# An Overview of Vascular Compression Syndromes and Associations with Autonomic Dysfunction: A Review

## TL;DR

This review explores how vascular compression syndromes may contribute to dysautonomia and highlights the need for better recognition and treatment.

## Contribution

The paper synthesizes evidence linking vascular compression syndromes with dysautonomia and proposes potential mechanistic pathways.

## Key findings

- Vascular compression syndromes are prevalent but underdiagnosed in patients with dysautonomia like POTS.
- Symptoms of vascular compression syndromes often overlap with HSD and dysautonomia, suggesting shared mechanisms.
- Targeted interventions like surgical decompression may improve outcomes in some patients, though more research is needed.

## Abstract

Background: Vascular compression syndromes are increasingly recognized as underdiagnosed contributors to morbidity in patients exhibiting dysautonomia. Underlying vascular compression syndromes affecting the head and neck, abdomen, pelvis, and lower extremities may influence venous return, neurohormonal signaling, and autonomic regulation. There is considerable clinical overlap among these syndromes, as well as between hypermobility spectrum disorders (HSD) and dysautonomia, indicating possible shared or interacting pathophysiological mechanisms. Purpose/Aims: This hypothesis-generating narrative review synthesizes current evidence linking vascular compression syndromes with dysautonomia, highlights potential mechanistic pathways, identifies patterns of syndromic overlap, and emphasizes the importance of systematic evaluation in affected patient populations. Key Findings: Evidence from retrospective studies, case series, and clinical observations indicates that vascular compression syndromes may be prevalent among patients with dysautonomia, particularly postural orthostatic tachycardia syndrome (POTS) and HSD, yet are often unrecognized. Proposed mechanisms based on limited data include impaired venous capacitance and preload reserve, increased intracranial pressure, altered renin–aldosterone and cortisol signaling, underlying autoimmune and systemic diseases, and sympathetic ganglion irritation. Several compression syndromes show symptom overlap and frequent co-occurrence, especially in patients with connective tissue disorders. Emerging data suggest that targeted interventions, such as surgical decompression or venous stenting, may improve orthostatic intolerance and quality-of-life measures in selected patients, though high-quality prospective data remain limited. Conclusions: Vascular compression syndromes may be an important yet underappreciated contributor to dysautonomia. Increased clinical awareness and systematic screening may reduce diagnostic delays and morbidity in this underserved population. Prospective studies are needed to clarify prevalence, establish causal relationships, and determine the impact of targeted treatments on autonomic outcomes.