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)

From 1983 to 1997, we have studied ten children with complete atrioventricular block likely due to myocarditis in order to assess its prognosis and to define a therapeutic strategy. Their age ranged from 6 days to 16 years (median: 4.1 years). All were admitted for sudden complete block, with symptoms in seven: syncope or fainting, seizures, collapse. Three had an asymptomatic bradycardia which was detected on routine auscultation in children with fever or already hospitalized; fever was present in 5. The disease was related to infection on biological data in 4 cases (1 listeriosis and 3 seroconversions for Epstein Barr or cytomegalic or Coxsackie B viruses), on a myocardial biposy in 1 case and on scintigraphic data in 1 case. In the remaining 4, indirect arguments were considered such as infectious context, normal recent ECG, favourable outcome. Five children were given intravenous isoprenalin with ventricular tachycardia in 3. Five were treated with steroids and 3 with specific antiviral agents. Seven patients were paced temporarily. One child died, 6 recovered totally and 3 have a permanent block with a definitive pacemaker implanted in 2. In conclusion, sudden acquired complete atrioventricular blocks are often ill-tolerated in children and have to be treated with transient pacing. Recovery occurs as a rule but some of these blocks may be definitive. Infective myocarditis is likely to be the cause of the disease even if the pathogen agent cannot always be identified.
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PMID:[Therapy and prognosis of infectious complete atrioventricular block in children]. 1085 52

Status epilepticus is common and associated with significant mortality and complications. It affects approximately 50 patients per 100,000 population annually and recurs in >13%. History of epilepsy is the strongest single risk factor for generalized convulsive status epilepticus. More than 15% of patients with epilepsy have at least one episode of status epilepticus and low antiepileptic drug levels are a potentially modifiable risk factor. Other risks include young age, genetic predisposition, and acquired brain insults. Fever is a very common risk in children, as is stroke in adults. Mortality rates are 15% to 20% in adults and 3% to 15% in children. Acute complications result from hyperthermia, pulmonary edema, cardiac arrhythmias, and cardiovascular collapse. Long-term complications include epilepsy (20% to 40%), encephalopathy (6% to 15%), and focal neurologic deficits (9% to 11%). Neuronal injury leading to temporal lobe epilepsy is probably mediated by excess excitation via activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors and consequent elevated intracellular calcium that causes acute necrosis and delayed apoptotic cell death. Some forms of nonconvulsive status epilepticus may also lead to neuronal injury by this mechanism, but others may not. Based on clinical and experimental observations, complex partial status epilepticus is more likely to result in neuronal injury similar to generalized convulsive status epilepticus. Absence status epilepticus is much less likely to result in neuronal injury, and complications because it may be mediated primarily through excess inhibition. Future research strategies to prevent complications of status epilepticus include the study of new drugs (including NMDA antagonists, new drug delivery systems, and drug combinations) to stop seizure activity and prevent acute and delayed neuronal injury that leads to the development of epilepsy.
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PMID:Status epilepticus: risk factors and complications. 1088 37

Contrary to a century-old belief that dendritic spines are stable storage sites of long term memory, the emerging picture from a recent flurry of exciting observations using novel high resolution imaging methods of living cells in culture is that of a dynamic structure, which undergoes fast morphological changes over periods of hours and even minutes. Concurrently, the nature of stimuli which cause formation or collapse of dendritic spines has changed from a mysterious Hebbian-governed plasticity producing stimulus to the more trivial activation of the synapse by strong/weak stimulation. The molecular mechanisms underlying spine plasticity are beginning to emerge; the role of presynaptic and/or postsynaptic activity, genetic, central or local factors in the formation and retraction of spines are currently being analyzed. A common mechanism for both, formation/elongation and pruning/retraction of spines, involving changes in intracellular calcium concentration ([Ca(2+)](i)), is emerging. It appears that [Ca(2+)](i) is related to changes in spines in a bell shape form: lack of synaptic activity causes transient outgrowth of filopodia but eventual elimination of spines, a moderate rise in [Ca(2+)](i) causes elongation of existing spines and formation of new ones, while a massive increase in [Ca(2+)](i) such as that seen in seizure activity, causes fast shrinkage and eventual collapse of spines. Nuclear signals (e.g. CREB), activated by an increase in [Ca(2+)](i), are involved in the central regulation of spine formation, while spine shrinkage and elongation are probably triggered by local [Ca(2+)](i) changes. This hypothesis provides a parsimonious explanation for conflicting reports on activity-dependent changes in dendritic spine morphology. Still, the many differences between cultured neurons, with which most of current studies are conducted, and the neuron in the real brain, require a cautious extrapolation of current assumptions on the regulation of spine formation.
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PMID:Rapid plasticity of dendritic spine: hints to possible functions? 1104 Apr 18

