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)

General principles of antiepileptic drug (AED) therapy are reviewed, current issues involving the use and monitoring of AEDs are examined, promising investigational agents are briefly reviewed, and situations that require potentially difficult decisions about long-term care are discussed. The initial treatment should be monotherapy with a first-line AED for the particular seizure disorder. The usual approach is to maximize seizure control and minimize the adverse effects of AED therapy. Current issues involving the pharmacokinetics, use, and monitoring of the conventional AEDs phenytoin, phenobarbital, primidone, carbamazepine, valproic acid, ethosuximide, benzodiazepines, and acetazolamide are discussed. AED therapy may have adverse effects on behavior and cognition. The risk of teratogenicity with well-monitored AED therapy is probably low, and severe hepatotoxicity is uncommon. Because carbamazepine, phenobarbital, phenytoin, and primidone all have enzyme induction properties, a number of clinically important interactions are possible. Issues related to discontinuing AED therapy, serum concentration monitoring, and generic interchange of AED products are addressed. Whether AEDs should be used to prevent recurrent febrile seizures, alcohol withdrawal seizures, or seizures in patients with head trauma or stroke must be considered. The treatment of seizure disorders is a complex process involving identification of the seizure disorder, selection and monitoring of an appropriate AED(s), and consideration of adverse effects and drug interactions. Whether therapy should be discontinued after a prolonged seizure-free period, compliance issues, and whether to treat certain conditions prophylactically also must be considered.
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PMID:Current issues in the treatment of epilepsy. 191 28

A 12 year old girl with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke like episodes (MELAS) is reported. After a normal childhood, at 9 years of age she developed generalized and hemilateralized seizures. Posteriorly, these episodes became more frequent and were accompanied by headache, homonimous hemianopsia, ataxia, vomiting, photophobia, left hemiparesis, slurred speech and even convulsive status. Laboratory tests evidenced lactic acidosis, brain lucencies at CT Scan and ragged skeletal muscle fibers at muscle biopsy.
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PMID:[Mitochondrial encephalomyopathy, lactic acidosis and features of cerebrovascular disorders]. 207 86

Clinical evidence implicates the cerebral cortex in the genesis of ECG changes and cardiac arrhythmias. Such findings are not infrequent following acute cortical stroke and during partial seizures. Electrical stimulation of the cerebral cortex, however, only rarely and inconsistently results in cardiac changes. When encountered, attendant alterations in blood pressure and respiration occur; consequently, it is unclear whether the cardiac effects are primary or secondary to these. Phasic insular cortex microstimulation linked to the ECG cycle, a new technique, elicits only heart rate effects, eliminating confounding variables. The insular cortex was chosen for study because of its profuse autonomic and limbic connectivity. Cardiac chronotropic sites were demonstrated in 37 chloralose-anesthetized rats, with tachycardia represented in the rostral posterior insula, and bradycardia in the caudal posterior insula. Both effects were abolished by atenolol but not by atropine, implying their mediation by respective increases or decreases in sympathetic activity. This is the first report of the demonstration of a cortical region wherein stimulation affects heart rate and no other parameter.
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PMID:Cardiac chronotropic organization of the rat insular cortex. 208 34

It is essential to image the carotid bifurcation adequately in patients with symptomatic carotid territory ischaemia if they are being considered for carotid endarterectomy. Optimal resolution is achieved by selective intraarterial contrast angiography which is an invasive procedure carrying some risk. The overall risk-benefit of carotid endarterectomy is currently being investigated in several large randomised trials in Europe and North America. Because cerebral angiography is a prerequisite for carotid endarterectomy, the risks of cerebral angiography will need to be added to those of surgery when considering whether carotid endarterectomy is effective in the management of these patients. This study evaluated prospectively 382 patients with symptomatically mild carotid ischaemia who had cerebral angiography to visualise a potentially resectable lesion at the carotid bifurcation. Complications followed 14 cerebral angiograms in 13 patients (3.4%); two complications were local (0.5%), two systemic (0.5%) and 10 were neurological (2.6%). The neurological complications were transient (TIA 1, generalised seizure 1) in two patients (0.5%), reversible (stroke) in three (0.8%) and permanent (stroke) in five patients (1.3%). There were no deaths. The significant risk factors for post angiographic stroke were (1) stroke before angiography compared with transient ischaemic attacks of the eye or brain and (2) the presence of greater than or equal to 50% diameter stenosis of the symptomatic internal carotid artery; unfortunately it may be the latter patients who are most at risk of stroke as part of the natural history of their disease and therefore most in need of prophylactic carotid endarterectomy (which requires cerebral angiography). The absolute risk of post-angiographic stroke of patients for cerebral angiography using clinical evaluation and Duplex carotid ultrasound screening.
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PMID:Complications of cerebral angiography for patients with mild carotid territory ischaemia being considered for carotid endarterectomy. 194 Sep 58

