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

Although preischemic hyperglycemia is known to aggravate damage due to transient ischemia, it is a matter of controversy whether or not this is a result of the exaggerated acidosis. It has recently been reported that although tissue acidosis of a comparable severity could be induced in normoglycemic dogs by an excessive rise in arterial CO2 tension, short-term functional recovery was improved, rather than compromised. In the present experiments we induced excessive hypercapnia (PaCO2, approximately 300 mm Hg) in normoglycemic rats before inducing forebrain ischemia of 10-min duration. This reduced the brain extracellular pH to values normally encountered in hyperglycemic rats subjected to ischemia. The events induced by hypercapnia clearly enhanced ischemic brain damage, as assessed histologically after 7 days of recovery. We hypothesize that the decisive event was an exaggerated decrease in extra- and intracellular pH and that the results thus demonstrate an adverse effect of acidosis. However, since postischemic seizures did not occur in the hypercapnic ischemic rats, the results also demonstrate that changes in intra-extracellular pH and bicarbonate concentrations modulated ischemic damage in an unexpected way.
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PMID:Acidosis induced by hypercapnia exaggerates ischemic brain damage. 811 21

When glucose utilisation is impaired due to decreased insulin effect, ketones are produced by the liver from free fatty acids to supply an alternate source of energy. This adaptation may be associated with severe metabolic acidosis and tends to occur in patients with type I (insulin-dependent) diabetes mellitus. In addition, hypovolemia is an almost invariable finding with marked hypoglycemia and is primarily induced by the associated glucosuria. Ketoacidosis stimulates both the central and peripheral chemoreceptors controlling respiration, resulting in alveolar hyperventilation (Kussmaul's respiration). With the ensuing fall in pCO2 the patient tries to raise the extracellular pH. A fruity odor of acetone on the patient's breath sometimes suggests that ketoacidosis is present. The classical triad of symptoms associated with hyperglycemia are polyuria, polydipsia, and weight loss. Circulatory insufficiency with hypotension is not uncommon due to the marked fluid loss and acidemia. In more severely affected patients, neurologic abnormalities may be seen, including lethargy, seizures or coma. Some patients also have marked vomiting and abdominal pain. The history and physical examination may provide important clues to the presence of uncontrolled diabetes mellitus. Once suspected, the diagnosis can be easily confirmed by measuring the plasma glucose concentration. Glucosuria and ketonuria can be semiquantitatively detected with reagent sticks. Blood gas analysis and anion gap give objective information as to the severity of the metabolic acidosis. Therapy must be directed toward each of the metabolic disturbances: hyperosmolality, ketoacidosis, hypovolemia and potassium, and phosphate depletion. The mainstays of therapy are the administration of low-dose insulin and volume repletion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ketoacidotic diabetic metabolic dysregulation: pathophysiology, clinical aspects, diagnosis and therapy]. 817 67

A 59-year-old female had been treated for epilepsy over 20 years. She had frequent convulsive seizures in spite of medication and was admitted to our hospital in status epilepticus. CT showed low density cyst with calcified wall at right suprasellar region and irregular ring enhancement in the frontal lobe which was continuous with the cyst. Angiography revealed tumor stain in the venous phase. The frontal mass was removed with evacuation of the cyst. Pathological findings were suggestive of squamous cell carcinoma arising from the epithelial component of the pre-existing dermoid cyst. The patient died six months after the operation with severe hyperglycemia, ketoacidosis and hypotension probably due to chemical meningitis and hydrocephalus.
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PMID:A squamous cell carcinoma originated from intracranial dermoid cyst. 844 93

