Fifty-three cases of non-accidental head injury in children were subjected
to detailed neuropathological study, which included immunocytochemistry for
microscopic damage. Clinical details were available for all the cases. The
re were 37 infants, age at head injury ranging from 20 days to 9 months, an
d 16 children (range 13 months to 8 years). The most common injuries were s
kull fractures (36% of cases), acute subdural bleeding (72%) and retinal ha
emorrhages (71%); the most usual cause of death was raised intracranial pre
ssure secondary to brain swelling (82%). On microscopy, severe hypoxic brai
n damage was present in 77% of cases. While vascular axonal damage was foun
d in 21 out of 53 cases, diffuse traumatic axonal injury was present in:onl
y three. Eleven additional cases, all of them infants, showed evidence of l
ocalized axonal injury to the craniocervical junction or the cervical cord.
When the data were analysed by median age at head injury, statistically si
gnificant patterns of age related damage emerged. Our study shows that infa
nts of 2-3 months typically present with a history of apnoea or other breat
hing abnormalities, show axonal damage at the craniocervical junction, and
tend also to have a skull fracture, a thin film of subdural haemorrhage, bu
t lack extracranial injury. Children over 1 year are more likely to suffer
severe extracranial, particularly abdominal, injuries. They tend to have la
rger subdural haemorrhages, and where traumatic axonal injury is present, s
how patterns of hemispheric white matter damage more akin to those reported
in adults. Diffuse axonal injury is an uncommon sequel of inflicted head i
njury in children.