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)

Cases of N-acetylcysteine overdose have been reported before. In some cases, these overdoses have led to death if an anaphylactoid reaction was present. A healthy 30-month-old girl allegedly ingested acetaminophen at 418 mg/kg. Because the emergency physician feared the time of ingestion might not be accurate, he decided to start the 20.5-hour intravenous N-acetylcysteine protocol 8 hours after ingestion. He mistakenly prescribed the maximum milliliter-per-kilogram volume of the dextrose 5% diluent for the milliliter-per-kilogram volume of N-acetylcysteine 20% to be administered. Five hours after the error was detected (19.5 hours postingestion), the patient started developing myoclonus on the left side of her body, with left eye deviation. This condition persisted intermittently for 3 hours despite treatment with diazepam, lorazepam, and phenytoin. A first computed tomographic scan result was normal. A few hours later, she sustained shorter recurrences of the myoclonus. At 30 hours after ingestion, she started to have irregular breathing and became unresponsive to pain. A repeated computed tomographic scan showed diffuse cerebral edema. A postmortem examination showed the presence of acute anoxic encephalopathy with marked cerebral edema and the beginning of uncal herniation that confirmed the clinical diagnosis of intracranial hypertension and brain death. A cumulative intravenous dose of 2,450 mg/kg of N -acetylcysteine was associated with status epilepticus, intracranial hypertension, and death in a child.
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PMID:Status epilepticus after a massive intravenous N-acetylcysteine overdose leading to intracranial hypertension and death. 1545 24

An 84-year-old Asian woman with hypertension and chronic renal failure was evaluated for incoherent speech, followed by intermittent interruptions of consciousness, and then status epilepticus after ingesting one star fruit (Averrhoa carambola) each day for 3 days. Conventional first-line anticonvulsants and hemodialysis were administered without significant control of the patient's seizures. Treatment was started with propofol, an intravenous agent that induces anesthesia with rapid onset and elimination from the central nervous system; this resulted in complete control of the seizures. Propofol may be an effective alternative when dialysis and conventional first-line anticonvulsants are unsuccessful in treating the symptoms of neurotoxicity.
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PMID:Management of star fruit-induced neurotoxicity and seizures in a patient with chronic renal failure. 1650 56

We report a patient of a 20-year-old woman of Takayasu's arteritis and hypertensive encephalopathy. The symptoms started with headache and vomiting following status epilepticus. On arrival at the emergency room in our hospital, fever was apparent and cerebrospinal fluid examination revealed pleocytosis. After the admission, the patient presented with hypertension, decreased right brachial pulse and the difference between bilateral brachial arterial blood pressures on examination. There had been no history of arterial hypertension. The MR angiography revealed stenoses of the bilateral cervical, especially right cervical, right middle cerebral and left renal arteries. Brain MRI showed transient hyperintense lesions of the left fronto-parieto-occipital cortices and subcortical white matter in FLAIR and diffusion weighted images. These alterations suggested the presence of reversible vasogenic edema induced by hypertensive encephalopathy. We need to be aware of young patients with convulsion, especially young women, who has arterial hypertension as well as the difference with blood pressures between extremities.
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PMID:[Case of unilateral alteration due to hypertensive encephalopathy]. 1838 28

Posterior reversible encephalopathy syndrome (PRES) is an acute disorder characterised by a variable association of neurologic symptoms with potentially reversible oedematous abnormalities mainly in the parieto-occipital regions of the brain. Despite the significant incidence of seizures, the EEG characteristics of epileptic disorders related to PRES have rarely been investigated. We report the case of an 85-year-old man who presented with generalised tonic-clonic seizures and prolonged disturbances of consciousness as clinical manifestations of PRES due to moderate exacerbation of chronic hypertension. An EEG performed during an alteration of mental function displayed a pattern of partial status epilepticus (SE) in both temporo-parieto-occipital regions. The seizure activity originated from two independent epileptic foci located in the occipital area of each hemisphere and could be related to the parenchymal abnormalities of PRES. The EEG pattern of partial SE related to independent occipital foci illustrates a distinctive seizure disorder that could be characteristic of PRES in adult patients.
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PMID:Partial status epilepticus related to independent occipital foci in posterior reversible encephalopathy syndrome (PRES). 1906 21

