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

We report three patients presented with meningoencephalitis associated with polyradiculoneuropathy with increased HSV IgG antibody titer. The first patient was a 27-year-old woman with meningoencephalitis who developed status epilepticus. The CSF showed pleocytosis and increase in HSV IgG antibody titer. Herpes encephalitis was suspected, and she was treated with acyclovir. The symptoms of meningoencephalitis improved, but she developed flaccid tetraplegia. The NCV study was compatible with polyradiculoneuropathy. About two months later from the onset, muscle atrophy appeared in her all limbs. The second patient was a 23-year-old woman with meningoencephalitis, which was followed by ascending motor paralysis. The CSF showed pleocytosis and increase in HSV IgG antibody titer. The symptoms of meningoencephalitis improved by administration of acyclovir, but paralysis didn't improve. About two months later from the onset, muscle atrophy of all limbs appeared. The NCV study was compatible with polyradiculoneuropathy. The third patient was a 43-year-old man presenting somnolence, neck stiffness and ascending motor paralysis developing into flaccid tetraplegia. The CSF showed pleocytosis and increase in HSV IgG antibody titer. Somnolence and neck stiffness improved by administration of acyclovir but tetraplegia didn't improve. The NCV study was compatible with polyradiculoneuropathy. Immuno-absorption therapy and administration of prednisolone were performed. Meningoencephalitis associated with increased HSV IgG antibody titer is rare. Auto-allergic process which is initiated by HSV infection may be involved in the pathogenesis of polyradiculoneuropathy in these patients.
 ...
PMID:[Meningoencephalitis associated with polyradiculoneuropathy with increased HSV IgG antibody--report of three cases]. 812 8

Human status epilepticus (SE) is consistently associated with cognitive problems, and with widespread neuronal necrosis in hippocampus and other brain regions. In animal models, convulsive SE causes extensive neuronal necrosis. Nonconvulsive SE in adult animals also leads to widespread neuronal necrosis in vulnerable regions, although lesions develop more slowly than they would in the presence of convulsions or anoxia. In very young rats, nonconvulsive normoxic SE spares hippocampal pyramidal cells, but other types of neurons may not show the same resistance, and inhibition of brain growth, DNA and protein synthesis, and of myelin formation and of synaptogenesis may lead to altered brain development. Lesions induced by SE may be epileptogenic by leading to misdirected regeneration. In SE, glutamate, aspartate, and acetylcholine play major roles as excitatory neurotransmitters, and GABA is the dominant inhibitory neurotransmitter. GABA metabolism in substantia nigra (SN) plays a key role in seizure arrest. When seizures stop, a major increase in GABA synthesis is seen in SN postictally. GABA synthesis in SN may fail in SE. Extrasynaptic factors may also play an important role in seizure spread and in maintaining SE. Glial immaturity, increased electronic coupling, and SN immaturity facilitate SE development in the immature brain. Major increases in cerebral blood flow (CBF) protect the brain in early SE, but CBF falls in late SE as blood pressure falters. At the same time, large increases in cerebral metabolic rate for glucose and oxygen continue throughout SE. Adenosine triphosphate (ATP) depletion and lactate accumulation are associated with hypermetabolic neuronal necrosis. Excitotoxic mechanisms mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors open ionic channels permeable to calcium and play a major role in neuronal injury from SE. Hypoxia, systemic lactic acidosis, CO2 narcosis, hyperkalemia, hypoglycemia, shock, cardiac arrhythmias, pulmonary edema, acute renal tubular necrosis, high output failure, aspiration pneumonia, hyperpyrexia, blood leukocytosis and CSF pleocytosis are common and potentially serious complications of SE. Our improved understanding of the pathophysiology of brain damage in SE should lead to further improvement in treatment and outcome.
 ...
PMID:Pathophysiological mechanisms of brain damage from status epilepticus. 838 2

We present six adult patients from three separate families, with a remarkably uniform heredo-ataxic syndrome, developing in three stages and ending in early death. The initial stage is determined by severe sensory neuropathy. The second stage is characterized further by progressive external ophthalmoplegia (PEO), probably caused by ocular myopathy, and progressive ataxia. During a short last stage there is epilepsia, and particularly myoclonic status epilepticus, of which four patients died unexpectedly. Sural nerve biopsies showed severe loss of myelinated fibres in a rather early stage of disease. Skeletal muscle biopsies (and a specimen of ocular muscle) revealed ragged-red fibres. Autopsy examination in two patients revealed multisystemic involvement of the nervous system, with, in particular, degeneration of spinal dorsal columns and spinocerebellar tracts. Pedigree data were compatible with an autosomal recessive disorder. Additional findings, particularly elevation of CSF lactate, suggested mitochondrial cytopathy as an essential feature of the multisystem degeneration in these patients.
 ...
PMID:Mitochondrial cytopathy presenting as hereditary sensory neuropathy with progressive external ophthalmoplegia, ataxia and fatal myoclonic epileptic status. 867 7

