Biomedical subjects
A Torvik
Publications and source records attributed to A Torvik.
The effects of ageing, cachexia and neoplasms on striated muscle. Quantitative histological and histochemical observations on an autopsy material.
The effects of ageing, cachexia and neoplasms on striated muscle were examined in histological sections of an autopsy material. Paraffin sections were examined from four separate muscles of 30 previously healthy subjects who died suddenly, from eight cases with cachexia and from 16 cases with cachexia and neoplasms. In addition, ATP-ase stained cryostat sections were examined from two muscles from most of the cases. All the sections were evaluated with regard to atrophy, myopathic changes and fibre type grouping. Furthermore, the exact size of 100 fibres of each type was determined in the enzyme stained sections. Myopathic changes were found in a few muscles, mainly in the normal cases. They were considered incidental findings without clinical significance. Fibre type grouping could not be evaluated in the anterior tibial muscle because large clusters of the same fibre type occur normally in this muscle. In the biceps brachii only two normal cases and none of the cachectic cases showed fibre type grouping. A moderate small grouped muscle fibre atrophy was found in normal cases with increasing age. The cases with cachexia showed a marked small grouped atrophy which involved both fibre types. There were only small and uncertain differences between cases with cachexia and tumours and those with cachexia alone. Thus, no changes were observed which could be ascribed to tumours alone. The small grouped atrophy in ageing and cachexia resembled that seen in denervation atrophy but the exact mechanism of the changes remains obscure.
Brain lesions in alcoholics. A neuropathological study with clinical correlations.
Among 8735 autopsies performed during a 5-year period at Ullevål Hospital in Oslo there were 70 cases of Wernicke's encephalopathy (0.8%) and 152 cases of alcoholic cerebellar atrophy (1.7%). Cerebellar atrophy was found in 26.8% of all examined alcoholics. Twenty-two of the cases with Wernicke's encephalopathy were active (acute and subacute) and 48 were inactive (chronic). Examination of the clinical records showed that stupor and coma were the dominating symptoms in active cases. A pure Korsakoff's psychosis with a selective memory defect was present in about one-third of the cases with inactive encephalopathy while the remaining had more or less pronounced global dementia ("alcoholic dementia"). It is suggested that inactive Wernicke's encephalopathy is the main underlying lesion both in Korsakoff's psychosis and "alcoholic dementia" but that additional lesions are present in the latter group. The brain weight in 545 male alcoholics was compared with that of 586 controls. Cases with non-alcoholic brain lesions were excluded from both groups. In alcoholics the brain weight was significantly lower than in controls in all age groups below 70 years. The mean weight difference was 31 g. The study thus confirmed the existence of a generalized alcoholic brain atrophy.
Watershed infarcts in the brain caused by microemboli.
Multiple vascular occlusions are frequently found in the leptomeningeal arteries over watershed infarcts in the brain. These occlusions have largely been interpreted as thrombi secondary to slowing of the blood flow. This report suggests that most of the occlusions are microemboli, which may lodge preferentially in these areas, and that they are the cause of the infarcts rather than secondary events. These suggestions are based upon the analysis of three groups of patients. The first group consists of four cases, two of which had atheromatous masses and the other two, tumor emboli in the overlying leptomeningeal arteries. These cases prove beyond doubt that microemboli can lodge preferentially in the watershed areas and cause infarcts in the brain. The second group consists of the cases of watershed infarcts that were precipitated by hypotensive episodes. Only one of these showed occlusion of the overlying arteries, although all of them obviously had slowing of the blood flow during the acute phase. These cases thus discredit the concept that stagnation thrombosis is a frequent event. Finally, three cases with watershed infarcts and vascular occlusions interpreted as platelet microemboli are presented to demonstrate different pathogenetic mechanisms effective in the process of embolization.
[Foreign bodies in the brain. 20-year autopsy material].
