Prevalence and related factors of blood pressure regulation abnormalities in Parkinson's disease: Orthostatic hypotension and supine hypertension

Abstract

Background

Orthostatic hypotension (OH) and supine hypertension (SH) are common in patients with Parkinson's disease (PD), contributing to disease-related morbidity and mortality. However, initial OH, a transient blood pressure that decreases immediately after standing, is often unrecognized, and the interactions among OH, SH, and anti-hypertensive therapy remain unclear.

Methods

This single-centre retrospective observational study included 183 patients with PD who underwent an active supine-to-stand test with beat-to-beat blood pressure monitoring. Logistic regression was used to identify factors associated with OH and SH, and linear regression was performed to examine the determinants of postural blood pressure decline and changes in cerebral haemodynamics.

Results

OH occurred in 72.1% of patients, including 27.9% with symptomatic OH; SH was present in 21.9%. Female sex (P = 0.013) and anti-hypertensive therapy (P = 0.026) were associated with lower odds of OH. Older age (P = 0.017), arterial hypertension (P = 0.002), and a high Hoehn and Yahr stage (P = 0.006) were associated with higher odds of SH (AUC 0.80). Increased supine systolic and diastolic blood pressure were associated with increased postural decline (β = 0.40, P < 0.001; β = 0.31, P = 0.001), whereas anti-hypertensive therapy was associated with decreased postural decline. Among patients with complete middle cerebral artery monitoring data, changes in the pulsatility index were correlated with reductions in cerebral blood flow velocity (β = −11.24; P = 0.002).

Conclusions

This study comprehensively characterized the prevalence and determinants of OH and SH in patients with PD. SH was associated with greater decreases in postural blood pressure, whereas anti-hypertensive therapy was associated with smaller decreases. Pulsatility index variation may serve as a physiological marker of cerebral haemodynamic adaptation during an orthostatic challenge.

Plain language summary title

Understanding Blood Pressure Changes in People with Parkinson's Disease

Plain language summary

Purpose and Aim:

This study looked at blood pressure regulation problems in people with Parkinson's disease (PD), especially blood pressure dropping when standing up, called orthostatic hypotension (OH), and blood pressure being high when lying down, called supine hypertension (SH). The aim was to find out how common these problems are and which clinical factors are associated with them.

Background:

Blood pressure changes are common in PD but are often overlooked. They may cause dizziness, fainting, falls, and other health problems. In some patients, blood pressure may also become high while lying down. Better understanding of these patterns may help clinicians assess cardiovascular risk and manage symptoms more effectively.

>Methods:

We reviewed medical records from 183 patients with PD who completed an active supine-to-stand test with continuous beat-to-beat blood pressure monitoring. Statistical analyses were used to examine factors associated with OH, SH, and the degree of blood pressure change after standing. In a subgroup with complete middle cerebral artery monitoring data, we also assessed changes in cerebral haemodynamics.

Results and Significance:

OH was found in 72.1% of patients, including 27.9% with symptoms, and SH was present in 21.9%. Female sex and anti-hypertensive therapy were associated with lower odds of OH, whereas older age, arterial hypertension, and more advanced PD were associated with higher odds of SH. Higher supine blood pressure was associated with larger blood pressure drops after standing. These findings show that abnormal blood pressure regulation is common in PD and may support more individualized clinical assessment.

Keywords

Parkinson's disease orthostatic hypotension supine hypertension active supine-to-stand test

Introduction

Parkinson's disease (PD) is a complex neurodegenerative disorder involving both motor and nonmotor symptoms.¹ Among these domains, cardiovascular autonomic dysfunction is increasingly recognized as a major nonmotor domain. Orthostatic hypotension (OH), one of the most frequent autonomic manifestations, affects approximately 30–50% of patients^2,3 and contributes to increased risks of falls, hospitalizations and mortality.⁴ Previous studies have linked OH in PD patients to older age, longer disease duration, initiation and dose of levodopa, and comorbidities such as hypertension and diabetes.^5–7 OH is typically defined as a sustained decrease in systolic blood pressure (SBP) of ≥20 mmHg or diastolic blood pressure (DBP) of ≥10 mmHg within 3 min of standing or during a ≥ 60° head-up tilt.⁸ However, initial orthostatic hypotension (IOH) is often overlooked, and is defined as a rapid decline of >40 mmHg in SBP or >20 mmHg in DBP within 15 s after active standing. Orthostatic symptoms are not consistently associated with OH; not all PD patients with OH experience classic orthostatic symptoms such as dizziness, lightheadedness, or near-syncope.⁹

In addition to OH, supine hypertension (SH) frequently coexists with OH in PD and other forms of primary autonomic failure, such as multiple system atrophy and pure autonomic failure.⁴ SH is closely associated with cognitive decline in patients with PD.¹⁰ Recent studies have identified SH as a novel risk factor for enlarged perivascular spaces, which may mediate both cognitive and motor symptoms in PD patients.¹¹ In addition, SH is linked to target-organ damage, cardiovascular events, and increased mortality.¹² SH may exacerbate morning OH through nocturnal pressure diuresis, further complicating blood pressure management.⁴ Hypertension is the most common comorbidity in cohorts with OH.¹³ Anti-hypertensive therapy (AHT) is still controversial. Some studies in hypertensive patients suggest that AHT does not worsen OH and may even reduce its risk.^14,15 Routine clinical measurements are typically performed seated, and many patients have normal seated blood pressure, potentially masking SH.

