Stroke Incidentally Identified Using Improved Positron Emission Tomography for Microglial Activation

A 42-year-old man enrolled in a research study using [11C]PBR28, an improved positron emission tomography (PET) radioligand to measure microglial activation. History included HIV infection, diabetes, hypertension, hypercholesterolemia, 12 pack-year smoking history, and remote use of cocaine and heroin. Medical and neurological exam were normal except for elevated blood pressure of 157/100 mmHg. Brain MRI showed occasional foci of mild chronic white matter ischemia but was otherwise unremarkable (Fig A). Figure 1 (A) The original T1-weighted MRI has mild white matter ischemic changes (not seen at the level shown) but is otherwise unremarkable. (B) [11C]PBR28 PET scan performed 6 weeks later shows increased binding in right basal ganglia. Repeat T1-weighted (C) ... The patient then underwent PET imaging of the brain with [11C]PBR28. Surprisingly, a small (1.3 cm3) focus of increased signal in the right basal ganglia was apparent on the PET scan (Fig B). Modeling of radioligand kinetics revealed that the total distribution volume (VT) of [11C]PBR28 in the right basal ganglia was 76% higher than in the left. VT is proportional to the amount of microglial activation. Based on the PET findings, the patient returned to the referring center, where he recalled a previously unreported episode of mild weakness in his left face and left hand. This weakness occurred 12 days before the PET scan and had resolved completely within twenty-four hours. Repeat MRI demonstrated a new lesion in the same region as the increased PET signal (Fig C, D). The MRI findings were consistent with a subacute infarction occurring between the first MRI and the PET scan.