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Coeliac Plexus in POTS : Insights into MALS, SMA and Nutcracker Syndrome in POTS

  • Writer: Graham Exelby
    Graham Exelby
  • May 24
  • 19 min read

Dr Graham Exelby, with Deborah Calleja and Michelle Hill


Abstract

Postural Orthostatic Tachycardia Syndrome (POTS) is increasingly recognized as a disorder of systemic dysautonomia, implicating both central and peripheral autonomic networks. Among the peripheral relay centres, the coeliac plexus and its associated ganglia play a crucial yet underexplored role. This paper integrates emerging anatomical, pathophysiological, and clinical evidence linking coeliac plexus dysfunction to the symptomatology of POTS, particularly in patients with overlapping mechanical syndromes such as Median Arcuate Ligament Syndrome (MALS), Superior Mesenteric Artery Syndrome (SMA), and Nutcracker Syndrome (NCS).


We propose that coeliac plexus disruption—through hypoperfusion, mechanical compression, or neuroimmune dysregulation—may mediate splanchnic vasodilation, preload failure, and systemic autonomic imbalance. Special attention is given to the interdependence between thoracic spinal segments (e.g., T8), the sympathetic chain, and neurovascular compression syndromes in perpetuating coeliac plexus pathology.

Implications for therapeutic intervention, including thoracic alignment, fascial release, and autonomic rebalancing, are discussed as part of an integrated management model.


Contents:

1.     Introduction

2.     Brainstem Hypoxia as a Central Driver of Dysautonomia

3.     Functional Continuum with Cardiac and Coeliac Plexuses

4.     Splanchnic Vaso-regulation and Preload Failure- Splanchnic Vasodilation via Parasympathetic Dysregulation: Consequences in POTS

5.     Coeliac Plexus

6.     Coeliac Ganglia -As Distinguished from Coeliac Plexus

7.     Median Arcuate Ligament Syndrome (MALS)

8.     Superior Mesenteric Artery Syndrome (SMA, Wilkie Syndrome)

9.     Nutcracker Syndrome (NCS)

10.  T8 Activation and Coeliac Plexus- a critical pathway for backpacks, rotational work and body armour

11.  The role of backpacks

12.  Integrated Physiotherapy/Osteopathy/Lymphatic Management Model in Coeliac Plexus-Associated POTS

13.  Conclusion


Introduction

Postural Orthostatic Tachycardia Syndrome (POTS), Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), and Long COVID represent a spectrum of disorders with shared autonomic, immune, and metabolic dysfunction. Central to these syndromes is brainstem hypoperfusion, which disrupts autonomic nuclei such as the nucleus tractus solitarius (NTS) and the rostral ventrolateral medulla (RVLM), leading to parasympathetic withdrawal and sympathetic overdrive. However, this central dysregulation does not occur in isolation.  This hypoperfusion triggers maladaptive autonomic responses—including baroreflex failure, sympathetic overactivation, and parasympathetic withdrawal—which cascade through interconnected anatomical networks.


The cardiac and coeliac plexuses, anatomically linked via descending thoracic sympathetic pathways and sharing vagal innervation from central nuclei, serve as key peripheral mediators.   The activation and dysfunction of the coeliac and cardiac plexuses in POTS—and particularly in patients with overlapping syndromes such as MALS, Long COVID, and trauma-induced dysautonomia are emerging as critical but under-recognized features in the complex pathophysiology of POTS.   


The coeliac plexus—situated around the origin of the coeliac trunk and the root of the superior mesenteric artery.  The coeliac ganglion has two major poles, each about 20–25 mm by 10–15 mm, and about 3–5 mm thick, which lie either side of the coeliac nerve trunk.


The coeliac plexus integrates sympathetic and parasympathetic input from T5-T12 and the vagus nerve—functions as a critical downstream hub in autonomic regulation. It governs splanchnic perfusion, adrenal secretion, gastrointestinal motility, and renal blood flow.


Importantly, mechanical changes in structure or function such as MALS, SMA, and NCS, as well as spinal segmental dysfunction (notably T8), may compound central autonomic injury by triggering local inflammation, neuroimmune activation, and perineural fibrosis. The resulting coeliac plexus dysfunction may manifest clinically as gastrointestinal dysmotility, orthostatic intolerance, and visceral pain.


