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)

Acute hepatic failure develops as a disease entity of rather diverse origin. With disease progression, toxic bilirubin levels may cause severe complications which include AV-nodal blockage, cardiac arrhythmia, impaired consciousness, generalized seizures, and status epilepticus. Treatment choices to prevent clinical deterioration comprise of costly and limited available orthotopic liver transplantation, utilization of extracorporeal bioartificial liver support devices and haemoperfusion/plasmaperfusion treatment with activated charcoal/anion exchange filters. Here, we present a patient with acute drug-induced cholestatic hepatitis. Excessively elevated bilirubin levels were accompanied by cardiac and cerebral complications. Extracorporeal resin perfusion treatment (Plasorba, BR-350) was successfully performed over a 50-day period without activation of the coagulation system or side effects. Bilirubin levels were lowered to a minimum of 225 micromol/l, with concurrent clinical improvement. In conclusion, extracorporeal anion exchange plasmaperfusion may be a viable long-term treatment for hyperbilirubinaemic side effects in overt cholestatic hepatitis.
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PMID:Long-term extracorporeal bilirubin elimination: A case report on cascade resin plasmaperfusion. 1034 81

The interactions between sleep and epilepsy are well known. A nodal point of the relationship between sleep and epilepsy is represented by pharmacological treatment. Sleep disturbances such as drowsiness are among the most frequent side effects of treatment with antiepileptic drugs, since they can deeply modify both sleep architecture and the sleep-wake cycle. Severe daytime somnolence affects patients' activities and it may facilitate the occurrence of seizures. These considerations underline the importance of antiepileptic drugs having anticonvulsant properties that do not negatively influence sleep and daytime somnolence. In this paper we review some relevant aspects of the effects of antiepileptic drugs on sleep.
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PMID:Effect of antiepileptic drugs on sleep. 1099 64

Sinus histocytosis with massive lymphadenopathy, also known as Rosai-Dorfman Disease (RDD), is an idiopathic histiocytic proliferation affecting lymph nodes. Although extranodal involvement has been reported in diverse sites, central nervous system (CNS) manifestation, particularly in the absence of nodal disease is uncommon. We report 11 cases of RDD primary to the CNS without evidence of other sites of involvement. The cases included 7 males and 4 females ranging in age from 22 to 63 years (mean: 41 y). The patients presented with headaches, seizures, numbness, or paraplegia. Eight cases involved the cranial cavity and three cases, the spinal canal. Lesions were most often extra-axial and dura based. Only one presented in the CNS parenchyma. Histologically, the lesions consisted of variable numbers of pale-staining histocytes with emperipolesis often overshadowed by extensive lymphoplasmacytic infiltrates and fibrosis in the background. Special stains for organisms were negative. By immunohistochemical analysis, the characteristic histiocytes were positive for S100 protein and CD68 and negative for CD1a. Treatment consisted of surgical biopsy or excision. Follow-up, available for 10 cases with intervals ranging from 5 days to 42 months (mean: 15 mo), disclosed one patient dying of operative complications 5 days after biopsy and nine patients with no evidence of disease progression RDD should be considered in the differential diagnosis of inflammatory lesions of the CNS. Our study suggests that this entity may have been misdiagnosed in the past as plasma cell granuloma or inflammatory pseudotumor.
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PMID:Rosai-Dorfman disease isolated to the central nervous system: a report of 11 cases. 1126 22

A coupled ordinary differential equation lattice model for the CA3 region of the hippocampus (a common location of the epileptic focus) is developed. This model consists of a hexagonal lattice of nodes, each describing a subnetwork consisting of a group of prototypical excitatory pyramidal cells and a group of prototypical inhibitory interneurons connected via on/off excitatory and inhibitory synapses. The nodes communicate using simple rules to simulate the diffusion of extracellular potassium. Both the integration time over which a node's trajectory is integrated before the diffusional event is allowed to occur and the level of inhibition in each node were found to be important parameters. Shorter integration times lead to total synchronization of the lattice (similar to synchronous neural activity occurring during a seizure) whereas longer times cause more random spatiotemporal behavior. Moderately diminished levels of inhibition lead to simple nodal oscillatory behavior. It is postulated that both the lack of inhibition and an alteration in conduction time may be necessary for the development of a behaviorally manifest seizure. (c) 1999 American Institute of Physics.
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PMID:A coupled ordinary differential equation lattice model for the simulation of epileptic seizures. 1277 75

