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

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

We evaluated the newborn lamb's cerebral cellular activity and metabolism following acute insulin-induced hypoglycemia. Eleven animals received an insulin bolus followed by a continuous infusion to maintain a plasma glucose of 1 mM/l for 2 h, while 8 other animals received an equivalent dose of saline. Following the induction of hypoglycemia, the animals became quiet and transient seizures were observed in 3 animals. A significant increase in heart rate (p less than 0.01), and a decrease in arterial PaCO2 at 30 min (p less than 0.01), and pH at 2 h (p = 0.02), following hypoglycemia, were observed in the experimental group. Hypoglycemia did not significantly alter the cerebral blood flow, mitochondrial respiratory control ratio or the state-3 activity. The cerebral arteriovenous difference (CAVD) for oxygen did not change, while the glucose CAVD was significantly reduced from 0.47 +/- 0.21 to 0.24 +/- 0.16 mM/l (p less than 0.05) at the end of the hypoglycemia period, suggesting consumption of alternate substrates of energy by the brain. Insulin-induced hypoglycemia was associated with a significant increase in arterial lactate (p less than 0.01), and a significant correlation (p less than 0.01) between arterial and CAVD for lactate and beta-hydroxybutyrate (BOB) was observed. Cerebral consumption of alternate substrates of energy was inconsistent, and only observed for lactate in 5 and for BOB in 3 experimental animals following hypoglycemia. These data indicate that the newborn lamb's cerebral cellular activity is not affected by the degree of hypoglycemia achieved in these studies.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral metabolic response and mitochondrial activity following insulin-induced hypoglycemia in newborn lambs. 265 16

Pre- and post-prandial circulating concentrations of metabolic fuels and plasma insulin are documented in 59 patients with severe epilepsy while receiving either a normal diet, the classical high-fat ketogenic diet, a medium-chain triglyceride (MCT) diet, or a modified MCT diet. All three therapeutic diets improved the control of epilepsy and induced a significant increase in the concentrations of blood aceto-acetate and 3-hydroxybutyrate, the greatest elevation being seen in patients on the classical diet. The classical diet also caused a significant decrease in blood alanine values, which was not observed with the other therapeutic diets. The only consistent change to occur in all patients on therapeutic diets was an increase in plasma uric-acid. The mechanism by which ketogenic diets improve seizure control remains to be elicited.
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PMID:Metabolic effects of three ketogenic diets in the treatment of severe epilepsy. 266 Dec 88

Serum cortisol, prolactin (PRL), TSH, GH, LH and FSH levels were measured before and immediately after daily ACTH-Z therapy (0.01 mg/kg/day, 1-2 weeks) for 5 patients with infantile spasms and one patient with myoclonus epilepsy. Total number of ACTH-Z therapy were 8 times, and all patients became seizure free after ACTH-Z therapy. In 6 occasions, TRH, LH-RH and insulin tolerance tests were performed before and after daily ACTH-Z therapy. Serum cortisol levels were significantly increased after daily ACTH-Z therapy but all other hormone levels were significantly decreased. In TRH and LH-RH tolerance tests, peak levels and increments of PRL, LH and FSH were significantly decreased after daily ACTH-Z therapy and those of TSH were mildly decreased. In one case insulin tolerance test revealed an adequate decrease of blood glucose before and after ACTH-Z therapy, and there was a poor GH response after ACTH-Z therapy. Daily ACTH-Z therapy was thought to suppress secretion of anterior pituitary hormones.
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PMID:[Changes in anterior pituitary function during ACTH therapy of patients with infantile spasms]. 280 96

Plasma epinephrine, norepinephrine, and dopamine responses were studied in insulin-dependent diabetic patients at rest, on standing and during insulin-induced hypoglycemia. beta-Adrenergic sensitivity was evaluated by the isoproterenol sensitivity test. Five men who had adrenergic symptoms during hypoglycemia and no severe hypoglycemic accidents (coma, seizures) (group A) and five men who had repeated severe hypoglycemic accidents but lack of adrenergic symptoms of hypoglycemia (group B) were studied. The mean resting plasma epinephrine was lower in group B (147 +/- 22 pmol/L, SEM) than in group A (398 +/- 98 pmol/L, P less than 0.02). On standing plasma epinephrine increased significantly in both groups. During hypoglycemia blood glucose decreased identically in the two groups; plasma epinephrine and norepinephrine increased significantly and to the same extent in both groups; the mean maximal heart rate was significantly greater in group A than in group B. Isoproterenol sensitivity (defined as the dose of isoproterenol required to increase heart rate by 25 beats/min) was lower in group B (5.87 +/- 1.12 micrograms) than in group A (2.37 +/- 0.22 micrograms, P less than 0.01). The group B patients had significantly fewer hypoglycemic symptoms during insulin-induced hypoglycemia than did group A patients. We conclude that decreased beta-adrenergic sensitivity contributes to the lack of adrenergic symptoms of hypoglycemia in insulin-dependent diabetic patients.
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PMID:Lack of hypoglycemic symptoms and decreased beta-adrenergic sensitivity in insulin-dependent diabetic patients. 282 5