Brainstem Hypoxia as a Central Driver of Dysautonomia

Persistent hypoxia is increasingly recognized as a central mechanism in the chronic neuroimmune dysfunction seen in Postural Orthostatic Tachycardia Syndrome (POTS), Long COVID, and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). At the molecular level, hypoxia triggers a cascade of inflammatory and metabolic stress signals, most notably through activation of the Receptor for Advanced Glycation End Products (RAGE). This receptor integrates signals from tissue injury, oxidative stress, and immune activation.


In parallel, neuropeptides such as Substance P, CGRP, and VIP—released from sensory and autonomic neurons—exacerbate inflammation by activating mast cells, glial cells, and endothelial cells. Together, these pathways promote blood-brain barrier breakdown, neuroinflammation, and autonomic instability.


A key feature of this model is the persistence of inflammation in brain regions critical to autonomic control (e.g., the brainstem), even after systemic recovery.  Hypoxia and its downstream immune and neurovascular effects form a self-sustaining loop—one that may explain the chronicity of symptoms across multiple systems.


Functional Continuum with Cardiac and Coeliac Plexuses

The medulla oblongata and rostral ventrolateral medulla (RVLM) in the brainstem coordinate cardiovascular, respiratory, and autonomic function. Chronic or dynamic hypoperfusion compromises neuronal viability and reflex integration.- discussed in Brainstem Hypoperfusion in POTS, CFS, Fibromyalgia, Long COVID and GWS-a Key Role (1).


The downstream consequences of brainstem hypoxia extend beyond central autonomic nuclei and permeate peripheral autonomic relay systems. Given the longitudinal continuity of the sympathetic chain and shared parasympathetic pathways, disturbances originating in the rostral medulla and nucleus tractus solitarius (NTS) can propagate functionally through spinal intermediolateral columns, ultimately manifesting as aberrant signalling in downstream plexuses.


A critical but often overlooked concept is the gastrocranial hydraulic continuum, which links abdominal venous and lymphatic congestion to central neurovascular dysfunction. In this model, mechanical or vascular compression syndromes such as Nutcracker Syndrome (NCS) or Superior Mesenteric Artery Syndrome (SMA) disrupt venous outflow from the splanchnic circulation and left renal vein.


 Given the valveless architecture of the vertebral and paravertebral venous systems, this venous congestion may propagate cranially, contributing to cerebrospinal fluid impedance, intracranial hypertension (ICH), and impaired glymphatic clearance. The coeliac plexus, anatomically and functionally proximal to these vascular bottlenecks, becomes a critical relay in this continuum—subjected to mechanical stress, neuroinflammation, and sympathetic overdrive.


This gastrocranial pathway provides a plausible mechanistic link between abdominal autonomic dysfunction, impaired venous return, and brainstem hypoperfusion observed in POTS, ME/CFS, and Long COVID. Recognition of this continuum underscores the need for integrated imaging approaches and orthostatic haemodynamic assessments when evaluating these patients


The cardiac and coeliac plexuses serve as principal nodal points within this distributed autonomic hierarchy. They relay centrally-derived signals into somatovisceral outputs—regulating cardiac contractility, vascular tone, splanchnic perfusion, adrenal output, and gastrointestinal motility.


Importantly, the structural and functional integrity of these plexuses is susceptible to both central influences (e.g., hypoperfusion-induced parasympathetic withdrawal) and regional mechanical perturbations (e.g., MALS, SMA compression, thoracic vertebral dysfunction). In syndromes like POTS and ME/CFS, the combined effect of descending sympathetic hyperactivation and vagal suppression precipitates a multilevel dysautonomia, where both cardiac and coeliac plexus dysfunction converge to shape the systemic phenotype—characterized by preload failure, postprandial hypotension, and central-peripheral mismatched autonomic tone.


There is descending sympathetic continuity along the thoracic sympathetic chain from T1–T12, with inter-ganglionic communication. The cardiac plexus governs chronotropy, inotropy, and coronary vascular tone.  It receives sympathetic innervation from T1–T4 via cervical and stellate ganglia.  Parasympathetic fibres arise from the vagus, converging near the base of the heart.


The coeliac plexus receives preganglionic sympathetic fibres from T5–T12 via greater, lesser, and least splanchnic nerves, Integrates vagal efferents and phrenic input, and modulates mesenteric, renal, and adrenal perfusion and gut motility.


Overactivity or dysfunction in the upper thoracic ganglia (affecting cardiac plexus) can propagate signals caudally, influencing the splanchnic sympathetic outflow.  This becomes highly relevant in central autonomic syndromes such as POTS, where a spinal or brainstem signal may be amplified and relayed across both cardiac and coeliac levels.

