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

Three boys are reported who showed typical autonomic manifestations of hypoglycemia in association with stupor or convulsive seizures two to four hours after eating a meal. During glucose tolerance tests all three children had high peaks in plasma glucose within the first hour and subsequently developed symptoms typical of their clinical disorders on at least one occasion. Two of the boys showed appropriate responses of plasma insulin to oral glucose loading; the third showed a delay in peak plasma insulin. All three children responded promptly and completely to simple dietary management.
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PMID:The prevention of postprandial seizures in children. 93 48

Systematic exercise increased the organism's sensitivity to the metabolic effect of insulin. When trained animals were subjected to low doses of insulin they showed a more significant decrease in the blood sugar and the free fatty acid contents as compared with the control (i.e. unadapted to systematic exercise) animals. No visible difference in glycogen contents was found due to the effect of hypoglycemic seizures which developed rather rapidly and were more obvious in trained animals. Administration of large doses of insulin did not cause any difference in the metabolic reactions of trained and untrained animals.
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PMID:[The effect of adaptation to increased muscular activity on bodily sensitivity to insulin]. 122 97

Eleven men with disabling reactive hypoglycemia, in a range of 12 to 50 mg per 100 ml, were treated an average of seven years after gastric surgery with a 10 cm reversed jejunal segment. The reversal was placed at the gastric outlet in six patients and just below the ligament of Treitz in five. The former technic produced a somewhat better correction of hypoglycemia than did the latter. A good result was obtained in all eleven and none has had recurrence of seizures or fainting. Whereas the average minimal blood sugar before reversal was 34 mg per 100 ml, after reversal it was increased to 64 mg per 100 ml. The most severe hypoglycemia was noted in a patient after vagotomy and pyloroplasty. We recommend that all patients with dumping syndrome undergo glucose tolerance tests and plasma insulin determinations to ascertain whether they have reactive hypoglycemia. It is our conclusion that introduction of a reversed jejunal segment can control refractory reactive hypoglycemia resulting from previous gastric surgery.
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PMID:Treatment of postoperative reactive hypoglycemia by a reversed intestinal segment. 124 49

A functional, insulin-secreting pancreatic (islet cell) carcinoma was diagnosed in a 17-year-old male Siamese cat. Diagnosis was made on the basis of clinical signs (i.e., seizures and stupor) that resolved temporarily after correction of hypoglycemia with feeding or intravenous administration of glucose, the finding of an inappropriately increased serum insulin concentration in the face of hypoglycemia, and prolonged resolution of hypoglycemia after surgical removal of the tumor. Primary islet cell tumor of the pancreas was confirmed by biopsy. The cat died 18 months later, and necropsy revealed metastases to regional lymph nodes and liver. Specimens of the tumor and metastatic lesions both stained positively for insulin.
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PMID:Insulin-secreting pancreatic (islet cell) carcinoma in a cat. 132 Jan 19

The clinical features of seven patients with non-ketotic hyperglycaemia who developed focal seizures are presented. All patients were alert except one who was mildly confused. Glucose values varied from 17.8 to 55.1 mmol/l, while calculated osmolarity values were elevated in all cases to a mild or moderate extent (299.1 to 346.5 mmol/l). In three cases diabetes mellitus was a new diagnosis. Four patients had recurrent episodes of focal seizures when glycaemic control was lost. Movement induced or kinesigenic seizures were seen in three cases and epilepsia partialis continua in one case. Seizures associated with hyperglycaemia are resistant to anticonvulsant treatment and respond best to insulin and rehydration. Focal seizures in adults may indicate diabetes mellitus.
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PMID:Focal seizures and non-ketotic hyperglycaemia. 156 79

The EEG data were compared among 260 epileptic patients, including 94 patients loaded with schizophrenia, 71 patients loaded with epilepsy, 95 patients without revealed hereditary loading with mental diseases, and among 32 schizophrenics in whom epileptic seizures could be seen during insulin therapy. Hereditary loading with epilepsy or schizophrenia in epileptic patients together with latent epileptic schizophrenia ++predisposition influence the characteristics of the electroencephalogram.
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PMID:[ECG characteristics in epilepsy of homo- and heterospecific hereditary origin and schizophrenia with latent epileptic predisposition]. 166 76

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 case of a non diabetic 6-year-old boy affected by Down's syndrome, who developed hyperosmolar hyperglycemic non-ketotic coma following the infusion of hypertonic dextrose solution during general anesthesia for a surgical procedure for cryptorchidism is reported. Following surgery, the patient remained deeply comatose and generalized seizures occurred. Hyperosmolarity due to hyperglycemia and acidosis were reduced by administration of insulin at low rate, hypotonic saline and sodium-bicarbonate solutions. The patient's clinical conditions promptly improved following normalization of blood glucose levels. An oral glucose tolerance test performed three months later was normal. The authors emphasize the potential risk of hyperosmolar hyperglycemic non-ketotic coma also in non diabetic patients treated with hypertonic dextrose solutions, during surgery events.
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PMID:A case of hyperglycemic hyperosmolar non-ketotic coma during anesthesia: a possible cause of failed re-awakening. 168 69

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

Major histocompatibility complex (MHC) molecules are not normally expressed in the central nervous system (CNS). However, aberrant expression has been observed in multiple sclerosis lesions and could contribute to the destruction of myelin or the myelinating cells known as oligodendrocytes. The mechanism of cell damage associated with aberrant MHC molecule expression is unclear: for example, overexpression of class I and class II MHC molecules in pancreatic beta cells in transgenic mice leads to nonimmune destruction of the cells and insulin-dependent diabetes mellitus. We have generated transgenic mice that express class I H-2Kb MHC molecules, under the control of the myelin basic protein promoter, specifically in oligodendrocytes. Homozygous transgenic mice have a shivering phenotype, develop tonic seizures and die at 15-22 days. This phenotype, which we term 'wonky', is due to hypomyelination in the CNS, and not to involvement of the immune system. The primary defect appears to be a shortage of myelinating oligodendrocytes resulting from overexpression of the class I MHC molecules.
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PMID:Dysmyelination in transgenic mice resulting from expression of class I histocompatibility molecules in oligodendrocytes. 192 55


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