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Biomedical subjects

Y Olsson

Publications and source records attributed to Y Olsson.

At least 181 records · Page 10Linked to original sources
PubMed1982

Light- and electron microscopic findings in the distal end of human cross-face sural nerve grafts.

In five patients with long-standing facial palsy we have tried to improve the possibility of elevating the angle of the mouth by bringing regenerating axons from the facial nerve on the normal side through a sural nerve graft to a transplanted free muscle in the paralyzed cheek. In order to expect clinical improvement a sufficient number of axons must grow into and through the sural nerve graft, neuromuscular contacts must be formed, and the transplanted muscle must be vascularized and survive. In order to find out if axons had regenerated, light- and electronmicroscopic examinations of a biopsy from the tip of the sural nerve graft were carried out at the time of muscle transplantation. All the cases showed a very large number of unmyelinated axons located within the fascicles of the sural nerve graft. A considerable fraction of myelinated axons were, however, present particularly in biopsies removed 12-13 months after the nerve operation. There was also a marked increase in endoneurial collagen and at the very tip a neuroma was present. This investigation thus shows that regeneration of a substantial number of axons had occurred and that they had reached the zone which was surgically sutured to the transplanted muscle. One essential requirement for reinnervation of the transplanted muscle therefore exists in these patients, but the clinical outcome has not yet been evaluated due to the short follow-up period.

Adolescent↗
PubMed1981

Pathogenesis of brain lesions caused by experimental epilepsy. Light- and electron-microscopic changes in the rat cerebral cortex following bicuculline-induced status epilepticus.

Status epilepticus was induced in rats by the GABA receptor blocking agent, bicuculline, during artificial ventilation and with closely monitored physiologic parameters. After 1 or 2 h of status epilepticus the brains were fixed by perfusion with glutaraldehyde and processed for light and electron microscopy. In the cerebral cortex two different types of changes were present, i.e., nerve cell injuries and status spongiosus. Type 1 injured neurons, mainly in the areas of most marked sponginess (layer 3), displayed progressive condensation of both karyo-and cytoplasm. In the most advanced stages the nucleus could no longer be distinguished from the cytoplasm in the light microscope, and vacuoles of apparent Golgi cisterna origin appeared in the darkly stained cytoplasm. This type of injured neurons comprised 41 and 56% of the cortical neurons after 1 or 2 h of status epilepticus, respectively. Seven to 9% of the neurons showed another type of injury (type 2). They were mainly located in the deeper cortical layers, and showed slit-formed cytoplasmic vacuoles chiefly due to swelling of the endoplasmic reticulum including the nuclear envelope. Marked sponginess of the cortex developed principally in layer 3 and it spread into deeper layers with longer duration of status epilepticus, but the outermost layers retained a compact structure. As judged by electron microscopy, the sponginess resulted mainly from swelling of astrocytes and their processes causing both perivascular and perineuronal vacuolation. The structural changes observed are considered to be caused by astrocytic and to a lesser extent intraneuronal edema related to the seizure activity. Although the exact pathogenetic mechanisms are not known, our findings indicate that hypoxia-ischemia is not a major determinant of the tissue damage observed.

Animals↗
PubMed1981

Brain lactic acidosis and ischemic cell damage: 2. Histopathology.

The influence of severe tissue lactic acidosis during incomplete brain ischemia (30 min) on cortex morphology was studied in fasted rats. Production of lactate in the ischemic tissue was varied by preischemic infusions (i.v.) of either a saline or a glucose solution. The brains were fixed by perfusion with glutaraldehyde at 0, 5, or 90 min of recirculation. In saline-infused animals (tissue lactate about 15 mumol g-1), changes observed at 0 and 5 min of recirculation were strikingly discrete: slight condensation of nuclear chromatin, mild to moderate mitochondrial swelling, and only slight astrocyte edema. These changes had virtually disappeared after 90 min recirculation and, at this time, only discrete ribosomal changes were observed. In contrast, glucose-infused rats (tissue lactate about 35 mumol g-1) showed severe changes: marked clumping of nuclear chromatin and cell sap in all cells was already evident at 0 and 5 min recirculation, while mitochondrial swelling was mild to moderate. Although tissue fixation was inadequate at 90 min, the ultrastructural appearance indicated extensive damage. It is concluded that excessive tissue lactic acidosis during brain ischemia exaggerates structural alterations and leads to irreversible cellular damage. A tentative explanation is offered for the paucity (less than 0.2%) of condensed neurons with grossly swollen mitochondria, previously considered a hallmark of ischemic cell injury.