The sympathetic chain continuity permits vertical signal propagation from upper thoracic segments to abdominal plexuses.  The loss of vagal tone (from brainstem hypoperfusion) concurrently depresses parasympathetic output to both plexuses.


Splanchnic Vaso-regulation and Preload Failure- Splanchnic Vasodilation via Parasympathetic Dysregulation: Consequences in POTS

The splanchnic circulation holds up to 30% of total blood volume, acting as a dynamic capacitance reservoir.   Under sympathetic stimulation, splanchnic vasoconstriction mobilizes blood toward the heart.


Hyper-sympathetic activation of the coeliac plexus (e.g., T8 rotational injury, trauma, or spinal facilitation) can cause paradoxical splanchnic vasodilation via aberrant reflex arcs or vasopressin resistance, leading to orthostatic blood sequestration.


The coeliac plexus acts as a key relay in sympathetic outflow to the abdominal viscera.  While splanchnic sympathetic activation typically causes vasoconstriction, paradoxical splanchnic vasodilatation in POTS may occur when:

  • There is chronic sympathetic overdrive, leading to desensitization or downregulation of α1-adrenergic receptors, creating functional vasoparalysis.

  • Vagal withdrawal occurs due to:

    • Brainstem hypoperfusion (NTS/nucleus ambiguus dysfunction)

    • Baroreflex uncoupling from cardiac afferents

    • Persistent stressor activation (including RAGE-TLR4–driven neuroinflammation)

  • This imbalance allows unopposed vasodilatation in the splanchnic bed, especially postprandially or orthostatically, leading to:

    • Blood pooling

    • Preload failure

    • Orthostatic intolerance


Doppler studies by Tani et al 2000 (14 ) show increased SMA blood flow at rest in POTS, and suggests compensatory mechanisms underpin the vasodilatation and preload failure.  In POTS and similar disorders, the coeliac plexus dysregulation may lead to:


Autonomic Dysregulation

  • Hyperadrenergic states (via splanchnic sympathetic overdrive

  • Hypotension or orthostatic intolerance (due to dysregulated splanchnic vasodilation or venous pooling)

  • Gastrointestinal symptoms (nausea, bloating, early satiety), often mimicking functional GI disorders.  48% of POTS patients exhibit rapid gastric emptying, while 18% have delayed emptying.


Visceral Pain and Central Sensitization

MALS-induced plexus compression may lead to:

  • Referred epigastric pain (radiating to the back or flanks)

  • Postprandial pain, exacerbated by exercise, resulting in fear of eating and malnutrition

  • Central amplification via spinal and brainstem nociceptive circuits, contributing to central sensitization, common in POTS, fibromyalgia, and CFS.


Venous and Lymphatic Congestion

Compression of the coeliac artery and/or nearby venous structures may lead to:

  • Venous hypertension in the splanchnic circulation, enhancing abdominal pooling

  • Lymphatic stagnation, particularly when combined with thoracic duct outflow obstruction at the venous angles

  • Mast cell activation in the gut and peritoneum, further compounding neuroimmune dysfunction


Nutrient Absorption and Metabolism

Reduced perfusion and impaired autonomic coordination may impair:

  • Chylomicron trafficking via mesenteric lymphatics

  • Fat-soluble vitamin absorption and intestinal immune tolerance

  • Enteric dopamine/serotonin synthesis, linking to fatigue, dysphoria, and nausea

In this model, sympathetic dysfunction is not purely overactivity, but an unstable or “leaky” control of vascular tone due to neuroimmune and neurovascular disintegration.


Coeliac Plexus

The coeliac plexus, the largest autonomic plexus, is situated around the origin of the coeliac artery, and forms the primary autonomic relay for sympathetic and parasympathetic innervation of the splanchnic organs, including the liver, pancreas, stomach, intestines, kidneys, and adrenal glands.  In POTS, dysfunction of this plexus/ ganglia is frequently driven by mechanical compression syndromes such as Median Arcuate Ligament Syndrome (MALS) and Superior Mesenteric Artery (SMA) entrapment, which irritate the plexus directly or via altered perfusion.


This leads to aberrant splanchnic vasomotor tone, excessive catecholaminergic signalling, and maladaptive gastrointestinal symptoms such as postprandial hypotension, nausea, and bloating.


