The non-astrocytic cells which proliferate in the rat brain after the induction of an area of necrosis have been characterized and counted by means of combined in vivo bromodeoxyuridine (BrdU) administration and immunohistochemical demonstration of glial fibrillary acid protein (GFAP), vimentin, Ricinus communis agglutinin 120 (RCA-1), Griffonia simplicifolia B4 isolectin (GSI-B4), keratan sulphate (KS), carbonic anhydrase C (CA.C), transferrin (TF) and ferritin. Two days after the injury, 7.5% of the proliferating cells were GFAP-positive reactive astrocytes, 5.7% were RCA-1-positive cells and 17.4% were GSI-B4-positive cells. Lectin-binding cells had the microscopic and ultrastructural aspects of microglia; they proliferated around the needle track and in the corpus callosum. Microglia represented a large fraction of the proliferating cells. Evidence is presented for the origin of at least a proportion of perilesional astrocytes and microglia from the periventricular matrix, and of microglia from blood precursors. Other non-proliferating microglia cells transiently appeared in the normal brain around the wound, in agreement with the existence of two different microglia cell populations reacting with different modalities to an area of necrosis.

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Widespread neuritic dystrophy is a hallmark of Alzheimer's disease (AD) and, in a less severe form, of brain ageing in various mammalian species. By immunohistochemistry, diffuse dot-like staining for ubiquitin (Ubq), a polypeptide involved in the degradation of abnormal and short-lived proteins, has been associated with human brain ageing. The nature of the Ubq deposits was investigated by immunogold electron microscopy on autopsy samples from aged human and dog brains. Most of the dot-like staining was localized to the white matter and corresponded to myelinated dystrophic neurites filled by Ubq-labelled lysosomal dense bodies. They did not contain paired helical filaments or multilamellar bodies. A minority of Ubq deposits was represented by amorphous densities in focal enlargements of the myelin sheaths. Our findings show that the spectrum of Ubq changes in ageing brain is wider than formerly recognized, and support the hypothesis that a defective regulation of the lysosomal system might be involved in the pathogenesis of structural abnormalities both in the ageing brain and in Alzheimer's disease.

Medulloblastoma is a highly malignant cerebellar tumor of children and, less frequently, of adults, with a tendency to early recurrence and dissemination through the cerebrospinal fluid. The prognosis has improved significantly in recent decades, in parallel with the improvement in neurosurgical techniques and the use of postoperative radiotherapy. An overview is given of the prognostic role of clinical and pathological features of individual cases as reported in the literature. Apart from the presence or absence of metastases at diagnosis and the radiotherapy modality, none of the factors studied was generally thought to have a definite significant prognostic role. The extent of surgical excision seems to influence survival more in pediatric cases than in adults. Ongoing cytogenetic studies and molecular biology investigations are aimed at better categorization of medulloblastomas and individualized postoperative treatment.

The increasing prevalence of brain tumours and longer duration of survival achieved by recent advances in treatment prompt a critical analysis of the impact of functional rehabilitation on patients with brain tumours. In this review brain tumours and outcome of brain tumour patients are discussed from a rehabilitation perspective, taking into account not only life expectancy but also the direct and indirect causes of functional impairment. Results of functional rehabilitation and factors involved in its effectiveness are presented and analysed to serve as a basis to neurologists involved in the management of patients with brain tumours.