Targeted Temperature Management for Poor Grade Aneurysmal Subarachnoid Hemorrhage: A Pilot Study.

OBJECTIVE: We assessed the effectiveness and safety of target temperature management (TTM) in treating patients with poor-grade aneurysmal subarachnoid hemorrhage (aSAH). The primary objective was to evaluate the neurological outcome at 3 months. Secondary objectives were to assess mortality, delayed cerebral ischemia, cerebral edema, hydrocephalus, midline shift, and laboratory indicators related to TTM. METHODS: A single-blind, nonrandomized controlled trial was conducted. After admission, patients with poor-grade aSAH (Hunt-Hess scores IV âˆ¼ V) were assigned to a TTM group or a control group in a 1:1 ratio. TTM with core temperatures ranging from 36°C to 37°C was performed immediately and maintained until microclipping or endovascular embolization. Subsequently, rapid induction to 33°C ∼ 35°C was carried out and maintained for 3 to 5 days. Then, the patients underwent slow rewarming to 36°C ∼ 37°C and maintained at that temperature for a minimum of 48 hours. RESULTS: Sixty patients (30 treated with TTM and 30 with standard treatment) were included in the study. At 3 months, a favorable prognosis (modified Rankin scale score 0 to 3) was significantly higher in the TTM group than in the control group (n = 14, 46.7% vs. n = 6, 20.0%, P = 0.028). Adjusted multivariate logistics regression analysis indicated that TTM (odds ratio = 0.20, 95% confidence interval: 0.05-0.77, P = 0.019) reduced the number of unfavorable prognoses 3 months after admission. CONCLUSIONS: This study demonstrated the effectiveness and safety of TTM in patients with poor-grade aSAH, and its implementation improved neurological outcomes. Multicenter randomized controlled studies with a large number of patients are needed to confirm these observations.

Effects of carotid artery stenting on cognitive impairment in patients with severe symptomatic carotid artery stenosis.

The effect of carotid artery stenting and medication on improvement of cognitive function in patients with severe symptomatic carotid artery stenosis is unknown. To investigate the effect of stenting compared with medication alone for severe carotid atherosclerotic stenosis on cognitive impairment. Patients with carotid stenosis and cognitive impairment were prospectively randomly divided into 2 groups of stenting or medication alone. Cognitive function was evaluated with the Montreal cognitive assessment (MoCA), Mini-Mental State Examination, and Barthel Index of Activities of Daily Living (BI). Continuous data in normal distribution were tested with the t-test but with the Mann-Whitney U test if not in normal distribution. Categorical data were presented as frequency and percentages and tested with the Fisher exact test. A P value < .05 was regarded as statistical significant. Carotid artery stenting was successfully performed in all patients (100%) in the stenting group. Compared with before treatment, the Mini-Mental State Examination, MoCA and BI scores at 6 months in the medication alone group and at 1, 3, and 6 months in the stenting group were significantly (P < .005) improved. The stenting group had significantly (P < .05) better scores than the medication alone group at the same time. At 6-month follow-up, the visuospatial/executive functions (3.69 ±â€…1.42 vs 2.42 ±â€…1.23), attention (5.24 ±â€…1.52 vs 3.63 ±â€…1.47), and language (2.64 ±â€…0.71 vs 1.96 ±â€…0.69) were significantly (P < .05) improved in the stenting group compared with the medication alone group. Carotid artery stenting may significantly improve cognitive impairment and neurological function compared with medication alone in patients with severe carotid atherosclerotic stenosis concurrent with cognitive impairment.

Hypersensitivity toward bacterial stimuli in patients with age-related macular degeneration.

Although the pathogenesis of age-related macular degeneration (AMD) is unclear, genetic screening has revealed that polymorphisms in the complement system may be associated with AMD development. Production of autoantibodies was also found in AMD patients. In this study, we analyzed the antibody response in AMD patients. We found that purified B cells from AMD patients tended to respond to lower concentrations of bacterial antigen stimulation, and produced higher amounts of antibodies, especially in IgM and IgA secretions. When examining clinical symptoms, patients with more severe wet-form AMD tended to exhibit higher sensitivity to bacterial antigens and secreted more IgM and IgA antibodies than those with less severe dry-form cases. In conclusion, our study discovered an altered B-cell antibody production in response to bacterial antigens in AMD patients, which potentially contributes to AMD pathogenesis.