Cocaine, derived from the leaves of the shrub Erythroxylon coca, which grows on the slopes of the Andes, remains one of the most widely abused illicit drugs (Johnson et al., 1993). Its abuse appears to be increasing and as a result, so is its trafficking across borders, with ever-increasing sophistication of concealment (Rouse, 1992). Over the past few years, cases of cocaine intoxication have been reported, resulting from ruptured packets of cocaine that have been swallowed, or inserted into the vagina or rectum by couriers (drug smugglers), so called 'body packers' or 'mules' (Westli and Mittleman, 1981; Ricaurte and Langston, 1995). Cocaine is a powerful sympathomimetic and central nervous system stimulant, an overdose of which causes primarily cardiac, neurological and psychiatric effects (Ricaurte and Langston, 1995). Acute toxicity is dose-related and is characterized in the first place by its sympathomimetic effects, which include tachycardia, hypertension and hyperthermia arrythmias, followed by seizures. Brainstem depression and cardio-respiratory collapse, stroke, coma, intracranial vasculitis, myocardial infarction and sudden death have all been reported in cocaine abuse (Ricaurte and Langston, 1995). We present a fatal case with neurological and psychiatric symptoms, but without the usual cardiac and systemic signs.
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PMID:Body packer: cocaine intoxication, causing death, masked by concomitant administration of major tranquilizers. 1105 42

The death of a 36-year-old alcoholic man who died after developing seizure activity while being treated with tramadol, as well as with venlafaxine, trazodone, and quetiapine, all of which interact with the neurotransmitter serotonin, is reported. The decedent, who had a history of chronic back pain, alcoholism, depression, mild hypertensive cardiovascular disease, and gastritis, had just been discharged from the hospital after 4 days of alcohol detoxification treatment. During the admission, no withdrawal seizures were noted. The morning after discharge, a witness observed the decedent exhibiting seizure activity and then collapsing. An autopsy was performed approximately 6 hours after death, and the anatomic findings were consistent with seizure activity and collapse, which included biting injuries of the tongue and soft-tissue injuries of the face. Toxicologic analysis identified tramadol, venlafaxine, promethazine, and acetaminophen in the urine; tramadol (0.70 mg/L) and venlafaxine (0.30 mg/L) in the heart blood, and 0.10 mg of tramadol in 40 ml of submitted stomach contents. No metabolites, such as acetate, acetone, lactate, and pyruvate, were found in the specimens that would be characteristically found in a person with alcohol withdrawal syndrome. The threshold for seizures is lowered by tramadol. In addition, the risk for seizure is enhanced by the concomitant use of tramadol with selective serotonin reuptake inhibitors or neuroleptics, and its use in patients with a recognized risk for seizures, i.e., alcohol withdrawal. The cause of death in this individual was seizure activity complicating therapy for back pain, depression, and alcohol withdrawal syndrome. The data in Adverse Event Reporting System of the Food and Drug Administration from November 1, 1997 to September 8, 1999 was reviewed along with a MEDLINE search from 1966 to the present. This case appears to be the first reported death caused by seizure activity in a patient taking tramadol in combination with drugs that affect serotonin.
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PMID:Lethal combination of tramadol and multiple drugs affecting serotonin. 1111