Given this background, the present study used the active standing test to assess the full spectrum of OH, including IOH, and to determine its frequency in patients with PD. This study further identified factors associated with OH, with separate analyses of symptomatic and asymptomatic OH, and investigated the determinants of SH to aid early recognition of high-risk patients. Particular attention was given to the role of supine blood pressure and anti-hypertensive therapy in postural blood pressure responses. Because OH and SH often coexist and complicate clinical management, this study aimed to provide a more comprehensive understanding of cardiovascular autonomic dysfunction, identify clinically relevant predictors, and inform strategies for individualized blood pressure control in patients with PD.

Materials and methods

Study subjects

This was a single-centre retrospective observational study conducted between January 2023 and June 2025. The inclusion criteria were: (1) age ≥18 years; (2) a confirmed diagnosis of PD according to the UK Parkinson's Disease Society Brain Bank clinical diagnostic criteria;¹⁶ and (3) availability of supine-to-stand test data with simultaneous transcranial Doppler (TCD) monitoring. The exclusion criteria were: (1) incomplete or technically inadequate standing test data precluding reliable analysis; (2) substantial missing clinical data for the study variables; and (3) comorbid conditions that could substantially affect haemodynamic assessment, including severe heart failure, recent myocardial infarction, stroke, severe arrhythmia, or cardiac pacemaker implantation. The study protocol was approved by the local ethics committee.

Supine-to-stand test and continuous haemodynamic monitoring

Patients rested in a supine position for ≥5 min to allow for a steady-state. Afterwards, they quickly stood independently and remained standing for at least 10 min. Blood pressure (BP), heart rate, cerebral blood flow velocity (CBF_v), and the pulse index (PI) were continuously monitored throughout the procedure, and symptoms were documented in the recording ﬁle.

Continuous noninvasive finger arterial pressure (FinAP) measurement is the preferred approach for evaluating the active standing response and identifying OH and all its variants.¹⁷ The beat-to-beat BP was measured using a finger photoplethysmography system (Finometer^®, Arnhem, The Netherlands). The baseline BP was calibrated using brachial pressure measured with a sphygmomanometer.

TCD signals and continuous finger arterial blood pressure were recorded simultaneously, with event markers used to indicate the timing of postural changes. Real-time cerebral blood flow velocity was assessed using TCD (EMS-9DPro; Delica Medical, Shenzhen, China). The TCD device consisted of a pulsed probe (2 mHz), mounted on an adjustable headband holder. Sonographers usually aim for the middle cerebral artery in the bilateral temporal window at a depth of 50–56 mm.¹⁸ In patients with poor temporal window penetration, the examiner manually held the probe to monitor alternative vessels, such as the vertebrobasilar artery.

Types of active standing responses

Based on reference [⁸], the definitions used in this paper are as follows:

Initial OH (IOH): IOH is defined as a transient decrease in SBP of >40 mmHg and/or > 20 mmHg in DBP within 15 s of standing in the absence of sustained OH.

Delayed recovery: Delayed recovery is defined as the inability of the SBP to recover to within ≤20 mmHg of the supine baseline values at 30–40 s after standing but does not meet the criteria of classical OH; recovery occurs within 3 min of standing.

Classical OH (COH): Classical OH is defined as a sustained decrease of ≥20 mmHg in SBP (or ≥30 mmHg in those with baseline hypertension) and/or ≥10 mmHg (≥15 mmHg in those with baseline hypertension) in DBP (or SBP <90 mmHg) occurring between 60 and 180 s of standing.

Delayed OH (DOH): The diagnostic criteria for BP reduction are identical to those for COH; however, the decrease occurs after 180 s of standing.

SH: SH is defined as SBP ≥140 mmHg and/or DBP ≥90 mmHg measured after ≥5 min of supine rest.

In this study, we defined IOH as transient OH and classified delayed recovery, classical OH, and delayed OH as persistent OH. Symptomatic OH was defined as a patient meeting the blood pressure criteria for OH during the supine-to-stand test, with symptoms of orthostatic intolerance (e.g., dizziness upon standing) documented in the examination report.

