Asymptomatic congenital isolated cerebellar malformations diagnosed in adults are very rare.1 A 62-year-old woman without any cerebellar symptom or sign but with subjective memory complaints and a family history of Alzheimer disease (AD) participated in an AD imaging study. Amyloid and tau PET scans were negative. An incidental cerebellar dysplasia, subtle on MRI, was striking on translocator protein (TSPO) PET (Figure). Dysplastic tissue displaced normal tissue, which allowed for normal function. TSPO is highly expressed by activated microglia and astrocytes. The signal on TSPO PET likely corresponded to the abundant astrocytes present in these malformations, as microglia are not increased.2
Figure. MRI, 18F-FDG, and 11C-ER176 PET.

MRI shows right hemispheric cerebellar dysplasia with abnormal folia orientation (red arrow) and decreased myelination (asterisk) but no increased fluid-attenuated inversion recovery (FLAIR) signal suggestive of inflammation. Dysplastic tissue displaced normal tissue (white arrow). PET is coregistered to MRI. FDG = fluorodeoxyglucose; SUV = standardized uptake value; VT = total distribution volume, calculated with the Logan plot and a metabolite-corrected arterial input function.
Appendix. Authors

Study Funding
The study was funded by the Moody Foundation and the Chao, Graham, Harrison, and Nantz Funds from the Houston Methodist Foundation.
Disclosure
B. Pascual, T. Hodics, Q. Funk, M.D. Cykowski, and M.O. Nakawah report no disclosures. J.C. Masdeu is a consultant for Biogen and has received research support from AVID Radiopharmaceuticals. Go to Neurology.org/N for full disclosures.
References
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