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)

We studied 80 hospitalized patients over 60 years old with either new-onset or newly diagnosed seizures that were generalized tonic-clonic in approximately half the cases and partial with or without secondary generalization in the other half. The etiology of seizures was acute symptomatic in 33 (41%), remote symptomatic in 32 (40%), progressive encephalopathy in nine (11%), and idiopathic in six (8%). Convulsive status epilepticus occurred in five cases (6%). The most common single cause of seizures was infarction or hemorrhage (54%). Morbidity and mortality were highest in the acute symptomatic group (p < 0.03). Nine (11%) of the subjects died within 3 months of admission, including two of the five with status epilepticus. Of the patients with acute symptomatic etiologies, 21% died compared with 6% of those in the remote symptomatic group. New neurologic deficits were present in eight (11%) of the 71 who survived, including five acute symptomatic, one remote symptomatic, and two progressive encephalopathy cases. No patient with idiopathic seizures died or had new neurologic deficits. We conclude that seizures in the elderly requiring hospitalization occur mainly with acute and remote symptomatic neurologic insults and are associated with a significant morbidity and mortality. In the absence of any associated neurologic insults, the morbidity is low.
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PMID:New-onset seizures in an elderly hospitalized population. 829 81

Status epilepticus (SE) occurs most commonly in infancy and childhood. Children with prior neurological abnormalities are most susceptible. More than 90% of cases are convulsive and the majority are generalized. SE may occur in the setting of an acute illness, in patients with established epilepsy or as a first unprovoked seizure. The etiology can be classified as idiopathic, remote symptomatic, febrile, acute symptomatic, or associated with a progressive encephalopathy. The morbidity and mortality of status have dramatically declined in recent years. Overall mortality in recent pediatric series was 3-10%, with almost all fatalities associated with acute central nervous system insults or progressive neurologic disorders. Neurological sequelae in children with idiopathic or febrile status are rare. Neurologically normal children with SE as their first unprovoked seizure have the same risk of experiencing subsequent seizures of any type as children who present with a brief first seizure. The risk of recurrent episodes of convulsive SE approaches 50% in neurologically abnormal children but is very low in neurologically normal children. The favorable outcome of SE in children may be related to advances in therapy and to the resistance of the immature brain to damage from seizures.
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PMID:Convulsive status epilepticus in children. 846 88

Two asthmatic children who developed status epilepticus during theophylline treatment followed by semi-coma were reported. They suffered from severe neurological sequelae. A two-year-old male received oral maintenance theophylline therapy and a four-year-old male received intravenous theophylline therapy at the time of seizures. Theophylline blood levels measured several hours after the onset of seizures were within or below the therapeutic level; 12.7 and 8.8 micrograms/ml. They had febrile convulsions prior to the onset of episode and one of them was mildly delayed in psychomotor development. Brain CT scans showed diffuse cortical low-density in the acute period. Follow up CT scans revealed progressive cortical low-density in the subacute period and subsequently reached to the peak in the 10th day and 19th day of illness respectively. We consider that the progressive and long-lasting severe cortical edema on brain CT scan is characteristic of theophylline-associated encephalopathy.
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PMID:[Two cases of theophylline-associated encephalopathy in childhood: clinical and CT findings]. 851 90