A 40-year-old conductor was admitted because of increasing drowsiness and confusion. Two years before admission he had had a first seizure. One year before admission he had a generalized convulsive status epilepticus; the following months he was less able to concentrate. A second status epilepticus was followed by transient weakness of his left arm and a depressed level of consciousness for several weeks. After awakening, he had delusions, and his wife found him demented. In the following months his confusion and drowsiness gradually deteriorated. He had previously had gonorrhoea, an episode of fever and exanthema, and was found to have oligospermia as cause of his infertility. On examination he was disoriented, and he had dysarthria. His left pupil was smaller, but both pupils reacted normally. There was left hemianopia and cerebellar ataxia. CT and MR showed large ventricles and periventricular diffuse lesions in the white matter. CSF examination revealed leucocytosis and increased protein content. Further examination were focussed on serological evidence of syphilis, and finally neurosyphilis was diagnosed. After treatment with penicillin, the patient started to recover.
 ...
PMID:[Clinical judgment and decision making in clinical practice. A music conductor with epilepsy followed by memory disorders]. 921 89

Effects of pentylenetetrazole (PTZ)-induced convulsive status epilepticus on free amino acids changes in venous blood, CSF and interstitial fluid (IF) of the brain were examined in dogs. A volume of brain IF sufficient for analysis was obtained by chronically implanted tissue cages. The onset of PTZ-induced convulsive seizures seemed mainly related to a marked increase of glutamate, aspartate, taurine, glycine and phosphoserine while, the maintenance and frequency of seizures seemed related to a marked increase of serine and glycine, in combination with a moderate rise of glutamate. L-alpha-Aminoadipate was recovered in moderate amount in epileptic brain IF, while, in controls, this compound was present in minimal amount. The observed complex temporal variation of the amino acidic pattern may play a role in PTZ-induced seizures and, possibly, in pharmacological kindling and brain structural alterations induced by PTZ.
 ...
PMID:Co-variation of free amino acids in brain interstitial fluid during pentylenetetrazole-induced convulsive status epilepticus. 929 15

Neuron-specific enolase (NSE) is a sensitive marker of brain damage in stroke, global ischemia, and coma. Serum NSE is also correlated with the duration and outcome of status epilepticus (SE). CSF-NSE levels have not been previously reported in SE. We report the CSF concentrations of NSE in 11 patients with cryptogenic/remote symptomatic SE. CSF obtained within 24 hours of SE showed increased concentrations of NSE in 9 of 11 patients. The mean CSF-NSE for the group was elevated compared with the levels for normal control subjects (30.8 +/- 18.33 versus 10.76 +/- 3.08 ng/mL; p = 0.002). Further, CSF-NSE levels were elevated compared with simultaneous serum levels in the same group of patients (p = 0.01). In addition, the CSF/serum albumin ratio (QAlb), a measure of the integrity of the blood-brain barrier, was increased in SE patients compared with control individuals (33.4 versus 4.79 x 10(-3); p = 0.0001). An increase of QAlb correlated with CSF-NSE (rs = 0.66, p = 0.04) and serum NSE levels (rs = 0.83, p = 0.004). CSF-NSE is a promising in vivo marker for brain injury after SE.
 ...
PMID:Status epilepticus increases CSF levels of neuron-specific enolase and alters the blood-brain barrier. 959 92

We report a case of non convulsive status epilepticus after an intrathecal injection of fluorescein. The clinical presentation was a confusional state--the epileptic origin of which was confirmed by the electroencephalogram. This rare and relatively benign complication should not bring about worry concerning the fluorescein test used for the diagnosis of a dural defect and the identification of the site of a CSF leak.
 ...
PMID:Non convulsive status epilepticus following intrathecal fluorescein injection. 1051 Jun 91

We reported a 37-year-old man who presented complex partial status epilepticus as the initial symptom of mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS). He showed fluctuating consciousness disturbance, left homonymous hemianopsia, and paroxysmal conjugated eye deviation to the left. The lactic acid level was elevated in blood and CSF, and ragged-red fibers were observed in the biopsied muscle. MRI demonstrated T2-prolonged lesions in the right occipito-parieto-temporal lobes. Since a mutation of mitochondrial DNA (A3243G) was identified, he was diagnosed as having MELAS. On an ictal record, high amplitude, rhythmic sharp waves were observed at right parieto-temporo-occipital region. High amplitude slow waves were also observed on the right hemisphere, especially in the right frontal lobe. These ictal discharges gradually decreased at their amplitude and in frequency, and then ictal EEG turned to the interictal EEG. During an ictal period, conjugated eye deviation to the left side and consciousness loss were observed. These seizures were observed once every several minutes. During the interictal period, sharp waves and sharp-wave complexes were observed frequently at right parietal and posterior temporal lobes. The venous injection of diazepam (10 mg) normalized EEG quickly. When consciousness loss, especially fluctuating, was observed in the patients of MELAS, complex partial status epilepticus should be considered.
 ...
PMID:[A case of MELAS presenting complex partial status epilepticus]. 1188 32

