Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of therapy have been analyzed in a series of 192 patients admitted for status epilepticus over 7 years in two intensive care units. Most (142 cases without any prior epilepsy) corresponded to secondary forms. In 2/3 of the cases, the patients were admitted because of failure of benzodiazepines and/or phenobarbitone. Sodium thiopentone achieved control of seizures in 75%; short-acting barbiturates should be especially prescribed in grand mal status with impending brain anoxia. Diphenylhydantoin would appear suitable in non-life-threatening conditions such as serial seizures or partial status. Chlormethiazole often succeeds in controlling convulsive status which has proved refractory to other treatment. Supportive management is mandatory: 52% of patients required respiratory assistance. Fatalities (36%) exclusively correspond to the underlying cerebral conditions and systemic disorders.
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PMID:[Treatment of status epilepticus in the adult. Retrospective analysis of 192 cases treated in intensive care units]. 286 66

The association of truncal ataxia with a number of different factors has been studied in a group of 95 epileptic outpatients on chronic anticonvulsant treatment. The 28 patients showing truncal ataxia had been epileptic for a longer period of time, received a significantly larger number of drugs, and had higher serum levels of phenobarbital than the non-ataxic group. Serum folate levels were significantly lower in the ataxic group. A role is postulated for anticonvulsant-induced folate deficiency in the appearance of truncal ataxia presenting after prolonged anti-convulsant therapy, either by increasing the serum levels of the anticonvulsants or through other, unknown mechanisms. The presence of tonic-clonic seizures, presumably associated with brain anoxia, was not associated with the appearance of truncal ataxia.
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PMID:Truncal ataxia in chronic anticonvulsant treatment. Association with drug-induced folate deficiency. 621 66

The ultrastructure and the blood-brain-barrier (BBB) permeability were studied in mice suffering from lymphocytic choriomeningitis (LCM). Brains and meninges from mice suffering from LCM virus-induced lymphocytic choriomeningitis were studied by investigating the BBB function and by electron and light microscopy. The cellular exudate in the leptomeninges was located in the subarachnoid space, in arachnoidea and pia, and it was dominated by proliferated pial cells and mononuclear cells, most of which were lymphocytes, while there were only a few neutrophil granulocytes. Many intravascular lymphocytes were seen adhering to as well as penetrating the vessel walls. Many of these lymphocytes were morphologically compatible with T cells. Lymphocytes and larger mononuclear cells were also accumulated in the choroid plexus, and lymphocytes were present in the ventricular system with a tendency to adhere to ependymal epithelial cells. Inspection of the ultrathin sections incubated for horseradish peroxidase (HRP)-activity revealed that the overwhelming part of the peroxidase activity was localized in the extracellular space of the meningeal vessel walls and especially in the abundant intercellular fluid which, like the inflammatory cells, was found in the subarachnoid space in arachnoidea and in pia. In the neuropil, only very small quantities of reaction product were seen intercellularly in the most superficial layers of the cortex. The tight junctions were always intact, but the possibility of a non-demonstrable opening is discussed. Evaluation of the BBB permeability for 2-amino[1-14C]isobutyric acid (AIB) was made by quantitative autoradiography, and it was demonstrated convincingly that AIB concentrations in the subpial and perichorodial tissues were markedly increased in diseased animals as compared to the controls. Our results seem to contradict previous theories on the cause of death resulting from the LCM disease. The findings presented here do not speak in favor of a pronounced brain edema, just as results obtained by us and others do not speak for the possibility of the death being caused by convulsive seizures with subsequent brain anoxia. However, our observations are compatible with the hypothesis that cytotoxic T cells may interact in vivo with virus-infected targets, which are essential for the regulation of the composition of the cerebrospinal fluid. On the other hand, the dysfunction of the BBB demonstrated adds a new element to the pathologic mechanism in a model for the study of virus-induced meningitis.
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PMID:The permeability of the blood-brain barrier in mice suffering from fatal lymphocytic choriomeningitis virus infection. 646 79

Management of neurocritical care patients is focused on the prevention and treatment of secondary brain injury, i.e. the number of pathophysiological intracerebral (edema, ischemia, energy dysfunction, seizures) and systemic (hyperthermia, disorders of glucose homeostasis) events that occur following the initial insult (stroke, hemorrhage, head trauma, brain anoxia) that may aggravate patient outcome. The current therapeutic paradigm is based on multimodal neuromonitoring, including invasive (intracranial pressure, brain oxygen, cerebral microdialysis) and non-invasive (transcranial doppler, near-infrared spectroscopy, EEG) tools that allows targeted individualized management of acute coma in the early phase. The aim of this review is to describe the utility of multimodal neuromonitoring for the critical care management of acute coma.
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PMID:[Multimodal neuromonitoring for the critical care management of acute coma]. 2563 29