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  • 1
    Electronic Resource
    Electronic Resource
    Hypoglycemic brain injury (1980)
    Springer
    Acta neuropathologica 50 (1980), S. 31-41 
    Details
    ISSN: 1432-0533
    Keywords: Hypoglycemia ; Nerve cell injury ; Biochemistry ; Light microscopy ; Rat cerebral cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Profound hypoglycemia causing the disappearance of spontaneous EEG activity was induced by insulin in rats. For analysis of cerebral cortical concentrations of labile phosphates, glycolytic metabolites and amino acids, the brain was frozen in situ. For microscopic analysis of the corresponding cerebral cortical areas the brain was fixed by perfusion. Hypoglycemia with an isoelectric EEG for 30 and 60 min caused severe perturbation of the cerebral energy metabolites. After both 30 and 60 min of isoelectric EEG, two microscopically different types of nerve cell injury were seen. Type I injury was characterized by angulated, darkly stained neurons with perineuronal vacuolation, mainly affecting small neurons in cortical layer 3. Type II injured neurons, mainly larger ones in layers 5–6, were slightly swollen with vacuolation or clearing (depending on the histotechnique used) of the peripheral cytoplasm, but had no nuclear changes. Recovery was induced by glucose injection. Improvement in the cerebral energy state occurred during the 30 min recovery period even after 60 min of hypoglycemia. However, the persisting reduction in the size of adenine nucleotide and amino acid pools after 30 or 180 min recovery suggested that some cells remained damaged. In confirmation many type I injured neurons persisted during the recovery suggesting an irreversible injury. The disappearance of virtually all type II injuries indicated reversibility of these histopathological changes. The microscopic changes in hypoglycemia were different from those in anoxia-ischemia suggesting a dissimilar pathogenesis in these states despite the common final pathway of energy failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688532
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  • 2
    Electronic Resource
    Electronic Resource
    Pathogenesis of brain lesions caused by experimental epilepsy (1981)
    Springer
    Acta neuropathologica 54 (1981), S. 219-231 
    Details
    ISSN: 1432-0533
    Keywords: Status epilepticus ; Nerve cell injury ; Brain edema ; Rat cerebral cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 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.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00687745
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  • 3
    Electronic Resource
    Electronic Resource
    Influence of systemic factors on experimental epileptic brain injury (1983)
    Springer
    Acta neuropathologica 60 (1983), S. 81-91 
    Details
    ISSN: 1432-0533
    Keywords: Brain injury ; Status epilepticus ; Hyperoxia ; Hypoxia ; Hypotension ; Vitamin E
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A previous study from the laboratory showed that status epilepticus induced by bicuculline administration to ventilated rats produced astrocytic swelling and nerve cell changes (“type 1 and 2 injury”) particularly in layers 3 and 5 of the neocortex (Söderfeldt et al. 1981). The type 1 injured neurons were characterized by condensation of cyto-and karyoplasm and the less common type 2 cells were characterized by swelling of endoplasmic reticulum including the nuclear envelope. In the present study we explored whether changes in cerebral oxygen availability altered the extent or character of the cellular alterations. Animals with 2 h of status epilepticus were made either hyperoxic (administration of 100% O2), hypoxic (arterialpO2 50 mm Hg) or hypotensive (arterial blood pressure of either 70–75 or 50 mm Hg). Furthermore, we explored whether “oxidative” damage occurred by manipulating tissue levels of α-tocopherol, a known free radical scavenger. Non-epileptic control animals exposed to comparable degrees of hypoxia or hypotension showed no or minimal structural alterations. In the epileptic animals the results were as follows.Hyperoxia did not change the quality or extent of the structural alterations previously observed in normoxic epileptic animals. Neither administration nor deficiency ofvitamin E did modify this pattern of alterations. Inhypoxia the extent of cell damage was the same or somewhat larger than in normoxic, epileptic animals. In addition, neurons often showed cytoplasmic microvacuoles due to swelling of mitochondria. The hypoxic animals also showed swelling of astrocytic nuclei with clumped chromatin. Changes similar to those observed in hypoxic animals also appeared in moderatehypotension (mean arterial blood pressure 50 mm Hg), whereas mild hypotension (70–75 mm Hg) did not