Sodium channel beta1 subunits modulate alpha subunit gating and cell surface expression and participate in cell adhesive interactions in vitro. beta1-/- mice appear ataxic and display spontaneous generalized seizures. In the optic nerve, the fastest components of the compound action potential are slowed and the number of mature nodes of Ranvier is reduced, but Na(v)1.6, contactin, caspr 1, and K(v)1 channels are all localized normally at nodes. At the ultrastructural level, the paranodal septate-like junctions immediately adjacent to the node are missing in a subset of axons, suggesting that beta1 may participate in axo-glial communication at the periphery of the nodal gap. Sodium currents in dissociated hippocampal neurons are normal, but Na(v)1.1 expression is reduced and Na(v)1.3 expression is increased in a subset of pyramidal neurons in the CA2/CA3 region, suggesting a basis for the epileptic phenotype. Our results show that beta1 subunits play important roles in the regulation of sodium channel density and localization, are involved in axo-glial communication at nodes of Ranvier, and are required for normal action potential conduction and control of excitability in vivo.
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PMID:Mice lacking sodium channel beta1 subunits display defects in neuronal excitability, sodium channel expression, and nodal architecture. 1510 18

The National Neonatal Perinatal Database (NNPD) network is a collaborative group of leading neonatal units in India involved in the prospective collection of morbidity and mortality data on uniform protocols. The present article reports the morbidity and mortality profile of outborn neonates in the year 2000. Ten centers provided data on outborn neonates. The data were analysed at the nodal center using Epi-Info statistical software version 6 and Excel 97. A total of 3831 neonates were admitted at the participating institutions. A majority of them (87.2 per cent) were delivered in nursing homes and small hospitals. Most of the admissions (68.7 per cent) were male. Nearly half of them (48.7 per cent) were low birthweight and one-third (32.1 per cent) were preterm. Overall mortality was 16.4 per cent, while 7.5 per cent left hospitals against medical advice. Nearly half of all neonatal deaths occurred within the first 48 h following admission. Common primary causes of deaths (n = 630) included: infections (36.0 per cent), prematurity related conditions (26.5 per cent), perinatal hypoxia (10.0 per cent), and malformations (7.8 per cent). Systemic infections (28.4 per cent), hyperbilirubinemia (27.9 per cent), seizures (11.7 per cent), hypoglycemia (11.5 per cent), hypoxic ischemic encephalopathy (8.3 per cent), anemia (8.9 per cent), and hypocalcemia (8.6 per cent) were common morbidities observed. Of systemic infections, 39.2 per cent were culture positive and 51.4 per cent were early onset (< 72 h). Sick babies were managed with antibiotics (75 per cent), oxygen administration (45.3 per cent), phototherapy (34.9 per cent), and assisted ventilation (16.3 per cent). In conclusion, the present study describes the morbidity and mortality profile of a large multicentric cohort of outborn neonates from a developing country.
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PMID:Morbidity and mortality among outborn neonates at 10 tertiary care institutions in India during the year 2000. 1523 94

Rosai-Dorfman disease (RDD) is an idiopathic proliferation of histiocytes that affects the lymph nodes. Central nervous system involvement in the absence of nodal disease is extremely rare. On neuroimaging studies, intracranial RDD appears as solitary or multiple well-circumscribed, dura-based lesions. The authors report on two cases of RDD with locally aggressive features including dural sinus invasion, which to their knowledge has never before been described. A 60-year-old woman presented with progressive dizziness and vertigo that had lasted for 1 week. Cranial computerized tomography and magnetic resonance imaging revealed an extraaxial homogeneous lobulated enhancing mass involving the right occipital lobe and the right cerebellar hemisphere. Invasion of the right transverse sinus was identified on a cerebral digital subtraction angiogram. A 59-year-old man with no prior medical illness experienced progressive weakness of both upper extremities and a partial complex seizure. Magnetic resonance imaging of his brain revealed a well-circumscribed enhancing mass in the left frontal lobe with extension to the right frontal lobe and invasion of the superior sagittal sinus. Both patients underwent resection of their brain masses. Pathological studies identified the disease as RDD in both patients.
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PMID:Rosai-Dorfman disease with dural sinus invasion. Report of two cases. 1579 95