Activation from sympathetic afferents from the thoracic spine, from T5–T9—particularly via the greater splanchnic nerve at T8—may contribute to coeliac plexus overdrive, while impaired vagal balance exacerbates visceral hypersensitivity and immune dysregulation.  

The coeliac plexus is a convergence point for neuroimmune activation, with chronic inflammation and mast cell infiltration perpetuating a feed-forward loop of autonomic dysfunction. In this context, the coeliac plexus acts as a visceral amplifier of dysautonomia, linking abdominal vasoplegia (low systemic vascular resistance, where vessels are dilated, a well-known complication after cardiac surgery (Omar et al 2015 (2)), immune perturbation, and central autonomic instability in POTS pathogenesis.  


Coeliac Plexus -Anatomy and Function

The coeliac plexus—also known as the solar plexus—is a dense network of autonomic nerves situated around the origin of the coeliac trunk, just below the diaphragm, and anterior to the aorta at approximately the level of T12–L1.   It includes a number of smaller plexuses- the hepatic plexus, splenic plexus, gastric plexus, pancreatic plexus and suprarenal plexus.  Others derived from the coeliac plexus include the renal plexus, testicular/ovarian plexus and superior mesenteric plexus.  It comprises both sympathetic fibres (from greater, lesser, and least splanchnic nerves) and parasympathetic fibres (mainly from the vagus nerve).


Figure 1. The coeliac ganglia with the sympathetic plexuses of the abdominal viscera radiating from the ganglia


Source. Henry Vandyke Carter, Public domain, via Wikimedia Commons. https://upload.wikimedia.org/wikipedia/commons/6/63/Gray848.png


The plexus communicates bilaterally with the adrenal medulla, renal plexus, mesenteric ganglia, and the aorticorenal and intermesenteric plexi. It governs mesenteric, splanchnic, adrenal, renal, and gastric function, forming the abdominal sympathetic outflow.  It receives:

  • Preganglionic sympathetic input from the greater splanchnic nerves (T5–T9), lesser (T10–T11), and least splanchnic nerves (T12).

  • Parasympathetic vagal branches and fibres from the phrenic nerve.


Figure 2. Lower Half of Right Sympathetic Cord

Source. Henry Vandyke Carter, Public domain, via Wikimedia Commons. https://commons.wikimedia.org/wiki/File:Gray849.png


Figure 3.  Diagram of Efferent Sympathetic Nervous System

Source. Henry Vandyke Carter, Public domain, via Wikimedia Commons.

 

Coeliac Ganglia-As Distinguished from Coeliac Plexus

The coeliac ganglia two discrete aggregations of neuronal cell bodies within the plexus; one on each side of the aorta at the level of the diaphragmatic crura.  They are the main sympathetic relay stations, receiving splanchnic input and modulating outflow to upper abdominal viscera.  They are histologically composed of neuronal cell bodies and satellite glial cells, surrounded by a dense fibrous capsule.


In chronic compression (e.g., MALS), this region is subject to:

  • Neuroinflammatory changes

  • Fibrotic encapsulation

  • Wallerian degeneration of postganglionic fibres

  • Perineural fibrosis, especially along the exiting fibres to the SMA and renal plexuses.


Distinguishing between coeliac plexus dysfunction and coeliac ganglia dysfunction is essential in refining the pathophysiological model of Nutcracker Syndrome (NCS)-associated autonomic instability in POTS and immune-neurovascular dysregulation. Both terms are often used interchangeably in literature, but from a neuroanatomical and pathophysiological standpoint, they denote distinct yet interrelated levels of dysfunction. (Mehr et al 2018 (13))


The dense fibrotic changes around the ganglia, rather than just the general plexus, are thought to be key drivers of:

  • Autonomic dysregulation

  • Sympathetic vasoconstriction

  • Visceral hypersensitivity and referred pain


The functional impact—including sympathetic dysautonomia, visceral pain, and vascular dysregulation—derives from ganglion-centric pathology, not diffuse fibrotic changes across the entire plexus.  Vagal nerve stimulation may rebalance input in the coeliac plexus, but not in the ganglia.


