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)

A 59-year-old female had been treated for epilepsy over 20 years. She had frequent convulsive seizures in spite of medication and was admitted to our hospital in status epilepticus. CT showed low density cyst with calcified wall at right suprasellar region and irregular ring enhancement in the frontal lobe which was continuous with the cyst. Angiography revealed tumor stain in the venous phase. The frontal mass was removed with evacuation of the cyst. Pathological findings were suggestive of squamous cell carcinoma arising from the epithelial component of the pre-existing dermoid cyst. The patient died six months after the operation with severe hyperglycemia, ketoacidosis and hypotension probably due to chemical meningitis and hydrocephalus.
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PMID:A squamous cell carcinoma originated from intracranial dermoid cyst. 844 93

Status epilepticus (SE) is one of the most common neurologic emergencies in children, adolescents, and young adults. SE may be due to acute neurologic conditions such as meningitis, encephalitis, or stroke, complicated febrile seizures, intractable epilepsy, degenerative diseases, intoxication, or may be the first manifestation of epilepsy. Initial treatment of convulsive SE is usually with an intravenous benzodiazepine (BZD) [lorazepam (LZP) or diazepam (DZP)], phenobarbital (PB), or phenytoin (PHT). LZP is less likely to cause respiratory depression than DZP and is therefore preferred. Sequelae and risk for recurrence of SE are primarily related to the underlying cause. Refractory SE (RSE) is most often symptomatic of an acute neurologic condition or neurodegenerative disease. Treatment for RSE is difficult, usually requiring intensive support of vital functions. Reported treatments for RSE include very high dose PB, continuous infusions of pentobarbital or BZDs (DZP, midazolam), lidocaine, inhalation anesthesia, and propofol. Outcome is related to underlying cause. Nonconvulsive SE may present as confusion or may mimic psychiatric illness. Response to BZDs is usually rapid but may not be sustained. Rapid initiation of oral or rectal valproate may be useful. Epilepsia partialis continua (EPC) is almost always due to an acute or chronic destructive lesion. Surgical treatment may be the only effective modality in some children with EPC. Acute treatment of breakthrough seizures and clusters of seizures at home with rectal BZDs (usually DZP, 0.2-0.5 mg/kg) may prevent progression to SE in some children and adolescents and reduce the need for visits to emergency facilities.
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PMID:Status epilepticus and acute repetitive seizures in children, adolescents, and young adults: etiology, outcome, and treatment. 864 55

Sixty-three children with new-onset temporal lobe epilepsy (TLE) underwent extensive clinical, EEG, and neuroimaging investigation as part of a prospective, community-based cohort study of the natural history of TLE in childhood. Complex partial seizures occurred in 94% of the children, and tonic-clonic seizures occurred in 14%. Developmental, behavioral, or learning problems were present in 38%. Eighteen children (29%) had a significant illness/event prior to the onset of TLE, including febrile status epilepticus in seven, meningitis in four, respiratory arrest in two, and head injury in one. Magnetic resonance imaging or computed tomography revealed structural abnormalities of the temporal lobe in 24 children (38%), including hippocampal sclerosis (HS) in 13 and tumor in eight. There was a strong association between HS and a history of significant illness/event prior to the onset of TLE (p < 0.001). Analysis of past history and neuroimaging findings led us to propose three etiologically defined subgroups of TLE; developmental TLE (10 children with long-standing, nonprogressive temporal lobe tumors and malformations), TLE with HS/significant antecedents (18 children with HS or a history of a significant illness/event), and cryptogenic TLE (34 children with normal neuroimaging findings and no significant past history). Etiologic differences between children with new-onset TLE may confer prognostic information that will be useful for counselling families and planning treatment.
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PMID:Temporal lobe epilepsy in childhood: clinical, EEG, and neuroimaging findings and syndrome classification in a cohort with new-onset seizures. 933 74