Mutations that reduce the function of KCNQ2 channels cause neuronal hyperexcitability, manifested as epileptic seizures and myokymia. These channels are present in nodes of Ranvier in rat brain and nerve and have been proposed to mediate the slow nodal potassium current I(Ks). We have used immunocytochemistry, electrophysiology and pharmacology to test this hypothesis and to determine the contribution of KCNQ channels to nerve excitability in the rat. When myelinated nerve fibres of the sciatic nerve were examined by immunofluorescence microscopy using antibodies against KCNQ2 and KCNQ3, all nodes showed strong immunoreactivity for KCNQ2. The nodes of about half the small and intermediate sized fibres showed labelling for both KCNQ2 and KCNQ3, but nodes of large fibres were labelled by KCNQ2 antibodies only. In voltage-clamp experiments using large myelinated fibres, the selective KCNQ channel blockers XE991 (IC50 = 2.2 microm) and linopirdine (IC50 = 5.5 microm) completely inhibited I(Ks), as did TEA (IC50 = 0.22 mm). The KCNQ channel opener retigabine (10 microm) shifted the activation curve to more negative membrane potentials by -24 mV, thereby increasing I(Ks). In isotonic KCl 50% of I(Ks) was activated at -62 mV. The activation curve shifted to more positive potentials as [K+]o was reduced, so that the pharmacological and biophysical properties of I(Ks) were consistent with those of heterologously expressed homomeric KCNQ2 channels. The ability of XE991 to selectively block I(Ks) was further exploited to study I(Ks) function in vivo. In anaesthetized rats, the excitability of tail motor axons was indicated by the stimulus current required to elicit a 40% of maximal compound muscle action potential. XE991 (2.5 mg kg(-1) i.p.) eliminated all nerve excitability functions previously attributed to I(Ks): accommodation to 100 ms subthreshold depolarizing currents, the post-depolarization undershoot in excitability, and the late subexcitability after a single impulse or short trains of impulses. Due to reduced spike-frequency adaptation after XE991 treatment, 100 ms suprathreshold current injections generated long trains of action potentials. We conclude that the nodal I(Ks) current is mediated by KCNQ channels, which in large fibres of rat sciatic nerve appear to be KCNQ2 homomers.
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PMID:KCNQ channels mediate IKs, a slow K+ current regulating excitability in the rat node of Ranvier. 1652 53

A few series in the literature were published before 1987 on syndrome of inappropriate antidiuretic hormone secretion (SIADH) in small cell lung cancer (SCLC). This study examines the outcome in more recent era. From 1981-1998, there were 1417 new cases of SCLC diagnosed in the provincial registry, of which 244 were of limited stage (LS). A chart review and statistical analyses were performed using Mann-Whitney test, chi-square test and Kaplan-Meier method. Fourteen LS patients (group A) had SIADH at presentation. Group B consisted of 230 LS patients without SIADH. There were more patients with poorer performance status (ECOG 2-4) in group A than B (28.6% versus 7.8%, P=0.03). Otherwise, sex, age at diagnosis, nodal spread, pleural effusion, bronchial obstruction, superior vena cava obstruction, performance status, weight loss, and lactic dehydrogenase at presentation, were comparable between the two groups. Treatments given, e.g., extent of surgical resection (if performed, whether complete/incomplete), total number of chemotherapy cycles, radiotherapy doses, were comparable (P>0.05). The response to chemo-radiation was not significantly different (P=0.7). Five-year overall survival (8% versus 19%, P=0.08), and cause-specific survival (16% versus 20%, P=0.13) showed that group A patients had a worse outcome, though of borderline significance. Symptoms related to SIADH included: weakness, 4 patients; tiredness, 3; change in level of consciousness, 1; seizure, 1. The range of lowest sodium level was 110-129. Two patients also had paraneoplastic myopathy. SIADH resolved in 12 patients at 1.6-44.7 weeks (median: 4.3). Among the 14 patients who initially presented with SIADH and recurred later, 10 had recurrence of SIADH at the time of tumor recurrence. Serum sodium was useful for post-treatment surveillance in SCLC patients who presented with SIADH, with 71% (10/14) developing SIADH again at the time of recurrence. SIADH is a poor prognostic factor for LS SCLC.
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PMID:Syndrome of inappropriate antidiuretic hormone secretion (SIADH) in patients with limited stage small cell lung cancer. 1678 84

Grayanotoxin intoxication, which is mostly seen in the eastern Black Sea region of Turkey, stems from the "mad honey" made by bees from the rhododendron plant flowers. In low doses, this causes dizziness, hypotension, and bradycardia, and in high doses, impaired consciousness, seizures, and atrioventricular block (AVB). This case study was designed as a series of cases of patients (6 women, 2 men) aged between 35 and 75 years. All of the patients' physical examinations revealed hypotension; 4 patients had sinus bradycardia, 3 had nodal rhythm, and 1 had complete AVB. In all patients, except for the patient with AVB, heart rate and blood pressure returned to normal limits within 2 to 6 hours. Two patients were monitored in the coronary intensive care unit. Of these 2, 1 was discharged on the second day. The other was fitted with a temporary pacemaker and was discharged on the third day. All the other patients were kept in for a 6-hour observation period and were then discharged from the ED. To date, 58 such cases have been reported, but we saw 8 patients within 2005. It is commonly seen in the east of the Black Sea region, although cases may occur from all over the eastern Black Sea region of Turkey. So far, no cases of death have been reported, although grayanotoxin causes adverse effects on the cardiovascular and respiratory systems and is therefore of considerable importance.
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PMID:Mad honey poisoning. 1693 99


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