anticonvulsants/fever

We studied the effects of phenobarbital (PB), valproic acid (VPA), and phenytoin (PHT) on the electroencephalograms and behaviorally defined seizure threshold temperatures in rat pups exposed to ambient hyperthermia on the fifth day of life. Animals injected with 10, 20, or 40 micrograms PB/g body

The effect of prostaglandins (PGs) A1, E1, E2, F1alpha, and F2alpha administered intraventricularly at doses of 0.02--4.0 mug/rat were studied in some behavioral, antinociceptive and anticonvulsant tests in rats. Exploratory and locomotor activity were decreased by all PGs except A1 and F2alpha

OBJECTIVE Mutations in the SCN1A gene, which encodes the α1 subunit of voltage-gated sodium channels, cause generalized epilepsy with febrile seizures plus (GEFS+) and severe myoclonic epilepsy of infancy (SMEI). N1417H-Scn1a mutant rats are considered to be an animal model of human FS+ or GEFS+. To

Although the anticonvulsant hypersensitivity syndrome was first described in 1950, confusion still abounds regarding the syndrome. The triad of fever, rash and internal organ involvement occurring 1 to 8 weeks after exposure to an anticonvulsant heralds this rare (1 in 1,000 to 10,000 exposures) but

Anticonvulsant hypersensitivity syndrome (AHS) is an acute, life-threatening, idiosyncratic drug reaction seen within 1-8 weeks after administration of an aromatic antiepileptic drug. The authors present the case of a 16-month-old boy who developed prolonged fever, a generalised pruritic rash and

In this study, we document a case of phenobarbital-induced anticonvulsant hypersensitivity syndrome (AHS), which has been rarely reported in veterinary medicine. A 2-year-old, 5.4 kg, neutered male Russian Blue cat was diagnosed with idiopathic epilepsy and started on phenobarbital treatment. Eight

An 8-year-old previously healthy girl with Streptococcus pneumoniae meningitis developed probable anticonvulsant hypersensitivity syndrome (AHS) within 5 days of starting fosphenytoin. She experienced fever, rash, periorbital edema, profound hepatotoxicity and coagulopathy. Her sudden and dramatic

Anticonvulsant hypersensitivity syndrome (AHS) is a rare, potentially fatal, idiosyncratic drug reaction characterized by fever, morbilliform rash, lymphadenopathy, hepatitis, and hematologic abnormalities. Aromatic antiepileptic agents, such as phenytoin, carbamazepine, and phenobarbital are the

OBJECTIVE To report a case of anticonvulsant hypersensitivity syndrome (AHS) precipitated by exposure to phenobarbital. METHODS An 11-year-old girl receiving phenobarbital developed fever, exfoliative skin rash, mucous membrane lesions, alopecia, and hepatic inflammation. Investigations ruled out an

Aromatic anticonvulsants such as phenytoin, phenobarbital and carbamazepine are associated with a hypersensitivity syndrome (fever, rash lymphadenopathy, hepatitis) suggestive of an immune component. We have identified immunoglobulin G antibodies in the sera of nine affected patients which recognize

The anticonvulsant hypersensitivity syndrome (AHS) is an idiosyncratic immunologic reaction to certain anticonvulsant medications, in which internal organ involvement may lead to fatal multisystemic failure. This syndrome has been associated with the use of aromatic ring-containing agents such as

OBJECTIVE To investigate the antipyretic and anticonvulsant activities of n-hexane fraction of Viola betonicifolia (V. betonicifolia). METHODS The antipyretic effect was scrutinized using brewer's yeast induced pyrexia and anticonvlsion effect was tested using pentylenetetrazol and strychnine

This study involved cases of unexplained fever for which an infectious disease consultation was requested and for which an untoward drug reaction was thought responsible. Twelve cases that met strict criteria for drug-induced fever are presented. Antimicrobial agents were responsible for eight