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

1. Imidazole 4-acetic acid (IMA) is a naturally occurring metabolite in brain, although it is unclear what biochemical pathways are involved in its biosynthesis and breakdown. Some evidence, however, suggests that IMA is an oxidation product of histamine. 2. The compound has pronounced neuropharmacological properties, many of which are consistent with an activation of GABA(A) receptors. Indeed, IMA is able to displace [3H]GABA from GABA(A) sites in a potent manner. 3. IMA displays definite partial agonist characteristics as an enhancer of benzodiazepine binding to the GABA(A) receptor complex in membrane preparations. In addition, it has an affinity for GABA(C) receptors, where it seems to act as an antagonist, and perhaps as a weak partial agonist. A third recognition site for IMA in brain is the I1-imidazoline receptor. 4. Parenteral administration to experimental animals leads to a sleep-like state which can often be accompanied by seizures. In addition, central application of IMA has been associated with a dose-related reduction in arterial pressure and sympathetic nervous discharge. 5. No specific receptor site or uptake system for IMA has yet been discovered, adding uncertainty to its role in central nervous system function. Yet the possibility cannot be overlooked that IMA plays a role in regulating blood pressure.
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PMID:Pharmacology and function of imidazole 4-acetic acid in brain. 979 7

Parenteral injection of endotoxin has been used as a model to examine the role of pro-inflammatory cytokines in the centrally controlled responses to Gram-negative bacterial infection. However, the events that occur following mucosal exposure to live bacteria have received little attention. In this study, we have used a murine model to demonstrate that respiratory infection with Bordetella pertussis, which is associated with a number of systemic complications including fever, seizure and encephalopathy in children, resulted in persistent expression of mRNA transcripts for IL-1beta and TNFalpha and transient expression of IL-6 in the hippocampus and hypothalamus. These changes correlated with elevated levels of cytokine protein in the same brain areas. The results demonstrate that infection at a mucosal surface can result in the induction of pro-inflammatory cytokine production in the brain and suggest that these locally synthesized mediators may contribute to the centrally controlled clinical manifestations of B. pertussis infection.
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PMID:Induction of inflammatory cytokines in the brain following respiratory infection with Bordetella pertussis. 1063 86

A hypertensive emergency is a situation in which uncontrolled hypertension is associated with acute end-organ damage. Most patients presenting with hypertensive emergency have chronic hypertension, although the disorder can present in previously normotensive individuals, particularly when associated with pre-eclampsia or acute glomerulonephritis. The pathophysiological mechanisms causing acute hypertensive endothelial failure are complex and incompletely understood but probably involve disturbances of the renin-angiotensin-aldosterone system, loss of endogenous vasodilator mechanisms, upregulation of proinflammatory mediators including vascular cell adhesion molecules, and release of local vasoconstrictors such as endothelin 1. Magnetic resonance imaging has demonstrated a characteristic hypertensive posterior leucoencephalopathy syndrome predominantly causing oedema of the white matter of the parietal and occipital lobes; this syndrome is potentially reversible with appropriate prompt treatment. Generally, the therapeutic approach is dictated by the particular presentation and end-organ complications. Parenteral therapy is generally preferred, and strategies include use of sodium nitroprusside, beta-blockers, labetelol, or calcium-channel antagonists, magnesium for pre-eclampsia and eclampsia; and short-term parenteral anticonvulsants for seizures associated with encephalopathy. Novel therapies include the peripheral dopamine-receptor agonist, fenoldapam, and may include endothelin-1 antagonists.
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PMID:Hypertensive emergencies. 1105 14

Acute isoniazid (INH) poisoning is uncommon in children. Although most physicians are aware of INH hepatotoxicity, acute INH poisoning and its treatment are not well recognized. INH is increasingly being used to control the spread of tuberculosis, and physicians should know its potentially fatal effects. INH overdose is known to result in rapid onset of seizures, metabolic acidosis and prolonged obtundation. We report two cases of obtundation secondary to INH overdose that was immediately reversed by pyridoxine. Parenteral pyridoxine administration is an effective method in INH intoxication. The intravenous form of pyridoxine must be available in the emergency care units, and INH toxicity should be suspected in any patient with refractory seizures and metabolic acidosis.
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PMID:Acute isoniazid neurotoxicity in childhood. 1185 81

We report pilomotor seizures in two patients who presented with piloerection or gooseflesh spreading in a pattern similar to the 'Jacksonian march'. Gooseflesh was confined to the ipsilateral side in most of the episodes. Occasionally it spread to the contralateral side. It was also associated with other autonomic symptoms and complex partial features of temporal lobe origin. Simple partial status that progressed to complex partial status occurred in the second patient. Very rarely secondary generalization occurred. The cause was left sphenoid meningioma and temporal tip contusion in the first case. It was idiopathic in the second case, although a positive family history of complex partial seizures was obtained in this patient. Interictal electroencephalogram (EEG) showed left temporal focus in the first and bitemporal foci with right fronto-temporal dominance in the second. Parenteral phenytoin controlled the partial complex status in the second and carbamazepine controlled the episodes in both cases. To our knowledge all reported cases were symptomatic and our case of idiopathic aetiology is the first to be recorded. We endorse that pilomotor seizures are autonomic in nature and constitute a subtype of simple partial seizures. These autonomic simple partial seizures may progress to, or be a component of, complex partial seizures of temporal lobe origin. Based on their dominance in such a symptom complex and careful interpretation of the ictal history, it can be logically concluded that pilomotor seizures may be underestimated by both patients and physicians.
Seizure 2002 Oct
PMID:Pilomotor seizures: symptomatic vs. idiopathic report of two cases and literature review. 1223 74

