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

A 38-year-old man with progressive psychiatric disturbances, dysarthria, myoclonus, rigidity and terminal generalized seizures died 4 years after onset. At post-mortem, severe leucodystrophy of the centrum semi-ovale, corpus callosum and internal capsule was found. In the demyelinated areas, abundant mononuclear phagocytes were found filled with dark yellow or brown pigment granules, staining with PAS and Sudan black, autofluorescent in paraffin sections, and orthochromatic with toluidine blue in paraffin and frozen sections and positive with Fontana's silver method. Iron deposits were present in a few cells. Electron micrographs of a biopsy showed massive storage of lipofuscin and ceroid with fingerprint profiles in macrophages and, to a lesser degree, in astrocytes as well. Oligodendroglia were depleted in demyelinated areas but prominent in the subcortical regions and in small foci in the deep cerebral white matter; they contained intracytoplasmic inclusions with fingerprint profiles. From these morphological findings it is suggested that lipofuscin and ceroids are the lipopigments stored in the pigmentary type of orthochromatic leucodystrophy.
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PMID:Leucodystrophy with pigmented glial and scavenger cells (pigmentary type of orthochromatic leucodystrophy). 322 79

Eleven cases of cerebral cavernous angiomas (cavernomas) were observed within a period of 3 years. Two patients presented with cerebral hemorrhage, five with epilepsy, three each with a progressive focal neurological deficit, and one with papilledema. The unruptured lesions had a heterogeneous density on computed tomography with relatively little contrast enhancement. Two lesions contained major cysts. In one of these cases, the cyst measured 5.5 cm in diameter, had an enhancing membrane, and was surrounded by brain edema. Angiography did not show hypervascularity in any instance. During exploration and histological processing, special attention was paid to signs of previous silent hemorrhages and to the degree of encapsulation of the lesion. Iron deposits (signs of previous hemorrhages) were seen to varying degrees inside all cavernomas as well as in the surrounding gliotic cerebrum, and a causal relation between iron deposits and epileptic seizures seems likely. Encapsulation was minimal with the ruptured cavernomas and particularly prominent with the cystic lesions. The membrane of the giant cystic lesion with peripheral brain edema had a histological structure similar to that of the membranes of chronic subdural hematomas. It is suggested that continuous growth of cavernoma cysts is the result of recurrent hemorrhages from sinusoids of the malformation and from the neocapillary network of the cyst membranes.
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PMID:Clinicopathological relations of cerebral cavernous angiomas: observations in eleven cases. 332 50

Intracortical injection of iron salts causes lipid peroxidation, focal edema, necrosis, gliosis, and the development of behavioral and electrographic seizures. Tocopherol pretreatment prevents the histopathologic perturbations associated with iron injection, and appears to accelerate the resolution of focal accumulation of peroxidation products. In this experiment, rats were pretreated with 500 mg/kg DL-alpha-tocopherol acetate prior to the injection of 3 microliter of 100 mM FeCl2 into the dorsal hippocampus, or induction of convulsive seizures by s.c. injection of 0.8 mg/100 g bicucullin. Tocopherol pretreatment prevented the occurrence of convulsive seizures in a significant number of iron-salts injected animals. Lipid peroxidation measured in the dissected hippocampus was significantly increased in untreated rats developing iron-induced seizures and in rats treated with tocopherol, but developing convulsive seizures. Tocopherol failed to prevent bicucullin-induced seizures. Further, convulsive seizures induced by bicucullin failed to alter hippocampal fluorescence levels. Hence, we concluded that the epileptogenic effects of hippocampal injection of iron salts appear to be related to the induction of peroxidation of neural lipids within the injection site.
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PMID:The role of iron-induced hippocampal peroxidation in acute epileptogenesis. 375 26

Small, anodal electrolytic lesions in the dorsal hippocampus were produced in rats, and continuous electrographic records were made from contralateral hippocampal electrodes for as long as 48 h following the lesion. Intense spontaneous epileptiform activity was observed, which developed from isolated spiking and spindling, to phasic spike trains, recurrent paroxysmal discharges and, in some cases, continuous ictal activity lasting to 7 h. Spontaneous clonic convulsions were observed in two cases. Epileptiform activity usually subsided after 12 h, but electrographic abnormalities such as spontaneous spiking and high-amplitude spindling persisted as long as 12 days. Such effects were reliably produced with iron-depositing lesions using stainless-steel electrodes, but not with platinum electrodes, suggesting that ionic deposition is critical for the lesion-induced seizure development. These results pose interpretive difficulties for the use of ion-depositing lesions in the study of limbic brain function.
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PMID:Epileptogenic effects of electrolytic lesions in the hippocampus: role of iron deposition. 649 91