change the character of the tissue injury from that seen in hyperoxic or normoxic epileptic rats. The present results demonstrate that the neuronal cell damage that can be observed when the brain is fixed by perfusion after status epilepticus of 2 h duration is not exaggerated by hyperoxia or vitamin E deficiency nor is it ameliorated by a moderate restriction in cerebral oxygen supply or by vitamin E administration. If anything, hypoxia (or moderate hypotension) appears to increase the extent of damage and it clearly alters its ultrastructural characteristics. However, although the results fail to support the notion that epileptic cell damage is “oxidative”, definite conclusions must await information on the cell damage that remains upon arrest of the epileptic activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00685351
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  • 4
    Electronic Resource
    Electronic Resource
    Pathogenesis of brain lesions caused by experimental epilepsy (1983)
    Springer
    Acta neuropathologica 59 (1983), S. 11-24 
    Details
    ISSN: 1432-0533
    Keywords: Status epilepticus ; Nerve cell injury ; Brain edema ; Rat hippocampal formation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Status epilepticus with a duration of 1 or 2 h was induced in rats by i. v. injection of the GABA receptor blocking agent, bicuculline. Immediately there-after, or following a 2 h recovery period, the brains were fixed by vascular perfusion and processed for light and electron microscopy to characterize the type and distribution of morphological changes in the hippocampal formation. In a previous study (Söderfeldt et al. 1981) astrocytic edema and wide-spread neuronal changes of two different kinds occurred in the fronto-parietal cortex of the same animals. Type 1 injured neurons were characterized by condensation of karyoplasm and cytoplasm (type 1a), which in some neurons became so intense that the nucleus could no longer be clearly discerned (type 1b). The type 2 injured neurons had slitformed cytoplasmic vacuoles chiefly caused by dilatation of the rough endoplasmic reticulum. In the hippocampus the most conspicuous alteration was astrocytic edema which was most marked around the perikarya of pyramidal neurons in CA1-CA4 and subiculum. In the dentate gyrus the edema was less pronounced and, when present, affected particularly the hilar zone of the stratum granulosum. The nerve cell changes were less pronounced than in the cerebral cortex. The vast majority of the hippocampal pyramidal neurons in CA1-CA4 showed minor configurational and tinctorial abnormalities (incipient type 1a change). Severe nerve cell alterations (type 1b) were present but very rarely affected the pyramidal neurons of CA1-CA4 and subiculum, whereas in the dentate gyrus pyramidal basket neurons of stratum granulosum and pyramidal nerve cells in stratum polymorhe showed the severe type 1b changes. As compared with the frontoparietal cortex (Söderfeldt et al. 1981) the type 2 changes were extremely rare. In the early recovery period after 1 h of status epilepticus the astrocytic edema and the incipient type 1a changes had almost entirely disappeared, whereas a few condensed and dark-staining type 1b injured neurons remained. Thus, in this model of status epilepticus the most marked response in the hippocampal formation is astrocytic edema in the layers where pyramidal perikarya are located. Incipient, mild nerve cell changes which appear to be reversible were frequent and widespread in the entire hippocampal formation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690312
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  • 5
    Electronic Resource
    Electronic Resource
    The firing rate of motor units in neuromuscular disorders (1981)
    Springer
    Journal of neurology 225 (1981), S. 269-276 
    Details
    ISSN: 1432-1459
    Keywords: Neuromuscular disease ; Motor unit ; Firing rate ; Electromyography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Entladungsfrequenz und die Variationen zwischen den Intervallen motorischer Einheiten wurden sowohl bei Patienten, die an Störungen peripherer Neuromuskulatur leiden, als auch bei Normalfällen im Vergleich untersucht. Während einer leichten Muskelkontraktion wiesen die an myopathischen Störungen leidenden Patienten, verglichen mit den Normalfällen, eine höhere Entladungsfrequenz motorischer Einheiten auf, trotz der unbedeutenden Unterschiede in Intervallvariationen zwischen den Untersuchungsgruppen. Eine größere Steigerung der Entladungsrate wurde auch bei neurogenen Läsionen festgestellt, in diesem Zusammenhang hatten auch die Abweichungen zwischen den Intervallen beträchtlich zugenommen. Die Entladungscharakteristika motorischer Einheiten können einen wertvollen Beitrag zur Differentialdiagnostik bei neuromuskulären Störungen liefern.
