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

Accounts of so-called "spontaneous" seizures by individual Mongolian gerbils during open-field tests resemble descriptions of magnesium tetany. A possible association between relative magnesium deficiency and tendency toward "spontaneous" seizures was explored through feeding groups of gerbils different rates of magnesium and subjecting the groups to open-field tests at intervals. Hypomagnesemia was related in degree of severity to length of survival, onset of seizing, and frequency of seizures.
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PMID:"Spontaneous" seizing in open-field tests by mongolian gerbils fed magnesium at different rates. 74 75

Magnesium is an essential cofactor for many enzymatic reactions, especially those involved in energy metabolism. Deficits of magnesium are prevalent due to inadequate intake or malabsorption and due to the renal loss of magnesium that occurs in certain disease states (alcoholism, diabetes) and with drug therapy (diuretics, aminoglycosides, cisplatin, digoxin, cyclosporin, amphotericin B). Protracted deficits of magnesium in humans and animals result in neurological disturbances, including hyperexcitability, convulsions and various psychiatric symptoms ranging from apathy to psychosis, some of which can be reversed with magnesium supplementation, others requiring correction of the dysregulation mechanism. Although the role of magnesium in neuronal function is not completely understood, a lowering of CSF or brain magnesium can induce epileptiform activity and there is an association between decreased CSF magnesium and the development of seizures. CSF concentrations of magnesium are normally higher than magnesium plasma ultrafiltrate (diffusible) concentrations due to the active transport of magnesium across the blood-brain barrier. Under conditions of magnesium deficiency, CSF concentrations decline, although this decline lags behind and is less pronounced than the changes observed in plasma magnesium concentrations. Decreases in CSF magnesium concentrations correlate with the alterations observed in extracellular brain magnesium concentrations in animals following the dietary deprivation of magnesium. CSF magnesium concentrations can readily be repleted following magnesium supplementation, although high dose magnesium therapy, such as that used in the treatment of convulsions in eclampsia, will only increase CSF magnesium concentrations to a very limited degree (approximately 11-18 per cent) above physiological concentrations. Greater increases in CSF magnesium may occur in neonates since neonatal swine, following treatment with magnesium, have CSF magnesium concentrations that are similar to their plasma concentrations. There has been a recent resurgence of interest in magnesium deficiency and its neurological consequences due to the finding that magnesium, at physiological concentrations, blocks N-methyl-D-aspartate (NMDA) receptors in neurones. NMDA receptors are normally activated by glutamate and/or aspartate which represent the principal neurotransmitters for excitatory synaptic transmission in vertebrate CNS. Magnesium deficiency produces epileptiform activity in the CNS which can be blocked by NMDA receptor antagonists. Other mechanisms, including alterations in Na+/K(+)-ATPase activity, cAMP/cGMP concentrations and calcium currents in pre- and postsynaptic membranes, may also be at least partially responsible for the neuronal effects associated with low brain magnesium. Further studies are necessary to increase our understanding of the neurological implications of magnesium deficit in the central nervous system.
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PMID:Brain and CSF magnesium concentrations during magnesium deficit in animals and humans: neurological symptoms. 129 67

Clinical and experimental investigations have shown that magnesium depletion causes a marked irritability of the nervous system, eventually resulting in epileptic seizures. Although magnesium deficiency as a cause of epilepsy is uncommon, its recognition and correction may prove life-saving. Two case reports are presented which emphasize the importance of recognizing hypomagnesaemia in patients with acute intractable seizures.
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PMID:Magnesium deficiency as a cause of acute intractable seizures. 191 10

