Inflammatory changes have been found in Parkinson's disease, in humans intoxicated with the parkinsonian toxin MPTP, and in animal models of the disease. However, it is still not known whether inflammatory changes are responsible for active nerve cell death or if they have a protective role against neurodegeneration. In this study, we analyzed the glial reaction in the substantia nigra pars compacta (SNpc) and the striatum of monkeys rendered parkinsosian by chronic MPTP injections. At postmortem examination 1 year after the last MPTP injection, the density of astroglial cells and activated microglial cells in the SNpc, but not in the striatum, of MPTP-intoxicated animals was significantly higher than in the two control animals. These data suggest that neurodegeneration was still active despite the absence of the agent triggering cell death and that the glial reaction is associated with long-term neurodegeneration.

The degeneration of nigral dopaminergic neurons in Parkinson's disease is believed to be associated with a glial reaction and inflammatory changes. In turn, local factors may induce changes in vascularization and contribute to neuronal vulnerability. Among these factors, Vascular Endothelial Growth Factor (VEGF) is released in adults under pathological conditions and is thought to induce angiogenesis. In order to determine whether changes in brain vasculature are observed in the affected brain regions in parkinsonism, we quantitatively analysed the VEGF-expressing cells and blood vessels in the substantia nigra of monkeys rendered parkinsonian by MPTP injection and compared the results with those obtained in control monkeys. Using stereological methods, we observed an increase in the number of VEGF-expressing neurons and an increase of the number of blood vessels and their volume occupying the substantia nigra pars compacta of monkeys rendered parkinsonian by chronic MPTP intoxication. These changes in vascularization may therefore modify the neuronal availability of blood nutrients, blood cells or toxic substances and neuronal susceptibility to parkinsonism.

Atretic cephalocele appears as an unimportant and benign lesion. This malformation consists of meningeal and vestigial tissues (arachnoid, glial, or central nervous system rests). The authors report the findings in 16 cases (seven parietal and nine occipital) of rudimentary cephaloceles. Twelve patients presented with associated brain abnormalities detected by either computerized tomography (CT) or magnetic resonance imaging (MR). Nine lesions also exhibited an anomalous vascular component demonstrated by CT or MR imaging or at surgery. The existence of this tiny malformation in five cases was the main diagnostic clue to a severe complex of cerebral anomalies, namely cerebro-oculomuscular (Walker-Warburg) syndrome. An occipital location of the atretic cephalocele was associated with the worst prognosis, with only two children developing normally. However, a parietal location carried a better prognosis, which is contrary to the outcome reported in the current literature. The authors classify atretic cephaloceles into two types based on histological examination of the surgical specimens, and suggest that these types represent different stages in the development of this malformation. It is concluded that, in the evaluation of the atretic cephalocele, the neurosurgeon is obliged to proceed to a detailed neuroradiological study of the patient and that the prognosis does not depend on the existence of the cephalocele itself, but rather on associated "occult" brain anomalies.

We report a series of 46 children who were treated for one of the diverse forms of cranium bifidum during a period of 22 years. The purpose of the survey was to investigate pathogenetic factors involved in the development of cranial dysraphism and to analyze clinical and pathological factors that influence the patients' outcome. We also investigated the existence of associated intracranial anomalies, in a systematic way, using modern methods of neuroimaging, and related the findings to the patients' final results. The lesions were classified as encephalocele (n = 15), cranial meningocele (n = 3), atretic cephalocele (n = 26), cranium bifidum occultum (n = 1), and exencephaly (n = 1). There was an excess of the atretic form of cephaloceles in our series, a fact that probably reflects geographical variations described for cephaloceles in general. The location of the lesions was occipital in 29 children, parietal in 16, and temporal and frontobasal in one case each. In seven cases there was parental consanguinity. A familial history of malformations of the central nervous system was encountered in eight instances. Associated systemic abnormalities were present in 23 patients, while central nervous system anomalies were found in 36 children. Cephalocele repair was undertaken on 35 occasions. There were no surgical fatalities in the series. The mean follow-up time was of 7 years. Overall mortality for the whole group was of 17/46 or 36%. Twenty of the 29 survivors had no neurological sequelae, but only 18 children exhibited a competitive intelligence level. A good outcome was found to correlate well with: an average head size at birth, a normal initial neurological condition, operability of the lesions, and an absence of disorders of the neuronal migration. Neurological outcome depended also on the occurrence or not of hydrocephalus, while the intelligence level was mainly related to the absence of cerebral tissue within the sac of the malformation.

Classically meningiomas present and evolve with a progressive course. Meningiomas manifest themselves mainly in middle and old age when the incidence of strokes is higher. The authors report three instances of meningioma with acute haemorrhagic onset. The clinical picture of our cases consisted of subarachnoid bleeding, subdural hematoma and intracerebral haemorrhage respectively. The diagnostic difficulties encountered when assessing these patients are discussed. The current literature regarding meningioma associated with haemorrhage is reviewed. One of our cases seems to be the first reported case of subarachnoid haemorrhage originating from a meningioma of the petrous bone.