Sodium imaging intensity increases with time after human ischemic stroke

Hussain, Muhammad Shazam; Stobbe, Robert W.; Bhagat, Yusuf A.; Emery, Derek; Butcher, Ken; Manawadu, Dulka; Rizvi, Nasir; Maheshwari, Perkash; Scozzafava, James; Shuaib, Ashfaq; Beaulieu, Christian

doi:10.1002/ana.21648

Cited by 79 publications

(91 citation statements)

References 33 publications

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“…Other groups have applied linear (11,13) or sigmoid (7) models to fit their data, but none have measured a delay before the TSC increased. The nature of the actual increase may deviate from linear, particularly when approaching an assumed upper limit of 140 mM, and indeed previous studies have reported such a leveling-off of the TSC increase during the subacute phase between 24 to 48 h after stroke in humans (7) and rats (4).…”

Section: Discussionmentioning

confidence: 96%

“…Human studies have been limited by the heterogeneity of the disease in man and the uncertainty of perfusion status in serial studies (7). Studies where TSC sampling is delayed a number of hours after stroke will also fail to identify any acute delays in 23 Na accumulation or transitions from slow to more rapid 23 Na accumulation in tissue (11).…”

Section: Discussionmentioning

confidence: 99%

“…Studies where TSC sampling is delayed a number of hours after stroke will also fail to identify any acute delays in 23 Na accumulation or transitions from slow to more rapid 23 Na accumulation in tissue (11). 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).…”

Section: Discussionmentioning

confidence: 99%

“…The ability to measure elevated 23 Na levels (7,8) and to accurately quantify the tissue sodium concentration (TSC-a measure related to combined intracellular and extracellular 23 Na concentrations) in humans using 23 Na-MRI has demonstrated considerable potential to provide such a direct marker for tissue viability in stroke (1,9). However, the clinical role of 23 Na-MRI in assessing stroke patients remains unclear, due primarily to the lack of temporally resolved 23 Na data in these studies coupled with the difficulty in correlating the TSC measurements in man with histological data, and consequently, 23 Na-MRI is not an established diagnostic technique in hospitals.…”

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confidence: 99%

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

Wetterling

Gallagher

Macrae

et al. 2011

Magnetic Resonance in Med

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A technique for noninvasively quantifying the concentration of sodium (23Na) ions was applied to the study of ischemic stroke. 23Na‐magnetic resonance imaging techniques have shown considerable potential for measuring subtle changes in ischemic tissue, although studies to date have suffered primarily from poor signal/noise ratio. In this study, accurate quantification of tissue sodium concentration (TSC) was achieved in 23Na images with voxel sizes of 1.2 μL acquired in 10 min. The evolution of TSC was investigated from 0.5 to 8 h in focal cortical and subcortical ischemic tissue following permanent middle cerebral artery occlusion in the rat (n = 5). Infarct volumes determined from TSC measurements correlated significantly with histology (P = 0.0006). A delayed linear model was fitted to the TSC time course data in each voxel, which revealed that the TSC increase was more immediate (0.2 ± 0.1 h delay time) in subcortical ischemic tissue, whereas it was delayed by 1.6 ± 0.5 h in ischemic cortex (P = 0.0002). No significant differences (P = 0.5) were measured between TSC slope rates in cortical (10.2 ± 1.1 mM/h) and subcortical (9.7 ± 1.1 mM/h) ischemic tissue. The data suggest that any TSC increase measured in ischemic tissue indicates infarction (core) and regions exhibiting a delay to TSC increase indicate potentially salvageable tissue (penumbra). Magn Reson Med, 2012. © 2011 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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

Wetterling

Gallagher

Macrae

et al. 2011

Magnetic Resonance in Med

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“…Indeed, Na spin density-weighted images with reasonable signal to noise ratio (SNR) and spatial resolution can now be obtained in the brain in less than 10 minutes using standard 3 T clinical imaging platforms (1) , and a growing number of groups worldwide are working to push the boundaries of this exciting technique ever further. Examples of clinical application areas which have been investigated to date include cerebral stroke (2,3,4) , brain tumour (5,6) , breast tumour (7) , cardiac infarction (8) , Alzheimer's disease (9) , multiple sclerosis (10) , kidney (11,12) , osteoarthritis in cartilage (13,14) , while the first whole body sodium images were recently presented (15) .…”

Section: Introductionmentioning

confidence: 99%

How can sodium MRI techniques help us understand acute stroke?

Fagan

2012

Imaging in Medicine

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SUMMARYThis article addresses the potential usefulness of sodium MRI in the acute phase of stroke, asking whether the additional time required to acquire high quality sodium images is justified in the time-critical minutes following the presentation of a patient with symptoms. It begins with a description of the pathophysiology of stroke and the implications of the increasing bioenergetic failure on the sodium content in tissue. Recent studies which have aimed at imaging the subtle changes in this sodium content in stroke patients are then reviewed, followed by experiments in animal models of stroke which circumvent some of the limitations of the human studies. Finally, steps which will likely be required to translate these latest model findings into human studies are discussed, including new MR imaging techniques which may provide a boost in signal and allow for the introduction of relaxationtime contrast and quantification of the sodium concentration.

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Density gradients of vesicular glutamate‐ and GABA transporter‐immunoreactive boutons in calbindin‐ and μ‐opioid receptor‐defined compartments in the rat striatum

Wouterlood

Härtig

Groenewegen

et al. 2012

J of Comparative Neurology

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Cortical and subcortical inputs to the striatum are functionally highly organized and they obey to some extent striatal patch-matrix topography. Whether this organization is reflected in the density of various glutamatergic endings is unknown. We therefore mapped boutons expressing the vesicular glutamate transporters VGluT1 and VGluT2, together with boutons immunoreactive for vesicular γ-aminobutyric acid (GABA) transporter (VGAT) in patch and matrix throughout the striatum. We used triple-immunofluorescence staining followed by multichannel, high-magnification confocal laser scanning and 3D object recognition. Densities of VGluT1 and VGluT2 boutons were on average higher in matrix than in patches in all striatal sectors. The dorsal one-third of the striatum contained the highest densities of VGluT1 boutons. Subsequent 3D surface plotting revealed patterns of density "valleys" in the dorsomedial striatum coinciding with patch locations in the patch-matrix mapping. The density of VGluT1 boutons increased along three axes: ventrolateral-to-dorsomedial, ventral-to-dorsal, and lateral-to-medial. In contrast, VGluT2 showed a global increase in density from lateral to medial and a relatively high density in the ventral striatum. VGAT appeared more evenly distributed in the striatal patch-matrix than the VGluTs, with a tendency of bouton density to increase from medial to lateral. We noted a good correlation between the high VGluT1 bouton density dorsomedially with inputs from dorsal medial prefrontal cortex and related thalamic regions, and the enhanced VGluT2 input ventromedially with input from ventral medial prefrontal cortex and thalamic, amygdaloid, and hippocampal sources.

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Sodium imaging intensity increases with time after human ischemic stroke

Abstract: Increases of sodium signal intensity within the ischemic lesion are related to time after stroke onset. Thus, noninvasive imaging of sodium may be a novel metabolic biomarker related to stroke progression. Ann Neurol 2009;66:55-62.

Cited by 79 publications

References 33 publications

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

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

How can sodium MRI techniques help us understand acute stroke?

Density gradients of vesicular glutamate‐ and GABA transporter‐immunoreactive boutons in calbindin‐ and μ‐opioid receptor‐defined compartments in the rat striatum

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