Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seizures are a documented complication to cerebral ischemia. After 10 min of forebrain ischemia in rats, preischemic hyperglycemia invariably leads to severe, most often fatal epileptic attacks. This outcome is related to the exaggerated lactic acidosis, which has been suggested as a possible contributor to severe membrane changes and widespread edema. To find out if circulating hormones or plasma energy substrates modulate this additive damage caused by the hyperglycemia, plasma concentrations of of corticosterone, epinephrine, norepinephrine, dopamine, glucagon, insulin, glucose, free fatty acids (FFA), 3-hydroxybutyrate, and acetoacetate were measured before and in the early recirculation period after 15 min of forebrain ischemia in the rat. Plasma corticosterone levels did not differ between the normo- and hyperglycemic groups. Although not significantly different from control, the catecholamine levels showed a tendency to be higher in the hyperglycemic groups. Therefore, because catecholamines have been reported to have a protective effect during ischemia the present result cannot explain why hyperglycemia aggravates the ischemic damage. Insulin levels seemed to increase during ischemia but not significantly. Levels quickly returned to normal after 30 min of recirculation. FFA concentrations were reduced after the induction of ischemia and appeared lower in all hyperglycemic groups. The level of one of the ketone bodies, 3-hydroxybutyrate, showed a significant decrease in hyperglycemic ischemia in all groups compared with normoglycemic ischemia. The same tendency was seen for acetoacetate. Results are compatible with a protective role of ketone bodies in ischemia. It is concluded that among the hormones and substrates studied only the ketone body concentrations qualify as a modulator of the exaggerated brain damage after ischemia in hyperglycemic subjects.
 ...
PMID:Ischemia in normoglycemic and hyperglycemic rats: plasma energy substrates and hormones. 211 Apr 23

Four insulin-treated diabetic patients presented over a 2-year period in hypoglycaemic coma and died secondary to this. At autopsy, there were widespread neuropathological changes, in all four cases consistent with hypoglycaemic damage. Abnormalities were also found in areas regarded as generally being spared in hypoglycaemic brain injury, particularly the brain stem, thalamus, globus pallidus, and cerebellum, and these lesions may relate to seizure activity and cardio-respiratory depression secondary to the hypoglycaemia. Although more than one aetiological factor may be contributing, it is concluded that the neuropathological changes in diabetic patients dying in hypoglycaemic coma are extremely diverse.
 ...
PMID:Fatal hypoglycaemia in insulin-treated diabetes mellitus: clinical features and neuropathological changes. 214 89

We have reported the case of a 69-year-old woman with a hugh benign fibrous tumor of the left pleura and hypoglycemic seizures. Increased preoperative levels of insulin-like growth factor (IGF II) were present; insulin level was low and plasma levels of somatomedin C were normal. After resection of the 2,400 gm tumor, blood sugar level has remained normal, and IGF II has fallen to normal limits. This appears to be the first reported case documenting elevated serum IGF II in association with a benign fibrous pleural tumor.
 ...
PMID:Benign fibrous pleural tumor with elevation of insulin-like growth factor and hypoglycemia. 216 71

Many classes of pharmacological agents have been implicated in cases of drug-induced seizures. The list includes antidepressant drugs, lithium salts, neuroleptics, antihistamines (H1-receptor antagonists), anticonvulsants, central nervous system stimulants, general and local anaesthetics, antiarrhythmic drugs, narcotic and non-narcotic analgesics, non-steroidal anti-inflammatory drugs, antimicrobial agents, antifungal agents, antimalarial drugs, antineoplastic drugs, immunosuppressive drugs, radiological contrast agents and vaccines. For each of these classes of drugs, this article offers a revision of the literature and emphasises in particular the frequency of the adverse reaction, its clinical presentation, its presumed epileptogenic mechanism and the therapeutic strategy for the management of drug-induced seizures. An attempt is also made to distinguish seizures induced by standard dosages from those provoked by accidental or self-induced intoxication. For some classes of drugs such as antidepressants, neuroleptics, central nervous system stimulants (e.g. theophylline, cocaine, amphetamines) and beta-lactam antibiotics, seizures are a well recognised adverse reaction, and a large body of literature has been published discussing exhaustively the major aspects of the issue; sufficient data are available also for the other classes of pharmacological agents mentioned above. In contrast, several other drugs [e.g. allopurinol, digoxin, cimetidine, protirelin (thyrotrophin releasing hormone), bromocriptine, domperidone, insulin, fenformin, penicillamine, probenecid, verapamil, methyldopa] have not been studied thoroughly under this aspect, and the only source of information is the occasional case report. This review does not address the issue of seizures induced by drug withdrawal.
 ...
PMID:Clinical features, pathogenesis and management of drug-induced seizures. 218 49

"A neuroendocrine hypothesis to explain the clinical activity of convulsive therapy is described. The hypothesis is based on the diabetes/insulin model and suggests that hypothalamic dysfunction with an insufficiency of a mood-maintaining peptide is the basis for affective disorders. Repeated seizures enhance the production and release of the hypothalamic peptide antidepressin - the active principle that relieves both neuroendocrine and behavioral abnormalities.
 ...
PMID:A neuroendocrine view of ECT. 227 10

