Traumatic Brain Injury and Concussion Flashcards
is there a higher incidence of TBIs in males or females?
males
there is an increased incidence of TBIs in males to females by __:___ ratio
2:1
t/f: a lower socioeconomic status is associated with a higher rate of injury
true
what is the lifetime cost for an individual with TBI?
$4 million
what is the annual cost of all TBIs in the US?
$60 billion
what are the 4 types of TBIs?
1) closed head injuries
2) severe acceleration injuries
3) blast injuries
4) open head injuries and penetrating brain injuries
what are closed head injuries?
external forces hitting the head or the head hitting an object hard enough to cause brain movt
what are the 2 subtypes of closed head injuries?
w/ or w/o skull fx
coup and contracoup
what is a coup injury?
injury at the site of impact
“impact” lesion
contusion resulting directly from the impact
on the side of the impact
what is a contracoup injury?
injuries distant from the site of impact
“rebound” lesion
surface hemmorrhage sustained on the opposite side of the brain from the impact, resulting from the deceleration forces
what does severe acceleration/deceleration of the head w/o impact result in?
axonal shear
what are open head injuries and penetrating brain injuries?
objects cause direct cellular and vascular damage; including damaging the blood supply to the brain
the severity of TBI may range from ____ to _____
mild, severe
what is a mild TBI?
a brief change in mental status or consciousness
what is a severe TBI?
an extended period of unconsciousness or memory loss after injury
what is primary injury in TBI?
brain damage from external forces that may cause brain tissue to make direct contact w/object, rapid acceleration/deceleration or blast/explosion
what are common areas of focal (primary injury) in TBIs?
anterior temporal poles
frontal poles
lateral and inferior temporal corticies
orbital frontal corticies
what is secondary injury in TBI?
cell death occuring as a result of cellular changes
the cascade of biochemical, cellular, or molecular changes
what happens as a result of brain inflammation/chemical changes
secondary processes due to hypoxemia, hypotension, ischemia, edema, and elevated ICP
how long does it take for secondary processes to progress?
hours to days
what things cause secondary processes progress over hours to days?
glutamate neurotoxicity
influx of excitatory NTs
free radical release
inflammation
t/f: the rigid structure of the skull can prevent pressure release in TBIs
true
what can cause elevated ICP?
swelling
abnormal brain fluid dynamics
hematoma (epidural, subdural, intracerebral)
what is normal ICP?
5-15 mmHg
if ICP is high enough, what may result?
emergency management like decompression
what is excitotoxicity?
excessive activation of neuronal amino acid receptors that are tocic to the cell and inhibit typical neurotransmission
what is a principle excitatory NT in the brain affected by TBI?
glutamate
what is the typical role of glutamate?
open ion channels
what is the result of too much glutamate following TBI?
too much Ca+ influx–>neuronal Ca+ overload–>membrane depolarization–>more ATP needed–>stimulates release of multiple enzymes–>neuronal self-digestion by protein breakdown, free radical formation, and lipid perioxidation
what is oxidative stress?
blood supply has been diminished while demand for blood/glucose has been increased leading to less ATP and production of reactive oxygen species damaging cell structures (lipids, membranes, proteins, DNA)
mobilization of pts post TBI is often very dependent on what?
VS response (ICP monitoring)
what is apoptosis?
after a brain injury, many regional neurons will undergo programmed necrotic cell death
the apoptotic cell % reaches up to ____% of all cells in the peri-infarct area (like the penumbra)
26
t/f: the peri-infarct area is an area of vulnerability that we can activate/stimulate
true
what are the 2 areas of the brain that can be affected by TBI causing disorders of consciousness?
1) damage to the cerebrum including basal forebrain, hypothalamic/thalamic activating areas, and fxn of the entire cerebral cortex
2) damage to the BS affecting the reticular formation and/or axons of the reticular activating system
what areas of the cerebrum can be damaged in TBI causing disorders of consciousness?
basal forebrain
hypothalamic/thalamic activating areas
entire cerebral cortex
what are areas of the BS can be damaged in TBI causing disorder of consciousness?
the reticular formation and/or axons of the reticular activating system
when the systems of consciousness (cerebrum and reticular areas) are activated, what happens?
arousal
when the systems of consciousness (cerebrum and reticular areas) are depressed or damaged, what happens?
sleep or coma
coma occurs when there is a lesion to…
upper BS reticular formation
BL regions of cerebral cortex (specifically the anterior cingulate cortex)
BL lesions of thalamus (specifically the intralaminar thalamic nuclei)
what area of the cerebral cortex specifically can cause coma when damaged?
the anterior cingulate cortex
what area of the thalamus specifically can cause coma when damaged?
the intralaminar thalamic nuclei
the intralaminar thalamic nuclei are essential for what?
arousal, awareness, thinking, and motor behavior
what are the minimally conscious states?
lethargy
obtunded
stupor
what is confusion?
progressive disordientation, forgetfulness, difficulty following commands, and restless/agitated state
what is lethargy?
