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

The relation of endotoxicosis to insulin responsiveness was evaluated in male Holtzman rats. Salmonella enteritidis lipopolysaccharide at 0.5 or 1.0 mg per 300 g rat increased lethality in convulsive seizure deaths to 0.25, 0.50, or 1.0 U insulin sc. The hypoglycemic nadir induced by 0.05, 0.10, or 0.25 U of insulin sc was greater in rats rendered endotoxic with 1 mg of lipopolysaccharide IV. Oxidation of U-14C-D-glucose to 14 CO2 by endotoxic tissues in vitro was augmented in liver slices, epididymal fat pads, hemidiaphragms, and spleen slices; no pronounced glucose oxidation increases occurred in lung, heart, stomach, cerebrum, kidney, or whole blood. Epididymal fat pads from endotoxic rats (100 g) manifested increased basal glucose oxidation as well as an enhanced maximal response to incremental insulin doses of 0.01 to 25 mU/ml. It is suggested that altered tissue responsiveness in concert with hyperinsulinemia underlie the profound alterations in glucose homeostasis during endotoxicosis.
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PMID:Increased insulin responsiveness in endotoxicosis. 37 53

The diagnosis of nesidioblastosis was established in a 9-month-old male child with a history of recurrent convulsive seizures and hypoglycemia. After unsuccessful subtotal pancreatectomy, treatment was started with the long-acting somatostatin derivative Sandostatin (Octreotide, Sandoz) at a dosage of 25 micrograms t.i.d. spaced between carbohydrate-enriched meals. With this regime, blood glucose was maintained at the low normal range and seizures ceased. During a 30-month observation period, growth velocity and weight progression were well within the predicted limits. A 24-hour hormone profile recorded at the end of the observation period revealed the following: (1) failure to improve blood glucose with carbohydrate-enriched food due to reactive hyperinsulinemia; (2) hyperglycemic reaction after administration of Sandostatin caused by a reduction of plasma insulin; this effect was particularly marked during sleep; (3) low mean GH, decreased spiking frequency and reduced area covered by the nocturnal peaks by recognized standards, and (4) normal somatomedin C levels for age. Interpretation of growth hormone (GH) data is hindered by the lack of pertinent information from the patient's age group. Recording of normal growth progression in the case illustrated here can only be explained by the capability of a reduced GH secretory rate to maintain full biological activity as shown by the normal plasma level of somatomedin C. Indeed, recent evidence has been provided elsewhere for normal growth progression in the presence of low GH secretion, although other factors unrelated to this hormone may also be operative at this early age. Further reports concerning the treatment of non-GH-dependent conditions with somatostatin derivatives will certainly contribute to the better understanding of the mechanisms governing growth in the postnatal period.
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PMID:Growth progression and 24-hour hormone profile in an infant treated chronically with a long-acting somatostatin derivative. 168 92

The medical records of six cases of nesidioblastosis were examined to determine the diagnostic approach, treatment, and neurologic sequelae. All six patients were male, and their ages at the onset of the disease ranged from one day to six months (mean 3.36 +/- 2.5 mo.). Initial clinical features were seizure, cyanosis, poor feeding, and apnea. Other subsequent symptoms were developmental delay, hyperactivity, and cold sweating. The Birth weight of the neonatal onset group was heavier than the postneonatal onset group (4.4 +/- 0.3 vs 3.26 +/- 0.04 kg). Before the diagnosis of hyperinsulinism, steroids of ACTH proved effective for seizure control. Initially, hyperinsulinemia (serum insulin greater than 10 microU/ml) was detected in four cases, but another two cases also showed hyperinsulinism by insulin/glucose(I/G) ratio greater than 0.3 during the fasting test. The glucagon response performed in 2 cases, showed normal and partial responses. Euglycemia was obtained by near total pancreatectomy (95% pancreatic resection)without malabsorption or persistent diabetes. In one case, nesidioblastoma coexisted with nesidioblastosis. Developmental delay was noted in three cases. In this group, the mean duration between symptom onset and operation was longer than the group without developmental delay (1.25 +/- 0.47 vs 0.38 +/- 0.19 yr).
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PMID:A study on nesidioblastosis in hyperinsulinemic hypoglycemia--diagnosis, treatment, and neurologic sequelae. 171 Sep 1

