# Should Neurogenic Supine Hypertension Be Treated? Insights from Hypertension-Mediated Organ Damage Studies—A Narrative Review

**Authors:** Cristiano Fava, Federica Stocchetti, Sara Bonafini

PMC · DOI: 10.3390/biomedicines14010040 · Biomedicines · 2025-12-24

## TL;DR

This review explores whether treating neurogenic supine hypertension in neurodegenerative diseases can prevent organ damage without worsening other symptoms.

## Contribution

The paper provides insights into individualized treatment decisions for neurogenic supine hypertension based on hypertension-mediated organ damage evidence.

## Key findings

- Neurogenic supine hypertension may drive vascular, cardiac, renal, and cerebral injury.
- Antihypertensive therapy could prevent subclinical organ damage but risks worsening orthostatic hypotension.
- Current guidelines lack clarity on treating persistent neurogenic supine hypertension.

## Abstract

Neurodegenerative synucleinopathies—including Parkinson’s disease, multiple system atrophy, pure autonomic failure, and dementia with Lewy bodies—often feature cardiovascular autonomic dysfunction. Neurogenic orthostatic hypotension (nOH) is common and symptomatic, while neurogenic supine hypertension (nSH) is less frequent but may carry long-term cardiovascular risks. Lifestyle measures are first-line for managing nSH, yet persistent hypertension unresponsive to nonpharmacological strategies presents a treatment dilemma. Limited trial data and unclear guidelines make it difficult to determine when antihypertensive therapy is appropriate. Evidence from studies on hypertension-mediated organ damage (HMOD)—assessed through markers such as carotid intima-media thickness, pulse wave velocity, left ventricular hypertrophy, estimated glomerular filtration rate, and white matter hyperintensities—suggests that nSH, rather than the underlying neurodegenerative disorder, drives vascular, cardiac, renal, and cerebral injury. Therefore, treatment decisions should be individualized. While antihypertensive therapy may help prevent subclinical organ damage, clinicians must balance this benefit against the risk of worsening nOH and further compromising overall prognosis.

## Linked entities

- **Diseases:** Parkinson’s disease (MONDO:0005180), multiple system atrophy (MONDO:0007803), pure autonomic failure (MONDO:0018608), dementia with Lewy bodies (MONDO:0007488)

## Full-text entities

- **Diseases:** cardiovascular autonomic dysfunction (MESH:D002318), Organ Damage (MESH:D000092124), Parkinson's disease (MESH:D010300), vascular, cardiac, renal, and cerebral injury (MESH:D006322), left ventricular hypertrophy (MESH:D017379), Neurodegenerative synucleinopathies (MESH:D019636), multiple system atrophy (MESH:D019578), HMOD (MESH:D006973), Neurogenic orthostatic hypotension (MESH:D007024), autonomic failure (MESH:D012791), white matter hyperintensities (MESH:D056784), Lewy bodies (MESH:D020961), dementia with (MESH:D003704)

## Full text

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## References

68 references — full list in the complete paper: https://tomesphere.com/paper/PMC12839373/full.md

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Source: https://tomesphere.com/paper/PMC12839373