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

Islet cell dysmaturation syndrome (ICDS) encompasses the causes of infantile hyperinsulinemic hypoglycemia histologically described as islet cell hyperplasia, pancreatic adenomatosis and nesidioblastosis. Eleven infants underwent 14 pancreatic resections for ICDS from 1965 to 1990 at the University of California at Los Angeles Medical Center for severe hypoglycemia unresponsive to medical therapy. Seizures were the presenting symptoms of hypoglycemia in eight infants. Six patients had nesidioblastosis, four had islet cell hyperplasia and one patient had an adenoma with histologically normal pancreatic islet cells. Four neonates underwent 80 per cent pancreatic resection; three with nesidioblastosis required reoperation (90 to 95 per cent resection). Four older infants underwent 80 per cent pancreatic resection but required diazoxide for less than six months postoperatively. Three infants underwent 90 to 95 per cent pancreatic resection. None have required reoperation or postoperative medications. All infants are normoglycemic without pancreatic exocrine insufficiency and none had postoperative complications. Five infants had preoperative neurologic impairment, with three having severe retardation; all showed some improvement postoperatively, but only one infant now has normal findings on neurologic examination. Early diagnosis and aggressive surgical resection should minimize neurologic complications of the ICDS.
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PMID:Surgical management of islet cell dysmaturation syndrome in young children. 221 37

Quinidine, procainamide and disopyramide are antiarrhythmic drugs in the class 1A category. These drugs have a low toxic to therapeutic ratio, and their use is associated with a number of serious adverse effects during long term therapy and life-threatening sequelae following acute overdose. Class 1A agents inhibit the fast inward sodium current and decrease the maximum rate of rise and amplitude of the cardiac action potential. Prolonged Q-T interval and, to a lesser extent, QRS duration may be observed at therapeutic concentrations of quinidine. With increasing plasma concentrations, progressive depression of automaticity and conduction velocity occur. 'Quinidine syncope' (a transient loss of consciousness due to paroxysmal ventricular tachycardia, frequently of the torsade de pointes type) occurs with therapeutic dosing, often in the first few days of therapy. Extracardiac adverse effects of quinidine include potentially intolerable gastrointestinal effects and hypersensitivity reactions such as fever, rash, blood dyscrasias and hepatitis. Procainamide produces electrophysiological changes that are similar to those of quinidine, although Q-T interval prolongation with the former is less pronounced at therapeutic concentrations. Hypersensitivity reactions including fever, rash and (more seriously) agranulocytosis are associated with procainamide, and a frequent adverse effect requiring cessation of therapy is the development of systemic lupus erythematosus. Of the 3 drugs, disopyramide has the most pronounced negative inotropic effects, which are especially significant in patients with pre-existing left ventricular dysfunction. As with quinidine, unexpected 'disopyramide syncope' at therapeutic concentrations has been described. Anticholinergic side effects are common with this drug and may require cessation of therapy. Disopyramide therapy may unpredictably induce severe hypoglycaemia. Severe intoxication with the class 1A agents may result from acute accidental or intentional overdose, or from accumulation of the drugs during long term therapy. Acute overdose can result in severe disturbances of cardiac conduction and hypotension, frequently accompanied by central nervous system toxicity. Decreased renal function can cause significant accumulation of procainamide and its active metabolite acecainide (N-acetyl-procainamide), resulting in severe intoxication. Mild to moderate renal dysfunction is less likely to lead to quinidine or disopyramide intoxication, unless renal failure is severe or concurrent hepatic dysfunction is present. Management of acute intoxication with class 1A drugs includes gut decontamination with provision of respiratory support and treatment of seizures as needed. Hypertonic sodium bicarbonate, by antagonising the inhibitory effect of quinidine on sodium conductance, may reverse many or all manifestations of cardiovascular toxicity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Poisoning due to class IA antiarrhythmic drugs. Quinidine, procainamide and disopyramide. 228 95

Two new cases of diffuse hyperplasia of the pancreas are reported. This infrequent condition is caused by intermittent and variable insulin hypersecretion. The hyperinsulinism is responsible for severe, lasting and intractable hypoglycemia that causes seizures and mental retardation. Onset usually occurs in the neonatal period. The diagnosis of hyperinsulinism rests on four criteria: the presence of increased insulin levels in the face of hypoglycemia, the low urinary excretion of ketone bodies during hypoglycemic episodes, the need for more than 15/mg/kg/min glucose to maintain the serum glucose level above 2 mmol/l, and a positive response to glucagon. The topographic diagnosis is often disappointing. Medical treatment of the hypoglycemia with diazoxide is a transient measure. Subtotal pancreatectomy is indispensable. Postoperative results are variable. Insulin deficiency diabetes mellitus is common and unusual in that insulin induces an exaggerated response. Recovery can be observed. If hypoglycemia recurs, diazoxide is often effective.
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PMID:[Nesidioblastosis. Apropos of 12 new cases]. 229 91