Cerebral contusion, cortical laceration, intracerebral hematoma formation, and hemorrhagic cortical infarction cause extravasation of red blood cells, followed by hemolysis, decompartmentalization of iron, formation and deposition of hemosiderin, and an increased incidence of epilepsy. In this experiment, 10 microliter of an aqueous solution containing 100 mmol/L FeCl2, 100 mmol/L CoCl2, or 0.9% (wt/vol) NaCl were injected at a depth of 1.8 mm into rat isocortex. The rate of formation of fluorescent compounds was measured in chloroform-methanol extracts of isocortical homogenates. Significant increases in the quantity of fluorescent products of lipid peroxidation were found 120 min after the injection of 100 mmol/L FeCl2. Cobaltous chloride and saline injection had no effect on the levels of fluorescent products found in the cortical homogenates. Although the intracortical deposition of aqueous solutions containing CoCl2 or FeCl2 in rodent cortex causes acute epileptiform discharges, the epileptogenic effect of CoCl2 is transient, while the injection of iron salts causes persistent seizures. Since CoCl2 injection failed to cause formation of lipid peroxidation products while the isocortical injection of iron caused significant increase in fluorescence within the injected hemisphere, we suggest that the occurrence of iron-induced lipid peroxidation may be of importance in initiation of recurrent seizures in the rat.
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PMID:In vivo lipid peroxidation in rat brain following intracortical Fe2+ injection. 669 47

Head trauma, intracerebral hematoma formation, and hemorrhagic cerebral infarction cause extravasation of the intravascular contents, red blood cell (RBC) hemolysis, hemosiderin deposition within the neuropil, and an increased incidence of epilepsy. Reports conflict regarding the efficacy of the administration of prophylactic anticonvulsant drugs to head-injured patients to prevent the development of posttraumatic epilepsy. In this study, rats received a 10-microliter injection of 100 mM FeCl2 at a depth of 1.8 mm into the isocortex, or an equal volume of saline. Rats were then treated with 30 mg/kg methylprednisolone (MPS), 90 mg/kg MPS, 100 mg/kg phenytoin, or with an equal volume of propylene glycol. Behavioral or electroencephalographic (EEG) seizures occurred in all control-treated iron-injected rats within 93 +/- 6 minutes of injection. Brain injury responses as measured by the occurrence of fluorescent product formation from iron-induced lipid peroxidation showed 6.6 +/- 0.8 units/gm in the saline-injected animals, and 16.7 +/- 2.5 units/gm in the control-treated iron-injected rats. Of the 90-mg/kg MPS-treated rats, 8% had seizures; fluorescence in those animals was 5.7 +/- 0.5 units/gm. Phenytoin treatment prevented the occurrence of convulsive and EEG seizures; however, lipid peroxidation was unaffected (16.5 +/- 4.1 units/gm). If posttraumatic epilepsy develops because of RBC extravasation, hemolysis, parenchymal deposition of heme compounds, and initiation of lipid peroxidation, then treatments designed to prevent peroxidation may be more effective for epilepsy prophylaxis than administration of anticonvulsant drugs that mask convulsive seizures while biochemical brain injury continues.
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PMID:Effect of phenytoin and corticosteroids on seizures and lipid peroxidation in experimental posttraumatic epilepsy. 669 90

