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

The technique of direct stimulation mapping of the cortex is used to identify regions of language representation in the dominant cerebral hemosphere and the Rolandic cortex in either hemisphere. The use of electrocorticography to remove epileptogenic zones in patients with difficult-to-control seizures is described. The article presents the authors' experience with brain mapping during glioma surgery to maximize the extent of tumor resection and minimize surgical morbidity.
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PMID:Neurophysiological monitoring during astrocytoma surgery. 213 74

Extracellular adenosine acts through specific cell surface receptors to modulate numerous physiological processes in both the CNS and peripheral tissues (e.g. neurotransmitter release and blood flow). Activation of A1 or A2 adenosine receptors leads to decreased or increased intracellular cAMP levels, respectively. Fos and Jun are nuclear proto-oncogene products, which, like cAMP, appear to act as intermediates in a number of signal transduction pathways. Since increases in both adenosine release and Fos and Jun expression occur in the brain following seizures, we wanted to determine whether Fos and Jun induction might occur as a result of adenosine receptor activation. 3T3 fibroblasts and NG108-15 neuroblastoma-glioma hybrid cells were chosen for study, since they were known to respond to adenosine agonists with changes in cAMP levels. The membranes of NG108-15 cells were shown to have A2-like binding activity in a competitive binding assay. Cultures of each cell line were treated with the adenosine agonists, CHA (A1-selective) and NECA (non-selective adenosine agonist). Both lines responded with a concentration-dependent transient increase in c-fos, but not c-jun, mRNA content after treatment with either agonist. The kinetics of the response were much more rapid for 3T3 cells (peak between 15 and 30 min) than for NG cells (peak between 60 and 90 min). The slower, more prolonged response in the NG108-15 cells is more similar to the time interval between adenosine release and the peak of c-fos mRNA induction in brains of animals following the administration of seizure-promoting drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Activation of adenosine receptors induces c-fos, but not c-jun, expression in neuron-glia hybrids and fibroblasts. 217 6

We reviewed retrospectively a series of 100 inpatients with onset of epileptic seizure after the age of 60. All of them were investigated by EEG and 96 by CT scan. The most frequent cause of seizure was previous stroke, with 25 cerebral infarcts and 5 hemorrhages. Neoplastic lesions were present in 18 cases, with glioma (high grade), meningioma and metastases in the same proportion. Other etiologies included toxico-metabolic (18 cases), post-traumatic (9 cases), cerebral atrophy (4 cases) and miscellaneous (14 cases). The causes of seizure remained unknown in 7 patients, of whom 6 had focal signs in either clinical examination or EEG. Focal seizures (with or without secondary generalization) accounted for 65% of all cases and generalized seizures for 35%. The EEG was normal in 12 patients and abnormal in 88, with diffuse slowing in 55 patients and focal signs in 70 (some patients had both diffuse slowing and focal signs). Fourteen patients presented status epilepticus. Ten died during hospitalization. We conclude that epileptic seizure with onset after age 60 is nearly always symptomatic, and neuroradiologic investigations are necessary in the search for cerebral lesions. In our study, the prevalence of "idiopathic epilepsy" is lower than previously described.
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PMID:[Initial epileptic crisis after the age of 60: etiology, clinical aspects and EEG]. 234 61

A 33-year-old male patient showed increasing frequency of seizures 12 years after a blunt head injury. From findings of x-ray computed tomography, the lesion was thought to be a benign glioma. Removal of the lesion was performed with the guidance of electrocorticography. Histological diagnosis was gliotic scar with calcification. Diffuse iron particles were detected in layers II-V of the cortex by hematoxylin and Berlin-Blue stain. These findings suggest progressing traumatic epilepsy which may be explained by the mechanism of Willmore's model.
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PMID:Iron in cicatrix and abnormal CT findings in a patient with posttraumatic epilepsy. 250 49

Cisplatin (DDP) is a chemotherapeutic agent that has shown efficacy against primary CNS malignancies. Intra-arterial (IA) administration of DDP to patients with brain tumors should produce higher peak levels of drug than intravenous (IV) administration of an identical dose and reduce systemic toxicity. Twelve patients with malignant glioma were entered into the study. All had failed irradiation, 11 had failed IA BCNU. Each patient received IA DDP, 58-100 mg/m2, into the internal carotid artery at four to six week intervals. One of 12 patients had a partial response of 6 months. The remaining 11 patients had progressive disease or severe complications. Toxicity included seizures in four patients, weakness and/or aphasia in four patients, coma in two patients, and visual deterioration in two patients. IA DDP has very limited efficacy in patients with malignant gliomas after failure of nitrosoureas and is associated with an unacceptable level of toxicity. IA DDP may be more effective when used as initial chemotherapy of malignant gliomas.
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PMID:Intra-arterial cisplatin for the treatment of malignant gliomas. 254 32

