Chronology of MRI Findings in Stroke | Walif Chbeir

                                                                   Walif Chbeir Radiology Notes

                                                                                                December 25, 2016





There is any actual or potential conflict of interest to disclose including any financial, personal or other relationships with other people or organizations.

The articles and notes in this website  are intended to be used for educational purposes only. The medical informations provided correspond simply to personal notes based on the mentioned bibliography and cannot be guaranteed for accuracy and completeness. Therefore they don’t represent a reference source for scientific articles , neither a medical advice and cannot therefore substitute for the advice of a medical professional.   If errors are encountered please send a message to me, so I can make the changes.   



“Time is brain”: IV rTPA window < 3 hours.  IA window < 6 hours. Therefore, diagnostic tests must be fast, reliable, and operationally efficient.   


Patient selection most important factor in outcome:  Symptom onset < 6 hours, No parenchymal hematoma on CT,  well-established acute infarct involving less than 1/3 of affected vascular territory.


Strong evidence supports the use of MR imaging to improve the safety profile and cost-effectiveness of intra-arterial treatment, which relies primarily on the greater accuracy of DWI to depict acute brain infarction. Using a simplified protocol, MR imaging can provide all the necessary information for treatment decision-making and can be performed without a significant time delay.


Conventional brain MRI (T1WI, T2WI) study is not very good at detecting cytotoxic or intracellular edema that is seen in the acute or less than 24 hour phase of stroke.    


Gradient recalled-echo T2* WI and Susceptibility WI are highly sensitive to blood-breakdown products.   In acute stroke, gradient recalled-echo T2*WI has been shown to be as accurate as NCCT for the detection of acute intracranial hemorrhage and is superior to CT in the detection of chronic hemorrhage.  MRI is therefore an excellent technique for distinguishing ischemic and hemorrhagic stroke.


Documenting Proximal Artery Occlusion. Occlusive thrombus in the proximal intracranial arteries is the target of intra-arterial therapy. Therefore, noninvasive vessel imaging is critical for the rational delivery of this treatment.   Moreover, it provides important pretreatment data for the neurointerventionalist, who can choose

the appropriate access tools in the case of arterial tortuosity or when treatment is required for steno-occlusive disease at the carotid bifurcation.  Although CTA provides the best noninvasive evaluation of the intracranial vessels,  MRA appears sufficient for decision-making regarding intra-arterial therapy.  3D TOF MRA has been  shown to have high sensitivity and specificity for identifying proximal artery occlusion.  Contrast-enhanced MRA offers faster acquisition times, wider coverage, and less flow related signal loss but has lower spatial resolution and venous contamination.


DWI is used to detect early ischemic changes (acute stroke; early ischemic change; cytotoxic edema) with greater conspicuity than standard MRI.  MRI with diffusion is quickly becoming the gold standard in acute stroke imaging.  MR diffusion improves ischemic stroke detection from 50% to more than 95% (6).  Diffusion MR noninvasively detects ischemic changes within minutes of stroke onset.  It is necessary to use ADC maps because some areas of high signal such as vasogenic edema can appear bright on the initial diffusion image signaling. This is because the diffusion sequence is T2 based and this “shine through” can cause some bright signals, but these areas of high signal that are not secondary to acute infarct are easily identified on the ADC maps as dark signal and allow for an accurate initial diagnosis.


Over time, the appearance of the diffusion and ADC abnormalities will reverse as the stroke moves into a subacute phase (more than 24 hours to 5 days). The specific injury patterns that are identified on MRI diffusion  help to date the time of onset, progression and resolution of strokes.


DWI allows to differentiate acute ischemic stroke from other stroke mimics such as a hemiplegic migraine headache, Todd’s paralysis (seizure) and peripheral or cranial nerve disorders.


Perfusion imaging (PWI) in which MMT ( mean transit time ) or TTP (Time –to –peak) perfusion maps are generated for the entire brain.  It can identify the ischemic penumbra. The ischemic penumbra is the difference between the DWI defect (cytotoxic edema – irreversible ischemia- the ischemic core) and the perfusion defect analogous to MTT or TTP. The penumbra is the DWI-PWI mismatch. The accurate identification of this ischemic penumbra will help guide future ischemic stroke therapy and potentially aide in extending the time window for treatment.


