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  • phenobarbital  (2)
  • Key words Carbon monoxide poisoning  (1)
  • 1
    ISSN: 1126-5442
    Keywords: Key words Carbon monoxide poisoning ; Delayed neurologic sequelae ; Magnetic resonance imaging
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The clinical and neuroradiological outcome of carbon monoxide (CO) intoxication was evaluated prospectively in 30 patients over a follow-up period of 3 years. Among the patients studied, 22 had been acutely exposed to CO while 8 were chronically exposed. One month after CO poisoning, 12 of the 22 patients with acute intoxication showed magnetic resonance imaging (MRI) abnormalities: 6 also had neurological sequelae and 6 were asymptomatic. The remaining 10 patients showed neither MRI abnormalities nor neurological sequelae. During the 3-year follow-up, 4 of the patients with both MRI abnormalities and neurological sequelae improved in both clinical features and MRI findings. One of the 6 asymptomatic patients with MRI abnormalities developed a progressive cognitive impairment 2 months after acute intoxication, with a concomitant severe worsening of the MRI lesions. Among the 10 patients with neither MRI abnormalities nor neurological sequelae, only 1 developed neurological sequelae after a clear period of 4 months. In the group of patients who experienced chronic CO intoxication, only 1 presented with a neuropsychiatric syndrome which improved at follow-up. Brain MRI showed white matter lesions which remained unchanged at control scan after 1 year. In conclusion, we observed that some patients with severe CO poisoning and neurological sequelae may fully regain normal functions after approximately 1 year. The presence of MRI lesions 1 month after CO poisoning did not accurately predict the subsequent outcome. The observation of a clear period longer than the usual 2–40 day interval in 2 patients should be considered for careful planning of follow-up and for prognosis in CO-poisoned patients.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Neurological sciences 13 (1992), S. 755-760 
    ISSN: 1590-3478
    Keywords: Posttraumatic epilepsy ; prophylaxis ; phenobarbital ; head injury ; late seizures
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Sommario 390 pazienti con gravi traumi cranici sono stati trattati con phenobarbital (PB) per via orale, per un periodo di 12 mesi, al fine di verificare se tale farmaco potesse ridurre l'incidenza dell'epilessia post-traumatica (PTE). Il PB è stato somministrato per via intramuscolare, entro 24 ore dopo il trauma, alla dose di 2.5–3 mg/kg/die; dopo 5 giorni o un periodo di tempo maggiore se il coma persisteva, il farmaco è stato somministrato per via orale. Il mantenimento del livello plasmatico, quando necessario, è stato ottenuto monitorando le concentrazioni plasmatiche del farmaco che sono state mantenute tra 5 e 30 μg/ml. 293 pazienti hanno completato lo studio. Il 66% presentava un solo fattore di rischio, mentre il 34% presentava due o più fattori di rischio associati. 6 pazienti (2.04%) hanno presentato almeno una crisi epilettica entro i 12 mesi. I livelli plasmatici del farmaco al momento della crisi, variavano fra 20 e 28 μg/ml, con una eccezione di 15 μg/ml. I risultati dello studio indicano che il PB somministrato durante i primi 12 mesi dopo il trauma, anche a dosi relativamente basse, può avere un effetto profilattico sulla PTE.
    Notes: Abstract 390 patients with severe head injuries were treated with phenobarbital (PB) orally for a period of 12 months in order to determine whether this drug could reduce the incidence of posttraumatic epilepsy (PTE). An intramuscular PB dose of 2.5–3 mg/kg body weight per day was administered within 24 hours after the trauma; after 5 days, or longer if the coma persisted, the drug was administered orally. Maintenance dosage adjustments, when necessary, were based on serial plasma concentrations of the drug, sustained at between 5 and 30 μg/ml. 293 patients completed the study. 66% of these presented one risk factor, while 34% presented two or more. 6 patients (2.04%) had at least one seizure during the twelve months. Plasma drug levels at the time of the seizure, with one exception of 15 μg/ml, ranged from 20 to 28 μg/ml. The results of the study indicate that PB administered during the first twelve months after the trauma, even at relatively low doses, can have a prophylactic effect on PTE.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1590-3478
    Keywords: gynecomastia ; anticonvulsant drugs ; phenobarbital ; phenytoin ; fluoresone ; drug-induced ; hyperprolactinemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Sommario Una ginecomastia insorta in due epilettici viene riportata. Il quadro si è sviluppato alcuni mesi dopo che ad un precedente trattamento con PB e PHT si era aggiunto fluoresone alla dose di 750 mg/die per os. Le comuni malattie sistemiche che possono determinare una ginecomastia sono state escluse. I rilievi ormonali hanno evidenziato soltanto in un caso un'iperprolattinemia ed un aumento del rapporto estrogeni-androgeni circolanti. La relazione temporale fra somministrazione del fluoresone e comparsa del quadro appare cruciate, tuttavia il meccanismo patogenetico resta da chiarire.
    Notes: Abstract Gynecomastia developed in two epileptic patients some months after the addition of oral fluoresone 750 mg daily to the phenobarbital and phenytoin already being administered. The common systemic diseases that may give rise to gynecomastia were excluded. One of the patients presented hyperprolactinemia and a raised estrogen/androgen ratio but the hormone levels were not raised in the other. The onset of symptoms after fluoresone in both cases is highly suggestive, although the pathogenetic mechanism is not clear.
    Type of Medium: Electronic Resource
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