anti inflammatory/seizures

Targeting pro-inflammatory events to reduce seizures is gaining momentum. Experimentally, antagonism of inflammatory processes and of blood-brain barrier (BBB) damage has been demonstrated to be beneficial in reducing status epilepticus (SE). Clinically, a role of inflammation in the pathophysiology

The effects of drugs on the convulsions induced by the combination of a new quinolone antimicrobial, enoxacin, and a nonsteroidal anti-inflammatory drug, fenbufen, were studied in mice. The combination of enoxacin at 30 or 100 mg/kg, p.o. and fenbufen at 100 mg/kg, p.o. induced convulsions; and the

Comparing with other pyridonecarboxylic acids (PCAs), the neurotoxicity of (+/-)-7-(3-amino-1-pyrrolidinyl)-6-fluoro-1-(2,4-difluorophenyl)-1,4- dihydro-4-oxo-1,8-naphthyridine-3-carboxylic acid p-toluenesulfonate hydrate (T-3262), which is a new PCA, was investigated in mice in a combination with

OBJECTIVE The central nervous system has been described as the coordinator of the inflammatory response to infection through the hypothalamo-pituitary axis and the autonomic nervous system. Brain lesions have been associated with impaired immunity and postoperative infections. We studied alterations

The muscarinic cholinergic agonist pilocarpine induces in rats seizures and status epilepticus followed by widespread damage to the forebrain. The present study was designed to investigate the effect of 5 non-steroidal anti-inflammatory drugs, sodium salicylate, phenylbutazone, indomethacin,

Prostaglandins and their inhibitors may affect convulsive phenomena. Thus, the aim of this study was to examine possible interactions between non-steroidal anti-inflammatory drugs and two conventional antiepileptic drugs in terms of their anticonvulsive activity and side-effects. Also, the plasma

As a crucial component of brain innate immunity, neuroinflammation initially contributes to neuronal tissue repair and maintenance. However, chronic inflammatory processes within the brain and associated blood-brain barrier (BBB) impairment often cause neurotoxicity and hyperexcitability. Mounting

The combined administration of enoxacin, a new quinolone, and fenbufen, a non-steroidal anti-inflammatory drug induced convulsions in mice, but convulsion did not occur when a single administration of each drug was given. Inhibition by enoxacin of [3H]muscimol binding to mouse and human brain

Convulsant activity of pazufloxacin mesilate (PZFX mesilate), a new quinolone antibacterial agent for intravenous use, in combination with nonsteroidal anti-inflammatory drug (NSAID) was investigated in mice after intravenous or intracerebroventricular administration. Following results were

Febrile seizures are childhood convulsions resulting from an infection that leads to an inflammatory response and subsequent convulsions. Prenatal stress has been shown to heighten the progression and intensity of febrile seizures. Current medications are costly and have adverse effects associated

Recent evidence has shown that proinflammatory and anti-inflammatory molecules are synthesized during epileptic activity in glial cells in CNS regions where seizures initiate and spread. These molecules are released and interact with specific receptors on neurons. Since various cytokines have been

Activation of proinflammatory and anti-inflammatory cytokines network seems to have a role in febrile seizures (FS). The present meta-analysis was aimed to pool the inconsistent data provided with case-control studies on the relationship of proinflammatory and anti-inflammatory cytokines and

OBJECTIVE Pro- and antiinflammatory cytokines regulate the febrile response during infection. Febrile seizures (FSs) conversely are associated with rapid onset of high fever. Activation of the cytokine network has been shown in previous studies of FSs and cytokines. In this study, the association

A young female subject with ineffective pharmacological regulation of chronic vasoconstrictive-induced epilectic-like seizures was effectively treated with a dietary regimen targeted to promote vasodilatation and attenuate vascular inflammation. The intervention consisted of complete cessation of