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.
 ...
PMID:[Nesidioblastosis. Apropos of 12 new cases]. 229 91

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.
 ...
PMID:Hypoglycemic hemiplegia. 235 82

Acromegaly was diagnosed in 14 middle-aged to old cats of mixed breeding. Thirteen (93%) of the cats were male and one was female. The earliest clinical signs in the 14 cats included polyuria, polydipsia, polyphagia, all of which were associated with untreated diabetes mellitus. All developed severe insulin resistance within a few months; peak insulin dosages required to control severe hyperglycemia ranged from 20 to 130 U per day. Other clinical findings weeks to months after diagnosis included enlargement of one or more organs (e.g., liver, heart, kidneys, and tongue) (n = 14), cardiomyopathy (n = 13), increase in body size and weight gain (n = 8), nephropathy associated with azotemia and clinical signs of renal failure (n = 7), degenerative arthropathy (n = 6), and central nervous system signs (i.e., circling and seizures) caused by enlargement of the pituitary tumor (n = 2). The diagnosis of acromegaly was confirmed by demonstration of extremely high basal serum growth hormone concentrations (22 to 131 micrograms/l) in all cats. Computerized tomography disclosed a mass in the region of the pituitary gland and hypothalamus in five of the six cats in which it was performed. Two cats were treated by cobalt radiotherapy followed by administration of a somatostatin analogue (octreotide), whereas two cats were treated with octreotide alone. Treatment had little to no effect in decreasing serum GH concentrations in any of the cats. Eleven of the 14 cats were euthanized or died four to 42 months (median survival time, 20.5 months) after the onset of acromegaly because of renal failure (n = 2), congestive heart failure (n = 1), concomitant renal failure and congestive heart failure (n = 3), progressive neurologic signs (n = 2), persistent anorexia and lethargy of unknown cause (n = 1), the owner's unwillingness to treat the diabetes mellitus (n = 1), or unknown causes (n = 1). Results of necropsy examination in ten cats revealed a large pituitary acidophil adenoma (n = 10), marked left ventricular and septal hypertrophy (n = 7), dilated cardiomyopathy (n = 1), arthropathy affecting the shoulder, elbow, or stifle (n = 5), and glomerulopathy characterized by expansion of the mesangial matrix and variable periglomerular fibrosis (n = 10).
 ...
PMID:Acromegaly in 14 cats. 240 66

Fifteen children with infantile spasms and a hypsarrhythmic EEG defined by EEG-videotelemetry monitoring received a regimen of high-dose (150 IU/m2/d) ACTH for their seizures. We carried out an endocrinologic evaluation before and after initiation of the ACTH and conducted a time course study of plasma ACTH and cortisol levels after ACTH dosing. Spasms were controlled and the EEG normalized in 14 of the 15 children. Prior to starting ACTH therapy all the patients had normal prolactin, insulin, cortisol, and ACTH levels in plasma and normal thyroid function. Although the pattern of rise of ACTH levels in plasma after ACTH dosing was similar in all the children, there was great individual variation in the absolute concentrations. However, both the pattern of rise and absolute level of cortisol in plasma after ACTH was highly predictable in all patients. Plasma cortisol rose rapidly within 1 hour of ACTH administration and continued a slower rise for 12 to 24 hours after the ACTH dose. High-dose ACTH therapy seems quite effective in infantile spasms, perhaps because of a sustained high level of plasma cortisol. This sustained plateau of cortisol may be more effective in controlling infantile spasms than the pulse effect expected with oral steroids or lower doses of ACTH.
 ...
PMID:Treatment of infantile spasms with high-dose ACTH: efficacy and plasma levels of ACTH and cortisol. 254 19

Eighteen cases of insulinoma treated at the Instituto Nacional de la Nutricion in Mexico City are presented. The cases were operated on between 1959 and 1988, and include 10 women and 8 men with a mean age of 38. The duration of symptoms ranged between 4 and 96 months with a median of 27; 78% of the patients had neuropsychiatric symptoms, 61% seizures, and 55% loss of consciousness. One of the patients had evidence of type I multiple endocrine neoplasia. Diagnosis was established in all the patients with the demonstration of Whipple's triad and also with an elevated insulin determination in the last nine patients. In six cases the insulinoma was enucleated; in two a Whipple procedure was performed; in nine a distal pancreatectomy and in the remaining patient only resection of hepatic metastases; 67% of the tumors were diagnosed as benign solitary adenomas, 16.5% as carcinomas and the same number as hyperplasia. Operative mortality was 5.5%, and morbidity 44%. The three carcinomas survived 6, 8 and 36 months. Disappearance of the hypoglycemic symptoms was obtained in 93% of the cases of adenoma and hyperplasia.
 ...
PMID:[Surgical treatment of insulinoma. Experience at the Salvador Zubiran National Nutrition Institute]. 255 Oct 25


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>