The inflammatory system has been implicated in the pathophysiology of a variety of psychiatric conditions. Individuals with PTSD, depression, and other fear-and anxiety-related disorders exhibit alterations in peripheral circulating inflammatory markers, suggesting dysregulation of the inflammatory system. The relationship between inflammation and PTSD has been investigated almost exclusively in the periphery, and has not been extensively explored in human postmortem brain tissue. Interleukins (ILs) represent a subtype of cytokines and are key signaling proteins in the immune and inflammatory systems. Based on prior research implicating IL signaling in PTSD and depression, we performed a preliminary investigation of IL gene expression in a region of the cortex involved in emotion regulation and PTSD, the dorsolateral prefrontal cortex (dlPFC), using tissue from the newly established VA National PTSD Brain Bank. Gene expression analyses were conducted on post-mortem tissue from the dlPFC from 50 donors: 13 controls, 12 PTSD cases, and 25 depressed cases. RNA was extracted from frozen dlPFC tissue, reverse transcribed to cDNA, and quantitative polymerase chain reaction (qPCR) was performed to assess gene *
The elderly population faces an increasing number of cases of chronic neurological conditions, such as epilepsy and Alzheimer’s disease. Because the elderly with epilepsy are commonly excluded from randomized controlled clinical trials, there are few rigorous studies to guide clinical practice. When the elderly are eligible for trials, they either rarely participate or frequently have poor adherence to therapy, thus limiting both generalizability and validity. In contrast, large observational data sets are increasingly available, but are susceptible to bias when using common analytic approaches. Recent developments in causal inference-analytic approaches also introduce the possibility of emulating randomized controlled trials to yield valid estimates. We provide a practical example of the application of the principles of causal inference to a large observational data set of patients with epilepsy. This review also provides a framework for comparative-effectiveness research in chronic neurological conditions.
Background: Pressure ulcers resulting from continuous EEG (cEEG) monitoring in hospitalized patients have gained attention as a preventable medical complication. We measured their incidence and risk factors. Methods: We performed an observational investigation of cEEG-electrode-related pressure ulcers (EERPU) among acutely ill patients over a 22-month period. Variables analyzed included age, sex, monitoring duration, hospital location, application methods, vasopressor usage, nutritional status, skin allergies, fever, and presence/severity of EERPU. We examined risk for pressure ulcers vs monitoring duration using Kaplan-Meyer survival analysis, and performed multivariate risk assessment using Cox proportional hazard model. Results:Among 1,519 patients, EERPU occurred in 118 (7.8%). Most (n 5 109, 92.3%) consisted of hyperemia only without skin breakdown. A major predictor was monitoring duration, with 3-, 5-, and 10-day risks of 16%, 32%, and 60%, respectively. Risk factors included older age (mean age 60.65 vs 50.3, p , 0.01), care in an intensive care unit (9.37% vs 5.32%, p , 0.01), lack of a head wrap (8.31% vs 27.3%, p 5 0.02), use of vasopressors (16.7% vs 9.64%, p , 0.01), enteral feeding (11.7% vs 5.45%, p 5 0.04), and fever (18.4% vs 9.3%, p , 0.01). Elderly patients (71-80 years) were at higher risk (hazard ratio 6.84 [1.95-24], p , 0.01), even after accounting for monitoring time and other pertinent variables in multivariate analysis. Conclusions: EERPU are uncommon and generally mild. Elderly patients and those with more severe illness have higher risk of developing EERPU, and the risk increases as a function of monitoring duration. Neurol Clin Pract 2017;7:15-25
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