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Median Arcuate Ligament Syndrome: Navigating Diagnostic Uncertainty and Multidisciplinary Management - A Narrative Revie

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20 September 2026

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20 September 2026

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Abstract
Median Arcuate Ligament Syndrome (MALS) is characterised as an intra‑abdominal vascular compression syndrome in which the caudad migration of the Median Arcuate Ligament (MAL) impinges the coeliac artery and/or coeliac plexus, causing foregut ischaemia, neuropathic pain and dysautonomia. Clinically, MALS can present with postprandial epigastric pain, weight loss, nausea, vomiting, upper abdominal bloating and dysautonomia. Its common comorbidities are Postural Orthostatic Tachycardia Syndrome (POTS), Ehlers-Danlos syndrome (EDS), Mast Cell Activation Syndrome (MCAS), other abdominal vascular compression syndromes such as nutcracker and Superior Mesenteric Artery Syndrome (SMA), along with anxiety, and functional gastrointestinal disorders. Surgical decompression of the median arcuate ligament, with or without coeliac plexus intervention or endovascular stenting, can provide meaningful pain reduction and functional improvement; however, postoperative symptom recurrence, persistent dysautonomia and variable long‑term outcomes are common.This narrative review synthesises current evidence on MALS pathophysiology, symptom presentation, diagnostic imaging and management, with a particular focus on autonomic dysfunction and the emerging role of osteopathic and manual therapies. It highlights the current knowledge gap regarding autonomic pathophysiology and conservative non-surgical care in MALS, as only a limited number of case reports and series systematically assess dysautonomia or evaluate osteopathic and manual therapy. This paper aims to critically assess vascular, neurogenic, connective‑tissue, and autonomic mechanisms, evaluate current diagnostic and surgical pathways with an autonomic nervous system focus, and examine the theoretical rationale and preliminary clinical data for osteopathic and manual therapies as adjunctive or non-invasive options, thereby outlining priorities for future multimodality, phenotype‑based management and research.
Keywords: 
median arcuate ligament syndrome
;  
coeliac artery compression
;  
coeliac plexus compression
;  
manual therapy
;  
osteopathic manipulation
Subject: 
Medicine and Pharmacology  -   Complementary and Alternative Medicine

Strengths and Limitations of This Study

  • This review synthesises a broad and clinically important literature on median arcuate ligament syndrome (MALS) with a specific, currently underexplored focus on autonomic nervous system involvement and the emerging role of osteopathic and manual therapy.
  • The search strategy drew on nine databases (PubMed, Cochrane, EBSCOhost, PEDro, ScienceDirect, BMJ, SpringerLink, Wiley Online Library, BMJ and SAGE), spanning several decades of literature.
  • As a narrative rather than systematic review, study identification and selection were not duplicated by independent reviewers or formally quality-appraised, and the review is therefore susceptible to selection and publication bias favouring positive surgical outcomes.
  • The evidence specifically supporting osteopathic and manual therapy in MALS is limited to isolated case reports and small case series with heterogeneous techniques, unclear dosing, and no validated, standardised outcome measures, so conclusions about efficacy remain preliminary.
  • Reporting of autonomic nervous system assessment across the reviewed literature is inconsistent and often absent, limiting this review’s ability to draw firm conclusions about autonomic mechanisms or treatment effects in MALS.

