3.1 Traumatic Brain Injury

TBI: One of the most complex to treat bc of __

secondary complications

TBI: Lvl of arousal & behavior (What changes)

Lvl of arousal → inc or dec

Behavior → aggressive

__% does not go back to N function

40%

TBI: An alteration in brain function, or other evidence of brain pathology caused by __

external force

TBI: Prevalence: its the leading cause of __ in the US

injury-related death and disability

TBI: Prevalence: __ ppl visit the ER for TBI annually

1.7 milllion

TBI: Prevalence: __ ppl die as a result of the injury

approx. 50,000

TBI: Prevalence: __ require hospitalisation

approx 300,000

TBI: Prevalence: NOTE: True incidence likely underestimated

Doesnt include military, non-ED visits, or many sports related injuries

TBI: Causes: Leading causes of TBI:

• Falls (32%)

• MVA / traffic accidents (19%)

• Struck by / against events (18%)

• Assaults (10%)

TBI: Causes: High risk groups:

• Children (0-4)

• Adolescents and young adults (<25)

• Older adults (65+)

TBI: Causes: High risk groups: Most common population affected

Children

TBI: Causes: High risk groups: __: Hospitalization and death as a result of TBI is most common

Older adults (65+)

TBI: Long Term Impact: __ ppl in the US live c TBI related disability

5.3 million

TBI: Long Term Impact: 1 year after injury

• __ not working

• __ struggle c social integration (changes in personality and behavior)

40%
33%

TBI: Long Term Impact: __ need help c adls

25%

TBI: Long Term Impact: __ report poor physical and mental health

40%

MOI & Pathophysiology: What kind of injury is it

heterogenous

MOI & Pathophysiology: Mechanisms

Wide variety of pathophysiological mechanisms

MOI & Pathophysiology: Brain damage results from external forces that cause brain tissue to make __ contact c an object (bony sull or penetrating object), __ forces, or __.

• Direct contact

• Rapid acceleration or deceleration forces

• Blast waves from explosions

MOI & Pathophysiology: Brain tissue damage categories

• Primary injury

• Secondary injury

MOI & Pathophysiology: Primary injury d/t

Direct trauma to parenchyma

MOI & Pathophysiology: Secondary injury d/t a cascade of __, __, __, events that evolve over time d/t the initial injury and injury-related __, __, __,

• Biochemical, cellular, molecular events

• Hypoxia, edema, elevated ICP

MOI & Pathophysiology: Primary injury damage:

BAT COZ HIT BY A BAT

• BBB dysfunction

• Axonal shearing

• Tissue damage

MOI & Pathophysiology: Secondary injury damage

BERII "→ “berry” but with 2 i’s coz 2º

• Brain edema

• Excitotoxicity

• Reactive oxygen species

• Inflammatory cytokines

• Immunosuppression

MOI & Pathophysiology: Diagram

1. Primary injury

2. Secondary injury

3. Hypermetabolism and hypercatabolism

4. Increased morbidity and mortality

Optimal nutritional support → #1,2,3

MOI & Pathophysiology: Primary injury types

• Contact injuries

• Acceleration / deceleration injuries

MOI & Pathophysiology: Primary injury: __ (type): Contusions

Contact injuries

MOI & Pathophysiology: Primary injury: __ (type): Lacerations

Contact injuries

MOI & Pathophysiology: Primary injury: __ (type): Hematomas

Contact injuries

MOI & Pathophysiology: Primary injury: __ (type): DAI (diffuse axonal injury)

Acceleration / deceleration

MOI & Pathophysiology: Primary injury: Common areas of focal injury:

AFLO

• Anterior temporal poles

• Frontal poles

• Lateral and inferior temporal cortices

• Orbital frontal cortices

MOI & Pathophysiology: Primary injury: If frontal is affected =

Behavior

MOI & Pathophysiology: Primary injury: If lateral is affected =

Expression

MOI & Pathophysiology: Primary injury: Acceleration / deceleration: __: Predominant mechanism of injury in most indivs c severe to moderate TBI

DAI

MOI & Pathophysiology: Primary injury: Acceleration / deceleration: __: Common in high-speed MVAs and can be seen in some sports-related TBIs

DAI

MOI & Pathophysiology: Primary injury: Acceleration / deceleration: __: Often occurs in __ areas

DAI

• Discrete

MOI & Pathophysiology: Primary injury: Acceleration / deceleration: DAI: Discrete areas

