Bilateral traumatic caroticocavernous fistulae: total resolution following unilateral occlusion

Balloon occlusion is the accepted treatment for direct post-traumatic caroticocavernous fistula. We present a case of bilateral traumatic fistulae associated with a pseudoaneurysm. Resolution of both fistulae occurred following treatment of one of them by balloon occlusion of the internal carotid artery. This case highlights the importance of considering a more conservative approach to bilateral fistulae or those associated with a pseudoaneurysm. We review other treatment options. Received: 1 October 1999/Accepted: 20 October 1999     

Potential impact of PET/CT on the initial staging of lymphoma

Purpose

The aim of this study was to investigate the potential impact of PET/CT on the initial staging of lymphoma with comparison to each of the PET and CT components alone.

Materials and methods

PET/CTs from 37 patients with lymphoma undergoing initial staging were studied. Review of PET, CT and PET/CT images were done and staging of each patient by each modality was assigned and compared together. Clinical follow-up, additional imaging and histology served as the standard of reference.

Results

PET/CT correctly diagnosed 83 nodal regions as positive for lymphomatous involvement versus 61 and 57 detected by PET and CT respectively. The respective sensitivities, specificities, and accuracies for the detection of nodal involvement were: PET: 88.4%, 65%, 94%, CT 89.1%, 60.1%, 96.1%, PET/CT 96.3%, 88.3%, 98.2%. PET/CT also correctly identified more extra-nodal lesions (n = 24) than CT (n = 16) and PET (n = 15). Correct staging was more accurate at PET/CT (n = 31) in comparison to PET alone (n = 23) and CT alone (n = 21).

Conclusions

PET/CT was superior to PET and CT in the initial staging of lymphoma with significant better performance compared to PET and CT to clarify nodal and extra-nodal involved sites. The application of PET/CT rather than CT or PET is likely to be more beneficial.     

Entrapment of Guide Wire in an Inferior Vena Cava Filter: A Technique for Removal

Entrapment of a central venous catheter (CVC) guide wire in an inferior vena cava (IVC) filter is a rare, but reported complication during CVC placement. With the increasing use of vena cava filters (VCFs), this number will most likely continue to grow. The consequences of this complication can be serious, as continued traction upon the guide wire may result in filter dislodgement and migration, filter fracture, or injury to the IVC. We describe a case in which a J-tipped guide wire introduced through a left subclavian access without fluoroscopic guidance during CVC placement was entrapped at the apex of an IVC filter. We describe a technique that we used successfully in removing the entrapped wire through the left subclavian access site. We also present simple useful recommendations to prevent this complication.     

Brain-immune interactions and ischemic stroke: clinical implications

Increasing evidence shows that the central nervous system and the immune system interact in complex ways, and better insight into these interactions may be relevant to the treatment of patients with stroke and other forms of central nervous system injury. Atherosclerosis, autoimmune disease, and physiological stressors, such as infection or surgery, cause inflammation that contributes to vascular injury and increases the risk of stroke. In addition, the immune system actively participates in the acute pathogenesis of stroke. Thrombosis and hypoxia trigger an intravascular inflammatory cascade, which is further augmented by the innate immune response to cellular damage occurring in the parenchyma. This immune activation may cause secondary tissue injury, but it is unclear whether modulating the acute immune response to stroke can produce clinical benefits. Attempts to dampen immune activation after stroke may have adverse effects because central nervous system injury causes significant immunodepression that places patients at higher risk of infections, such as pneumonia. The activation of innate immunity after stroke sets the stage for an adaptive immune response directed against brain antigens. The pathogenic significance of adaptive immunity and its long-term effects on the postischemic brain remains unclear, but it cannot be ruled out that a persistent autoimmune response to brain antigens has deleterious and long-lasting consequences. Further research will be required to determine what role, if any, immunity has in long-term outcomes after stroke, but elucidation of potential mechanisms may open promising avenues for the development of new therapeutics to improve neurological recovery after brain injury.     