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51

Convulsions are characteristic of magnesium deficiency and hypocalcemia. In this study, weanling rats were fed magnesium deficient diets with varying concentrations of calcium and phosphorus. Diets were either normal (Mg =) or low (Mg-) in magnesium and were either low (Ca- or P-), normal (Ca = or P =) or high (Ca+ or P+) in calcium or phosphorus. After consuming the diets for 17 days, the rats were tested for audiogenic seizures and blood was then drawn for serum mineral analyses. Rats fed Mg-Ca = P =, Mg-Ca = P-, Mg-Ca+P = or Mg-Ca+P+ diets had high incidences of seizures. Those fed Mg-Ca-P =, Mg-Ca-P-, Mg-Ca = P+, Mg-Ca-P+ or Mg-Ca+P- diets had low incidences of seizures. In general, animals with low serum magnesium and calcium levels and high serum potassium levels were susceptible to audiogenic seizures. In this model, serum magnesium level is the most important determinant of seizure susceptibility, followed by calcium and potassium.
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PMID:Dietary calcium and phosphorus and seizure susceptibility of magnesium deficient rats. 365 67

A controlled study was conducted to quantitate plasma catecholamines in magnesium-deficient weanling rats experiencing the seizure-shock episode. Eighty-four male Sprague-Dawley rats each weighing 35.6 +/- 0.3 g (mean +/- SEM) were fed purified diets to which was added 150 mg magnesium/100 g (Mg-150) or no magnesium (Mg-0). Studies were conducted between d 5 and 8. Plasma and bone magnesium and calcium were measured by atomic absorption spectrophotometry, and plasma catecholamines by radioenzymatic assay using 3H. Compared with Mg-150 rats, the Mg-0 rats showed reduced weight gain (P less than 0.001); reduced plasma magnesium (P less than 0.001) and reduced bone magnesium (P less than 0.001) with no corresponding changes in calcium concentration; and a 25% mortality by d 8. Pair-feeding and 80-dB noise provoked no changes in plasma catecholamines in Mg-150 rats, but both strychnine-induced seizures in Mg-150 rats and seizures induced by 80-dB noise in Mg-0 rats were accompanied by massive increases in plasma catecholamines. In contrast, 80-dB noise in Mg-0 provoked a massive increase in plasma catecholamines (P less than 0.001). However, gross pulmonary pathology developed only in Mg-0-shocked rats, not Mg-150-shocked animals. The study provides no evidence for a role of catecholamines in the pathogenesis of Mg-0 shock. The weanling rat displayed the ability to release massive quantities of three catecholamines during the final stages of acute magnesium deficiency and to normalize the plasma catecholamine levels within 16 h after seizure shock.
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PMID:Plasma catecholamines in acute magnesium deficiency in weanling rats. 377 20

Mice of the DBA/2/M strain are audio-sensitive only for a short period (5 to 10 days). When this period is over, 100 p. 100 audiogenic seizures can be obtained with experimental magnesium deficiency. When AKR/R, OF1 and C57BL/R mice were deprived of magnesium for 15 or 21 days, they manifested an audiogenic attack only when given amphetamine sulfate, caffeine or isonicotinylhydrazine. If they had been deprived for 43 days, it was no longer necessary to administer these substances. The audiogenic attack could be prevented by correcting the deficiency with magnesium chloride or by preliminary administration of a single dose of various barbiturics, anti-convulsives, tranquillizers or parachlorophenylalanine, but not neuroleptics.
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PMID:[Audiogenic seizure in the mouse according to strain and sex: the effect of the magnesium ration and neuromediators]. 613 May 80

