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Biomedical subjects

A Torvik

Publications and source records attributed to A Torvik.

At least 19 recordsLinked to original sources
PubMed1992

Neuronal uptake of plasma proteins in brain contusions. An immunohistochemical study.

Twenty-five cases of cerebral contusions of various age were examined immunohistochemically for neuronal uptake of albumin and fibrinogen. The neurons in the damaged areas were heavily stained in all cases, even in those of only a few minutes' survival, and they remained positive for serum proteins until they disappeared from the lesions. In hematoxylin and eosin-stained sections, neuronal changes were observed from the first minutes after the lesion but they were indistinguishable from the shrunken "dark" neurons that occur as artifacts in poorly fixed material. However, in contrast to the artificially changed cells, the truly damaged ones took up serum proteins. It is concluded that staining with antisera against serum proteins may serve as early markers for neuronal injury before reliable histological changes have developed.

Adolescent↗
PubMed1992

Affection of the hippocampal granule cells in pontosubicular neuron necrosis.

The dentate fascia of the hippocampus was studied in 25 infants with pontosubicular necrosis and in 21 control cases without hypoxic cerebral lesions. Of the control cases 19 were completely normal and 2 showed one single necrotic cell in the granule cell layer. In contrast 15 of the cases with pontosubicular necrosis showed varying degrees of neuronal karyorrhexis in the dentate fascia. The severity of these changes largely parallelled those in the subiculum but there were exceptions to this rule. It is concluded that the dentate fascia is frequently involved in pontosubicular necrosis.

Blood Glucose↗
PubMed1992

Neuronal uptake of plasma proteins in cryogenic brain lesions. An immunoelectron microscopic study.

A previous light microscopic study on cryogenic brain lesions in rats demonstrated uptake of plasma proteins into damaged neurons within a few minutes after the lesion. The protein concentration was much higher inside the nerve cell bodies than in the surrounding neuropil. This is puzzling since the neuropil to a large extent consists of damaged neuronal processes. The present investigation describes the intracellular localization of albumin in this model using a post-embedding immunoelectron microscopic technique. The distribution of albumin in the lesions was studied after 1, 6 and 12 h survival periods. The intraneuronal albumin was mainly bound to the particulate elements of the cytoplasm and nuclei, while the watery parts of the cells showed no immunoreactivity. The intracellular organelles contained very little albumin, indicating that their membranes may be more resistant to freezing than those of the cells. Most of the neuronal and glial processes in the neuropil were swollen and contained almost no albumin. This explains the contrast between the strong immunoreactivity of the neurons and the vague reactivity of the neuropil in light microscopy.

Animals↗
PubMed1992

Protective effect of low-grade hypothermia in experimental skeletal muscle ischemia.

In the present study, a rat hindlimb tourniquet model was used to investigate the effect of moderate hypothermia on ischemic muscle necrosis. Complete circulatory arrest was maintained for 4.5 h. During the ischemic period the animals were kept in an infant incubator at different temperatures. After 72 h survival the percentage of necrosis in the anterior tibial muscle was measured morphometrically on histological slides. At an ambient temperature of 24 degrees C there was 80% necrosis in the anterior tibial muscle. At 22 degrees C the necrosis was reduced to 29%. This reduction corresponds to more than 30 min shortening of the ischemia time. Differences in tissue temperature may explain some of the discrepancies reported in tolerance limits for muscle ischemia. To achieve consistent results in experimental muscle ischemia, it is necessary to control the ambient temperature.

Animals↗
PubMed1992

Plasma proteins in normal neurons. Immunohistochemical studies on autopsy material and experimental animals.