    Notes: Summary The firing frequency and interval variability of motor units was studied in healthy controls and in patients suffering from peripheral neuromuscular disorders. In patients with myopathic disorders, the motor unit reached a higher firing frequency than in the controls during a slight muscle contraction although interval variability did not differ significantly from controls. In neurogenic lesions the firing rate also reached a higher level than in controls; in addition the interval variability was significantly increased. The firing characteristics of motor units may prove to be a valuable aid in the differential diagnosis of neuromuscular diseases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00313299
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  • 6
    Electronic Resource
    Electronic Resource
    Bicuculline-induced epileptic brain injury (1983)
    Springer
    Acta neuropathologica 62 (1983), S. 87-95 
    Details
    ISSN: 1432-0533
    Keywords: Status epilepticus ; Nerve cell injury ; Bicuculline ; Rat cerebral cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It was earlier shown that bicuculline-induced status epilepticus gives rise to profound acute changes in the rat cerebral cortex, i.e. edema and neuronal alterations. In the present study, we explored to what extent interruption of the seizure activity reverses the changes observed. To that end, status epilepticus of 1 and 2 h duration was induced by bicuculline before the seizures were arrested by i.v. injection of diazepam. The brain was then fixed by vascular perfusion either 5 min (1 h of seizures) or 2 h (1 and 2 h of seizures) of recovery and cerebral cortical tissue was studied by light (LM) and electron microscopy (EM). Already 5 min following the arrest of seizure activity most of the astrocytic edema had disappeared, and the number of injured neurons was clearly reduced. After 2 h of recovery, following 1 h of status epilepticus, the edema was virtually absent, and only few injured cells were found (only about 1% of the neuronal population). When recovery was instituted after 2 h of status epilepticus, numerous dark, triangular neurons were found. In the last group an adequate blood pressure could not be obtained. Therefore, the cellular alterations observed were probably not the result of the seizure activityper se. After 5 min of recovery, EM studies showed condensed, dark-staining injured neurons, similar to those previously observed in non-recovery animals. However, an increased incidence of swollen mitochondria was observed. After 2 h of recovery a few severely injured neurons remained which showed signs of progressive injury with fragmentation of the cell body.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00684924
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  • 7
    Electronic Resource
    Electronic Resource
    Reply to the remarks by J. B. Brierley and A. W. Brown (1981)
    Springer
    Acta neuropathologica 55 (1981), S. 323-325 
    Details
    ISSN: 1432-0533
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00690997
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  • 8
    Electronic Resource
    Electronic Resource
    The brain in extreme respiratory acidosis (1982)
    Springer
    Acta neuropathologica 58 (1982), S. 87-94 
    Details
    ISSN: 1432-0533
    Keywords: Hypercapnia ; Rat brain ; Ultrastructure ; Cerebral edema
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It is presently debated how much cellular acidosis contributes to brain cell damage during ischemia and hypoxia. To study the influence of acidosis occurring in the absence of energy failure, extreme hypercapnia was produced in anesthetized, artificially ventilated, and well oxygenated rats by increasing the inspired CO2 concentration until arterialPCO2 reached 150 or 300 mm Hg. At these CO2 tensions intracellular pH falls from a control value of about 7.05 to about 6.85 and 6.65, respectively. After 45 min the brains were fixed in perfusion and processed for light and electron microscopy. AtPaCO2 150 mm Hg no clear neuronal abnormality was detected, but atPaCO2 300 mm Hg some neuronal changes were observed. Notably, the nuclei showed slightly coarser chromatin than normally. In a few nerve cells mild swelling of mitochondria and dispersion of polysomes as well as detachment of ribosomes from the endoplasmic reticulum appeared. In both groups, slight to moderate astrocytic edema developed. Thus, even extreme hypercapnia, with its acompanying marked tissue acidosis, alters ultrastructure in the brain only to such a moderate extent that irreversible cell damage is unlikely. We conclude, therefore, that acidosis occurring during ischemia or hypoxia is detrimental only if pH is further lowered and/or if it occurs in conjunction with cerebral energy failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691646