We used northern and western blotting to measure the quantity of glutamate and GABA transporters mRNA and their proteins within the hippocampal tissue of rats with epileptogenesis. Chronic seizures were induced by amygdalar injection of kainic acid 60 days before death. We found that expression of the mRNA and protein of the glial glutamate transporters GLAST and GLT-1 were down-regulated in the kainic acid-administered group. In contrast, EAAC-1 and GAT-3 mRNA and their proteins were increased, while GAT-1 mRNA and protein were not changed. We performed in vivo microdialysis in the freely moving state. During the interictal state, the extracellular glutamate concentration was increased, whereas the GABA level was decreased in the kainic acid group. Following potassium-induced depolarization, glutamate overflow was higher and the recovery time to the basal release was prolonged in the kainic acid group relative to controls. Our data suggest that epileptogenesis in rats with kainic acid-induced chronic seizures is associated with the collapse of extracellular glutamate regulation caused by both molecular down-regulation and functional failure of glutamate transport.
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PMID:Collapse of extracellular glutamate regulation during epileptogenesis: down-regulation and functional failure of glutamate transporter function in rats with chronic seizures induced by kainic acid. 1115 61

Electroencephalography (EEG) is a valuable diagnostic test to identify functional disturbances in brain activity. The purpose of this study was to assess the validity of EEG as a diagnostic indicator of intracranial diseases in horses. The validity of EEG was estimated by comparing clinical, clinicopathologic, and histopathologic findings to EEG findings in 20 horses examined for seizures. collapse, or abnormal behavior between 1984 and 1997. A bipolar left-to-right, back-to-front montage and a bipolar circular montage were recorded from sedated (4) and anesthetized (16) horses. Visual and semiquantitative masked analysis of EEG recording Ist was validated on 10 horses presented for problems other than intracranial diseases. EEG pattern was normal in 7 of the 20 clinically affected horses. Abnormal EEG patterns included high-voltage slow waves and discrete paroxysmal activity with or without generalized activity in 13 horses. Histopathologic diagnoses in 10 horses included meningoencephalitis, neuronal necrosis, congenital anomalies. cerebral edema. and abscess. All of these horses had abnormal EEG patterns (sensitivity, 100%) with a positive neuroanatomic correlation in 7 animals. Localization of histopathologic and EEG abnormalities did not correlate in 15% of the horses (3/20). The cause of neurologic signs could not be explained at postmortem examination in 10 animals and the EEG pattern was normal in 7 of these horses (specificity, 70%). In conclusion, equine EEG was a sensitive tool in the diagnosis of intracranial disorders.
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PMID:Diagnostic validity of electroencephalography in equine intracranial disorders. 1146 98

We report a case of fatal intoxication with 2% viscous lidocaine. A 18 month old infant was admitted after malaise and cardiorespiratory arrest at home. He was resuscitated, then seizures appeared before arrival at the hospital. Treatment was symptomatic, including cardiorespiratory resuscitation and administration of anticonvulsants. Identification of lidocaine and its metabolite monoethylglycinexylidide (MEGX) MEGX was performed after organic extraction by High Performance Liquid Chromatography (HPLC) with Diode Array Detection (DAD); the serum concentrations, determined by Fluorescence Polarisation Immuno Assay (FPIA), were: 1.1 micrograms/ml for lidocaine and 0.94 microgram/ml for MEGX (H + 7) and 0.30 microgram/ml for the lidocaine (Day + 1). Neurotoxic manifestations appear at lower concentrations than cardiotoxic symptoms which are correlated with plasma levels of lidocaine. The toxic symptoms begin with headache, hallucinations, seizure, coma, respiratory arrest and circulatory collapse. The toxic symptoms can persist even after the decrease of lidocaine concentration under therapeutic levels. There is no antidote and acute lidocaine toxicity is managed with supportive therapy (diazepam for seizures, intubation, chronotropic agents). Considering the gravity of these poisonings which remain rare, the 2% viscous lidocaine prescription is forbidden for children under 6 years old.
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PMID:[Fatal intoxication after accidental ingestion of viscous 2% lidocaine in a young child]. 1197 45

