In adults with suspected PPAoS, what imaging findings might support a neurodegenerative etiology of AOS?

• A. Left-dominant perisylvian atrophy or hypometabolism in frontal speech planning regions on MRI or FDG-PET.
• B. Right-dominant parietal atrophy.
• C. No consistent imaging findings.
• D. Bilateral cerebellar hyperactivity on functional imaging.

Answer: (B)

Imaging that supports a neurodegenerative cause of apraxia of speech in adults typically shows left-dominant atrophy or reduced metabolism in the frontal speech planning regions, located in the left perisylvian network. On MRI you’d expect focal atrophy in areas such as the left inferior frontal gyrus (opercular part), insula, and involved premotor and supplementary motor areas; on FDG-PET you’d see hypometabolism in these same left frontal regions. This left-sided degradation matches the disruption of neural planning for speech that characterizes PPAoS, making it the best evidence for a neurodegenerative etiology.

Right-dominant parietal atrophy would not align with the typical left-hemisphere speech planning disruption; no consistent imaging findings would argue against a neurodegenerative AOS pattern; and bilateral cerebellar hyperactivity is not the signature imaging clue for neurodegenerative AOS.