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)

Seven patients with cancer complicated by nonmetastatic sagittal sinus thrombosis were encountered in a 7-year period. Five had hematologic malignancies and two had solid tumors. There were two different presentations. In the first, neurologic signs and symptoms (e.g., headaches, seizures, hemiparesis, lethargy) occurred suddenly in five patients shortly after initiation of cancer therapy. Four of these five patients recovered with minimal residua; the fifth died as a direct result of the sinus thrombosis. The second presentation occurred in the two patients with terminal cancer who declined gradually without focal signs; both patients died. Only arteriography can reliably establish the diagnosis of sagittal sinus occlusion. In patients with cancer, sagittal sinus occlusion probably results from a "hypercoagulable state" associated with the systemic neoplasm.
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PMID:Nonmetastatic superior sagittal sinus thrombosis complicating systemic cancer. 28 38

Cytarabine is an effective drug in the treatment of certain hematologic malignancies and its common toxicities are myelosuppression and gastrointestinal disturbance. In the past decade, neurotoxicity has been an increasingly recognized cytarabine effect. Intrathecal (IT) cytarabine may result in myelopathy that is incompletely reversible. Combined IT drug and cranial irradiation may lead to necrotizing leukoencephalopathy. Intravenous (IV) therapy may cause a peripheral neuropathy that varies greatly in its severity. The high IV cytarabine doses now commonly used can cause seizures, cerebral dysfunction, or an acute cerebellar syndrome with an incidence up to 14%. Patient age (greater than 60 years) appears to be the most important risk factor, but drug dose/schedule, cumulative drug dose, renal and hepatic dysfunction, and concomitant use of neurotropic antiemetic agents may also influence the risk of neurotoxicity. A better understanding of the pathophysiology and pharmacology of such cytarabine-induced neuronal injury will allow this drug to be used with greater efficacy and safety.
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PMID:Cytarabine and neurologic toxicity. 172 19

Etoposide (VP-16-213) has been used in the treatment of many solid tumors and hematologic malignancies. When used in high doses and in conjunction with autologous bone marrow transplantation, this agent has activity against several treatment-resistant cancers including malignant glioma. In six of eight patients (75%) who we treated for recurrent or resistant glioma, sudden severe neurologic deterioration occurred. This developed a median of 9 days after initiation of high-dose etoposide therapy. Significant clinical manifestations have included confusion, papilledema, somnolence, exacerbation of motor deficits, and sharp increase in seizure activity. These abnormalities resolved rapidly after initiation of high-dose intravenous dexamethasone therapy. In all patients, computerized tomographic (CT) brain scans demonstrated stability in tumor size and peritumor edema when compared with pretransplant scans. This complication appears to represent a significant new toxicity of high-dose etoposide therapy for malignant glioma.
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PMID:Acute neurologic dysfunction after high-dose etoposide therapy for malignant glioma. 328 26

Neurological complications are frequent in the course of malignant hematological diseases. Five cases occurring in children are reported here: 4 presented with acute lymphoblastic leukemia and 1 with lymphoma. The clinical pattern was remarkably acute, with fever, seizures and a neurological deficit. Brain CT scan showed a limited hypodensity sometimes with a contrast uptake in the involved area in the first days or weeks. Seroconversion for measles virus occurred in 3 cases, associated with the presence of helix-like bodies in the cerebrospinal fluid and/or cerebral tissue. These case reports are discussed with respect to the neurological complications already reported in patients with hematologic malignancies. The hypothesis of measles-virus related encephalitis seems likely.
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PMID:[Acute neurological deficit in treated malignant hemopathies]. 658 9

Between July 1991 and January 1994, 52 patients with hematologic malignancies underwent BMT using BU/CY2 as conditioning regimen. Median patient age was 38 years. Eleven patients underwent autologous BMT, 22 HLA-identical allogeneic BMT, and 19 patients underwent a MUD or an allogeneic mismatched BMT. GVHD prophylaxis was with cyclosporine/methylprednisone in 26 patients; T cell depletion was used in 15 patients. VOD was observed in 7.5% of patients, IP in 12%, seizures in 4%. The overall incidence of grade II-IV acute GVHD was 35%. Delayed platelet engraftment was observed in seven of 11 patients who underwent autologous BMT. Graft failure was seen in seven of 19 (37%) patients who underwent MUD or allogeneic mismatched BMT. Six of the seven patients received T cell depletion as GVHD prophylaxis. BU/CY2 transplantation from an unrelated or family-mismatched donor with T cell depletion is associated with a high incidence of graft failure.
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PMID:Toxicity of busulfan and cyclophosphamide (BU/CY2) in patients with hematologic malignancies. 870 82