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

The hypoglycemias caused by organic hyperinsulinism are predominantly manifested by means of neuropsychiatric disorders. They include losses of consciousness and seizures occurring in the period of hunger. The method of choice in the treatment of this disorder is surgical treatment of pancreatic neoplasms. This implies the need of early diagnostic procedure.
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PMID:[Organic hyperinsulinism as a diagnostic problem in neuropsychiatric practice]. 263 87

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

Hyperinsulinemia, a common cause of persistent hypoglycemia in infants and children, can result in permanent damage to the central nervous system. Thus, early diagnosis and treatment are important. The typical clinical manifestation of hyperinsulinemic hypoglycemia is symptomatic hypoglycemia that responds poorly to medical therapy. Affected infants may have tremors, jitteriness, apnea, cyanosis, or seizures. If initial medical therapy (frequent feedings, large amounts of intravenously administered glucose, diazoxide, and glucocorticoids) fails to stabilize plasma glucose levels, subtotal pancreatectomy is indicated. This surgical intervention does not completely correct the hypoglycemia in all patients, but it effectively reduces the severity of the condition. Surgical treatment of pediatric patients with Cushing's syndrome or aldosteronoma has also been effective. In our experience, survival of patients with adrenocortical adenomas has been 100%, whereas only five of nine children with adrenocortical carcinomas survived, and four of the five were younger than 10 years of age.
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PMID:Endocrine disorders of the pancreas and adrenal cortex in pediatric patients. 287 83

Hypoglycemia of infancy and childhood represents a treatable cause of mental retardation and seizures. Most neonates with hypoglycemia have transient disorders, but with persistent hypoglycemia one must consider hyperinsulinism, hypopituitarism, or hereditary hepatic enzyme deficiencies. Outside of the neonatal period, ketotic hypoglycemia is the most common cause of hypoglycemia in childhood. One cannot overemphasize the value of obtaining certain diagnostic tests at the presentation of spontaneous hypoglycemia, including blood for insulin, cortisol, growth hormone, and urine for ketone bodies. Supportive treatment with intravenous glucose to maintain the blood glucose greater than 50 mg/dl is important until a diagnosis is established allowing specific therapy aimed at the underlying disorder.
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PMID:Hypoglycemia of infancy and childhood. 330 1

A historical cohort study was undertaken to determine the risk of epilepsy in a population of 18 newborns with neonatal hypoglycemia due to insulin excess. Follow-up was 3 years 8 months (range 7 years-1 year 3 months). Insulin excess was associated with maternal diabetes in 13 infants, with an isolated macrosomia in 2 infants, in one case with probable Langerhans hyperplasia, and in 2 newborns only prolonged beta-sympathomimetic therapy was the possible cause of insulin excess. Newborns with anoxia, brain malformation or small for date were excluded. Two newborns had hypoglycemia with epileptic clonic seizures, but only one was later epileptic. In this case, hypoglycemia was severe and persistent (16 hours). Hyperinsulinism was related to Langerhans hyperplasia. CT scan made at ages one and 6 months showed large hypodensity of the frontal and occipital white matter. Visual evoked responses were also abnormal. Visual evoked responses and CT scan normalized at 1 year. In other children, asymptomatic hypoglycemia (n = 11) or symptomatic hypoglycemia without epileptic seizures (n = 5) did not increase the epileptic risk as none of them had epileptic seizure later on. Thus, seizures associated with neonatal hypoglycemia alone seem to increase the epileptic risk with duration and severity of hypoglycemia being also essential prognostic factors.
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PMID:[Neonatal hypoglycemia caused by hyperinsulinism and subsequent epilepsy]. 357 76

The usefulness of ACTH in the treatment of childhood epilepsy is assessed by improvement in the EEG and in the clinical condition. However, pronounced side effects, even serious ones, must be encountered. The most common complications are Cushing syndrome, infections, and arterial hypertension. We report on seven patients with infantile myoclonic seizures, who exhibited myocardial hypertrophy with increased left ventricular function during ACTH treatment. These changes were detected and followed by serial echocardiographic investigations. Within a period of 5 months after the termination of ACTH therapy the abnormal echocardiographic findings disappeared. We believe that the cardiac hypertrophy is ACTH-induced. Based on the various biological effects of ACTH different explanations are proposed: oedema or deposition of glycogen in the myocardial tissue, hyperinsulinism, arterial hypertension and increased inotropic stimulus. Because of our observations, we suggest careful monitoring of children treated with ACTH by performing serial echocardiographic investigations.
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PMID:Cardiac hypertrophy secondary to ACTH treatment in children. 608 43


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