Introduction

Median Arcuate Ligament Syndrome (MALS), also known as coeliac artery compression syndrome, Dunbar syndrome, and coeliac axis syndrome, is an intra-abdominal vascular compression syndrome characterised by extrinsic impingement of the coeliac artery and/or coeliac plexus due to caudad migration of the median arcuate ligament. The median arcuate ligament (MAL) is a fibrous band formed by the medial tendinous fibres of the diaphragmatic crura that crosses anterior to the aorta, forming the aortic hiatus, at approximately T12 to L1. Commonly, this is superior to the coeliac trunk origin. In some individuals, anatomical variants such as a relatively high coeliac trunk, low median arcuate ligament, thickened ligamentous tissue or atypical branching of the coeliac axis can create compression at the coeliac artery and surrounding plexus. Structures close to this region include the thoracic duct, azygos venous system, cisterna chyli and the dense autonomic coeliac plexus, making the coeliac axis a clinically important neurovascular and lymphatic junction [1,2].
In MALS, the clinical challenge is that anatomical compression alone does not define the syndrome. Radiological evidence of coeliac artery compression has been reported in 10-24% of asymptomatic populations, and in selected cohorts at higher rates, while the estimated clinical incidence of symptomatic MALS is much lower at 2 per 100,000 people [3,4,5,6]. This discrepancy explains why MALS remains diagnostically contested. Patients may have marked imaging findings with few symptoms or disabling symptoms with only modest stenosis. Therefore, MALS is better understood as a clinical syndrome in which compatible symptoms, exclusion of common gastrointestinal and vascular disorders, dynamic imaging and the broader autonomic phenotype must be interpreted together.
Clinically, MALS presents with a heterogeneous group of symptoms that closely overlap and mirror more common gastrointestinal and autonomic disorders such as gastroparesis, gastroesophageal reflux disease, biliary pathology, Helicobacter pylori infection, peptic ulcer disease, and inflammatory bowel disease, which complicates recognition and contributes to frequent misdiagnosis [7,8]. These more common features include postprandial and epigastric pain, nausea, vomiting, weight loss, anorexia and abdominal, especially upper quadrant bloating [1,3,4,5,6]. Often these symptoms are attributed to foregut ischaemia, with an impaired haemodynamic response of the coeliac axis following gastric stimulation demonstrated in affected individuals [9,10]. In addition, involvement of the coeliac plexus may produce features of autonomic dysregulation, also known as dysautonomia, including orthostatic intolerance, tachycardia, gastrointestinal dysmotility, and fatigue.
MALS also appears to occur within a broader multisystem phenotype. The co-occurrence of MALS with conditions such as Postural Orthostatic Tachycardia Syndrome (POTS), Ehlers-Danlos Syndrome (EDS), Mast Cell Activation Syndrome (MCAS), other functional gastrointestinal disorders and intra-abdominal vascular compressions such as Nutcracker and Superior Mesentery Artery Syndrome (SMA) further complicate clinical interpretation [6,9,11]. Psychiatric conditions, such as panic disorder, post-traumatic stress disorder, and particularly anxiety and depression, are common and often secondary to chronic abdominal pain and dysautonomia [12,13]. There is a marked female predominance noted across both adult and paediatric cohorts, comprising approximately 73-94% of cases, though the reasons for this disparity remain unclear [4,6,11,14,15]. These features support a biopsychosocial and multisystem model rather than a purely structural vascular model.
The objective of this narrative review is to describe the clinical presentation, diagnostic phenotypes and challenges, management of Median Arcuate Ligament Syndrome, highlight common co-morbidities and examine the contribution of autonomic nervous system dysfunction to symptom persistence, while exploring the theoretical and emerging clinical rationale for manual therapy as part of multidisciplinary care.

Methods

This narrative review drew on English-language literature identified through searches of PubMed, Cochrane, EBSCOhost, PEDro, ScienceDirect, BMJ, SpringerLink, Wiley Online Library and SAGE, from 1953 to June 2026. Search terms and subject headings included combinations of ‘median arcuate ligament syndrome’, ‘coeliac artery compression’, ‘Dunbar syndrome’, ‘paediatric’, ‘surgical outcomes’, ‘treatment’, ‘manual therapy’ and ‘osteopathic’. Reference lists of relevant reviews and key articles were also screened to identify additional studies. Included literature comprised narrative and systematic reviews, observational studies, surgical outcome studies, case reports, case series and relevant anatomical or mechanistic literature. Findings were synthesised narratively around four themes: clinical features and diagnosis, treatment options, autonomic nervous system involvement, and the potential role of osteopathic/manual therapy.

Diagnosis and Clinical Phenotype

Median arcuate ligament syndrome is traditionally diagnosed using Doppler ultrasound, computed tomography with contrast, also known as Computed Tomography Angiography (CTA), multidetector computed tomography, or magnetic resonance angiography [1,16]. Evaluation is multifactorial which includes imaging to demonstrate compression at the proximal end of the coeliac artery during deep respiration [5]. In the expiratory phase, caudad displacement of the median arcuate ligament accentuates extrinsic compression of the coeliac trunk, producing a rise in peak systolic flow velocity within the vessel. During inspiration, cranial excursion of the ligament diminishes this compression, permitting relative normalisation of coeliac arterial haemodynamics. This respiratory dependent change in coeliac stenosis and flow helps rule in MALS with the peak systolic velocity (PSV) ≥ 200 cm/sec and an end diastolic velocity (EDV) ≥55 cm/sec on Doppler being reported as a threshold for hemodynamically significant stenosis [14,17].
While there is no universally accepted diagnostic criterion set for MALS, it is diagnosed radiologically, incorporating clinical symptoms, exclusion of other causes, and compatible vascular imaging. In a subset of patients with MALS, compensatory vasodilation distal to the stenotic segment resulted in characteristic post-stenotic dilatation [18,19]. Additional positive findings on CT, MRA, and US imaging include focal narrowing of the proximal coeliac artery commonly accompanied by the inferior displacement of the median arcuate ligament, which gives rise to the distinctive ‘hook’ shape. These additional anatomical variations are not required for a positive MALS diagnosis [20,21]. MALS compressions are best visualised in the sagittal plane and may be missed on axial views. The hooked contour helps distinguish this condition from atherosclerotic narrowing. Other diagnostic signs include post-stenotic dilatation of the coeliac artery and its branches, and accessory collateral vascular formation from the superior mesenteric artery to support arterial flow. A median arcuate ligament thickness exceeding 4 mm is also medically considered abnormal [22]. Clinically, the most useful question is not simply whether coeliac compression is present, but whether the patient’s symptoms, respiratory-dependent imaging findings, autonomic profile and exclusion of alternative diagnoses form a coherent syndrome. This is particularly important before recommending high-risk invasive procedures or, conversely, before dismissing symptomatic patients whose imaging appears only moderate.