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Combined modality therapy of operated astrocytomas grade III and IV. Confirmation of the value of postoperative irradiation and lack of potentiation of bleomycin on survival time: a prospective multicenter trial of the Scandinavian Glioblastoma Study Group.
In a controlled, prospective, randomized investigation, started in 1974, 118 patients with supratentorial astrocytoma Grade III--IV were divided into three groups. Groups 1 and 2 received 45 Gy postoperatively to the whole supratentorial brain. Bleomycin in 15-mg doses and a total dose of 180 mg or placebo was given intravenously three times a week, one hour prior to radiotherapy, during weeks 1, 2, 4 and 5. Group 3 received conventional care but no radiotherapy or chemotherapy. Median survival rates of patients were 10.8 months in Groups 1 and 2, and 5.2 months in Groups 3, a statistically significant difference. With regard to performance, the patients in Group 3 deteriorated faster than patients in Groups 1 and 2. Bleomycin had no positive or negative influence on survival.
The pathology of experimental obstructive hydrocephalus. A scanning electron microscopic study.
Obstructive hydrocephalus was produced in 14-day old rabbits by injection of kaolin into the cisterna magna. The ependymal lining was studied by scanning electron microscopy. Marked hydrocephalus was present 1 or 2 weeks after the kaolin injection. The ependymal lining adapted remarkably well to the rapid expansion by increasing the surface area of the ependymal cells. No breaks or denudement of the ependymal lining was observed except at the sites of ruptured ventricular synechiae. Generally, these findings confirm previous light and electron microscopic observations on the same model (Torvik et al. 1976; Torvik and Stenwig 1977). The results are discussed in relation to current theories concerning the pathophysiology of acute hydrocephalus.
Subarachnoid hemorrhage and cerebrovascular spasm. Morphological study of intracranial arteries based on animal experiments and human autopsies.
Artificial subarachnoid hemorrhage (SAH) produced by injection of autologous blood into the cisterna magna in dogs gave rise to considerable narrowing or spasm of the basilar artery and its branches, including the posterior cerebral arteries, as demonstrated by cerebral angiography. Repeated cisternal injections of blood at various intervals produced more severe spasm than a single injection. After perfusion-fixation of the brain, the cerebral arteries were examined by light and electron microscopy. None of the animals showed abnormalities in the intima or media of the vessel walls. Previously reported findings of morphological changes due to spasm could not be confirmed. Postmortem examination of brain vessels from nine patients with SAH and arterial spasm showed no specific changes that could be ascribed to spasm.
Encephalomyelitis with polyneuropathy.
Four cases of progressive polyneuropathy and bulbar encephalitis and/or myelitis are described. A carcinoma was found in only one of the cases. It is emphasized that this syndrome may occur in the absence of malignant tumors.
The relationship between cerebrospinal fluid creatine kinase and morphologic changes in the brain after transient cardiac arrest.
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Lack of labelling of microglial cells following microinjection of [3H] beta-alanine: an electron microscopic autoradiographic study.
Following axotomy of the facial nerve, the uptake of [3H] beta-alanine into different types of glial cells in the facial nucleus was studied by autoradiography. A marked proliferation of microglial cells, predominantly in a satellite position to neurons, was accompanied by a localization of [3H] beta--alanine over astrocytes and oligodendrocytes but not over microglial cells. Microglial cells therefore appear to be a functionally distinct cell type and should not be classified with the macroglia.
A tribute to Kristian Kristiansen.
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Transitory block of the arachnoid granulations following subarachnoid haemorrhage. A postmortem study.
The arachnoid granulations of the superior sagittal sinus were examined for blockage by erythrocytes in 43 cases of subarachnoid haemorrhage. Ten cases had survived for more than two weeks after the haemorrhage. Among 33 cases with acute haemorrhage, 17 had evidence of blocking of the granulations. The severity of the block varied from complete clogging of nearly all granulations to slight filling of a few of them. Cases with some days' survival showed evidence of phagocytosis of the entrapped erythrocytes by macrophages. Several of the cases with old haemorrhage had groups of haemosiderin macrophages in the granulations but none showed fibrosis (except for one single villus). It is concluded that clogging of the arachnoid granulations may contribute to the raised intracranial pressure in some cases of acute subarachnoid haemorrhage. However, the observations do not support the hypothesis that the haemorrhage may lead to fibrosis or scarring of the granulations with chronic impairment of the cerebrospinal fluid resorption and subsequent hydrocephalus.