The systemic consequences of status epilepticus occur in two stages: the first stage is a hyperadrenergic period (high blood pressure, tachycardia, arrhythmia, hyperventilation, hypermetabolism, hyperthermia), the second stage a collapsus period, sometimes with acute circulatory failure, and hypoxemia. Symptomatic resuscitation aimed at restoring vital functions should be undertaken. Resuscitation must be started immediately before hospital transfer, by a trained emergency team. Respiratory care includes at least oxygen intake, but it can also require oral intubation (crash induction) and mechanical ventilation. The arterial blood gas objectives are SaO(2)> or =95%, and 35mmHg< or =PaCO(2)< or =40mmHg. Fluid and electrolyte care includes intravenous infusion of normal saline, with control of sodium and calcium levels as well as blood pH within normal limits. Heart rate and blood pressure must be monitored. Mean blood pressure must be kept between 70 and 90mmHg, first by means of plasma volume expansion, and then norepinephrine if necessary. Hyperthermia must be corrected to prevent further neuronal damage. Cerebromeningeal sepsis should be ruled out. Capillary glucose (most often elevated) must be corrected using a pre-established insulin infusion algorithm. Rhabdomyolysis is rare, but can result in hyperkaliemia, acidosis, and acute renal failure. In case of associated intracranial hypertension (traumatic, vascular or infectious injury), status epilepticus is considered as a secondary insult for the brain, that can worsen neuronal damage. Numerous compounds have experimental neuroprotective properties, but none have proven significant efficacy in clinical conditions. Nevertheless, convulsion cessation is considered as a neuroprotective measure.
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PMID:[Non specific treatment of status epilepticus]. 1924 65

Prolonged seizure activity (status epilepticus; SE) can result in increased susceptibility to lethal ventricular arrhythmias for an extended period of time following seizure termination. SE is accompanied by acute, intense activation of the sympathetic nervous system (SymNS) and results in myocyte myofilament damage, arrhythmogenic alterations in cardiac electrical activity, and increased susceptibility to ventricular arrhythmias. However, the mechanisms mediating the changes in cardiac function, and the specific arrhythmogenic substrate produced during SE are unknown. To determine if detrimental cardiac effects of SE are mediated by SymNS stimulation of the heart, we examined the effects of B-adrenergic blockade (atenolol) during seizure activity on blood pressure, heart rate, myocyte myofilament injury (cardiac troponin I, cTnI), electrocardiographic activity, and susceptibility to arrhythmias. Furthermore, we determined if SE was associated with altered expression of the Kv4.x potassium channels, which are critical for action potential repolarization and thereby contribute significantly to normal cardiac electrical activity. Lithium-pilocarpine induced SE was associated with acute tachycardia, hypertension, and cardiomyocyte damage. Arrhythmogenic alterations in cardiac electrical activity accompanied by increased susceptibility to experimentally induced arrhythmias were evident during the first 2 weeks following SE. Both were prevented by atenolol treatment during seizures. Furthermore, one and two weeks after SE, myocyte ion channel remodeling, characterized by a decreased expression of cardiac Kv4.2 potassium channels, was evident. These data suggest that the cardiac effects of prolonged and intense SymNS activation during SE induce myofilament damage and downregulation of Kv4.2 channels, which alter cardiac electrical activity and increase susceptibility to lethal arrhythmias.
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PMID:Autonomic and cellular mechanisms mediating detrimental cardiac effects of status epilepticus. 2228 14

