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)

An elderly man had focal motor status epilepticus secondary to a frontal lobe hematoma. Phenytoin, phenobarbital, and diazepam did not stop the seizures. Intravenous lidocaine by bolus injection and continuous infusion rapidly controlled the seizures.
South Med J 1979 Dec
PMID:Lidocaine: a neglected anticonvulsant? 11 54

A 51-year-old housewife developed symptoms of a cold followed by high fever, delirium, coma, rigidity of extremity muscles, positive Babinski sign and generalized convulsions, while complement-fixing antibody titre to herpes simplex virus in the sera raised over 128 X and declined to 8 X in the course. She finally expired of bronchopneumonia following status epilepticus after 94 days of illness. Severe necrosis with extensive hemorrhage in the white matter was predominant in the temporal, insular and orbitofrontal cortex, thalamus and globus pallidus. Focal rarefaction of the cerebral cortex with a very few eosinophilic intranuclear inclusions in the oligodendroglia and nerve cells, nerve cell destruction in the substantia nigra with glial nodules and perivascular inflammatory cell cuffs were observed. Abundant cytomegalic inclusion cells, originating from hypertrophic astrocytes, were present in the necrotic areas of cerebrum as well as in the rarefied tissue in the subependymal layers of the brainstem and cerebellum. Electron-microscopic study of the cytomegalic cells demonstrated the presence of numerous virions in both nucleus and cytoplasm. Fortuitour infection of the brain by cytomegalovirus with necrotizing encephalitis by herpes simplex virus is unique. The cause of double viral infections and severe lesions by less virulent strains is discussed.
Acta Neuropathol 1975 Dec 08
PMID:Double encephalitis with herpes simplex virus and cytomegalovirus in an adult. 17 28

The influence of hypercapnia, hypoxia and status epilepticus on cerebral cortex concentrations of adenosine, adenine nucleotides and cyclic AMP was studied on lightly anaesthetized (70% N2O) and artificially ventilated rats. Neither hypercapnia (arterial PCO2 about 80 and about 300 mmHg) nor hypoxia (minimal values of 19 mmHg) altered tissue concentrations of AMP, cyclic AMP or adenosine. Bicuculline-induced status epilepticus was accompanied by increased concentrations of cyclic AMP but adenosine concentration did not change. Experiments with ischemia, and those in which tissue hypoxia was exaggerated by unilateral carotid artery ligation, showed that tissue adenosine concentrations were elevated only when AMP concentration rose. It is concluded that the marked increase in cerebral blood flow which occurs in hypoxia and status epilepticus is unrelated to changes in tissue adenosine concentration and that the increase in cyclic AMP during neuronal hyperactivity is triggered by other mechanisms than adenosine accumulation.
Acta Physiol Scand 1978 Dec
PMID:Adenosine and cyclic AMP in cerebral cortex of rats in hypoxia, status epilepticus and hypercapnia. 21 98

EEG operant conditioning in an alumina-gel monkey model (N = 14) to decrease EMG, to increase 9 Hz or decrease 9 Hz, and to increase 23 Hz (18 Hz and 26 Hz in 2 pilot monkeys), respectively, was not consistently beneficial in reducing seizures. The data suggested: (1) that desynchronization of the EEG by reinforcing 18-26 Hz decreased in some animals the extent and severity of seizures while increasing seizure frequency; (2) that attending during conditioned EMG suppression reduced seizures somewhat; and (3) that the operant conditioning setting became stressful to the majority of monkeys under certain conditions, precipitating status epilepticus, gastrointestinal disturbances, and shock, which culminated in the death of 3 animals. Certain precautions are discussed in the therapeutic application of this technique to epileptic patients.
Epilepsia 1977 Dec
PMID:EEG operant conditioning in a monkey model: I. Seizure data. 41 66

Disseminated intravascular coagulation is here reported as a complication of status epilepticus. Other features of this case were rhabdomyolysis, hyperthermia, myoglobinuria and renal failure.
Thromb Haemost 1977 Dec 15
PMID:Disseminated intravascular coagulation in status epilepticus. 57 96

Electroencephalographic activity of the frontal cortex, cerebellar vermis, and superior vestibular nucleus was recorded in awake rats during the high pressure nervous syndrome (HPNS) by means of permanently implanted electrodes. Power-spectrum analysis revealed a decline in the faster frequencies and an increase in the slow frequences as the seizure end-point was approached. Effects of compression to 4500 fsw varied from severe tremor and myoclonic jerks to status epilepticus, with seizures occurring at an average depth of 3560 fsw. In all animals, multifocal-spiking activity progressed in severity with increasing depth. The predominant seizure pattern observed was a spike and slow-wave pattern reminiscent of absence seizures. Initial evidence of generalized seizure activity was equally divided between the cerebellum and cortex. It is concluded that the cerebellum participates in HPNS seizures. Possible evolution of the syndrome by loss of Purkinje cell inhibitory influence on subcortical sites that modulate cortical excitability is discussed.
Undersea Biomed Res 1977 Dec
PMID:Cerebellar and cerebral electroencephalogram during the high pressure nervous syndrome (HPNS) in rats. 60 10

