NEUROIMAGING / MAGNETIC RESONANCE

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.

• 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?

• 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)    
• 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)

• 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

• 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

• 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

• 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

• 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)

• 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