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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Compr+Physiol
2014 ; 4
(2
): 805-26
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Dysautonomia in Parkinson disease
#MMPMID24715569
Goldstein DS
Compr Physiol
2014[Apr]; 4
(2
): 805-26
PMID24715569
show ga
Dysautonomias are conditions in which altered function of one or more components
of the autonomic nervous system (ANS) adversely affects health. This review
updates knowledge about dysautonomia in Parkinson disease (PD). Most PD patients
have symptoms or signs of dysautonomia; occasionally, the abnormalities dominate
the clinical picture. Components of the ANS include the sympathetic noradrenergic
system (SNS), the parasympathetic nervous system (PNS), the sympathetic
cholinergic system (SCS), the sympathetic adrenomedullary system (SAS), and the
enteric nervous system (ENS). Dysfunction of each component system produces
characteristic manifestations. In PD, it is cardiovascular dysautonomia that is
best understood scientifically, mainly because of the variety of clinical
laboratory tools available to assess functions of catecholamine systems. Most of
this review focuses on this aspect of autonomic involvement in PD. PD features
cardiac sympathetic denervation, which can precede the movement disorder. Loss of
cardiac SNS innervation occurs independently of the loss of striatal dopaminergic
innervation underlying the motor signs of PD and is associated with other
nonmotor manifestations, including anosmia, REM behavior disorder, orthostatic
hypotension (OH), and dementia. Autonomic dysfunction in PD is important not only
in clinical management and in providing potential biomarkers but also for
understanding disease mechanisms (e.g., autotoxicity exerted by catecholamine
metabolites). Since Lewy bodies and Lewy neurites containing alpha-synuclein
constitute neuropathologic hallmarks of the disease, and catecholamine depletion
in the striatum and heart are characteristic neurochemical features, a key goal
of future research is to understand better the link between alpha-synucleinopathy
and loss of catecholamine neurons in PD.