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

This paper reports late effects and health status of 198 children who had cancer or leukemia diagnosed under 2 years of age and their therapies electively withdrawn. This series (92 neuroblastoma [NBL], 57 Wilms' tumor [WT], 46 acute lymphoblastic leukemia [ALL], and 3 non-Hodgkin's lymphoma) was followed for 1-12 years after discontinuation of therapy. Thirty-three children were diagnosed before 1973, 92 between 1973 and 1977, and 73 after 1977 in 16 Italian Pediatric Oncology Centers. As of December 1983, 176 children were reported to be alive and without evidence of primary cancer by physicians responsible for their care. One child died from a second primary tumor, two from late recurrences of the primary cancer, and three from other causes; eight were alive with evidence of primary cancer; and eight were lost to follow-up. Kyphoscoliosis was found in 22 children and other musculoskeletal anomalies in 8. Neurological sequelae were observed in 8 out 35 children with ALL treated with radiotherapy (RT) and intrathecal methotrexate. All but one were in continuous complete remission when they developed seizures (three cases), leukoencephalopathy (three cases), or intracerebral calcifications (two cases). One child had cardiomyopathy and subsequently died from cardiac failure: he had received doxorubicin (400 mg/m2) and mediastinal RT (13 Gy) for NBL. Growth impairments were observed in children with NBL and WT.
 ...
PMID:Health status of young children with cancer following discontinuation of therapy. 347 May 93

Methotrexate may cause seizures, dementia, and leukoencephalopathy when given in toxic doses to children with leukemia or solid tumors. Even in therapeutic doses, treatment with this drug is associated with an increased incidence of seizures in children with leukemia. To study mechanisms of injury, juvenile rats were given multiple intraventricular injections of methotrexate and the brains were analyzed for histopathology and biogenic amine metabolites of dopamine and serotonin. Disruption of monoamine metabolism has been proposed as a cause of brain dysfunction from this chemotherapy. Multiple injections (1 or 2 mg/kg) produced convulsions in an increasingly larger percentage of animals at higher cumulative doses, and five doses produced the neuropathological changes seen in human leukoencephalopathy. A single dose reduced the concentration of brain metabolites of dopamine, but not serotonin, six hours later. The effect was less pronounced after five doses. This rodent model should be useful for studying the metabolic basis of methotrexate encephalopathy.
 ...
PMID:A model of methotrexate encephalopathy: neurotransmitter and pathologic abnormalities. 359 35

An autopsy case of Nasu-Hakola's disease (membranous lipodystrophy) is reported. A 43-year-old Japanese man, whose parents were not consanguineous, had been suffering from frequent long bone fractures since the age of 10. Neuropsychiatric symptoms, which were characterized by euphoria, disturbance of attention and dementia, appeared at his thirties and generalized and/or localized seizures and apallial syndrome at the later stage. The neuropathology revealed diffuse leukoencephalopathy of the cerebrum. The peculiar aspects in this case were membranocystic changes in the lungs [Yagishita et al. Virchows Arch [A] 408:211-217 (1985)], diffuse degeneration of the cerebral cortex, chiefly in frontal and temporal lobes, and many axonal spheroids throughout the cerebral cortex. The ultrastructure of spheroids in the cerebral cortex demonstrated aggregations of mitochondria, dense bodies and minute concentric bodies and a small amount of neurofilaments.
 ...
PMID:Nasu-Hakola's disease (membranous lipodystrophy). 367 22

Intracarotid BCNU (100 mg/m2) and cisplatin (60 mg/m2) were administered to 36 patients with malignant brain tumors recurrent or progressive after cranial irradiation. Courses of therapy were repeated at 4-6 week intervals. Of 23 evaluable patients with recurrent glioma, 9 (39%) had tumor regression by CT scan and 3 had stable disease. The median time to tumor progression for responding patients was 37 weeks. For all patients with primary tumors it was 14 weeks. Six of 9 patients with no prior chemotherapy had a response and 1 had stable disease. Of 14 patients who had received prior chemotherapy, 3 had a response and 2 had stable disease. Survival ranged from 9 weeks to 95+ weeks (median 34 weeks) from start of therapy. Six of 23 patients with primary tumors are alive 1 year or more following therapy. Four of 11 patients with brain metastases had a response and 2 had stable disease. Major neurologic toxicity of intracarotid BCNU and cisplatin appeared cumulative and consisted of reversible hemiparesis in 3% of 118 courses, TIA in 1%, expressive aphasia in 9%, lethargy in 3%, seizures in 12%, and reversible confusion in 1%. Retinal toxicity consisted of mild blurring of vision in 4 patients and ipsilateral blindness in 5 patients. Three of 22 patients who had received supraophthalmic infusion later developed evidence of leukoencephalopathy. Intracarotid BCNU and cisplatin appears to have modest increase in activity over intracarotid cisplatin alone (Cancer 54:794, 1984), however, neurologic and retinal toxicity may also be increased.
 ...
PMID:Phase II trial of intracarotid BCNU and cisplatin in primary malignant brain tumors. 370 37