Table 1: Differentiating Coeliac Plexus and Ganglia


Feature

Coeliac Plexus

Coeliac Ganglia

Definition

A large autonomic nerve plexus surrounding the coeliac trunk, SMA, and renal arteries

Two discrete aggregations of neuronal cell bodies within the plexus; one on each side of the aorta

Composition

Network of preganglionic and postganglionic fibres, both sympathetic and parasympathetic

Mostly sympathetic postganglionic neurons, receiving input from thoracic splanchnic nerves

Function

Integrates autonomic control to viscera of upper abdomen (stomach, pancreas, liver, kidneys, intestines)

Acts as the primary relay centre for sympathetic output to upper abdominal organs

Innervation

Sympathetic: greater, lesser, least splanchnic nerves; Parasympathetic: vagus nerve (posterior trunk)

Mainly receives input from preganglionic splanchnic fibres (T5–T12)

Clinical Targeting

Coeliac plexus block (CPB) targets nerve transmission in the plexus

Neurolytic procedures may specifically target the ganglia in chronic pain or neoplastic syndromes

Dysfunction Implication

Impaired integration of reflexes, gut dysmotility, baroreflex failure, visceral pain

Disinhibition or hyperactivation of sympathetic efferents, triggering vasoconstriction, gut ischemia, pain


Median Arcuate Ligament Syndrome (MALS) 

The Coeliac Artery (or Coeliac Axis or Coeliac Trunk) is a major artery in the abdominal cavity supplying the foregut.   Arising from the Aorta, it branches into the Left Gastric Artery, Splenic Artery and Common Hepatic Artery.   When visualized on ultrasound, which would show displacement and variable narrowing of the Coeliac Axis, it is an indirect sign of compression of the over-riding Coeliac Ganglion.


The median arcuate ligament  is the fibrous arch that unites the diaphragmatic crura forming the anterior arc of the aortic hiatus.  The coeliac trunk is a major branch of the abdominal aorta, originating anteriorly near the level of the diaphragm and usually in close proximity to the median arcuate ligament.  There is considerable variation in positioning of both the coeliac trunk and the diaphragm.  In some, the ligament is positioned more inferiorly relative to the coeliac artery, resulting in compression. The degree of compression typically varies with respiration, most accentuated during end-expiration when the two structures move closer together.( Gaillard et al (3))  Others include where the coeliac artery originates higher than usual from the aorta.(Upshaw et al 2023 (4))


Median Arcuate Ligament Syndrome is caused by compression of the coeliac ganglion, a web of nerves in the upper abdomen located immediately below the diaphragm.   Arching over the aorta is the arcuate ligament.  Movement of the diaphragm while breathing may irritate the coeliac ganglion leading to pain and autonomic symptoms.(5)

 

The distinction between coeliac ganglion and coeliac plexus in the context of MALS (Median Arcuate Ligament Syndrome) has historically been blurred, but anatomically and functionally, the differentiation is crucial—and the literature does indeed vary in its terminology depending on the author’s focus (vascular surgery vs neurology vs autonomic science).

 

There are both vascular and neurogenic symptoms from the compression, vascular compression potentially causing reduced blood flow to abdominal organs, and intimal hyperplasia and stenosis of the coeliac artery lumen.  Neurogenic compression of the coeliac ganglia may affect neural control of digestion, delayed gastric emptying and disordered autonomic activity.(4)    Sympathetic excitation, and mesenteric vasospasm may create a functional splanchnic underfill state despite adequate volume.


Beyond ischaemic compression of the artery, a critical feature of MALS is direct irritation or compression of the coeliac ganglia, inducing splanchnic dysmotility, chronic sympathetically-mediated visceral pain syndrome and may become source of cardiac arrythmia. This neuropathic component is often underappreciated.(Mehr et al 2018 (13))


Repeated mechanical stress from the ligament may incite neuroinflammation, and potentially periganglionic mast cell activation, perpetuating pain and autonomic instability.  Fibrosis is often described as affecting the plexus but the fibrosis is more precisely localized to the peri-ganglionic region, the tissue encasing the coeliac ganglia which are structurally embedded within the broader plexus.


Figures 4,5. Median Arcuate Ligament Compression



Courtesy of Dr Matt Skalski, <a href="https://radiopaedia.org/?lang=us">Radiopaedia.org</a>. From the case <a href="https://radiopaedia.org/cases/36837?lang=us">rID: 36837</a>



Courtesy of Domenico Nicoletti, <a href="https://radiopaedia.org/?lang=gb">Radiopaedia.org</a>. From the case <a href="https://radiopaedia.org/cases/45205?lang=gb">rID: 45205</a>


Symptoms may include, and not always associated with intake of food, are clearly related to autonomic dysfunction.  It is very commonly misdiagnosed as an eating disorder, but a sound history will usually elucidate the problem.  The pain can often be relieved by positional changes, eg standing, and aggravated by lying.  Symptoms may include:

  •  Abdominal pain below the sternum which sometimes radiates like a belt or even into the chest

  • Loss of appetite

  • Rapid fullness while eating

  • Weight loss

  • Syncope and pre-syncope

  • Sweating

  • Tachycardia

  • Short-lived bouts of diarrhoea.(Scholbach (5))


Functional Links Between MALS and the Coeliac Plexus

The coeliac plexus lies directly adjacent to the coeliac trunk and superior mesenteric artery—a known compression point in MALS.


