Traumatic Brain Injury

Dan Sprando
Andres Tabares
 Epidemiology
• Leading cause of death in North America for
ages 1-45
• Approximately 1.7 million sustain a TBI each
year
• Most prevalent in ages 0-4, 15-24, 65+

• Falls affected the youngest and oldest age

groups the most

• Among TBI-related deaths, motor vehicle

crashes were the second leading cause of TBI-
related deaths
Mechanisms
• Closed (dura intact)
• Blunt
• Low energy vs high energy
• Coup/countercoup
• Linear vs Rotational forces
• Sheering forces
• Open (dura is disrupted)
• Penetrating
• Low vs. high velocity
Pathophysiology
• Primary
• Shearing mechanisms → Diffuse axonal injury
• Focal cerebral contusions
• Extra-axial
• Epidural hematoma
• Subdural hematoma
• Subarachnoid hemorrhage
• Intraventricular hemorrhage
Low Energy Blunt Trauma
• Baseball bat, brick, rock, falls
• Coup/countercoup
• Cerebral Contusion
• Inferior frontal lobe

• Temporal Pole

• Extra Axial Injuries

• Skull Fractures

• Epidural/Subdural Hematoma

• Subarachnoid hemorrhage
Low Energy Blunt Trauma
High Energy Blunt Trauma
• Rapid Acceleration/Deceleration Force
• Linear or Rotational
• Seen in MVCs
• Shearing Force
• Diffuse Axonal Injury
• Shearing of Grey-White Matter Junctions

• Multiple locations

• Profound Coma Coma and Poor prognosis

Penetrating Trauma
• Low Velocity (Low energy)
• Nailgun, arrow, pipe ect
• Limited to tissue disrupted
• Usually better prognosis

• High Velocity (High Energy)

• Gunshot wound, bullet, explosive projectile
• Cavitation Caused by pressure wave
• Larger amount of tissue damaged
Pathophysiology
• Secondary
• Glutamate excitotoxicity
• Electrolyte imbalance
• Inflammation
• Mitochondrial dysfunction
• Apoptosis
• Secondary ischemia
• Increased ICP due to
•Edema/swelling
•Excess blood due to hemorrhage
•Accumulation of CSF due to blockage of outflow
Increased ICP
• Can lead to herniation
• Subfalcine herniation
• Can compress ACA

• Transtentorial herniation (Uncal)

• Midbrain & PCA compression

• Decerebrate posturing
CPP (cerebral perfusion pressure) is reciprocally
• Tonsillar herniation
related to ICP
• Cardiac & Respiratory failure
CPP = MAP - ICP
● ICP → CPP → Ischemia → Edema
• Brainstem herniation
Severity
• Length of loss of consciousness (LOC)
• Posttraumatic amnesia (PTA)
• Glasgow Coma Scale
• Mild ( >13)
• Moderate (9-12)
Eye Opening
• Severe (<8)
4. Spontaneous
3. Response to verbal command
2. Response to pain
1. No eye opening
● Mild TBIs more prevalent (> 85%
TBIs)
○ Many of them go untreated
Best Verbal Response Best Motor Response
5. Oriented 6. Obeys commands
4. Confused 5. Localizing response to pain
3. Inappropriate words 4. Withdrawal response to pain
2. Incomprehensible sounds 3. Flexion to pain
1. No verbal response 2. Extension to pain
1. No motor response
Severity
Neuroimaging Findings
• Focal
• Skull fracture

• Cerebral contusions/lacerations

• Intracranial hemorrhage

• Epidural/Subdural hematomas

• Subarachnoid hemorrhage

• Intraparenchymal hemorrhage
• Intraventricular hemorrhage
• Diffuse
• Global ischemic injury
Contusion/Laceration

Contusions vs. Laceration

● Contusion → bruising of the surface of the brain in which
the pia mater is intact
● Lacerations → the pia mater is torn
Epidural Hematoma

Image: Skull cap removed to show that the

hematoma lies on the surface of of the dura

● Most commonly associated with fracture

of the squamous temporal bone resulting
in damage to the middle meningeal artery
Subdural Hematoma

