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)

Fourteen patients, aged from 5 to 14 years, with syndrome of electrical status epilepticus during slow sleep (ESESS) have been studied. The absence of epileptic attacks was observed in 21.5% of patients and diagnosis was established by a combination of continuous diffuse epileptiform activity with marked cognitive disturbances. In 78.5% patients, epileptic attacks presented as follows: pharyngeal and oral, hemicephalgia (100% patients with attacks), hemiclonic (18%), atypical absences (27%), negative myoclonus (18%), automotor (18%), focal adverse with vomiting (18%), secondary generalized (36%). Drugs of choice were valproate (depakine) and topamax in patients with attacks; suxilep and frisium in the absence of attacks and in case of continuous diffuse epileptiform activity on the sleep EEG. Two variants have been singled out by the character of ESESS syndrome. The first one, a "symptom variant", was featured by mostly hemiclonic, secondary generalized and automotor epileptic attacks, presence of continuous regional or lateral, less frequent diffuse epileptiform activity, detected by the local structural lesions in MRI, marked cognitive disturbances persisting after stopping of the attacks. The second ("idiopathic") variant is characterized by normal development of children before attack manifestation, appearance of mostly "rolandic" attacks, atypical absences and negative myoclonus, presence of exclusively continuous diffuse epileptiform activity in the phase of slow sleep, standard MRI results (moderate cortical subatrophy in single cases), cessation or substantial decrease of cognitive disturbances after attack stopping. It is emphasized that prognosis of ESESS syndrome should be considered separately with regard to attacks and cognitive disturbances. A prognosis for attacks is always favorable. Cognitive disturbances despite the therapy can persist for a long time.
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PMID:[Epilepsy with electrical status epilepticus during slow sleep: diagnostic criteria and approaches to therapy]. 1673 53

To study clinical and EEG features of children with ictal vomiting and no underlying brain lesions (Panayiotopoulos syndrome). The subjects were 36 children aged 2-13 years. The onset of seizures occurred between 1 and 5 years of age. Fourteen children (38.8%) had a single seizure. Fourteen children (38.8%) had autonomic status epilepticus. Impairment of consciousness was reported in 30 (83.3%) children, eye deviation in 10 (27.7%) other autonomic symptoms and head deviation in 9, generalization in 8, visual symptoms in one child, and, speech arrest or hemifacial motor symptoms in 8 cases. The EEG showed occipital spikes or spike-wave complexes in 27 (75.0%) children, blocked by opening of the eyes in 8 (22.2%) cases. Nine patients (25%) also had rolandic spikes and 3 had extraoccipital spikes. Six (16.6%) patients had normal EEG. No clinical differences were observed between patients having occipital or extraoccipital spikes. In children only with autonomic seizures, the spikes are predominantly occipital but blockage by opening of the eyes is a less frequent feature. In some children there is an overlapping of different focal childhood idiopathic syndromes.
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PMID:Autonomic seizures and autonomic status epilepticus in early onset benign childhood occipital epilepsy (Panayiotopoulos syndrome). 1705 74

We encountered an 11-year-old girl with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) who developed occipital lobe epilepsy at the age of 7 years and 4 months. Thereafter she had repeated status epilepticus associated with stroke-like episodes. Status epilepticus consisted of repetitive complex partial seizures with or without secondarily generalized tonic clonic seizures. The seizures did not respond to conventional anticonvulsive drugs, including diazepam, midazolam, phenytoin, lidocaine, chloral hydrate, and thiamylal sodium, and lasted for several hours (mean 9.5 hours). At the age of 11 years, intravenous infusion of L-arginine (0.5 g/kg body weight) was first given five hours after the onset of status epilepticus. The seizures and electroencephalographic abnormalities improved dramatically. After the introduction of L-arginine, in addition to shortened duration of status epilepticus (mean 3 hours), clinical recovery from the status epilepticus was prompt, and the average hospitalization periods could be shortened. There were no obvious adverse effects, including vomiting, hypotension, and urticaria. Our experience suggests that early intravenous administration of L-arginine may be useful in the treatment of status epilepticus associated with stroke-like episode in patients with MELAS.
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PMID:[Usefulness of L-arginine infusion for status epilepticus in mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes]. 1722 17

A 34-year-old man with MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) showed chronic intestinal pseudo-obstruction (CIPO), which was improved by the administration of distigmine bromide. He exhibited generalized tonic clonic seizures at the age of 21, and mitochondrial DNA analysis showed the MELAS mutation. At the age of 34, he became akinetic mutism after nonconvulsive status epilepticus and needed enteral nutrition through a nasogasrtic tube. However, he developed abdominal distention and vomiting, and was diagnosed as CIPO, therefore tube feeding was stopped. Although the administration of domperidone, mosapride citrate, butyric acid bacteria, sodium picosulfate, prostaglandin F2 alpha, pantothenic acid, dioctyl sodium sulfosuccinate, and so on, was ineffective, the administration of distigmine bromide improved his bowel motion disturbance and abnormal distention. The present case is the first MELAS patient with CIPO to be ameliorated by distigmine bromide, which might work acetylcholine receptor on the interstitial cells of Cajal.
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PMID:[Distigmine bromide improves chronic intestinal pseudo-obstruction in a case of MELAS]. 1751 Dec 91