Induction of messenger RNA encoding the 70-kDa heat shock or stress protein, hsp70, and the product of the proto-oncogene c-fos was evaluated in gerbil hippocampus by in situ hybridization at various recirculation intervals after 5 minutes of ischemia. Striking increases in c-fos RNA were observed in dentate granule cells within 15 minutes of recirculation and remained evident through 1 hour, returning to undetectable control levels by 3 hours. Modest c-fos hybridization was seen in CA1 and CA3 neurons during the same time course. These results are consistent with the rapid and transient stimulation-induced c-fos expression observed in many experimental systems. Hsp70 expression showed a longer time course, being strongly induced in all major hippocampal neuron populations within 3 hours and persisting for approximately 12 hours in dentate granule cells and through 24 hours in CA3 pyramidal neurons. Notably, the most prolonged expression of hsp70 RNA was observed in vulnerable CA1 neurons that minimally accumulate the immunoreactive protein, with hybridization detected essentially until the death of this cell population at 3-4 days. These studies demonstrate an overlapping distribution of hsp70 and c-fos expression in gerbil hippocampus after ischemia, although there are differences in time course and in the relative induction observed in different neuron populations. The transient increase in c-fos hybridization in dentate granule cells is identical to that seen in various seizure paradigms and provides further support for activation of hippocampal circuitry after ischemia. The prolonged time course of hsp70 messenger RNA expression in vulnerable CA1 neurons may provide a molecular correlate of proposed excitotoxic mechanisms mediating delayed neuronal death.
Stroke 1990 Nov
PMID:70-kDa heat shock protein and c-fos gene expression after transient ischemia. 212 54

The pattern of epilepsy and other convulsive disorders in 1,000 consecutive Saudi nationals is described. These disorders were common with a hospital frequency rate of 8 per 1,000. Men were more frequently affected than women and 60% of the patients were under 10 years old at the onset of their illness. The epilepsies were the commonest type (74%). Febrile convulsions (20%) presented mainly between the ages of one and five years. Isolated seizures (3%) and acute symptomatic convulsions (3%) were uncommon. In the epileptic group, generalised seizures (71%) were more frequent than partial (29%) and complex partial seizures occurred mainly in those above 21 years old. Absences (4%), infantile spasms (3%) and atonic seizures (3%) were uncommon. No specific etiology of the epilepsy was determined in the majority of the cases (63%). The identified major etiologic factors of the epilepsies were perinatal encephalopathy (21%), cerebral trauma (11%), sequelae of meningitis or encephalitis (2%), brain tumors (0.5%), and vascular lesions such as stroke and arteriovenous malformation. Perinatal encephalopathy accounted for 40% of the epilepsies in children less than 5 years old, and trauma for 20% of those above 20 years old. A family history of epilepsy in close relations was obtained in 23% of the cases, and the consanguinity rate among the parents was 53%. The high incidence of associated perinatal encephalopathy found in this study suggests that perinatal factors play a major role in the pathogenesis of epilepsy in Saudi Arabia. The high frequency of cerebral trauma was also striking. Although consanguinity of the parents appeared not to be a major factor in the genetics of convulsive disorders in this environment, it might have potentiated the tendency of familial aggregation of convulsive disorders in this community. Consanguinity may be an important factor in the production of some of these disorders but its precise role has not been determined.
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PMID:Epilepsy and other convulsive disorders in Saudi Arabia: a prospective study of 1,000 consecutive cases. 212 16