Treatment Options

Surgical

Surgical treatment for MALS aims to fully decompress the coeliac artery, restore stable blood flow, and reduce both neuropathic pain and any secondary aneurysmal disease risk. Decompression is achieved by dividing the median arcuate ligament and associated fibrotic tissue around the coeliac axis, often combined with coeliac ganglionectomy or neurolysis when neurogenic pain is suspected. Surgical release may be performed through open, laparoscopic or robotic approaches and may be combined with coeliac ganglionectomy, neurolysis, coeliac plexus intervention or subsequent endovascular treatment when residual stenosis persists [11,18,19,23,24]. Laparoscopic release is now widely used and has been associated with shorter hospital stay and fewer major perioperative complications than open surgery in some series, while robotic release offers enhanced visualisation and dexterity around the coeliac axis but has limited and mixed comparative evidence [25,26,27]. Surgical outcomes are generally favourable but variable. The systematic review by Metz et al. (2022), which included adult and paediatric surgical and coeliac plexus block studies, reported symptom improvement in more than 70% of many surgical series, although the evidence was largely observational, heterogeneous and often at unclear risk of bias [11].
Surgical intervention for MALS is not without its risks or side effects. Fernstrum et al. (2020) conducted a 5-year follow-up of 27 patients and showed that 24% had symptom recurrence after initial resolution, with 8% requiring repeat surgical intervention (28). “Similarly, in a retrospective cohort of 41 patients undergoing open, laparoscopic, or robotic median arcuate ligament release, 82.9% reported overall clinical improvement; persistent pain was reported by 5 patients (12.2%), and pain recurred in 13 of 36 patients with follow-up (36.0%)”. Proposed explanations for suboptimal outcomes include residual coeliac or visceral artery stenosis, incomplete division of the ligament, secondary periarterial fibrosis, or irreversible arterial wall damage after prolonged compression. Complications from open surgery included persistent pain, postoperative thrombosed bypass graft with stroke, gastroesophageal reflux disease, pancreatitis, hemothorax, and splenic infarction. Other complications arising from the laparoscopic approach include coeliac artery bleeding, pneumothorax, aortic puncture, phrenic artery laceration, and gastric artery bleeding [29].

Conservative and Rehabilitation Strategies

Rehabilitation strategies are underreported in the literature. Management of MALS is likely to be optimised within a multidisciplinary model of care that includes vascular surgery, gastroenterology, pain medicine, psychology, autonomic assessment, nutrition, osteopathic or other manual therapy. The need for this broader approach is strongest in patients with dysautonomia, EDS, MCAS, persistent postoperative pain, deconditioning, food fear, anxiety, depression or overlapping vascular compression syndromes. Surgery may reduce mechanical compression, but it may not fully reverse central sensitisation, autonomic instability, gastrointestinal dysmotility or musculoskeletal adaptations developed during prolonged illness. Therefore, MALS management may need a multimodal pathway rather than a single procedure. Nutritional support may be required when food avoidance, early satiety or weight loss is prominent. Pacing and graded activity are also relevant because prolonged symptoms, orthostatic intolerance and fear of symptom flares may reduce physical capacity. Psychological support is not an implication that symptoms are non-organic; rather, it recognises that persistent abdominal pain, diagnostic uncertainty, misdiagnosis and repeated investigations can amplify distress and disability.