Refractory status epilepticus was observed in two patients who underwent vestibular neurectomy. We investigated the relationship with the use of an aluminum containing bone cement during the procedure. Two patients developed focal and thereafter generalized seizures in the late postoperative period of vestibular neurectomy (respectively after 42 and 35 days). A cement (1 g aluminum-calcium fluorosilicate) was used during the procedure to bridge bone defects. Both patients presented cerebrospinal fluid fistula. Investigations excluded common etiologies, in particular infections, and a toxic origin was suspected. Aluminum concentration was determined repeatedly in serum urine, cerebrospinal fluid and retroauricular fistula. The highest aluminum values were respectively in case 1 and 2, 112 and 63 micrograms/L for the cerebrospinal fluid, 495 and 1440 micrograms/L for the fistula, 4.4 and 4.4 micrograms/L in serum. Desferrioxamine was used as chelating agent and aluminum elimination was analyzed in the urine. Status epilepticus became refractory to intensive care therapy. The patients never recovered normal consciousness. Case 1 died 143 days after the procedure and case 2 at 80 days from brain failure. Brain post-mortem examination was obtained in Case 2. Brain aluminum concentration was 2.5 micrograms/g (wet weight) (0.85 micrograms/g in a control non exposed cadaver). The cement (0.2 g) was incubated in vitro (16 h-37 degrees C) with the cerebrospinal fluid of a control patient (cerebrospinal fluid aluminum 8 micrograms/L): aluminum concentration reached 2750 micrograms/L. A close contact between an aluminum containing cement and the cerebrospinal fluid may have resulted in encephalopathy and fatal status epilepticus in these two patients.
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PMID:Fatal encephalopathy after otoneurosurgery procedure with an aluminum-containing biomaterial. 852 86

We studied the seizure and polygraphic patterns of 18 patients with Angelman's syndrome. All patients showed movement problems. Eleven patients were also reported to have long-lasting periods of jerky movements. The polygraphic recording showed a myoclonic status epilepticus in nine of them. Seven patients had partial seizures with eye deviation and vomiting, similar to those of childhood occipital epilepsies. These seizures and electroencephalographic patterns suggest that Angelman's syndrome occurs in most of the patients as a nonprogressive, age-dependent myoclonic encephalopathy with a prominent occipital involvement. These findings indicate that, whereas ataxia is a constant symptom in Angelman's syndrome, the occurrence of a transient myoclonic status epilepticus may account for the recurrence of different abnormal movements, namely the jerky ones.
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PMID:Seizure and EEG patterns in Angelman's syndrome. 857 58

A previously healthy 8-month-old girl developed exanthem subitum and acute encephalopathy with status epilepticus, quadriplegia and bilateral abducens nerve palsies. Human herpesvirus-6 DNA was found in the cerebrospinal fluid by the polymerase chain reaction at the acute stage. Cranial computed tomography showed low density areas in the thalami and in the cerebellar and abducens nuclei. The distribution of the lesions was consistent with acute necrotizing encephalopathy. As for the thalamic lesions, a T2 weighted magnetic resonance image on the 24th day of the illness demonstrated low signal intensity surrounded by high intensity; 99mTc-ECD SPECT showed hypoperfusion, which suggested irreversible tissue damage. The patient is now 1 year 6 months old and has spastic quadriparesis with mental retardation and abducens nerve palsies.
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PMID:Serial neuroimages of acute necrotizing encephalopathy associated with human herpesvirus 6 infection. 857 24

Between August 12 and September 27, 1994, five children in South Florida were hospitalized at a single hospital because of encephalopathy, presenting as status epilepticus, associated with cat-scratch disease (CSD). Diagnoses were confirmed by using an indirect fluorescent antibody test to detect antibody to Bartonella henselae, the causative agent of CSD. These cases represent the first cluster of CSD encephalopathy cases to be recognized in the United States. The patients lived within 7 miles of each other and all reported contact with pet or stray cats before developing regional lymphadenopathy and encephalopathy. All recovered fully. A high proportion of 124 cats from the local area were seropositive (62%) or bacteremic (22%). This study suggests that B. henselae can be associated with geographically focal clusters of CSD encephalitis and should be considered in the evaluation of children with acute encephalopathy.
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PMID:Cluster of five children with acute encephalopathy associated with cat-scratch disease in south Florida. 858 13

