Brain Advance Access originally published online on January 5, 2005
Brain 2005 128(2):338-344; doi:10.1093/brain/awh376
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Brain Vol. 128 No. 2 © Guarantors of Brain 2005; all rights reserved
Involvement of medullary regions controlling sympathetic output in Lewy body disease
1 Department of Neurology, 2 Robert H. and Clarice Smith and Abigail Van Buren Alzheimer's Disease Research Program of the Mayo Foundation and 3 Department of Anatomic Pathology, Mayo Clinic, Rochester, MN, USA
Correspondence to: Eduardo E. Benarroch, MD, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA E-mail: benarroch.eduardo{at}mayo.edu
We sought to determine the involvement of medullary regions controlling sympathetic output in pathologically confirmed diffuse Lewy body disease (LBD). We studied eight limbic or neocortical stage LBD and eight multiple system atrophy (MSA) cases, confirmed neuropathologically, and eight age-matched controls. Five of the LBD cases and all MSA cases had orthostatic hypotension. Serial 50-µm sections obtained from the medulla rostral to the obex were immunostained for tyrosine hydroxylase, tryptophan hydroxylase and 
-synuclein. Analysis was focused on the ventrolateral medulla and medullary raphe nuclei. In LBD cases, there were Lewy bodies and neurites, as well as dystrophic neurons in the ventrolateral medulla, but the number of catecholaminergic and serotonergic neurons was not significantly reduced. All these groups were depleted in MSA. There were Lewy body pathology and dystrophic neurons in the raphe in all LBD cases. Cell numbers were reduced in both the raphe obscurus and raphe pallidus. Our findings suggest that, although LBD affects medullary autonomic areas, it does so less severely than MSA, particularly in the case of the VLM, which controls sympathetic outputs maintaining arterial pressure. In LBD, orthostatic hypotension may be due primarily to involvement of sympathetic ganglion neurons rather than ventrolateral medulla neurons.
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