Generalized seizures can induce both hypertension and hyperglycemia which may aggravate preexisting cerebral or medical conditions in patients. In vivo fluorescent imaging of regional cortical blood flow and brain intracellular pH (pHi) was performed in fasted New Zealand rabbits (n = 35) in which either mean arterial blood pressure (MABP) or serum glucose was the covaried factor during pentylenetetrazole induced status epilepticus under 1.5% inspired halothane. Baseline brain pHi and regional cortical blood flow were 7.02 +/- 0.02 and 51.1 +/- 1.7 ml/100 g/min, respectively. Following seizure induction, MABP increased to 105 mm Hg and brain pHi fell to 6.79 +/- 0.03 within 15 min and remained at this level for 1 h (P < 0.001). With normalization of MABP during ongoing seizures, there was no worsening in brain pHi despite a significant decrease in regional cortical blood flow. Hyperglycemia decreased pHi to 6.71 +/- 0.02 compared to 6.84 +/- 0.04 in normoglycemic animals (P < 0.001). Using pHi as a cerebral metabolic index, these data suggest that normalization of MABP does not increase metabolic injury while hyperglycemia does significantly worsen brain acidosis. Therefore, administration of glucose to patients with status epilepticus should be avoided unless there is documented hypoglycemia.
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PMID:Effect of arterial blood pressure and serum glucose on brain intracellular pH, cerebral and cortical blood flow during status epilepticus in the white New Zealand rabbit. 845 50

Generalized convulsive status epilepticus (GCSE) is accompanied by a marked increase in plasma catecholamines. This produces a number of changes in general systemic physiology including hypertension, tachycardia, cardiac arrhythmias, hyperglycemia, acidosis, and hyperpyrexia. If SE is stopped quickly, these changes are self-correcting and do not produce an increased risk of neuropathology. However, if seizures continue, many of the early physiologic changes reverse, and late status epilepticus is marked by hypotension, hypoglycemia, pulmonary edema and a continued acidosis and elevation of body temperature. Prevention of serious hypoglycemia, maintenance of adequate systemic blood pressure to provide adequate cerebral perfusion, and normalizing the body temperature will minimize or prevent neuropathologic sequelae to SE of extended duration.
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PMID:Systemic effects of generalized convulsive status epilepticus. 846 91

The present experiments were undertaken to study how preischemic hyperglycemia, which is known to exaggerate ischemic damage and to trigger delayed postischemic seizures affects the bioenergetic state and the intracellular pH (pHi) of brain tissue at early (6 h) and late (18 h) recirculation times. To that end, normo- and hyperglycemic rats were subjected to 10 min of forebrain ischemia, and neocortical tissue was frozen in situ for analyses of labile energy metabolites. Animals with preischemic hyperglycemia failed to show a postischemic reduction of the phosphorylation state of the adenine nucleotide pool, or a rise in tissue lactate content, nor did they show a change in tissue redox state. However, the hyperglycemia led to a rise in phosphocreatine (PCr) content after 6 h of recirculation. Calculations of intracellular pH (pHi) from the creatine kinase (CK) equilibrium showed a rise in pHi above normal, a finding which was supported by a limited number of 5,5-dimethyl[2-14C]oxazolidine-2,4-dione (DMO) measurements. The preischemic hyperglycemia also blunted the postischemic rise in tissue glycogen content, which is usually observed in normoglycemic rats. The results thus fail to reveal that the hyperglycemia-triggered, massive exaggeration of ischemic brain damage, which is heralded by generalized seizures after 18-24 h of recirculation, is preceded by mitochondrial dysfunction of a degree which affects the bioenergetic state or the redox potential of the tissue. However, the results suggest that the hyperglycemia enhances and/or prolongs the postischemic alkalosis. It is discussed whether the rise in pH contributes to the mitochondrial dysfunction which subsequently develops.
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PMID:Changes in labile energy metabolites, redox state and intracellular pH in postischemic brain of normo- and hyperglycemic rats. 883 45