Compression by the median arcuate ligament (especially during expiration) results in:

  • Ischaemia of splanchnic autonomic nerves.

  • Mechanical neuropathic irritation or chronic afferent barrage from plexal afferents.

  • Coactivation of adrenal medullary output (via splanchnic nerves), triggering catecholamine surges and sympathetic overdrive.


Feedback Amplification:

Chronic nerve irritation likely initiates central sensitization in brainstem–hypothalamic circuits, including:

  • Nucleus of the Solitary Tract (NTS)

  • Paraventricular Nucleus (PVN)

  • Locus Coeruleus (LC) → These circuits are heavily connected to the coeliac-cardiac axis through both afferent vagal and efferent sympathetic links.


Superior Mesenteric Artery Syndrome (SMA, Wilkie Syndrome)

The Superior Mesenteric Artery Syndrome (SMA) is compression of the 3rd part of the duodenum between the abdominal aorta and the superior mesenteric artery, and is an unusual cause of proximal intestinal obstruction.  Duodenal compression is usually due to the loss of the intervening mesenteric fat pad between the aorta and SMA, which in turn, results in a narrower angle between the vessels. The fat pad cushion functions to hold the SMA off the spine and protect it from duodenal compression.(Van Horne & Jackson 2023 (6))


SMA compression is usually accompanied by left renal vein compression and may have a Nutcracker and/or Pelvic Congestion Syndrome.   The Nutcracker is sometimes postural, and may not be seen on supine CTv, requiring dynamic ultrasounds for confirmation, as frequently only in an erect posture.


The SMA may compress the third part of the duodenum (Wilkie's syndrome) or left renal vein (Nutcracker syndrome), both of which may mechanically disrupt venous return, splanchnic drainage, or lymphatic outflow, indirectly aggravating plexus irritation or perfusion instability.


The SMA shares autonomic integration via the superior mesenteric ganglion, which lies just inferior to the coeliac ganglia, and is thus functionally linked in POTS-related dysautonomia through: It may indirectly compress the superior mesenteric plexus, disrupting gut-derived autonomic feedback.

  • Impaired splanchnic pooling regulation

  • Dysfunctional baroreceptor modulation of GI perfusion

  • Reduced gut motility (via extrinsic autonomic dysfunction)

Figure 6. Compression of Left Renal Vein and Duodenum in Superior Mesenteric Artery Syndrome (SMA)



Source: courtesy Dr Zane Sherif. Mermaid Beach Radiology

 

Symptoms are usually vague and non-specific, and can be acute or gradual and is commonly misdiagnosed as an eating disorder.   They may include:

  • Epigastric pain

  • Nausea

  • Vomiting

  • Abdominal distension

  • Weight loss

  • Early satiety

  • Post-prandial pain worse in supine position

 

Initial treatment is usually conservative.  IV fluids and sometimes nasogastric tube feeding may be required when severe.   Conservative treatment is aimed at restoring the fat pad.   It is likely that many of the young teen POTS that “grow out of it” after 2 years reflect an SMA and with increased age, an increase in the fat pad.  This is complicated with continuing weight loss and poor diagnoses of eating disorders which increases stress on the patient and not uncommonly leads to PTSD.

 

Nutcracker Syndrome (NCS)

 The Nutcracker phenomenon is an entrapment of the left renal vein between the aorta and the superior mesenteric artery.    It is seen frequently in young girls, young and slender women, pregnant women, people with soft connective tissue and overweight people.   Within this angle between the aorta and the superior mesenteric artery runs the left renal vein and the duodenum.