A+Ox3, sluggish, sleep frequently, but awakens to voice/gentle shaking
what is obtunded?
extreme drowsiness, minimally responsive, barely follows commands, requires vigorous stimulation to awaken, stays awake for mere minutes
what is stupor?
min movt, responds in groans and moans, awakens briefly only w/repeated stimulation
what is coma?
doesn’t respond to verbal stimuli, doesn’t speak, decorticate/decerebrate/no response to pain
what is unresponsive wakefulness syndrome (vegetative state)?
appear awake
may have eyes open but no meaningful responses coming forth
automatic and reflexive responses only
not aware or interactive w/environment
what is a minimally conscious state?
minimal/inconsistent awareness
follows simple commands but not consistently
show some purposeful movt but relatively inconsistent
what are the closed head injuries?
concussion
contusion
coup lesion
contracoup lesion
axonal shearing
hematomas
what is a concussion?
trauma that induces an alteration in mental status (physical/cognitive abilities) that may/may not involve a loss of consciousness
what is a contusion?
“bruising” or small vessel hemorrhages of the surface of the brain resulting from impact
t/f: accleration/deceleration forces associated with coup and contracoup injuries results in further vessel damage, occlusion and edema
true
axonal shearing occurs from what forces?
hyperflexion/extension or rotation
what is axonal shearing?
diffuse axonal injury or death can disconnect the BS activating centers from the modulation of the cerebral hemispheres
what are the areas most susceptible to shear?
corpus callosum
basal ganglia
superior cerebellar peduncles
periventricular white matter
what structures of the brain are less susceptible to axonal shearing?
midbrain structures
what are hematomas?
vascular hemmorrhage resulting from impact
what are the 2 types of hematomas that can result from TBI?
epidural hematoma
subdural hematoma
what is an epidural hematoma?
typically a rupture of the middle meningeal artery resulting from severe MVA or blow to the side of the head
what are the typical characteristics of an epidural hematoma?
period of unconsiousness, followed by an alert/lucid period, followed by a rapid decline as the blood continues to leak and the hematoma enlargens
which hematoma usually results in death within hours?
epidural hematoma
which type of hematoma causes damage to the arterial system?
epidural hematoma
which hematoma is much more dangerous?
epidural hematoma
what is a subdural hematoma?
acute venous hemmorhage resulting in hematoma bw the dura and the arachnoid
which type of hematoma cuases blood to leak from the venous system accumulating slowly over hours to weeks?
subdural hematoma
t/f: subdural hematoma is very common post fall w/a blow to the head
true
describe the onset of symptoms of a subdural hematoma?
slow, insidious, and fluctuant
t/f: subdural hematoma can cause changes like a cognitive decline bw sessions
true
in what population is a blast injury common?
military populations
what is a blast injury?
when a solid/liquid explosive material explodes and turns into a gas
what is the mechanism of a blast injury?
when a solid/liquid explosive material explodes and turns into a gas
gas expands and forms a high pressure wave (overpressure wave) that travels at supersonic speed
pressure then drops, creating a relative vacuum (blast overpressure wave) that results in a reversal of airflow followed by a second overpressure wave
t/f: blast injury can cause stress and shear injuries
true
what is an example of a blast injury result?
rupture of the tympanic membrane and lung and GI injuries
t/f: the exact mechanism of blast injuries is known and set
false, it is unknown and variable
what is the suspected mechanism of injury for blast injury?
axonal shearing and shearing of vascular structures
what are the 2 types of penetrating object injuries?
high velocity penetrating injuries
low velocity penetrating injuries
what is a high velocity penetrating injury?
bullets/shrapnel from explosives cause primary tissue damage on contact, as well as additional damage remote from the areas of impact as a result of shock waves
what is a low velocity penetrating injury?
foreign objects such as sticks and sharp toys cause direct damage to the tissues they contact
what are some consequences of TBI (secondary injury/sequelae)?