Acidosis↗
PubMed1981

Hypoglycemic brain injury: metabolic and structural findings in rat cerebellar cortex during profound insulin-induced hypoglycemia and in the recovery period following glucose administration.

Previous results have shown that severe, prolonged hypoglycemia leads to neuronal cell damage in, among other structures, the cerebral cortex and the hippocampus but not the cerebellum. In order to study whether or not this sparing of cerebellar cells is due to preservation of cerebellar energy stores, hypoglycemia of sufficient severity to abolish spontaneous EEG activity was induced for 30 and 60 min. At the end of these periods of hypoglycemia, as well as after a 30 min recovery period, cerebellar tissue was sampled for biochemical analyses or for histopathological analyses or for histopathological analyses by means of light and electron microscopy. After 30 min of hypoglycemia. the cerebellar energy state, defined in terms of the phosphocreatine, ATP, ADP, and AMP concentrations, was better preserved than in the cerebral cortex. After 60 min, gross deterioration of cerebellar energy state was observed in the majority of animals, and analyses of carbohydrate metabolites and amino acids demonstrated extensive consumption of endogenous substrates. In spite of this metabolic disturbance, histopathologic alterations were surprisingly discrete. After 30 min, no clear structural changes were observed. After 60 min, only small neurons in the molecular layer (basket cells) were affected, while Purkinje cells and granule cells showed few signs of damage. The results support our previous conclusion that the pathogenesis of cell damage in hypoglycemia is different from that in hypoxia-ischemia and indicate that other mechanisms than energy failure must contribute to neuronal cell damage in the brain.

Adenosine Diphosphate↗
PubMed1981

Reliability of computed tomography in assessing histopathological features of malignant supratentorial gliomas.

A new method was developed whereby close comparisons can be made between components of a computed tomography (CT) image and neuropathological findings. This was achieved by a combination of intravital (terminal) CT, postmortem CT, and whole brain sectioning of formalin-fixed tissue. The method was applied in seven cases of malignant supratentorial astrocytic gliomas (Kernohan Grades III and IV) and in one case of thalamic ependymoma. The glioblastoma-like parts of the astrocytic gliomas were usually correctly delineated by postcontrast CT, although there were exceptions to this rule. Tumor components consisting of diffusely growing malignant astrocytoma were difficult or impossible to delineate by CT. Necrotic areas within the tumors were accurately outlined by postcontrast CT. Peritumoral edema was correctly delineated by CT, but growth of diffuse astrocytoma or the presence of astrocytic gliosis within this edematous area seems difficult or impossible to evaluate by current CT techniques.

Adult↗
PubMed1980

Differences between the peripheral and the central nervous system in permeability to sodium fluorescein.

Sodium fluorescein (SF) was used as a very small tracer (mol wt 376; 5 A diameter) to examine diffusion barriers in peripheral nerves and to compare them to those in other regions of the nervous system. The technique involved immobilization of the tracer by rapid freezing, followed by freeze-drying and vacuum embedding in paraffin. The localization of the SF was then determined in tissue secretions using fluorescence microscopy. Even at the highest doses of intravenously (IV) injected tracer, no extravasation could be detected in the cerebral cortex. On the other hand, SF penetrated very rapidly into peripheral ganglia and into the epineurium and perineurium of large peripheral nerves. The penetration of SF into the endoneurium of large nerves was, however, much more restricted with tracer detectable within the endoneurium only at high doses and long survival times. Even in such cases, the level of SF fluorescence was much lower within nerve fascicles than in the epineurium and the perineurium, and a sharp gradient in fluorescence intensity persisted at the inner border of the perineurium. The extent of extravasation into the endoneurium varied markedly betwen different fascicles of the same nerve and between different nerves in the same animal. Experiments involving injection of high doses of SF adjacent to the nerve indicated relatively little movement of SF across the perineurium, which indicates that the observed accumulation of tracer within the endoneurium was the result of direct extravasation of SF from the endoneural blood vessels. Small nerve branches (< 100 mu diameter) showed an earlier and more extensive penetration of SF into the endoneurium than large nerves like the sciatic, hypoglossal, or ventral tail nerve. This may be due to a diffusion of SF along the extracellular space of the endoneurium from nerve terminals where the perineurial barrier is open-ended. In experiments involving IV injection of a solution containing both green fluorescent SF and red fluorescent Evans Blue (Evans Blue-serum albumin conplex, EBA = mol wt. 69,000), the distribution of SF could be directly compared at various sites and sacrifice times to that of EBA, a much larger tracer. SF appeared more rapidly and extensively than EBA in the various compartments in ganglia and peripheral nerve. The distribution of EBA was the same as is typically seen when this tracer is injected alone, indicating that there was no change in vascular permeability associated with IV injection of SF. Since SF is of very small size, freely diffusible, nontoxic, and detectable at very low concentrations, it should be a useful complement to existing tracers. When tissues are processed according to the indicated procedure, one can obtain a very sensitive and reliable localization of this tracer which should be of value for studies in the nervous system concerning various pathological conditions associated with permeability alterations.