We reviewed records of 387 patients with cancer who had Ommaya reservoirs placed between October 1967 and December 1982. Complications of reservoir placement were reported in 27 patients, including intracranial hemorrhage (5 patients) and reservoir malfunction (15 patients). In 15 of 19 patients with meningitis, the infection was linked to the reservoir. The organism most frequently implicated was Staphylococcus epidermidis. Seizures, leukoencephalopathy, and pericatheter necrosis were seen in 10 patients who had received intraventricular chemotherapy.
 ...
PMID:Ommaya reservoirs in 387 cancer patients: a 15-year experience. 383 73

We evaluated the CNS complications in 118 adults with acute leukemia who received IV high-dose Ara-C therapy. Fourteen (12%) had cerebellar signs, encephalopathy, seizures, or leukoencephalopathy. Symptoms usually occurred within 24 hours after the last treatment. Patients receiving a cumulative dose in excess of 24 g/m2 had more severe or irreversible symptoms. After lower cumulative doses, symptoms often resolved even though treatment was continued. The incidence of CNS complications of high-dose Ara-C is acceptable and is potentially reversible if appropriate precautions are taken.
 ...
PMID:Central nervous system toxicity with high-dose Ara-C. 403 29

17 patients suffering from the presenile dementia characterised by polycystic lipomenbranous osteodysplasia and sclerosing leukoencephalopathy were studied neurophysiologically. Noteworthy findings were diffuse slowing, the accentuation of 6-8 Hz parasagittal activity, slowing of the dominant occipital rhythm and, in the late phase when 13 of patients got epileptic seizures, there was paroxysmal activity in the EEG.
 ...
PMID:Neurophysiological findings in the hereditary presenile dementia characterised by polycystic lipomembranous osteodysplasia and sclerosing leukoencephalopathy. 641 4

From 1972-1974, 228 children began treatment for acute lymphocytic leukemia and were prospectively assessed for neurologic complications. After CNS irradiation (2,400 rad) and intrathecal methotrexate (MTX), they received weekly intravenous maintenance therapy with MTX alone (40-60 mg/m2; 20 patients) or MTX (10-30 mg/m2) with other drugs (208 patients). Signs of leukoencephalopathy appeared in 11 children (nine without CNS leukemia) after 4-15 months of IV MTX alone, and included lethargy, seizures, spasticity, paresis, drooling, and dementia. Before or during the clinical onset, EEG frequencies slowed (all ten patients tested). Radionuclide scans showed periventricular accumulation of 99mTc (9/11 patients) and remained abnormal for greater than or equal to six months in eight patients. Cranial computed tomograms or neuropathology findings (five patients each) demonstrated leukoencephalopathy (nine patients) and radiation-related microangiopathy (ten patients). Severe neurologic and neuropsychologic dysfunctions were present in four long-term survivors.
 ...
PMID:Progression of methotrexate-induced leukoencephalopathy in children with leukemia. 693 56

Seven patients with bone or soft tissue sarcomas but without metastatic CNS disease developed a chronic leukoencephalopathy after high-dose (8000-15,000 mg/m2) iv methotrexate (MTX) chemotherapy with leucovorin (LV) rescue. Approximately 12 MTX-LV treatments were administered over a 3-7 month period. None of the patients had cranial irradiation. The syndrome usually began several months after the initiation of chemotherapy with subtle personality changes followed by a progressive dementia, focal seizures, pseudobulbar palsy, spastic quadriparesis, and stupor. Computerized tomographic scans revealed diffuse white matter hypodensity in five patients and atropic changes in five patients. Serum MTX concentrations were elevated in four of six patients prior to several MTX-LV treatments, suggesting that MTX persisted in tissues for a long time. Abnormally high levels of MTX were detected in the cerebrospinal fluid of all four patients several days after an MTX-LV treatment, at a time when their encephalopathy was most severe. Pathologic brain material was obtained from three patients and revealed a spectrum of abnormalities. The syndrome observed in our patients clinically resembles the one described in children with acute lymphatic leukemia who received cranial irradiation and large cumulative amounts of low-dose (12-20 mg/m2) systemic MTX without LV.
 ...
PMID:Leukoencephalopathy following high-dose iv methotrexate chemotherapy with leucovorin rescue. 697 Jun 16

Although cerebral amyloid angiopathy is a well-known cause of cerebral lobar hemorrhage, subacute dementia, seizures, and acute encephalopathy without lobar hemorrhage are infrequently recognized as manifestations of this disease. In this report, we describe a case of cerebral amyloid angiopathy in a 74-year-old woman who had subacute progressive dementia and a superimposed rapid acute neurologic deterioration associated with seizures and the presence of cerebral edema on computed tomographic scans and leukoencephalopathy and cortical petechial hemorrhages on magnetic resonance imaging. A diagnosis of cerebral amyloid angiopathy in conjunction with small cortical infarcts and petechial hemorrhages was confirmed by antemortem biopsy. This clinical and radiologic picture is being increasingly recognized as characteristic of cerebral amyloid angiopathy.
 ...
PMID:Cortical petechial hemorrhage, leukoencephalopathy, and subacute dementia associated with seizures due to cerebral amyloid angiopathy. 773 Dec 59


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>