Several factors involved in the regulation of ornithine decarboxylase (ODC) activity in adult rat brain tissue have been identified by using the in vitro hippocampal slice preparation. The same amino acids that have previously been reported to induce ODC in tissue culture, i.e., asparagine and glutamine, were found to produce a concentration- and time-dependent increase in ODC activity that reached a 100 fold the control value after 6 h of incubation. The effect of asparagine was totally blocked by inhibition of either protein or RNA synthesis, suggesting that the inducing amino acids increase ODC activity by stimulating the transcription of genes directly or indirectly regulating ODC activity. The effect of the inducing amino acids was potentiated by a variety of factors which by themselves did not modify ODC activity. In particular, opioid peptides markedly potentiated the effect of asparagine. Although the opiate antagonists naloxone and naltrexone totally blocked the effects of the opioid peptides on ODC induction, they also produced an inhibition of the asparagine-mediated increase in ODC activity. Other factors like dibutyryl cyclic AMP and insulin also potentiated the effects of asparagine on ODC activity. These results provide the first description of ODC induction in an in vitro preparation of adult brain tissue and indicate that the hippocampal slice preparation could be used to study the molecular mechanisms which regulate the expression and activity of ODC in the adult central nervous system. Moreover the data suggest possible mechanisms which may be involved in the induction of ODC in hippocampus by seizure activity.
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PMID:Induction of ornithine decarboxylase in adult rat hippocampal slices. 285 84

A nine-year-old mixed breed dog was presented with a history of mild generalized seizures, weakness, and muscle fasciculations, following periods of excitement and exercise. Investigative procedures included haematology, chemical pathology, faecal analysis, urinalysis, cerebrospinal fluid analysis, hormone assays, computerized axial tomography and scintigraphic imaging. Results of these investigations revealed hypoglycaemia (blood glucose 1.9 mmol l-1, hyperinsulinism (111 muu ml-1) and an amended insulin-glucose ratio of 2643. The glucagon tolerance test was typical for an insulin producing pancreatic islet cell tumour and pancreas scintigraphic imaging revealed focal lesions in the pancreas and liver. Seizures were initially controlled by dietary means and by limiting exercise. Eventual control was obtained by treatment with prednisolone (1 mg kg-1 on alternate days) and diazoxide (10 mg kg-1 in divided doses daily). Post mortem examination confirmed the presence of a pancreatic islet cell adenocarcinoma with hepatic metastasis.
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PMID:An insulinoma causing hypoglycaemia and seizures in a dog: case report and literature review. 285 64

An 8-year-old boy with insulin-dependent diabetes mellitus and a seizure disorder demonstrated transient visual loss after severe seizure activity. The role of hypoglycemia in relation to his transient cortical blindness remains indeterminate. The nature of the cortical involvement, the rate of visual recovery, and prior reports of postictal phenomena emphasize the relatively benign nature of this condition in children.
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PMID:Transient postictal cortical blindness. 295 7

The mean age of the 13 patients studied (9 women, 7 men) was 50.5 +/- 15.7 years. The disease was discovered on account of malaise (3 cases), behavioural disorders (4 cases), coma (3 cases), syncope (1 case) or right hemiparesis (1 case) or in the course of systematic examination (1 case). Eleven patients consulted for evaluation of hypoglycaemia and 2 for behavioural disorders. The history was characteristic, with malaise, loss of consciousness, severe neurological disorders (seizures, hemiparesis, hemiplegia or coma) and psychiatric disorders. These symptoms typically occurred in the morning before breakfast or between meals in 9 patients, and atypically at any point of time or after meals in 4 patients. Their hypoglycaemic nature was demonstrated by blood glucose determination in 11/13 cases and by response to ingestion of sugar in 12/13 cases. The mean period elapsed between the initial symptoms and the final diagnosis was 20.3 +/- 17.3 months. Inappropriate insulin secretion was elicited a.m. before breakfast, during Conn's diet or fasting test, or by calculating the blood insulin/glucose ratio or Turner's coefficient. Prior to surgery, the insulinoma was located by ultrasonography in 3/8 cases, by computerized tomography in 2/6 cases, by selective arteriography in 6/11 cases, and by phlebography with spleno-portal catheterization and staged sampling for insulin and C-peptide assays in 8/9 cases. Histological examination after surgery (11 cases) or necropsy (1 case) showed an adenoma without evidence of malignancy.
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PMID:[Insulinoma: diagnostic elements. 13 cases]. 299 55

Insulinoma was diagnosed in a 7-year-old female ferret examined because of generalized seizures, intermittent paraplegia, and abnormal behavior. Low serum glucose, high serum insulin, and infinite amended insulin/glucose ratio values in this ferret supported the clinical diagnosis of insulinoma. Histologic examination of the pancreas confirmed the diagnosis of insulinoma. The clinical signs and laboratory evaluations in this case and in a previously reported case of insulinoma in a ferret were consistent with variations reported in dogs with insulinoma.
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PMID:Insulinoma in a ferret. 302 97


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