Clonidine Use for the Treatment of Nightmares in Posttraumatic Stress Disorder.

INTRODUCTION: While clonidine is used clinically for the treatment of nightmares in posttraumatic stress disorder (PTSD), few case reports demonstrating this indication exist, and there have been few studies investigating clonidine's mechanism of action for controlling nightmare symptoms. Case Report. In order to further characterize clonidine's role in treating nightmare symptoms in PTSD, we offer this case report describing one United States veteran who presented to an inpatient psychiatric unit after a suicide attempt. At that time, she described a remote history of PTSD symptoms, including nightmares, flashbacks, hyperarousal, and avoidance behaviors which had been well controlled on sertraline and clonidine. Upon her admission, her home sertraline and alprazolam were continued but her home clonidine was not continued. On day two of her hospital stay, she stated that her nightmares had returned. Her home clonidine was restarted on day two. On day three and thereafter, the patient no longer complained of nightmares. CONCLUSION: Our patient's nightmare symptoms had been controlled for years after beginning clonidine as an outpatient, but off clonidine, she had a return of her nightmare symptoms. Her nightmares again resolved once clonidine was resumed. Given this pattern in the patient's response to clonidine, this case may serve as additional evidence in the literature that clonidine has a role in treating nightmares in PTSD. Current proposed mechanisms of action for clonidine's ability to control nightmare symptoms in PTSD include that clonidine may alter the proportions of REM and non-REM sleep in a dose-dependent manner or that clonidine may play a role in memory consolidation. Further formal medication trials are the ideal future direction for establishing this role for clonidine.

The dangers of sublethal carvacrol exposure: increases in virulence of Bacillus cereus during endophthalmitis.

Bacillus cereus can cause endophthalmitis through secretion of virulence factors, including hemolysin BL (Hbl) and nonhemolytic entertoxin (Nhe). Carvacrol is an extract from oregano oil, with potential for curtailing B. cereus endophthalmitis, due to antimicrobial and anti-inflammatory qualities. However, sublethal levels of carvacrol increases B. cereus virulence. The goal of this study was to investigate the increase in B. cereus virulence potential in response stress induced by a subinhibitory concentration (SIC) of carvacrol. Enterotoxin production and tissue damage were examined during ocular infections in vitro and in vivo. We hypothesized that the SIC of carvacrol would significantly increase toxin production in B. cereus without progressing systemically. RT-PCR determined SIC carvacrol-treated B. cereus had significantly higher hblC and nheA mRNA expression levels than controls in vitro. ELISA and RPLA analysis revealed a 46.8% and 50% increase in NheA and HblC toxin levels, respectively, in SIC-treated cultures. Caenorhabditis elegans-fed SIC carvacrol-treated B. cereus had a significantly higher mean mortality rate than nematodes fed untreated B. cereus. Significantly higher TNF-α levels were observed in SIC carvacrol-treated B. cereus mice compared to other treatment groups except for mice infected with B. cereus alone. Significantly higher IL-6 levels were also found in SIC-B. cereus mice. Histological analysis using Rose-Bengal and DAPI determined that the eyes of mice infected with SIC carvacrol-treated B. cereus had significantly more damage than eyes treated with B. cereus alone. The SIC of carvacrol increased B. cereus virulence in vitro and in vivo, with a mild systemic infection noted.