Interaction between serine phosphorylated IRS-1 and beta1-integrin affects the stability of neuronal processes

Tumor necrosis factor-alpha (TNFalpha) released in the brain by HIV-activated macrophages/microglia is suspected to compromise neuronal survival. Previously, we have demonstrated that activated receptor for insulin-like growth factor I (IGF-IR) protects neurons from TNFalpha-induced neuronal damage (Wang et al. [ 2006] J. Neurosci. Res. 83:7-18). Because TNFalpha triggers phosphorylation of insulin receptor substrate 1 (IRS-1) on serine residues (pS-IRS-1; Rui et al. [ 2001] J. Clin. Invest. 107:181-189), and pS-IRS-1 binds integrins (Reiss et al. [ 2001] Oncogene 20:490-500), we asked how these events affect neuronal processes. We show that beta1-integrin and pS-IRS-1 colocalize in PC12 cells and in primary cortical neurons. TNFalpha treatment elevated membrane-associated pS-IRS-1, enhanced pS-IRS-1 interaction with beta1-integrin, and attenuated cell attachment to collagen IV. In contrast, IGF-I inhibited pS-IRS-1-beta1-integrin complexes and improved cell attachment. The domain of IRS-1 involved in beta1-integrin binding mapped between amino acids 426 and 740, and the expression of 426-740/IRS-1 mutant attenuated neuronal outgrowth. Our results indicate that TNFalpha facilitates the interaction of pS-IRS-1 and beta1-integrin and destabilizes neuronal processes. IGF-I counteracts TNFalpha-mediated accumulation of pS-IRS-1-beta1-integrin complexes supporting the stability of neuronal processes.     

VEGF and mRNA VEGF expression in CSF from Behçet's disease with neurological involvement

Vascular endothelial growth factor (VEGF) stimulates angiogenesis, but is also pro-inflammatory and plays an important role in the development of neurological disease, where it can have both attenuating and exacerbating effects. Several studies have indicated that VEGF-A (VEGF) may play a role in the pathogenesis of neurological inflammatory diseases.To assess the role of VEGF in patients with Behçet's disease with neurological involvement, VEGF was measured in the cerebrospinal fluid (CSF) of 32 patients compared to a group of 12 patients with noninflammatory neurological diseases (NIND) and 14 patients with multiple sclerosis (MS). We have also studied the expression of mRNA-VEGF (VEGF-A) in CSF and in peripheral blood mononuclear cells.The mean VEGF_CSF was significantly increased in neuro-BD and MS patients compared to NIND patients. There was an association between neuro-BD-VEGF_CSF, and leukocyte count. A significant correlation was also observed between neuro-BD-VEGF_CSF and CSF_%CD4 cells. As a measure of the integrity of the blood-brain barrier Q_albumin was found correlated to VEGF_CSF. VEGF mRNA was significantly increased in neuro-BD patients compared to NIND patients.These results indicate that, VEGF may be associated with the increased percentages of CD4 cell subpopulation. The role of VEGF is within the inflammatory cascade in the mediation of blood-brain barrier disruption and not specific to Behçet's.     

Contribution des facteurs génétiques et nutritionnels dans les hyperhomocystéinémies dans la population algérienne saine

The particular genetic polymorphisms associated to homocysteine metabolism enzymes, or more usually, a relative lack in different vitamins B group, are the main cause of the increase in this sulfur amino acid in the blood. As a fact, hyperhomocysteinemia are associated to many pathologies. The aim of this study is to determine the frequencies of the different genotypes caused by these polymorphisms, folate and vitamin B12 status and their eventual connections to hyperhomocysteinemia among a healthy adult population. The investigation has been applied to 165 apparently healthy volunteers. The homocysteine concentration was determined by IMx fluorescence polarization immunoassay. The genotypes determination was done by real-time PCR (RT-PCR) (Light Cycler 480). Folates and vitamin B12 were analyzed by SimulTRAC-SNB immunoassay. The homocysteine level was 14,69 ± 7,30 μmol/L. 22.5% of the subjects exhibited a moderate hyperhomocysteinemia (> 15 μmol/L). The major nutritional determinants of the plasmatic homocysteine rates among these subjects were blood folate and vitamin B12 levels. Blood homocysteine was the highest for the homozygote (TT) individuals for the MTHFR gene than for the heterozygote (CT) and homozygote (CC) subjects in particular for the lowest blood folate quartile. These two assessments have to be taken in consideration when evaluating the predisposition of the Algerian population for morbid and/or mortal pathologies and allow emphasizing on the necessity of screening out and eventually treating vitamin deficiencies on folates vitamin B12.     

