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

Adequate analgesia and sedation with adequate respiratory and hemodynamic control are needed during brain surgery in awake patients. In this study, a protocol using clonidine premedication, intraoperative propofol, remifentanil, and labetalol was evaluated prospectively in 25 patients (aged 50 +/- 16). In all but one patient, no significant problems regarding cooperation, brain swelling, or loss of control were noticed, and it was not necessary to prematurely discontinue any of the procedures. One patient, who was uncooperative and hypertensive, became apneic with increasing sedation, and needed a laryngeal mask airway inserted. Patients were hemodynamically stable; elevated systolic blood pressure (>or= 150 mm Hg) was measured infrequently, and there were no events of significant hypotension, tachycardia, or bradycardia. Events of hypoxemia (SAO2 <or= 95%), severe hypoxemia (SaO2 <or= 90%), or hypoventilation (respiratory rate <or=8 minute), were frequent in the first ten patients, but the incidence decreased significantly in subsequent patients (P < .001). Three patients developed a focal neurologic deficit, and two patients experienced intraoperative seizures. Nausea and vomiting were not recorded in any of the patients. Although these findings attest to the safety of awake craniotomy, they demonstrate the difficulty of achieving adequate sedation without compromising ventilation and oxygenation. The learning curve of using a new protocol and a new potent anesthetic drug is emphasized.
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PMID:Monitored anesthesia care using remifentanil and propofol for awake craniotomy. 1142 2

Leukoencephalopathy with severe hypertension is a recently described entity in nephrology, with only a few case reports to date in children. We prospectively studied 18 children with severe hypertension to evaluate the clinical features, severity, reversibility, and prognosis. All were subjected to clinical and biochemical tests, magnetic resonance imaging (MRI), and magnetic resonance angiography (MRA). Headache was reported in 16 children, 13 had confusion and drowsiness, 12 had nausea and vomiting, and 9 had visual disturbances, seizure, and dyspnea. Only 2 had focal neurological deficit (1 with right facial palsy and another with right lateral rectus palsy). Of these 18 children, 14 patients had hypertensive retinopathy and 4 had normal fundus. MRI revealed leukoencephalopathic changes in 16 of 18 patients. These changes were bilateral occipito-parietal in 9 patients, diffuse white/gray matter lesion in 2, brain stem hyperintensity in 2, and hemorrhagic lesion in 3. On MRA, 11 of 18 patients had attenuation of cerebral arteries of different degree. On follow-up, MRI findings resolved in all except 3 patients and all patients had normal MRA, except for 1 with persistent minimal attenuation and another with spasm in all vessels. We conclude that leukoencephalopathy with severe hypertension is reversible both clinically and radiologically in the majority of children after the control of hypertension. However, a few patients may have residual damage and may need psychometric analysis and follow-up for neurodevelopmental sequelae.
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PMID:Is reversible posterior leukoencephalopathy with severe hypertension completely reversible in all patients? 1450 62

We present 2 cases, one eclamptic patient and one noneclamptic patient, of headache, cortical blindness, and seizures. Both patients demonstrated findings consistent with posterior leukoencephalopathy syndrome. Posterior leukoencephalopathy syndrome is a rapidly evolving neurologic condition that is characterized by headache, nausea and vomiting, seizures, visual disturbances, altered sensorium, and occasionally focal neurologic deficits. Posterior leukoencephalopathy syndrome can be triggered by numerous conditions, including preeclampsia-eclampsia, and can be seen in the postpartum period. It is characterized predominately by white matter vasogenic edema of the occipital and posterior parietal lobes. This condition can be difficult to differentiate clinically from cerebral ischemia, and magnetic resonance imaging with diffusion-weighted imaging and apparent diffusion coefficient are needed to do so. In most cases of posterior leukoencephalopathy syndrome, the prognosis is excellent, with full resolution of symptoms.
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PMID:Postpartum blindness: two cases. 1474 15