Guanidinosuccinic acid (GSA) is a guanidino compound found in mammalian central nervous system and physiological fluids. Its level has been found to be greatly increased in serum and cerebrospinal fluid of patients with renal failure, and the compound is suggested to play a role in uremic encephalopathy. In this report we examined the behavioral, electrographic and morphological effects of intrahippocampal GSA injection in unanesthetized rats. Intrahippocampal administration of 2 microliters GSA solution (3.5 nM) was followed by behavior observation, and electrohippocampographic and electrocorticographic recording. GSA-injected animals showed partial clonic seizures leading to generalized clonic seizures, and eventually status epilepticus. These were accompanied by epileptiform electrographic discharges. During generalized clonic seizures, the electrohippocampogram showed arythmic bursting spikes. Epileptiform electric activity persisted even after the generalized clonic convulsions had stopped, and lasted until the animals were killed, 5 days following injection. Microscopic examination of brain slices of these rats revealed severe neural damage in CA1 area of hippocampus. Treatment of rats with the non-competitive NMDA receptor antagonist ketamine prevented both partial and generalized clonic seizures, epileptiform electrographic discharges, and GSA-induced hippocampal damage.
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PMID:Epileptiform activity and hippocampal damage produced by intrahippocampal injection of guanidinosuccinic acid in rat. 876 97

Reversible bilateral lesions of the claustrum and external capsule in a 12-year-old girl suffering from a severe, transitory encephalopathy are reported. After a prodromal stage of feeling uncomfortable a sudden onset of status epilepticus occurred, followed by recurrent complex partial and myoclonic seizures for 3 weeks, with psychotic symptoms and temporary loss of vision, speech and hearing. After treatment with phenytoin the patient became free of seizures and recovered completely without neurological deficit. The initial cranial CT was normal; however, cranial MRI 7 days later showed bilateral selective lesions of the claustrum and external capsule, which disappeared completely 5 weeks later. The aetiology of these lesions remains obscure; repeated cerebrospinal fluid and blood tests were negative for herpes simplex virus and other infectious agents. The clinical and radiological improvement were concomitant. This may indicate a functional disturbance of the claustrum grey matter, rather than lesions of the white matter of the external and extreme capsules.
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PMID:Severe transitory encephalopathy with reversible lesions of the claustrum. 892 73

Clinical electroencephalography is a relatively simple and inexpensive diagnostic tool with a high sensitivity for diffuse organic encephalopathy of various aetiologies but with a rather low specificity for the type of diagnosis. The highest sensitivity is shown in DAT and Parkinson dementia, and in these conditions the degree of EEG abnormality is correlated with the disease severity. Quantification of EEG makes these correlations more reliable and provides a method for monitoring therapeutic effects. Dementias with predominantly frontal pathology show much less EEG abnormality, and in these conditions the EEG is often normal despite obvious clinical dementia. Also, alcohol dementias often show normal EEG patterns. At an early stage of clinical evaluation, EEG may be useful in the discrimination of organic dementia from pseudodementia, because EEG is usually normal in depression, confusion, agitation and other psychiatric conditions. In pseudodementia due to intoxication with sedatives the EEG is usually dominated by diffuse beta activity. At the stage of differential diagnosis of an organic brain disorder, EEG cannot reliably discriminate between encephalopathies secondary to hydrocephalus, AIDS, cerebrovascular disease, B12 deficiency and primary degenerative diseases such as DAT. More specific EEG patterns are seen in acute cerebrovascular lesions, metabolic encephalopathies, i.e. of hepatic origin, Creutzfeldt-Jakob disease, herpes encephalitis, and nonconvulsive status epilepticus as possible causes of a rapidly deteriorating mental and neurological condition. Repeated EEG recordings over time would add significantly to the diagnostic information. New techniques such as topographical brain mapping, analysis of the EEG during REM sleep, coherence analysis of the EEG activity, and the combination of quantified EEG techniques with evoked potentials and event-related potentials will presumably add to the sensitivity as well as the specificity of the electrophysiological methods in the diagnosis of dementia.
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PMID:Electroencephalography as a diagnostic tool in dementia. 906 24


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