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classification of BRain injury
acquired brain injury
TBI
NTBI
acquired brain injury
not hereditary, congenital, degenerative or induced by birth trauma
result in changes in neuronal activity affecting the physical integrity, metabolic activity or functional ability of neurons
traumatic brain injury
injury caused by external forces
impact to the head directly
inertial forces that damage the brain
nontraumatic brain injury
caused by internal forces
anoxia
exposure to toxins
infections
pressure from tumor
stroke
epimediology
2.8 million TBI-related ED visits, hospitilazations, and deaths
TBI related ED visits increased by 54% (2006-2014)
812,00 children treated in EDs for sprots and recreation-related injuries (concussion or other TBI)
causes of TBI in 2014
falls (children and older adults
being struck by or against object
motor vehicle crashes
leading cause of TBI-related deaths: intentional self-harm
health inequities and TBI
Native american: highest rates of TBI-related hospitalizations and deaths
racial and ethnic minority groups are less likely to receive follow-up care and rehab
prisoners, homeless, DV, service members/veterans, low income/health insurance, rural
risk factors
young (0-4, 15-19) elderly (75+)
male
lower SES
psychiatric diagnosis
dementia
contact sports, not using helmets
classification of injury severity
mild
moderate
severe
criteria to calssify severity
structural imaging
loss of consciousness
alteration of consciousness/mental state
post-traumatic amnesia
Glasgow coma scale
slide 15
posttraumatic amnesia
a period of disorientation and difficulty consistently making new memories
resolution: consistently oriented and able to make new memories
Glascow Coma Scale subscales
eye opening
motor response
verbal response
slide 17
posturing
abnormal flexion/extension
swelling in one hemisphere compressing diencephalon
asymmetrical motor response
ipsilateral hand tries to remove
babinski on contralateral foot
bilateral damage to diencephalon-upper midbrain
decorticate
flexion of bilateral elbows, wrists, fingers
toes pointed bilateral extending
bilateral damage to upper midbrain
deceretbrate
uppers and lowers are extended
if there is a change in a day like decorticate to decerebrate
means a deterioration of the condition,
a change in their status,
extension of damage into the brainstem
factors interfereing with GCS
pre-exsiting factors
effects of current treatment
effects of other injuries or lesions
pre-existing factors
language or cultural differences
intellectual or neurological deficit
hearing loss or motor speech impairments
effects of current treatment
physical (intubation or trach
pharmological (sedation or paralysis)
effects of other injuries or lesions
orbital/cranial fracture
dysphasia or hemiplegia
spinal cord damage
raccoon’s eyes
periorbital ecchymosis (brusisng)
basilar slull fracture, more anterior
Battle’s sign
retroauricular ecchymosis)
basilar skull fracture, more posterior
mild TBI
traumatically induced physiological disprution brain function, as manifested by at least one of the following:
any period of loss of conscoiusness
any loss of memory for events immediately before or after the accident
any alteration in mental state at the time of the accident
focal neurological deficits that may or may not be transient, but where the severity of the injury doesn’t exceed the following
loss of consciousness of 30 minutes or less
after 30 min. an initial GCS of 13-15
PTA not greater than 24 hours
primary injury
axonal shearing (diffuse axonal injury)
contusion
epidurmal hematoma (EDH)
subdurmal hematoma (SDH)
subarachnoid hemorrhage
hypoxic-ischemic
coup-contrecoup injury
a primary impact creates an acceleration of the brain that caues the front of the cranium to hit the front of the skull then ricochet to hit the back of the skull (secondary)
happen at 180 degrees form one another
contusion
difuse axonal injury
diffuse axonal injury
• Widespread shearing and retraction of damaged axons
• Sudden acceleration then deceleration of brain
• Shaken baby syndrome
contusion
brusie on the brain
EDH
collection of blood between dura and cranium
brief loss of consciousness followed by lucid interval, then headache, obtunded, hemiparesis
if not treated can lead to death
SDH
between dura mater and arachnoid mater
headache, altered mental status, hemiparesis
could lose consciousness
SAH
bleeding into subarachnoid space
often seen with aneurysms, but can be caused by TBI
hypoxic-ischemic injury
NTBI
systemic hypotension as a result of anoxia/hypoxia which can result in global damage
secondary injury
cerebral herniation
ischemic CVA from vascular compression
excitotoxicity
apoptosis
inflammation due to trauma
coagulopathy
major goal of medical management
prevent secondary injuries
intracranial pressure
increased ICP is caused by abnormality of brain fluid dynamics adn hematoma
normal is 4-15 mmHG
herniation of brain
supratentorial
infratentorial
prinary goals of acute medical management
prevent 2nd injury by surgiclal management
ICP monitoring
CVP/respiratory support
management of concomitant injuries
