MR-DWI in the acute stroke diagnosis

David Goldemund M.D.
Updated on 01/06/2024, published on 24/05/2021

Diffusion-weighted imaging (DWI) is a common MRI sequence used to evaluate acute ischemic stroke. Increased DWI signal in ischemic brain tissue is usually observed within minutes of arterial occlusion.

Technical notes

  • ischemia leads to diffusion restriction due to the energetic failure of Na+/K+ membrane pumps, causing water molecules to remain inside the cells
  • the intensity of each voxel on the Diffusion-Weighted Imaging (DWI) sequence reflects the degree of water diffusion ⇒ restricted diffusion on DWI serves as a sensitive indicator of acute ischemia
    • acute lesions with restricted diffusion are hyperintense on DWI and hypointense on the Apparent Diffusion Coefficient (ADC) map (the lower the value, the greater the restriction)
    • CT or conventional MRI sequences (T1, T2) may not reveal the lesion in the first hours after the stroke onset
  • DWI is acquired within 2 minutes and is less susceptible to motion artifacts compared to other sequences
  • the diffusion defect is not stroke-specific and has been described in various neurological disorders (refer to the table below)
  • always assess all MRI sequences (DWI, ADC map, T1, T2) and exclude artifacts (e.g., T2 shine-through phenomenon)
  • when evaluating DWI images, consider the following aspects:
    • location and shape of the lesion (does it correspond to a specific vascular territory?)
    • is the DWI lesion hyperintense diffusely, centrally, or peripherally?
    • does a bright signal on DWI correspond to a dark signal on the ADC map?
    • isolated or multifocal lesion? (multiple territories x symmetric or even diffuse involvement?)
    • presence of edema on T2/FLAIR images? – typically observed in the tumors and abscesses
    • post-contrast enhancement on T1C+ sequences?
Adult Children
  • acute ischemia   Corpus callosum infarction and intraventricular hemorrhage
    • arterial/venous infarction
    • hypoxic-ischemic encephalopathy (e.g., after cardiac surgery with extracorporeal circulation – ECC) 
  • abscess Brain abscess with prominent diffusion restriction on DWI
    • central DWI restriction
    • typical ring enhancement, oval shape
    • T2 hyposignal rim
  • lymphoma CNS lymphoma with diffusion restriction on DWI
    • substantial diffusion restriction, typically multiple lesions
    • postcontrast enhancement
  • Creutzfeldt-Jakob disease  Creutzfeldt-Jakob disease
    • persistent  hyperintense DWI lesions, progressing over time
    • typically in the basal ganglia, thalamus, and various cortical areas, often symmetrical
  • diffuse axonal injury (DAI)
    • in the gray/white matter junction, corpus callosum, and brainstem
    • microbleeds
  • metastasis, glioblastoma  Glioblastoma multiforme
    • DWI hyperintensity is usually in the periphery + vasogenic edema and postcontrast saturation of the lesion
  • hyperacute hematoma
    • the hyperintense ring surrounding the hematoma (reactive vascular and metabolic changes)
    • the hematoma may be DWI hyperintense in the hyperacute stage (including hypointensity on the ADC map due to intracellular oxyhemoglobin ) and then in the late subacute stage   Late subacute ICH with hyperintense lesion on DWI
  • encephalitis (viral)
  • PRES
    • typical T2 lesions, hyperintense DWI lesion is rarely described (prognostically unfavorable)
    • more likely, there is DWI positivity caused by the  T2 -shine through phenomenon
  • Wernicke’s encephalopathy
    • diffusion restriction near the 3rd ventricle or around the diencephalon  T2 shine through in a patient with Wernicke's encephalopathy
    • ADC hyperintense (often only T2 shine through phenomenon)
    • concomitant T2 hyperintense lesions in the mamillary bodies, medial thalamus, and around the aqueduct
  • osmotic demyelination syndrome (ODS)
    • pons or basal ganglia
    • hyperintense on DWI and T2 sequences
  • CO poisoning (cortex, basal ganglia)  Acute CO poisoning

