= CEREBRAL CONTUSION = BRAIN CONTUSION

= traumatic injury to cortical surface of brain

Incidence: most common type of primary intraaxial lesion; in 21% of head trauma patients; children÷adults = 2÷1

Pathogenesis: capillary disruption leads to extravasation of whole blood, plasma (edema) and RBCs

Path: petechial hemorrhage (= admixture of blood with native tissue) followed by liquefaction + edema after 4–7 days, tissue necrosis

Mechanism: linear acceleration-deceleration forces / penetrating trauma

1. Coup (same side as impact)
   = small area of direct impact on stationary brain
   Associated with: skull fracture
2. Contrecoup (180° opposite to side of impact)
   = broad area of impact as a result of moving brain against stationary calvarium
   Associated with: fall

Location: multiple bilateral lesions;

• common: along anterior + lateral + inferior surfaces of frontal lobe (in orbitofrontal, inferior frontal, and rectal gyri above cribriform plate, planum sphenoidale, lesser sphenoid wing) and temporal lobe (just above petrous bone / posterior to greater sphenoid wing)
• less frequent: in parietal + occipital lobes, cerebellar hemispheres, vermis, cerebellar tonsils
• often bilateral / beneath an acute subdural hematoma
• confusion (mild initial impairment), focal cerebral dysfunction
• seizures, personality changes
• focal neurologic deficits (late changes)

CT (sensitive only to hemorrhage in acute phase):

• Look for scalp swelling to focus your attention on the location of the coup!
• “salt and pepper lesion” = mottled / speckled densities as focal / multiple (29%) poorly defined areas of low attenuation with irregular contour (edema) intermixed with a few tiny areas of increased density (petechial hemorrhage)
• diffuse cerebral hypodensity + swelling without hemorrhage in immediate posttraumatic period (common in children) ← hyperemia / ischemic edema
• some degree of contrast enhancement ← leaking new capillaries
• hemorrhage isodense after 2–3 weeks
• true extent of lesions becomes more evident with progression of edema + cell necrosis + mass effect over ensuing weeks

MR (best modality for initial detection of contusional edema with accurate portrayal of extent of lesion):

• hemorrhagic lesion (detected in 50% of all contusions):
  • initially decreased intensity (← deoxyhemoglobin of acute hemorrhage) surrounded by hyperintense edema on T2WI
  • hyperintense on T1WI + T2WI in subacute phase ← Met-Hb
  • hyperintense gliosis + hypointense hemosiderin on T2WI in chronic phase
• nonhemorrhagic lesion hypointense on T1WI + hyperintense on T2WI

Cx:

1. Progression to cerebral hematoma
2. Encephalomalacia (= scarred brain)
3. Porencephaly (= formation of cystic cavity lined with gliotic brain and communicating with ventricles / subarachnoid space)
4. Hydrocephalus ← adhesions ← subarachnoid blood