Patients with Parkinson disease (PD) often have manifestations of autonomic failure. About 40% have neurogenic orthostatic hypotension (NOH), and among PD+NOH patients virtually all have evidence of cardiac sympathetic denervation; however, whether PD+NOH entails extra-cardiac noradrenergic denervation has been less clear.
Conclusions
The results support the concept of generalized noradrenergic denervation in PD+NOH, with similar severity to that seen in PAF [pure autonomic failure]. In contrast, the parasympathetic cholinergic and adrenomedullary hormonal components of the autonomic nervous system seem intact in PD+NOH.
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The movement disorder in Parkinson disease (PD) is well known to result from loss of nigrostriatal dopaminergic neurons; however, there is increasing recognition that PD also entails several non-motor symptoms.
About 90% of PD patients complain of symptoms of autonomic nervous system dysfunction,1and about 40% have orthostatic hypotension.2 Among PD patients in whom orthostatic hypotension is neurogenic (neurogenic orthostatic hypotension, NOH),3virtually all have a loss of sympathetic noradrenergic nerves in the heart.4, 5 Post-mortem histological studies have confirmed these observations and have consistently demonstrated a profound loss of tyrosine hydroxylase immunoreactive cardiac innervation in patients with PD6, 7 as well as involvement of autonomic ganglia.8, 9.
PMCID: PMC2667619
NIHMSID: NIHMS65719
PMID: 18661549
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aspergerian13
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"Dopamine agonists appear to act by not only direct stimulation of postsynaptic DA receptors but also presynaptic receptors. Dopamine agonists cause orthostatic hypotension through the activation of dopamine receptors, determining cutaneous, mesenteric and renal vasodilation, but also through other mechanisms such as a reduced central sympathetic tone which causes a small reduction in heart rate and an impaired release of renin and aldosterone "
In my personal case the autonomic impairment persisted for a month after quitting and I also suffered supine hypertension so a straight out lowering of BP is not the whole story.
Signs or symptoms of impaired autonomic regulation of circulation often attend Parkinson disease (PD). This review covers biomarkers and mechanisms of autonomic cardiovascular abnormalities in PD and related alpha-synucleinopathies.
The clearest clinical laboratory correlate of dysautonomia in PD is loss of myocardial noradrenergic innervation, detected by cardiac sympathetic neuroimaging. About 30-40% of PD patients have orthostatic hypotension (OH), defined as a persistent, consistent fall in systolic blood pressure of at least 20 mmHg or diastolic blood pressure of at least 10 mmHg within 3 min of change in position from supine to standing.
Neuroimaging evidence of cardiac sympathetic denervation is universal in PD with OH (PD+OH). In PD without OH about half the patients have diffuse left ventricular myocardial sympathetic denervation, a substantial minority have partial denervation confined to the inferolateral or apical walls, and a small number have normal innervation.
Among patients with partial denervation the neuronal loss invariably progresses over time, and in those with normal innervation at least some loss eventually becomes evident. Thus, cardiac sympathetic denervation in PD occurs independently of the movement disorder.
PD+OH also entails extra-cardiac noradrenergic denervation, but this is not as severe as in pure autonomic failure. PD+OH patients have failure of both the parasympathetic and sympathetic components of the arterial baroreflex.
OH in PD therefore seems to reflect a "triple whammy" of cardiac and extra-cardiac noradrenergic denervation and baroreflex failure. In contrast, most patients with multiple system atrophy, which can resemble PD+OH clinically, do not have evidence for cardiac or extra-cardiac noradrenergic denervation.
Catecholamines in the neuronal cytoplasm are potentially toxic, via spontaneous and enzyme-catalyzed oxidation. Normally cytoplasmic catecholamines are efficiently taken up into vesicles via the vesicular monoamine transporter. The recent finding of decreased vesicular uptake in Lewy body diseases therefore suggests a pathogenetic mechanism for loss of catecholaminergic neurons in the periphery and brain.
Parkinson disease (PD) is one of the most common chronic neurodegenerative diseases of the elderly, and it is likely that as populations age PD will become even more prevalent and more of a public health burden.
Severe depletion of dopaminergic neurons of the nigrostriatal system characterizes and likely produces the movement disorder (rest tremor, slowness of movement, rigid muscle tone, and postural instability) in PD. Over the past two decades, compelling evidence has accrued that PD also involves loss of noradrenergic neurons in the heart.
This finding supports the view that loss of catecholaminergic neurons, both in the nigrostriatal system and the heart, is fundamental in PD. By the time PD manifests clinically, most of the nigrostriatal dopaminergic neurons are already lost. Identifying laboratory measures-biomarkers-of the disease process is therefore crucial for advances in treatment and prevention.
Deposition of the protein, alpha-synuclein, in the form of Lewy bodies in catecholaminergic neurons is a pathologic hallmark of PD. Alpha-synucleinopathy in autonomic neurons may occur early in the pathogenetic process. The timing of cardiac noradrenergic denervation in PD is therefore a key issue.
This review updates the field of autonomic cardiovascular abnormalities in PD and related disorders, with emphasis on relationships among striatal dopamine depletion, sympathetic noradrenergic denervation, and alpha-synucleinopathy.
PMID 22094370 [Indexed for MEDLINEPMCID PMC3299874.
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