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)

Carisbamate is a novel drug with neuromodulator activity that is currently under development for the treatment of epilepsy, diabetic neuropathy and neuralgia. The compound possessed a promising pharmacological profile in tests in vivo, and demonstrated broad anticonvulsant activity in preclinical studies, both elevating seizure threshold and preventing seizure spread. Carisbamate was also effective in protecting against spontaneous recurrent seizures in kainate-treated animals and in genetic models of epilepsy, and displayed antiepileptic and neuroprotective activity in the lithium-pilocarpine model of status epilepticus. In a phase I clinical trial, orally administered carisbamate demonstrated efficacy at high doses of 500 to 1000 mg. A phase II clinical trial confirmed that oral carisbamate was efficacious at a 300- to 1600-mg dose range. The preliminary evaluations of carisbamate in humans indicated complete absorption, extensive metabolism, and carbamate ester hydrolysis. The most frequently reported side effects associated with carisbamate are dizziness, headache, somnolence and nausea. In clinical trials, carisbamate did not display any significant interactions with commonly used antiepileptic drugs such as carbamazepine, valproate and lamotrigine. At the time of publication, a phase III clinical trial for carisbamate in the treatment of epilepsy was ongoing, as well as phase II trials in neuropathy and neuralgia. Data from preclinical brain injury studies with carisbamate and the analog RWJ-333369-A have also been reported. This drug profile will focus on the development of carisbamate in epilepsy.
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PMID:Carisbamate, a new carbamate for the treatment of epilepsy. 1789 91

We describe the cases of three children with encephalitis associated with Coxiella burnetii infection. Neurologic features ranged from status epilepticus and coma to headache and pseudotumor cerebri syndrome. Patients had good response to antibiotic treatment with doxycycline and recovered fully. Q fever should be included in the differential diagnosis of children with encephalitis, and routine serological testing should be considered, especially in endemic areas.
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PMID:Acute Q fever in children presenting with encephalitis. 1805 92

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

The relationship between epilepsy and migraine is complex and remains to be determined. We report 3 cases that address 2 questions on this topic. The first and second cases showed an association between migraine without aura and the onset of epileptic seizures. The third case report describes a patient in whom migraine with aura occurred and was followed by the development of status epilepticus, which occurred 2 or 3 hours after the attack of migraine with aura. We discuss the present definition of migralepsy and reassess its definition by suggesting possible extensions to its current definition.
Headache 2008 Jul
PMID:Migralepsy: is the current definition too narrow? 1870 28

A 50-year-old woman presented with confusion, fever and drowsiness following an episode of headache and dizziness. On admission, neurological examination found positive pyramidal tract signs, meningeal irritation, and bilateral myoclonus in her arms. Laboratory tests revealed liver dysfunction, positive inflammatory reaction, elevated serum IgM antibody against cytomegalovirus, and increased cerebrospinal fluid protein of 67 mg/dl. MRI of brain by diffusion weighted imaging showed a wide spread hyperintense lesion in white matter and limbic areas. We administered aciclovir, ganciclovir and steroid pulse therapy that showed a limited effect in the initial stage. In spite of all these therapies, she suffered from status epilepticus, followed by persistent disturbance of consciousness for about 2 months. However, her level of consciousness and motor deficit were gradually improved by continuous administration of ganciclovir. The present case indicates that prolonged disturbance of consciousness due to cytomegalovirus encephalitis could be restored with continuous ganciclovir administration.
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PMID:[A case of probable cytomegalovirus encephalitis who restored from persistant disturbance of consciousness]. 1871 81

