Basal ganglia subacute infarct

Case contributed by Assoc Prof Frank Gaillard


One week headache. Fever last week. Afebrile now.

Patient Data

Age: 30 years
Gender: Male

Peripherally enhancing lesion within the right basal ganglia with associated abnormal diffusion restriction. In addition, cortically based T2/FLAIR hyperintensity and abnormal diffusion restriction involving the right frontal, parietal and temporal gyri, extending into the right cerebral peduncle are also present. These demonstrate gyral enhancement post-contrast. Occluded right middle cerebral artery on MRA (obtained the following day) - on the initial study there appeared to be preserved flow voids on T2.


The appearances are most in keeping with a subacute MCA territory infarct. It is possible that this represents a basal ganglia abscess with secondary M1 arteritis and distal artery-to-artery embolism although the lack of significant leptomeningeal enhancement around the artery makes this less likely. It is also possible that this was an embolic stroke with subsequent superimposed infection (e.g. from bacterial endocarditis).

Regardless of the microbiology of the aspirate, this requires stroke workup and an echo of the heart is recommended. 

Case Discussion

The patient went on to have a needle biopsy/aspiration due to A) the concern for infection and B) the original report suggesting atypical infection as the likely cause. 


The sections show brain parenchyma with necrosis and mixed inflammation including neutrophils, plasma cells histiocytes and lymphocytes. There are no granulomata. No organisms are seen on H&E section. There is no evidence for malignancy.

PAS, Gram and FITE stain are negative. No acid-fast bacilli (AFB) identified.

Microbiology (on aspirate) 

  • Polymorphs ++
  • No organisms
  • No growth of bacteria, fungi or AFB

Blood cultures negative including aerobic, anaerobic and MGIT.

Mycobacterium PCR: negative.

Peripheral blood: normal white cell count.



This is an important case and highlights the importance of not just looking at the dominant lesion, but examining the whole scan for clues and for patterns of involvement. There the distribution is very reminiscent of a M1 occlusion with dominant perforator infarction. Subacute imaging is not common and misinterpretation is common. 

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