L2 Mod/Severe TBI Flashcards
types of mod/severe brain injuries
acquired brain injury
stroke
blunt trauma
coup-contra coup injury
shaken baby syndrome
diffuse axonal injury
anoxic brain injury
occlusion of oxygen
15 s can cause loss of consciousness
4 minutes severe injury
hypoxic brain injury
caused by not enough O2 saturation in air like at altitude
suffocation
causes of TBI
falls
blunt trauma
car accident
assault
incidence of TBI - population
highest in teenagers/20s and after 75 due to falls
immediate damage after brain trauma
scalp laceration
fracture
cerebral contusion
cerebral laceration
intercranial hemorrhage
diffuse axonal injury
delayed secondary damage after brain trauma
ischemia
hypoxia
cerebral swelling
infection
events evolving over time
+ elevated ICP and edema
diffuse axonal injury - primary damage
axons are sheared by deceleration/acceleration/rotational injuries
axons twist and tear leading to neuronal death
white matter injury
grades of DAI
1: mild, microscopic changes in midbrain
2: local lesions, corpus callosum
3: severe focal lesions on brainstem
recovery after DAI
prognosis, % of people recovering
50% of people have good recovery
dural hematoma - primary damage
skull fracture can tear menigeal arteries/vessels/sagittal sinus
causes bleed until the dura or above
penetrating brain injuries - primary damage
can survive puncture in cerebrum with memory and cognition changes
brain stem injury mostly fatal
cellular complications with TBI
inflammation/ROS generation
excitotoxicity
BBB damage
mitochondrial dysfunction
damage causes glutamate increase and excitotoxicity with reactive oxygen species, neutrophils and microglia cross BBB, cerebral edema, death
microglia activity after injury
increasing up to 30 days after injury, specifically the neurotoxic type
primary types of injury in TBI
- DAI (3 grades of severity)
- Dural hematoma
- penetrating injury
Secondary damage after TBI includes:
cerebral edema/vasospasm/ICP increase
increased glutamate release
excitotoxicity
inflammation and ROS generation
impaired GLC metabolism
BBB damage
cascade of secondary damage after TBI (order of events)
TBI causes:
1. exocytosis
2. structural damage
3. BBB damage and glutamate affected permeabiliity
4. glutamate transporter impairment
Then:
glutamate levels increase due to brain trauma
Then:
glutamate receptors are excessively activated
leading to: excitotoxicity
How does excitotoxicity affect the brain physiologically?
increases Ca entry into cells
cerebral edema
cell death
how is BBB affected by TBI?
inflammatory markers, ROS, glutamate lead to larger gaps in the BBB
these allow neutrophils and activated microglia to enter
increasing risk of infection and inflammation
microglia activity after TBI
immediate: protective microglia levels increase over 1-2 days then decrease; low level of toxic microglia
10-12 days post injury: toxic microglia increase for up to a month as protective microglia have decreased levels
microglia levels determine degree of secondary injury
TBI contributes to what condition later in life?
dementia, Alzheimer’s, chronic neurocognitive impairment
mTBI mechanism contributing to dementia
repetitive mTBI
creates edema
axonal alterations/protein aggregates
neurofibrillary tangles form + genetic influence
dementia onset or Alzheimer’s
severe TBI mechanism contributing to Alzheimer’s
impaired neuronal homeostasis over long term leads to protein aggregates
Amyloid beta plaques form
Alzheimer’s develops
prefrontal cortex control:
working memory
self control/irritability
decision making
amygdala controls:
emotional regulation
fear response
hippocampus controls:
learning
memory
motor impairments can come from damage in these areas of the brain:
brainstem
mid brain
cerebellum
cortex
BG
neurocognitive impairments in brain injury include:
memory: STM, LTM, procedural
judgment
language/aphasia
sleep/wake cycle, arousal
behavioral impairments in brain injury include:
impulsivity
irrational
out of context behaviors
personality changes
motor impairments from brain injury include:
hemiparesis
ataxia
synergistic movement
hypertonia - spasticity, contractures
tremors
- impairments depend on damaged area(s)
reticular activating system control:
waking: thalamic input increases to increase arousal; pt increases attention and appropriate responses to stimuli
sleeping: reduction in sensory info and atonia to not activate movement
fight or flight: ANS function with hypothalamus and circadian rhythm
reticular formation functions
integration, relay, coordination center for life functions
including: circadian rhythm, sleep/wake cycle, coordinate somatic motot movements, CV/resp control, pain modulation, habituation to sensation
CN motor nuclei for respiration
CN involved in respiration
trigeminal, facial, glossopharyngeal, vagus, hypoglossal
mechanism of sleep dysfunction after TBI
frontal temporal lobe primary and secondary damage results in reduced melatonin
hypothalamus damage: suprachiasmistic nucleus assists circadian rhythm by making melatonin
long pathway damage interrupts melatonin production
type of memory disruption common in mild/mod TBI
STM, learning
type of memory disruption common in severe TBI
LTM due to hippocampus and cortex damage
will need to relearn procedural memory like walking, bed mobility, etc
mechanism of memory loss in TBI
hippocampus and cortex/pre-frontal cortex interact w hippocampus retrieving, storing, and recalling spatial info and identification info + procedural memory
damage to any of these areas can disrupt this process
how to improve memory in therapy for mod/severe TBI
incorporate memory into therapy exercises
ex) ask pt to recall where they put an object
work on compensatory strategies like memory book
What neurochemicals increase w exercise to benefit healing in TBI?