Four cases of pleomorphic xanthoastrocytoma (PXA), a low-grade leptomeningeal glioma with a reported favorable prognosis affecting young patients, are reported together with a discussion and review of management and prognosis. A literature review has confirmed a favorable prognosis in at least 50% of patients with this disorder. Seventeen of 35 reported patients are still alive and often seizure-free for a mean period of 7.4 years (range 2 to 18 years) after diagnosis. Five patients have died within 2 years and four between 9 and 25 years after diagnosis of PXA. In some cases in which death followed shortly after diagnosis, there may have been histological confusion between PXA and a malignant glioma with heavily lipidized tumor cells. Nonetheless, transformation of PXA into a malignant astrocytoma or glioblastoma with eventual death may occur many years after initial diagnosis. From the currently reported cases it does not appear possible on clinicopathological grounds to predict which patients will have a favorable prognosis. Optimal management of PXA seems to be primary surgical resection with later surgery for residual or recurrent tumor. The role of radiotherapy in the management of PXA is at this time uncertain.
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PMID:Pleomorphic xanthoastrocytoma. Report of four cases. 264 2

Photoirradiation treatment depends on exposing tumors to a photosensitizer and light to achieve selective tumor kill. We evaluated the kinetics of uptake of a photosensitizer, hematoporphyrin derivative (HpD), in an animal model of cerebral glioma to ascertain the optimal time for photoirradiation therapy. Animal models of cerebral glioma were established by implanting cells from the rat C6 glioma cell line into rat brains or as xenografts in adult mouse brains. C6 cells (10(7] injected into the frontal lobe of adult Wistar rats produced intracranial tumors greater than 5 mm in diameter in 90% of the animals at 21 days. Tumors greater than 4 mm in diameter developed in adult mouse brains within 14 days after 10(6) cells were implanted into the frontal lobe. These two tumor models were used to investigate the localization of HpD. After HpD administration, its presence was detected in fresh, unfixed specimens by fluorescence emission after excitation with an ultraviolet lamp. Fluorescence was determined quantitatively by an image analysis method using an optical data digitometer. The fluorescence, which was highly localized selectively to the intracerebral tumor, was just detectable 5 minutes after an intravenous injection of HpD. Patchy, bright fluorescence was evident 4 hours after injection, and the tumor was uniformly fluorescent after 6 hours. A minimal dose of 0.5 mg of HpD per kg of body weight was necessary to produce detectable fluorescence, and the dose of HpD necessary to produce detectable fluorescence was 4 mg/kg of body weight. The intracarotid route of administration was unsatisfactory because seizures were induced, and intrathecal injection did not produce significant fluorescence in the tumor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Uptake and retention of hematoporphyrin derivative in an in vivo/in vitro model of cerebral glioma. 293 41

A retrospective study was performed to evaluate the efficacy of prophylactic anticonvulsants in preventing seizures in 68 patients with supratentorial astrocytomas who had been treated with operation and irradiation and who had no previous history of convulsions. Thirty-three patients received prophylactic anticonvulsants and 38 patients did not. The incidence of all types of seizures (generalized convulsions or partial) was lower in patients receiving anticonvulsants. No seizures with an impairment of consciousness occurred in the patients with documented therapeutic anticonvulsant blood levels. The overall incidence of seizures was 39% in untreated patients and 21% in treated patients. The incidence of major seizures including tonic/clonic or partial complex seizures with impairment of consciousness was zero in patients with therapeutic anticonvulsant levels and 18% in untreated patients. Regarding the overall incidence of seizures in both groups, there tend to be fewer seizures in older patients, females, patients with a higher grade of malignancy, and patients who had a more radical resection of the tumor. This study suggests that seizures are a frequent occurrence after operation and irradiation for supratentorial glioma and that anticonvulsants may be effective in reducing the incidence of those seizures.
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PMID:Postoperative prophylactic anticonvulsant therapy in cerebral gliomas. 298 99

Twenty-one patients with documented neurofibromatosis had MR examinations to evaluate possible intracranial disease. In five cases the indication was a known or suspected optic glioma. Two patients were examined because of a history of seizures; the rest were examined as part of a baseline evaluation. Eighteen patients showed evidence of signal hyperintensity on T2-weighted images. Lesions involved the optic nerves, optic chiasm, optic tracts, lateral geniculate body, optic radiations, basal ganglia, periventricular white matter, cerebellar white matter, and dentate nucleus of the cerebellum. Comparison between MR and concurrent CT scans showed MR to be superior in demonstrating the posterior extent of optic-pathway gliomas. In addition, MR showed focal areas of hyperintensity in the basal ganglia, internal capsule, cerebellum, and/or white matter that were not detected on CT. Although we found MR to be superior to CT in detecting intracranial tumors in patients with neurofibromatosis, and in evaluating the extensive involvement of known lesions, the full clinical implications of our findings remain to be determined.
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PMID:MR imaging of optic pathways in patients with neurofibromatosis. 312 May 29

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


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