Relationship between sodium intensity and perfusion deficits in acute ischemic stroke

Abstract

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.

Sodium-23 Magnetic Resonance Imaging Has Potential for Improving Penumbra Detection but Not for Estimating Stroke Onset Time

“…10 Recent studies involving human sodium MRI in the acute stroke period showed that sodium signal levels measured in the core tissue, defined by visibly increased DWI signal, remained normal up to 7 hours after arterial occlusion before eventually increasing. 8,9 This is consistent with the current and previous 13,17 rat stroke studies, where variable delay times were measured before TSC increased, coupled with early small decreases in sodium levels in the penumbra, suggesting that any increase above normal levels (we propose this as a viability threshold level) would indicate irreversible damage. In this case, permanent tissue damage would not be directly correlated with SOT, that is, the time of arterial occlusion, but rather the time at which sodium signal begins to increase above normal levels.…”

“…Recent patient data indicate that the sodium signal remains unchanged in presumed penumbra tissue 8,9 and that sodium signal changes in the core do not reverse after reperfusion. 19 During acute stroke it has been reported that the lesion identified from increased sodium concentration can be smaller than the lesion identified from decreased ADC.…”

Regional and temporal variations in tissue sodium concentration during the acute stroke phase

“…Taking these factors into consideration, in human stroke, a lag in the increase in 23 Na signal intensity has been identified with increases of less than 10% in the first 7 h increasing to 23% beyond 9 h and eventually leveling at 69% (7). A recent article reported no 23 increase in penumbral tissue as defined by the diffusion/perfusion-mismatch within 4-7 h after stroke onset (25). In the ischemic core (not defined as cortex or subcortex) in a rabbit embolic model, an acute (11%) decrease in signal during the first 40 min of ischemia was followed by a 12%/h increase, culminating in a 25% increase over baseline by 4 h poststroke (15).…”

The design of a double-tuned two-port surface resonator and its application to in vivo Hydrogen- and Sodium-MRI

“…The potential diagnostic benefits of 23 Na-MR imaging have recently been demonstrated for common pathological conditions such as tumor [5,6], stroke [7][8][9], Alzheimer disease [10], paramyotonia [11], arthritis [12], multiple sclerosis [13] and functional renal imaging [14] in humans. In addition, pre-clinical in vivo 23 Na MRI enables one to temporally follow pathological progression in animal models of common human disease [14][15][16].…”