Skull fractures: 33.3 – 75 ft lb to produce a single linear fracture.
Soft and flexible surface: 268 – 581 ft lbs.
With increasing force get simple linear fracture, circular fracture and stellate fracture.With smaller surface area get depressed skull fracture.
Growing fracture: entrapment of dura in fracture line or escape of blood from an epidural through a fracture to create a scalp hematoma results in enlargement of the fracture after healing as the periosteal edges are deprived of the dural-based blood supply.
Hinge fractures: Type I coronal, Type II front to back, Both through sella. Type III coronal but not through sella. Type I most common: assoc impact on side of head or on tip of chin.
Ring fractures: impact to vertex, buttocks or tip of chin. Most cases fractures of mandible not present.
Hinge and ring fractures can be produced by impacts anywhere on the circumference ofthe head.
Diastatic fractures: rarely produced by cerebral edema in infants and young children.
Contre-coup fractures. (12%) All cases have fractures at impact site.
Involve crests of gyri and extend into white matter as wedge-shaped lesions.
Most common locations: frontal and temporal poles.
Not usually seeen in infants: instead see lacerations.
Coup: at site of impact
Contrecoup: opposite side of impact (assoc w/falls). Often more severe than the coup.
Fracture contusions: may be displaced from point of impact, underlying fracture line.
Intermediary coup contusions: in white matter, basal ganglia, corpus callosum or brainstem along line of impact.
Gliding: dorsal cortex and white matter, mostly frontal, usu assoc w/DAI. Independent of site and direction of impact.
Herniation: at uncus or tonsils, also independent of site and direction of impact.

Lacs of corpus callosum or septum pellucidum can occur without skull fracture (usu younger individuals).
Lacs often blood-less due to vasospasm.
Hyperextension injury: lacs to brainstem esp at ponto-medullary junction,

Primarily impact injuries. 90-95% assoc w/fracture.
Rare in very old and very young (< 2 yo). Unassoc w/fracture more common in the very young (elastic bones don’t break).
Primarily arterial blood (middle meningeal) but may be venous (diploic veins, middle meningeal and dural sinuses).
Gross: disc shaped, convex.
Classic symptoms: lucid interval (1/3).
Chronic epidurals are rare. (by def discovered > 48 – 72 hrs from injury).

Subdural Hematoma
Often assoc w/contrecoup contusions in a fall.
Often not assoc w/fractures.
Caused by angular acceleration over a short period of time.
72% assoc with falls and assaults vs. 24% due to MVAs.
Tears of parasagittal bridging veins.
Gross: Cerebral convolutions retain normal contours, concave.
Rebleeding and formation of chronic subdural from thin walled-sinusoidal blood vessels.
Subdural Hygroma: accumulation of spinal fluid in subdural space. Can occur secondary to trauma or meningtis.
Clinical Classification:

  • Acute: 12 – 24 hrs
  • Subacute: 24 hrs – 7 days
  • Chronic: 7+ days

Organization and Histologic Dating:

Up to 24 hoursThin fibrin layer, few PMNs, swelling of endothelial cells.
2 - 5 daysClot becomes adherent.Rare fibroblasts, mononuclear cells in fibrin, rare hemosiderin-laden macrophages, no RBC in fibrin layer.
5 - 10 days3-5 cell fibroblast layer; some sinusoidal capillaries; more hemosiderin-laden cells.
10-20 daysVisible inner membrane.>5 cells fibroblast layer; well-formed capillaries.
3- 4 weeksAtachnoid membrane as thick as dura.fibroblast layer = dura in outer membrane; 2-4 cells thick in inner membrane.
1 - 3 monthsliquified clot 4 - 5 wks; membrane hyalinizedouter membrane complete with aggregates of hemosiderin-laden macrophages.

Diffuse Axonal Injury
Def: trauma induced diffuse injury of axons assoc w/immediate LOC and coma > 6hrs.
– Mild: 6 – 24hrs.
– >24 hrs w/o brainstem dysfunction
– > 24 hrs with brain stem signs.
caused by angular acceleration over a long period of time
not associated with a lucid interval
primate model exists.
89% assoc with MVA (only 10% assoc with falls or assaults).
Gross: multiple small white matter perivascular hemorrhages (diffuse vascular injury), hemorrhages or tears in corpus callosum, dorsolateral rostral brainstem, gliding contusions.
Micro: histologically apparent after 12-24 hrs survival by silver stains or H&E; At 3-4 hrs if use b-APP (as early as 1.5 hrs). [not specific to DAI: can be seen in hypoxia!]
axonal spheroid s(“retraction balls”) in corpus callosum, long white matter tracts and brainstem. Peak at 2 -3 wks after injury, then replaced by gliosis.

Concussion: trauma induced alteation in mental status that may or may not involve a LOC.
Second-impact syndrome: usu in sports, 1st concussion followed by succesive impact and coma. Mortality 50%
Concussion aloe or in combination with alcohol can cause post-traumatic apnea.

Subarachnoid Hemorrhage
Due to trauma usually thin and on convexities.
May cause secondary communicating hydrocephalus from interference with arachnoidal villi reabsorption of CSF.
If massive at base of brain consider vertebral artery laceration. (Abrasions about ear in 50%).
Carotid injury: usu assoc w/MVA, hyperextension or spinal fracture.

Traumatic Brain Swelling
Congestive brain swelling: due to vasodilation
– more common in infants and children (has been contested: they have a more benign course).
– results from increased intracranial blood volume due to vascular congestion and may increase brain weight
– does not necessarily correspond to the extent of injury

Boxing Injuries
“Punch-drunk syndrome”: slurred speech, ataxia, impaired memory, dementia, broad-based gait, Parkinsonian-like
– fenestrated septum pellucidum cavum
– scarring or cerebral hemispheres and cerebellum with gliosis and hydrocephalus ex vacuo
– degeneration or loss of cells in substantia nigra
– NF tangles in cortex esp medial temporal gray matter

Hyperostosis frontalis:
Yellow skull: Tetracycline for acne