MALS and the Autonomic Nervous System

MALS can disturb autonomic regulation at the coeliac axis through interacting vascular and neurogenic mechanisms, which likely coexist from early in the disease process rather than acting in isolation. The coeliac plexus receives sympathetic input from the thoracic splanchnic nerves and parasympathetic input from the vagal trunks, coordinating vasomotor tone, motility, and nociception for foregut-derived viscera [4,24]. A caudal or thickened median arcuate ligament may chronically compress the coeliac artery and coeliac plexus, providing recurrent mechanical irritation. Histopathological series of resected coeliac ganglia in MALS show perineural inflammation, fibrosis, and small-fibre proliferation, supporting a neuropathic and autonomic contribution alongside haemodynamic factors [7,30]. Mechanistically, this has been compared to maladaptive autonomic reflex patterns, in which heightened peripheral afferent input may drive an exaggerated sympathetic outflow and impaired parasympathetic function [24]. In MALS, abnormal afferent signalling from sensitised coeliac ganglia and splanchnic nerves may contribute to increased sympathetic tone, altered vasomotor control, disordered gastrointestinal motility, and reduced thresholds for visceral pain [30,31]. Clinically, this mixed neurogenic-vascular model aligns with MALS symptoms such as postprandial epigastric pain, upper-predominant bloating, nausea, vomiting, early satiety, weight loss, constipation, gastroparesis-like symptoms, and conditioned food avoidance [32].
Classically, MALS has been described as an intrabdominal vascular compression syndrome in which expiratory coeliac artery narrowing limits postprandial hyperaemia and predisposes to foregut ischaemia. However, diagnostic imaging and surgical series demonstrate inconsistent correlation between the degree of anatomical stenosis and symptom severity, with some highly symptomatic patients showing only mild narrowing and others with marked stenosis remaining minimally symptomatic [6,33,34]. In parallel, surgical outcome studies suggest that symptom improvement may relate more closely to coeliac ganglionectomy or extensive neurolysis than to restoration of arterial calibre alone, and that patients with pronounced perineural fibrosis may exhibit more prominent neuropathic and autonomic features pre-operatively [24,35]. Together, these findings support an emerging mixed vascular-neurogenic model in which ischaemia, autonomic dysregulation, and central sensitisation each contribute to the clinical presentation.
Visceral afferents from the foregut travel with sympathetic fibres in the thoracic splanchnic nerves to the thoracic spinal cord, where they converge with somatic inputs and may cause central sensitisation, diffuse and poorly localised pain [26,33,36]. This tissue anastomosis may help explain typical epigastric pain radiating to the back or flanks, as well as less common patterns involving the chest, neck, or temporomandibular region [37]. Observational and survey data in abdominal vascular compression syndromes also demonstrate frequent co-occurrence of POTS, EDS, and MCAS. These associations are largely derived from cross-sectional data, suggesting a broader systemic phenotype characterised by connective tissue laxity, altered extracellular matrix structure, susceptibility to multiple vascular compression syndromes, and baseline autonomic vulnerability, highlighting the somato-visceral reflex. In this context, MALS may act as a contributing or exacerbating factor in dysautonomia rather than a singular causal mechanism in all cases [24,30,31].
Diaphragmatic motion and the median arcuate ligament are mechanically coupled, such that the respiratory cycle dynamically modifies compression of the coeliac artery and plexus. During expiration, cephalad diaphragmatic motion increases extrinsic compression of the coeliac trunk, which may also irritate adjacent celiac plexus structures, whereas inspiration may partially decompress this impingement. These changes can be seen on dynamic Doppler ultrasound and CT angiography [20,22,38]. Given this significant respiratory involvement, dysfunctional or paradoxical breathing patterns may represent a consequence, a compensatory adaptation, or a perpetuating factor in MALS [9,20,22]. Diaphragmatic mechanics also influence autonomic regulation by affecting intrathoracic pressure, venous return, baroreflex sensitivity, and vagal afferent input. Evidence from case reports and small case series describes manual therapy approaches targeting the diaphragm, rib cage, and thoracic spine, with particular focus applied to the coeliac innervated region such as rib raising at T5-T9, myofascial techniques, and other coeliac plexus-directed interventions reporting improvements in pain, gastrointestinal symptoms, and dysautonomia flares, particularly in post-surgical populations [29,39,40,41,42]. These findings should be interpreted with caution, given the limited evidence, but suggest that optimisation of thoracoabdominal mechanics may influence autonomic function in selected patients [43,44].
The autonomic dysregulation features found in MALS overlap substantially with functional gastrointestinal disorders and primary dysautonomia, so diagnostic evaluation should integrate dynamic vascular imaging, autonomic assessment, and symptom chronology to distinguish MALS from isolated functional GI presentations and primary dysautonomia [6,14,15,44,45].