Depression and the subsequent risk of Parkinson's disease in the NIH‐AARP Diet and Health Study

We conducted a case‐control study to examine the association between depression and Parkinson's disease (PD). Participants included 992 PD cases diagnosed after 2,000 and 279,958 individuals without PD from the NIH‐AARP Diet and Health Study follow‐up survey. Physician‐diagnosed depression and PD were self‐reported with information on the year of diagnosis in the following categories: before 1985, 1985–1994, 1995–1999, and 2000–present. Only PD cases diagnosed after 2000 were included in the analysis. Odds ratios (ORs) and 95% confidence intervals (CIs) were derived from logistic regression models, adjusted for age, gender, educational level, marital status, smoking, and coffee drinking. Individuals with depression diagnosed after 2000 were more likely to report a concurrent diagnosis of PD than those without depression (OR = 4.7, 95% CI = 3.9, 5.7). Depression diagnosed before 2000 was also associated with higher odds of PD diagnosed after 2000 (OR = 2.0, 95% CI = 1.6, 2.4). This association was stronger for depression diagnosed in 1995–1999 (OR = 2.7, 95% CI = 2.0, 3.6), but was also noted for depression diagnosed in 1985–1994 (OR = 1.6, 95% CI = 1.1, 2.3) or even before 1985 (OR = 1.7, 95% CI = 1.3, 2.3). This association was not modified by other factors and persisted in an analysis excluding participants who reported poor health status. The results suggest that depression may either be a very early symptom of PD or share common etiological factors with PD. © 2010 Movement Disorder Society     

Time from Onset of SIRS to Antibiotic Administration and Outcomes after Subarachnoid Hemorrhage

Introduction

The interval from presentation with systemic inflammatory response syndrome (SIRS) to the start of antibiotic administration affects mortality in patients with sepsis. However, patients with subarachnoid hemorrhage (SAH) often develop SIRS directly from their brain injury, making it a less useful indicator of infection. We therefore hypothesized that SIRS would not be a suitable trigger for antibiotics in this population.

Methods

We examined the time from the development of SIRS until antibiotic initiation and its relationship to long-term neurological outcomes in patients with nontraumatic SAH. Patients’ baseline characteristics, time of antibiotic administration, and hospital course were collected from retrospective chart review. The primary outcome, 6-month functional status, was prospectively determined using blinded, structured interviews incorporating the modified Rankin Scale (mRS).

Results

Sixty-six of 70 patients with SAH during the study period had 6-month follow-up and were included in this analysis. SIRS developed in 57 patients (86 %, 95 % CI 78–95 %). In ordinal logistic regression models controlling for age and illness severity, the time from SIRS onset until antibiotic initiation was not associated with 6-month mRS scores (OR per hour, 0.994; 95 % CI 0.987–1.001).

Conclusions

In this cohort of patients with SAH, time from SIRS onset until antibiotic administration was not related to functional outcomes. Our results indicate that SIRS is nonspecific in patients with SAH, and support the safety of withholding antibiotics in those who lack additional evidence of infection or hemodynamic deterioration.     

Peptidoglycan recognition protein genes and risk of Parkinson's disease

Increased gut permeability, inflammation, and colonic α‐synuclein pathology are present in early Parkinson's disease (PD) and have been proposed to contribute to PD pathogenesis. Peptidoglycan is a structural component of the bacterial cell wall. Peptidoglycan recognition proteins (PGRPs) maintain healthy gut microbial flora by regulating the immune response to both commensal and harmful bacteria. We tested the hypothesis that variants in genes that encode PGRPs are associated with PD risk. Participants in two independent case‐control studies were genotyped for 30 single‐nucleotide polymorphisms (SNPs) in the four PGLYRP genes. Using logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI) adjusted for potential confounding variables, we conducted analyses in each study, separately and pooled. One SNP failed the assay, and three had little to no variation. The ORs were similar in both study populations. In pooled analyses, three of seven PGLYRP2 SNPs (rs3813135, rs733731, rs892145), one of five PGLYRP3 SNPs (rs2987763), and six of nine PGLYRP4 SNPs (rs10888557, rs12063091, rs3006440, rs3006448, rs3006458, and rs3014864) were significantly associated with PD risk. Association was strongest for PGLYRP4 5'untranslated region (UTR) SNP rs10888557 (GG reference, CG OR 0.6 [95%CI 0.4‐0.9], CC OR 0.15 [95%CI 0.04‐0.6]; log‐additive P‐trend, 0.0004). Common variants in PGLYRP genes are associated with PD risk in two independent studies. These results require replication, but they are consistent with hypotheses of a causative role for the gut microbiota and gastrointestinal immune response in PD. © 2014 International Parkinson and Movement Disorder Society