Retracted: Characteristics of orthostatic hypotension in Parkinson's disease

Abstract

Clinical symptoms of Parkinson's disease (PD) include not only motor distress but also autonomic dysfunction. Orthostatic hypotension (OH) occurs in one-fifth to one-half of all patients with PD. We examined the relation of this type of hypotension to clinical features and cardiovascular parameters such as cardiac 123I-meta-iodobenzylguanidine (MIBG) uptake, changes on the Valsalva maneuver, and plasma norepinephrine concentrations on head-up tilt-table testing (HUT). We performed HUT in 55 patients with PD and divided them into two groups according to the presence or absence of OH, defined as a drop in systolic blood pressure (SBP mmHg) by 20 mmHg or more on standing. We evaluated cardiac sympathetic function by 123I-MIBG scintigraphy and assessed cardiovascular autonomic function by using the Valsalva maneuver in all subjects. We also performed HUT, 123I-MIBG scintigraphy and assessed cardiovascular autonomic function by using the Valsalva maneuver in 20 controls. The results of HUT showed that 20 patients had OH and 35 did not. The hypotension was associated with gender, older age, longer disease duration, posture and gait instability phenotype, low mini-mental state examination scores and visual hallucinations. Cardiac 123I-MIBG uptakes were lower in patients with OH. SBP fell further during early second phase in patients with OH than in patients without the condition and their increase in SBP during the late second phase and the overshoot of SBP during the fourth phase were lower. The blood pressure recovery time during the fourth phase on the Valsalva maneuver was longer in patients with OH than in those without OH. There was, however, no association between the fall in SBP on HUT and baroreflex sensitivity or the plasma norepinephrine concentrations, adjusted by age, disease duration, disease severity and dopaminergic medication using multiple regression analyses. Patients without OH already had impaired cardiac sympathetic and baroreceptor reflex functions as early abnormalities of cardiovascular autonomic control. Our results suggest that pronounced vasomotor and cardiac sympathetic dysfunction is the primary cause of OH in PD, although baroreceptor reflex failure may also make a minor contribution. It was unclear whether vasomotor and cardiac sympathetic dysfunction in patients with PD was caused primarily by the impairment of preganglionic or postganglionic lesions.

Imaging Approaches to Parkinson Disease

“…Oka et al (125) examined the association between myocardial 123 I-MIBG uptake and orthostatic hypotension, pulse, and blood pressure changes during the Valsalva maneuver and erect and supine plasma norepinephrine concentrations in PD patients. Mean myocardial 123 I-MIBG uptake was significantly lower in PD patients with orthostatic hypotension and an abnormal Valsalva response.…”

Arterial Baroreflex Dysfunction Fails to Mimic Parkinson’s Disease in Rats

“…For example, orthostatic hypotension is a common symptom of cardiovascular dysfunction in patients with PD, which appears to arise from a combination of vasomotor-, cardiac sympathetic-, and baroreflex-dysfunction (13). Importantly, attenuated baroreflex function in PD may even precede the behavioral and motor symptoms of PD (14,15).…”

Effect of Subthalamic Nucleus Deep Brain Stimulation on the Autonomic Nervous System in Parkinson’s Disease Patients Assessed by Spectral Analyses of R-R Interval Variability and Blood Pressure Variability

“…Impairments of the autonomic nervous system such as OH are frequently observed in patients with PD [18,19,20]. The autonomic cardiovascular function in PD was demonstrated previously using various tests.…”

“…Many investigators have reported that the plasma norepinephrine concentration is lower in PD patients [24]. The plasma norepinephrine concentration during standing responses is low in PD patients [18,19,24,25]. Cardiac (123)I-metaiodobenzylguanidine (123I-MIBG) is a pharmacologically inactive analogue of norepinephrine, which is similarly metabolized in noradrenergic neurons.…”