The C10orf2 gene encodes the mitochondrial DNA helicase Twinkle, which is one of the proteins important for mitochondrial DNA maintenance. Dominant mutations cause multiple mitochondrial DNA deletions and progressive external ophthalmoplegia, but recent findings associate recessive mutations with mitochondrial DNA depletion and encephalopathy or hepatoencephalopathy. The latter clinical phenotypes resemble those associated with recessive POLG1 mutations. We have previously described patients with infantile onset spinocerebellar ataxia (MIM271245) caused either by homozygous (Y508C) or compound heterozygous (Y508C and A318T) Twinkle mutations. Our earlier reports focused on the spinocerebellar degeneration, but the 20-year follow-up of 23 patients has shown that refractory status epilepticus, migraine-like headaches and severe psychiatric symptoms are also pathognomonic for the disease. All adolescent patients have experienced phases of severe migraine, and seven patients had antipsychotic medication. Epilepsia partialis continua occurred in 15 patients leading to generalized epileptic statuses in 13 of them. Eight of these patients have died. Valproate treatment was initiated on two patients, but had to be discontinued because of a severe elevation of liver enzymes. The patients recovered, and we have not used valproate in infantile onset spinocerebellar ataxia since. The first status epilepticus manifested between 15 and 34 years of age in the homozygotes, and at 2 and 4 years in the compound heterozygotes. The epileptic statuses lasted from several days to weeks. Focal, stroke-like lesions were seen in magnetic resonance imaging, but in infantile onset spinocerebellar ataxia these lesions showed no predilection. They varied from resolving small cortical to large hemispheric oedematous lesions, which reached from cerebral cortex to basal ganglia and thalamus and caused permanent necrotic damage and brain atrophy. Brain atrophy with focal laminar cortical necrosis and hippocampal damage was confirmed on neuropathological examination. The objective of our study was to describe the development and progression of encephalopathy in infantile onset spinocerebellar ataxia syndrome, and compare the pathognomonic features with those in other mitochondrial encephalopathies.
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PMID:Recessive twinkle mutations cause severe epileptic encephalopathy. 1930 94

Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) is a mitochondrial disorder commonly caused by the A3243G mutation. We report a patient who initially presented with visual hallucinations, headaches, and nonconvulsive status epilepticus originating in left occipital lobe who subsequently progressed to have multifocal seizures. His magnetic resonance imaging (MRI) showed subtle T2 hyperintensity at first presentation that subsequently fully resolved. He then had more typical diffusion restriction not conforming to vascular territories. Evolution of his neuroimaging and electroencephalogram (EEG) is discussed with a brief review of literature. Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes should be suspected early with occipital lobe seizures.
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PMID:MELAS with A3243G mutation presenting with occipital status epilepticus. 1940 52

Endosulfan is an organochloride insecticide, widely used in insect control. It is responsible for many severe intoxication and several deaths. We present a case series of endosulfan poisoning, admitted to our emergency department with different clinical courses. Two patients presented with status epilepticus and were successfully treated with thiopental sodium to control seizures. One patient required also hemodialysis. All patients were discharged following a complete recovery of their health. Endosulfan is a highly toxic insecticide that produces tonic-clonic convulsions, headache, dizziness and ataxia. It can cause also life threatening metabolic disturbances. Treatment is symptomatic and supportive (Tab. 2, Ref. 11). Full Text (Free, PDF) www.bmj.sk.
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PMID:Unintentional endosulfan poisoning. 1950 67

A 40-year-old woman was diagnosed with iron deficiency anemia (hemoglobin 3.5 g/dl) induced by uterine myomas, and admitted to the Department of Gynecology of our hospital. During admission, she underwent the daily intravenous administration of saccharated ferric oxide for 3 weeks, and monthly GnRH analogue administration was started. Her hemoglobin level acutely increased to 9.3 g/dl over the next 18 days with normal blood pressure. Thirteen days after the 3rd administration of the GnRH analogue, she suddenly developed marked headache. Just before the onset, she had been driving a car, and spun the steering wheel to avoid a traffic accident on a busy street. This headache was so severe that she was brought to our hospital by ambulance. During transport to the hospital, her blood pressure was normal. Soon after arriving, she developed generalized convulsions, followed by status epilepticus. A brain MRI showed vasogenic edema in the posterior and parietal cortices including white matter bilaterally, and minimum subarachnoid hemorrhage was indicated in the bilateral frontal lobe and right temporal lobe. CSF analysis was unremarkable. Anticonvulsants, one course of steroid pulse therapy and glycerol were started, and status epilepticus disappeared on the same day. Abnormal areas on MRI decreased gradually. However, hyperintensity on T1- and FLAIR images remained in the right parietal lobe and bilateral occipital lobe white matter at 15 months after the onset Judging from the clinical and radiological findings, this patient was diagnosed as reversible posterior leukoencephalopathy syndrome (RPLS) accompanied with subarachnoid hemorrhage. This case suggests that an unexpected prompt physical activity or astonishment would induce RPLS in a patient treated with GnRH analogue.
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PMID:[Acutely developed reversible posterior leukoencephalopathy syndrome following a prompt physical activity to avoid a traffic accident: a case report]. 1992 86

Occasionally, patients with Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) present atypical features such as confusion, coma, or nonconvulsive status epilepticus. Acute focal neuropsychological syndrome revealing the disease has been poorly documented. We report the atypical presentation of two patients in whom CADASIL was revealed by an episode of headache followed by focal neuropsychological impairment.
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PMID:Acute headache followed by focal neuropsychological impairment in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). 2012 31


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