Immunohistochemical Methods in the Differential Diagnosis of Primary

Overview

In a 22-year-old man, driver of a personal motor vehicle, who died within 39 hours after a trafficinjury, the authors made histological and immunohistochemical examinations of the brain focu-sed on differentiation of primary traumatic and subsequent secondary changes. In haematomasthe authors revealed the presence bi-and trivalent iron by Turnbull´s and Perl´s reaction as wellas glycophorin by immunohistochemical reactions.White matter lesions were evaluated histologically by staining according to Palmgren and immu-nohistochemically by detection of neuron-specific enolase, beta-amyloid protein precursor andlow molecular neurofilaments.Minor contusion foci in the corpus callosum and in the peripheral portion of the pons revealedthe presence of extracellular bivalent iron and exceptionally also the presence of intracellulariron. Glycophorin was present not only in erythrocyte membranes but also in the form of lumpssignalizing haemolysis.In the haematoma in the median portion of the pons neither iron nor free glycophorin weredetected.At all investigated sites (subcortical areas of the white matter of the hemispheres, capsula inter-na, corpus callosum, pons Varolii) the authors detected numerous axonal deformities (oedema orformation of retraction spheroids) which revealed on immunohistochemical examination an in-tense reaction with antibodies in particular against neuron-specific enolase and beta-amyloidprotein precursor, and to a smaller extent against low-molecular neurofilaments.The combination of the mentioned immunohistochemical examinations seemed a suitable methodfor differentiating primary cerebral injury (diffuse axonal injury and minor contusion foci in thecorpus callosum and the margin of the pons) from secondary changes (haemorrhages in themedian portion of the pons) which developed shortly before death as a manifestation of haemody-namic disorders associated with cerebral oedema)

Key words:
immunohistochemistry - diffuse axonal injury - neuron-specific enolase - beta-amyloid