Crossed Cerebellar Diaschisis in Alzheimer’s Disease

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.

Cite this article as:

Reesink F.E.*, García Vállez D. , Sánchez-Catasús C.A., Peretti D.E., Willemsen A.T., Boellaard R. , Meles S.K., Huitema R.B., de Jong B.M., Dierckx R.A. and De Deyn P.P. , Crossed Cerebellar Diaschisis in Alzheimer’s Disease, Current Alzheimer Research 2018; 15 (13) . https://dx.doi.org/10.2174/1567205015666180913102615