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  • 9
    Electronic Resource
    Electronic Resource
    Brain lactic acidosis and ischemic cell damage: Quantitative ultrastructural changes in capillaries of rat cerebral cortex (1983)
    Springer
    Acta neuropathologica 60 (1983), S. 232-240 
    Details
    ISSN: 1432-0533
    Keywords: Brain ; Incomplete ischemia ; Acidosis ; Capillaries ; Morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Excessive tissue lactic acidosis has earlier been shown to aggravate structural damage of both neurons and glial cells in the rat cerebral cortex. To study the reactions of cortical capillaries, light- and electronmicroscopic morphometry was used. Rats were subjected to severe incomplete ischemia (cerebral blood flow below 5% of normal) for 30 min by clamping their carotid arteries and by lowering the blood pressure. Lactate production during ischemia was modified by preischemic administration of either saline (low lactic acidosis group) or glucose (high lactic acidosis group). In the animals with low lactic acidosis, only minimal vascular changes were seen after both 5 min and 90 min recirculation. In the high lactic acidosis group, the endothelial cells were swollen after 5 min of recirculation, and the changes grew markedly worse during 90 min of recirculation. Nuclear chromatin coarsened and mitochondria swelled up. Morphometry showed that the lumen narrowed as a result of endothelial swelling. In spite of variable degree of perivascular astrocytic edema, the outer capillary diameter was little changed in the experimental groups. It seems likely that endothelial swelling hampers postischemic circulation in incomplete ischemia accompanied by high lactic acidosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00691871
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  • 10
    Electronic Resource
    Electronic Resource
    Hypoglycemic brain injury (1980)
    Springer
    Acta neuropathologica 50 (1980), S. 43-52 
    Details
    ISSN: 1432-0533
    Keywords: Hypoglycemia ; Nerve cell injury ; Electron microscopy ; Rat cerebral cortex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Severe hypoglycemia was induced in rats by insulin. The brain was fixed in situ by perfusion after the spontaneous EEG had disappeared for 30 or 60 min or after recovery had been induced for 30 or 180 min by glucose injection. Samples from the cerebral cortex from the area corresponding to the previous metabolic studies were processed for electron microscopy. The light-microscopic finding of two different types of nerve cell injury, reported in a preceding communication (Agardh et al. 1980), was also verified at the ultrastructural level. The type I injury was characterized by cellular shrinkage, condensation of the cell sap and nuclei, and perineuronal astrocytic swelling. No swelling of mitochondria occurred. The slightly swollen type II injured neurons showed contraction of mitochondria, disintegration of ribosomes, loss of RER, and appearance of membrane whorls, while their nuclear chromatin remained evenly distributed. No transition from one type to the other was observed. Neither type of nerve cell injury in hypoglycemia was like that commonly seen in anoxic-ischemic insults indicating a different pathogenesis in these states despite the common final pathway of energy failure. The loss of endoplasmic membranes and disintegration of ribosomes suggests that these structures might be sacrificed for energy production in the absence of normal substrates. During recovery, though, the number of type I injured neurons decreased while some of the remaining ones appeared even more severely affected, suggesting irreversible damage. Type II injured neurons were no longer seen indicating reversibility of these changes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688533
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