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

Currently, limited data exist on the role of tacrolimus (FK506) in pediatric allogeneic marrow transplantation. Forty-one patients who received tacrolimus as prophylaxis were reviewed, with a median age of 9 years (range 0.2-16 years). Twenty-one patients underwent related donor transplants and 20 underwent unrelated donor transplants. All patients received tacrolimus beginning the day prior to transplant at a dose of 0.03 mg/kg/day by continuous i.v. infusion. When clinically possible, patients were switched to oral therapy in two divided doses, at four times the intravenous dose. Tacrolimus levels were monitored twice a week, and dosages adjusted to maintain serum levels 5-15 ng/ml. Common adverse effects included hypomagnesemia (98%), hypertension (49%), nephrotoxicity (34%), and tremors (32%). Less common side-effects (<10% cases) included seizures and hyperglycemia. The median time to ANC recovery (ANC >500 x 106/l) was 15 days. For the related donor group, the incidence of grade II-IV acute GVHD was 33%, and grade III-IV GVHD 19%. For the unrelated donor group, the incidence of grade II-IV acute GVHD was 55%, and grade III-IV GVHD 30%. Overall, tacrolimus therapy was well tolerated as prophylaxis for acute GVHD in pediatric patients undergoing allogeneic transplantation.
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PMID:Tacrolimus (FK506) and methotrexate as prophylaxis for acute graft-versus-host disease in pediatric allogeneic stem cell transplantation. 1091 26

On any given day a patient seen by the dental hygienist has the potential of experiencing a life-threatening medical emergency. All dental hygiene practitioners should be aware of potential risks that a patient may present, take steps to prevent life-threatening events from occurring, and plan for problems in advance of their happening. The primary goal of this course is to help dental hygienists carry out the ethical, moral, legal, and professional obligation owed any patient. The course will review the basics of medical emergencies, with particular emphasis on those that are most likely to occur in the dental office. Discussion will center on general aspects of prevention and preparation, and will focus on the recognition and emergency treatment of specific conditions. Vasodepressor syncope, orthostatic hypotension, acute adrenal insufficiency, hyperventilation, asthma, heart failure and acute pulmonary edema, cerebrovascular accident seizures, hyperglycemia, hypoglycemia, myocardial infarction, angina pectoris, and anaphylaxis will be emphasized.
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PMID:Medical emergencies in the oral health care setting. 1131 57

Here we describe five patients with Greig cephalopolysyndactyly syndrome (GCPS), including one pair of monozygotic twin boys with a de novo microdeletion involving the chromosomal band 7p13, where various clinical manifestations, in addition to GCPS, were recognized. Besides the twin pair, all patients are unrelated. Since there is a considerable lack of well-defined clinical delineation of the few patients with microdeletions involving 7p13 with GCPS described so far, we focus on the symptoms that are not typically related to GCPS, such as moderate psychomotor retardation, seizures, muscle fiber anomalies, cardiac anomalies, hyperglycemia, and hirsutism. Our observations suggest that in all cases of atypical GCPS, the presence of a cytogenetically detectable microdeletion or a submicroscopic deletion of 7p13 should be suspected.
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PMID:Phenotype of five patients with Greig syndrome and microdeletion of 7p13. 1148 1

Epilepsia partialis continua (EPC) may occur during nonketotic hyperglycemia but has not been described with diabetic ketoacidosis. The authors report a patient with EPC associated with ketotic hyperglycemia. Brain MRI showed two areas of abnormal signal intensity in the left precentral gyrus and in the right cerebellar hemisphere. Hyperglycemia may reduce seizure threshold because of the increase in gamma-aminobutyric acid metabolism and may trigger epileptic discharges.
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PMID:Ketotic hyperglycemia and epilepsia partialis continua. 1150 30

A recent study reported that hyperglycemia of a brief duration worsens, and of long duration reduces, ischemic brain damage. To test whether this is a valid conception, we induced 10 min of transient forebrain ischemia, recorded postischemic seizures, and evaluated brain morphology. The results showed that administration of glucose 2 h before ischemia aggravated brain damage, induced seizures, and caused animal death in the same manner as was previously observed when glucose was given 30 min before ischemia. Thus, the conclusion that the influence of glucose on an ischemic transient is dependent upon the duration of hyperglycemia is unsubstantiated.
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PMID:Does long-term glucose infusion reduce brain damage after transient cerebral ischemia? 1153 37

Focal epileptic seizures can be the first manifestation of a diabetic disorder. Metabolic disturbances, including hyperglycemia, mild hyperosmolality, hyponatremia, and lack of ketoacidosis contribute to the development of partial focal seizures. A review of the medical literature for partial focal seizures is presented, followed by a case study of a patient who developed clonic seizures of the right foot secondary to hyperglycemia, hyponatremia, and hyperosmolality.
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PMID:Clonic focal seizure of the foot secondary to nonketotic hyperglycemia. 1184 63