Pyridoxine-dependent seizure is a rare autosomal recessive disorder that usually presents with neonatal intractable seizures. This syndrome results from an inborn abnormality of the enzyme glutamic acid decarboxylase, which results in reduced pyridazine-dependent synthesis of the inhibitory neurotransmitter gamma amino butyric acid. The full range of symptomatology is unknown; but can be associated with autism, breath holding and severe mental retardation, bilious vomiting, transient visual agnosia, severe articulatory apraxia motor dyspraxia, microcephaly and intrauterine seizures. Parenteral pyridine injection test is a highly effective and reproducible test in confirming the diagnosis. Pyridoxine should be administered as a diagnostic test in all cases of convulsive disorders of infancy in which no other diagnosis is evident. Epileptic seizure discharges subside within 2-6 minutes after the intravenous injection of 50-100 mg of pyridaoxine. Once the diagnosis is confirmed, maintenance therapy should be continued indefinitely and doses increased with age or intercurrent illnesses. The maintenance dose of Bg needed is still not clear. There is a relatively wide range for the daily B6 dose necessary to control the seizure i.e., 10-200 mg/day.
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PMID:Pyridoxine-dependent seizures: a review. 1288 19

Parenteral injection of kainic acid (KA), a glutamate receptor agonist, causes severe and stereotyped behavioral convulsions in mice and is used as a rodent model for human temporal lobe epilepsy. The goal of this study is to examine the potential anti-convulsive effects of the neuro-active amino acid taurine, in the mouse model of KA-induced limbic seizures. We found that taurine (43 mg/Kg, s.c.) had a significant antiepileptic effect when injected 10 min prior to KA. Acute injection of taurine increased the onset latency and reduced the occurrence of tonic seizures. Taurine also reduced the duration of tonic-clonic convulsions and mortality rate following KA-induced seizures. Furthermore, taurine significantly reduced neuronal cell death in the CA3 region of the hippocampus, the most susceptible region to KA in the limbic system. On the other hand, supplementation of taurine in drinking water (0.05%) for 4 continuous weeks failed to decrease the number or latency of partial or tonic-clonic seizures. To the contrary, we found that taurine-fed mice showed increased susceptibility to KA-induced seizures, as demonstrated by a decreased latency for clonic seizures, an increased incidence and duration of tonic-clonic seizures, increased neuronal death in the CA3 region of the hippocampus and a higher post-seizure mortality of the animals. We suggest that the reduced susceptibility to KA-induced seizures in taurine-injected mice is due to an increase in GABA receptor function in the brain which increases the inhibitory drive within the limbic system. This is supported by our in vitro data obtained in primary neuronal cultures showing that taurine acts as a low affinity agonist for GABA(A) receptors, protects neurons against kainate excitotoxic insults and modulates calcium homeostasis. Therefore, taurine is potentially capable of treating seizure-associated brain damage.
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PMID:Prevention of epileptic seizures by taurine. 1290 38

Parenteral phenobarbitone is an integral part of the management of status epilepticus, especially in the context of resource-poor countries. It is highly effective at controlling seizures. It is safe, cheap, can be given by rapid intravenous push or intramuscular route, boluses can be repeated, and it is recommended as part of the Advanced Paediatric Life Support guidelines. The proposed alternatives lack efficacy, practicality and/or place the child in status epilepticus at risk of respiratory compromise. The impact of the loss of parenteral phenobarbitone would be increased cardiac complications, lack of early seizure control, prolonged seizures resulting in brain damage and systemic complications. Increased numbers of patients will require artificial ventilation in centres without facilities, and centres with facilities will be unable to cope with the load of ventilated patients because of lack of safe transport systems and bed space.
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PMID:Withdrawal of parenteral phenobarbitone--implications for resource-poor countries. 1634 20

Parenteral phenytoin is an effective agent used to manage seizures, but it is associated with adverse effects and must be given intravenously. Fosphenytoin is higher in drug cost, but is more soluble, better tolerated and can be infused at rates three times that of phenytoin. When infusion rate is not an issue the adverse effect risk becomes a focus of concern, as well as cost. The determination of the point at which the treatment costs of infusion-related adverse effects of phenytoin outweigh the drug costs of fosphenytoin has been attempted through various clinical economic analyses. Strategies developed to promote the safe use of intravenous phenytoin are based on patient selection, recommended administration methods and patient monitoring. When rapid attainment of serum phenytoin levels is required or in patients at high risk of adverse effects secondary to parenteral phenytoin, fosphenytoin is clearly preferred. This review will focus on the implications of the use of parenteral phenytoin products in the nonemergent setting where potential adverse effects of parenteral phenytoin may be avoided with use of established criteria for patient selection and administration.
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PMID:Cost-effectiveness of nonemergency use of phenytoin. 1980 94

Hypertensive crisis is an acute, life-threatening condition associated with a substantial sudden increase in blood pressure. If the increase is accompanied by a damage of brain, cardiovascular system, eye ground or kidneys, it is referred to as an emergent hypertensive situation. In case of complaints comprising chest pain, shortness of breath, headache, epistaxis, weakness, faintness or seizure alone without organ damage, it is referred to as an urgent hypertensive situation. Treatment of emergent situations is parenteral and is conducted under a permanent monitoring in an intensive care unit. Nitrates, urapidil, diuretics, angiotensin-converting enzyme inhibitors, calcium channel blockers, beta blockers and clonidin are used with respect to organ damage and accompanying diseases. Rate of blood pressure reduction and target values depend on a type of organ damages. An escalation of per oral medication is used in the treatment of urgent situations. Parenteral medication is indicated only in case of failure of this approach.
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PMID:[Hypertensive crisis--the present view]. 1989 22


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