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BACKGROUND: Cerebral microdialysis (MD) provides valuable information about brain metabolism under normal and pathologic conditions. The CMA 600 microdialysis analyzer received US Food and Drug Administration (FDA) approval for clinical use in the United States in 2005. Since then, cerebral MD has been increasingly utilized nationally in the multimodal monitoring of traumatic brain injury (TBI), stroke, aneurysmal subarachnoid hemorrhage, and brain tumors. We describe a 5-year, single-institutional experience using cerebral MD at a community-based hospital, Legacy Emanuel Medical Center (LEMC). Implications for the adoption and utility of MD in medical centers with limited resources are discussed. METHODS: This is a retrospective chart review and data analysis of 174 consecutive patients who had cerebral MD as part of multimodal brain monitoring. All cerebral MD catheters were placed by board-certified, attending neurosurgeons at LEMC. Clinical severity in the TBI patients was reported using initial Glasgow Coma Scale (GCS); radiologic severity was graded with the Marshall CT grading scale. Measures of the risks of MD placement included post-placement hemorrhage, cerebral infection, and dislodgement. RESULTS: Between July 2005 and July 2010, 248 cerebral MD catheters were placed in 174 patients undergoing multimodal brain monitoring. One hundred and eighty-five catheters were placed at the time of open craniotomy. None were associated with cranial infection. Patients ranged in age from 5 months to 90 years, with a mean of 49 years. The male to female ratio was 1.4:1. The underlying pathologies were: TBI (126), cerebral vascular accident (24), aneurysmal subarachnoid hemorrhage (17), and tumor (7). CONCLUSIONS: Cerebral MD was readily implemented in a community-based hospital. No cerebral hemorrhages or infections were attributed to cerebral MD. Examples of how MD may be a useful adjunct in the clinical decision making of patients with brain injuries are presented.
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BACKGROUND: This paper introduces the 7/5/2011al Pupil index (NPi), a sensitive measure of pupil reactivity and an early indicator of increasing intracranial pressure (ICP). This may occur in patients with severe traumatic brain injury (TBI), aneurysmal subarachnoid hemorrhage, or intracerebral hemorrhage (ICH). METHODS: 134 patients (mean age 46 years, range 18-87 years, 54 women and 80 men) in the intensive care units at eight different clinical sites were enrolled in the study. Pupillary examination was performed using a portable hand-held pupillometer. RESULTS: Patients with abnormal pupillary light reactivity had an average peak ICP of 30.5 mmHg versus 19.6 mmHg for the normal pupil reactivity population (P = 0.0014). Patients with "nonreactive pupils" had the highest peaks of ICP (mean = 33.8 mmHg, P = 0.0046). In the group of patients with abnormal pupillary reactivity, we found that the first evidence of pupil abnormality occurred, on average, 15.9 hours prior to the time of the peak of ICP. CONCLUSIONS: Automated pupillary assessment was used in patients with possible increased ICP. Using NPi, we were able to identify a trend of inverse relationship between decreasing pupil reactivity and increasing ICP. Quantitative measurement and classification of pupillary reactivity using NPi may be a useful tool in the early management of patients with causes of increased ICP.
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BACKGROUND: Age-related macular degeneration (AMD) is the leading cause of vision loss in elderly people over 60. The pathogenesis is still unclear. It has been suggested that lysosomal stress may lead to drusen formation, a biomarker of AMD. In this study, ARPE-19 cells were treated with chloroquine to inhibit lysosomal function. RESULTS: Chloroquine-treated ARPE-19 cells demonstrate a marked increase in vacuolation and dense intracellular debris. These are identified as chloroquine-dilated lysosomes and lipid bodies with LAMP-2 and LipidTOX co-localization, respectively. Dilation is an indicator of lysosomal dysfunction. Chloroquine disrupts uptake of exogenously applied rhodamine-labeled dextran by these cells. This suggests a disruption in the phagocytic pathway. The increase in LAMP protein levels, as assessed by Western blots, suggests the possible involvement in autophagy. Oxidative stress with H2O2 does not induce vacuolation or lipid accumulation. CONCLUSION: These findings suggest a possible role for lysosomes in AMD. Chloroquine treatment of RPE cells may provide insights into the cellular mechanisms underlying AMD.
