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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The dynamics of ultrastructural changes in axonal endings were studied after experimental epileptic seizures. Mice and rats from strains with genetically--determined audiogenic epilepsy were used as a model of epilepsy. The animals were divided into 3 groups: in group 1 only one seizure was evoked, in group 2 eight seizures within 4 hours, group 3 served as control. The animals were killed immediately after the last seizure, 30 min. after it or 1 hour after the seizure. Hippocampal gyrus cortex was impregnated with zinc-iodide-osmium tetroxide and synapses were examined under electron microscope. The number of synaptic vesicles showing positive reaction with zinc iodide was calculated in 20 synaptic boutons in each group. A significant correlation was demonstrated between the frequency of seizures and the survival time after the seizure on the one hand, and synaptic changes, on the other. In the control group 97% of synaptic vesicles were filled with neurotransmitter substance giving positive reaction with zinc iodide. Immediately after the single seizure 46% of synaptic vesicles were found emptied, 30 min. later the neurotransmitter substance was demonstrated in 79% of vesicles, 1 hour later 82% of vesicles had normal appearance. Immediately after serial seizures 91% of vesicles were found empty, 30 min. later the neurotransmitter was present in 50% of vesicles, 1 hour later in 78%. In another group of animals seizures were evoked once daily for 40 days (chronic epilepsy model). Synaptic changes were different: the synaptic boutons were swollen, the number of vesicles was reduced, greatly enlarged vesicles and clear membrane-bound vacuoles appeared. They evidenced degenerative character of changes. It is suggested that degenerative synaptic changes may be a substrate of epileptic dementia.
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PMID:[Dynamics of synaptic changes in experimental audiogenic epilepsy]. 1 11

The observation in 14 dialysis patients of an encephalopathy associating myoclonia, dysarthria, generalised seizures in some cases, worsening over a few months, led to an aetiological inquiry based upon comparative study of patients with or without encephalopathy treated in the same centre or at home, and controls. Higher levels of aluminium were found in the frontal cortex grey matter of encephalopathy patients as compared to the control group. The same applies to manganese in the white matter. Copper, zinc and iron contents were not different. Aluminium levels in blood, dialysis bath and tap water supply were higher in center dialysis than in home dialysis. Blood aluminium levels at the end of hemodialysis were correlated with bath aluminium levels. The ingestion of alumine gels was not greater in the encephalopathy patients than in other hemodialysis patients; its estimation, in each case, was not related to the blood aluminium levels at the begining of hemodialysis. These finding indicate the need of a routine measure of metal content - mainly aluminium and manganese - in tap water used for dialysis, in order to treat this water if necessary.
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PMID:[Progressive myoclonic encephalopathy in dialysis patients. The role of the water used for haemodialysis (author's transl)]. 65 14

Acute plumbism include recurrent seizures, cerebral palsy and mental retardations. The impairment of the central nervous system (CNS) with increased lead absorption is of paramount concern which remains unsolved because of the lack of specific and sensitive neurochemical/biochemical indicators of the effect of lead on the CNS. In our experimental acute lead-zinc poisoning, significant increase in noradrenaline and slight decrease in dopamine have been found in the brains of rats, which suggest that there is change in neurotransmitter metabolism in lead poisoning.
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PMID:Dopamine and noradrenaline levels in the brains of lead and zinc poisoned rats. 67 13

We determined zinc, copper, magnesium, and calcium concentrations by atomic absorption spectrophotometry in the plasma of 30 patients hospitalized for treatment of seizures during a period of alcohol withdrawal. Those patients who developed delirium tremens or a prolonged hallucinatory state had significantly higher plasma copper concentrations (P = 0.026), significantly lower zinc concentrations (P = 0.004), and significantly higher copper/zinc ratios (P = 0.001) than the patients who recovered uneventfully. Zinc deficiency may be one of the factors that contribute to the neurologic complications of alcoholism. A determination of the plasma copper/zinc ratio early in the course of alcohol withdrawal could be of value in indicating which patients have the most substantial underlying disease or metabolic imbalance and therefore may be at greatest risk of developing delirium tremens or prolonged hallucinosis.
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PMID:Plasma calcium, copper, magnesium, and zinc concentrations in patients with the alcohol withdrawal syndrome. 68 16

We examined CSF copper and zinc concentrations in 30 children with acute febrile illness and meningism (control group) and in 37 patients with shortlasting seizures, febrile or not, and acute viral meningitis. The trace elements were quantitatively measured by means of atomic absorption spectrophotometry. 1. It was shown that the concentrations of copper and zinc in CSF remain constant during childhood.--2. No increase could be found in the concentrations of copper and zinc in CSF caused by the neurological diseases of our patients. These data suggest that permanent cerebral lesions as a consequence of shortlasting seizures and viral meningitis would be very unlikely and that a transient dysfunction of metabolism does not liberate copper- and zinc-metallo-proteins in CSF. 3. There was no correlation between the protein concentration in CSF and copper and zinc concentrations in CSF.
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PMID:[Copper and zinc in cerebrospinal fluid of children with neurological diseases (author's transl)]. 73 23