    • T1 hypointense lesions
    • T2/FLAIR hyperintense lesions
    • DWI hyperintense lesion in the acute phase
  • hypo/hyperglycemia

    • hypoglycemia – cortical lesions (P – O)
    • hyperglycemia – BGG
  • multiple sclerosis
    • rarely in acute plaques, the lesion shows postcontrast enhancement (unlike stroke lesions)
  • prolonged seizure/status epilepticus    Post-epileptic lesion in corpus callosum
  • cyanide, ethylene glycol, methanol poisoning
  • hyperammonemia
  • chemotherapy
  • some diseases seen in adult patients (ischemia, tumor, encephalitis, etc.)
  • neonatal adrenoleukodystrophy  → more
  • Canavan disease   →  more
  • methylmalonic acidemia (MMA)
  • Leigh syndrome
  • Pantothenate Kinase-Associated Neurodegeneration (PKAN)   → more

DWI in acute stroke

  • DWI visualizes impaired (restricted) diffusion of water molecules (or protons) caused by the energetic failure of Na+/K+ membrane pumps
  • it is highly sensitive and specific (88-100%) for detecting acute cerebral infarction within minutes of onset, with a maximum of 4-6 hours
  • acute ischemia is hyperintense (bright) on DWI (b factor around 1000 s/mm2) and hypointense (dark) on calculated ADC maps
    • an ADC <620×10-3 mm/s is likely to identify ischemia
    • following recanalization, an increased signal is often observed on ADC maps in the ischemic area  (visible on both DWI and FLAIR)     After recanalization, there is often an increase in ADC at the site of ischemia (visible on both DWI and FLAIR) [Albers]
  • the extent of the DWI lesion in acute stroke approximately corresponds to the size of the tissue likely to be irreversibly affected
    • however, the reversibility of DWI changes (early DWI reversal) following early reperfusion has been repeatedly documented
  • DWI allows the differentiation of acute, subacute, and chronic lesions
    • initially bright DWI signal decreases within a few days to become hypointense in later stages
    • low signal on the ADC map increases during the subacute stage, with temporal pseudo-normalization of the ADC map occurring in the second week; in the chronic stage, ADC values remain increased
  • DWI allows for the assessment of ischemic penumbra (demonstrated by DWI/FLAIR or DWI/PWI mismatch)
  • DWI changes are not specific to ischemia; they can occur in any transport disorder (e.g., edema). Such changes are often reversible, and lesions are not hypointense on the ADC map (refer to the table above)
Acute (0-7 days)
  • marked hyperintensity on DWI and hypointensity on ADC images
  • early DWI reversal may occur after reperfusion; in most cases, it represents DWI pseudonormalization
Subacute (7-21 days)
  • ADC pseudonormalization occurs after 5-7 days; ADC values rise and return near the baseline; later continue to rise (ischemia becomes hyperintense¨)
  • DWI remains hyperintense (due to T2 shine-through)
Chronic ( >3 weeks)
  • ADC signal is increased
  • DWI signal decreases (as T2 shine-through is resolved)
DWI in acute, subacute and chronic ischemia
  • DWI is inherently T2-weighted; T2 changes may influence the appearance of DWI independent of tissue diffusibility, causing artifacts
    • increased T2 signal can lead to T2 shine-through and T2 washout
    • decreased T2 signal leads to the T2 blackout phenomenon (hypointense area on DWI)
      • e.g., iron deposition, bleeding
      • infections (abscess, toxoplasmosis, aspergillosis)
      • certain metastases

DWI/FLAIR mismatch (DFM)

