Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The extreme medical emergency situation in the dental setting is cardiac arrest. The need to provide dental treatment to the medically compromised patients, suffering from very high risk heart diseases at special oral medicine hospital dentistry units, expose the dental and medical teams to the possibility of patients' death. Cardiac and cardiorespiratory arrest in these units faces the dentists with the need to perform basic and/or advanced cardiopulmonary resuscitation (CPR). Various etiologies are responsible for cardiac arrests. This article describes our experience and the outcome of six patients who have suffered cardiac arrests pre, during or post dental treatment in two special oral medicine centers. Two patients, suffering from severe congestive heart failure experienced fatal ventricular arrhythmia, both of them underwent CPR with early cardiac defibrillation, following which one patient completely recovered, and the other one expired. Two young and healthy patients experienced severe neurocardiogenic syncope with heart standstill for more than 40 seconds followed by spontaneous uneventful recovery. The fifth patient, who suffered from ventricular fibrillation as a result of an acute coronary ischemia, was resuscitated successfully. The last patient, a young woman, suffered from a severe status epilepticus causing bradycardia, which led to cardiac arrest, but recovered following CPR. All patients who did not recover spontaneously underwent methodical advanced CPR with early defibrillation. Only one patient out of the six died.
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PMID:[Cardiac arrest in dental offices. Report of six cases]. 1185 53

We report a 12-year-old child with episodes of migraine-like headaches with visual and motor auras a year after the surgical resection and radiation therapy for medulloblastoma The patient presented with an episode of headache, prolonged aphasia, right hemiparesis, status epilepticus, and salt wasting. There was no evidence of a structural lesion. The neurologic deficits resolved over a period of 6 weeks. Because of the progressive deterioration in neurologic deficits, the patient underwent an extensive battery of laboratory tests and multiple neuroimages, all of which were normal. The unusually prolonged neurologic deficit in this patient without demonstrable structural lesions and his eventual complete recovery were most likely caused by ischemia in the left hemisphere secondary to vasospasm. This presentation mimics migraine headache. Evidence suggesting that this represents a long-term complication of treatment of children with central nervous system neoplasia is presented.
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PMID:Pseudomigraine with prolonged aphasia in a child with cranial irradiation for medulloblastoma. 1195 86

Postictal aphasia has been described in left temporal lobe seizures. It may be of fluent, non-fluent or global type. We present here a patient who displayed signs of mixed transcortical aphasia (MTCA). The patient was a 67 year old man who underwent excision of a left frontal parasagittal meningioma in 1987. Since then he has been treated with phenytoin for generalized tonic-clonic seizures (GTCS). He was admitted in status epilepticus. On awakening, the patient was non-fluent with palilalia and echolalia. His repetition was relatively preserved but all the other language functions were impaired. This picture faded away within a few hours. Brain CT, performed during this postictal state, was normal except for signs related to frontal craniotomy. SPECT, which was performed after language functions returned to normal, displayed left frontal, cingular and insular hypoperfusion. The postictal language dysfunction of the patient corresponded to MTCA. Although our case has frontal, he had no other structural lesion that could explain either diffuse ischemia of the left hemisphere or watershed areas secondary to the generalized seizures. The uniqueness of this case is the combination of postictal MTCA with good prognosis.
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PMID:Postictal mixed transcortical aphasia. 1202 78

The outcomes of devastating neurological emergencies such as stroke and subarachnoid hemorrhage may be measurably improved by timely treatment in a neurointensive care unit (NICU). Optimal care requires a multidisciplinary approach, with attention to a wide range of treatment issues. This review examines the key therapeutic concerns in the NICU management of acute ischemic and hemorrhagic stroke and subarachnoid hemorrhage, including mechanical ventilation, blood pressure management, cardiac monitoring, intracranial pressure assessment, vasospasm, seizures, sedation, fluids, electrolytes, and nutrition. The discussion of mechanical ventilation includes rapid sequence induction and intubation, indication for intubation and extubation, and prognostic factors in mechanical ventilation. Differing blood pressure management concerns in hemorrhagic and ischemic events are discussed, and specific target blood pressures and pharmacologic interventions are reviewed. The discussion of cardiac monitoring includes concurrent stroke and cardiac ischemia and arrhythmias, cardiac imaging, anticoagulation, and vasopressor therapy. The importance, monitoring and management of cerebral blood flow and intracranial pressure (ICP) are discussed, and strategies for treatment of elevated ICP are outlined in detail. The discussion of vasospasm includes evaluation, prophylaxis, and treatment with medications, hypervolemic hemodilution, and angioplasty. Management of seizure and status epilepticus in stroke and subarachnoid hemorrhage are reviewed and current algorithms are presented. The management of fluids, electrolytes and enteral nutrition are also reviewed.
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PMID:Critical care issues in stroke and subarachnoid hemorrhage. 1207 37

Selective neuronal loss following status epilepticus was first described just under 100 years ago. The acute pathology following status epilepticus was shown to be 'ischemic cell change' and was assumed to arise through hypoxia/ischemia. Less than 30 years ago it was proposed, from experiments in primates, that the selective neuronal loss in hippocampus and cortex resulted from the abnormal electrical discharges. Selectively vulnerable neurons show swollen, calcium-loaded mitochondria in the soma and focally in dendrites. Burst firing with a massive Ca2+ entry needs to be sustained for 30-120 min to produce necrotic cell death. Lesser stress may produce apoptosis or immediate early gene expression with enhanced expression of many enzymes and receptor subunits. Changes in enzyme, transporter, ion-channel or receptor function or in network properties may lead to altered vulnerability to the effects of seizures. This type of modification and the cumulative effect of oxidative damage to proteins and lipids may explain the long-term consequences of repetitive brief seizures.
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PMID:Concept of activity-induced cell death in epilepsy: historical and contemporary perspectives. 1214 50