Image: The blue arrows show the cut edges

of the dura, revealing the bleeding

● Due to rupture of bridging veins (cortical veins passing

from cortical surface to dural sinus
Subarachnoid hemorrhage Intraventricular hemorrhage

Intraparenchymal hemorrhage
Global ischemic injury
• Can develop due to:

• Increasing cerebral swelling

• Cardiorespiratory arrest

• Hypotension

• Neurons of the hippocampus are the most susceptible to ischemic injury

 Diffuse Axonal Injury (DAI)
● Contributes to about 35% of the mortality and morbidity of TBI cases
without space-occupying lesions
● One of the major causes of severe disability and vegetative state
● Classified into mild, moderate, and severe
○ Grade 1: microscopic changes in the white matter of cerebral
cortex, corpus callosum, brainstem, and cerebellum
○ Grade 2: Grossly focal lesions isolated to the corpus callosum
○ Grade 3: Additional focal lesions in the dorsolateral quadrants of
the rostral brainstem
● May be diagnosed clinically when loss of consciousness (coma) lasts
> 6 hours in absence of evidence of intracranial mass or ischemia
Brain swelling/edema
● May be due to:
○ increase in the cerebral blood volume
○ Edema

● Edema can be identified as areas of hypodensity or

indirectly by findings such as effacement of cortical sulci,
disappearance of the normal gray--white matter
demarcation, midline shift, or effacement of basal cistern

Image: Right-sided edema

 CT Findings Image: Fourth ventricle and
prepontine cistern
compressed
• What to look for?
• Intracranial hematomas
• Appearance of the cisterns
• Sulcal patterns and evidence of midline shift
• Review of ventricles
• Assess bones of the cranium (Fractures?)

• These findings can then be used to classify injuries

Image: Epidural hematoma,
• Marshall scale midline shift & fracture
Marshall Scale
Rotterdam Score
Neuroimaging Findings
• Even though CTs are useful in detecting acute abnormalities, they
are poor indicators to the long-term outcome in mTBI
• Not useful in detecting microstructural white matter damage
• Failure to identify deficits in cerebral perfusion

• Other imaging available:

• MRI, fMRI
• FLAIR imaging
• DWI imaging
Long Term Consequences

a. Compared with preinjury levels in the 1 to 3-year period post-TBI

b. Including unemployment, diminished social relationships, and decrease in the ability to live independently
Long Term Consequences

c. Primarily hypopituitarism
d. Particularly unemployment and diminished social relationships
e. Subset of patients admitted into or discharged from rehabilitation or receive disability services
g. In the 2 to 3-year period post-TBI
Long Term Consequences
Long Term Consequences
• Alteration of the developmental potential of the brain to develop in
young kids that may later result in substance abuse, mood and
conduct disorders
• Associated increased risk of late-life dementia and Alzheimer's
• Alzheimer → A 10-fold increase in the risk of AD was associated with BOTH
apolipoprotein-epsilon 4 and a history of traumatic head injury, compared
with a two-fold increase in risk with apolipoprotein-epsilon 4 alone.

• Posttraumatic epilepsy may manifest years after the initial TBI

Areas of Function
Questions
Sources
• Centers for Disease Control and Prevention. Centers for Disease Control and
Prevention, 22 Jan. 2016. Web. 21 June 2016.
<http://www.cdc.gov/traumaticbraininjury/get_the_facts.html>.

• Vos, Pieter. Traumatic Brain Injury (1). Somerset, GB: Wiley-Blackwell, 2014. ProQuest ebrary.
Web. 21 June 2016.

• Greenberg, Mark S., and Mark S. Greenberg. Handbook of Neurosurgery. Tampa, FL:
Greenberg Graphics, 2010. Print.

• Mayeux R, ottman R, Maestre G et al. (1995). Synergistic effects of traumatic head

injury and apolipoprotein-epsilon 4 in patients with Alzheimer’s disease. Neurology 45:
555-557

• Rosen, C. Head Injury. [Lecture Powerpoint and Recording] West Virginia University
School of Medicine. 2016.

• Sarani B, Phan N. Traumatic brain injury: epidemiology, classification and

pathophysiology. In: UpToDate. Aminoff, M, Wilterdink, J (Eds). UpToDate. Waltham,
MA. (Accessed June 18, 2016)