*  0-6 Hours, HyperAcute:    


  • T1:  No abnormality.
  • T2:  Absence of flow voids,  No parenchymal abnormality.
  • FLAIR: Intraarterial Flair Hyperintensity: early sign of major vessel occlusion or slow flow. No Parenchymal Abnormality.
  • T2* GRE:   Detection of acute blood products of intracranial hemorrhage as an area of abnormal blooming (Hypointensity due to paramagnetic effect of the hemosiderin)   .Arterial “ Blooming ”  ( Thrombosed Vessel) from clot susceptibility. May see susceptibility from Ca++ embolus.
  • T1 with gadolinium: Intravascular enhancement (stasis of contrast material within vessels in the affected territories).
  • Diffusion-weighted imaging (DWI): Hyperintense cytotoxic edema. Improves hyperacute stroke detection to 95%.  Usually correlates to “ Infarct Core” ( final Infarct Size).  Some Diffusion abnormalities reversible ( TIA, Migraine). May have reduced sensitivity in brainstem and medulla in first 24 hours.  Restriction typically lasts 7-10 days. Hypointense Cytotoxic Edema.


  • PWI:   Bolus Tracking T2* Gadolinium Perfusion Imaging  with CBV (cerebral blood volume) MAP: ↓ 75% larger than DWI abnormality.   DWI/PWI “mismatch”: Penumbra or “at-risk” tissue.


  • Diffusion tensor imaging (DTI):  Multidirectional diffusion-weighted images; at least 6 directions can be used to calculate DTI trace and ADC maps.  Higher spatial resolution.   May be more sensitive for small ischemic foci, emboli, cortical strokes.
  • MRA: Major vessel occlusions, stenoses, status of collaterals. It can detect high grade atherosclerotic lesions in the neck and head. It is also helpful for detecting less common causes of ischemic stroke such as carotid and vertebral artery dissection, fibromuscular dysplasia, and venous thrombosis.


* 6-24 Hours, Acute:

    • T1 :  No abnormality


  • T2 : Cortical swelling,  Hyperintensity develops by 12-24 hours.  Rare subcortical white matter hypointensity.
  • Flair:  Parenchymal hyperintensity appears (6 hours post ictus) while other sequences normal.  Rare subcortical white matter hypointensity.  Useful in the initial evaluation of the acute stroke patient suspected of having a subarachnoid hemorrhage. Subarachnoid hemorrhage appears bright on FLAIR images and so becomes readily apparent.
  • T1 with gadolinium:  Vascular Enhancement.  Meningeal enhancement (pial collateral flow appears in 24-48 hours, resolves over 3-4 days).  
  • DWI: Hyperintense.
  • ADC :  Hypointense.
  • MR T2* perfusion:  ↓ rCBV.


* Early Subacute, 1-7 Days    Standard MRI images(T1 and T2) are good at detecting vasogenic edema that is present in the subacute phase of stroke and is seen at greater than 24 hours to several days.

  • T1: Hypointense edema with mass effect,  Gyral thickening and swelling,  Sulcal effacement,  Loss of GM-WM borders,  Mass effect,  ± gyral hyperintensity (ies)  from petechial hemorrhage,  May see gyriform ↑ signal ( PseudoLaminar Necrosis).
  • T2: Hyperintense edema with mass effect,  Hyperintense gyral thickening, sulcal effacement, ± gyral hypointensity from petechial hemorrhage.  “ Fogging Effect =  Normal T2WI with striking enhancement on T1WIC+, 1-2 Weeks following ictus.  Early Wallerian Degeneration can occur: Look for well defined hyperintense band in corticospinal tract.
  • Flair: Hperintense edema with mass effect,  Hyperintense gyral thickening,  Sulcal effacement, Mass effect,  Gyral hypointensity(ies) from petechial hemorrhage,  Hyperintensity ( “ DOT Sign” ) in slow flowing/ Occluded vessels.  By 1 week, final infarct volume corresponds to Flair-Defined abnormality. 
  • T2* GRE:  May see blooming if Hemmorrhagic Transformation has occurred
  • T1 with gadolinium:  Intravascular enhancement; disappears at 3-4 days as vessels recanalize.             