Anatomical data now strongly suggest that the common factor in curative ablative operations for the commonest (i.e. ammonshorn-sclerosis) form of temporal-lobe epilepsy is the cutting of the ipsilateral temporoammonic perforant path's "nozzle" where it leaves the entorhinal cortex to "spray" along the length of the ammonshorn. This substantially deafferences ipsilateral dentate granule-cells and hence the unsclerosed pyramidal neurons notably in "resistant sector" CA2, which are probably the source of the seizures. Stereo-chemoding of long-lasting (experimentally tested) chelates along the zone of peculiarly zinc-rich synapses of the mossy fibre system should block the commissural as well as the ipsilateral inputs to these residual neurons, to give higher percentage cures, and could probably be performed bilaterally (where indicated, in adults) without endangering memory function.
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PMID:Anatomical rationale of ablative surgery for temporal lobe seizures and dyscontrol: suggested stereo-chemode chelate-blockade alternative. 79 6

The effects of pyridoxine deficiency and the administration of supplemental vitamin B6 on audiogenic and electroconvulsive seizures were studied in two inbred strains of mice and their F1 hybrids. Pyridoxine deficient diets increased seizure risk, whereas supplemental vitamin B6 protected these animals against seizures. Penicillamine and thiosemicarbazide, at doses which lowered brain levels of pyridoxine by only 10%, increased seizure risk. Diets deficient in zinc and copper did not alter susceptibility to either audiogenic or electroconvulsive seizures. DBA/2J mice, genetically susceptible to audiogenic seizures, have the same endogenous levels of pyridoxine in the brain as do C57Bl/6J mice, which are resistant to audiogenic seizures.
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PMID:Levels of pyridoxine and susceptibility to electroconvulsive and audiogenic seizures. 117 97

Zinc is a potent inducer of the 72 kD heat shock protein (HSP72). In brain, pathological conditions such as ischemia and seizures increase extracellular zinc. The present study examines the effect of zinc on HSP72 expression in rat primary cortical astrocyte culture. Astrocytes were grown to confluence and exposed to zinc chloride in CO2-equilibrated Earle's buffered salt solution. Expression of HSP72 was examined using immunocytochemistry. HSP72 was induced with zinc concentrations of 5 to 100 microM after 4 h exposures, or 200 to 300 microM after 15 min exposures. At the lower concentrations expression occurred in small clusters of contiguous cells. At concentrations high enough to cause cell death, HSP72-positive astrocytes formed a continuous margin around patches of dead cells. These patterns of HSP72 expression are similar to the patterns seen after cerebral ischemia in vivo. Exposure to zinc at 100 microM for 4 h or 400 microM for 15 min caused greater than 90% cell death. Increases in extracellular zinc may contribute to HSP72 induction and astrocyte death under ischemia and other pathological conditions in brain.
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PMID:Zinc toxicity and induction of the 72 kD heat shock protein in primary astrocyte culture. 133 69

This paper reviews chemical models of epilepsy and their relevance in the identification and characterization of anticonvulsants. For each convulsant we discuss possible modes of administration, clinical type(s) of seizures induced, proposed mechanism(s) of epileptogenesis and, where available, responsiveness of the induced seizures to anticonvulsants. The following compounds are reviewed: pentylenetetrazol, bicuculline, penicillin, picrotoxin, beta-carbolines, 3-mercaptopropionic acid, hydrazides, allylglycine; the glycine antagonist strychnine; gamma-hydroxybutyrate; excitatory amino acids (glutamate, aspartate, N-methyl-D-aspartate, quisqualate, kainate, quinolinic acid); monosubstituted guanidino compounds, metals (alumina, cobalt, zinc, iron); neuropeptides (opioid peptides, corticotropin releasing factor, somatostatin, vasopressin); cholinergic agents (acetylcholine, acetylcholinesterase inhibitors, pilocarpine); tetanus toxin; flurothyl; folates; homocysteine and colchicine. Although there are a multitude of chemical models of epilepsy, only a limited number are applied in the routine screening of potential anticonvulsants. Some chemical models have a predictive value with regard to the clinical profile of efficacy of the tested anticonvulsants. Some chemical models may contribute to a better understanding of possible mechanisms of epileptogenesis.
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PMID:Chemical models of epilepsy with some reference to their applicability in the development of anticonvulsants. 139 44

Multiple morphological and neurochemical changes are found in the dentate gyrus of humans with temporal lobe epilepsy (TLE). Three basically different types of changes will be discussed and some interrelationships considered. Neuronal loss in several regions of the hippocampal formation in human TLE has been recognized for many years, but only recently have the polymorph or hilar neurons been evaluated as a distinct group of neurons, and cell loss in this region is now being documented in many cases with severe TLE. Reorganization of afferents within the molecular layer of the dentate gyrus is also found in a high percentage of TLE specimens. The apparent reorganization of mossy fibers from the dentate granule cells is particularly striking, and aberrant innervation of the inner part of the molecular layer by zinc- and dynorphin-containing mossy fibers has been reported in human tissue by several groups of investigators. In a subpopulation of TLE specimens, there is also disorganization of the granule cell layer. Rather than being arranged in the compact, highly organized layer that is characteristic of control tissue, the granule cell bodies in some TLE cases are dispersed. In some additional cases, a bilaminar pattern of granule cells is observed. Each of these changes could contribute to altered circuitry within the dentate gyrus of humans with TLE, and such alterations could influence seizure susceptibility within the hippocampal formation.
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PMID:Morphological changes in the dentate gyrus in human temporal lobe epilepsy. 146 68


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