The possible role of systemic physiological changes (occurring secondarily during status epilepticus) in the causation of epileptic brain damage has been evaluated in rats. Animals were anaesthetized, paralysed and mechanically ventilated; sustained electrocortical seizure discharges were induced by the intravenous injection of bicuculline, 1.2 mg/kg. After two hours of seizure activity brains were fixed by perfusion for histology. Physiological variables were maintained within certain limits from the end of the initial seizure phase (approximate duration twenty minutes) until two hours after onset of seizure to provide six groups: (1) Standard: mean arterial pressure above 120 mmHg, no hypoxia or hypoglycaemia, rectal temperature close to 37 degrees C. (2) Moderate Hypotension: mean arterial pressure at 70-75 mmHg. (3) Severe Hypotension: mean arterial pressure at 50 mmHg. (4) Hypoxia: arterial oxygen tension at 50 mmHg. (5) Hypoglycaemia: non-fed animals, with blood glucose close to 3.0 mumol/g. (6) Hyperthermia: rectal temperature at 40 degrees C. Microvacuolation and ischaemic cell change were identified by light microscopy in scattered neurons in the cortex (principally in the outer layers) in animals in three groups (Standard, Severe Hypotension and Hyperthermia). Similar neuronal changes were seen in the hippocampus (predominantly in the h1 or Sommer sector) in the Standard and Hyperthermia Groups. It is tentatively proposed that neuronal damage in animals with unrestricted cerebral oxygen and glucose availability is due to oxidative mechanisms in cells with excessively enhanced neuronal activity and that lesions caused by failing energy production do not appear until severe degrees of hypoxia are reached.
Brain 1978 Dec
PMID:Epileptic brain damage: the role of systemic factors that modify cerebral energy metabolism. 73 25

The role of glucose metabolism in alleviating the complications of status epilepticus (SE) was investigated in developing rats. Pretreatment with glucose reduced mortality from SE by 90% in rats under 1 week of age, 80% in 10-day-old rats, 50% in 15- to 20-day-olds, and not at all in adults. In 4-day-old animals, brain DNA synthesis during seizures, and in survivors, brain weight, DNA, RNA, protein, and cholesterol contents at 7 days of age were reduced less in glucose-treated than in saline-treated littermates. In the saline group, seizures caused a progressive fall in brain glucose level but no fall in blood glucose level, suggesting that glucose transport from blood to brain could not keep pace with glycolytic demands. In glucose-treated rats, blood and brain glucose concentrations remained elevated throughout the convulsive period. There was no reduction of brain adenosine triphosphate levels in either group. Thus, the protection by glucose appears to be related to its roles as a carbon source rather than an energy source. It is concluded that in immature animals, depletion of brain glucose can occur in the absence of hypoglycemia, and may be an important and potentially treatable complication of status epilepticus.
Arch Neurol 1976 Dec
PMID:Status epilepticus in immature rats. Protective effects of glucose on survival and brain development. 99 45

Four unrelated children were thought to have valproate-associated hepatotoxicity. They presented with recurrent partial secondarily generalized status epilepticus and epilepsia partialis continua followed by mental and motor regression. Despite treatment with multiple antiepileptic medications, they continued to have seizures. After initiation of valproic acid (VPA), all 4 manifested liver failure within 3 months. Two of these children each had 1 sibling who was not exposed to VPA, but who developed the same clinical picture including liver failure. At the time of autopsy, all 6 children had similar neuropathological findings with focal areas of spongiosis and neuronal loss, diffuse gliosis, and Alzheimer type II cells. One VPA-treated patient underwent a successful liver transplantation only to die from relentlessly progressive neurological deterioration. We propose that many of the reported patients with VPA-associated hepatotoxicity represent undiagnosed patients with early childhood hepatocerebral degeneration, the Huttenlocher variant of Alpers' syndrome. This disease manifests by obstinate partial seizures, recurrent partial secondarily generalized status epilepticus, epilepsia partialis continua, psychomotor deterioration, and hepatic dysfunction that is exacerbated by VPA administration. The accelerated demise from liver failure in the nontransplanted patients before the central nervous system pathology fully evolves makes the diagnosis of this rare condition difficult. The occurrence of disease in the unexposed siblings suggests recessive inheritance.
Ann Neurol 1992 Dec
PMID:Early childhood hepatocerebral degeneration misdiagnosed as valproate hepatotoxicity. 147 67

A series of 5 generalized tonic-clonic seizures within 30 min was induced by repeated transauricular electrical stimulation in mice. In this model, the anticonvulsant potency of intravenous valproate was compared with diazepam and phenytoin. All 3 drugs proved capable of rapidly suppressing the seizures after intravenous bolus injection. Potent anticonvulsant activity of diazepam and valproate was already obtained after 30 s, while phenytoin's onset of action was somewhat slower. In contrast to diazepam, valproate and phenytoin suppressed the seizures at non-sedative doses. ED50s for blockade of generalized tonic-clonic seizures throughout the 30-min period of repeated electrical stimulation were 6.6 mg/kg for diazepam, 28 mg/kg for phenytoin and 212 mg/kg for valproate. Determination of valproate in plasma and brain demonstrated that the rapid onset of anticonvulsant action after intravenous bolus injection was related to rapid drug penetration into brain tissue. The data indicate that an intravenous formulation of valproate might be a useful alternative to phenytoin as a non-sedative anticonvulsant for diazepam-resistant status epilepticus.
Epilepsy Res 1992 Dec
PMID:Intravenous valproate: onset and duration of anticonvulsant activity against a series of electroconvulsions in comparison with diazepam and phenytoin. 149 84


1 2 3 4 5 6 7 8 9 10 Next >>