To assess the association between team sport participation and behavioral, psychological, and social health outcomes in young athletes. A systematic review and meta-analysis was undertaken to ident...
22 August 2013 in Neurology Research International
Cerebral vasospasm (CVS) is a potentially lethal complication of aneurysmal subarachnoid hemorrhage (aSAH). Recently, the symptomatic presentation of CVS has been termed delayed cerebral ischemia (DCI), occurring as early as 3-4 days after the sentinel bleed. For the past 5-6 decades, scientific research has promulgated the theory that cerebral vasospasm plays a primary role in the pathology of DCI and subsequently delayed ischemic neurological decline (DIND). Approximately 70% of patients develop CVS after aSAH with 50% long-term morbidity rates. The exact etiology of CVS is unknown; however, a well-described theory involves an antecedent inflammatory cascade with alterations of intracellular calcium dynamics and nitric oxide fluxes, though the intricacies of this inflammatory theory are currently unknown. Consequently, there have been few advances in the clinical treatment of this patient cohort, and morbidity remains high. Identification of intermediaries in the inflammatory cascade can provide insight into newer clinical interventions in the prevention and management of cerebral vasospasm and will hopefully prevent neurological decline. In this review, we discuss current theories implicating the inflammatory cascade in the development of CVS and potential treatment targets.
1 September 2016 in British Journal of Sports Medicine
OBJECTIVE: Sport-related concussion (SRC) has become a major public health concern. Prolonged recovery after SRC, named postconcussion syndrome (PCS), has been associated with several biopsychosocial factors, yet the role of both family and personal psychiatric histories requires investigation. In a cohort of concussed high school athletes, the authors examined the role(s) of family and personal psychiatric histories in the risk of developing PCS.METHODS: A retrospective cohort study of 154 high school athletes with complete documentation of postconcussion symptom resolution or persistence at 6 weeks was conducted. PCS was defined as 3 or more symptoms present 6 weeks after SRC. Three groups were defined: 1) positive family psychiatric history and personal psychiatric history (FPH/PPH), 2) positive FPH only, and 3) negative family and personal psychiatric histories (controls). Three bivariate regression analyses were conducted: FPH/PPH to controls, FPH only to controls, and FPH/PPH to FPH. Post hoc bivariate regression analyses examined specific FPH pathologies and PCS.RESULTS: Athletes with FPH/PPH compared with controls had an increased risk of PCS (χ2 = 8.90, p = 0.018; OR 5.06, 95% CI 1.71–14.99). Athletes with FPH only compared with controls also had an increased risk of PCS (χ2 = 6.04, p = 0.03; OR 2.52, 95% CI 1.20–5.30). Comparing athletes with FPH/PPH to athletes with FPH only, no added PCS risk was noted (χ2 = 1.64, p = 0.247; OR 2.01, 95% CI 0.68–5.94). Among various FPH diagnoses, anxiety (χ2 = 7.48, p = 0.021; OR 2.99, 95% CI 1.36–6.49) and bipolar disorder (χ2 = 5.13, p = 0.036; OR 2.74, 95% CI 1.14–6.67) were significantly associated with the presence of PCS.CONCLUSIONS: Concussed high school athletes with FPH/PPH were greater than 5 times more likely to develop PCS than controls. Athletes with only FPH were over 2.5 times more likely to develop PCS than controls. Those with an FPH of anxiety or bipolar disorder are specifically at increased risk of PCS. These results suggest that not only are athletes with FPH/PPH at risk for slower recovery after SRC, but those with an FPH only—especially anxiety or bipolar disorder—may also be at risk. Overall, this study supports taking a detailed FPH and PPH in the management of SRC.
In recent decades, a large body of research has focused on the role of nitric oxide (NO) in the development of cerebral vasospasm (CV) following subarachnoid hemorrhage (SAH). Literature searches were therefore conducted regarding the role of NO in cerebral vasospasm, specifically focusing on NO donors, reactive nitrogen species, and peroxynitrite in manifestation of vasospasm. Based off the assessment of available evidence, two competing theories are reviewed regarding the role of NO in vasospasm. One school of thought describes a deficiency in NO due to scavenging by hemoglobin in the cisternal space, leading to an NO signaling deficit and vasospastic collapse. A second hypothesis focuses on the dysfunction of nitric oxide synthase, an enzyme that synthesizes NO, and subsequent generation of reactive nitrogen species. Both theories have strong experimental evidence behind them and hold promise for translation into clinical practice. Furthermore, NO donors show definitive promise for preventing vasospasm at the angiographic and clinical level. However, NO augmentation may also cause systemic hypotension and worsen vasospasm due to oxidative distress. Recent evidence indicates that targeting NOS dysfunction, for example, through erythropoietin or statin administration, also shows promise at preventing vasospasm and neurotoxicity. Ultimately, the role of NO in neurovascular disease is complex. Neither of these theories is mutually exclusive, and both should be considered for future research directions and treatment strategies.
Study Design: Retrospective cohort. Objective: The purpose was to investigate the incidence of and risk factors for complications associated with vertebroplasty (VP) or kyphoplasty (KP) for osteoporotic vertebral compression fracture (OVCF) using the American College of Surgeons National Surgical Quality Improvement Program (ACS-NSQIP) database. Methods: A cohort of patients undergoing VP/KP was constructed from the 2011-2013 ACS-NSQIP dataset using Current Procedural Terminology (CPT) codes. The incidences of minor complications (i.e. urinary tract infection, pneumonia, renal insufficiency, superficial infection, wound dehiscence), major complications (i.e. reoperation, deep vein thrombosis, pulmonary embolism, sepsis, dialysis, cardiac arrest, deep infection, stroke), and mortality within 30 days post-surgery were investigated, and their risk factors were assessed using logistic regression modeling. Results: Of 1932 patients undergoing VP/KP, 166 (8.6%) experienced a complication, including minor complications in 53 (2.7%), major complications in 95 (4.9%), and death in 40 (2.1%). Multivariate logistic regression analysis indicated that the adjusted odds ratios (95% confidence interval [CI]) of mortality was significantly associated with ASA 4: 16.604 (1.956-140.959) and increased creatinine (≥ 1.3 mg/dL): 3.494 (1.128-10.823). History of chronic obstructive pulmonary disease was associated with minor complications. Increased WBC count and hypoalbuminemia (<3.0 g/dL) were also associated with major complications. Conclusions: The major complication and mortality rates associated with VP/KP were 4.9% and 2.1% respectively, higher than previous reports. Increased creatinine and ASA 4 were independently associated with mortality after VP/KP. Therefore, cautious monitoring and counseling is needed for elderly, patients with preexisting kidney disease or ASA 4 undergoing VP/KP.