Statistical analysis

All the statistical analyses were conducted in R (version 4.5.0; R Foundation for Statistical Computing, Vienna, Austria) using RStudio (version 2024.12.1). Continuous variables are expressed as the means ± standard deviations or medians (interquartile ranges) as appropriate, and categorical variables are expressed as counts and percentages. Group comparisons were conducted using parametric or nonparametric tests for continuous variables, and chi-square or Fisher's exact tests for categorical variables. Univariable logistic regression was used to screen candidate factors, which, together with clinical relevance and prior evidence, were subsequently entered into multivariable logistic regression to identify independent risk factors for OH and SH. The predictive value of the model for SH was assessed using receiver operating characteristic (ROC) curve analysis. For symptomatic OH and OH subtypes classified by duration, univariable analyses and logistic regression were performed, and the variables selected, and those in previous studies were included in multivariable models. Multivariable linear regression was employed to examine factors associated with postural blood pressure decline and changes in time-averaged maximum mean velocity (TAMMV). Among 112 patients whose middle cerebral artery flow was monitored, 90 with complete data were included in the analysis of cerebral haemodynamics. A two-tailed P˂ 0.05 was the threshold for significance.

Results

A total of 186 patients with PD met the inclusion criteria between January 2023 and June 2025. Of these, 3 were excluded: 1 because of cardiac pacemaker implantation and 2 because of inadequate blood pressure signal quality during the supine-to-stand test, which precluded reliable analysis. Ultimately, 183 patients were included in the final analysis (Figure 1).

Figure 1.

Flowchart of participant selection.

Frequencies of OH and symptomatic OH

Among 183 patients with PD, 132 (72.1%) were diagnosed with OH, 9 (4.9%) with orthostatic hypertension (OHT), 1 (0.5%) with postural tachycardia syndrome (POTS), and 41 (22.4%) with a normal blood pressure response. Within the OH group, 104 patients had IOH (transient type), 9 had delayed recovery OH, 18 had COH, and 1 had DOH, resulting in 28 patients with persistent OH overall. On the basis of the results of the supine-to-stand test, the frequency of OH was 72.1% (n = 132/183), and the frequency of symptomatic OH was 27.9% (n = 51/183); 6.6% (n = 12/183) of patients exhibited orthostatic symptoms without meeting the diagnostic threshold for OH (Figure 2). Overall, OH is highly prevalent in PD patients, with asymptomatic OH observed more commonly than symptomatic OH. When patients were stratified by age (˂65, 65–74, and ≥75 years), no significant differences were observed in the incidence of OH (χ² = 0.85, P = 0.654) or symptomatic OH (χ² = 1.02, P = 0.601) among patients with PD.

Figure 2.

Prevalence of OH and symptomatic OH in PD patients. OI = orthostatic intolerance. The black section represents patients who experience dizziness and other symptoms of orthostatic intolerance upon standing.

Clinical characteristics and related factors of OH

The clinical characteristics of PD patients with OH and those with a normal blood pressure response are presented in Table 1. PD patients who developed OH after active standing reported significantly less use of anti-hypertensive medications than did those with normal responses (P = 0.041). Variables such as age, sex, duration of PD, Hoehn and Yahr stage, arterial hypertension, diabetes, sleep disturbances, urinary dysfunction, use of anti-hypertensive medications, use of anxiolytics and/or antidepressants and SH were entered into the multivariate logistic regression model. In the multivariate analysis, female sex (OR = 0.37; 95% CI: 0.17–0.81; P = 0.013) and the use of anti-hypertensive medications (OR = 0.22; 95% CI: 0.06–0.84; P = 0.026) were associated with lower odds of OH.

Table 1.

Clinical characteristics of PD patients with OH or a normal response.

	OH (n = 132)	Normal (n = 41)	P value
Demographic characteristics
Sex (male)	75(56.8%)	16(39.0%)	0.051
Age (years)	68.04 ± 10.13	69.27 ± 9.60	0.493
PD duration (years)	4.64 ± 3.77	4.79 ± 4.28	0.961
Hoehn and Yahr stage			0.691
I/I.5	19(14.4%)	4(9.8%)
II/II.5	45(34.1%)	12(29.3%)
III	52(39.4%)	18(43.9%)
IV	16(12.1%)	7(17.1%)
Nonmotor symptoms
Sleep disturbances	92(69.7%)	23(56.1%)	0.130
Constipation	71(53.8%)	21(51.2%)	0.858
Urinary dysfunction	34(25.8%)	13(31.7%)	0.547
Comorbidities
Arterial hypertension	64(48.5%)	22(53.7%)	0.595
Diabetes	30(22.7%)	10(24.4%)	0.834
Coronary heart disease	20(15.2%)	7(17.1%)	0.807
Renal failure	8(6.1%)	3(7.3%)	0.724
Medication use
Anti-hypertensive medications	43(32.6%)	21(51.2%)	0.041*
Anxiolytics and/or antidepressants	44(33.3%)	11(26.8%)	0.565
Sleep medications	36(27.3%)	14(34.1%)	0.433

Note: OH = orthostatic hypotension; Sleep disturbances = difficulties falling asleep, poor sleep duration and quality, and their impact on daytime functioning; Urinary dysfunction = frequent urination, nocturia, urinary incontinence; *P < 0.05.

