Thoracic Outlet Syndrome, Abdominal Vascular Compression Syndromes and the Functional Continuum in Dysautonomia

Dr Graham Exelby May 2025

Functional Continuum with Brainstem and Cardiac Plexus Involvement:

Emerging evidence and clinical observation suggest that these abdominal compression syndromes are not isolated phenomena but operate along a functional continuum that extends cranially to the cardiac plexus and brainstem nuclei.

Venous hypertension from Nutcracker Syndrome may propagate cephalad through the valveless spinal venous plexus, increasing central venous pressure and impacting the posterior fossa, where vital autonomic centres reside.

Coeliac plexus dysfunction can amplify sympathetic tone via the thoracolumbar outflow and intersect with cardiac plexus regulation, leading to inappropriate sinus tachycardia, vagal dysregulation, and baroreflex failure.

Furthermore, the interaction of coeliac plexus compression with systemic inflammation (e.g., from post-viral states) can trigger a RAGE–TLR4–CCL2–NF-κB immune activation loop. This loop sustains neuroinflammation and microvascular dysregulation, contributing to brainstem hypoxia.

The brainstem autonomic nuclei—particularly the nucleus tractus solitarius (NTS), dorsal motor nucleus of the vagus, and locus coeruleus—are highly sensitive to perfusion shifts and oxidative stress.

Chronic afferent signalling from the coeliac plexus or its compression may therefore maintain a pathological loop between abdominal autonomic input, cardiac dysregulation, and cerebral hypoperfusion.

Clinically, patients with overlapping abdominal vascular compression and POTS or Long COVID phenotypes often report fluctuating fatigue, PEM, palpitations, syncope, and migraine-like symptoms, which may reflect this multi-level dysfunction. Recognizing and addressing this continuum is essential in guiding investigations and formulating comprehensive treatment plans.

Integration with Thoracic Outlet Syndrome and Cardiac Plexus Dysfunction:

The functional continuum between the coeliac plexus and brainstem extends through the cardiac plexus, particularly in cases of thoracic outlet syndrome (TOS). The cardiac plexus receives autonomic fibres from the vagus and sympathetic trunks and is anatomically adjacent to the thoracic outlet.

Mechanical compression or neural irritation in TOS can therefore influence cardiac autonomic signalling, contributing to dysrhythmias, presyncope, and central autonomic sensitization.Compression of the subclavian vein or artery in venous or arterial TOS can exacerbate preload failure and reduce cerebral perfusion—especially in upright posture—further contributing to brainstem hypoxia.

In patients with underlying connective tissue fragility or hypermobility, this cascade may also trigger or worsen POTS and sensitization syndromes.Clinically, this interplay may manifest as exertional presyncope, coat-hanger pain, palpitations, and fluctuating fatigue, especially in patients with overlap between vascular compression syndromes, autonomic dysfunction, and post-viral sensitization.

Addressing the thoracic outlet and optimizing shoulder girdle and cervical mechanics may reduce afferent overload to the cardiac plexus, stabilize autonomic tone, and improve tolerance to activity.

Nutcracker Syndrome:

Nutcracker Syndrome involves compression of the left renal vein between the abdominal aorta and the superior mesenteric artery (SMA). This obstruction impairs venous outflow from the left kidney, causing retrograde blood flow through the gonadal and collateral veins.

It may lead to pelvic congestion, flank pain, haematuria, and has been associated with autonomic symptoms through activation of vagal afferents and spinal venous reflux. Nutcracker physiology can also impact cerebral and spinal venous return due to valveless venous systems.

Superior Mesenteric Artery (SMA) Syndrome:

SMA Syndrome is caused by compression of the third portion of the duodenum between the SMA and the aorta, typically due to loss of the intervening mesenteric fat pad.

It results in post-prandial pain, nausea, vomiting, early satiety, and weight loss. This syndrome often coexists with Nutcracker Syndrome and shares the same anatomical compression point, exacerbating gastrointestinal and autonomic dysfunction.

Median Arcuate Ligament Syndrome (MALS):

MALS arises from compression of the coeliac artery and more importantly the coeliac plexus by the median arcuate ligament of the diaphragm. Symptoms are often neurogenic and include epigastric pain, early satiety, syncope, nausea, and sympathetic overdrive.

The coeliac plexus is a dense autonomic nerve network that modulates visceral pain, vagal tone, and neuroimmune signalling. Compression leads to both mechanical vascular compromise and neurogenic inflammation.

Interrelationship and Coeliac Plexus Involvement:

Nutcracker, SMA Syndrome, and MALS often coexist anatomically and functionally. The common denominator is their impact on the coeliac plexus, which resides near the origin of these vessels.

Compression syndromes in this area result in not only vascular impedance but also aberrant autonomic signalling. Stimulation or irritation of the coeliac plexus can result in dysautonomia, gut dysmotility, postural tachycardia, and widespread pain syndromes.

Additionally, venous hypertension from Nutcracker physiology may propagate upward into the spinal venous system and exacerbate intracranial hypertension or CSF drainage resistance.

Clinical Implications:

These syndromes may present with vague or overlapping symptoms, with a functional continuum with the autonomic dysregulation from the brainstem hypoxia.

A high index of suspicion is needed in patients with unexplained abdominal pain, weight loss, autonomic dysfunction, or post-exertional flares.

Dynamic imaging, including Doppler ultrasound and CT/MR angiography in appropriate postures, is essential.

Management may include dietary modification, postural interventions, autonomic modulation, and in select cases, surgical decompression.

Integrated Clinical Applications:

Understanding the continuum between thoracic, cardiac, and abdominal plexus dysfunction provides a more cohesive framework for addressing multisystem symptoms in Long COVID, POTS, and connective tissue disorders.

Clinically, this model suggests that seemingly disparate symptoms—such as palpitations, coat-hanger pain, brain fog, exertional fatigue, and syncope—may originate from overlapping mechanical, vascular, and neuroimmune disruptions.

Key applications include:

• Consider screening for TOS and venous thoracic outlet involvement in patients with POTS and unexplained cardiac symptoms, especially when exacerbated by posture or arm movement.

• Investigate for venous compression syndromes (Nutcracker, May-Thurner) in patients with persistent fatigue, pelvic congestion, head pressure and postural hypotension.

• Recognize that brainstem hypoperfusion in these patients may be driven not only by central causes, but also by compound effects of thoracic and abdominal venous congestion.

• Incorporate postural and mechanical assessments (e.g., cervical spine alignment, shoulder mechanics, vertebral rotation at T6–T9) into routine evaluation.

• Adopt a systems-based approach to autonomic instability by layering vascular decompression, autonomic pacing, dietary histamine control, mitochondrial support, and vagal tone restoration.

  
  

By integrating mechanical, immune, and autonomic perspectives, clinicians can more effectively identify upstream contributors to dysautonomia and better personalize interventions to restore network stability.