Lethal cardiac arrhythmias contribute to mortality in a number of pathological conditions. Several parameters obtained from a non-invasive, easily obtained electrocardiogram (ECG) are established, well-validated prognostic indicators of cardiac risk in patients suffering from a number of cardiomyopathies. Increased heart rate, decreased heart rate variability (HRV), and increased duration and variability of cardiac ventricular electrical activity (QT interval) are all indicative of enhanced cardiac risk. In animal models, it is valuable to compare these ECG-derived variables and susceptibility to experimentally induced arrhythmias. Intravenous infusion of the arrhythmogenic agent aconitine has been widely used to evaluate susceptibility to arrhythmias in a range of experimental conditions, including animal models of depression and hypertension, following exercise and exposure to air pollutants, as well as determination of the antiarrhythmic efficacy of pharmacological agents. It should be noted that QT dispersion in humans is a measure of QT interval variation across the full set of leads from a standard 12-lead ECG. Consequently, the measure of QT dispersion from the 2-lead ECG in the rat described in this protocol is different than that calculated from human ECG records. This represents a limitation in the translation of the data obtained from rodents to human clinical medicine. Status epilepticus (SE) is a single seizure or series of continuously recurring seizures lasting more than 30 min, and results in mortality in 20% of cases. Many individuals survive the SE, but die within 30 days. The mechanism(s) of this delayed mortality is not fully understood. It has been suggested that lethal ventricular arrhythmias contribute to many of these deaths. In addition to SE, patients experiencing spontaneously recurring seizures, i.e. epilepsy, are at risk of premature sudden and unexpected death associated with epilepsy (SUDEP). As with SE, the precise mechanisms mediating SUDEP are not known. It has been proposed that ventricular abnormalities and resulting arrhythmias make a significant contribution. To investigate the mechanisms of seizure-related cardiac death, and the efficacy of cardioprotective therapies, it is necessary to obtain both ECG-derived indicators of risk and evaluate susceptibility to cardiac arrhythmias in animal models of seizure disorders. Here we describe methods for implanting ECG electrodes in the Sprague-Dawley laboratory rat (Rattus norvegicus), following SE, collection and analysis of ECG recordings, and induction of arrhythmias during iv infusion of aconitine. These procedures can be used to directly determine the relationships between ECG-derived measures of cardiac electrical activity and susceptibility to ventricular arrhythmias in rat models of seizure disorders, or any pathology associated with increased risk of sudden cardiac death.
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PMID:Methods for ECG evaluation of indicators of cardiac risk, and susceptibility to aconitine-induced arrhythmias in rats following status epilepticus. 2150 5

The posterior reversible encephalopathy syndrome is an increasingly recognised disorder. Most patients have several symptoms; seizures are the most frequent, often multiple or status epilepticus. A combination of seizures, visual disturbance and/or headache, in particular, should lead to an early brain MRI to reveal the typical pattern of bilateral hyperintensities on fluid attenuated inversion recovery imaging, predominantly in the parieto-occipital region. There seem to be many possible triggers, including abrupt arterial hypertension, impaired renal function, pregnancy, immunosuppressive therapies and various inflammatory conditions. The clinical outcome is excellent, with recovery within a few days, while the MRI abnormalities resolve much more slowly. Little is known about the best management. Seizures do not normally progress to chronic epilepsy so antiepileptic drugs should be discontinued after about 3 months.
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PMID:The posterior reversible encephalopathy syndrome: what's certain, what's new? 2155 Nov 7

Cerebral venous thrombosis is a rare but potentially severe condition in children. We present the case of a teenager with corticodependent nephrotic syndrome diagnosed at five months of age and treated with cyclosporine A. In the context of recurrence of nephrotic syndrome he presented with headache, vomiting and severe intracranial hypertension. While the raised intracranial pressure and the status epilepticus were controlled, the brain imaging revealed venous thrombosis of all venous sinus, with absence of venous drainage. He was submitted to local thrombolysis with recombinant tissue plasminogen activator, with recanalization of the venous sinuses. The outcome was favourable, without neurological deficits. In this case, the early radiologic intervention was crucial, enabling a full neurological recovery, in a teenager whose initial prognosis was very poor.
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PMID:[Endovascular thrombolysis for massive cerebral venous thrombosis in a teenager with nephrotic syndrome]. 2162 91

Neurocysticercosis (NCC) is the most common cause of acquired epilepsy in developing countries. It can present variably depending on the location and stage of cysts in the nervous system, and the host immune response. The most common presentation of parenchymal NCC is with seizures that are usually focal and brief; status epilepticus occurs in some cases. About a third of cases have headache and vomiting. Diagnosis is made by either CT or MRI. Single, small, contrast enhancing lesions are the most common; visualization of a scolex is diagnostic. Some cases have multiple cysts with a characteristic starry-sky appearance. Although treatment with cysticidal therapy continues to be debated, there is increasing evidence that it helps through increased and faster resolution of CT lesions; whether there is any improvement in long-term seizure control needs further study. It should not be used in cysticercus encephalitis or in ophthalmic NCC and used with caution in extraparenchymal NCC. It is of no use in calcified lesions. Corticosteroids are used simultaneously to reduce cerebral oedema. Seizures respond well to a single antiepileptic, and the seizure recurrence rate is low in cases with single lesions; those with multiple, persistent or calcified lesions usually have recurrent seizures. Extraparenchymal NCC is often associated with intracranial hypertension, hydrocephalous and chronic meningitis; it has a guarded prognosis; surgical intervention is required in many cases. Management of NCC needs to be individualized. NCC is potentially eradicable; proper sanitation, hygiene and animal husbandry are warranted.
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PMID:Neurocysticercosis. 2169 5


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