Orthostatic hypotension was not significantly associated with symptoms of orthostatic intolerance (P = 0.276). Patients were categorized into three groups: symptomatic OH, asymptomatic OH, and normal response. Multinomial logistic regression analysis was performed, in which age, sex, use of anti-hypertensive medications, and sleep disturbances were included as covariates. Sleep disturbances emerged as an independent risk factor for symptomatic OH (OR = 3.15; 95% CI: 1.23–8.04; P = 0.017). Sex was not independently associated with symptomatic OH (OR = 0.71; 95% CI: 0.30–1.68; P = 0.439). Instead, female sex was independently associated with lower odds of asymptomatic OH (OR = 0.37; 95% CI: 0.17–0.81; P = 0.013).

Factors associated with transient/persistent OH

The clinical characteristics of patients with transient and persistent OH are summarized in Supplementary Table 1. Urinary dysfunction (P = 0.028), creatinine levels (P = 0.009), and uric acid levels (P = 0.024) significantly differed between the two groups. Patients with PD were categorized into transient OH, persistent OH, and normal response groups. Multinomial logistic regression analysis was performed, including sex, use of anti-hypertensive medications, and sleep disturbances. Compared with male sex, female sex was significantly associated with a lower risk of persistent OH (OR = 0.24; 95% CI: 0.08–0.70; P = 0.008). In the transient OH group, females also exhibited a protective trend (OR = 0.55), although this did not reach statistical significance (P = 0.117).

Prevalence and associated factors of SH

Among the 183 patients with PD, 21.9% (n = 40) met the diagnostic criteria for SH. Among these, 28 patients had OH, 3 had orthostatic hypertension, and 9 had a normal blood pressure response. However, OH was not associated with supine hypertension (P = 0.920). Thirty-one patients had concomitant arterial hypertension, and 7 did not. In the multivariable logistic regression model including age, arterial hypertension, and Hoehn and Yahr stage, age (OR = 1.06; 95% CI: 1.01–1.11; P = 0.017) and arterial hypertension (OR = 4.68; 95% CI:1.77–12.38; P = 0.002) were independently associated with SH. When stages I and II were merged and used as the reference group, there was a significant linear trend across the Hoehn and Yahr stages. A higher stage was associated with an increased risk of SH (OR = 3.49; 95% CI:1.43–8.51, P = 0.006). The increase in risk was significant for stage IV disease (OR = 5.87; 95% CI:1.67–20.65; P = 0.006), whereas that for stage III disease did not significantly differ from that for the reference stage (OR = 2.34; 95% CI:0.93–5.89; P = 0.072). The multivariable model showed moderate-to-good discrimination (AUC 0.80). In contrast, a model including age alone identified an optimal cut-off of 69.5 years with moderate discrimination (AUC 0.70), as illustrated in Figure 3.

Figure 3.

Receiver operating characteristic curves for predicting supine hypertension. SH = supine hypertension; multi_mod = multivariable model including age, arterial hypertension, and Hoehn and Yahr stage; age_mod = age alone model.

Predictors of blood pressure decline after standing

A total of 168 patients whose complete records were available were included in the standing-induced blood pressure change analysis. In a multivariable linear regression model incorporating sex, use of anti-hypertensive medications, supine SBP, history of tumor, constipation, and total cholesterol, supine SBP was positively associated with ΔSBP (β = 0.40; P < 0.001), whereas the use of anti-hypertensive medications was negatively associated with ΔSBP (β = −8.99; P < 0.001). In a separate model including sex, use of anti-hypertensive medications, use of anxiolytics and/or antidepressants, supine DBP, red blood cell count, and haematocrit, supine DBP was positively associated with ΔDBP (β = 0.31; P = 0.001), whereas the use of anti-hypertensive medications was negatively associated with ΔDBP (β = −4.74; P = 0.008) (Table 2). Overall, higher supine BP was associated with greater postural decline, whereas patients receiving anti-hypertensive therapy exhibited smaller reductions after standing.

Table 2.

Multivariable linear regression analysis of changes in SBP/DBP in the supine-to-stand test.