Japanese encephalitis (JE) causes at least 10 000 deaths each year. Death is presumed to result from infection, dysfunction and destruction of neurons. There is no antiviral treatment. Seizures and raised intracranial pressure (ICP) are potentially treatable complications, but their importance in the pathophysiology of JE is unknown. Between 1994 and 1997 we prospectively studied patients with suspected CNS infections referred to an infectious disease referral hospital in Ho Chi Minh City, Vietnam. We diagnosed Japanese encephalitis virus (JEV), using antibody detection, culture of serum and CSF, and immunohistochemistry of autopsy material. We observed patients for seizures and clinical signs of brainstem herniation, measured CSF opening pressures (OP) and, on a subset of patients, performed EEGs. Of 555 patients with suspected CNS infections, 144 (26%) were infected with JEV (134 children and 10 adults). Seventeen (12%) patients died and 33 (23%) had severe sequelae. Of the 40 patients with witnessed seizures, 24 (62%) died or had severe sequelae, compared with 26 (14%) of 104 with no witnessed seizures [odds ratio (OR) 4.50, 95% confidence interval (CI) 1.94-10.52, P < 0.0001]. Patients in status epilepticus (n = 25), including 15 with subtle motor seizures, were more likely to die than those with other seizures (P = 0.003). Patients with seizures were more likely to have an elevated CSF OP (P = 0.033) and to develop brainstem signs compatible with herniation syndromes (P < 0.0001). Of 11 patients with CSF OP > or =25 cm, five (46%) died, compared with seven (9%) of 80 patients with lower pressures [OR 8.69, 95% CI 1.73-45.39, P = 0.005). Of the 50 patients with a poor outcome, 35 (70%) had signs compatible with herniation syndromes (including 19 with signs of rostro-caudal progression), compared with nine (10%) of those with better outcomes (P < 0.0001). Of 11 patients with CSF OP > or =25 cm, five (46%) died, compared with seven (9%) of 80 patients with lower pressures (OR 8.69, 95% CI 1.73-45.39, P = 0.005). The combination of coma, multiple seizures, brainstem signs and illness for 7 or more days was an accurate predictor of outcome, correctly identifying 42 (84%) of 50 patients with a poor outcome and 82 (87%) of 94 with a better outcome. These findings suggest that in JE, seizures and raised ICP may be important causes of death. The outcome may be improved by measures aimed at controlling these secondary complications.
 ...
PMID:Seizures and raised intracranial pressure in Vietnamese patients with Japanese encephalitis. 1196 Aug 97

Ceftriaxone is recommended in children with acute bacterial meningitis (ABM) for 10 days. However, the drug is expensive, and shorter duration of therapy, if equally effective, would cut costs of therapy and hospitalization. The aim of this study was to compare the outcome of 7 days vs. 10 days' ceftriaxone therapy in children with ABM. Seventy-three children aged 3 months to 12 years with ABM, consecutively admitted to hospital were enrolled. Ceftriaxone was given for 7 days to all. Randomization to group I (7 days) and group II (10 days) therapy was done on the seventh day. At the end of 7 days' therapy in group I and 10 days in group II, children were evaluated using a clinical scoring system. Children with a score of more than 10 were labelled as 'treatment failures' and were continued on ceftriaxone. If a score was less than 10, the antibiotic was stopped. Complications were appropriately evaluated and managed. All children were followed-up 1 month after discharge: neurodevelopmental assessment, Denver Development Screening Tests, IQ and hearing assessment were done. After excluding four patients, there were 35 children in group I and 34 in group II. The two groups were comparable with respect to age, sex, nutritional status, presenting clinical features, and CSF parameters. Organism identification was possible in 38 per cent of children: (Streptococcus pneumoniae, 21 per cent; Haemophilus influenzae, 13 per cent; meningococcus, 4 per cent). Treatment failure rate was comparable in both groups (9 in group I and 8 in group II) as was the sequelae at discharge and at 1 month (9 in group I, 15 in group II,p > 0.1). Status epilepticus and focal deficits at presentation were significantly associated with treatment failures and sequelae in both the groups (p < 0.05). Length of hospital stay was shorter in group I (10.8 +/- 6.0 days) as compared with group II (14.4 +/- 7.2 days,p < 0.05) and frequency of nosocomial infection was significantly more in group II (p < 0.05). It was concluded that clinical outcome of patients treated with 7 days' ceftriaxone therapy is similar to that of 10 days' therapy, and is associated with lesser nosocomial infection and earlier hospital discharge. Seven days ceftriaxone therapy may be recommended for uncomplicated ABM in children in developing countries.
 ...
PMID:Seven days vs. 10 days ceftriaxone therapy in bacterial meningitis. 1240 69


<< Previous 1 2 3 4 5 6 Next >>