Abstract
It has been suggested that autonomic dysfunction constitutes a biomarker for early
detection of the disease process in Parkinson disease (PD). Recent findings based
on cardiac sympathetic and striatal dopaminergic imaging in the same patients indicate
that this view is overly simple. Although evidence of cardiac sympathetic denervation
is associated with other non-motor manifestations such as anosmia, REM behavior disorder,
dementia, baroreflex failure, and orthostatic hypotension (OH), across individual
patients the severities of OH and of the cardiac sympathetic lesion (indicated by
thoracic 6-[18F]fluorodopamine PET scanning) are unrelated to the severity of the putamen dopaminergic
lesion (indicated by brain 6-[18F]fluorodopa PET scanning). Moreover, whereas cases have been reported with neuroimaging
evidence of cardiac sympathetic denervation several years before motor onset of PD,
in other cases loss of cardiac sympathetic innervation progresses approximately concurrently
with the movement disorder or can even occur as a late finding. Bases for independent
sympathetic noradrenergic and striatal dopaminergic lesions in Lewy body diseases
remain poorly understood. In elderly patients with unexplained OH or other evidence
of autonomic failure, it is reasonable for clinicians to look for subtle signs of
parkinsonism, such as masked facies, cogwheel rigidity, and shuffling gate.
Abbreviations:
DOPAL (dihydroxyphenylacetaldehyde), OH (orthostatic hypotension), MSA (multiple system atrophy), PAF (pure autonomic failure), PD (Parkinson disease)Keywords
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Article info
Publication history
Published online: April 29, 2011
Accepted:
April 3,
2011
Received in revised form:
March 2,
2011
Received:
January 30,
2011
Identification
Copyright
Published by Elsevier Inc.