increased ICP
acute hydrocephalus
cerebral hypoxia/ischemia
intracranial hemorrhage –>hypoxia, metabolic byproducts
infections (open head injury)
electrolyte imbalances–> secondary death (necrosis, apoptosis)
seizures from pressure and scarring
how does electrolyte imbalance lead to secondary death?
through necrosis and apoptosis
what are the autonomic sequelae of TBI (autonomic dysregulation)?
changes in pulse and RR or regularity
temp elevations
BP changes
excessive sweating, salivation, tearing, and sebum secretion
dilated pupils
vomiting
if autonomic dysregulation is severe, what can it lead to?
sympathetic storming
what often causes autonomic dysregulation in athletes?
exercise intolerance
what is post-traumatic amnesia (PTA)?
time lapsed bw the accident and the point at which the fxns concerned w/memory have been restored
the duration of PTA is an indicator of what?
severity of injury
when PTA is longer, are the outcomes more or less favorable?
less
when PTA is shorter, are the outcomes more or less favorable?
more
what are the two types of amnesia that result from TBI?
retrograde amnesia
anterograde amnesia
what is retrograde amnesia?
a partial/total loss of the ability to recall events that have occured during the period immediately preceding brain injury
t/f: the duration of retrograde amnesia may progressively decrease
true
how does the duration of retrograde amnesia progressively decrease?
forgetting a week b4 the injury-> forgetting a few days b4 the injury–>forgetting a few hours before the injury–>eventually re-establishing all memory
what is anterograde amnesia?
inability to form new memories
t/f: the capacity for anterograde memory is frequently the last fxn to return after recovery from loss of consciousness
true
what are the key principles of the examination of brain injury?
multifactorial phenomenon
pts post TBI are treated across the continuum of care
successful treatment requires a strong interdisciplinary team
PT interventions primarily address physical limitations
what is the multifactorial phenomenon?
multiple body systems are involved (multiple areas of assessment)
where are post TBI pts treated?
across the continuum of care:
ICU, acute care, acute rehab, outpatient, homecare, etc
what aspect of TBI is often the most disabiling?
the cognitive and behavioral limitations
what tends to be the most challenging aspect of care for TBI pts?
the cognitive and behavioral limitations
what are general concerns of acute care for moderate to severe TBI?
medical stability
neurologic and neurochemical stability
behavioral stability
physical assessment and mobilization
t/f: medical stability in moderate to severe TBI is often fluctuant
true
what is a key part of medical stability in moderate to severe TBI?
prevention of secondary sequelae
what is key to neurologic and neurochemical stability?
adequate brain rest, particularly in acute care
t/f: behavioral stability is often fluctuant and unpredictable in TBI recovery
true
what is one of the most challenging components of the exam and intervention of moderate to severe TBI?
the behavioral stability component
t/f: early mobilization in moderate to severe TBI is critical
true
what is involved in pt/family education in moderate to severe TBI?
positioning, stimulation, and arousal strategies
what is involved in emergency medial management?
surgical decompression and evacuation of intracranial hematomas
ICP monitoring to prevent diffuse cerebral ischemia
MAP monitoring
mechanical ventilation
prevention measures (DVT and pressure sores)
nutrition/feeding interventions (PEG tube)
VP shunt, fx fixation, debridement of penetrating injury/gunshot wound/foreign bodies
CN repair
intrathecal baclofen pump placement for spasticity
what is involved in medical stability in acute care of TBIs?
prevention of the complications associated w/TBIs as previously outlines
what meds can prevent complications of TBI?
sedating meds
antispasticity meds
mood stabilizers
amantadinen
beta blockers
what sedating meds can prevent complications of TBI?
glutamate receptor antagonists
calcium antagonists
cyclosporine
what antispasticity meds can prevent complications of TBI?
tizanidine
SSRIs
anxiolytics
what is a mood stabilizer used to prevent complications of TBI?
carbamazepine
what is a dopamine agonist that is considered effective in improving cognitive fxn related to arousal, memory, and aggression in moderate to severe TBIs?
amantadine
t/f: early and continuous beta blocker therapy is found to lead to increased survival and significantly better long-term fxnal outcomes compared to controls bc of the autonomic stability that it can establish
true
why does beta blocker therapy increase survival and increase long term fxnal outcomes compared to controls?
bc of the autonomic stability it can establish
what is the goal of external ventricular draining (EVD)?
monitoring ICP
what is ICP?
pressure around the brain
what is cerebral perfusion pressure (CPP)?
pressure at which the brain is perfused
what is normal CPP?
60-80 mmHg
what is normal ICP?
5-15 mmHg