	Parameter estimate (β)	Standard error	95% CI	P value
ΔSBP
Sex (male)	−3.98	2.29	(−8.49, 0.54)	0.084
SBP_supine	0.40	0.07	(0.25, 0.54)	< 0.001*
Anti-hypertensive medications	−8.99	2.42	(−13.77, −4.20)	< 0.001*
History of tumor	8.16	5.68	(−3.06, 19.38)	0.153
Constipation	−4.50	2.27	(−8.95, −0.05)	0.052
TC	−2.12	1.15	(−4.40, 0.16)	0.068
N = 168, R² = 0.23, Adjusted R² = 0.20, F(6, 161) = 8.01, P＜0.001
ΔDBP
Sex (male)	−2.84	1.71	(−6.22, 0.53)	0.098
DBP_supine	0.31	0.09	(0.12, 0.49)	0.001*
Anti-hypertensive medications	−4.74	1.76	(−8.21, −1.28)	0.008*
Anxiolytics and/or antidepressants	2.43	1.88	(−1.29, 6.14)	0.199
RBC	3.22	2.65	(−2.02, 8.46)	0.227
HCT	−0.46	0.41	(−1.27, 0.36)	0.271
N = 168, R² = 0.18, Adjusted R² = 0.15, F(6, 161) = 5.94, P＜0.001

Note: ΔSBP = change in SBP; ΔDBP = change in DBP; SBPsupine/ DBPsupine = SBP/DBP in the supine position; TC = total cholesterol; RBC = red blood cell count; HCT = haematocrit; ΔDBP regression estimated with HC3 heteroskedasticity-robust standard errors.

Cerebral haemodynamic changes in the supine-to-stand test

As shown in Table 3, patients with OH, irrespective of the presence of orthostatic symptoms, had significantly lower mean blood pressure (MBP) in the standing position than patients in the normal response group did (P˂0.05). Moreover, the reduction in the MBP and TAMMV after standing was significantly greater in the OH group than in the normal response group (P˂0.05).

Table 3.

Cerebral haemodynamic changes in PD patients in the supine-to-stand test.

	N	Supine			Stand			Supine to stand
	N	MBP	TAMMV	PI	MBP	TAMMV	PI	ΔMBP	ΔTAMMV	ΔPI
symptOH	29	88.76 ± 14.52	53.83 ± 14.04	1.08 ± 0.26	56.52 ± 12.58 *	45.72 ± 15.17	1.42 ± 0.35	−32.24 ± 8.86 *	−8.10 ± 8.47 *	0.34 ± 0.25
asymptOH	42	89.86 ± 10.98	51.79 ± 16.94	1.06 ± 0.26	57.64 ± 13.23 *	42.74 ± 14.92	1.36 ± 0.31	−32.21 ± 11.46 *	−9.05 ± 9.47 *	0.29 ± 0.25
normal	19	87.74 ± 11.86	50.21 ± 17.96	1.05 ± 0.21	71.16 ± 13.89	48.05 ± 19.83	1.34 ± 0.30	−16.58 ± 7.83	−2.16 ± 6.86	0.29 ± 0.31

Note: symptOH = symptomatic orthostatic hypotension; asymptOH = asymptomatic orthostatic hypotension; MBP = mean blood pressure; TAMMV = time-averaged mean of the maximum velocity; PI = pulsatility index, defined as (peak systolic velocity – end diastolic velocity) divided by the mean flow velocity. *Compared with the normal response group, P<0.05 (Benjamini–Hochberg FDR correction).

Univariable linear regression analysis revealed that the MBP in the standing position (β = 0.34; P˂0.001), the change in the MBP (ΔMBP) (β = 0.33; P = 0.002) and the pulsatility index (ΔPI) (β = −0.40; P˂0.001) from supine to standing were significantly associated with the corresponding change in the TAMMV (ΔTAMMV). After adjustment for age and sex in the multivariable linear regression, the ΔPI remained independently associated with the ΔTAMMV (β = −11.24; 95% CI: (−18.10, −4.37); P = 0.002). Specifically, a greater increase in the PI upon standing was associated with a greater decrease in cerebral blood flow velocity. Among the haemodynamic variables examined, ΔPI showed the strongest association with ΔTAMMV, highlighting its potential relevance as an indicator of cerebral haemodynamic adaptation during postural change. The ΔTAMMV was not related to symptoms of orthostatic intolerance (P = 0.898).

Discussion

In this study, the prevalence of OH and symptomatic OH in patients with PD was estimated, and risk factors for OH and its subtypes were identified. The incidence of OH was 72.1%, with asymptomatic OH being more common than symptomatic OH. This relatively high prevalence may be explained by several factors. Patients with PD are at increased risk of OH because of cardiovascular autonomic dysfunction. In addition, the marked heterogeneity in reported prevalence across studies may reflect differences in clinical practice and research methodology, particularly in case definitions and the timing of blood pressure measurements after standing.^19,20 In this study, OH was assessed across the full poststanding time course, including IOH, which may have increased the detection rate. Previous studies have shown that the incidence of IOH in patients with PD may be at least comparable to that of classical OH.²¹ The presence of OH was not consistently accompanied by orthostatic symptoms, which is consistent with previous reports,^22–25 possibly reflecting preserved cerebral autoregulation that maintains cerebral perfusion within a compensatory range.²⁶ Previous studies have shown that a decrease in blood pressure within the first minute of standing is closely associated with orthostatic symptoms and several long-term adverse outcomes.^21,27 Both symptomatic and asymptomatic OH have been linked to unfavorable outcomes, including falls and cognitive impairment.²⁸ Higher symptom scores in patients with symptomatic OH correlate with poorer postural stability⁶ and a greater risk of disability.²⁹ Notably, patients with asymptomatic OH exhibit impairments in activities of daily living (ADL) and instrumental activities of daily living (iADL) comparable to those with symptomatic OH.³⁰ Therefore, asymptomatic OH should not be underestimated simply because clinical symptoms are absent, as it may represent an early or compensated stage of cardiovascular autonomic dysfunction.

