Evaluation of Febrile Seizures: A Therapeutic Review of Current Modalities.

As benign as its nature is, a febrile seizure (FS) can be one of the most frightening experiences for parents to witness. It is a seizure that occurs in infants and children aged six months to five years, accompanied by a fever (with a temperature of at least 100.4°F or 38.0°C by any method), without any infection in the central nervous system. FS is typically benign and tends to resolve on its own. Overall, the risk of recurrence after an FS is high, so there is still a sizable knowledge discrepancy that needs to be addressed for better understanding and management of the disease. Thus, the objective of this review is to evaluate current therapeutic modalities available for FS and summarize recent recommendations on the management of this condition. On June 25, 2023, a review was undertaken using the Medical Subject Headings Tool (MeSH), and the following keywords yielded 867 results: seizures, febrile/drug therapy [Mesh] and seizures, and febrile/therapy [Mesh]. A total of 21 relevant articles were chosen for the research. Seizures were classified as simple and complex FS (CFS) based on clinical features. CFS usually results in recurrence. Certain investigations like computed tomography (CT) scans, magnetic resonance imaging (MRIs), and electroencephalography (EEG) are helpful, along with laboratory investigations, to rule out other causes of FS. After reviewing the current literature, we have tried to conclude whether the current pharmacotherapy is effective in treating FS.

Preconditioning with the BKCa channel activator NS-1619 prevents ischemia-reperfusion-induced inflammation and mucosal barrier dysfunction: roles for ROS and heme oxygenase-1.

Activation of large-conductance Ca2+-activated K+ (BKCa) channels evokes cell survival programs that mitigate intestinal ischemia and reperfusion (I/R) inflammation and injury 24 h later. The goal of the present study was to determine the roles of reactive oxygen species (ROS) and heme oxygenase (HO)-1 in delayed acquisition of tolerance to I/R induced by pretreatment with the BKCa channel opener NS-1619. Superior mesentery arteries were occluded for 45 min followed by reperfusion for 70 min in wild-type (WT) or HO-1-null (HO-1-/-) mice that were pretreated with NS-1619 or saline vehicle 24 h earlier. Intravital microscopy was used to quantify the numbers of rolling and adherent leukocytes. Mucosal permeability, tumor necrosis factor-α (TNF-α) levels, and HO-1 activity and expression in jejunum were also determined. I/R induced leukocyte rolling and adhesion, increased intestinal TNF-α levels, and enhanced mucosal permeability in WT mice, effects that were largely abolished by pretreatment with NS-1619. The anti-inflammatory and mucosal permeability-sparing effects of NS-1619 were prevented by coincident treatment with the HO-1 inhibitor tin protoporphyrin-IX or a cell-permeant SOD mimetic, Mn(III)tetrakis (4-benzoic acid) porphyrin (MnTBAP), in WT mice. NS-1619 also increased jejunal HO-1 activity in WT animals, an effect that was attenuated by treatment with the BKCa channel antagonist paxilline or MnTBAP. I/R also increased postischemic leukocyte rolling and adhesion and intestinal TNF-α levels in HO-1-/- mice to levels comparable to those noted in WT animals. However, NS-1619 was ineffective in preventing these effects in HO-1-deficient mice. In summary, our data indicate that NS-1619 induces the development of an anti-inflammatory phenotype and mitigates postischemic mucosal barrier disruption in the small intestine by a mechanism that may involve ROS-dependent HO-1 activity.NEW & NOTEWORTHY Antecedent treatment with the large-conductance Ca2+-activated K+ channel opener NS-1619 24 h before ischemia-reperfusion limits postischemic tissue injury by an oxidant-dependent mechanism. The present study shows that NS-1619-induced oxidant production prevents ischemia-reperfusion-induced inflammation and mucosal barrier disruption in the small intestine by provoking increases in heme oxygenase-1 activity.

Rhinorrhea not responding to nasal corticosteroids.

A woman with multiple illnesses including allergic rhinitis presented for a follow-up visit at our clinic with constant rhinorrhea for 2 weeks despite regular use of nasal corticosteroids. Two weeks earlier, after alcohol drinking and doubling some of her medications for missed doses, she fell on her face. The Emergency Department records documented headache, bradycardia, hypotension, dehydration, and right infraorbital swelling. She was admitted for hydration and observation, and was discharged after two days without radiologic evaluation of the head. At our clinic, physical examination revealed pale turbinates bilaterally and clear watery discharge from the right nostril. Cerebrospinal fluid (CSF) rhinorrhea was suspected, but glucose testing was not available at our clinic. The patient was immediately admitted into the hospital. A beta-2-transferrin test confirmed CSF from the right nostril. High resolution sinus CT revealed fluid in the right sphenoid sinus, a large cyst in the left maxillary sinus, a cribriform plate dehiscence on the right side, and fluid collection adjacent to the middle turbinate. A lumbar drain was placed to release the pressure and antibiotic prophylaxis was started. Nasal endoscopy revealed CSF leak from the cribriform plate with bone dehiscence and a dural tear. A graft from nasal septal cartilage and temporalis fascia was applied using Tisseal fibrin glue. The persistent rhinorrhea resolved and on follow-up visits, the patient remained asymptomatic. Thinking of CSF rhinorrhea in the differential diagnosis of rhinitis would lead to early diagnosis and prevention of serious medical complications and potential legal liabilities.