The pathology of experimental obstructive hydrocephalus. Electron microscopic observations.
Obstructive hydrocephlus was produced in 10-14 day-old rabbits by injection of kaolin into the cisterna magna and the ependyma and subependymal tissue was studied by electron microscopy. Generally, the study confirmed recent light microscopic observations on similar models (Torvik et al., 1976). In contrast to most previous reports, it was found that the ependyma adapted remarkably well to ventricular dilatation. No true ependymal defects occurred even in extensive hydrocephalus except at the sites of the ventricular synechiae which sometimes ruptured. The specialized ependymal junctions remained intact but outside the junctions the intercellular clefts were widened, particularly along the lateral wall of the lateral ventricle. The density of the microvilli and cilia decreased, probably because of the increase in the surface area of the ependyma. Dense bundles of filaments developed in the ependymal cells of the hydrocephalic animals. The extracellular space of the subependymal white matter appeared increased but there was no evidence of destruction of fibres or cells. Thus, the reduction of the cerebral mantle thickness was probably mainly caused by pre-sure atrophy.
A case of chronic demyelinating polyneuropathy resembling the Guillain-Barré syndrome.
A case of demyelinating polyneuropathy is reported which was clinically and pathologically indistinguishable from the Guillain-Barré syndrome, with the exception that the symptoms progressed steadily for 7 months. Pathologically, the peripheral nerves and intraspinal roots showed selective demyelination with axonal sparing and patchy mononuclear inflammation. The posterior columns of the spinal cord also showed selective demyelination with axonal sparing. The simultaneous destruction of central and peripheral myelin is discussed in relation to the immune theory for the Guillain-Barré syndrome. Numerous anterior horn cells showed severe chromatolysis although there was little axon loss. It is suggested that chromatolysis may occur after severe and longstanding demyelination.
The spinal cord central canal in kaolin-induced hydrocephalus.
In order to study the cause of the great individual variations in kaolin-induced hydrocephalus, the lower brain stem and upper spinal cord were examined histologically in a series of young rabbits that had received injections of kaolin into the cisterna magna. Animals with complete occlusion of the outlets from the fourth ventricle into the subarachnoid space showed only a moderate ventricular dilatation, while cases with marked hydrocephalus also plugs of kaolin in the caudal part of the fourth ventricle. The intraventricular kaolin was adherent to the roof of the fourth ventricle by strands of connective tissue and it is suggested that the plugs served as valves that initially occluded the opening of the central canal and were then lifted away as the ventricle dilated and the roof moved posteriorly. The animals with marked hydrocephalus also had extensive dilatation of the central canal with cleft formation in the posterior columns. The observations support the concept that in hydrocephalus the central canal may serve as an alternative resorption route for the cerebrospinal fluid through communication with the spinal subarachnoid space.
The origin of reactive cells in retrograde and Wallerian degeneration. Experiments with intravenous injection of 3H-DFP-labeled macrophages.
In order to examine the possible haematogenous origin of phagocytes in anterograde and retrograde degeneration, rabbit peritoneal macrophages were labeled in vitro with 3H-DFP and injected intravenously into host animals. Four or five days prior to the injection, the facial nerve was avulsed and the sciatic nerve ligated in five recipients. The animals were killed 24 h after the injection of the macrophages. Labeled cells were found in that part of the sciatic nerve which was mechanically damaged and in the liver and spleen but not in areas with retrograde or Wallerian degeneration. The possible interpretation of these findings is discussed.
[Editorial: An infectious form of presenile dementia].
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