Pheochromocytomas are frequently associated with inherited cancer syndromes such as von Hippel-Lindau disease (VHL). Retinal angioma and hemangioblastomas of the central nervous system are hallmarks of VHL, but its clinical variety is remarkably broad. Pheochromocytomas as the sole or first manifestation of VHL are rare but have been observed. In this case report, the authors describe an unusual case of initial collapse, seizures, and hypertensive crisis in a child who later was found to have multiple extraadrenal pheochromocytomas. Molecular diagnostics revealed a novel point mutation in the VHL gene (VHL nt. 406 T-->G). Only 7 months after the first lesions had been removed, a new paraganglioma developed in the contralateral periadrenal region. When encountering pheochromocytomas in children, the clinician should be aware that an associated tumor syndrome might be present, and appropriate molecular screening should be initiated. Molecular genetics aid in the clinical decision-making and clinical management of individual patients with pheochromocytoma.
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PMID:Recurrent polytopic chromaffin paragangliomas in a 9-year-old boy resulting from a novel germline mutation in the von Hippel-Lindau gene. 1199 Jul 3

Regional anesthesia has become a routine part of the practice of anesthesiology in infants and children. Local anesthetic toxicity is extremely rare in infants and children; however, seizures, dysrhythmias, cardiovascular collapse, and transient neuropathic symptoms have been reported. Infants and children may be at increased risk from local anesthetics compared with adults. Larger volumes of local anesthetics are used for epidural anesthesia in infants and children than in adults. Metabolism and elimination of local anesthetics can be delayed in neonates, who also have decreased plasma concentrations of alpha(1)-acid glycoprotein, leading to increased concentrations of unbound bupivacaine. Most regional anesthetic procedures in infants and children are performed with the patient heavily sedated or anesthetized; because of this, and because a test dose is not a particularly sensitive marker of intravenous injection in the anesthetized patient, detection of intravascular local anesthetic injection is extremely difficult. The same local anesthetics used in adult anesthetic practice are also used in infants and children. Because of its extremely short duration of action, chloroprocaine has been used primarily for continuous epidural techniques in infants and children. The use of tetracaine has generally been limited to spinal and topical anesthesia. Lidocaine (lignocaine) has been used extensively in infants and children for topical, regional, plexus, epidural and spinal anesthesia. The association between prilocaine and methemoglobinemia has generally restricted prilocaine use in infants and children to the eutectic mixture of local anesthetics (EMLA). Because of its greater degree of motor block compared with other long-acting local anesthetics, etidocaine has generally been limited to plexus blocks in infants and children. Mepivacaine has been used for both plexus and epidural anesthesia in infants and children. Because postoperative analgesia is often the primary justification for regional anesthesia in infants and children, bupivacaine, a long-acting local anesthetic, is the most commonly reported local anesthetic for pediatric regional anesthesia. Given the lower toxic threshold of bupivacaine compared with other local anesthetics, the risk-benefit ratio of bupivacaine may be greater than that of other local anesthetics. Two new enantiomerically pure local anesthetics, ropivacaine and levobupivacaine, offer clinical profiles comparable to that of bupivacaine but without its lower toxic threshold. The extreme rarity of major toxicity from local anesthetics suggests that widespread replacement of bupivacaine with ropivacaine or levobupivacaine is probably not necessary. However, there are clinical situations, including prolonged local anesthetic infusions, use in neonates, impaired hepatic metabolic function, and anesthetic techniques requiring a large mass of local anesthetic, where replacement of bupivacaine with ropivacaine, levobupivacaine or (for continuous techniques) chloroprocaine appears prudent.
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PMID:Benefit and risks of local anesthetics in infants and children. 1226 41


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