  • a positive DWI with negative findings on FLAIR indicates that the stroke probably occurred within the previous 4.5 hours [Aoki, 2010] [Thomalla, 2009]
  • may be useful to guide intravenous thrombolysis (IVT) in patients with stroke of unknown onset or wake-up stroke (WUS)
  • WAKE-UP      WAKE-UP trial (Thomalla, 2018)  WAKE-UP trial (Thomalla, 2018)
    • DWI/FLAIR mismatch is present (DWI positive in <1/3 of the MCA territory, FLAIR still negative)
    • n=503 ( 254 tPA vs. 249 placebo), median NIHSS 6
    • good outcome 53.3 vs. 41.8 (placebo), median mRS/3m 1 vs. 2
    • mortality 4.1% vs. 1.2% (placebo)
    • sICH 2% vs. 0.4% (placebo)
    • DWI/FLAIR mismatch (DWI positive in <1/3 of the MCA territory, FLAIR either negative or showing only minimal lesion)
    • IVT administered within 4.5 hours of symptom onset
    • n = 80, sICH 1.25% (as defined by ECASS III)
DWI/FLAIR mismatch (DFM)

DWI/PWI mismatch

  • Perfusion-weighted imaging (PWI) quantifies the concentration of gadolinium as it passes through the cerebral microcirculation
    • colored maps are generated representing MTT, TTP, CBF, and CBV; these values are relative to the contralateral (healthy) side 
    • noninvasive techniques using Blood Oxygen Level-Dependent (BOLD) or Arterial Spin Labeling (ASL) are much less commonly used
  • the ischemic penumbra is characterized by the perfusion-diffusion (PWI-DWI) mismatch
    • the DWI lesion represents the ischemic core; the remainder of the PWI lesion (with a TTP delay > 4s) is a probable penumbra (more likely a combination of penumbra and benign oligemia)
    • the core may expand to reach the size of the baseline PWI lesion unless early reperfusion is achieved
    • DWI lesions may exhibit some degree of reversibility (normalization x pseudonormalization)
  • major recanalization trials using advanced imaging have used CT perfusion; no such robust data are available for DWI/PWI mismatch yet

ADC pseudonormalization

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Early DWI reversal

  • the phenomenon occurs in the early phase of stroke, specifically during successful reperfusion within 3-6 hours after stroke onset [Pham, 2015]
  • true regression is relatively rare; more commonly observed are DWI pseudonormalization  (fluctuation) or partial regression
Fluctuation of DWI findings (pseudonormalization)

T2 shine-through

  • falsely increased signal on DWI, that is not attributable to diffusion restriction but rather to the shining through of the T2 prolongation (commonly observed in subacute to chronic infarction)
  • T2 and ADC maps should be evaluated simultaneously
    • ADC is decreased in acute ischemia
    • ADC is either normal or increased in T2 shine-through
T2 shine through
T2 shine through in a patient with Wernicke's encephalopathy

T2 washout

  • present in the subacute phase of ischemic stroke (between days 10-15) or in tumors accompanied by collateral vasogenic edema  [Hiwatashi, 2003]
  • normal-appearing DWI (b = 1000) despite abnormal ADC maps
  • prolonged (hyperintense) T2, causing T2 shine through, is counterbalanced by higher ADC values  ⇒ normal-appearing DWI  [Casey, 2001]
  • DDx:
    • early DWI reversal – typically appears 3-6 hours post-stroke
    • ADC pseudonormalization – occurs around day 7 post-stroke
  • beyond stroke, the T2-washout phenomenon can also be observed in Posterior reversible encephalopathy syndrome (PRES)   
    • isointense lesions result from a balance of T2 effects and increased water diffusibility  (Provenzale, 2001)

T2 blackout

  • the actual DWI signal (determined by ADC values) is reduced due to the presence of a low  (hypointense) T2 signal ⇒ DWI appears hypointense (dark)
  • the T2 blackout phenomenon is present in conditions such as hematomas, degenerative diseases with iron accumulation, etc.
  • T2 blackout is mainly caused by susceptibility effects
T2 blackout - hypointense DWI in intracerebral bleeding
T2 blackout on DWI
Hemorrhagic transformation (DWI with T2 blackout)

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MR-DWI in the acute stroke diagnosis