Which MRI findings are characteristic of the hyperacute phase (0-24 h) of acute stroke?

Updated: Dec 19, 2018
  • Author: Souvik Sen, MD, MPH, MS, FAHA; Chief Editor: Helmi L Lutsep, MD  more...
  • Print
Answer

Answer

DWI is able to detect ischemic changes within minutes of onset (see the image below). Reduced proton motion is detected as a decreased ADC.

Magnetic resonance imaging in acute stroke. Left: Magnetic resonance imaging in acute stroke. Left: Diffusion-weighted MRI in acute ischemic stroke performed 35 minutes after symptom onset. Right: Apparent diffusion coefficient (ADC) map obtained from the same patient at the same time.

Early in the process of cerebral ischemia, PWI, using first-pass contrast bolus injection or spin tagging of the protons in the water in blood, reveals reductions in CBF and CBV and an increase in MTT of blood through the brain (see the image below).

Magnetic resonance imaging in acute stroke. Left: Magnetic resonance imaging in acute stroke. Left: Perfusion-weighted MRI of a patient who presented 1 hour after onset of stroke symptoms. Right: Mean transfer time (MTT) map of the same patient.

Matched diffusion- and perfusion-weighted abnormalities correlate with the region of infarction and are indicative of permanent neuronal death. Mismatched diffusion and perfusion abnormalities with the perfusion abnormality larger than the diffusion abnormality may be indicative of a region of reversible ischemic penumbra (see the image below).

Magnetic resonance imaging in acute stroke. Diffus Magnetic resonance imaging in acute stroke. Diffusion-perfusion mismatch in acute ischemic stroke. The perfusion abnormality (right) is larger than the diffusion abnormality (left), indicating the ischemic penumbra, which is at risk of infarction.

A popular paradigm is to subject patients presenting beyond the 3-hour window to multimodal MRI to detect DPM; patients with mismatch may be candidates for stroke treatment. Two clinical trials have been completed that tested the hypothesis that patients with ischemic penumbra as detected by DPM mismatch may benefit from thrombolysis beyond the 3-hour treatment window.

Both studies seemed to show lack of benefit, suggesting that patients selected based on DWI/PWI mismatch do not benefit from intravenous thrombolysis beyond the 3-hour window. Both the studies, the EPITHET and the DEFUSE trials, randomized patients presenting 3-6 hours with greater than 20% DWI/PWI mismatch to intravenous tissue-type plasminogen activator (tPA) or placebo. [7] The ECASS-3 trial did not use such an MRI paradigm and has shown benefit of intravenous tPA in acute ischemic stroke 3-4.5 hours from onset. [8]

These trials raise several technical issues with DWI/PWI mismatch, particularly with regard to (1) most appropriate DWI/PWI ratio, (2) the most appropriate PWI threshold, (3) the coregistration of DWI and PWI, and (4) the online automated assessment of mismatch. EPIPHET and DEFUSE failed to show the utility of DPM in selecting patients for IV tPA beyond the traditional 3-hour window. [7] The MR RESCUE similarly showed that DPM was not a useful tool in selecting patients who may benefit from interventional stroke management. [9]

Newer MRI techniques are being developed to assess regions of reversible ischemia. Susceptibility-weighted imaging, such as BOLD functional MRI (BOLD-fMRI), is considered to provide a surrogate for brain OEF measurement and is one such emerging technique. [10]

A few hours after stroke onset, a loss of arterial void signal is sometimes observed (30-40% of patients); it is best observed on T2-weighted imaging (T2-WI). At 2-4 hours, T1-weighted imaging (T1-WI) shows subtle effacement of the sulci due to cytotoxic edema. At 8 hours, T2-WI shows hyperintense signal due to cytotoxic and vasogenic edema. At 16-24 hours, T1-WI shows hypointense signal due to cytotoxic and vasogenic edema.

Contrast-enhanced images show arterial enhancement followed by parenchymal enhancement. The arterial enhancement can be very early (in >50% of patients) and is due to slow blood flow; it typically disappears after 1 week.

Parenchymal enhancement differs in complete and incomplete infarctions. In complete infarction, it starts 5-7 days after the stroke and persists for several months. In incomplete infarctions, it can be observed within 2-4 hours and usually is more intense than in complete infarction.

Although conventional MRI sequences most often do not show evidence of stroke in the acute phase, conventional MRI may show signs of intravascular thrombus, such as absence of flow void on T2-WI, vascular hyperintensity on FLAIR, and hypointense vascular sign on gradient-recalled echo (GRE) sequence.

MRI findings arising from acute ischemic changes are summarized in the table below.


Did this answer your question?
Additional feedback? (Optional)
Thank you for your feedback!