Although several studies have reported an association between age and OH,^31,32 our analysis revealed no significant differences in the incidence of OH or symptomatic OH across age groups. This discrepancy may reflect the combined influence of neurodegenerative progression, disease duration and severity, and medication use. Compared with male patients, female patients had significantly lower rates of OH, asymptomatic OH, and persistent OH, and female sex emerged as an independent protective factor. However, the association between sex and OH has been inconsistent across previous studies, with some reporting a higher prevalence in men,^33,34 and others in women,^35,36 with others finding no significant sex difference.³⁷ The mechanisms underlying these sex-related differences remain unclear. Previous studies have suggested that sex-related variation in autonomic and vascular regulation may contribute to orthostatic blood pressure responses, although the available findings have been heterogeneous.^38–40 In addition, differences in cerebral autoregulation and the maintenance of cerebral perfusion during orthostatic stress may also play a role, but the current evidence remains conflicting.^41,42 Taken together, our findings suggest that female sex may be associated with a lower susceptibility to OH in patients with PD; however, the underlying mechanisms require further investigation.

After adjusting for sex and the use of anti-hypertensive medications, sleep disturbances were identified as an independent risk factor for symptomatic OH. In the present study, sleep disturbances were defined broadly on a clinical basis and were not equivalent to polysomnography-confirmed rapid eye movement sleep behavior disorder (RBD). Nevertheless, evidence from studies of specific sleep disorder subtypes, particularly RBD, may provide mechanistic insight into the observed association. In patients with RBD, neurodegeneration involving the locus coeruleus and dorsal motor nuclei may disrupt sympathetic and parasympathetic regulation, resulting in nocturnal blood pressure variability, impaired cardiovascular reflexes, and reduced baroreflex sensitivity, thereby exacerbating OH.⁴³ Previous studies have also demonstrated that RBD is an independent predictor of OH in PD patients,⁴⁴ with affected patients showing greater decreases in SBP upon standing and higher orthostatic symptom scores.⁴⁵ However, our findings are limited by the lack of polysomnographic evaluation. Future studies incorporating sleep monitoring are warranted to clarify the impact of sleep disturbances on cardiovascular autonomic regulation in PD patients.

We found that anti-hypertensive therapy was an independent protective factor against OH. Multivariate linear regression analysis further demonstrated that patients who received anti-hypertensive therapy exhibited a significantly smaller decrease in BP when they were standing. This observation appears counterintuitive to clinical expectations, as anti-hypertensive agents are traditionally viewed as potential contributors to OH. Most OH is nonneurogenic and is usually triggered by hypovolemia or the use of medications that affect BP, such as antihypertensives and psychotropic drugs; in contrast, neurogenic OH is typically observed in conditions that impair autonomic function, including PD, multiple system atrophy, pure autonomic failure, and diabetes.^46,47 In the context of PD, neurogenic mechanisms are clinically relevant and are thought to involve cardiac and extracardiac noradrenergic denervation and baroreflex failure.^48,49 Although neurogenic mechanisms are clinically relevant in PD, the present study did not formally distinguish neurogenic from nonneurogenic OH; therefore, neurogenic OH was discussed only as pathophysiological context rather than as a separate study outcome.

In most patients with PD, OH likely results from a combination of autonomic reflex dysfunction, relative volume depletion, and medication effects. Notably, arterial hypertension frequently coexists with OH; in our cohort, 48.5% of patients with OH had arterial hypertension, and 32.6% were receiving anti-hypertensive therapy. Clinicians often adopt a conservative approach to control blood pressure in patients with OH to avoid exacerbating orthostatic symptoms. However, accumulating evidence suggests that achieving lower BP targets in patients with primary hypertension does not necessarily increase the risk of OH and may even reduce its incidence.^15,50–52 Patients with severe or symptomatic OH are generally excluded from hypertension trials. The observed protective effect of anti-hypertensive therapy against OH may be related to long-term cardiovascular adaptations, such as improvements in myocardial remodelling, baroreflex sensitivity⁵³ and arterial stiffness.⁵⁴ These effects likely develop gradually, whereas short-term haemodynamic changes following drug initiation may transiently worsen OH. This temporal discrepancy does not negate the long-term benefits of anti-hypertensive therapy. Therefore, anti-hypertensive therapy should not be withheld solely out of concern for exacerbating OH; rather, appropriate drug selection and individualized dosing schedules are important for optimizing blood pressure control while minimizing orthostatic symptoms. Different classes of anti-hypertensive agents may have different effects on OH.^55,56 Angiotensin-converting enzyme inhibitors/angiotensin receptor blockers (ACEIs/ARBs) and calcium channel blockers (CCBs) may be less likely to aggravate OH than α- or β-adrenergic blockers and may therefore be preferable in hypertensive patients with coexisting OH.⁵⁷ In addition, although the timing of anti-hypertensive drug administration has been investigated in relation to cardiovascular outcomes, no consensus has been reached regarding the optimal dosing time.^58,59

