27 research outputs found
Serum miRNA125a-5p, miR-125b-5p, and miR-433-5p as biomarkers to differentiate between posterior circulation stroke and peripheral vertigo
BACKGROUND:
Acute vertigo is a common presentation of inner ear disease. However, it can also be caused by more serious conditions, especially posterior circulation stroke. Differentiating between these two conditions by clinical presentations and imaging studies during the acute phase can be challenging. This study aimed to identify serum microRNA (miRNA) candidates that could differentiate between posterior circulation stroke and peripheral vertigo, among patients presenting with acute vertigo.
METHODS:
Serum levels of six miRNAs including miR-125a-5p, miR-125b-5p, miR-143-3p, miR-342-3p, miR-376a-3p, and miR-433-5p were evaluated. Using quantitative reverse-transcription polymerase chain reaction (RT-qPCR), the serum miRNAs were assessed in the acute phase and at a 90 day follow-up visit.
RESULTS:
A total of 58 patients with posterior circulation stroke (n = 23) and peripheral vertigo (n = 35) were included in the study. Serum miR-125a-5p (P = 0.001), miR-125b-5p (P < 0.001), miR-143-3p (P = 0.014) and miR-433-5p (P = 0.0056) were present at significantly higher levels in the acute phase, in the patients with posterior circulation infarction. Based on the area under the receiver operating characteristic curve (AUROC) only miR-125a-5p (0.75), miR-125b-5p(0.77), and miR-433-5p (0.71) had an acceptable discriminative ability to differentiate between the central and peripheral vertigo. A combination of miRNAs revealed no significant improvement of AUROC when compared to single miRNAs.
CONCLUSION:
This study demonstrated the potential of serum miR-125a-5p, miR-125b-5p, and miR-433-5p as biomarkers to assist in the diagnosis of posterior circulation infarction among patients presenting with acute vertigo
FP06-MO-06 Prevalence and risk factors of extracranial internal carotid and intracranial artery stenosis in asymptomatic Thai subjects
PO12-TU-04 Carotid duplex ultrasound flow velocities and other parameters in healthy Thai subjects
FP23-TU-02 Association between apolipoprotein E (APOE), angiotension-converting enzyme (ACE), and methylenetetrahydrofolate reductase (MTHFR) polymorphisms and atherosclerosis of cervicocerebral arteries among different vascular locations
Serum NfL (Neurofilament Light Chain) Levels and Incident Stroke in Adults With Diabetes Mellitus
Hyperacute matrix metalloproteinase-2 levels predict early neurological deterioration in acute ischemic stroke
Depressive symptoms due to stroke are strongly predicted by the volume and location of the cerebral infarction, white matter hyperintensities, hypertension, and age: A precision nomothetic psychiatry analysis
Objectives: To delineate the effects of white matter hyperintensities (WMHs) as measured by Fluid-attenuated inversion recovery (FLAIR) and infarction volume as measured by Diffusion-weighted imaging (DWI) on post-stroke depression symptoms. Methods: Baseline National Institutes of Health Stroke Score (NIHSS) and Modified Rankin Scale (mRS) scores, and FLAIR and DWI MRIs to assess WMHs and acute infarct volumes, respectively, were assessed in 47 patients (≥55 years) with acute ischemic stroke and 17 normal controls. The Montgomery–Åsberg Depression Rating Scale (MDRS) was assessed three months after the stroke. Results: The MADRS score was significantly increased in stroke patients as compared with normal controls. The MADRS scale is not unidimensional and cannot be used as an accurate indicator of depression severity in stroke patients. Three months after stroke, key depressive (sadness and inability to feel) and concentration-tension symptoms, and lassitude are significantly predicted by the infarct volume. Right side infarction strongly predicts key depressive symptoms and left side infarction strongly predicts concentration-tension and lassitude scores. Total WMHs significantly predict key depressive and concentration-tension symptoms, and lassitude, with these effects being mediated by right and left DWI stroke volumes and associated disabilities. Conclusions: Interactions between age, hypertension, a chronic atherosclerotic process, and acute stroke account for the onset of key depressive symptoms three months after the acute infarct. Chronic and acute neuro-immune and neuro-oxidative stress pathways associated with the formation of WMHs and acute stroke may explain the incidence of post-stroke key depressive and concentration-tension symptoms, and lassitude