Reflex seizures are a rare form of epilepsy, the pathogenesis of which is unclear. They have been reported in the setting of non-ketotic hyperglycemia (NKH) and are considered to be neuroendocrine in origin. We report a diabetic patient with movement-induced seizures whose presentation suggests that brain ischemia may be the precipitating event in focal seizures seen in the setting of NKH. We recommend that in such instances a focal lesion such as stroke should be ruled out.
Seizure 2002 Jan
PMID:Reflex seizures and non-ketotic hyperglycemia: an unresolved issue. 1188 64

The clinical and laboratory findings of 21 children with amitraz poisoning were evaluated retrospectively. Poisoning route, signs and symptoms of poisoning, duration of hospitalization and outcome were recorded. The mean age was 3.5 +/- 1.9 years and the ratio of males to females was 1.63. In all cases poisoning was via the oral route. The time from ingestion to onset of symptoms was 30-180 min. Drowsiness (100%) and loss of consciousness (100%) were the most common clinical findings, followed by vomiting (61.9%). Hypotension was observed in 66.7% of cases, bradycardia in 61.9%, respiratory depression in 42.9%, hypothermia in 9.3%, and 14.3% had generalized seizures responsive to diazepam. Hyperglycaemia and glycosuria were detected in 47.6% and 38.1% of cases, respectively. Minimally elevated transaminases and alkaline phosphatase levels were detected in 23.8% of cases. All patients recovered completely and were discharged within 1.0-5.2 days (mean, 2.1 +/- 1.1).
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PMID:Amitraz poisoning in children: retrospective analysis of 21 cases. 1202 30

Mice lacking ClC-3 chloride channels, encoded by the Clcn3 gene, undergo neurodegeneration of the hippocampal formation and retina [Neuron, 29 (2001) 185-196; Genes Cells, 7 (2002) 597-605]. We independently created a mouse lacking the Clcn3 gene which demonstrated similar central nervous system abnormalities, including early postnatal degeneration of retinal photoreceptors. However, we observed a characteristic spatial-temporal sequence of hippocampal neurodegeneration that differs from the pattern previously reported. Anterior-to-posterior degeneration and astrogliosis of the dentate gyrus and hippocampus progressed over months. Sequential loss of hippocampal neuronal subpopulations began in the dentate gyrus and progressed to CA3, followed by CA1 neurons. Projection neurons of the entorhinal cortex degenerated, secondary to the loss of their synaptic targets within the hippocampal formation. Other characteristics of the Clcn3(-/-) mice included an abnormal gait, kyphosis, and absence of hindlimb escape extension upon tail elevation. Spontaneous seizures were observed in four adult Clcn3(-/-) mice, and one mouse died during the event. We hypothesized that neuronal injury may be related to recurrent seizures. Clcn3(-/-) mice had normal serum electrolytes and pH, and exhibited neither hyperglycemia nor rebound hypoglycemia following a glucose load. They displayed a greatly reduced susceptibility to pentylenetetrazole-induced seizures and an abnormally prolonged sedation to benzodiazepines. There was no change in vulnerability to kainic acid-induced seizures. Immunostaining revealed a progressive loss of GABA synthesizing cells in the dentate gyrus. The death of these cells was preceded by increased GABA(A) receptor immunoreactivity. These data suggest that GABA(A) inhibitory neurotransmission is altered in Clcn3(-/-) mice. The increase in GABA(A) receptor density may represent a compensatory response either to chronic excessive excitatory stimuli or reduced inhibitory input from local GABAergic interneurons within the dentate gyrus.
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PMID:Altered GABAergic function accompanies hippocampal degeneration in mice lacking ClC-3 voltage-gated chloride channels. 1247 Aug 59

In adult diabetic patients, periods of hyperglycemia may be associated with exacerbation of focal seizures. Our objective was to determine in the adult rats the correlation between seizure susceptibility and extracellular glucose concentration in two models of seizures. Male rats were injected with two doses of streptozocin (40 mg/kg IP) on 2 consecutive days to induce diabetic hyperglycemia. Controls either received vehicle or were not injected. After 2 weeks, blood glucose concentration was measured, and the rats were subjected to flurothyl seizure test. Another group of rats received glucose solution (20%, 5 ml IP) 30 minutes before testing to induce nondiabetic hyperglycemia. Thresholds for flurothyl-induced clonic and tonic-clonic seizures were determined. Finally, in vitro epileptiform activity was induced in the entorhinal cortex-hippocampal slices from naive rats by perfusing with magnesium-free medium with various glucose concentrations. In additional slices, paired-pulse paradigm was determined in the perforant path. Susceptibility to clonic and tonic-clonic flurothyl-induced seizures positively correlated with blood glucose concentrations as the increased glucose concentration was associated with proconvulsant effects. Similarly, in the in vitro experiments, epileptiform activity was promoted by increased and suppressed by decreased glucose concentrations. Data indicate that, in the adult rats, high glucose concentrations are associated with proconvulsant effects.
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PMID:Correlation between extracellular glucose and seizure susceptibility in adult rats. 1250 52


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