PCP

• Parasagittal white matter of the cerebral cortex

• Corpus callosum

• Pontine-mesencephalic junction adjacent to the superior cerebellar peduncles

MOI & Pathophysiology: Primary injury: Acceleration / deceleration: T or F: DAI is easy to detect due to its nature

FALSE - Not easy coz it occurs in cellular level

MOI & Pathophysiology: Primary injury: Acceleration / deceleration: DAI: Mechanism is __, so often there are minimal initial findings on CT & MRI

Microscopic

MOI & Pathophysiology: Primary injury: Acceleration / deceleration: DAI: The forces cause disruption of __ within the axon leading to __ degeneration

Neurofilaments

Wallerian-type axonal degeneration

MOI & Pathophysiology: Primary injury: Acceleration / deceleration: DAI: What happens to other cells

Degen will cause toxins to infect other cells

MOI & Pathophysiology: Primary injury: Acceleration / deceleration: DAI: Types of forces

• Tensional (stretching)

• Rotational (twisting)

• Shearing (horizontal pulling)

MOI & Pathophysiology: Primary injury: __: Signature injury of the US military conflicts in the middle east

Blast injury

MOI & Pathophysiology: Primary injury: Blast injury: When an explosive device detonates a __ is produced, which can cause brain damage

Transient shock wave

MOI & Pathophysiology: Primary injury: Type of blast injuries:

• Primary blast injury

• Secondary blast injury

• Tertiary blast injury

MOI & Pathophysiology: Primary injury: Blast injury: __ (type): Direct effect of blast overpressure on organs (brain)

Primary blast injury

MOI & Pathophysiology: Primary injury: Blast injury: __ (type): Shrapnel and other objects being hurled at the individual

Secondary blast injury

MOI & Pathophysiology: Primary injury: Blast injury: __ (type): Occurs when the victim is flung backward and strikes an object

Tertiary blast injury

MOI & Pathophysiology: Primary injury: Blast injury: __ (type): Once the body stops, the brain continues to move in the direction of the force, hitting the interior of the skull and then bouncing back into the opposite side, causing a __

Blast injury

• Coup-countercoup injury

MOI & Pathophysiology: Primary injury: Blast injury: Mechanisms

1. Direct transcranial wave propagation

2. Transfer of kinetic energy

3. Elevations in CSF or venous pressure

MOI & Pathophysiology: Primary injury: Blast injury: Mechanisms: Explain Ttansfer of kinetic energy

From the blast wave through the vasculature, which triggers pressure oscillations in the BVs leading to the brain

MOI & Pathophysiology: Primary injury: Blast injury: Mechanisms: Explain elevations in CSF or venous pressure

Caused by compression of the thorax & abd & by propagation of a shock-wave through BVs of CSF

MOI & Pathophysiology: Primary injury: Blast injury: Mechanisms: Blast-related brain injury can result in:

• Contusion

• DAI

• Edema

• Hematomas

• Hemorrhage

MOI & Pathophysiology: Primary injury: Blast injury: Mechanisms: A wide spectrum of injury severities ranging from __ can result from blast TBI

Mild (blast concussion) → Severe and fatal

MOI & Pathophysiology: __: Occurs hours to days after initial trauma

Secondary injury

MOI & Pathophysiology: Secondary injury: Triggered by

HHIIE

• Hypoxia

• Hypotension

• Ischemia

• Inc ICP

• Edema

MOI & Pathophysiology: Secondary injury: Cellular-level changes

GIFC

• Glutamate toxicity

• Calcium influx

• Free radical release

• Inflamatory cytokines

MOI & Pathophysiology: Secondary injury: Cellular level changes: __: Release of metabolic & catabolic wastes

Glutamate toxicity

MOI & Pathophysiology: Secondary injury: Elevated ICP caused by

• Brain swelling

• Hematoma

• CSF imbalance

MOI & Pathophysiology: Secondary injury: Normal ICP

5-20 cm H2O

MOI & Pathophysiology: Secondary injury: High ICP can lead to

• Brain herniation (uncal, central, tonsilar)

• Requires emergency tx

MOI & Pathophysiology: Secondary injury: High ICP can lead to: Brain herniation: __: Pons gets stuck, making it hard to breather

Tonsilar (TONS = PONS)

