BackgroundMigraine is a common disorder in general population. Presence of white matter hyperintensities (WMHs) in brain MRI of migraine patients was not studied clearly. Detection of the prevalence of white matter hyperintensities in migraine patients determines its correlation with migraine severity, type and duration.MethodsCross sectional analytic study was conducted on migraine patients attending neurology clinic Suez Canal University Hospital. Sixty-five patients with migraine aged from 18 to 50 years were included. We excluded smokers and patients with hypertension, cardiac disease, diabetes mellitus, endocrine dysfunction, oncological and hematological diseases, infectious diseases, demyelinating disorders, and Alzheimer disease. Brain MRI and laboratory investigation was done for all patients.ResultsWhite matter hyperintensities were significant more frequent in migraine with aura than those without aura. According to MIGSEV scale, white matter hyperintensities were highly significantly more frequent in grade III severity than grades II and I. The number of white matter hyperintensities increases significantly with increase intensity of pain during attack. The number of white matter hyperintensities increases significantly with increase intensity of nausea, disability, tolerability during attack and age. Resistance to treatment also shows statistically significant difference in increase number of WMHs.ConclusionsWhite matter hyperintensities are present in 43.1% of migraine patients. Age, presence of aura, nausea, disability during attack, resistance to treatment, and severity of headache and duration of migraine are considered a risk factor for development of white matter hyperintensities.

MicroRNAs regulate the expression of many genes and subsequently control various cellular processes, such as the immune response to viral infections mediated by type I interferon (IFN). In this study, the expression pattern of two interferon-related microRNAs, miR-146a and miR-155, was examined in healthy and HCV-genotype-4-infected peripheral blood mononuclear cells (PBMCs) using qRT-PCR. In contrast to other viral infections, the expression pattern was similar in both healthy and infected PBMCs. This could be attributed to attenuation of IFN pathway by HCV, which was assessed by investigating the expression of MxA, an interferon-stimulated gene, that showed lower expression in HCV-infected PBMCs. To determine the site of interference of HCV in the IFN pathway, expression of both microRNAs was examined following stimulation of PBMCs with IFN-α2a, an activator of the JAK/STAT pathway as well as with imiquimod, a toll-like receptor-7 (TLR-7) agonist that promotes interferon release. IFN stimulation induced the expression of miR-146a and miR-155 in HCV-infected and healthy PBMCs. Stimulation with imiquimod led to a down-regulation of both microRNAs in infected PBMCs, while it increased their expression in healthy PBMCs, indicating that HCV might interfere with miR-146a and miR-155 expression at sites upstream of interferon release, specifically in the TLR-7 pathway. The pattern of expression of both miR-146a and miR-155 was very similar with a strong positive correlation, but showed no correlation to the patients’ clinical or histopathological parameters or response to treatment. In conclusion, HCV infection might repress the induction of miR-146a and miR-155 by interfering with TLR-7 signaling.

DAAs are safe and effective in genotype 4 chronic HCV patients. It improves liver necro-inflammatory markers in cirrhotics and non-cirrhotics. Cirrhotic patients require careful observation being more vulnerable for treatment related complications.

BackgroundCentral post-stroke pain (CPSP) is an under-recognized complication of stroke although it can lead to deterioration in quality of life and impairment in activities of daily living. Its estimated prevalence varies between 18.6 and 49%.ObjectiveTo investigate the prevalence and predictors of CPSP in ischemic stroke patients and to find its relationship with somatosensory evoked potentials (SSEPs) and magnetic resonance imaging.Patients and methodsSixty five consecutive patients with recent first attack of ischemic stroke who were admitted to the Neurology Department, Suez Canal University Hospitals were recruited. Patients were subjected to clinical assessment, Hamilton depression rating scale, brain MRI, short-form McGill Pain Questionnaire (SF-MPQ), daily pain rating scale (DPRS), stimulus evoked pain, and SSEPs.ResultsThe total prevalence rate of CPSP was 35.4% (n = 23). The mean age of the patients developed CPSP was significantly lower than those without CPSP (p = 0.004). Deep sensory dysfunction was statistically significantly higher among CPSP group than non-CPSP group (p = 0.001). CPSP group showed statistically significant higher prevalence of thalamic stroke (p = 0.007), as well as significant abnormalities in inter-peak interval (IPL) of median and tibial nerves SSEPs (p < 0.05). Thalamic group showed higher abnormalities in IPL of median and tibial nerves compared to extra-thalamic group, but without statistically differences.ConclusionThe prevalence of CPSP was found to be 35.4%. Predictors of CPSP include; deep sensory dysfunction, prolongation of tibial N21–P40 IPL, smoking history, age < 50 years, presence of thalamic stroke and prolongation of median N9–N20 IPL.

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