Title:Crossed Cerebellar Diaschisis in Alzheimer’s Disease
Volume: 15
Issue: 13
Author(s): F.E. Reesink*, D. Vállez García, C.A. Sánchez-Catasús, D.E. Peretti, A.T. Willemsen, R. Boellaard, S.K. Meles, R.B. Huitema, B.M. de Jong, R.A. Dierckx and P.P. De Deyn
Affiliation:
- Department of Neurology, Alzheimer Research Center, University of Groningen, University Medical Center, Groningen,Netherlands
Keywords:
Cerebellar diaschisis (CCD), hypometabolism, supratentorial lesions, contralateral, dementia, Alzheimer's disease.
Abstract: 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.
