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General autopsy findings, brain weight and brain pathology were studied in 98 men and five women who had been exposed occupationally to organic solvents over several years and assessed by the Danish National Board of Industrial Injuries for chronic toxic encephalopathy. The findings were compared with a forensic control material and a hospital control material. As in the general population, the most common causes of death among the exposed workers were heart failure and other vascular diseases. Due to the composition of the material (forensic cases), the number of suicides and violent deaths was high. Atherosclerosis was the most common CNS finding, but in comparison with the two control materials, no increase in the frequency of atherosclerosis or of Alzheimer's disease was found. Brain weights of the exposed workers corresponded closely to brain weights in the control materials, after correction for body height, body weight and age. Chronic alcoholism was correlated with slightly reduced brain weight.

Six cases of completed ischemic stroke in the middle cerebral artery territory of more than two months' duration were selected for this study of neuropathology. Coronal brain slices of the entire brain were cut for histology and stained with Klüver-Barrera's stain. Neuronal and glial cell density, and cortex thickness were measured at various distances from the border of the infarct. Corresponding counting points in the contralateral hemisphere served as control in all cases. The density of histologically intact neurons was in all cases normal at a distance of 0.5 cm or more from the border of the infarcts. In one half of the cases the border zone between infarcted and normal tissue was less than a few cells in thickness. This study of old brain infarcts confirms the commonly held view that there is an abrupt transition between infarcted and normal tissue. This observation suggests that the wide zone of low blood flow and metabolism surrounding cerebral infarcts is not caused by selective loss of neurons. Instead, we hypothesize that such change in blood flow and metabolism is the result of neuronal disconnection and cortical deactivation.

Histopathology of eye, optic nerve and brain was performed in a patient with typical signs and symptoms of dominant optic atrophy. He belonged to a previously-reported family of 152 members in which optic atrophy was demonstrable in 14 persons, and probably present in a further 8 cases. In the eyes, fibrosis of the retinal ganglion cell layer and disc was found. Ultrastructural examination showed a few remaining cells in this layer, heavy fibrosis and in particular a highly condensed inner limiting membrane. The optic nerves, the optic chiasm and optic tracts showed an increased content of collagen tissue and a decreased number of neurofibrils and myelin sheaths. In the lateral geniculate body there was massive loss of ganglion cells, fibrillary gliosis and a great quantity of fine granular lipid in the cytoplasm of the ganglion cells. No changes in the calcarine cortex were observed. Examination of the intracranial part of both vestibulocochlear nerves showed a decreased number of neurofibrils and myelin sheaths. It is concluded that the histopathological changes of the visual system are similar to those in Leber's disease, but less pronounced. The study confirms earlier theories that dominant optic atrophy is a primary degeneration of the ganglion cell layer in the retina, with ascending optic atrophy.

During the years 1984-1987, a consecutive Danish autopsy material of 43 AIDS cases was analysed in order to investigate a possible coincidence of pathological changes in brain and eye. In the brain, nodular gliosis/encephalitis was most frequent, followed by cytomegalovirus infection, which occurred twice as frequently as toxoplasmic infection and four times as frequently as fungal infection. In the eye, cytomegalovirus infection was most frequent and the only opportunistic infection, followed by retinal gliosis and cytoid body lesion. Malignant lymphoma was present in the brain in three patients, and in the choroid in two of these. In 11 patients, no changes of the brain were found. In eight of these the eye was also without pathological findings, while three had minor changes. In 22 patients the eye was normal, but in only eight of these was the brain without changes. Eight had nodular gliosis, and four a specific infection, while multifocal leucoencephalopathy and unspecified abscess each occurred in one patient. Comparison of the three opportunistic infections--CMV, toxoplasmosis and mycosis--in the three-year period showed an overall decreasing frequency, attributed to better medical care. It is concluded that concomitance of identical pathological lesions in brain and eye is less frequent than was expected.

The reported findings of periphlebitis retinae (PR) at autopsy, in which brain autopsy was also performed, in 2 patients with multiple sclerosis (MS) are, so far as the authors are aware, the first histological account of this manifestation of the disease. The similarity between the cellular accumulations around the veins of the central nervous system seen in multiple sclerosis and the periphlebitic cellular accumulations here described suggests that periphlebitis is an initial event in plaque formation.

Nuclear size and density were determined in brain regions with different glial--neurone composition in rats up to 35 weeks after porto-caval anastomosis. In the white matter, i.e. corpus callosum, both the total cell count and the percentage of astrocytes and oligodendrocytes were unchanged. In the corpus striatum, where the glial/neurone ratio is about 1, the number of nuclei registered as astrocytes increased, and after 35 weeks astrocytes comprised 29% of glial cells (compared with 15% in controls). However, the number of oligodendrogial nuclei decreased simultaneously, leaving the total glial number unchanged. In the animals with longest experimental period there was a 15% loss of neurones. In a region with higher glial/neurone ratio, i.e. the Purkinje cell layer, the neurones showed a similar reduction, whereas the number of Bergmann astrocyte nuclei increased less than striatal astrocytes. A small group of animals with pronounced signs of encephalopathy had a higher loss of neurones and, furthermore, the glial number in corpus striatum and callosum was reduced, due to loss of oligodendrocytes. Despite the use of perfusion fixation, the size of astrocyte nuclei increased, this was reversible, as only slight changes were seen after 35 weeks. A possible explanation of the increase in astrocyte nuclear count and decrease in oligodendroglial count could be that nuclei normally considered to be oligodendroglial are transformed into nuclei with morphological characteristics of astrocytes.

Following injections of iodophendylate (Pantopaque) in adult rats, the contrast medium was shown to be refrained in the dilated cerebral ventricles for at least 180 days. Histological examination revealed macrophages containing phagocytosed lipid on the ependymal lining of the ventricles, but there was no leukocytic reaction to retained or encysted contrast material. The macrophages were considered to be involved in the removal of iodophendylate. The irritative reaction in the normal central nervous system was limited, as opposed to the severe reactions previously reported in animals with inflammation of the brain and meninges.

Previous clinical and histological studies have suggested that the aetiology of Meniere's disease should be sought not only in the endolymphatic hydrops, but also in pathological changes of the brain and brain stem. Moreover, neuropsychological studies have indicated some centralization of the disease, whether it be primary or secondary. In order to elucidate this problem further we have examined the temporal bones and brains of 4 patients with Meniere's disease, who died of diseases unrelated to the inner ear or the central auditory and vestibular pathways. Endolymphatic hydrops was found in 6 temporal bones to a varying degree, as well as degeneration of the ganglion cells. The brain stem was divided by many horizontal sections from the rostral border of the superior colliculi above, to 15 mm caudal to the border between pons and medulla below. The principal nuclei and fascicles, the intra- and extraparenchymatous vessels and the leptomeninges were examined. The morphology of ganglion and glial cells was studied. Myelin sheaths were investigated for focal or diffuse demyelination, and the axons were observed. In addition, vessels and leptomeninges were studied for atherosclerosis and fibrosis. The brain autopsies did not reveal any changes, either locally or diffusely, which could support central pathoanatomical lesions as being responsible for the symptoms in Meniere's disease.