Previous observations have shown that plasma proteins are taken up by damaged neurons after trauma, cold injury and anoxic lesions. The present study was undertaken to test whether such uptake also can occur in normal neurons. Normal human brains at different intervals after death as well as normal rat brains after perfusion and immersion fixation were studied. During the first 24 h after death, the human cases showed practically no immunostaining with anti-fibrinogen and vague and inconstant staining with anti-albumin in the cortex and hippocampus, while certain brain stem nuclei were stained with both antisera even at the shortest postmortem intervals. At longer intervals, increased immunostaining of the neurons in the cortex and hippocampus was also demonstrated. Generally, more cells were positive for albumin than for fibrinogen. Perfusion-fixed rat brains showed no immunostaining, whereas rat brains that were immersion-fixed 24 h after death showed positive staining, mainly located in the brain stem. It is concluded that the staining of normal neurons demonstrated with the present method is due to postmortem leakage of proteins. Since practically no uptake of fibrinogen occurs in the cortex or hippocampus during the first 24 h, a definite neuronal staining with anti-fibrinogen at these intervals probably indicates true neuronal damage. In the brain stem, on the other hand, this phenomenon can not be used to demonstrate neuronal damage even at the shortest postmortem intervals.

Adult↗
PubMed1991

[The carbohydrate deficient glycoprotein syndrome].

The carbohydrate-deficient glycoprotein syndrome is a newly described hereditary disorder which may be due to a defect in the glycoprotein metabolism. Predominant symptoms are mental retardation, epilepsy, cerebellar ataxia, polyneuropathy, squint, retinitis pigmentosa, retarded growth, hypothyroidism and liver steatosis. Increased serum glycoprotein-deficient transferrin is a marker of the disease and confirms the diagnosis. We describe four Norwegian children with this syndrome. Olivopontocerebellar degeneration was found upon examination of the brain in two patients who died.

Abnormalities, Multiple↗
PubMed1991

Uptake of plasma proteins into damaged neurons. An experimental study on cryogenic lesions in rats.

Preliminary observations on human autopsy material have indicated that damaged neurons may take up plasma proteins early after the injury. These observations prompted an experimental study under controlled conditions. Focal brain lesions were produced in rats by extracranial application of dry ice for 90 s. This caused an immediate disruption of the blood-brain barrier with leakage of plasma components into the tissue and sharply circumscribed areas of necrosis of the underlying cortex. Five minutes after the lesion, uptake of albumin, fibrinogen and fibronectin into damaged neurons was demonstrated by immunostains. These proteins were retained in the injured neurons until they were phagocytized 2-4 days later. In addition, normal neurons whose axons or axon collaterals passed through or terminated in the lesion were labeled. This labeling was generally weaker than in damaged neurons and no labeling of neuronal nuclei was observed in these cells in contrast to those of damaged cells. Apart from nerve cells labeled through retrograde axonal transport, no staining of normal neurons was observed. Intravenous injections of Evans blue, which binds to plasma proteins, confirmed that albumin was taken up into damaged neurons almost immediately after the injury and showed that this uptake continued for at least 20 h. It is concluded that uptake of plasma proteins into damaged neurons may serve as early (and late) markers of neuronal injury.

Animals↗
PubMed1991

Model for skeletal muscle ischemia in rat hindlimb: evaluation of reperfusion and necrosis.

In this study we describe a technique for complete arrest of blood flow in rat hindlimbs. After graded periods of ischemia, immediate reperfusion in the leg was demonstrated by direct microscopy and scintigraphy. Laser Doppler flowmetry indicated microvascular hypoperfusion in the anterior tibial muscle during the first 2 h of reperfusion. The extent and distribution of necrosis in the middle part of the anterior tibial muscle of the legs were determined histologically 3 days after the ischemic insult. We found a reproducible degree of necrosis under constant experimental conditions. The necrosis was most pronounced in the central part of the muscle, leaving the subfascial fibers undamaged. After 4.0 h of ischemia, 46% of the cross-section area was necrotic. After 4.5 h, the necrosis increased to 70%. This difference was significant. Two types of necrotic zones were detected. One type was characterized by numerous macrophages and partial resorption of the muscle fibers, the other by a lack of macrophages and no resorption. Most cases with little damage had only the first type of necrosis, while most cases with extensive damage had both types. The areas that had no signs of resorption and therefore had been without circulation during most of the postischemic period, measured 8% after 4.0 h of ischemia and 22% after 4.5 h.