The absence of osmotic diuresis modifies the effects of hyperglycemia on body fluids in patients with advanced renal failure. To determine the relationship between clinical manifestations and abnormalities in tonicity and extracellular volume in such patients, we analyzed 43 episodes of severe dialysis-associated hyperglycemia (serum glucose exceeding 600 mg/dL) treated only with insulin. The main manifestations were dyspnea in 22 cases (pulmonary edema in 19), nausea and vomiting in 15, coma in 13 and seizures in 3, while 5 patients had no symptoms. Treatment with insulin resulted in a decrease in serum glucose value from 913 +/- 197 mg/dL to 170 +/- 78 mg/dL, an increase in serum sodium level from 125 +/- 5 to 136 +/- 5 mmol/L, and a fall in calculated serum tonicity value from 300 +/- 13 to 282 +/- 11 mmol/kg (all at p < 0.001). The ratio of the change in serum sodium level over change in serum glucose concentration was -1.50 +/- 0.22 mmol/L per 100 mg/dL. The percent increase in extracellular volume secondary to hyperglycemia developing from the prior euglycemic state and calculated from changes in serum sodium and chloride concentrations, was 10.9% +/- 4.6% (1.5% +/- 0.6% per 100 mg/dL increase in serum glucose level). All clinical manifestations dissipated after correction of hyperglycemia in 42 patients. One woman developed during treatment a fatal myocardial infarction. Dialysis patients with severe hyperglycemia may develop symptoms as a result of hypertonicity and extracellular expansion. Insulin alone may be sufficient treatment for these symptoms. The changes in serum tonicity and electrolytes during treatment are consistent with theoretical predictions.
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PMID:Serum tonicity, extracellular volume and clinical manifestations in symptomatic dialysis-associated hyperglycemia treated only with insulin. 1552 Dec 14

Brain tumours are a frequent cause of intracraneal hypertension syndrome, clinically manifested by headache, nausea and vomiting, and a decrease in the level of consciousness. The keypoint sign of intracraneal hypertension is papilloedema. Other manifestations depend on the localization of the tumour, appearing as neurological focality and seizures. The causes of intracranial hypertension of tumoural origin are the mass effect of the tumour, brain edema, the possibility of intratumoural haemorrhage and hydrocephalus caused by obstruction in the circulation of cerebrospinal fluid. The treatments employed, medical or surgical, act against these causes.
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PMID:[Treatment of intracranial hypertension of malign tumour origin]. 1572 15

Abdominal epilepsy is an uncommon syndrome in which gastrointestinal complaints, most commonly abdominal pain, result from seizure activity. It is characterized by (1) otherwise unexplained, paroxysmal gastrointestinal complaints, (2) symptoms of a central nervous system disturbance, (3) an abnormal electroencephalogram with findings specific for a seizure disorder, and (4) improvement with anticonvulsant medication. We review the history of the syndrome and analyze all 36 cases reported in the English literature from the last 34 years. The most common gastrointestinal symptoms include abdominal pain, nausea and vomiting, while the most common neurological symptoms include lethargy and confusion. After exclusion of more common etiologies for the presenting complaints, workup should proceed with an electroencephalogram. Where the diagnosis is seriously considered, neurological consultation should be considered. Treatment typically begins with anticonvulsant medication, and resolution of symptoms with therapy helps to confirm the diagnosis.
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PMID:Abdominal epilepsy. 1583 92

We present a case of anesthesia for electroconvulsive (ECT) therapy that was complicated by emetic sensitivity to etomidate, fragile ictal threshold, and mild pseudocholinesterase deficiency. The anesthetic was designed in this patient taking all his issues in consideration. The mild pseudocholinesterase deficiency necessitated a (50-75%) reduction in succinylcholine dosage, careful monitoring of the train of four, and postictal amnestic coverage to prevent paralysis upon waking. The significant emetic response to etomidate prompted substitution to propofol and preemptive ondansetron. Propofol significantly raised the ictal threshold but significantly reduced the postprocedural emesis. Eventually, this clinical challenge was resolved with adjunctive use of low-dose etomidate and remifentanil. This combination preserved the ictal parameters, providing patient comfort, good clinical response, and therapeutic efficacy. Although seizure duration and quality often are restored with hyperventilation and caffeine, this case necessitated a return to etomidate for the restoration of satisfactory ictal parameters. Although this effect of remifentanil has been described with methohexital, and etomidate with alfentanil, to the best of our knowledge, this is the first reported case of adjunctive remifentanil with etomidate for preserving ictal threshold. The outpatient course of ECT was thus completed with all psychiatric and anesthetic goals satisfied: adequate seizure quality and duration, no paralysis upon waking, no post-ECT nausea and vomiting, and patient satisfaction. Anesthesiologists should be aware of factors influencing the seizure duration and, keeping in mind the coexisting medical conditions of the patient, adjustments should be made to get the best possible outcome.
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PMID:Customized anesthetic preservation of ictal threshold in electroconvulsive therapy: role of adjunctive remifentanil with etomidate. 1590 58

