Neuropathology of inflicted head injury in children. II. Microscopic brain injury in infants.

There are very few reports in the literature dealing with the neuropathology of infant head injury, and the question of whether diffuse traumatic brain damage [diffuse axonal injury (DAI)] occurs in such children has not yet been reliably established by detailed neuropathological studies. We report the findings in the brains of a series of 37 infants aged 9 months or less, all of whom died from inflicted head injuries, and 14 control infants who died of other causes. Axonal damage was identified using immunohistochemistry for beta-amyloid precursor protein.

Neuropathology of inflicted head injury in children. I. Patterns of brain damage.

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. There were 37 infants, age at head injury ranging from 20 days to 9 months, and 16 children (range 13 months to 8 years).

Neuronal cytoskeletal changes are an early consequence of repetitive head injury.

While neuropathological studies have established the pathology of dementia pugilistica to be similar to that of Alzheimer's disease, there is little information about the early histological changes caused by the repetitive trauma that eventually produces dementia pugilistica. We have examined the brains of four young men and a frontal lobectomy specimen from a fifth, age range 23-28 years, all of whom suffered mild chronic head injury. There were two boxers, a footballer, a mentally subnormal man with a long history of head banging, and an epileptic patient who repeatedly hit his head during seizures.

The diagnosis of diffuse axonal injury: implications for forensic practice.

The diagnosis of diffuse axonal injury (DAI), which may be of considerable importance in forensic medicine, necessitates widespread sampling of the brain for histology. Because a limited sampling method for screening brains for axonal damage would be of value for medico-legal work, the authors have tested the findings of an earlier study which suggested that a standard set of three blocks from above and below the tentorium could reliably be used in routine practice as a basis for the diagnosis of DAI. A series of 22 previously diagnosed cases of DAI, with a range of survival times, was studied using immunohistochemistry with antibodies to beta-amyloid precursor protein (beta APP), the microglial-associated antigen CD68 (PG-M1) and for GFAP.

Neurofibrillary tangles, but not Alzheimer-type pathology, in a young boxer.

The chronic neurological sequelae of boxing are well described, but there have been few neuropathological studies of boxers dying early in their career. We report the case of a 23-year-old boxer, whose brain showed neurofibrillary tangles in all neocortical areas, but remarkable sparing of medial temporal lobe structures. These tangles, assumed to be the result of repetitive head injury, were the only detectable abnormality: none of the other changes previously described in the brains of retired boxers were seen.