Neuroinvasion of emerging and re-emerging arboviruses: A scoping review.

Background: Arboviruses are RNA viruses and some have the potential to cause neuroinvasive disease and are a growing threat to global health. Objectives: Our objective is to identify and map all aspects of arbovirus neuroinvasive disease, clarify key concepts, and identify gaps within our knowledge with appropriate future directions related to the improvement of global health. Methods: Sources of Evidence: A scoping review of the literature was conducted using PubMed, Scopus, ScienceDirect, and Hinari. Eligibility Criteria: Original data including epidemiology, risk factors, neurological manifestations, neuro-diagnostics, management, and preventive measures related to neuroinvasive arbovirus infections was obtained. Sources of evidence not reporting on original data, non-English, and not in peer-reviewed journals were removed. Charting Methods: An initial pilot sample of 30 abstracts were reviewed by all authors and a Cohen's kappa of κ = 0.81 (near-perfect agreement) was obtained. Records were manually reviewed by two authors using the Rayyan QCRI software. Results: A total of 171 records were included. A wide array of neurological manifestations can occur most frequently, including parkinsonism, encephalitis/encephalopathy, meningitis, flaccid myelitis, and Guillain-Barré syndrome. Magnetic resonance imaging of the brain often reveals subcortical lesions, sometimes with diffusion restriction consistent with acute ischemia. Vertical transmission of arbovirus is most often secondary to the Zika virus. Neurological manifestations of congenital Zika syndrome, include microcephaly, failure to thrive, intellectual disability, and seizures. Cerebrospinal fluid analysis often shows lymphocytic pleocytosis, elevated albumin, and protein consistent with blood-brain barrier dysfunction. Conclusions: Arbovirus infection with neurological manifestations leads to increased morbidity and mortality. Risk factors for disease include living and traveling in an arbovirus endemic zone, age, pregnancy, and immunosuppressed status. The management of neuroinvasive arbovirus disease is largely supportive and focuses on specific neurological complications. There is a need for therapeutics and currently, management is based on disease prevention and limiting zoonosis.

Stealth invaders: unraveling the mystery of neurotropic viruses and their elusive presence in cerebrospinal fluid - a comprehensive review.

Neurotropic viruses are a threat to human populations due to ongoing zoonosis. A wide array of neurological manifestations can occur most often including parkinsonism, encephalitis/encephalopathy, flaccid myelitis, and Guillain-Barré syndrome. Neuroinvasion occurs through: transneural transmission, blood brain barrier (BBB) dysfunction, and 'trojan horse' mechanism or infected immune cell trafficking into the central nervous system (CNS). Transneural transmission occurs through virus mediated hijacking of intracellular transport proteins allowing retrograde viral transport. BBB dysfunction occurs through cytokine storm increasing membrane permissibility. Increased chemokine expression allows leukocyte trafficking to the BBB. Virally infected leukocytes may successfully pass through the BBB allowing the pathogen to infect microglia and other CNS cell types. We define cerebrospinal fluid (CSF) nondetection as a virus' ability to evade direct CSF detection but still causing significant neurological symptoms and disease. Mechanisms of CSF nondetection include: transneuronal propagation through trans-synaptic transmission, and synaptic microfusion, as well as intrathecal antibody synthesis and virus neutralization. Direct virus detection in CSF is associated with an increased neurological disease burden. However, the lack of CSF detection does not exclude CNS involvement due to possible neuroevasive mechanisms.

May-Thurner Syndrome.

This single-center, retrospective review identified 6 patients (n = 6, 100% female) treated by endovascular therapy for May-Thurner syndrome from June 2013 to September 2015. Patients consisted of 3 African American, 2 Caucasian and 1 Asian; mean age was 53.50 ± 8.31 years, range: 39-63 years. Clinical presentations consisted of left lower extremity deep vein thrombosis in 4, left lower extremity deep vein thrombosis with pulmonary embolism in 1 and pulmonary embolism with left common iliac vein thrombosis in 1 patient. All 6 patients were treated with catheter-directed thrombolysis and venous stenting to correct the underlying anatomical defect. Hypercoagulability work up revealed antiphospholipid antibody syndrome in 1 patient. No major periprocedural complications were observed. Median follow-up period was 22 ± 5.5 months (range: 13-30 months). One patient with pre-exiting antiphospholipid antibody syndrome developed stent thrombosis with secondary loss of patency. Endovascular therapy for May-Thurner syndrome in our adult cohort seemed safe and effective. One patient with pre-existing thrombophilia developed secondary loss of stent patency, suggesting need for further investigation in this subgroup.

Contrast-Induced Nephropathy After Cardiac Catheterization: Culprits, Consequences and Predictors.

BACKGROUND: Contrast-induced nephropathy (CIN) is a common complication after radiocontrast exposure. METHODS: A retrospective medical record review of 513 hospitalized patients who underwent cardiac catheterization from June-December 2014 was done, of which 38 patients with end-stage renal disease and 57 patients without preprocedural creatinine were excluded. Serum creatinine concentration before the procedure and each day for 3 days after the procedure was recorded. CIN was defined as an increase in serum creatinine concentration by ≥25% or ≥0.5mg/dL from the preprocedural value within 72hours of contrast exposure. RESULTS: A total of 418 patients (mean age: 69.1 ± 13.8 years, 55% males) were included in the study. Mean incidence of CIN was 3.7% (n = 16). CIN accounted for longer duration of hospitalization, lengthier intensive care unit admission, requirement of hemodialysis and higher mortality. Incidence of CIN was higher in the presence of preexisting atrial fibrillation (AF), congestive heart failure (CHF) and chronic kidney disease (CKD). When tested by univariate analysis, incidence of CIN was 13.8% in the AF group (P < 0.001), 8.6% in CHF group (P < 0.01) and 8.9% in CKD group (P < 0.002), compared with 2.3%, 1.9% and 2.4% in the absence of preexisting AF, CHF and CKD, respectively. On further testing using multivariate logistic regression model using AF, CHF and CKD as independent variables, development of CIN was strongly associated with preexisting AF with an odds ratio of 4.11, 95% CI: 1.40-12.07, P = 0.01. CONCLUSION: Identifying patients at risk is an important step in preventing CIN. Preexisting AF, independent of traditional risk factors, may increase the risk for CIN.