Given the close interplay between SH and OH, and the feasibility of bedside SH monitoring, we further investigated risk factors for SH and developed a predictive model to identify high-risk patients. In our cohort, older age, arterial hypertension, and advanced Hoehn and Yahr stage were independent predictors of SH, demonstrating good discriminative performance in the multivariable model. These findings align with previous findings that advanced age and a history of hypertension are independent risk factors for SH in newly diagnosed PD patients.⁶⁰ Approximately one-third of PD patients experience SH, and cardiovascular comorbidities markedly accelerate its development.⁶¹ SH is a common comorbidity in OH patients, while sympathetic failure primarily explains OH, SH may arise from independent pressor mechanisms.^4,48 Potential contributors include abnormal nocturnal blood pressure patterns, such as a failure to exhibit a normal ≥10% nocturnal decline (nondipping) or nocturnal hypertension (reverse dipping).^62,63 As noted in the introduction, SH is associated with poor prognosis in patients with PD. Therefore, identifying high-risk patients and performing continuous supine and nocturnal blood pressure monitoring may reveal a potential therapeutic target for managing blood pressure dysregulation in PD patients.

Moreover, our results revealed that supine blood pressure is significantly correlated with the magnitude of systolic and diastolic decreases during active standing, which is consistent with the findings of previous studies using tilt or active standing tests.⁶¹ Managing supine blood pressure may help mitigate orthostatic drops. Although no direct statistical association between OH and SH was observed, this may reflect the predominance of nonneurogenic OH in our cohort or an underestimation of SH incidence because of the reliance on a single measurement. Notably, nocturnal SH may exacerbate morning OH through pressure diuresis, leading to prominent orthostatic symptoms.⁶⁴ Most pharmacologic therapies for OH act by expanding blood volume or increasing vascular tone to maintain blood pressure; however, these agents carry the risk of aggravating SH. Common examples include midodrine, droxidopa, and fludrocortisone.⁶⁵

The coexistence of OH and SH thus presents a major therapeutic dilemma, requiring a balanced management strategy that addresses both conditions simultaneously. The therapeutic goal for OH should be to alleviate orthostatic symptoms and prevent excessive blood pressure drops without exacerbating SH. Nonpharmacologic interventions are generally recommended as first-line therapy. These include lifestyle modifications, physical countermanoeuvres, and the use of abdominal binders or compression garments.⁶⁶ Pyridostigmine is considered a relatively safe pharmacologic option, as it enhances cholinergic transmission at the autonomic ganglia and promotes sympathetic activation primarily in the upright position, thereby improving OH without increasing the risk of SH.⁶⁵ For the management of SH, short-acting antihypertensive agents administered at bedtime are preferred. Suitable agents include nitroglycerin patches, sildenafil, clonidine, nebivolol, short-acting nifedipine, losartan, and eplerenone.⁶⁷ These regimens aim to control nocturnal or supine hypertension while minimizing the potential worsening of morning OH.

We found that patients with OH, regardless of the presence of orthostatic symptoms, exhibited greater reductions in the CBFv during standing. The magnitude of the decrease in the CBFv was not associated with orthostatic symptoms. Multivariable linear regression further demonstrated that postural changes in the pulsatility index were independently correlated with changes in the CBFv. Most studies attribute orthostatic symptoms to cerebral hypoperfusion, with greater CBFv reductions in symptomatic patients.^68,69 Previous research has shown that cerebral perfusion may be compensatorily enhanced in early PD patients with OH, whereas differences in cerebral perfusion between those with and without OH become less pronounced in later disease stages.⁷⁰ Another study reported that in patients with autonomic dysfunction, symptoms of orthostatic intolerance were associated with resting cerebral hyperperfusion and reduced intracranial compliance.⁷¹ These findings suggest that mechanisms beyond simple hypoperfusion—including altered cerebrovascular reactivity and compliance—may contribute to orthostatic symptoms.

