Stroke Onset Time Using Sodium MRI in Rat Focal Cerebral Ischemia

Tissue sodium concentration increases in irreversibly damaged (core) tissue following ischemic stroke and can potentially help to differentiate the core from the adjacent hypoperfused but viable penumbra. To test this, multinuclear hydrogen-1/sodium-23 magnetic resonance imaging (MRI) was used to measure the changing sodium signal and hydrogen-apparent diffusion coefficient (ADC) in the ischemic core and penumbra after rat middle cerebral artery occlusion (MCAO). Penumbra and core were defined from perfusion imaging and histologically defined irreversibly damaged tissue. The sodium signal in the core increased linearly with time, whereas the ADC rapidly decreased by >30% within 20 minutes of stroke onset, with very little change thereafter (0.5–6 hours after MCAO). Previous reports suggest that the time point at which tissue sodium signal starts to rise above normal (onset of elevated tissue sodium, OETS) represents stroke onset time (SOT). However, extrapolating core data back in time resulted in a delay of 72±24 minutes in OETS compared with actual SOT. At the OETS in the core, penumbra sodium signal was significantly decreased (88±6%, P=0.0008), whereas penumbra ADC was not significantly different (92±18%, P=0.2) from contralateral tissue. In conclusion, reduced sodium-MRI signal may serve as a viability marker for penumbra detection and can complement hydrogen ADC and perfusion MRI in the time-independent assessment of tissue fate in acute stroke patients.

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A Magnetic Resonance Imaging Protocol for Stroke Onset Time Estimation in Permanent Cerebral Ischemia

Journal of Visualized Experiments ◽

10.3791/55277 ◽

2017 ◽

Cited By ~ 4

Author(s):

Bryony L. McGarry ◽

Kimmo T. Jokivarsi ◽

Michael J. Knight ◽

Olli H.J. Grohn ◽

Risto A. Kauppinen

Keyword(s):

Magnetic Resonance Imaging ◽

Cerebral Ischemia ◽

Magnetic Resonance ◽

Onset Time ◽

Time Estimation ◽

Stroke Onset ◽

Resonance Imaging ◽

Imaging Protocol ◽

Magnetic Resonance Imaging Protocol

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Inhibition of Reactive Astrocytes with Fluorocitrate Retards Neurovascular Remodeling and Recovery after Focal Cerebral Ischemia in Mice

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.2009.257 ◽

2009 ◽

Vol 30 (4) ◽

pp. 871-882 ◽

Cited By ~ 91

Author(s):

Kazuhide Hayakawa ◽

Takafumi Nakano ◽

Keiichi Irie ◽

Sei Higuchi ◽

Masayuki Fujioka ◽

...

Keyword(s):

Cerebral Ischemia ◽

Focal Cerebral Ischemia ◽

Behavioral Outcomes ◽

Reactive Astrocytes ◽

Stroke Onset ◽

Stroke Recovery ◽

Neurological Deficits ◽

Behavioral Recovery ◽

Glial Scarring ◽

Neurovascular Remodeling

Glial scarring is traditionally thought to be detrimental after stroke. But emerging studies now suggest that reactive astrocytes may also contribute to neurovascular remodeling. Here, we assessed the effects and mechanisms of metabolic inhibition of reactive astrocytes in a mouse model of stroke recovery. Five days after stroke onset, astrocytes were metabolically inhibited with fluorocitrate (FC, 1 nmol). Markers of reactive astrocytes (glial fibrillary acidic protein (GFAP), HMGB1), markers of neurovascular remodeling (CD31, synaptophysin, PSD95), and behavioral outcomes (neuroscore, rotarod latency) were quantified from 1 to 14 days. As expected, focal cerebral ischemia induced significant neurological deficits in mice. But over the course of 14 days after stroke onset, a steady improvement in neuroscore and rotarod latencies were observed as the mice spontaneously recovered. Reactive astrocytes coexpressing GFAP and HMGB1 increased in peri-infarct cortex from 1 to 14 days after cerebral ischemia in parallel with an increase in the neurovascular remodeling markers CD31, synaptophysin, and PSD95. Compared with stroke-only controls, FC-treated mice demonstrated a significant decrease in HMGB1-positive reactive astrocytes and neurovascular remodeling, as well as a corresponding worsening of behavioral recovery. Our results suggest that reactive astrocytes in peri-infarct cortex may promote neurovascular remodeling, and these glial responses may aid functional recovery after stroke.

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