Sudden incapacitations can affect a pilot and even a whole crew during a flight, preventing them from performing their task in complete safety. In some cases, they could even cause an accident. Our study examines the causes of sudden in-flight incapacitation in Air France pilots and flight engineers from 1968-88. Ten cases were reported out of a population of 1,800 cockpit crew, each flying an average of 600 h/year. These incapacitations were due to cardiac disorders (1 atrial fibrillation, 1 sinus tachycardia), epileptic attacks (2 generalized seizures), duodenal hemorrhages (2 cases), infection (1 case of severe vertigo due to viral labyrinthitis), metabolic disorders (1 case of hypoglycemia), and sometimes disorders affecting the whole crew (1 case of hypoxia due to a pressurization deficiency, 1 case of CO2 intoxication caused by the inadequate packaging of a container refrigerated in dry ice). Seven times out of ten, incapacitations occurred during cruising, twice during approach, and once on the ground before starting up, with closed doors (CO2 intoxication). Two of these incapacitations led to flight diversions. None of them caused an accident. In this series, incapacitations of a cardiac nature were rarer and less serious than those caused by gastrointestinal or neurological disorders. Prevention is based on detection during systematic medical check-ups, and on crews being trained to recognize subtle incapacitations early and to ensure that the flight continues safely when such a case occurs.
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PMID:Clinical aspects of inflight incapacitations in commercial aviation. 231 81

The usual signs and symptoms of hypoglycemia include tachycardia and profound diaphoresis. These will progress to include an altered mental status that can advance in severe cases to coma, seizures, and death. Occasionally, hypoglycemia may present with focal neurologic signs that can include hemiparesis or hemiplegia with preservation of mental status. In patients with the latter signs, the possibility of a cerebrovascular accident or other intracranial abnormality must be considered. The authors describe an elderly patient with hypoglycemic hemiplegia secondary to insulin administration. Their report includes observations on clinical presentation, the various mechanisms involved, and guidelines for the management of this syndrome.
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PMID:Hypoglycemic hemiplegia. 235 82

The specificity of the hypoglycemic response to the intrathecal (i.t.) administration of the naturally occurring (-)-enantiomer of morphine previously reported from our laboratory was studied in mice. (+)-Morphine HBr (50 micrograms) caused a behavioral syndrome (scratching, biting, seizures) comparable to that produced by (-)-morphine sulfate (50 micrograms), but did not cause hypoglycemia. Many opioids, at a dose of 50 micrograms i.t. in nonfasted mice, showed either a saline-like hyperglycemic response or no significant effect on blood glucose. (+)-Morphine, ketocyclazocine, U-50,488, (-)- and (+)-N-allyl-normetazocine, beta-endorphin, (-)- and (+)-naloxone and naltrexone caused hyperglycemia. Significant changes from basal blood glucose were not produced by [D-Pen2, L-Pen5]-enkephalin, [D-Ser2]-Leu-enkephalin-Thr or sufentanil in 50-micrograms doses, or by codeine (300 micrograms), levorphanol (400 micrograms) or methadone (200-400 micrograms). Agonists which produced both hypoglycemic and behavioral effects were, in order of decreasing potency, hydromorphone greater than normorphine greater than morphine greater than 6-acetylmorphine greater than oxymorphone much greater than heroin. Morphine-induced hypoglycemia was partially antagonized by the i.t. coadministration of naloxone methobromide (10 micrograms). Fasting for 24 hr increased the sensitivity to hypoglycemic and lethal effects of morphine. D-Ala2-N-Me-Phe4-Gly5-ol]-enkephalin (5-50 micrograms i.t.) tended to decrease blood glucose in both nonfasted and fasted mice, but these effects were moderate and appeared to be unrelated to dose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypoglycemia induced by intrathecal opioids in mice: stereospecificity, drug specificity and effect of fasting. 235 29