Cocaine abuse is associated with a variety of severe acute neurologic complications. These include ischemic stroke, subarachnoid and intraparenchymal hemorrhage, syncope, seizures, and death. Eleven adult patients with cocaine-related seizures are reported. All were seen during the 1987 calendar year at the King/Drew Medical Center and Urban Comprehensive Epilepsy Program of Los Angeles. Three apparent clinical circumstances with defined methods of intake and time course after usage were identified in our cases. Seizures occurred 1) as acute provoked convulsions in patients known to have epilepsy, 2) spontaneously in otherwise normal individuals after acute snorting or "crack smoking," and 3) agonally with massive ingestion.
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PMID:Cocaine-related seizures in adults. 212 13

Clinical, CT and EEG findings of 100 consecutive patients suffering from epileptic seizures following hemispheric cerebral infarction were evaluated retrospectively. All patients were followed up for an average of 49 months. Twelve patients suffered from cardiogenic brain embolism, 20 had an occlusive disease of the internal cerebral artery. Forty-seven patients had a single middle cerebral artery infarct, 6 each a posterior cerebral artery or watershed infarct. CT showed lacunes in only 6 cases, 8 had multiple larger infarcts and 27 were normal. Seventy-six patients suffered from generalized seizures, 54 from partial fits, predominantly focal motor seizures. Seventy-one patients had their first seizure within the 1st year after stroke, 30 within 2 weeks after the infarct. The interval between stroke and the first epileptic fit exceeded 1 year in the remaining 29 cases. If the first fit occurred in the acute phase after stroke, the risk of further ones was significantly lower than when the first fit occurred in the chronic stage. The frequency of fits mainly depended on the occurrence of epileptic potentials in the EEG and the interval between stroke and the first seizure. During follow-up 27 patients suffered a recurrent stroke, and 52 patients died. Cardiac failure was the predominant cause of death; only 4 patients died as a consequence of an epileptic fit.
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PMID:Epileptic seizures following ischaemic cerebral infarction. Clinical picture, CT findings and prognosis. 214 39

We retrospectively studied 19 cases of occlusive cervical carotid dissection encountered at our hospital between 1974 and 1984 and followed for 5-13 (mean 8.2) years to assess the long-term prognosis of the disease. Five patients had transient ischemic attacks, seven had minor stroke, six had major stroke, and one had epileptic seizures. Angiography demonstrated the typical string sign in 17 cases, a double lumen with occlusion in one, and multiple scalloped narrowings with distal occlusion in the other. Three patients died within 1 month and three remain severely disabled (overall mortality and major morbidity 32%), five have permanent deficits, and seven are neurologically intact; the remaining patient was lost to follow-up. Five patients were treated surgically (two had extracranial-intracranial bypass and three had cervical carotid exploration), and the other 14 were treated medically. The overall rate of reopening was 47% with eight of 10 patients demonstrating recanalization on control angiography and another patient demonstrating recanalization at surgery. These nine patients remain clinically stable on follow-up evaluations. However, vascular abnormalities in the healed arteries were notable and include kinking, fibromuscular dysplasia, dissecting aneurysms, intracranial occlusion, and a residual mural defect.
Stroke 1990 Apr
PMID:Long-term follow-up of occlusive cervical carotid dissection. 218 3

Neurologic consequences of cocaine use frequently present as medical emergencies in the form of stroke, repeated seizures, encephalopathy, acute headache, and unusual transient neurological deficits. The often fatal or disabling neurologic syndromes have only recently been recognized but are now well documented. Cocaine use is a significant cause of stroke in young adults, and the full, long-term ramifications of maternal cocaine use on the fetus will not be known for years to come. Unfortunately, there is not effective treatment other than abstinence, and our understanding of the pathophysiology of cocaine-associated neurologic illness remains limited.
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PMID:Neurologic consequences of cocaine use. 218 41


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