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

1. Starting with published data derived mainly from hippocampal slice preparations, we have used computer-modeling techniques to study hippocampal pyramidal cells (HPCs). 2. The dendrites of the HPC apparently have a short electrotonic length. Calcium spikes are apparently generated by a voltage-dependent mechanism whose kinetics are slow in comparison with those generating sodium spikes of the soma. Inward calcium currents are assumed to trigger a long-lasting potassium conductance. This slow calcium-potassium system, which in our model is located predominantly on the dendrites, provides a heuristic model to describe the mechanism for a) the after-depolarization following an HPC soma (sodium) spike, b) the long afterhyperpolarization following repetitive firing, c) bursts of spikes that sometimes occur after orthodromic or antidromic stimulation, and d) the buildup of the "depolarizing shift" during the strong synaptic input presumed to occur during seizures. 3. Fast prepotentials or d-spikes are shown to arise most probably from dendritic "hot spots" of sodium-regenerative membrane. The limited amplitude and short duration of these prepotentials imply that the hot spots are located on small dendrites. 4. Dendritic electroresponsiveness, first postulated for the HPC by Spencer and Kandel (52), is analyzed quantitatively here and is shown to provide rich integrative possibilities for this cell. Our model suggests that, for these nerve cells, alterations in specific membrane properties, particularly calcium electroresponsiveness, can lead to bursting behavior that resembles epileptogenic neuronal responses.
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PMID:Hippocampal pyramidal cells: significance of dendritic ionic conductances for neuronal function and epileptogenesis. 42 74

Growing, mongrel dogs were fed high fat (22%), low calcium (.1%) semipurified and purified diets with and without 77 ppm lead as lead acetate to experimentally induce the seizures and lead encephalopathy historically associated with accidental canine lead toxicity. Seizures were observed in 44% of the lead toxic dogs and microscopic encephalopathy was observed in 89% of the lead toxic dogs. The encephalopathy was characterized by bilaterally symmetrical areas of vacuole formation involving the neuropile especially in a laminar pattern at the tips of the gyri of the cerebral cortex. The spongy state was accompanied by capillary activation and gliosis. These lesions are similar to those reported in accidental lead toxicoses in other species but previous efforts to experimentally induce these lesions in young dogs fed low-calcium, normal-fat (16%) purified diets have been unsuccessful.
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PMID:Lead-induced encephalopathy in dogs fed high fat, low calcium diets. 46 67

Computerized cranial tomograms (CCTs) unexpectedly showed bilateral symmetrical calcifications in the basal ganglia and frontal areas in two unrelated epileptic patients 12 and 13 years of age. The patients presented with a variety of seizures, some with focal features; these seizures were resistant to medication in the first case. Subsequent testing revealed hypocalcemia and other biochemical and radiologic features of pseudohypoparathyroidism, despite absence of the usual phenotypic features, tetanic symptoms, and positive family history. The CCT scan may provide the first clue to an underlying hypocalcemic disorder in an epileptic patient even when the skull X-ray is normal. Early detection of this metabolic condition by CCT scanning allows specific treatment to restore serum calcium levels to normal, which usually eliminates seizures and favors optimal cerebral functioning. Serial CCT scanning also provides a useful means for following the intracerebral calcifications, which remained unchanged after 1 and 2 years of normocalcemia in our 2 patients.
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PMID:Pseudohypoparathyroidism and epilepsy: diagnostic value of computerized cranial tomography. 47 43

The effects of the intraventricularly administered cations (Mn2+, Ca2+, Mg2+ and Li+) against the seizure induced by ouabain (3 microgram) were investigated. Mn2+, Ca2+ and Mg2+ caused definite sedation and decreased locomotor activity. But Li+ was without significant behavioral effect at the doses applied. Among the cations used, Mn2+, Ca2+ and Mg2+ showed significant anticonvulsive effect on the ouabain-induced seizure. In comparison, on the dose and molar-to-molar basis, the potency of anticonvulsive action was in the following order: Mn2+ greater than Ca2+ greater than Mg2+. On the contrary, the higher dose of Li+ potentiated the ouabain-induced seizure. The importance of the increased Ca2+ level in the extracellular space or the inhibition of Ca2+ uptake as the anticonvulsive effect of Ca2+, Mn2+ and Mg2+ was discussed.
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PMID:Effects of manganese, calcium, magnesium and lithium on the ouabain-induced seizure. 60 66