Epilepsy and psychiatric problems can occur simultaneously and can, quite unexpectedly, trigger interactions that may lead to life-threatening situations. This became obvious in the case of a female patient who suddenly developed a status epilepticus while admitted to hospital. The seizure was probably connected with secret self-induced vomiting which led to a low intake of antiepileptic medication. She used the vomiting to control emotionally charged post-traumatic intrusions. Both the vomiting and the number of seizures were triggered by a life event (in this case emigration). In case of epilepsy, early screening for psychopathology seems advisable because there may be interactions with epileptic variables.
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PMID:[Interactions of epilepsy and psychiatric problems: life-threatening situations]. 1769 92

We describe a 26-year-old female patient, who had attempted suicide with Endosulfan, and who presented to the Emergency Department with status epilepticus. She subsequently developed hypotension refractory to inotropes, intravascular hemolysis, disseminated intravascular coagulation (DIC), metabolic acidosis and, finally, cardiac arrest and death. Endosulfan is a chlorinated insecticide that causes central nervous system hyperstimulation. It is absorbed from the gastrointestinal tract, skin, and respiratory tract, and leads to nausea, vomiting, paraesthesia, giddiness, convulsion, coma, respiratory failure, and congestive cardiac failure. Hepatic, renal and myocardial toxicity, agranulocytosis, aplastic anemia, cerebral edema, DIC, thrombocytopenia, and skin reaction also have been reported. Management includes decontamination of skin and gastrointestinal tract, supportive care including treatment of status epilepticus, dysrhythmias, and mechanical ventilation. Mortality and morbidity rates are very high and there is no specific antidote. Atropine and catecholamines should be avoided.
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PMID:Endosulfan poisoning with intravascular hemolysis. 1797 61

The vagus nerve stimulator has become a standard modality for intractable pediatric epilepsy. We reviewed our experience with major adverse events, after accidental puncture of a stimulator wire by an emergency room physician seeking intravenous access to treat status epilepticus. The Children's National Medical Center database was reviewed for patients undergoing vagus nerve stimulator placement between January 1988 and June 2006. Patient characteristics, duration of therapy, and treatment-limiting adverse events were noted. Of 62 patients implanted over 8 years, 22 (35%) had adverse events which led to a change in therapy. Adverse events included prominent drooling, coughing, throat discomfort, dysphagia, wound infection, difficulty breathing, vomiting, vocal-cord weakness, lead failure, and iatrogenic (piercing of wire; surgical clipping of wire during revision). Eight patients required nonroutine surgical intervention (13%). There were two unusual case presentations. In a 13-year-old boy with status epilepticus at an outlying emergency department, the stimulator line was pierced in search of intravenous access. In a 25-year-old housepainter, neck paresthesias upon right lateral neck turning were attributed to insufficient strain relief. Treatment-limiting adverse events occurred in approximately one-third of patients. Unanticipated adverse events included misidentification of the wire for intravenous access, clipping of the wire during surgical dissection, and cervical dysesthesias associated with head-turning.
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PMID:Misidentification of vagus nerve stimulator for intravenous access and other major adverse events. 1835 2

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

Star-fruit ingestion has been previously reported to cause severe neurotoxicity in uremic patients with symptoms ranging from hiccups, vomiting and consciousness disturbances to refractory status epilepticus, coma and death. MRI examinations of five uremic patients with severe neurological disturbances following star-fruit intoxication were reviewed. At the time of MRI, all patients presented with a confusional state, preceded by seizures in three cases. MRI showed focal (four patients) and diffuse (one patient) cortical hyperintensity on diffusion-weighted sequences, with a corresponding low apparent diffusion coefficient. An additional area of increased diffusion intensity was observed in the pulvinar (two patients) and hippocampus (two patients). MRI and diffusion-weighted imaging may be useful for the diagnosis of star-fruit neuro-intoxication which is associated with a poor prognosis and requires acute and appropriate treatment.
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PMID:[MRI findings in star-fruit intoxication]. 1843 5

Ingestion of star fruit (Averrhoa carambola) can induce severe intoxication in subjects with chronic renal failure. Oxalate plays a key role in the neurotoxicity of star fruit. We report the cases of two patients with unknown chronic renal insufficiency who developed severe encephalopathy after ingestion of star fruit. The two patients developed intractable hiccups, vomiting, impaired consciousness and status epilepticus. Diffusion-weighted MR imaging showed cortical and thalamic hyperintense lesions related to epileptic status. They improved after being submitted to continuous hemofiltration which constitutes the most effective treatment during the acute phase.
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PMID:[Star fruit (Averrhoa carambola) toxic encephalopathy]. 1875 86


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