The brain is a viscoelastic organ with different densities and complex geometry that impact how energy is transmitted through tissues to cause injury.
Areas most susceptible to injury include the frontal and temporal poles, corpus callosum, and brain stem.
Natural frequency of each tissue type also likely plays a role in which structures are damaged as does the nature of the force applied (blunt force, blast, whiplash, etc.)
Frontal lobe injury can lead to difficulties with executive functions (sustained and divided attention, planning, problem solving etc.)
Temporal lobe dysfunction can include difficulty with language and memory
Both areas are also involved in emotional regulation
Injury to subcortical white matter impairs intra and interhemispheric signaling and communication
Edema/ICP Elevation
After severe TBI w/ ↑ ICP → ⊕ feedback loop can ensue, leading ultimately to brain death.
This situation can be likened to a compartment syndrome w/i the noncompliant skull.
↑ of ICP (A) → impedes CBF → ischemia → cytotoxic edema caused in part by ATP–dependent Na+-K+ pump failure.
This in turn further ↑ ICP & ↓ CBF.
This situation can ultimately progress to brain death if ICP becomes so high that the cerebrum is not perfused.
✓ the value of different prognostic factors in TBI ⇒ the most powerful independent prognostic variables identified were age, GCS motor score, pupil response, and CT finding (Marshall classification), labs (PT & glu)(J Neurotrauma. 2007)
✓ effectiveness of DC in pts /w TBI & refractory ↑ ICP ⇒ DC ↓ mortality; ↑ risk of severe disability & vegetative state compared to medical Tx alone. (N Engl J Med 2016)
✓ ICP monitoring in pts /w severe TBI improves o/c ⇒ ICP focused Tx was not better to care based on CT and Px → routine ICP monitoring does not provide additional benefits for pts o/c (N Engl J Med 2012)
ICP monitoring in severe adult TBI - not recommended for comatose pts /w nml initial CT that can be f/u Px; recommended for pts w/ bifrontal contusions, s/p 2° DC, WUT is c/i(Acta Neurochir 2014)