Animals↗
PubMed1991

Wernicke's encephalopathy--prevalence and clinical spectrum.

Although easily preventable, Wernicke's encephalopathy (WE) remains a regrettably frequent and largely undiagnosed disorder in alcoholics. Unselected autopsy materials from the United States and Australia give prevalence figures of 2%. In Oslo, Norway, the corresponding figures are somewhat lower, 0.6%-0.8%. Only a fraction of the cases discovered at autopsy have been diagnosed clinically (1%-20%). One third of the cases in postmortem materials have been acute with signs of ongoing thiamine deficiency. In contrast to classical concepts, stupor and coma have been predominating symptoms in such cases. Two thirds have had chronic disease with marked variations in severity of the lesions and corresponding variations in severity of the symptoms, from Korsakoff's psychosis or global dementia in severe cases to a slight memory reduction in mild ones. The wide spectrum of the clinical symptoms has not been fully appreciated and this may in part explain the low level of diagnostic accuracy of the disease.

Acute Disease↗
PubMed1990

Necrosis of granule cells of hippocampus in adrenocortical failure.

A case of untreated and rapidly progressive Addison's disease in a 23-year old woman showed selective necrosis with karyorhexis of the granule cells in the hippocampus. We suggest that this unique lesion was caused by a severe adrenocortical insufficiency. This explanation is in accordance with a recent report of selective loss of hippocampal granule cells after complete adrenalectomy in rats. No evidence of nerve cell loss was found in three cases of Addison's disease that had received cortisone treatment, which is consistent with the experimental observation that even very low levels of cortisone in adrenalectomized rats are sufficient to prevent granule cell loss.

Adrenal Cortex Diseases↗
PubMed1989

Pathogenesis of carotid thrombosis.

We histologically examined specimens from 11 patients with recent occluding thrombi at the carotid bifurcation to study local factors in the vessel wall that precipitated the thrombi. The area of stenosis of the vessel lumen was determined morphometrically. Severe atherosclerotic stenosis was frequent but was not a prerequisite for thrombus formation since specimens from almost one half of the patients had only moderate narrowing of the lumen (less than 60% stenosis). Specimens from three patients showed ulcerations, those from one showed intraplaque hemorrhage, and those from one massive plaque rupture, all of which were thought to be important in thrombogenesis. All such types of plaque complications may thus precipitate thrombi but no single complication was particularly predominant, and specimens from one half of the patients showed no complications at all. Screening of the carotid arteries for stenosis can therefore detect only one half of the individuals who ultimately will develop thrombosis, and the risk caused by plaque complications seems to be moderate in unselected materials.

Aged↗
PubMed1989

Brain contusions: the time sequence of the histological changes.

Microscopical sections from 65 cases with brain contusions of known age were studied in order to obtain histological data for age determination of the lesions. The earliest histological alterations were observed within one hour after the lesion and they changed in an orderly fashion over the following hours, days and weeks. It is concluded that the age of brain contusions can be determined with reasonable accuracy from routinely stained histological sections.

Adolescent↗
PubMed1988

Infantile Refsum's disease: a generalized peroxisomal disorder. Case report with postmortem examination.