This article reviews current and future applications of continuous electroencephalography (cEEG) to monitor brain function and physiology in the neurologic intensive care unit. In comatose patients, cEEG may provide otherwise unobtainable information and influence therapeutic management, and also help determine the prognosis of patients with acute brain injury. This technique is best used for the detection of subclinical seizures, which may frequently occur during or after treatment of convulsive status epilepticus and after many types of acute brain injury, particularly trauma. The other main application of cEEG is as a primary monitor of brain function. cEEG can detect focal cerebral ischemia, such as that caused by vasospasm after subarachnoid hemorrhage, as well as global ischemia related to intracranial pressure elevation and insufficient cerebral perfusion pressure. Other potential applications include prognostication in coma and titration of continuous infusion sedative therapy. New technologic developments include continuous digital video EEG, automated seizure-detection software, and user-friendly online quantitative EEG analysis.
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PMID:Continuous electroencephalographic monitoring in neurocritical care. 1235 9

One of the oldest questions in epilepsy is whether seizures are a cause or a result of brain damage. Animal data have provided us with insights into the relationship between seizures and subsequent brain damage. It is now recognized that seizures can be caused by brain injury and that, in certain conditions, can cause brain damage. Whether seizures result in brain damage depends on a number of variables, including age of the animal, seizure type and duration, etiology of the seizures, and genetic substrate on which the seizures occur. Seizures lasting for hours can cause injury to the brain regardless of whether they are generalized or focal in onset. The cell loss that occurs after the seizure is secondary to excessive excitability, with seizures causing massive depolarization of neurons leading to excessive glutamate release. This glutamate release results in increased intracellular calcium, causing a cascade of changes that ultimately result in cell death. Hypoxia and ischemia can exacerbate the injury. However, even in animals that are well ventilated and oxygenated, prolonged seizures can lead to cell loss and subsequent reorganization of synaptic networks. Although prolonged seizures at any age can result in cell loss, the immature brain fares much better than the mature brain with regard to cell loss after a prolonged seizure. Evidence that prolonged seizures result in neuronal loss is firmly established. It is less clear how detrimental recurrent seizures are. Although cell loss and synaptic reorganization have been reported in recurrent seizure models, such as kindling, it is generally modest compared to status epilepticus. When seizure-induced changes do occur, the pathologic patterns in the brain differ from those in status epilepticus.
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PMID:Seizure-induced neuronal injury: animal data. 1242 25

A full-term neonate presented with status epilepticus at 12 hours of age after a symptom-free interval following transient asphyxia at birth. Conventional neuroimaging failed to detect structural correlates to support recent injury. However, diffusion-weighted magnetic resonance imaging studies revealed recent ischemic brain injury. Placental examination documented multiple subacute and chronic findings indicative of decreased maternal/fetal perfusion. These antepartum placental abnormalities may have been associated with this child's inability to withstand the stress of a prolonged second stage of labor, resulting in intrapartum asphyxia leading to brain injury. This child's clinical presentation highlights the delayed reperfusion phase after ischemia-induced brain injury.
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PMID:Delayed onset of status epilepticus after transient asphyxia in an asymptomatic full-term neonate. 1254 37

This study determined whether stroke and other types of insults produced a gene expression profile in blood that correlated with the presence of neuronal injury. Adult rats were subjected to ischemic stroke, intracerebral hemorrhage, status epilepticus, and insulin-induced hypoglycemia and compared with untouched, sham surgery, and hypoxia animals that had no brain injury. One day later, microarray analyses showed that 117 genes were upregulated and 80 genes were downregulated in mononuclear blood cells of the "injury" (n = 12) compared with the "no injury" (n = 9) animals. A second experiment examined the whole blood genomic response of adult rats after global ischemia and kainate seizures. Animals with no brain injury were compared with those with brain injury documented by TUNEL and PANT staining. One day later, microarray analyses showed that 37 genes were upregulated and 67 genes were downregulated in whole blood of the injury (n = 4) animals compared with the no-injury (n = 4) animals. Quantitative reverse transcription-polymerase chain reaction confirmed that the vesicular monoamine transporter-2 increased 2.3- and 1.6-fold in animals with severe and mild brain injury, respectively, compared with no-injury animals. Vascular tyrosine phosphatase-1 increased 2.0-fold after severe injury compared with no injury. The data support the hypothesis that there is a peripheral blood genomic response to neuronal injury, and that this blood response is associated with a specific blood mRNA gene expression profile that can be used as a marker of the neuronal damage.
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PMID:Blood genomic expression profile for neuronal injury. 1262 6

Overactivation of N-methyl-D-aspartate receptors is known to mediate excitotoxicity due to excessive entry of calcium, leading to the activation of several calcium-dependent enzymes. Calpains are calcium-activated proteases that appear to play a role in excitotoxic neuronal death. Several cellular proteins are substrates for these proteases, particularly the N-methyl-D-aspartate receptor. Recently, cleavage of NR2B subunits has been implicated in excitotoxic neurodegeneration in ischemia. In this work, we investigated the proteolysis by calpains of NR2B subunits of the N-methyl-D-aspartate receptor in the hippocampus of epileptic rats. Our results show that cleaved forms of NR2B subunits are formed after status epilepticus, in the same areas of the hippocampus where calpain activation was detected by immunohistochemical staining of calpain-specific spectrin breakdown products.
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PMID:Proteolysis of NR2B by calpain in the hippocampus of epileptic rats. 1572 44


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