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 quantitative 2-[14C]deoxyglucose autoradiographic method was applied to measure local cerebral metabolic rates of glucose (LCMRglc) in a model of genetic petit-mal-like seizures in a strain of Wistar rats. During the experimental period, epileptic rats exhibited synchronous spike-and-wave discharges, whereas the EEG pattern of control animals was normal. Overall, LCMRglc was consistently higher in epileptic rats than in the non-epileptic controls. The increase in LCMRglc was widespread and concerned all cerebral functional systems studied, whether they exhibit spike-and-wave discharges (neocortex and thalamus), or not (limbic system). These results are in good accordance with positron-emission tomography measurements in humans with typical childhood absence epilepsy. There appears to be a lack of anatomical correlation between areas demonstrating hypermetabolism and areas where spike-and-wave discharges are recorded. The administration of 200 mg/kg ethosuximide completely suppressed spike-and-wave discharges in epileptic rats and did not change the EEG pattern in controls. However, LCMRglc were increased to the same extent over control values in epileptic rats whether they were injected with ethosuximide or untreated. By contrast, when epileptic rats were given 2 mg/kg haloperidol, the frequency and the length of spike-and-wave discharges increased, inducing almost a permanent petit-mal status epilepticus. Haloperidol did not change EEG pattern in controls. In haloperidol-treated epileptic rats, LCMRglc decreased to levels comparable to those measured in untreated control rats. In the presence of haloperidol, LCMRglc were similar in both control and epileptic rats. Thus, the diffuse increase in cerebral energy metabolism in epileptic rats as compared to controls is not directly related to the occurrence of spike-and-wave discharges, and may rather be associated with inhibitory mechanisms involved in their termination and suppression, as well as their spread to limbic and motor structures.
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PMID:Mapping of cerebral energy metabolism in rats with genetic generalized nonconvulsive epilepsy. 151 92

Although midazolam has been proposed for the treatment of a variety of conditions such as anxiety, dyspnoea, hiccups and status epilepticus, terminal agitation is the only condition where its use is based on a reasonably large number of published clinical studies. A causal approach is generally recommended. Whenever possible, the aetiological condition (pain, fever, constipation, etc.) should be corrected. Such general measures as ensuring a peaceful, familiar environment, and the use of a night light, fluid therapy to counteract dehydration, and antipyretics for fever are beneficial. When symptomatic treatment is needed, drugs with little anticholinergic effect are to be recommended. The use of benzodiazepines as single drug treatment may exacerbate the condition. Haloperidol or risperidone (which has fewer side effects) are recommended. If the agitation is marked, a common strategy is to add lorazepam. Chlormethiazole is an alternative. Subcutaneous midazolam should be reserved for refractory cases. Attention should be paid to dosage, reduced doses being given to the elderly, patients on opioid medication, and patients with impaired liver or renal function. Overdosage may induce deep sedation, and result in carbon dioxide retention and subsequently heart failure and pulmonary oedema which may be fatal.
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PMID:[Midazolam (Dormicum) in terminal anxiety and agitation. The last choice alternative in palliative care]. 1035 70

Sedatives continue to be used on a routine basis in critically ill patients. Although many agents are available and some approach an ideal, none are perfect. Patients require continuous reassessment of their pain and need for sedation. Pathophysiologic abnormalities that cause agitation, confusion, or delirium must be identified and treated before unilateral administration of potent sedative agents that may mask potentially lethal insufficiencies. The routine use of standardized and validated sedation scales and monitors is needed. It is hoped that reliable objective monitors of patients' level of consciousness and comfort will be forthcoming. Each sedative agent discussed in this article seems to have a place in the ICU pharmacologic armamentarium to ensure the safe and comfortable delivery of care. Etomidate is an attractive agent for short-term use to provide the rapid onset and offset of sedation in critically ill patients who are at risk for hemodynamic instability but seem to need sedation or anesthesia to perform a procedure or manipulate the airway. Ketamine administered through intramuscular injection or intravenous infusion provides quick, intense analgesia and anesthesia and allows patients to tolerate limited but painful procedures. The risk/benefit ratio associated with the use of this neuroleptic agent must be weighed carefully. Ketamine is contraindicated in patients who lack normal intracranial compliance or who have significant myocardial ischemia. Barbiturates are reserved mainly to induce coma in patients at risk for severe CNS ischemia, which frequently is associated with refractory intracranial hypertension, or in patients with status epilepticus. When administered in high doses, these drugs have prolonged sedative and depressant effects. Judicious hemodynamic monitoring is required when barbiturate coma is induced. Haloperidol is indicated in the treatment of delirium. Patients should be monitored for extrapyramidal side effects and, when they require higher doses, for potential electrocardiographic prolongation of the QT interval. Dexmedetomidine may evolve into an agent with qualities comparable with midazolam and propofol, and it may even become a drug of choice in select patients. Further study is required, however. Propofol has many of the qualities of an ideal sedative agent. Benzodiazepines and narcotics often are used in concert with propofol to provide reliable amnesia and to relieve pain, respectively. Propofol frequently causes hypotension when administered as a bolus or infusion, particularly in patients with limited cardiac reserve or hypovolemia. More data must be obtained to identify potential deleterious effects of hypertriglyceridemia, and further evaluation of the potential benefits in certain patient populations, such as neurosurgical patients, is needed.
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PMID:Use of propofol and other nonbenzodiazepine sedatives in the intensive care unit. 1176 65

Hepatic encephalopathy represents a reversible decrease in neurological function caused by liver disease. Overall incidence of seizures in hepatic encephalopathy varies between 2% and 33%. Non-convulsive status epilepticus may be particularly common in these patients. Psychiatric disturbances manifest as agitation, personality change, delusions, etc. Aims of seizure management include treatment of basic disease, correction of precipitant factors, imaging of head, and choice of a pharmacologically safe agent. It is important to consider non-convulsive status epilepticus and rule it out by an EEG. Absolute data for safety profile of drugs in liver disease is still not clear, as changes of pharmacokinetics make choice of drugs difficult. Free drug concentrations may be higher, making plasma concentration monitoring essential in such circumstances. A single seizure may not require therapy. However when started, antiepileptic drugs are usually discontinued early. Drugs with sedative effects are best avoided because of a risk of precipitating coma. Phenytoin and gabapentin are relatively preferred drugs; however, monitoring of drug levels is desirable. Management of agitation includes physical restraint and medication. Benzodiazepines are best avoided. Haloperidol is a safer choice in the presence of liver disease. Overall management of neuropsychiatric state aims at management of underlying pathology, the resolution of which leads to improvement in the clinical symptomatology.
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PMID:Management of agitation and convulsions in hepatic encephalopathy. 1502 57