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

Carbonic anhydrase inhibitors used in the treatment of glaucoma, seizure disorders, and hypertension are rarely associated with blood dyscrasias. Several case reports of aplastic anemia with use of acetazolamide, and two cases with use of methazolamide, have appeared in the literature. This article describes two cases of aplastic anemia, at least one of which was almost certainly induced by the use of methazolamide, and one case of agranulocytosis related to the use of methazolamide.
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PMID:Aplastic anemia and agranulocytosis in patients using methazolamide for glaucoma. 44 45

Serum levels of mephenytoin (Mesantoin) and its metabolite nirvanol were correlated with effectiveness and side effects in 93 patients. Mean mephenytoin level was 8% of the combined mephenytoin plus nirvanol levels. "Total mephenytoin" level should be used clinically, as neither individual component is as well correlated with clinical phenomena. Serum levels of 25 to 40 mug/ml usually yield improvement in seizure control without discomfort, and three-quarters of patients had fewer seizures. Side effects frequently associated with phenytoin were absent, but drowsiness, an occasional rash, and a single, fatal case of aplastic anemia were found. Performance on psychological tests of cognitive-attentional skills showed a modest improvement during mephenytoin administration. The drug merits wider employment in refractory seizure problems, but vigilant follow-up is required.
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PMID:Mephenytoin: a reappraisal. 100 Dec 84

Three consecutive cases of severe aplastic anemia undergoing immunosuppressive therapy with cyclosporin A (CyA) and high-dose methylprednisolone (HDMP) developed grand mal seizures after receiving ketoconazole treatment. All the seizures were reversed after transient discontinuation of those drugs. To our knowledge, it has not been reported as yet that the combination of ketoconazole and HDMP may considerably increase the risk of CyA-induced seizure. We would advise that ketoconazole and HDMP not be taken concomitantly with CyA treatment, and whenever ketoconazole therapy is needed, CyA be started with as small a dose as possible.
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PMID:Ketoconazole and high-dose methylprednisolone predisposing to cyclosporine-induced seizures: report of 3 cases. 146 96

After an accidental or intentional ingestion of lindane, clinical manifestations of poisoning may include rapid onset of nausea and vomiting, coma, seizures, respiratory failure, and death. While rhabdomyolysis, secondary renal failure, and aplastic anemia have also been reported, coagulopathies have not been observed following poisoning with this pesticide. In this case report we describe a 43-year-old female who intentionally ingested 8 oz of a 20% lindane solution. Her serum lindane concentration reached 1.3 mcg/ml and her clinical manifestations included seizures, coma, rhabdomyolysis, secondary renal failure, and disseminated intravascular coagulation. The coagulopathy presented early in her clinical course and resolved when serum lindane levels fell. The patient died 11 days after the ingestion.
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PMID:Disseminated intravascular coagulation in a case of fatal lindane poisoning. 245 26

A total of 46 patients with aplastic anemia (34 severe; 12 moderate) were treated with antihuman thymocyte globulin (ATG), high-dose methylprednisolone, and oxymetholone. Early symptoms of ATG toxicity included fever, rash, and bronchospasm. Signs of serum sickness also developed in 23 patients. Complications associated with high doses of steroids were hyperglycemia, hypertension, fluid retention, gastrointestinal hemorrhage, and aseptic necrosis of the hip. Other morbidity possible associated with steroid administration included seizures, arrhythmias, and headache with papilledema. Studies of elevated liver function necessitated discontinuation of androgen therapy in eight patients. A complete or partial hematological response was noted in 19 patients (41%). Of these, three have had recurrent cytopenias, of whom one has developed a myelodysplastic syndrome. There are currently 34 patients surviving, and 12 who have died. Actuarial survival at three years is 65%. These response and survival data are comparable to those of previous trials using ATG and androgens without high-dose steroids. A prospective, randomized trial is needed to determine whether the addition of high-dose corticosteroids to ATG does significantly increase the rate and frequency of response in order to justify the toxicity of this additional immunosuppressive therapy in the treatment of aplastic anemia.
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PMID:Treatment of aplastic anemia with antithymocyte globulin, high-dose corticosteroids, and androgens. 349 72

Appropriate use of carbamazepine for the treatment of epilepsy is based on correct identification of the patient's seizure type. Carbamazepine is effective against partial seizures and against generalized tonic clonic seizures. Therapy should begin gradually, with initial doses increased slowly over 1 or 2 weeks, as tolerated. Side effects include fatigue, dizziness, ataxia, double vision, nausea, and vomiting. Most practitioners agree that, because of carbamazepine's relatively short half-life, the total dosage should be administered in at least two divided doses. This avoids too high a peak blood level that would occur with a single dose. Carbamazepine therapy is associated with the development of two hematologic conditions. Leukopenia, which may be transient or persistent, requires careful monitoring but is not cause for immediate discontinuation of therapy. Aplastic anemia occurs rarely but is potentially fatal, and therefore diligent monitoring of hematologic function is indicated. Aplastic anemia is an idiosyncratic, non-dose-related side effect that is most likely to occur within the first 3 or 4 months of initiating therapy. Once seizures are controlled, plasma levels of carbamazepine should be measured to establish optimum levels for individual patients being treated with this drug.
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PMID:How to initiate and maintain carbamazepine therapy in children and adults. 369 21

