Severe non-missile head injury commonly results in a form of brain damage known as diffuse axonal injury (DAI). The histological diagnosis of DAI is made by silver staining for the presence of axonal retraction balls. This feature takes about 24 h to develop and does not allow for the early histological diagnosis of DAI. We have used immunocytochemistry for the beta-amyloid precursor protein (beta APP) as a marker for axonal injury in formalin-fixed, paraffin-embedded sections of human brain. Axonal beta APP immunoreactivity was present in all cases which had survived for 3 h or more. This was true even where the degree of head injury did not appear to be severe, supporting the theory that DAI is a severe form of a more common phenomenon of axonal injury which occurs after cerebral trauma. beta APP immunoreactivity was also found in some non-head injured cases and so cannot be considered to be a specific marker for trauma. The results show that beta APP immunocytochemistry may be useful in the detection of traumatic axonal injury in its early stages, before the formation of axonal retraction balls, provided care is taken to exclude other causes of such immunoreactivity.

The authors present a case of neuromuscular hamartoma of the cochlear nerve, an unusual occurrence in the internal auditory meatus (IAM). A review of the literature shows no previous report of neuromuscular hamartoma of the cochlear nerve. This tumour was clinically and radiologically difficult to distinguish from acoustic neuroma. It is important to consider the diagnosis of these rare small tumours pre-operatively, as it may be appropriate to manage this conservatively.

We describe a cas e of angioleiomyoma of the internal auditory meatu s. Afinding ofthis tum or at this site is ve,y unusual. In fa ct, our review ofthe literature revealed that only 1 case has been previously reported. 1n our patient, the tumor was clinically and radiologically difficult to distingu ish frotn an acoustic neuroma. It would be important to recognize this rare small tumor preoperatively because it may be appropriate to manage it conservatively.

Introduction:  Amyloid β (Aβ) protein, a 38–42 amino acid peptide is the major component of senile plaques in Alzheimer's disease and has been suggested to exert its toxic effects via the direct and indirect production of reactive oxygen species. Materials and methods:  We have investigated the role of reactive oxygen species in the toxic actions of Aβ on a human neuronal cell line SHSY‐5Y, using the MTT assay for cellular viability and comparing the toxicity of Aβ with that of H2O2. Results:  The neurotoxic fragment of Aβ protein, Aβ25–35, had clear concentration‐ and time‐dependent toxic effects on SHSY‐5Y cells. The ability of antioxidants to reverse these toxic effects of 10 µm Aβ25–35 or 200 µm H2O2 were tested. Vitamin E (10–100 µm) did not affect either Aβ or H2O2. Trolox, a vitamin E analogue (5–200 µm) had protective effects on H2O2‐induced cell death but was ineffective in preventing the cell death induced by Aβ. Vitamin C (10–1000 µm) partially reversed H2O2‐induced toxicity but had no protective action when cells were exposed to Aβ. Discussion:  These results indicate that the mechanisms by which Aβ and H2O2 exert their toxic effects are different and suggest that in this experimental system, formation of reactive oxygen species do not have major role in Aβ‐induced cell death.