Cerebral blood flow is influenced by intracranial pressure (ICP), arterial blood pressure (ABP), and cerebrovascular resistance (CVR).⁷² Previous work has demonstrated that MBP and changes in MBP after standing are significantly associated with CBFv variations.⁶⁸ Although the PI is often interpreted as an indicator of downstream vascular resistance, accumulating methodological and clinical evidence suggests that it is a composite parameter reflecting not only distal arteriolar resistance but also cerebral perfusion pressure (ABP − ICP), vascular compliance, and heart rate.⁷³ In this study, a greater increase in the PI during standing was independently associated with a greater decrease in the CBFv, even after adjustment for age and sex. These findings suggest that compared with BP alone, postural changes in the PI may reflect the integrated cerebral haemodynamic response to orthostatic stress more comprehensively. As a composite index, the PI may therefore be a useful physiological marker for future studies investigating cerebral haemodynamic adaptation and possibly cerebral autoregulation during postural transitions.

This study has several limitations. First, the findings need to be validated in a larger sample to ensure robustness. Second, as this was a retrospective study, detailed symptom scores for symptomatic OH were not available, and information on classes of anti-hypertensive medications and blood pressure control was not recorded. Third, beat-to-beat blood pressure was measured noninvasively at the finger, which may be affected by signal instability during active standing and could introduce residual measurement error, although recordings with inadequate signal quality were excluded. Fourth, OH was not formally classified as neurogenic or nonneurogenic. Simultaneous ECG data were not available because of equipment limitations, and ΔHR/ΔSBP -based criteria have been applied mainly classical OH.⁷⁴ Finally, the predictive model for SH has not been externally validated, and estimates derived from a single-centre cohort may overstate its true performance.

Conclusion

In summary, using the active standing test, we comprehensively evaluated the full spectrum of OH, including IOH and its prevalence in PD patients. We further identified key risk factors for both OH and SH. Screening for high-risk SH patients and monitoring nocturnal and supine blood pressure may facilitate a deeper understanding of blood pressure dysregulation in PD patients. Although antihypertensive therapy has traditionally been viewed with caution, our findings suggest that it may confer long-term benefits for OH, warranting further confirmation in prospective studies. When OH and SH coexist, clinical management should adopt a comprehensive, individualized approach that addresses both conditions simultaneously, rather than neglecting either. Finally, postural changes in the PI may serve as a useful physiological markers for future studies of cerebral haemodynamic adaptation and cerebral autoregulation during orthostatic challenge.

Supplemental Material

sj-docx-1-pkn-10.1177_1877718X261457798 - Supplemental material for Prevalence and related factors of blood pressure regulation abnormalities in Parkinson's disease: Orthostatic hypotension and supine hypertension

Supplemental material, sj-docx-1-pkn-10.1177_1877718X261457798 for Prevalence and related factors of blood pressure regulation abnormalities in Parkinson's disease: Orthostatic hypotension and supine hypertension by Jinyu Jia, Jianmin Zeng, Yifan Gong, Huan Zhou, Xiuli Zeng and Jing Zou in Journal of Parkinson's Disease

Supplemental Material

sj-xlsx-2-pkn-10.1177_1877718X261457798 - Supplemental material for Prevalence and related factors of blood pressure regulation abnormalities in Parkinson's disease: Orthostatic hypotension and supine hypertension

Supplemental material, sj-xlsx-2-pkn-10.1177_1877718X261457798 for Prevalence and related factors of blood pressure regulation abnormalities in Parkinson's disease: Orthostatic hypotension and supine hypertension by Jinyu Jia, Jianmin Zeng, Yifan Gong, Huan Zhou, Xiuli Zeng and Jing Zou in Journal of Parkinson's Disease

Supplemental Material

Footnotes

ORCID iDs

Jinyu Jia

Jianmin Zeng

Yifan Gong

Huan Zhou

Xiuli Zeng

Jing Zou

Ethical considerations

This study was performed in line with the principles of the Declaration of Helsinki. Approval was granted by the Ethics Committee of the First Affiliated Hospital of Jinan University.

Consent to participate

This study was retrospective in design and was approved by the institutional ethics committee, which waived the requirement for informed consent.

Author contributions

Jinyu Jia and Xiuli Zeng conceived and designed the study; Jinyu Jia, Jianmin Zeng, and Yifan Gong collected and organized the data; Huan Zhou evaluated the quality of transcranial Doppler and active standing data; Jinyu Jia analysed and drafted the article; and Xiuli Zeng, Huan Zhou, and Jing Zou edited and revised the article. All the authors approved the final version of the article.

Funding

The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This work was supported by the Basic and Applied Basic Research Foundation of Guangdong Province, Medical Scientific Research Foundation of Guangdong Province, Grants from Youth S&T Talent Support Program of Guangdong Provincial Association for Science and Technology, Science and Technology Projects in Guangzhou, Guangzhou Science and Technology Project, Open Project Program of State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD) at Harbin Medical University (grant number 2025A1515012465, A2024127, SKXRC2025219, 2025A04J3801, 2024A04J4175, HDHY2025042).

Declaration of conflicting interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Supplemental material

Supplemental material for this article is available online.

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