The clinical, laboratory, and pathological features of aspergillosis of the central nervous system (CNS) were studied in a series of 17 autopsied patients. Two groups were defined. Group A consisted of 8 patients with diseases commonly associated with CNS aspergillosis: leukemia, lymphoma, aplastic anemia, and renal transplantation. Group B contained 9 patients with various illnesses not generally known to be associated with CNS aspergillosis. CNS aspergillosis was diagnosed and treated before death in only 1 patient. Patients in Group A received cytotoxic drugs, often had granulocytopenia, less commonly had focal neurological deficits, and seldom had seizures. Group B patients were not granulocytopenic, received no cytotoxic agents, underwent nontransplant surgery, and more frequently had focal neurological deficits. Eleven of the 17 patients (65%) had focal deficits, most of them hemiparesis. Meningeal signs were rare, but the cerebrospinal fluid was usually abnormal. The principal neuropathological process was Aspergillus invasion of blood vessels causing hemorrhagic infarction. Focal clinical deficits correlated neuroanatomically with Aspergillus lesions. In 2 patients, such lesions were detected by 99mTc-DTPA or cerebral angiography before computed tomographic scanning. The lungs were the usual portal of entry, but isolated CNS lesions occurred in 2 patients. CNS aspergillosis should be considered as a cause of new onset of focal neurological deficits in patients with illnesses that are more diverse than has generally been appreciated.
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PMID:Aspergillosis of the central nervous system: clinicopathological analysis of 17 patients. 393 42

A 10-year-old girl with aplastic anemia developed seizures and a mild hemiparesis following a bone marrow transplant. Based on serologic evidence and a computed tomography scan, which showed a left parietal lucency with ring enhancement, a diagnosis of toxoplasmosis was considered. A brain biopsy of the lucent area demonstrated the inflammation and necrosis but no organisms were seen. During a six-week course of pyrimethamine, sulfadiazine, and folinic acid therapy there was clinical and neuroradiologic resolution. The short course of therapy as well as the inadvertent substitution of folic acid for folinic acid and trimethoprim-sulfamethoxazole for sulfadiazine resulted in the reappearance of neurologic deficits. Reinstitution of appropriate therapy produced gradual improvement over a nine-month period. Serial computer tomography scans correlated with the clinical course. In the immunologically compromised host CNS toxoplasmosis should be considered in the differential diagnosis of an evolving CNS syndrome. Early detection and prolonged therapy with appropriate drugs can result in a favorable outcome. Computed tomography scanning may be helpful in diagnosis and follow-up.
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PMID:Toxoplasmosis: a treatable neurologic disease in the immunologically compromised patient. 701 42

Twenty-four patients, including two with aplastic anemia and 22 with malignancy, underwent marrow transplantation after preparation with mechlorethamine, 0.3 to 2.0 mg/kg body weight. Fourteen of the 21 neurologically evaluable recipients developed immediate neurotoxicity a median of 4 days after treatment (range, 0 to 34 days). Confusion and disorientation were observed in six patients, headache in six, hallucinations n four, lethargy in four, tremors in three, paraplegia in one, seizure in one, and vertigo in one. Whereas acute symptoms cleared in 11 patients, three remained symptomatic until death. Twelve evaluable patients survived more than 60 days; all six with previous acute toxicity subsequently developed delayed onset of new neurologic findings (personality change, confusion, seizure, diplopia, or dementia) a median of 169 days (range, 70 to 248 days) after treatment. Cerebrospinal fluid analysis was usually normal but cerebral computed tomographic scans showed ventricular enlargement and electroencephalograms showed diffuse slowing. Postmortem histologic examination of brain showed neuronal degenerative changes with increased vascularity, gliosis, and perivascular fibrosis. Neurotoxicity appeared to increase with age and mechlorethamine dose and was commoner in patients given additional procarbazine or cyclophosphamide.
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PMID:Immediate and delayed neurotoxicity after mechlorethamine preparation for bone marrow transplantation. 704 28

Several new antiepileptic drugs offer a worthwhile alternative when standard antiepileptic drugs have failed. Suggestions have been made to improve the risk-benefit ratio of the new antiepileptic agents. More specifically, vigabatrin, which is a very useful and well tolerated new antiepileptic drug for refractory partial epilepsy, should be started at a low dosage of 0.5 g/day with increments of 0.5 g/day every week. Daily dosages exceeding 3 g/day should be restricted to patients with improvement. If necessary, the daily dosage of vigabatrin should be withdrawn slowly, i.e. by not more than 1 g/week. Lamotrigine is also a beneficial new drug for refractory partial and generalized seizures. However, the drug is associated with rash. In patients also receiving valproic acid (sodium valproate) [which inhibits the metabolism of lamotrigine], the incidence of rash can be reduced by slow titration of 25mg every other day for the first week and 25mg per day for the second week. Rare hypersensitivity reactions, e.g. Stevens-Johnson syndrome, remain a problem. The risk-benefit ratio of felbamate has recently been compromised by fatal aplastic anaemia and fatal liver disease in a number of patients. In general, patients should be withdrawn from felbamate, if possible, until further clarification of its definitive risk-benefit ratio. Finally, gabapentin is a very safe add-on medication. Its remarkably low potential to cause adverse effects makes it a welcome addition for the treatment of refractory partial epilepsy.
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PMID:The new anticonvulsant drugs. Implications for avoidance of adverse effects. 772 52


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