A transient brain ischemia of 30-min duration was induced by the four-vessel occlusion technique in normally fed and in 48-hr-fasted rats. Evaluation of brain damage 72 hr after ischemia showed that fasting reduced neuronal necrosis in the striatum, the neocortex, and the lateral part of the CA1 sector of hippocampus. Signs of status spongiosis in the pars reticulata of the substantia nigra were seen in 75% of fed rats and in only 19% of fasted rats. The protective effect was associated with reduction in mortality and in postischemic seizure incidence. The metabolic changes induced by fasting were evaluated before and during ischemia. After 30 min of four-vessel occlusion, fasted rats showed a marked decrease in brain lactate level (14.7 vs 22.5 mumol/g in fed rats; P less than 0.001). The decrease in brain lactate concentration might explain the beneficial effect of fasting by minimizing the neuropathological consequences of lactic acidosis. Several factors may account for lower lactate production during ischemia in fasted rats: hypoglycemia, reduction in preischemic stores of glucose and glycogen, or increased utilization of ketone bodies aiming at reducing the glycolytic rate.
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PMID:Fasting prior to transient cerebral ischemia reduces delayed neuronal necrosis. 238 15

The activity of glutamate related enzymes and the concentration of glutamine, glutamate and gamma-amino n-butyric acid (GABA) were investigated in the cerebral cortex of rats, in different stages of insulin-induced hypoglycemia. Hypoglycemia was produced by intraperitoneal injection of insulin 0.05-100 units per kg body weight. The minimum required dose to produce irreversible severe hypoglycemia was 0.5 units/kg. In 85% of the cases an insulin induced hypoglycemic convulsion, was achieved 130-150 minutes after injection. Blood glucose levels during insulin induced seizures ranged between 8-15 mg%. In the range of 0.5-100 u insulin/kg the degree of hypoglycemia and the onset of convulsions were identical. The concentration of glutamine was significantly reduced during convulsive and postconvulsive stages. Glutamate and GABA concentrations were reduced significantly in all stages of insulin-induced hypoglycemia. The decrease in glutamine concentration was concurrent with an increase in the activity of its degradative enzyme, glutaminase. This was apparent at the preconvulsive, convulsive and postconvulsive stages. The activity of other enzymes related to energy production such as glutamate dehydrogenase (GDH), glutamate transaminase (GPT) and aspartate aminotransferase (AAT) were also increased. The activity of glutamine synthase (GS) was unaffected by hypoglycemia. Insulin induced changes in glutamine, glutamate and their related enzymes could not be attributed to convulsion since a similar pattern of changes was observed in the preconvulsive and postconvulsive stages, and no changes were detected following picrotoxin-induced seizures.
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PMID:Changes in the activity of glutamate related enzymes in cerebral cortex, during insulin-induced seizures. 257 18

Over a period of one year, 16,365 consecutively live born neonates were prospectively studied for evidence of birth asphyxia using the requirement of greater than one minute of positive pressure ventilation for identifying infants suffering from birth asphyxia. Asphyxia occurred in 2.8% of all neonates. Multivariate analysis of high risk factors associated with increased risk of asphyxia showed that low birth weight was the most significant predictor of asphyxia: asphyxia occurred in 68% of infants of less than 1,000 g birth weight and decreased to 1.2% in infants of 3-4 kg birth weight. Perinatal risk factors associated with a higher incidence of asphyxia include: postmaturity, birth weight (less than or equal to 2.5 kg) and with the presence of maternal and/or obstetric complications. The impact of asphyxia on neonatal mortality was most pronounced in more mature infants and the mortality was increased 3 fold in infants of less than 34 week gestation and greater than 27 fold for infants greater than 38 week gestation. Of the asphyxiated neonates, intrauterine growth retardation, fetal macrosomia, hypothermia, hyaline membrane disease, seizures, hypoglycemia and hyponatremia were significantly associated with an increased risk of death.
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PMID:Perinatal risk factors in birth asphyxia: relationship of obstetric and neonatal complications to neonatal mortality in 16,365 consecutive live births. 262 78

A female infant presented with poor feeding, hypotonia, prolonged jaundice, seizure and wandering nystagmus. A case of septo-optic dysplasia was proved by demonstrating the absence of septum pellucidum, small optic discs and hypothalamic-pituitary dysfunction at the age of three months. It is stressed that a diagnosis of septo-optic dysplasia must be entertained in infants who present with prolonged jaundice and hypoglycemia, particularly when rotatory nystagmus is associated.
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PMID:Septo-optic dysplasia: report of a case. 263 88


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