MOI & Pathophysiology: Secondary injury: Elevated ICP: Clinical features

• Cushing triad

• Altered LOC

• Headache

• Vomiting

• Papilledema

• Behavioral changes

MOI & Pathophysiology: Secondary injury: Elevated ICP: Clinical features: Cushing triad:

• Irregular breathing

• Widened pulse pressure (Htn) → big diff bw systole and diastole (>150 & <60)

• Bradycardia

MOI & Pathophysiology: Secondary injury: Elevated ICP: Clinical features in infants

• Macrocephaly

• Bulging fontanels

• Sunset sign

MOI & Pathophysiology: Secondary injury: Elevated ICP: Clinical features in infants: __: Always looking down bc CNs are damaged

Sunset sign

Sequelae of TBI: Impairments associated c TBI:

• Neuromuscular

• Cognitive

• Neurobehavioral

• Communication

• Swallowing

Sequelae of TBI: Impairments associated c TBI: Neuromuscular:

PareMAP (like asking for the map → tapping the arm to ask = neuromuscular)

• Paresis

• Motor function

• Abnormal tone

• Postural control

Sequelae of TBI: Impairments associated c TBI: Cognitive:

CAMEAL

• Concentration

• Attention

• Memory

• Executive functions

• Arousal level

• Learning

Sequelae of TBI: Impairments associated c TBI: Neurobehavioral:

I MADE AI (has an attitude → neurobehavioral)

• Impulsivity

• Mental inflexibility

• Apathy

• Disinhibition

• Emotional lability

• Agitation/aggression

• Irritability

Neuromuscular Impairments:

• Impaired motor function

• Abnormal, involuntary mvmts

• Impaired somatosensory function (possible but depends on location of lesion)

Neuromuscular Impairments: Impaired motor function:

Similar presentation c stroke bc same areas are damaged

• UE and LE paresis

• Impaired coordination

• Impaired postural control

• Abnormal tone

• Abnormal gait

*may be present as lifelong impairments

The mental process of knowing and applying information

Cognition

Cognitive impairments: Cognition: Involves:

• Arousal

• Attention

• Concentration

• Memory

• Learning

• Executive function (multitasking and prioritizing)

Cognitive impairments: Cognition: Categories:

CRISP

• Cognitive flexibility

• Response inhibition

• Initiation and self generation

• Serial ordering and sequencing

• Planning

Cognitive impairments: Cognition: Mainly controlled by the __, making them vulnerable in TBI

Frontal lobes

Cognitive impairments: __ are commonly seen

Altered LOC

Cognitive impairments: Disordered arousal states seen p severe brain injury

• Coma

• Vegetative state

• Minimally conscious state

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: Arousal system is not functioning (erratic changes to VS)

Coma

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: Pts eyes are closed

Coma

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: No sleep wake cycle

Coma

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: Pt is ventilator dependent

Coma

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: No auditory or visual function

Coma

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: No cognitive or communicative function

Coma

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: Abnormal and postural reflexes may be present

Coma

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: Usually not permanent

Coma

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: Pts may become brain dead, enter a vegetative or minimally conscious state, or go onto full recovery

Coma

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: Dissassociation bw wakefulness and awareness

Vegetative state

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: Higher CNS centers are not integrated c the brainstem

Vegetative state

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: __: able to manage basic cardiac, respiratory, and other vegetative functions and the pt can be weaned off the ventilator

Vegetative state

• Brainstem

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: Present sleep wake cycle (there are moments of VS adaptation)

Vegetative state

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: Eyes may be open through awareness of surroundings is absent

Vegetative state

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: Pts may startle to visual or auditory stimuli and briefly orient to sound or visual stimuli

Vegetative state

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: Meaningful cognitive and communication function is absent

Vegetative state

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: Reflexive smiling / crying may be present

Vegetative state

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: A withdraw response to noxious stimuli is present

Vegetative state

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: Although pts in vegetative state may appear to have purposeful mvmt, these are non-purposeful and reflexive in response to external stimuli (Not ballistic)

Vegetative state

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: Pts in a permanent vegetative state may have no meaningful motor or cognitive function and a complete absence of awareness of self or the environment for a period __ p TBI and __ p anoxic brain injury

1 year p TBI

>3 mos p anoxic brain injury

Cognitive impairments: Cognition: Disordered arousal states seen p severe brain injury: __: Ther eis minimal evidence of self or environmental awareness

Minimally conscious state