Seizures and epilepsy in the elderly are an important and increasingly common clinical problem. Major known causes include cerebrovascular disease, brain tumor, degenerative disorders such as Alzheimer disease and cerebral amyloid angiopathy, and toxic-metabolic syndromes such as nonketotic hyperglycemia, postcardiac arrest, and drug-induced seizures. Recognition of seizures may be complicated by relatively unique clinical presentations and differential diagnosis. Nonconvulsive status epilepticus may present as recurrent episodes of confusion. The electroencephalogram is less useful than in the pediatric age group, but has a role in the evaluation of a first seizure and may rarely show characteristic patterns, such as poststroke periodic lateralized epileptiform discharges. Convulsive status, especially that associated with drug toxicity, is associated with increased mortality in the elderly. Pharmacological treatment is complicated by age-related changes in pharmacokinetics and pharmacodynamics and drug-drug and drug-disease interactions. Some of the new antiepileptic drugs may offer advantages for use in the elderly. Oxcarbazepine has fewer drug interactions than carbamazepine, and gabapentin has one, a reduction of felbamate renal elimination. Vigabatrin causes little cognitive dysfunction, while drugs that reduce excitatory amino acid neurotransmission, such as lamotrigine and felbamate, have potentially protective effects in patients with ischemic cerebrovascular disease. The use of barbiturates, primidone, the benzodiazepine clobazam, and the calcium blockers flunarizine and cinnarizine should preferably be avoided in the elderly.
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PMID:Seizures and epilepsy in the elderly. 943 89

Severe partial seizures may be the presenting feature of nonketotic hyperglycemia in older adults, but cases in children are rare. We report three teenagers with well-controlled epilepsy who suddenly developed intractable partial seizures poorly responsive to anticonvulsants. Blood glucose levels were measured only after several days of hospitalization for frequent seizures when mild polyuria and polydipsia were first noted. Glucose levels were high with mild ketosis and acidosis in one patient and no ketosis in two. With institution of insulin, there was prompt cessation of seizures. The patients were diagnosed as having type I insulin-dependent diabetes mellitus and require ongoing insulin treatment. Hyperglycemia should be considered in children with epilepsy who develop intractable seizures.
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PMID:Insulin-dependent diabetes mellitus presenting in children as frequent, medically unresponsive, partial seizures. 913 91

Administration of endogenous corticosterone to intact animals induces calbindin-D28k protein in the hippocampal CA1-CA2 subfields. The fact that this effect on calbindin-D28k was shown to be specific for the hippocampus argues for a receptor-mediated effect on gene expression. In addition, chronic pretreatment with corticosterone aggravates ischemia-induced neuronal damage in the CA3-CA4 subfields. This effect is similar to that of preischemic hyperglycemia, which also induces postischemic seizures and aggravates brain damage, since corticosterone raises blood glucose level and enhances tissue lactic acidosis during ischemia. The energetically compromising qualities of corticosterone indicates that it is a key factor in hippocampal vulnerability. We assume that the increase of calbindin-D28k expression in the CA1-CA2 subfields in corticosterone-treated animals is an adaptive response to the exogenous stress. The lack of adaptive response in CA3-CA4 neurons endangers them by impairing the ability of these neurons to counteract the deleterious effects of calcium. This finding, supports: (1) the hypothesis that corticosterone treatment, when paired with an ischemic insult, causes a prolonged elevation of neuronal [Ca2+]i, in an energy dependent manner, probably through the reduction of calcium efflux and (2) that neurons which do contain calbindin-D28k are particularly predisposed to ischemic insults. The CA1-CA2 neurons express high amounts of calbindin-D28k under stress conditions because their activity may involve a high rate of calcium buffering.
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PMID:Synergy between chronic corticosterone treatment and cerebral ischemia in producing damage in noncalbindinergic neurons. 950 Sep 60

Reflex seizures induced by movement are typically evoked by sudden or unattended motor actions. However, tonic seizures may also be triggered by slow movements as observed in nonketotic hyperglycemia or in "praxis-induced epilepsy." We report the case of a young, nondiabetic patient affected by recurrent partial tonic postural seizures precipitated by slow movements which were unrelated to cognitive tasks. Ictal EEG did not permit location of the epileptogenic brain region. However, the clinical features suggest possible involvement of the supplementary motor area.
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PMID:Movement-induced seizures: a case report. 957 97


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