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INTRODUCTION: Ischemic cerebral stroke initiates a complex cascade of pathophysiological events, involving various forms of molecular shifts and oedema. Early intervention is pivotal in minimizing tissue loss and improving clinical outcomes. This study explores the temporal and spatial evolution of tissue sodium concentration (TSC) in acute ischemic lesions after acute therapy using 23Na MRI in addition to conventional 1H MRI. METHODS: Prospectively, from examined 58 patients with acute ischemic stroke with a combined 1H/23Na MRI within 72 hours of symptom onset after receiving acute therapy, 31 patients were included in the evaluation of this study. After coregistration of the 23Na-MRI images to the morphological 1H-MRI images, manual segmentation of the ischemic lesions was performed and the ADC and TSC measurements were quantified and correlated with the time of onset and lesion volume. RESULTS: The mean TSC in ischemic lesions correlated positively with lesion volume (r=0.52, p=0.002) and showed a significant association with the time of stroke onset (r=0.8, p<0.001). Patients who were treated only with i.v. rtPA showed homogenous sodium signal intensity in the ischemic lesions, whereas the patients who received mechanical recanalization exhibited distinctive sodium signal intensity patterns with focal significant TSC differences. CONCLUSION: The integration of 1H and 23Na MRI provides a nuanced understanding of temporal and spatial changes due to different types of oedema in ischemic stroke lesions following acute treatment. Further exploration of these findings may enhance our understanding of stroke pathophysiology and guide personalised therapeutic interventions.
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BACKGROUND AND PURPOSE: Alzheimer's disease (AD) is characterized by cognitive decline and mnestic deficits. The pathophysiology of AD is not fully understood, which renders the development of accurate tools for early diagnosis and effective therapies exceedingly difficult. In this study, we investigated the use of 23Na-MRI to measure the relative sodium signal intensities (rSSIs) in CSF in patients with AD and healthy controls. METHODS: We prospectively recruited 11 patients with biomarker-diagnosed early-stage AD, as well as 12 cognitively healthy age-matched controls. All participants underwent 23Na-MRI to measure rSSI. Statistical analyses were performed to compare CSF sodium signal intensities between groups and to evaluate the specificity and sensitivity of the rSSI in the diagnosis of AD. RESULTS: RSSIs in CSF were significantly higher in AD patients (mean = 68.6% ± 7.7%) compared to healthy controls (mean = 56.9% ± 5.5%) (p < .001). There was also a significant negative correlation between rSSI in CSF and hippocampus and amygdala volumes (r = -.54 and -.49, p < .05) as well as a positive correlation with total CSF volumes (r = .81, p < .05). Receiver operating characteristic analysis showed high diagnostic accuracy for rSSI in discriminating between AD patients and healthy controls (area under the curve = .94). CONCLUSION: Our study provides evidence that rSSI in CSF is increased in AD patients in comparison to healthy controls. rSSI may serve as a potential marker for early detection and monitoring of disease progression. Larger, longitudinal studies are needed to confirm our findings and to investigate the association between rSSI in CSF and the severity of cognitive impairment.