 

Figure 7.  Compression of Left Renal Vein between Superior Mesenteric Artery and Aorta (Nutcracker)

Source: courtesy Dr Zane Sherif. Mermaid Beach Radiology (Spectral CT)


The blood flow in the left renal vein becomes obstructed, blocking the outflow from the left kidney. Its blood is then forced into tributaries that normally bring blood from their organs towards the left renal vein. This sets these organs under pressure, they swell, their vessels become engorged and the walls of these vessels react with an inflammation. These so called collateral vessels enlarge and go baggy, become varicose veins, which are painful.  As Schonbach (5) describes, these fill other collateral vessels, including the spinal venous plexus, thus linking the head and neck to the abdominal “drivers” in POTS and chronic fatigue.

 

NCS compression may lead to:

  • Renal venous hypertension

  • Pelvic venous congestion (due to collateral flow especially the gonadal and adrenal veins)

  • Orthostatic intolerance (via underfilling)

  • Haematuria and flank pain

  • Left-sided varicocele in males, and pelvic congestion in females

  • Vertebral and paravertebral venous congestion which can cause Intracranial Hypertension (Scholbach (5))


Anatomical and Functional Links Between Nutcracker Syndrome and the Coeliac Plexus

In the evolving pathophysiology model of preload failure, central hypoperfusion, and autonomic dysregulation in POTS, Nutcracker syndrome may:

  • Act as a peripheral hydraulic disruptor that secondarily activates coeliac plexus dysfunction.

  • Promote a low-flow gut state, augmenting postprandial splanchnic pooling and worsening orthostatic tolerance.

  • Contribute to the sympathetic surges, nausea, vasoconstriction, and GI distress characteristic of hyperadrenergic POTS subtypes.


The Nutcracker Syndrome may initiate ganglion/plexus-level dysfunction through mechanical and vascular stress. Over time, repetitive inflammatory stimulation, oxidative damage, or RAGE/TLR4-mediated mechanisms may lead to structural or biochemical changes within the ganglia themselves, transforming a network dysregulation into a nodal pathology.


This shift is critical in chronic POTS or ME/CFS cases where:

  • Pain becomes fixed and sympathetically maintained

  • Splanchnic circulation becomes hypoperfused despite adequate cardiac output

  • Increasing central sensitization, likely via persistent afferent bombardment from dysfunctional ganglia


T8 Activation and Coeliac Plexus- a critical pathway for backpacks, rotational work and body armour

Another factor that may impact on “apparent clinical resolution” in teens with POTS comes from the increasingly heavy poorly fitted backpacks worn by this age group.   I believe this is also a factor in the use of military armour and similar causes.


Thoracic Sympathetic Anatomy at T8

  • Preganglionic fibres emerge from the intermediolateral column of the spinal cord at T5–T12 and form the greater (T5–T9), lesser (T10–T11), and least (T12) splanchnic nerves.

  • At T8, the sympathetic fibres predominantly travel through the greater splanchnic nerve, synapsing in the coeliac ganglion.

  • These fibres modulate:

    • Arteriolar vasoconstriction in the splanchnic bed

    • Visceral smooth muscle tone

    • Enteric blood flow, motility, and neuroimmune interaction (e.g., mast cells and enteric glia)

  • Musculoskeletal or postural activation (e.g., vertebral rotation, mechanical stress, or thoracic outlet-type compression at T8) can hyperactivate these fibres or cause segmental irritation of the sympathetic chain.


Impact on the Coeliac Plexus: Hyperactivation and Crosstalk

T6-T9 spinal segments house sympathetic preganglionic neurons (SPNs) that regulate splanchnic circulation (blood flow to abdominal organs) via the greater splenic nerve and coeliac ganglion.  


Repetitive thoracic rotation (e.g., in dental assistants or teachers) may cause mechanical irritation or misalignment at T8, leading to:

  • Sympathetic hyperexcitability - Loss of descending inhibitory control over SPNs, resulting in exaggerated sympathetic reflexes (Wulf & Tom 2023 (7)

  • Impaired splanchnic vasoconstriction- Disrupted regulation of gut blood flow, contributing to orthostatic blood pooling. (Stewart et al 2005 (8))(Stewart et al 2005 (9))


The role of backpacks

The impact of added weight eg backpacks in children, and body armour in soldiers and police is at present largely speculative, but there is a strong clinical correlation, with clinical findings of backpacks both activating and driving POTS.  These findings are hypothesized based on clinical and biomechanical modelling.


Backpacks exceeding 10-15% of a child’s body weight alter spinal alignment, increasing forward head posture, thoracic kyphosis, and lumbar flexion. (Suri et al 2019 (7)) (Ramprasad et al 2009. (10))     This associated with reduced craniovertebral angles (eg head protrusion) at loads ≥15% body weight, (Ramprasad et al 2009. (10)) and increased compressive forces on the lumbar spine (up to 64% at 30% body weight).