additional: reverse coagulopathy, DVT/PE prevention, early mobilization, nutrition
surgical management
reduce depressed skull fracture
remove penetrating bodies if accessible
EDH/SDH
craniotomy/craniectomy
burr hole/catheter
craniotomy/craniectiomy
cryopreservation or subcutaneous storage followed by cranioplasty
red flags
progressively declining level of consciousness
progressively declining neurological exam
pupillary asymmetry
seizures
repeated vomiting
double vision
worsening headaches
can’t recognize people or disoriented to place
behaves unusually or seems confused and irritable
slurred speech
unsteady on feet
weakness or numbness in arms/legs
biomed complications
seizures
sympathetic storming
hydrocephalus
heterotropic ossification
venous thromboembolism
seizures
electrical disturbances in the brain
multiple types (gneralized wit impaired awareness, focal awareness
may be subclinical
risk factors for seizures
hydrocephalus, intracranial hemorrhage, depressed skull fracture, hematoma evacuations, low GCS, dural penetration, parietal lesions, focal neuro deficits
sympathetic storming
paroxysmal sympathetic hyperactivity (PSH), dysautonomia
uninhibited sympathetic outflow after CNS injury
cycling of agitation/dystonia
clinical presentation of sypathetic stortming
tachycardia, tachypnea, hypertension, hyperthermia, diaphoresis/hyperhidrosis, posturing
diagnostic PSH-AM scale
hydrocephalus
CSF accumulation in the ventricles
may note
papilledema pressure that causes optic nerve swelling
decresed conscoiusness
memory deficits
headache
focal neuro deficits
impairments
physical: abnormal tone, sensory deficits, decreased motor control/learning, paresis/paralysis, impaired balance, spasticity
behavioral
emotional
cognitive
slide 45
Ranchos Los Amigos levels of cognitive functioning (LOCF)
most common
8-10 levels of cognitive and behavioral function
describes progress after TBI, but patient can skip levels or plateau at any level
LOCF levels
no response: total assistance
generalized response: total assistance
localized response: maximal assistance
confused-agitated: maximal assistance
confused-inappropriate: maximal assistance
confused appropriate: moderate assistance
automatic-appropriate: minimal assistance
purposeful-appropriate: standby assistance
purposeful-appropriate: standby assistance on request
purposeful-appropriate: modified independent
DRS
slide 50
mod-severe TBI
within 72 hours of admission and discharge
GOS: extended
51
consciousness
arousal
awareness of self/environment + motivation to respond
arousal
global state of wakefulness
stage 3 non-REM sleep to high vigilance
awareness
ability to perceive one or more specifc stimuli
• Visual
• Tactile
• Auditory
• Gustatory
• Olfactory
• Vestibular
• Proprioceptive
• Interoceptive
motivation
the drive to act on stimuli, both internal and external, that have entered conscious awareness
reticular formation
• Wakefulness
• Eye movements
• Swallowing/vomiting
• Posture/locomotion
• Respiration
• Blood pressure
• Sensory awareness
ascending arousal system
networkk of neurons that project to multiple brainstem source nuclei from within and next to RF to the cortex through thalamic and extrathalamic pathways
network is complex and diffuse
thalamic pathway
starts in RF, projects to thalamus then spreads out to cortical regions
extrathalamic pathway
RF to thalamus but mainly bypassing the thalamus. then hypothalamus, basal forebrain to cerebral cortices
thalamic specific fibers
both are cholinergic
pedunclulopontine tegmental nuclei (PPT)
lateraldorsal tegmental nuclei (LDT)
how does one become aware of stimuli
• Conscious awareness and arousal states interact
• No arousal: no awareness
• High arousal? Awareness can focus on one modality at expense of others
• Interactions between the cortex and specific and nonspecific thalamic nuclei (e.g., reticular, intralaminar)
ascending reticular activating system
originates in teh reticular formation, projections activate the cerebral cortex via glutamtergic relays in the thalamus
thalamus
Relay station and filters and modulates information
Coordinates activity in widespread areas
• Cortico-striatopallidal-thalamocortical loops
• Cortico-thalamocortical loops
frontal/parietal systems
function is movement planning/execution
Frontal eye fields (FEF)
Supplementary motor area (SMA)
Anterior cingulate cortex (ACC)
Posterior parietal cortex (PPC)
arousal systems
Basal forebrain (BF) and brainstem cholinergic (LDT/PPT)
Locus ceruleus (LC)
Mesencephalic reticularformation (MRF)
brainstem attention capture mechanism
redirects attention to peripheral sensory inputs
Pretectum (PT)-OKN
Cerebellar/vestibular orientation (VOR)
Acoustic startle (ASR)
Tendon somatosensory feedback afferents
Nociceptive afferents
Postural reflexes
thalamus interactions with striatum
strong and largest efference to striatum
provides connection to large cerebral networks: potential mechanism for translating sensory/motor activity to awareness
resting state networks
connnectomes
default mode
connectomes
spontaneous resting brain activity, functionally connected brain regions
default mode
what happens in your brain when you stop thinking about everything
