Purpose: To assess the relationship between sodium signal intensity changes and oligemia, measured with perfusion-weighted imaging (PWI), in ischemic stroke patients. Materials and Methods:Nine ischemic stroke patients (55 6 13 years), four with follow-up scans, underwent sodium and proton imaging 4-32 hours after symptom onset. Relative sodium intensity was calculated as the ratio of signal intensities in core (identified as hypertintense lesions on diffusion-weighted imaging [DWI]) or putative penumbra (PWI-DWI mismatch) to contralateral homologous regions.Results: Sodium intensity increases in the core were not correlated with the severity of hypoperfusion, measured with either cerebral blood flow (rho ¼ 0.157; P ¼ 0.61) or cerebral blood volume (rho ¼ À0.234; P ¼ 0.44). In contrast, relative sodium intensity was not elevated (4-7 hours 0.96 6 0.07; 17-32 hours 1.00 6 0.07) in PWI-DWI mismatch regions.Conclusion: Sodium signal intensity cannot be predicted by the degree of hypoperfusion acutely. Sodium intensity also remains unchanged in PWI-DWI mismatch tissue, indicating preservation of ionic homeostasis. Sodium magnetic resonance imaging (MRI), in conjunction with PWI and DWI, may permit identification of patients with viable tissue, despite an unknown symptom onset time.

This study used oculomotor, cognitive, and multi-modal magnetic resonance imaging (MRI) measures to assess for neurological abnormalities in current asymptomatic amateur Australian rules footballers (i.e., Australia's most participated collision sport) with a history of sports-related concussion (SRC). Participants were 15 male amateur Australian rules football players with a history of SRC greater than 6 months previously, and 15 sex-, age-, and education-matched athlete control subjects that had no history of neurotrauma or participation in collision sports. Participants completed a clinical interview, neuropsychological measures, and oculomotor measures of cognitive control. MRI investigation involved structural imaging, as well as diffusion tensor imaging and resting-state functional MRI sequences. Despite no group differences on conventional neuropsychological tests and multi-modal MRI measures, Australian rules football players with a history of SRC performed significantly worse on an oculomotor switch task: a measure of cognitive control that interleaves the response of looking towards a target (i.e., a prosaccade) with the response of looking away from a target (i.e., an antisaccade). Specifically, Australian footballers performed significantly shorter latency prosaccades and found changing from an antisaccade trial to a prosaccade trial (switch cost) significantly more difficult than control subjects. Poorer switch cost was related to poorer performance on a number of neuropsychological measures of inhibitory control. Further, when comparing performance on the cognitively more demanding switch task with performance on simpler, antisaccade/prosaccades tasks which require a single response, Australian footballers demonstrated a susceptibility to increased cognitive load, compared to the control group who were unaffected. These initial results suggest that current asymptomatic amateur Australian rules football players with a history of SRC may have persisting, subtle, cognitive changes, which are demonstrable on oculomotor cognitive measures. Future studies are required in order to further elucidate the full nature and clinical relevance of these findings.

Although GABA has figured prominently in theories of migraine pathogenesis, 1 brain levels of this transmitter have not been directly measured in migraineurs. This is of importance since, in migraine, neurophysiologic events account for brain hyperexcitability and subcortical disinhibition. 2,3 Magnetic resonance spectroscopy (MRS) measures levels of metabolites in the human brain and may map regional changes in their levels. 4 Accordingly, herein we used MRS to measure the levels of GABA in individuals with migraine with aura (MA), migraine without aura (MO), and in controls. MethodsIndividuals with MA (n = 9), MO (n = 10), and controls without headache (n = 9) were enrolled. Participants could not use migraine preventive drugs or any other on a daily basis. Subjects prospectively collected their headache information over 1 month, using a daily headache calendar. Disability was assessed with the Migraine Disability Assessment Questionnaire (MIDAS).Migraineurs were imaged no less than 72 hours after their last headache attack. Data were acquired at 4T using a MRS INOVA system. Details of the methods are described elsewhere. 5 Briefly, a volume of 3 × 3 × 1.5 cm 3 was used positioned within the midline of the occipital lobe using inversion recovery gradient echo images. Two 8.5-minutes acquisition were averaged to generate a final GABA spectrum, referenced to creatine (Cr) and to N-acetylaspartate (NAA).We conducted cross-sectional analysis examining occipital GABA levels by headache status. We also evaluated the relationship between GABA levels and variables prospectively obtained from headache diaries (e.g., severe headaches). We powered our study based on assumptions for the GABA levels, as published previously. 6 We had an 80% power to detect 15% change in the GABA levels in a two-sided t test. This study was approved by the Tables 1 and 2 display the GABA concentration (millimoles per liter), GABA/Cr ratio, and total GABA (millimoles), across the different groups. The differences were not significant. For GABA, the mean values were 0.61 mmol (95% CI = 0.49-0.75) in controls, 0.67 mmol (95% CI = 0.56 -0.78) in the MO group, and 0.74 mmol (95% CI = 0.58-0.89) in the MA group. Nonsignificant differences were found in the other variables as well.Pooling the MO and MA subjects, GABA concentration was lower in individuals with severe headaches in the previous month. In those with no severe headaches, it was 0.72 ± 17 mmol/L vs 0.52 ± 0.64 mmol/L in those with one or more (p = 0.03). It was also lower in individuals with headaches of at least moderate severity. Finally, migraineurs with impairment (MIDAS grades II to IV) had lower GABA concentrations compared to those with no impairment (0.50 ± 0.48 mmol/L vs 0.73 ± 15 mmol/L, p < 0.05). After scaling by the creatine and NAA content, the findings were similar. For example, GABA/Cr ratio was also significantly lower in those with severe headaches in the past month (0.056 ± 0.08 mmol/L vs 0.068 ± 0.017 mmol/L, p = 0.04). DiscussionWe found that the levels of GABA ...

BackgroundSeveral options are available for the treatment of chronic rhinosinusitis (CRS), but disease control remains elusive for many patients. Recently, literature has emerged describing anti-IgE monoclonal antibody as a potential therapy for CRS. However, its effectiveness and safety are not well known. The purpose of this systematic review was to assess the effectiveness and safety of anti-IgE therapy and to identify evidence gaps that will guide future research for the management of CRS.MethodsMethodology was registered with PROSPERO (No. CRD42014007600). A comprehensive search was performed of standard bibliographic databases, Google Scholar, and clinical trials registries. Only randomized controlled trials assessing anti-IgE therapy in adult patients for the treatment of CRS were included. Two independent reviewers extracted data using a pre-defined extraction form and performed quality assessment using the Cochrane risk of bias tool and the GRADE framework.ResultsTwo studies met our inclusion criteria. When comparing anti-IgE therapy to placebo, there was a significant difference in Lund-McKay score (p = 0.04) while no difference was seen for percent opacification on computed tomography (CT). At 16 weeks, treatment led to a decrease in clinical polyp score. No significant difference was seen with regard to quality of life (Total Nasal Symptom Severity (TNSS), p < 0.21; Sinonasal Outcome Test 20 (SNOT-20), p < 0.60), and no serious complications were reported in either trial. Based on the quality assessment, studies were deemed to be of moderate risk of bias and a low overall quality of evidence.ConclusionsThere is currently insufficient evidence to determine the effectiveness of anti-IgE monoclonal antibody therapy for the treatment of CRS.Electronic supplementary materialThe online version of this article (doi:10.1186/s13643-015-0157-5) contains supplementary material, which is available to authorized users.