NEUROIMAGING / MAGNETIC RESONANCE

MR-DWI in the acute stroke diagnosis

 Created 01.10.2019, last update 04.04.2022

  • ischemia leads to diffusion restriction (water molecules stay in the cells) because of energetic failure of Na+/K+ membrane pumps
  • the intensity of each image element (voxel) on the DWI sequence reflects the degree of water diffusion ⇒ restricted diffusion depicted on DWI is a sensitive indicator of acute ischemia
    • the acute lesion with restricted diffusion is hyperintense on DWI and hypointense on the ADC map (the lower the value, the greater is  the restriction)
    • CT or conventional MRI sequences (T1, T2) may not demonstrate the lesion in the first hours after the stroke onset
  • DWI is obtained within 2 minutes and is less susceptible to motion artifacts than other sequences
  • diffusion disturbance is not stroke-specific; it was described in many other neurological diseases (see table below)
  • always assess all MRI sequences (DWI, ADC map, T1, T2) and exclude artifacts (e.g., T2 shine through phenomenon)
  • when assessing DWI images, consider:
    • localization and shape of the lesion (does it correspond to a vascular territory?)
    • whether the DWI lesion is hyperintense diffusely, centrally, or in the periphery
    • whether the bright signal on DWI matches with a dark signal on the ADC map
    • whether the lesion is isolated or multifocal (multiple territories x symmetric or even diffuse involvement?)
    • whether the edema is present (hyperintense on T2/FLAIR) – typically in the tumors and abscesses
    • whether the lesion shows post-contrast enhancement  (T1C+)
Adult Children
  • acute ischemia   Corpus callosum infarction and intraventricular hemorrhage
    • arterial/venous infarction
    • hypoxic-ischemic encephalopathy (e.g., after cardiac surgery using extracorporeal circulation – ECC) 
  • abscess Brain abscess with prominent diffusion restriction on DWI
    • DWI restriction is usually localized centrally
    • typical ring enhancement, oval shape
    • T2 hyposignal rim
  • lymphoma CNS lymphoma with diffusion restriction on DWI
    • substantial restriction of diffusion, typically multiple lesions
    • postcontrast enhancement
  • Creutzfeldt-Jakob disease  Creutzfeldt-Jakob disease
    • persistent DWI hyperintense lesions, progressing over time
    • typically in the basal ganglia, thalamus, and different cortical areas, often symmetrical
  • diffuse axonal injury (DAI)
    • in the grey / white matter junction
    • in the corpus callosum and the brain stem
    • microbleeds
  • metastasis, glioblastoma  Glioblastoma multiforme
    • DWI hyperintensity is usually located at 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 in the ADC map due to intracellular oxyhemoglobin ) and then in the late subacute stage (with no ADC correlate)
  • 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 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)
    • the lesion in the pons or basal ganglia
    • hyperintense in 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 stage
  • hypo/hyperglycemia

    • hypoglycemia – cortical lesions (P – O)
    • hyperglycemia – BGG
  • multiple sclerosis
    • rarely in acute plaques, the lesion is postcontrast enhancing (unlike stroke lesions)
  • prolonged seizure / status epilepticus    Post-epileptic lesion in corpus callosum
  • cyanide, ethylene glycol, methanol poisoning
  • hyperammonemia
  • chemotherapy
  • some diseases are 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
  • MELAS

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 its onset, with a maximum of 4-6 hours
  • acute ischemia appears hyperintense (bright) on DWI (b factor around 1000 s/mm2) and hypointense (dark) on calculated ADC (apparent diffusion coefficient) maps
    • ADC <620×10-3 mm/s is likely to identify ischemia
    • after recanalization, there is often an increase of signal on ADC maps in the ischemic area  (visible on 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 corresponds approximately with the size of the probably irreversibly affected tissue
    • however, reversibility of DWI changes (early DWI reversal) in case of early reperfusion has been repeatedly described
  • DWI allows  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 in the subacute stage with temporal pseudo-normalization of the ADC map during the second week; in the chronic stage, ADC values remain increased
  • DWI allows assessment of ischemic penumbra (DWI/FLAIR and DWI/PWI mismatch)
  • DWI changes are not specific to ischemia – they can occur in any transport mechanisms impairment (edema), such changes are often reversible, and lesions are not hypointense in the ADC map) – see the table above
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  • artifacts – DWI depends on T2 signal
    • increased T2 signal can lead to T2 shine through and T2 washout
    • reduced T2 signal leads to T2 blackout phenomenon (hypointense DWI)
      • e.g. iron deposits
      • bleeding
      • infections (abscess, toxoplasmosis, aspergillosis)
      • some metastases

DWI/FLAIR mismatch (DFM)

  • positive DWI with still negative findings on FLAIR implies the stroke onset < 4.5 hours ago [Aoki, 2010] [Thomalla, 2009]
  • can be helpful in the indication of IV thrombolysis in stroke patients with unknown onset or wake-up strokes (WUS)
  • WAKE-UP      WAKE-UP trial (Thomalla, 2018)  WAKE-UP trial (Thomalla, 2018)
    • DWI / FLAIR mismatch (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%
    • sICH 2% vs 0.4%
  • MR WITNESS
    • DWI / FLAIR mismatch (DWI positive in <1/3 of the MCA territory, FLAIR negative or with only minimal lesion)
    • IVT administered within 4.5 hours of symptoms onset
    • n = 80, sICH 1.25% (as defined by ECASS III)
DWI/FLAIR mismatch (DFM)

DWI/PWI mismatch

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ADC pseudonormalization

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Early DWI reversal

  • it occurs in the early phase of stroke during successful reperfusion (within 3-6hrs of the stroke onset) [Pham, 2015]
  • actual regression is relatively rare; more often, pseudonormalization of DWI (fluctuation) or only partial regression is present
Fluctuation of DWI findings (pseudonormalization)

T2 shine through

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T2 washout

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T2 blackout

  • the actual DWI signal (given by ADC values) is reduced by the presence of a low  (hypointense) T2 signal ⇒ DWI is hypointense (dark)
  • the T2 blackout phenomenon is present in hematomas, degenerative diseases with iron accumulation, etc.
T2 blackout - hypointense DWI in intracerebral bleeding
T2 blackout on DWI
Hemorrhagic transformation (DWI with T2 blackout)

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