Basic Neuroscience and Neuropathology of Brain Injury
Core concepts
Know the primary versus secondary injury distinction: primary injury is the mechanical event (contusion, diffuse axonal injury, hematoma, penetrating injury); secondary injury is the downstream biochemical cascade (excitotoxicity, calcium influx, mitochondrial failure, oxidative stress, neuroinflammation, edema). Candidates must understand diffuse axonal injury (DAI) - shearing at gray-white junctions from angular acceleration, with axonal swelling and impaired axonal transport; classic locations are the corpus callosum, dorsolateral brainstem, and subcortical white matter. Understand coup/contrecoup contusions, epidural (middle meningeal artery, lens-shaped) versus subdural (bridging veins, crescent) hematomas, and the Monro-Kellie doctrine governing intracranial pressure.
Traps
Questions conflate cytotoxic edema (intracellular, early, ischemic) with vasogenic edema (blood-brain barrier breakdown, later). Remember that herniation syndromes are named for the structure being compressed, not the direction of shift alone - uncal herniation classically compresses CN III (blown pupil) before respiratory failure, whereas central herniation produces early altered consciousness. Do not confuse Wallerian degeneration (downstream of axonal injury) with retrograde changes.
Rule of thumb
For any localization question, ask: does the deficit fit a single vascular territory, a single tract, or a diffuse process? Diffuse processes with normal initial CT but prolonged coma suggest DAI - MRI (SWI, DTI) is more sensitive than CT.
Worked example
A patient with high-speed deceleration has a normal head CT but remains comatose for days. The best explanation is DAI, not contusion, because CT misses most axonal pathology.