pathophysiology of disorders of consciousness
slide 24
five basic wave forms
gamma
beta
alpha
theta
delta
frequency is the key characteristic
alert wakefulness
• Alpha waves (8–13 Hz, more posterior, prominent with EC and/or relaxation)
• Beta waves (13–30 Hz, more anterior, prominent with mentation)
• Gamma waves (more than 30 Hz, information processing during a cognitive task)
decrease in cortical arousal
• Theta waves (4–7 Hz, drowsy)
• Delta waves (less than 4 Hz, highest amplitude; deep, dreamless sleep: stages 3–4)
sleep wake cycle and EEG activity
alpha = awake
beta = REM sleep
theta = stage 1
delta = 2-4
sleep is 1/3 of life
• Suprachiasmatic nucleus of hypothalamus
• Reduced motor activity
• Decreased response to stimulation
• Relatively easy reversibility
Suprachiasmatic nucleus of hypothalamus
• Regulates circadian rhythm
• Melatonin released from pineal gland
• Light inhibits release of melatonin
• GABA inhibits neurons involved in wakefulness
Monoaminergic
• Maximum activity during wakefulness
• Decrease during non-REM sleep
• Almost zero activity during REM sleep
• Similar to motor neurons
• Dopaminergic activity patterns
Cholinergic
Difference from monoaminergic: activity increases during REM sleep
Sleep-Wake Cycle Neural Activity
Monoaminergic (NE, 5HT, Hist)
Cholinergic (Ach)
are brain injuries similar
no, no two are alike due to
remote injuries
hidden injuries
personal factors
cognition should not
limit functional goals
thus change how you approach intervention based on cognition
hiearchy of cognitive recovery
wakefulness
awareness
perception and recognition of info
speed o info processing
memory
reasoning and problem-solving
executive functioning
Patient exam
observation
history
systems review
funcitonal asessment
outcome measures
observation
really variable depending on setting and patient
could include: the room, lines and tue, people, vitals, surgical incision, trauma, patient repsponse when you walk into the room or talk
HPI
MOI
acuity of injury
PMH
clarify any precautions
diagnostic imaging: orthopedic injuries, CT/MRI
social history
social supports and home setup (helps to dictate discharge)
life roles and interests to get a picture of daily life and help with salience
systems review
cognition
cardiovascular
vitals
prolonged stay and immobility can impair upright tolerance
could be the first one getting the patient up
integumentary
effects of trauma
surgical site
bony prominences
implications of increased tone (pressure wounds)
MSK
precautions or fractures
ROM restrictions
pain
neuromuscular
gross coordination of movements/motor control
spontaneous vs. to command
muscle overactivity at rest and with mobility
outcome measures
core set for adults w/ neurologic conditions
TBI EDGE
Rehabilitation Measures Database
COMBI website
core set
berg
FGA
ABC
10MWT
6MWT
5STS
TBI EDGE
moderate to severe TBI
slides 20-21
rehab measures database
will give details on the measures themselves
COMBI
center for outcome measurement in brain injury
disorders of consciousness
coma, VS?UWS, MCS
many emerge from coma within 2-4 weeks, but might not recover consciousness quickly → DoC
deemed go have limited active participation in rehab and if documentation fails to detect progress beyonf VS and MCS → denied at inpatient rehabs
can return home or to SNF where follow-up care to determine state of consciousness is minimal to none
misdiagnosis
high rates are misdiagnosed as being in VS when they should be MCS
greater prognisis for mergence from MCS than from VS
level l
complete absence of observable change in behavior whren presented stimuli
coma
complete failure of arousal system with no spontaneous eye opening and inability to be awakened by vigorous sensory stimuli
Level II
generalized reflex response to painful stimuli
responds to repeated auditory stimuli with increased or decreased activity
responds to external stimuli with generalized physiollogical changes, movements or vocalizations
responses are the same regardless of the stimuli
could be delayed responses
VS/unresponsive wakefulness syndrome criteria
no evidence of sustained, reproducible, purposeful, or voluntary behavioral responses to stimuli
no evidence of language comprehension or expression
intermittent wakefulness manifested by the presence of sleep-wake cycles
sufficient preservation of autonomic function to permit survival with adequate medical care
bowel/bladder incontinence
variable preservation of cranial nerves and spinal reflexes
level III
demonstrates withdrawl or vocalization to painful stimuli
turns towards or away from auditory stimuli
blinks when strong light crosses visual field
follows moving object passed through visual field
responds to discomfort by pulling tubes or restraints
responds inconsistently to simple commands
responds directly related to type of stimulus
may respond to some persons
MCS
occasionally demonstrates clear cut signs of self or enviornmental awareness
diagnosis requires evidence of one or more of
simple command following
gestural or verbal “yes/no” responses
intelligible verbalizations
movements or affective behaviors that occur in contingent relation to relevant environmental stimuli