Phenytoin toxicity may result from intentional overdose, dosage adjustments, drug interactions, or alterations in physiology. Intoxication manifests predominantly as nausea, central nervous system dysfunction (particularly confusion, nystagmus, and ataxia), with depressed conscious state, coma, and seizures occurring in more severe cases. Cardiac complications such as arrhythmias and hypotension are rare in cases of phenytoin ingestion, but they may be seen in parenteral administration of phenytoin or fosphenytoin. Deaths are unlikely after phenytoin intoxication alone. A greatly increased half-life in overdose due to zero-order pharmacokinetics can result in a prolonged duration of symptoms and thus prolonged hospitalization with its attendant complications. The mainstay of therapy for a patient with phenytoin intoxication is supportive care. Treatment includes attention to vital functions, management of nausea and vomiting, and prevention of injuries due to confusion and ataxia. There is no antidote, and there is no evidence that any method of gastrointestinal decontamination or enhanced elimination improves outcome. Activated charcoal should be considered if the patient presents early; however, the role of multiple-dose activated charcoal is controversial. Experimental studies have proven increased clearance rates, but this effect has not been translated into clinical benefit. There is no evidence that any invasive method of enhanced elimination (such as plasmapheresis, hemodialysis, or hemoperfusion) provides any benefit. This article provides an overview of phenytoin pharmacokinetics and the clinical manifestations of toxicity, followed by a detailed review of the various treatment modalities.
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PMID:Phenytoin poisoning. 1617 88

We studied 30 pediatric patients with malignant (n = 16) or nonmalignant (n = 14) conditions. The preparative regimen consisted of fludarabine, intravenous (IV) busulfan (Bu) for 2 daily doses, and antithymocyte globulin before stem cell transplantation. A test dose of IV Bu (0.8 mg/kg), anticipated to target an area under the concentration-time curve (AUC) of 800 to 1200 micromol.min, was followed later by 2 daily doses adjusted according to the pharmacokinetics (PK) to target an AUC of 3200 to 4800 micromol.min. The median test dose AUC was 953 micromol.min (range, 439-1315 micromol.min). The median AUC of single daily doses was 3798 micromol.min (range, 1511-7254 micromol.min). PK-based dose modification was required in 20 patients: 12 were adjusted to a higher dose, and in 8 the dose was decreased. Nausea and vomiting were noted in 15 patients. No patient developed hepatic veno-occlusive disease or seizures. Full donor chimerism was attained in 20 patients (mean of 24.5 days), 3 achieved partial chimerism, 5 did not engraft, and in 2 it is too early to assess chimerism. Acute graft-versus-host disease developed in 11 patients, grades I to II developed in 10 patients, and grade III developed in 1. Four patients died of infection and 5 of progressive disease. Thus, PK of a test dose of IV Bu provided information to adjust subsequent daily doses of IV Bu: this resulted in a regimen that was feasible, safe, and convenient for administration to children.
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PMID:Pharmacokinetics of a test dose of intravenous busulfan guide dose modifications to achieve an optimal area under the curve of a single daily dose of intravenous busulfan in children undergoing a reduced-intensity conditioning regimen with hematopoietic stem cell transplantation. 1654 31

We report our experience with oral busulfan (BU) in 159 consecutive patients to evaluate the safety of home administration. Patients received a myeloablative BU-containing regimen, including oral anticonvulsant and antiemetic prophylaxis, followed by hematopoietic stem cell transplantation. Comprehensive verbal and written education was provided. Pharmacokinetic monitoring was performed and dose adjustments were made to target an area under the plasma concentration-time curve (AUC) of 900-1500 micromol.min/l. Safety was assessed by evaluating therapy-related toxicities, including seizures, venoocclusive disease (VOD) and patient tolerability. The utilization of pharmacokinetic monitoring was reviewed as a secondary end point. Of the 143 patients evaluated for BU-related seizures and VOD, only two (1.4%) experienced a generalized seizure and four patients (3%) were diagnosed with VOD. VOD resolved in three patients and was a contributing cause of death in one patient. Additional BU dosing owing to nausea and/or vomiting occurred in 28 patients (18%) and five patients (3%) were hospitalized. The median measured AUC was 1405 micromol.min/l, 68% of patients required a dose adjustment, and the median total administered BU dose was 13.6 mg/kg. In conclusion, high-dose oral BU can be safely administered on an outpatient basis.
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PMID:Home administration of high-dose oral busulfan in patients undergoing hematopoietic stem cell transplantation. 1732 33


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