Animals↗
PubMed1980

Axonal uptake of horseradish peroxidase isoenzymes during Wallerian degeneration.

Horseradish peroxidase isoenzymes were applied around crushed mouse hypoglossal nerves to study the influence of electrical charge on the uptake and ultrastructural distribution of macromolecules in axons distal to an injury. Both isoenzymes tested (Sigma type IX, cationic and type VII, anionic) were readily taken up into axons and moved in a distal direction along the nerve. Samples taken 1-3 mm below the crush showed that reaction products from both enzymes covered the inner surface of the axonal plasma membrane and were attached to organelles, particularly microtubules and neurofilaments. However, reaction product in the Schwann cell basement lamina and in the endoneurial collagen was much more dense with cationic peroxidase than with the anionic isoenzyme. Our study shows that both cationic and anionic macromolecules can move into axons distal to a nerve lesion. It can be assumed that also other agents can be taken up into axons and that 'wound substances' in this way may influence the processes by which axons are destroyed during Wallerian degeneration.

Animals↗
PubMed1980

Cerebral computed tomography in methanol intoxication.

In four of six patients with methanol intoxication, computed tomography (CT) showed necrotic changes in the area of the putamina. Hemorrhages were also seen in some cases. There was a clear relationship between the severity of the clinical symptoms and the CT findings, indicating the potential of CT for prognosis and possible therapy guidance.

Adult↗
PubMed1980

Effects of severe hypoglycemia on the human brain. Neuropathological case reports.

The neuropathological findings in two cases of irreversible hypoglycemic brain injury are described. A 26-year-old diabetic man injected insulin without adequate food intake and died after 2 months in coma. An 84-year-old nondiabetic man accidentally received 10 mg of glibenclamide and died after 3 months in relatively superficial coma. In the first case, an extensive necrotizing injury with gliosis was present in the cerebral cortex with temporal preponderance, as well as in the amygdalae and hippocampus. Lesions were also present in the putamen and caudate nucleus whereas the globus pallidus and thalamus were less severely destroyed. The distribution of the lesions was therefore somewhat different from that commonly seen in hypoxic-ischemic brain injury, which, together with some previously published data, suggests some difference in the pathogenesis of hypoglycemic vs. hypoxic-ischemic brain injury. In the second case only a slight loss of cortical neurons with secondary gliosis could be attributed to the hypoglycemic insult. This case demonstrates the danger of accidental intake of sulfonylurea preparations, which can cause an irreversible brain injury due to their prolonged hypoglycemic effect.

Adult↗
PubMed1980

A silver-gold impregnation technique for demonstration of striated muscle elements.

A silver-gold impregnation technique for demonstration of cross striations in skeletal muscles is presented. It is easily performed and all ingredients are chemically well characterized and easily available. The method has been successfully applied to formalin-fixed paraffin-embedded material from human muscles and can be of value in the histopathological diagnosis of rhabdomyosarcomas and other tumors of muscular origin.

Gold↗
PubMed1979

Familial subacute necrotizing encephalomyelopathy of the adult form (adult Leigh syndrome).

A family--mother and 2 sons--with a heredodegenerative neurological disease is described. The disease started with bilateral optic atrophy, central scotoma, and color blindness during the second decade. This was followed by a quiescent period until additional neurological symptoms appeared, around the age of 50 years in the case of the mother and 40 and 30 years, respectively, in the sons. The additional symptoms were ataxia, spastic paresis, clonic jerks, grand mal seizures, psychia lability, and slight dementia. The disease was progressive, resulting in permanent hospitalization within a few years. The mother died at the age of 63 years and the sons at 46 and 43 years of age. Neuropathological examination revealed lesions histopathologically characteristic of subacute necrotizing encephalomyelopathy (SNE, Leigh disease), and their distribution in the brain and brainstem also conformed to this disease. On the basis of the clinical course and neuropathological findings, we consider that these 3 patients represent the first reported familial cases of the adult form of SNE.

Adult↗