stores in cell
-> ptosis happens and nerve cell kills itself off

52
Q

what is the general risk of a second injury to a concussion and why

A

lead to more severe and permanent deficits -> can be just as severe as a mod-severe TBI
- cumulative concussion which impacts person more as new cascade is enacted before cells recovered from the first one

53
Q

what is the significance of PT in preventing a second injury

A

we play a large role in return to play guidelines
- which are important and vital in preventing this
- “concussion problem or concussion management problem?”

54
Q

what is second impact syndrome

A

2nd injury w/i days of first concussion
- diffuse cerebral swelling and catastrophic deterioration

55
Q

what is the pathophysiology behind second impact syndrome

A

vascular mechanism of irritation preventing blood flow from going into brain which causes local swelling and leads to herniation of cerebellum thru foramen magnum and places pressure on brainstem

56
Q

what is chronic traumatic encephalopathy (CTE)

A

progressive and degenerative dz of brain in (usually) athletes w hx of repetitive brain trauma including symptomatic concussions and asymptomatic subconcussive hits to head
- trauma triggers progressive degeneration of brain tissue and buildup of abnormal proteins (specifically tau protein)

57
Q

what patient population has CTE had research in

A

1920s boxers
most recently, football players

58
Q

when can CTE happen

A

months, years, and decades after last trauma or end of athletic involvement

59
Q

s/sx of CTE (7)

A

memory loss
confusion
impaired judgment
impulse control problems
aggression
depression
progressive dementia

Neuro Rehab 2 (48 decks)

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