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

"Fahr's Disease" is characterized by bilateral and symmetrical calcifications of the Globus Pallidus (systematically extending to the Commisura Anterior and the Capsula Interna, and less commonly to the Putamen, the Centrum Semi-Ovale and the Cerebral Cortex), and of the Cerebellar Nucleus Dentalus (with spreading to the White Matter and the Cortical Lamellae). Lesions or absence of Parathyroids are frequently related, with subsequent metabolic disorders of Phosphorus and Calcium, but idiopathic cases without hypoparathyroid disturbances are also found. A Morgagni-Morel Hyperostosis Frontalis Interna is often associated with "Fahr's Disease", and there could be a relationship between these two affections. We found in three cases the association between "Fahr's Disease" and Morel's Nodular Dysgenesis of the Frontal Cortex. Most of the cases are sporadic, but observations with a clear familial incidence are also found. Clinically, various Neurological Disorders (cerebellar, extrapyramidal, pyramidal, dysarthria, epileptic seizures) are often but not always observed; the Psychiatric Disorders found in some cases could be fortuitious associations (psychoses), connected to hypothyroidism (oligophrenia), and in aged patients, to unrelated cerebral vascular or degenerative lesions; very seldom, a dementing state could be connected to the spreading of calcifications to the Cerebral Cortex.
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PMID:[Pallido-dentate calcifications (apropos of 7 anatomo-clinical case reports)]. 69 68

Three children with primary hypomagnesemia are described. First symptoms of the disease were observed, when the children were 35, 19, and 20 days old, resp. The hypomagnesemia was accompanied by a severe hypocalcemia. Therapeutic trials with high doses of calcium given intravenously and vitamin D were without effect on the symptoms. The whole body retention and intestinal resorption of orally administered 28-Mg was greatly reduced in all three patients compared to healthy adults. Symptoms of tetany and seizures ceased immediately after intravenous application of magnesium. An oral Mg substitution with 42--85 mmol per day was necessary to maintain subnormal to normal serum magnesium levels. The patients are now 5, 4 3/12 and 1 5/12 years old, resp. Psychomotor development in all three children is normal. Height and weight are in the lower normal range around the 3rd percentile, while the oral Mg substitution sometimes caused frequent fluid stools. By family studies from these patients and from the literature an autosomal-recessive inheritance for primary hypomagnesemia is proposed.
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PMID:[Primary hypomagnesemia. Clinical, diagnostic and therapeutic studies in three children (author's transl)]. 75 40

Anticonculsant drug-induced disorders in mineral and bone metabolism are apparently quite common. Current evidence indicates that these drugs derange bone metabolism, both through induction of increased hepatic catabolism of vitamin D and its biologically active products, as well as by direct effects on membrane cation transport systems. The significant clinical manifestions of the disorder include rickets with defective bone development, decreased bone mass with increased risk of pathological fracture and reductions in serum calcium levels which may predispose to increased seizure frequency. There is a broad range of clinical presentation with a number of factors -- drug dose, duration of therapy, vitamin D intake, amount of sunlight exposure, degree of physical activity and presence of other concurrent diseases -- which appear to determine the severity of the clinical manifestations. Current evidence indicates that appropriate vitamin D and calcium supplementation can significantly reduce the clinical manifestations of this disorder. All patients receiving chronic anticonvulsant drug therapy should be carefully evaluted for the presence of drug-induced osteomalacia and treated appropriately with vitamin D. This is especially important in those patients in whom the presence of multiple risk factors indicates an increased likelihood of deranged mineral metabolism.
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PMID:Bone complications of anticonvulsants. 78 46

Seizures in the neonatal period are usually concomitants of serious neurological disease. The convulsive phenomena take certain distinctive and often subtle forms because of the status of the neuroanatomical and neurophysiological development of the neonatal brain. The predominant etiological process is hypoxic-ischemic encephalopathy, but intracranial hemorrhage, intracranial infection, development defects and metabolic disorders are also responsible for a considerable proportion of cases. Prognosis is related primarily to the neurological disease that underlies the seizures. Treatment may be specific for the underlying disorder, e.g., glucose, calcium, magnesium, pyridoxine, but whatever the cause, urgent control of the convulsions is important because they may have deleterious consequences. Phenobarbital is the single, most important anticonvulsant in the management of neonatal seizures.
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PMID:Management of neonatal seizures. 83

The effects of leptazol and bicuculline on the efflux of endogenous acetylcholine (ACh) from the surface of the cerebral cortex have been related to EEG activity in urethane-anaesthetised rats. During seizure activity there was a calcium dependent increase in ACh efflux which was related to increase EEG activity and clonic muscle movements. ACh release and EEG activity were reduced during convulsive activity by trimethadione but not phenytoin. Phenobarbitone reduced convulsive EEG activity but left ACh release relatively unaffected. Blood pressure changes induced by convulsant and anticonvulsant drugs were not consistently related to EEG activity or ACh release. It is suggested that ACh efflux from the cerebral cortex is closely related to the activity of neurones within the cortex where it is released from nerve endings. Comparison of EEG changes induced by anticonvulsants and urethane during control and convulsant activity showed that only trimethadione produces anticonvulsant activity unaccompanied by general CNS depression.
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PMID:Convulsant-anticonvulsant interactions on seizure activity and cortical acetylcholine release. 85 9


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