Magnesium deficiency was induced in a setting of an otherwise adequate diet in adult beagle dogs. Despite the development of severe hypomagnesemia (from 1.5 +/- 0.2 to 0.5 +/- 0.2 meq/liter) during the 10-wk study, Mg content of skeletal muscle fell only modestly (from 3.8 +/- 0.2 to 3.1 +/- 0.4, P less than 0.005, at 7 wk and 3.5 +/- 0.4 mM/100 g FFDS, NS, at 10 wk). The most pronounced muscle compositional changes were a loss of phosphorus (from 29.5 +/- 1.8 to 22.0 +/- 1.6, P less than 0.001, at 7 wk and 24.8 +/- 2.8 mM/100 G FFDS, P less than 0.001, at 10 wk) and gains of calcium (from 0.64 +/- 0.11 to 0.93 +/- 0.17, P less than 0.05, at 7 wk, and 0.85 +/- 0.26 mM/100 g FFDS, P less than 0.05, at 10 wk), sodium (from 13.2 +/- 2.6 to 22.9 +/- 4.7, P less than 0.001 at 7 wk and 17.8 +/- 2.0 meq/100 g FFDS, P less than 0.005, at 10 wk), and chloride (from 5.8 +/- 0.8 to 8.2 +/- 1.6, P less than 0.001, at 7 wk and 6.8 +/- 0.6 meq/100 g FFDS, P less than 0.05, at 10 wk). Cellular potassium content did not change (from 35.9 +/- 1.9 to 33.0 +/- 4.1, NS, at 7 wk and 36.3 +/- 2.0 meq/100 g FFDS, NS, at 10 wk). Muscle cell electrical hyperpolarization developed after 10 wk of Mg depletion. Convulsive seizures developed in three animals. Frank rhabdomyolysis in three animals and focal necrosis in four animals were present on terminal biopsy, with only four animals having completely normal histology.
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PMID:Skeletal muscle injury after magnesium depletion in the dog. 711 11

The effect of dietary magnesium deficiency has so far been studied preferentially in rapidly growing rodents or in adult animals. Since magnesium deficiency frequently occurs in elderly persons too, magnesium- and calcium-deficient diets were offered during 32 and 64 days to 'old' rats (34 months old, spontaneous mortality of 15 per cent). The calcium-deficient diet (2.5 per cent of the requirement) was well tolerated and no profound biochemical disturbances were noted. In contrast, dietary magnesium deficiency (12.5 per cent of the requirement) induced loss of body weight, formation of erythema, severe hypomagnesaemia and increase of tissue calcium levels. No seizures were noted and mortality did not increase, in contrast to growing magnesium-deficient rats. Histologically, age effects were present in bone tissues of old rats, however no additional dietary effects became visible. Tensile strength of femur and rib did not reveal treatment-related changes. Fourteen days preloading with high dietary magnesium increased plasma magnesium and also skeletal concentrations, although to an only small degree. Nevertheless, time until the appearance of erythema in 50 per cent of the rats subsequently fed the magnesium-deficient diet was significantly delayed.
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PMID:Influence of high and low dietary magnesium levels on functional, chemical and morphological parameters of 'old' rats. 778 86

The aim of our study was to analyse the possible implication of the serotoninergic system in the pathophysiology and the lethality of audiogenic seizures induced by magnesium deficiency, either by decreasing cerebral serotonin (5-HT) levels (p-chlorophenylalanine) or by increasing 5-HT levels in the brain (5-hydroxytryptophan, L-tryptophan, nialamide, fluoxetine). In magnesium-deficient mice, the percentages of audiogenic seizures and of fatal seizures were dependent on the time lapse between the p-chlorophenylalanine (PCPA) injection and the audiogenic test. The percentage was at least 24 h after the injection: in OF1 and C57BL/6 strains, PCPA fully protected the mice from seizure occurrence, whereas it only partially protected the animals of the other strains. 5-Hydroxytryptophan caused a decrease in the audiogenic seizures in magnesium-deficient OF1 mice as well as in control DBA/2 mice. In contrast L-tryptophan did not reduce the number of wild courses or of clonic and tonic seizures in either the magnesium-deficient OF1 strain or control DBA/2 mice. Nialamide and fluoxetine were only effective in decreasing the numbers of clonic and tonic convulsions of the audiogenic seizure without affecting the wild courses. The combination of nialamide and tryptophan caused a cessation of the audiogenic seizure phases in both magnesium-deficient OF1 and control DBA/2 mice. In contrast, the fluoxetine-tryptophan combination did not have the same effect on magnesium-deficient and non-magnesium-deficient mice. This work showed that the serotoninergic system plays a secondary role in the pathophysiology of audiogenic seizures in magnesium-deficient mice rather than in that of genetically audiosusceptible mice.
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PMID:Effect of various serotoninergically induced manipulations on audiogenic seizures in magnesium-deficient mice. 799 24


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