argyria/епилептични припадъци

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Argyria and convulsive seizures caused by ingestion of silver in a patient with schizophrenia.

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The case study of a schizophrenic patient with argyria which resulted from the chronic and excessive ingestion of antismoking pills contain silver, is presented. Convulsive seizures developed after the patient had been addicted to the pills for 40 years. An extremely high concentration of silver was

[Linkage analysis and gene mapping of one Chinese family with benign familial infantile convulsions].

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OBJECTIVE The present study performed linkage analysis and gene mapping to find the possible chromosome locus harboring in one family with benign familial infantile convulsions (BFIC) and investigate the possible molecular pathogenesis of BFIC. METHODS A four-generation family with BFIC was

19q13.33→qter trisomy in a girl with intellectual impairment and seizures.

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Rearrangements in chromosome 19 are rare. Among the 35 patients with partial 19q trisomy described, only six have a breakpoint defined by array. The 19q duplication results in a variable phenotype, including dysmorphisms, intellectual disability and seizure. In a female patient, although G-banding

Latency to onset of status epilepticus determines molecular mechanisms of seizure-induced cell death.

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The molecular mechanisms mediating degeneration in response to neuronal insults, including damage evoked by prolonged seizure activity, show substantial variability across laboratories and injury models. Here we investigate the extent to which the proportion of cell death occurring by apoptotic vs.

Glial activation precedes seizures and hippocampal neurodegeneration in measles virus-infected mice.

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Intracerebral injection of hamster neurotropic (HNT) measles virus in weanling Balb/C mice leads to an encephalitis, which is characterized by glial activation, behavioral seizures, selective neurodegeneration, and, after approximately 7 days, death. To provide a better understanding of the

Auditory and vestibular pathology of seizure-prone chicks.

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The mutant sex-linked lethal recessive px (paroxysmal) gene, expressed in White Leghorn chicks (Gallus domesticus) causes seizures beginning on approximately day 8 post-hatching. Seizures are spontaneous and inducible by auditory but not by photic stimulation. Prior to seizure onset px chicks are

A cupric silver histochemical analysis of domoic acid damage to olfactory pathways following status epilepticus in a rat model for chronic recurrent spontaneous seizures and aggressive behavior.

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The amnesic shellfish toxin, domoic acid, interferes with glutamatergic pathways leading to neuronal damage, most notably causing memory loss and seizures. In this study, the authors utilized a recently developed rat model for domoic acid-induced epilepsy, an emerging disease appearing in California

Spontaneous recurrent seizures after status epilepticus induced by soman in Sprague-Dawley rats.

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OBJECTIVE Exposure to toxic levels of organophosphorus (OP) nerve agents can lead to seizures, respiratory failure, and, if untreated, death. The cholinesterase inhibitor soman belongs to the class of OP nerve agents and can cause status epilepticus (SE) and brain damage due to neuroexcitotoxicity.

Hippocampal sclerosis dementia with tauopathy.

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In some elderly individuals with dementia, hippocampal sclerosis (HS) is the only remarkable autopsy finding. The cause of HS in this setting is puzzling, since known causes of HS such as seizures or global hypoxic-ischemic episodes are rarely present. We here describe a series of HS cases that have

Intrahippocampal cholinesterase inhibition induces epileptogenesis in mice without evidence of neurodegenerative events.

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The mechanisms of epileptogenesis remain largely unknown and are probably diverse. The aim of this study was to investigate the role of focal cholinergic imbalance in epileptogenesis. To address this question, we monitored electroencephalogram (EEG) activity up to 12 weeks after the injection of a

Electroconvulsive shock exposure prevents neuronal apoptosis after kainic acid-evoked status epilepticus.

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In the aftermath of prolonged continuous seizure activity (status epilepticus, SE), neuronal cell death occurs in the brain regions through which the seizure propagates. The vulnerability to adrenalectomy-induced apoptotic neuronal death was recently reported to be reduced by prior exposure to

Amygdala-kindling induces alterations in neuronal density and in density of degenerated fibers.

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Kindling is characterized by a progressive intensification of seizure activity culminating in generalized seizures following repeated administration of an initially subconvulsive electrical or chemical stimulus. Since it is known that epilepsy induces morphological alterations in the limbic system,

Partial trisomy 15 and temporal lobe syndrome in a retarded girl without gross malformations.

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A supernumerary small bisatellited chromosome was found in a girl with stunted growth and psychomotor retardation. The extra chromosome was identified as a deleted 15, del(15)(q21), with C-band positive heterochromatin and satellite-like appendages to the distal end of the long arm. This chromosome

Sequelae of parenteral domoic acid administration in rats: comparison of effects on different anatomical markers in brain.

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Brain damage following administration of domoic acid, a structural analog of the excitatory amino acids glutamic acid and kainic acid, was compared using different anatomic markers in adult rats. Seven days after administration of domoic acid (2.25 mg/kg i.p.) or vehicle, brains were collected and

Unintentional silver intoxication following self-medication: an unusual case of corticobasal degeneration.

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Silver toxicity is a rare condition. The most notable feature is a grey-blue discoloration of the skin, argyria, although harmful effects on the liver and kidney may be seen in severe cases. Neurological symptoms are an unusual consequence of silver toxicity. So far no effective treatment has been

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