Hemolytic uremic syndrome (HUS) in associated with infections of neuraminidase-producing streptococcus pneumoniae was rarely reported in the literature. We report two infants with proven pneumococcal meningitis associated with anemia, thrombocytopenia, renal failure, and T-antigen activation characteristic of neuraminidase activity. This supports a common pathogenesis in HUS following infection of neuraminidase-producing strains of S. pneumoniae. One infant complicated with status epilepticus died, and the other infant survived without sequelae. We recommend that neuraminidase production should be considered in case of pneumococcal meningitis associated with anemia and thrombocytopenia without diffuse bleeding tendency. Early recognition of HUS associated S. pneumoniae neuraminidase production is vital. The use of compatible washed red blood cells, meticulous supportive care and appropriate use of dialysis will improve survival.
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PMID:Pneumococcal meningitis complicated with hemolytic uremic syndrome: report of two cases. 955 96

Midazolam infusion was tried as the treatment for 48 episodes of refractory status epilepticus or a cluster of seizures in 16 children. The mean age of patients was 3.5 years (range, 1 month to 18 years). Nine children had epilepsy, one purulent meningitis, one encephalitis, one acute cerebral infarction, and the remaining four had acute phase of hypoxic ischemic encephalopathy. The type of the seizure was a generalized tonic clonic seizure (including a partial seizure secondarily generalized) in 41 episodes, a tonic seizure in 3, an atypical absence in 1, and a complex partial seizure in 3, respectively. All patients received intravenous midazolam at 0.15 mg/kg as bolus, followed by a continuous infusion at 0.1-0.15 mg/kg/hr initially. The dose was increased gradually up to 0.3 mg/kg/hr until the complete control of seizures was achieved. Fourty-one of the 48 episodes of seizures were controlled within 30 minutes after the initiation of midazolam therapy. The mean infusion rate of midazolam required was 0.22 mg/kg/hr. The mean duration of the treatment was 4.1 days. None of the patients had serious changes in the blood pressure or respiratory status attributable to the use of midazolam. In conclusion, midazolam infusion is an effective and safe therapeutic approach for the management of childhood status epilepticus.
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PMID:[Efficacy of continuous intravenous infusion of midazolam in the treatment of status epilepticus in children]. 969 22

We studied the efficacy and safety of midazolam given as a continuous infusion in the treatment of refractory generalized convulsive status epilepticus (RGCSE). We carried out a prospective, open study, in 19 patients (11 men) with RGCSE in the intensive care unit at Firat Medical Center in Elazig. When intravenous administration of 0.3 mg/kg diazepam (three times at 5-min intervals), 20 mg/kg phenytoin, and 20 mg/kg phenobarbital failed to bring the episode under control, patients were administered an intravenous bolus of midazolam (200 microg/kg) followed by a continuous infusion at 1 microg/kg min. The dose was increased by 1 microg/kg min every 15 min until the episode of seizure was brought under control. The time from beginning of treatment to control of seizures, infusion rate, and side-effects were monitored. The mean age of the patients was 40.4 years (range 16-87 years). The clinical etiology of RGCSE was idiopathic epilepsy (6 cases), anoxicischemic cerebral insult due to cardiac arrest (3), viral encephalitis (2), intrahemispheric hematoma due to hemorrhagic stroke (1), cerebral infarct due to ischemic stroke (1), pituitary adenoma (1), post-traumatic epilepsy (1), renal failure (1), tuberculous meningitis (1), and unknown (2). In eighteen (94.7%) patients, seizures were completely controlled in a mean time of 45 min (range, 5-120 min) at a mean infusion rate of 8 microg/kg min (range, 3-21 microg/kg min). In one patient seizures did not stop. Midazolam administration did not cause any significant change in blood pressure, heart rate, oxygen saturation, or respiratory status. The mean time to full consciousness for patients after stopping the infusion was 1.6 hours (range, 2.0-8.5 hours). The mean infusion duration of midazolam was 14.5 hours (range, 12-25 hours). Midazolam is an effective and safe drug to control RGCSE, and may represent a substantial improvement over current therapeutic approaches such as pentobarbital anesthesia.
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PMID:Continuous infusion of midazolam in the treatment of refractory generalized convulsive status epilepticus. 1253 86