Acute tumor lysis syndrome (TLS) occurs frequently in hematologic malignancies such as high-grade lymphomas and acute leukemia, which are rapidly proliferating and chemosensitive tumors. It occurs rarely in solid tumors and has never been reported in gastric adenocarcinoma. Typical biochemical findings of acute tumor lysis syndrome are hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia in patients with a malignancy. Rapid changes of these electrolytes may cause cardiac arrhythmia, seizure, acute renal failure and sudden death. Therefore, as soon as it is detected, it should be taken care of immediately. Until now almost all cases of TLS associated with solid tumor have developed after cytoreductive therapy in chemosensitive tumors. We report here a case of spontaneous acute tumor lysis in a patient of advanced gastric cancer with hepatic metastases and multiple lymphadenopathy. The biochemical finding of TLS improved with the management and tumor burden also showed slight response to the one cycled combination chemotherapy but the patient died of progressive pneumonia.
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PMID:Spontaneous acute tumor lysis syndrome with advanced gastric cancer. 1128 89

Interferon (IFN)-alpha is associated with central nervous system (CNS) side effects such as depression and suicide ideation, somnolence, confusion, drowsiness, psychomotor slowing, memory impairment and visual disorientation. More severe complications are uncommon and include frank paranoia, dementia, coma, seizures and neuropathy. With the increasing long-term and extensive use of interferon (IFN)-alpha several new neurologic adverse effects have been recognized. We report on two patients who developed severe subcortico-frontal impairment, associated in one case with choreic movements, after a long-term treatment with IFN-alpha 2b for hematologic malignancies. Our patients rapidly and completely recovered from their cognitive and motor symptoms after the discontinuation of the drug. The same neurologic symptoms reappeared when we attempted to reintroduce lower doses of IFN-alpha in one case. Although little is known regarding IFN-alpha actions in the CNS, several possible mechanisms may underlie its neurotoxicity and might result from complex direct and indirect effects involving brain vasculature, neuroendocrine system, neurotoxic secondary cytokines'release and neurotransmitters.
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PMID:[Sub-cortico-frontal encephalopathy and choreic movements related to recombinant interferon-alpha 2b]. 1207 24

Splenic lymphoma with villous lymphocytes (SLVL) is an indolent hematological malignancy. Persistent lymphocytosis and splenomegaly usually last for years before patients develop infectious complications. Organ involvement other than spleen and bone marrow is rare in SLVL. We report a case of SLVL-related meningitis occurring in a patient presenting with altered mental status and seizures. CNS involvement was documented by an MRI of the head and by the presence of atypical lymphocytes in the cerebrospinal fluid (CSF). Morphologic examination and immunophenotypic analyses were conducted to determine the nature of atypical lymphocytes in the peripheral blood, spleen, bone marrow and CSF. The patient improved after treatment with a combination of radiation and chemotherapy.
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PMID:Leptomeningeal involvement in a patient with splenic lymphoma with villous lymphocytes. 1215 5

We report a case and autopsy findings of posterior leukoencephalopathy (PL) developing during induction chemotherapy for B-cell acute lymphoblastic leukaemia (B-ALL) complicated by tumour lysis syndrome. PL may present with seizures, headache, altered mental status and occipital blindness, associated with transient parieto-occipital abnormalities on neuro-imaging studies. Precipitants include immunosuppressive agents, renal insufficiency, hypertension and fluid retention. It has also been reported in association with pre-eclamptic and eclamptic states, nephrotic syndrome and following liver and bone marrow transplantation. Only rare cases of PL developing during treatment for haematological malignancy have been reported and to our knowledge it has not been previously reported in association with tumour lysis syndrome. Since the condition is generally regarded as being fully reversible few autopsy findings have been reported.
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PMID:Posterior leukoencephalopathy in association with the tumour lysis syndrome in acute lymphoblastic leukaemia--a case with clinicopathological correlation. 1277 51

We have observed an increasing number of autopsies on patients with chemotherapy-related complications. One complication is toxic leukoencephalopathy, which is due to a direct toxic effect of chemotherapeutic agents on the central nervous system white matter. Autopsies of four cases of toxic leukoencephalopathy were performed following standard protocols. The brain and spinal cord were examined routinely, and histological sections were taken for evaluation. We report here three patients with hematologic malignancies and one patient with metastatic carcinoma with chemotherapy-induced leukoencephalopathy. The first was a 56-year-old male treated with multiple chemotherapeutics for multiple myeloma. He presented with confusion and focal seizures with a rapid progression to coma and decerebrate posturing. The second was a 36-year-old male who developed mental status changes, ataxia and dysarthria following treatment for lymphoma. The third was a 16-year-old male who developed a profound peripheral and central neuropathy after chemotherapy treatment for T-cell acute lymphoblastic leukemia. The fourth was a 49-year-old female patient who was treated with multiple chemotherapeutics for Stage II breast carcinoma and subsequently developed visual acuity and field defects. The neuropathologic findings in these cases, although similar, varied in severity and distribution. The white matter was affected by severe myelin pallor, edema, and a prominent macrophage infiltrate in each of the cases. The location and extent of the central nervous system pathology correlated with the type and severity of clinical symptoms. These four cases, with their varied presenting symptoms, clinical courses, and degree of pathology, emphasize the importance of considering toxic leukoencephalopathy as an etiology of acute neurologic deterioration following high-dose chemotherapy.
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PMID:Chemotherapy-induced toxic leukoencephalopathy causes a wide range of symptoms: a series of four autopsies. 1470 18


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