Infantile Refsum's disease (IRD) is a peroxisomal deficiency disease which is closely related to neonatal adrenoleukodystrophy (NALD) and the Zellweger syndrome (ZS). Recent observations suggest that NALD and ZS are separate genetic disorders but the delimitation towards IRD remains uncertain. We present here the first autopsy report of a patient who was clinically and biochemically diagnosed as having IRD, and we compare the findings with those from NALD and ZS. The main gross and microscopic findings comprised micronodular liver cirrhosis, small hypoplastic adrenals without degenerative changes, and large groups of lipid macrophages in liver, lymph nodes and certain areas of the cerebral white matter. The brain showed no malformations except for a severe hypoplasia of the cerebellar granule layer and ectopic location of the Purkinje cells in the molecular layer. A mild and diffuse reduction of axons and myelin was found in the corpus callosum and periventricular white matter, the corticospinal tracts, and the optic nerves. Large numbers of perivascular macrophages were present in the same areas but there was no active demyelination. The retina and cochlea showed severe degenerative changes. Peripheral nerves, skeletal system and kidneys were normal. Electron microscopy showed characteristic cytoplasmic inclusions with bilamellar profiles in macrophages in the liver, lymph nodes and brain but not in the adrenals. Similar inclusions were found in liver cells and astrocytes. The findings differ from ZS which shows cortical renal cysts, skeletal changes, liver changes, cerebral micropolygyria, neuronal heterotopias, and demyelination of the white matter. Cases with NALD show mild cerebral malformations, active demyelination, degenerative changes of the adrenals, liver changes, and bilamellar electromicroscopic inclusions in macrophages. Our cases thus resembled NALD but lacked active demyelination, cerebral cortical malformations and adrenal degenerative changes. Further autopsy studies will be necessary to determine whether these changes are consistent findings in IRD.

Adrenoleukodystrophy↗
PubMed1988

Atherosclerotic carotid disease in asymptomatic individuals: An histological study of 53 cases.

The carotid bifurcation was studied histologically in 53 consecutive autopsies from persons over 65 years of age who were asymptomatic for carotid artery disease and showed no carotid related brain infarcts. The autopsy material is considered to be representative for the population in Oslo. The area stenosis was determined morphometrically in histological sections and the cases were examined for the occurrence of atherosclerotic plaques, calcifications, plaque hemorrhages, ulcerations, and mural thrombi. About one half of the cases had more than 50% stenosis. There was increasing frequency of plaque hemorrhages, ulcerations and mural thrombi with increasing stenosis. When the stenosis exceeded 60%, most cases had small recent and old plaque hemorrhages and one half had ulcerations and mural thrombi. In addition, numerous healed ulcerations and organized thrombi were seen. It is concluded that plaque complications are frequent in cases with stenosis and that most of them apparently heal without giving rise to symptoms. The presence of such lesions in asymptomatic cases must therefore be interpreted with caution.

Aged↗
PubMed1987

Brain lesions in alcoholics: neuropathological observations.

Examination of the autopsy material from a city hospital in Oslo gave the following results: 1. The brain weight of male alcoholics was significantly lower than that of age-matched controls in all 10-year age groups from 40 to 69 years. The mean weight reduction was 31 g. 2. Combined morphometric and histologic studies demonstrated atrophy of the anterior vermis in 42 per cent of all male alcoholics under 70 years of age. In cases over 70 years, 33 per cent of the non-alcoholic controls showed atrophy of the anterior vermis. This is assumed to be a consequence of physiologic ageing. The prevalence of alcoholic cerebellar atrophy could therefore not be determined in this age group. 3. Wernicke's encephalopathy was found in 12.5 per cent of all alcoholics and in 0.8 per cent of all autopsies. One third of the Wernicke cases had acute and subacute lesions while two thirds were chronic. Most of the acute lesions were widespread and severe. The chronic lesions were more restricted but showed great variations in extent and severity within the affected areas. There were corresponding variations in the severity of the clinical symptoms.

Adult↗
PubMed1987

Congenital neuronal ceroid lipofuscinosis. A case report.

A case of congenital neuronal ceroid lipofuscinosis, a 9-day-old male child of Pakistani parents, is reported. Only 5 congenital cases have been described previously. The cerebral and cerebellar cortex showed extensive nerve-cell loss. Granular material with histochemical characteristics of ceroid-lipofuscin was deposited in neurons, macrophages and glial cells throughout the brain. Similar material was found in macrophages in the lymphoid system and in certain other organs. Ultrastructurally, the material was identical with that described in the infantile type of ceroid lipofuscinosis. It is pointed out that the metabolic exchange between the blood of the mother and the foetus is not sufficient to prevent the intra-uterine progression of the disease.

Brain↗