Fogging of middle cerebral artery

• Transient pseudonormalization of previously hyperintense cortical infarction on T2 MRI or non-contrast CT
• Temporal relationship: 3-36 days post-stroke with median of 10 days on MRI
• Geographic restriction to MCA territory with cortical involvement
• Persistent T2 hyperintensity in the clearance zone surrounding the normalizing core

• Non-contrast CT shows transient attenuation normalization of the infarcted cortex during the subacute phase (6-10 days post-infarction), related to macrophage and leukocyte infiltration with simultaneous angiogenesis and protein degradation.
• T2/FLAIR MRI demonstrates signal normalization in the infarction core (necrosis zone) between days 3-36, typically around day 10, while the ischemic border zone (clearance zone) remains hyperintense from angiogenesis and tissue liquefaction.
• The fogging effect reflects increased binding of free water by degraded proteins within the infarction, contrasting with the acute phase when free water causes edema-related hyperintensity.
• CT perfusion studies show increased cerebral blood volume (CBV) and cerebral blood flow (CBF) during the fogging phase, supporting active angiogenic and inflammatory processes.
• Ribbon-like gyral cortical enhancement is seen on contrast-enhanced CT during the evolution phase, representing breakdown of blood-brain barrier integrity.
• The phenomenon can occur immediately after endovascular stroke treatment in up to 24% of cases, likely from contrast extravasation, and does not necessarily exclude fogging effect.
• FLAIR imaging shows residual hyperintense signal within the infarction during the healing phase, persisting even as T2 signal normalizes in the core.
• Follow-up imaging 1-7 weeks after fogging shows developing volume loss and hypo-attenuated infarction core, confirming the ischemic nature of the process.

• Petechial hemorrhagic transformation (type 2 hemorrhagic infarction): distinguished by early timing (within 4 days), susceptibility artifact blooming on GRE sequences, and predominant cortical distribution without pseudonormalization pattern.
• Resolving tumor-associated vasogenic edema: differentiated by clinical and imaging history of neoplasm, lack of acute stroke presentation, and absence of subsequent cortical infarction evolution on follow-up.
• Resolving infection-associated vasogenic edema: distinguished by clinical sepsis/meningitis history, lack of vascular territory restriction, and imaging features of encephalitis or abscess.
• Treatment effect from primary tumor or infection: clarified by presentation timing, imaging features of the underlying mass or infection, and lack of stroke symptoms at onset.

Describe fogging effect as "transient pseudonormalization of the previously hyperintense MCA territory infarction on T2 imaging, consistent with subacute infarction in the fogging phase (expected 3-36 days post-stroke), with persistent hyperintensity in the border zone and expected evolution to volume loss and infarction hypo-attenuation on follow-up imaging in 1-7 weeks."

• Misinterpreting fogging effect as tissue recovery or incomplete infarction, when the pseudonormalization actually represents active biological transformation and ultimate progression to established infarction.
• Confusing fogging with petechial hemorrhagic transformation by overlooking the temporal pattern (fogging day 3-36 vs hemorrhagic infarction within 4 days) and lack of susceptibility blooming artifact on GRE sequences.
• Attributing pseudonormalization to successful treatment of an underlying tumor or infection without adequate clinical and imaging correlation to exclude acute stroke etiology.
• Failing to obtain appropriate follow-up imaging in the 1-7 week window to confirm fogging diagnosis and exclude masquerading pathology, potentially delaying diagnosis of complications.