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Thrombolytic treatment has been available for stroke treatment in Thailand since 1996. The use of intravenous thrombolysis in Thailand has dramatically increased during the past 10 years. This is mainly due to the stroke fast track program that has been implemented throughout the country. The “stroke fast track” program is designed for medical triage personnel at the hospital to identify stroke patients who presented early in order to immediately notify the stroke team for further investigation and management. The establishment of a telestroke network will be the next step to increase the accessibility of stroke patients to a better medical care as well as to decrease the rate of thrombolysis.

Introduction:In the United States, the risk of stroke is greater among Black compared to White adults. Furthermore, hypertension has a greater impact on stroke risk among Black adults. We hypothesized that race-specific metabolites may account for some of this observed disparity.Methods:This was a case-cohort study nested in the REasons for Geographic and Racial Differences in Stroke (REGARDS) study. Incident ischemic stroke cases (n=1,075) were compared with a random cohort sample (n=968). Metabolites were measured by liquid chromatography-tandem mass spectrometry. Weighted logistic regression and Cox proportional hazard model were used to identify race-specific metabolites in association with prevalent hypertension and incident stroke respectively. Candidate metabolites were assessed for mediation between hypertension and incident ischemic stroke. Linear regression was used to explore the association of metabolites with lifestyle factors.Results:A total of 162 plasma metabolites were quantified. Of these, gluconic acid was associated with prevalent hypertension in Black adults (OR=1.86, 95% CI=1.39-2.47, P=2.58x10-5) but not in White adults (OR=1.00, 95% CI=0.80-1.24, P=0.97; Pfor interaction=4.57x10-4). Gluconic acid was also associated with incident ischemic stroke among Black adults (HR=1.53, 95% CI=1.28-1.81, P=1.76x10-6) but not White adults (HR=1.16, 95% CI=1.00-1.34, P=0.057; Pfor interaction=0.019). Gluconic acid mediated 25.4% (95% CI=4.1%-46.8%, P=0.02) of the association between hypertension and ischemic stroke among Black adults. Specific lifestyle factors were linked to elevated gluconic acid level among Black adults in multivariable analysis, including a Southern diet (β=0.18, 95% CI=0.08-0.28, P<0.001), lower educational attainment (β=0.45, 95% CI=0.19-0.72, P=0.001), and lack of exercise (β=0.26, 95% CI=0.01-0.51, P=0.045).Conclusions:Gluconic acid is a lifestyle-related biomarker that is associated with prevalent hypertension, incident ischemic stroke, and mediates the relationship between hypertension and ischemic stroke in Black adults. Key factors linked to gluconic acid include Southern diet, low educational attainment, and low physical activity.

Stroke-like symptoms after COVID-19 vaccination was thought to be functional if there was no anatomical image abnormality. We aimed to analyze brain perfusion changes in these patients. A case-control study of brain perfusion single photon emission computed tomography (SPECT) of 12 vaccinated patients with left-sided stroke-like symptoms were compared with 12 age- and gender-matched normal interictal brain SPECTs using voxel-based analysis. Significant hyperperfusion was seen on the right side in postcentral, inferior parietal, mid temporal, parahippocampal, and caudate regions, and on the left side in the thalamus, hippocampus, and mid temporal areas. In addition, there were hypoperfused bilateral superior frontal gyri and right mid/posterior cingulate cortex (Family-wise-error corrected p-values  < .05). Both hypoperfusion and hyperperfusion in the brain are demonstrated. We hypothesize that these findings might be the result of the functional neurological disorder. However, based on other previous studies, circulating spike protein in the patients’ plasma early after vaccination might also be the cause.

Traumatic brain injury frequently causes traumatic axonal injury (TAI) in white matter tracts. Experimental TAI in the corpus callosum of adult mice was used to examine the effects on oligodendrocyte lineage cells and myelin in conjunction with neuroimaging. The injury targeted the corpus callosum over the subventricular zone, a source of neural stem/progenitor cells. Traumatic axonal injury was produced in the rostral body of the corpus callosum by impact onto the skull at the bregma. During the first week after injury, magnetic resonance diffusion tensor imaging showed that axial diffusivity decreased in the corpus callosum and that corresponding regions exhibited significant axon damage accompanied by hypertrophic microglia and reactive astrocytes. Oligodendrocyte progenitor proliferation increased in the subventricular zone and corpus callosum. Oligodendrocytes in the corpus callosum shifted toward upregulation of myelin gene transcription. Plp/CreERT:R26IAP reporter mice showed normal reporter labeling of myelin sheaths 0 to 2 days after injury but labeling was increased between 2 and 7 days after injury. Electron microscopy revealed axon degeneration, demyelination, and redundant myelin figures. These findings expand the cell types and responses to white matter injuries that inform diffusion tensor imaging evaluation and identify pivotal white matter changes after TAI that may affect axon vulnerability vs. recovery after brain injury.