Asymmetric loading (common in single-strap use) may induce thoracic rotation, potentially irritating T6-T9 sympathetic ganglia. (Ahmed et al 2024 (11))

Pain and autonomic crossover- 50-63% of children report musculoskeletal pain from backpacks, (Ahmed et al (11)) which may sensitize central pain pathways and amplify autonomic symptoms. (Perrone et al 20198 (12))


Sympathetic activation from T8 and adjacent segments feeds directly into the coeliac ganglion, increasing noradrenergic output to:

  • Mesenteric vessels (leading to systemic shunting or dysregulated GI perfusion)

  • Adrenal medulla (amplifying circulating catecholamines)

  • Spleen (modulating immunological tone)

  • Pancreas and liver (altering glucose and metabolic homeostasis)


Chronic overactivation or irritation (e.g., from scoliosis, vertebral misalignment, or inflammatory mediators at this level) may lead to:

  • Neuroplastic changes within the coeliac plexus

  • Neuroimmune activation (including macrophage and mast cell infiltration)

  • Periganglionic fibrosis or axonal hypersensitivity, perpetuating dysfunction even without ongoing mechanical insult


Integrated Physiotherapy/Osteopathy/Lymphatic Management Model in Coeliac Plexus-Associated POTS

An integrated physiotherapy/osteopathy/lymphatic approach to coeliac plexus-related POTS must target the mechanical, autonomic, and circulatory contributors that underlie symptom persistence. The model begins with postural and biomechanical screening, focusing on thoracic vertebral rotation (especially at T6–T9), thoracic outlet compression, diaphragmatic excursion, and evidence of compensatory cervical or lumbar strain. Manual therapies should aim to decompress the T8–T12 sympathetic axis, reduce myofascial tension overlying the diaphragmatic crura, and restore thoracoabdominal mobility—thus alleviating mechanical stress on the coeliac ganglion.


Neuromodulation strategies, including diaphragmatic breathing, vagal stimulation (e.g., via taVNS or slow-controlled breathing), and autonomic retraining, may help rebalance sympathetic-parasympathetic tone across the cardiac and coeliac plexuses. Kikko-Matsumoto acupuncture can play a vital role in reducing sympathetic overactivity, and reducing sensitisation.  Where appropriate, graded compression or decompression garments may be trialled to modulate venous return and reduce splanchnic pooling during upright activity.


Therapeutic exercise should incorporate proprioceptive control and spinal alignment training, progressing to dynamic anti-gravity loading as autonomic stability improves. Recognizing the interlink between lymphatic congestion and venous insufficiency, lymphatic drainage techniques and thoracic duct activation may also be valuable adjuncts. Crucially, therapist input must integrate with medical assessment of mechanical compression syndromes (MALS, SMA, NCS) and guide onward referral where surgical decompression is indicated.


Conclusion

The coeliac plexus serves not only as a peripheral relay in visceral regulation but as a dynamic participant in a broader neurovascular and neuroimmune continuum that spans from the abdominal splanchnic vasculature to the brainstem. In this integrated model, dysfunction in the coeliac plexus—through mechanical compression, vascular congestion, or neuroimmune activation—can feedback upon central autonomic centres, particularly under orthostatic stress or preload failure.


The gastrocranial hydraulic continuum highlights how venous obstruction below the diaphragm may propagate cranially, compromising vertebral and cranial venous outflow, impairing glymphatic clearance, and triggering intracranial hypertension.

Crucially, these haemodynamic and neuroimmune disruptions converge upon the medullary centres—particularly the NTS and RVLM—where hypoperfusion leads to parasympathetic withdrawal and sympathetic overactivation. This perpetuates a pathological loop of dysautonomia that is expressed clinically as fatigue, orthostatic intolerance, gastrointestinal dysmotility, and central sensitization.


Thus, POTS should not be viewed solely as a disorder of cardiac chronotropy but as a systemic failure of autonomic homeostasis spanning the sympathetic chain, vagal nuclei, and peripheral relay plexuses. Therapies aimed at restoring structural, hydraulic, and neuroimmune balance—through musculoskeletal correction, acupuncture, vagal modulation, and targeted immune regulation—are essential to breaking this continuum and restoring autonomic integrity.


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