Background:
We describe the phenomenon of crossed cerebellar diaschisis (CCD) in four
subjects diagnosed with Alzheimer’s disease (AD) according to the National Institute on Aging -
Alzheimer Association (NIA-AA) criteria, in combination with 18F-FDG PET and 11C-PiB PET imaging.
Methods:
18F-FDG PET showed a pattern of cerebral metabolism with relative decrease most prominent
in the frontal-parietal cortex of the left hemisphere and crossed hypometabolism of the right cerebellum.
11C-PiB PET showed symmetrical amyloid accumulation, but a lower relative tracer delivery (a
surrogate of relative cerebral blood flow) in the left hemisphere. CCD is the phenomenon of unilateral
cerebellar hypometabolism as a remote effect of supratentorial dysfunction of the brain in the contralateral
hemisphere. The mechanism implies the involvement of the cortico-ponto-cerebellar fibers. The
pathophysiology is thought to have a functional or reversible basis but can also reflect in secondary
morphologic change. CCD is a well-recognized phenomenon, since the development of new imaging
techniques, although scarcely described in neurodegenerative dementias.
Results:
To our knowledge this is the first report describing CCD in AD subjects with documentation of
both 18F-FDG PET and 11C-PiB PET imaging. CCD in our subjects was explained on a functional basis
due to neurodegenerative pathology in the left hemisphere. There was no structural lesion and the
symmetric amyloid accumulation did not correspond with the unilateral metabolic impairment.
Conclusion:
This suggests that CCD might be caused by non-amyloid neurodegeneration. The pathophysiological
mechanism, clinical relevance and therapeutic implications of CCD and the role of the
cerebellum in AD need further investigation.
Selection of the optimal intensity normalization region for FDG-PET studies of normal aging and Alzheimer’s disease