                                                   Parenchymal enhancement, typically patchy or gyral (appears after 24-72 hours, can persist for weeks/months). Can persist up to 8-10 weeks

  • DWI:  . Hyperintense. Gyral Hypointensity (ies)  from petechial Hemmorrhage.
  • ADC :  Hypointense ,  Reversing as it proceeds into/through subacute stage
  • DWI, T1WI C+  Complement each other in detecting subacute infarcts. Early subacute can be ↑ DWI and ↓ T1 C+
  • MR T2* perfusion:   Increase of CBV in subacute stage, reflecting reperfusion hyperemia.  


*  Late Subacute  (8 days to 34 days, 5 weeks)

  • T1: Hypointense, swelling resolves, gyral hyperintensity from petechial hemorrhage.
  • T2:   Hyperintense, swelling resolves. hyperintensity develops by 12-24 hours, may normalize 2-3 weeks post ictus (MR “fogging”)
  • Flair:  Hyperintense, swelling resolves.
  • T1 with gadolinium: Parenchymal enhancement, no vascular enhancement.
  • DWI: Hyperintense.
  • ADC :  Isointense, But after 10 days, T2 effect may predominate over low ADC: T2 “shine-through”.
  • MR T2* perfusion:   Increase of CBV


* Chronic (after 5 weeks = 35 days)

  • T1: Hypointense – isointense to CSF in affected areas, tissue cavitation.  Adjacent sulci become prominent; ipsilateral ventricle enlarges. Wallerian degeneration may be present.
  • T2:   Hyperintense (Isointense to CSF in affected areas), tissue cavitation. Borders of infarction may show ↑ signal secondary to gliosis/spongiosis. Differentiation of subacute from chronic infarction on standard SE/FSE sequences may be diffcult due to prolonged relaxation times in both.
  • Flair: Hyperintense gliotic white matter at margins with hypo-intense center from tissue cavitation.
  • T1 With Gadolinium : Parenchymal  Enhancement gone by 3 months.
  • DWI: Isointense to hypointense ( No Restriction) but high signal can persist up to 2 months post ictus.
  • ADC :  Hyperintense.
  • T2* GRE: May see hemosiderin staining in gliotic areas or along borders of infarction.
  • MR T2* perfusion:   CBV decreases again.




1 -Stroke and Cerebral Ischemia.      

in Clinical Magnetic Resonance Imaging e-edition, CHAP. 50

Clinical Magnetic Resonance Imaging: 3-Volume Set 3rd Edition

by Robert R. Edelman (Author), John Hesselink (Author), Michael Zlatkin (Author)

ISBN-13: 978-9996019494

ISBN-10: 0721603068


2 – Cerebral Ischemia and Infarction

Anne G. Osborn, MD, FACR    &  Edward P. Quigley, III, MD, PhD

STATdx: Brain > Diagnosis > Pathology-based Diagnoses > Stroke > Cerebral Ischemia and Infarction 8d062182adc943d3b64a54a4e2c3a278/print


3- State-of-the-Art Imaging of Acute Stroke.

Srinivasan et al.,,RadioGraphics 2006; 26:S75–S95


Published online 10.1148/rg.26si065501


4 -Subacute Cerebral Infarction ,

Karen L. Salzman, MD & Sheri L. Harder, MD, FRCPC

STATdx:   Brain > Diagnosis > Pathology-based Diagnoses > Stroke > Cerebral Ischemia and Infarction print


5- Chronic Cerebral Infarction

Sheri L. Harder, MD, FRCPC & Anne G. Osborn, MD, FACR

STATdx Brain > Diagnosis > Pathology-based Diagnoses > Stroke > Cerebral Ischemia and Infarction 6a6aefbc6dc34798aa591291723674a4/ print


6- Imaging in Acute Stroke.

Dale Birenbaum et al,West J Emerg Med. 2011 Feb; 12(1): 67–76.

PMCID: PMC3088377


7 – Multimodal Diagnostic Imaging for Hyperacute Stroke. 2015

K.D. Vo et al, AJNR Am J Neuroradiol 36:2206 –13 Dec 2015