Iron causes formation of superoxide radicals resulting in peroxidation of membranous components of tissue. Hemosiderin deposition in human brain often accompanies chronic posttraumatic seizures induced by trauma. We injected an aqueous solution of iron salts, the principal metallic iron of whole blood, into rat isocortex. Serial electroencephalographic recording showed than 94% of untreated animals developed epileptiform discharges. Pretreatment with alpha-tocopherol and with 2 ppm selenium prevented development of iron-induced epileptiform activity in 72% of animals. Histopathologic assessment of serial sections stained with Nissl, hematoxylin and eosin, and prussian blue showed cavitation, neuronal pyknosis and loss, and astrogliosis in untreated animals. The site of iron injection in animals treated with antiperoxidants contained only an area of neuronal pyknosis. The efficacy of antioxidants in preventing development of iron-induced cavitation, gliosis, and epileptiform discharges suggests that peroxidative injury may be important in the development of experimental epilepsy induced by isocortical injection of ferrous chloride.
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PMID:Antiperoxidant pretreatment and iron-induced epileptiform discharges in the rat: EEG and histopathologic studies. 719 26

In a patient with celiac disease, folate and iron deficiency, and epilepsy, CT over a 4-month period showed parietoocipital calcifications in the corticomedullary junctions. The calcification was progressive, but it and the seizures stabilized after institution of a gluten-free diet and iron and folic acid supplements.
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PMID:Bilateral occipital calcification associated with celiac disease, folate deficiency, and epilepsy. 748 40

Avoidance of homologous blood products and patients' demand for preoperative autologous blood donation programs are increasing. As many of these patients are older, with a compromised cardiovascular system and a slow response of the erythropoietic system when anemia occurs, the feasibility and benefit of autologous blood donation is often limited. Augmentation of preoperative blood donation by therapy with recombinant human erythropoietin (rHuEPO) has been described in animal models and in patients. METHODS. In a multicenter, controlled, randomized trial, 49 patients scheduled for orthopaedic or vascular surgery received 0 (control group, n = 9), 200 (n = 10), 300 (n = 11), 400 (n = 10) or 500 (n = 9) U/kg rHuEPO (Erypo, Cilag, Sulzbach, distributor Fresenius, Oberursel, Germany) subcutaneously twice a week for 3 weeks while every week 450 ml blood was collected. Iron sulphate 100 mg was prescribed orally twice a day. Patients were ineligible if they had uncontrolled hypertension, recent myocardial infarction, haematological disorders or a history of seizures. Blood donation had to be cancelled if the haematocrit was below 30%. RESULTS. There was a significant (ANOVA) drop of the haematocrit value only in the control group, and end-point values for haematocrit and haemoglobin were significantly elevated in the 400 and 500 U/kg groups compared with the control group (Table 9). DISCUSSION. The erythropoietic stimulus of phlebotomy for autologous blood donations is often not efficient enough to guarantee a constant haematocrit. Lowering of the preoperative haematocrit jeopardizes the aim of avoidance of homologous blood transfusions. rHuEPO increased the efficiency of autologous blood collections, as predonation haematocrit values could be preserved in the high-dosage groups. As a consequence, homologous transfusions could be avoided. However, there were broad interindividual differences in the erythropoietic response, possibly due to limitations in iron availability. Adverse effects of rHuEPO therapy, such as hypertension, thrombosis or neurologic disorders, are mostly reported in patients with terminal kidney failure. No such disturbances were observed in the present study. CONCLUSION. rHuEPO ameliorates the preoperative decrease of haemoglobin and haematocrit values due to autologous blood donations in a dose-related fashion. The individually adjusted dosage of rHuEPO and iron supplementation merits further investigation.
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PMID:[Erythropoietin therapy during frequent autologous blood donations. Dose-finding study]. 748 23

L-Arginine-derived nitrogen monoxide (NO) formation was determined in different regions of the rat brain during kainate-induced seizures. NO was trapped in vivo as a paramagnetic mononitrosyl-iron diethyldithiocarbamate complex, the concentration of which was determined ex vivo by cryogenic electron spin resonance spectroscopy. Basal NO formation (0.3-0.8 nmol g-1 tissue 30 min-1) was detected in the brain of control rats. In kainate-injected rats NO formation was increased six-fold within 30-60 min in the amygdala/temporal cortex region, and up to 12-fold, though more slowly, in the remaining cortex. The kainate-elicited convulsions and NO formation were attenuated in animals pretreated with either 7-nitroindazole, a specific inhibitor of neuronal NO synthase, or diazepam. These findings identify NO as a proconvulsant mediator in kainate-evoked seizures.
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PMID:Nitric oxide promotes seizure activity in kainate-treated rats. 753 56


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