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.

Detection of multidrug resistance gene product (P-glycoprotein) expression in ependymomas.

A neurosurgical series of 33 ependymal tumours was examined for expression of the membrane transport molecule P-glycoprotein, which is linked with the development of multidrug resistance in many human tumours. We employed the monoclonal antibodies JSB1 and C219, raised to two different epitopes of the P-glycoprotein molecule, and found P-glycoprotein expression both in normal ependyma and in 29 of the tumours. This is the first time that ependymal tumours have been demonstrated to express the protein, and we conclude that its expression may contribute to the reported failure of adjuvant chemotherapy to improve outcome in ependymomas.

Histochemical and immunocytochemical study of ubiquitinated neuronal inclusions in amyotrophic lateral sclerosis.

Ubiquinated cytoplasmic inclusions are a characteristic feature of the anterior horn cell pathology of amyotrophic lateral sclerosis. The underlying abnormality leading to the production of these inclusions in this neurodegenerative motor system disease is unknown. Despite the application of a wide range of histochemical and immunocytochemical techniques we have been unable to identify a core constituent protein in these intraneuronal inclusions.

Axonal injury in closed head injury by assault: a quantitative study.

Due to the controversy in the literature regarding the time course of axonal balloon formation in human material, we wished to determine if it was possible to diagnose axonal injury before the development of axonal balloonings. The hypothesis was that the presence of axonal swellings or axonal enlargements associated with a glial reaction could be used as a diagnostic aid in human axonal injury before 12 hours. The brains of eight individuals that survived for less than 48 hours following head injury, and also had evidence of axonal injury using the criteria of Vanezis et al.

The glial reaction in closed head injuries.

The development of the glial reaction in human closed head injury has been investigated using morphometry and statistical analysis. The brains of eight individuals that survived less than 48 h following closed head injury were analysed using immunoperoxidase for glial fibrillary acidic protein (GFAP). Controls were eight patients without neurological disease.

Selective and asymmetric vulnerability of corticospinal and spinocerebellar tracts in motor neuron disease.

The spinal cords of 10 cases of motor neuron disease were compared with those of six age-matched controls using myelin and silver impregnation methods, and the Marchi reaction for myelin degradation products. These studies revealed striking asymmetry in involvement of the lateral and anterior corticospinal tracts, without concordance in the pattern of involvement of these crossed and uncrossed corticospinal pathways. In addition there was prominent involvement of the posterior and anterior spinocerebellar tracts, but less marked abnormality was seen in the reticulospinal pathways.

Diffuse axonal injury in early infancy.

Diffuse axonal injury typified by retraction balls and axonal swellings was identified in the brains of a series of infants, 5 months old and younger, who had suffered closed head injuries. These axonal discontinuities were shown by using Nauomenko and Feigin's silver method, which is particularly useful for showing fine axons such as those found in the developing brain. Diffuse axonal injury in early infancy may occur in the same way as that described in adults.