Neuron-specific enolase (NSE) is a glycolytic enzyme present almost exclusively in neurons and neuroendocrine cells. NSE levels in cerebrospinal fluid (CSF) are assumed to be useful to estimate neuronal injury and clinical outcome of patients with serious clinical manifestations such as those observed in stroke, head injury, anoxic encephalopathy, encephalitis, brain metastasis, and status epilepticus. We compared levels of NSE in serum (sNSE) and in CSF (cNSE) among four groups: patients with meningitis (N=11), patients with encephalic injuries associated with impairment of consciousness (ENC, N=7), patients with neurocysticercosis (N=25), and normal subjects (N=8). Albumin was determined in serum and CSF samples, and the albumin quotient was used to estimate blood-brain barrier permeability. The Glasgow Coma Scale score was calculated at the time of lumbar puncture and the Glasgow Outcome Scale (GOS) score was calculated at the time of patient discharge or death. The ENC group had significantly higher cNSE (P=0.01) and albumin quotient (P=0.005), but not sNSE (P=0.14), levels than the other groups (Kruskal-Wallis test). Patients with lower GOS scores had higher cNSE levels (P=0.035) than patients with favorable outcomes. Our findings indicate that sNSE is not sensitive enough to detect neuronal damage, but cNSE seems to be reliable for assessing patients with considerable neurological insult and cases with adverse outcome. However, one should be cautious about estimating the severity of neurological status as well as outcome based exclusively on cNSE in a single patient.
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PMID:Use of neuron-specific enolase for assessing the severity and outcome in patients with neurological disorders. 1468 39

Neurocysticercosis is the most common parasitic infestation involving the central nervous system in tropical countries. Common presentations are seizure, meningitis and increased intracranial pressure. The authors report a case of a 52-year-old woman with racemose neurocysticercosis in the subarachnoid space at the cistern of the brain through the lumbar cistern. She presented with progressive paraparesis due to spinal cord compression and finally had progressive bilateral sensori-neural hearing loss. MRI brain and the whole spinal cord revealed numerous rim-enhancing cystic lesions at the basal cistern, prepontine cistern, bilateral cerebellopontine angle, internal acoustic canals, intramedullary lesion at the 5th cervical spinal level, lumbar cistern lesions and secondary syringomyelia at the thoracic spinal cord. The histopathologic examination confirmed cysticercosis. After treatment by albendazole and surgical removal, she still developed recurrent spinal compression at a higher level and obstructive hydrocephalus. Finally, she died from status epilepticus and septic shock.
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PMID:Spinal cord compression and bilateral sensory neural hearing loss: an unusual manifestation of neurocysticercosis. 1556 Jul 5

The child who presents with acute coma runs a high risk of cardiopulmonary insufficiency, direct brain injury or even cerebral herniation. The case-management of such child requires a coma-specific emergent evaluation, immediate treatment of any hypoxicischemic insults and of the underlying cause. The coma-specific examination includes performance of child-adapted Glasgow Coma Score, the evaluation of brain stem functions such as pupillary response to light, cough- and gag reflex, and determination of all vital signs including body temperature. Treatment of hypoxicischemic insults includes control of airways and ventilation in patient with coma defined as GCS <8; liberal treatment of impaired cardiovascular states with isotonic fluids such as 0.9% sodium chloride; and treatment of cerebral herniation with head elevation, mannitol, hypertonic sodium chlorid fluids, steroids and hyperventilation. Immediately treatable causes are hypoglycemia, meningitis/encephalitis, opioid overdose and status epilepticus. Exclusion of rapidly progressive intracranial lesions almost always requires referral to the tertiary centre with head CT-scan facilities. Finally, an extensive etiology search of the stable coma is performed by looking for disease or trauma of the brain, for metabolic causes, for intoxications and for cardiopulmonary problems.
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PMID:[The comatose child]. 1613 15

A 37-year-old man in a status epilepticus due to meningitis was admitted to Intensive Care because of respiratory insufficiency. Spinal fluid culture yielded Streptococcus salivarius. Despite extensive diagnostics, the source of this bacterium could not be found. However, the patient had recently undergone spinal anaesthesia for surgery on a toe ulcer, from which other bacteria were cultured. The patient died 2 weeks after admission with a picture of multiple organ failure. Bacterial meningitis following spinal anaesthesia may be the result of impairment of the blood-brain barrier due to a sudden drop of spinal fluid pressure during the puncture, or of the introduction of bacteria from the hair follicles or from a haematoma caused by the needle or the introducer. Hygienic measures and a proper technique when performing regional anaesthesia are important in preventing the dissemination of bacteria.
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PMID:[Bacterial meningitis following spinal anaesthesia]. 1668 97


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