BDNF, orexin A
+ neuroprotective microglia
+ antiinflammatory cytokines
effect of BDNF on brain
increased long term potentiation, plasticity, and neurogenesis in the hippocampus
leads to cognitive improvements, mood improvements, and prevention of neurodegeneration
helps repair after damage from TBI
effect of Orexin A on brain
increased long term potentiation, plasticity, and neurogenesis in the hippocampus
leads to cognitive improvements, mood improvements, and prevention of neurodegeneration
What neurochemicals decrease w exercise to benefit healing in TBI?
proinflammatory cytokines
neurotoxic microglia
extent of secondary injury timeline after TBI
days - months - years depending on pt, condition, social support, rehab
medical sequelae after TBI
increased ICP caused by: edema, hemorrhage, hematoma
must be monitored for acute hydrocephalus
red flag s/s of acute hydrocephalus
pupillary changes
headache
vomiting
mobilization with EVD
early mobilization improves outcomes after a craniotomy and extraventricular drain
a ventricular catheter monitors what?
ICP
brain bolt monitors
brain oxygenation
indications for decompressive craniectomy
massive ICP not relieved by burr hole
How to mobilize patient with EVD
must be clamped by nursing before mobilizing at all, including changing HOB height or bed mobility
monitor cerebral perfusion pressure, ICP, HR, BP, O2
basic ways ICP is monitored and lowered
monitored to be <20 mmHg
if high:
1. 30 degree HOB elevation, sedation, O2 sats 92%, decrease CO2, CSF drain
2. hyperventilation, mannitol, barbituates
3. hyperosmolar solution, hyperventilation, decompressive craniectomy, hypothermia
loss of consciousness defitinion
several minutes to hours/days
coma definition
complete paralysis of cerebral function
unresponsive state
GCS: eyes closed, no response to pain, sound, tactile stim
persistent vegetative state
reduced responsiveness with no evidence of cortical function
due to diffuse hypoxia, axonal white matter damage
mTBI GCS scores
13-15
mod TBI GCS scores
9-12
severe TBI GCS scores
<9
post traumatic amnesia, mTBI
<1 day
post traumatic amnesia, mod TBI
1-7 days
post traumatic amnesia, severe TBI
> 7 days
LOC time, mTBI
0-30 min
LOC time, mod TBI
30 min-24 hours
LOC time, severe TBI
> 24 hours
GCS: eye opening scores
1-4
4 - spontaneous
3 - to voice
2 - to pain
1 - no repsonse
GCS: verbal response
1-5
5: normal conversation
4: disoriented conversation
3: words, not coherent
2: sounds only
1: no response
GCS: motor response
1-6
6: normal
5: localized to pain
4: withdraws to pain
3: decorticate posture/flexor synergy
2: decerebrate posture/extensor synergy
1: no response
subgroups of severe brain injury
includes prolonged state of unconsciousness for days-months
-coma
-vegetative state
- persistent vegetative state
- minimally responsive state
- locked in syndrome
rancho los amigos levels of cognitive functioning (simplified)
1: no response
2: generalized response, inconsistent, not in response to stim
3: localized response to stim
4. agitated and confused
5. inappropriate, non agitated, confused
6. confused appropriate response to commands
7. automatic appropriate, person has minimal confusion
8. functioning memory, response to environment, unaware of some deficits
9. does daily routine, aware of need for assistance
10. normal function/modified independent, does daily routine with or without compensation
possible motor issues in TBI
weakness
contractures
spasticity/hypertonia
coordination from cerebellum or BG
balance
synergistic
postural misalignment
motor planning (prefrontal cortex)
cognitive assessment in mod/severe TBI should include:
arousability: what stim arouses pt
alertness
orientation: self, place, time
following directions: # of steps
memory: spatial, idetify, procedure
judgement: transfers/gait
agitated behavior scale (ABS)
assesses pts in the acute phase for issues such as: violence, anger
pulling at tubes, mood changes, impulsivity
each behavior scored 1-4 from absent to present to extreme level
functional assessment of mod/severe TBI should include:
bed mobility
transfers
upright stability
gait
what environmental factors could affect TBI treatment?
light
background noise
people in room
extra movement
