TBI - 1a Mild TBI Flashcards
what is a traumatic brain injury
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
what are 3 modes of injury
- impact loading
- impulsive loading
- static or quasi-static loading
what is impact loading
head hits an object in environment or an object hits the head
- impact causes trauma to brain or skull
what is impulsive loading
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
what is static or quasi-static loading
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
what are coup and contra coup injuries and when is this seen
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
what is the most common location for a coup injury
frontal lobe
what is the most common location for a contra coup injury
occipital lobe
mild TBI/concussion vs mod/severe TBI
mild/concussion:
- functional damage
- contusion
- nothing visible on imaging
mod/severe TBI
- structural damage
- hematoma
- visible on imaging
structural vs functional damage and when are they each seen
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
hematoma vs contusion and when are they seen
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
how would a diffuse axonal injury (DAI) present differently in mild TBI/concussion vs mod/severe TBI
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
what intracranial sites can hematomas form in mod/severe TBIs
intra-cerebral
epidural
subdural
subarachnoid (hemorrhage)
what is a diffuse axonal injury (DAI)
axonal shearing across brain w diffuse damage
- see tissue tearing, shearing
what are the mechanics of why DAIs happen
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
what is a common MOI for a DAI
high speed MVA
what locations in the brain are DAI commonly found in
high density of tracts (ascending and descending tracts):
- white matter
- pontine-mesencephalic junction
- corpus callosum
what is the result of a DAI on brain trauma
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
what is the physiology behind a concussion
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
what causes a neurophysiological cascade effect
nerve cell and axon distortion/strain/stretching
what happens physiologically if the concussion is caused by a rotational force
stretches and twists axons
- strains nerve cells more than linear/angular
what type of force to head is most common to cause concussion
rotational forces
why don’t helmets prevent concussions
it’s the whipping motion of the head that causes the brain to jostle around in skull
- helmet can’t prevent this
why can’t you see concussions on imaging
axonal dysfunction disrupts physiology of brain cells rather than anatomy
- no structural damage
why can you see a LOC from concussions
rotational forces centered on midbrain and thalamus which causes transient and disruptive components of the reticular activating system (RAS)
is a concussion more: coup/contra coup injury or a stretch/shear
stretch and shear
- white matter axon injury and not bruising to outer cortex like gray matter cell bodies
what are the 2 main phases in the neurophysiological cascade
excitatory phase
depressive phase
what happens during the excitatory phase of the neurophysiological cascade
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
what is a super simplified way to think of the neurophysiological cascade
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
what happens during the depressive phase of the neurophysiological cascade
- Ca in cell disrupts mitochondria’s ETC in making ATP
- massive drop in energy, ATP and energy stores plummet
- ATP getting used to reset ion balance, energy stores continue to plummet
- blood flow to brain restricted d/t edema -> not getting glucose to brain; causing disparity b/w glucose supply and demand = cellular energy crisis
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
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
what are sx of insufficient blood flow to brain
brain activity slows
- foggy cognition, dizziness, compromised balance
what is the significance of the neurophysiological cascade in terms of rehab
it can happen over days to weeks
- people might get worse before better
what is the significance of DAI recovery in the inner vs outer shell of brain cells
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
what are the 3 GCS TBI classifications
- mild = concussion (13-15)
- moderate (9-12)
- severe (3-8)
what are characteristics of a mild TBI per the GCS classification
dazed & confused
may or may not LOC
no change in imaging
what are characteristics of a moderate TBI per the GCS classification
LOC for min-hrs
confused for days - wks
physical, cog, behavioral issues may or may not be permanent
what are characteristics of a severe TBI per the GCS classification
prolonged LOC or coma
physical, cognitive, and/or behavioral issues w permanent damage
what are the 3 categories that the GCS looks at
eye opening response
verbal response
motor response
what is a mild TBI
no universal definition or standard dx criteria
neuropathological disturbances are functional and not structural
- neuroimaging is normal
what are the 4 criteria to dx a mild TBI or concussion
- LOC <30min
- initial GCS >13/15
- PTA is <24hrs
- normal imaging
for a mild TBI what is the significance of the force of impact
not necessarily related to the severity of the TBI
what are prognostic factors for a mild TBI/concussion (4)
body’s ability to heal
whether you rest after
report sx accurately
amt of ms support in neck (stability)
what is PTA and what is the significance of this sx
post traumatic amnesia
- can’t form new memories after injury
- indication of severity
- mod/severe TBI >24hrs
how do deficits present after a mild TBI/concussion
physical, emotional, cognitive deficits, and frequently changes in sleep patterns that usually resolve spontaneously
what was a concussion label (as opposed to a mild TBI label) significantly associated w
early hospital dc
early return to school
(independent of GCS score)
what does the label concussion (as opposed to mild TBI) imply
transient injury w no long-term effects
mild TBI vs concussion
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
why do individuals who have a concussion have a vulnerability to a second injury
physiological changes inc brain’s vulnerability to further injury
how long does it take to recover from a concussion
22-30days
why do the physiological changes after a concussion inc vulnerability to a second injury
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
what is the general risk of a second injury to a concussion and why
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
what is the significance of PT in preventing a second injury
we play a large role in return to play guidelines
- which are important and vital in preventing this
- “concussion problem or concussion management problem?”
what is second impact syndrome
2nd injury w/i days of first concussion
- diffuse cerebral swelling and catastrophic deterioration
what is the pathophysiology behind second impact syndrome
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
what is chronic traumatic encephalopathy (CTE)
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)
what patient population has CTE had research in
1920s boxers
most recently, football players
when can CTE happen
months, years, and decades after last trauma or end of athletic involvement
s/sx of CTE (7)
memory loss
confusion
impaired judgment
impulse control problems
aggression
depression
progressive dementia