Osteopathic and Manual Therapeutic Treatment

There is a small, but evolving body of evidence showing that manual therapy can support the management of MALS by modulating neurovascular compression, restoring autonomic balance, and taking a multisystem approach while focusing on mechanical and fluid disturbances [40,41].

Theoretical Mechanisms

Foregut sympathetic efferents to the coeliac plexus predominantly originate from the T5-T9 thoracic segments via the greater splanchnic nerves. Manual treatment strategies that address somatic dysfunction in this mid-thoracic region are theoretically positioned to influence sympathetic tone, viscerosomatic reflexes and perceived pain in patients with MALS [30]. This rationale aligns with osteopathic reports describing improvement in upper abdominal symptoms and neurovascular congestion following thoracic and diaphragmatic manipulative treatment in post-surgical MALS [29]. By improving thoracolumbar junction mobility, directly mobilising the coeliac region, reducing fascial tension around the median arcuate ligament, its associated vertebral segments and viscera, manual therapy may reduce mechanical load on the coeliac artery and ganglion and optimise downstream arterial inflow to the upper abdominal viscera and caudal structures via the abdominal aorta. This may reduce tension on the diaphragmatic crura and medial arcuate ligaments and enhance venous and lymphatic return via the lymphatic thoracic ducts, cisterna chyli, hemiazygos & azygos veins, and vertebral veins. This, in turn, may lead to a decrease in neurovascular congestion and sensitisation in the upper abdominal and lower thoracic segments.
From an autonomic standpoint, decompression and mobilisation of the coeliac plexus region may dampen aberrant sympathetic afferent signalling and help re-establish a more physiological balance between sympathetic outflow from T5-T9 and parasympathetic input via the Vagus to gastric, hepatic and splenic function. Sympathetic activity can exert both excitatory and inhibitory effects, so clinical changes may reflect either a reduction in sympathetic drive or a relative enhancement of parasympathetic tone [30]. Techniques such as rib raising at T5-T9, suboccipital release, and direct coeliac plexus fascial work are theorised to reduce sympathetic overactivity and facilitate parasympathetic tone, which in turn can normalise gastric myoelectric activity and motility that are known to be disturbed in MALS [31]. These neurophysiologic effects provide a coherent rationale for using manual therapy both in patients with MALS and those with persistent pain after technically adequate decompression.

Osteopathic Model and Specific Techniques

Osteopathic management of MALS engages the dynamic relationships among the circulatory, respiratory, neurological, musculoskeletal, fascial and visceral systems, recognising how altered structure-function interactions contribute to symptomatic expression [46]. Peeters (2010) describes three core aims: (1) restoring thoracolumbar flexion and de-coaptation to reduce mechanical strain at the MAL coeliac interface; (2) normalising diaphragmatic excursion, particularly inhalation, to lessen expiratory phase coeliac compression; and (3) decongesting and stretching tissues ventral to T12-L1 to improve mobility and trophic status of the coeliac plexus zone [41]. To implement these aims, he details active coeliac trunk mobilisation in kneeling flexion, standing and supine myofascial techniques over the coeliac plexus, and lift/mobilisation of the duodenojejunal angle, all designed to improve regional circulation and reduce fibrotic tethering while respecting vascular contraindications such as arteriosclerosis.
Contemporary case reports apply this theory to MALS postsurgical and dysautonomia dominant presentations. Volokitin and Bergman (2024) describe an autonomic focused osteopathic treatment incorporating rib raising at T5-T9, suboccipital myofascial release to influence vagal tone, Chapmann’s reflex work, and coeliac plexus fascial release in a 23year-old woman with recurrent postoperative pain flares. This treatment normalised musculoskeletal segmental and reflex findings and produced sustained symptom resolution over several months. Other reports highlight the value of combining spinal, rib, visceral and postural correction techniques (including exercises and rib raising) to address recurrent postsurgical symptoms linked to hip dysplasia, excessive lumbar lordosis, and exercise-induced abdominal pain, suggesting that manual therapy can mitigate biomechanical drivers of neurovascular stress in MALS [29,39,40,41].
Table 1. Manual techniques used in the treatment of MALS. 
Table 1. Manual techniques used in the treatment of MALS. 
Patient context Intervention dose (sessions, duration) Techniques Outcomes reported
53 y/o female with MALS and lumbar lordosis and hip dysplasia/arthritis; multisystem symptoms included pain with eating, dyspnoea, oedema, dizziness, palpitations, and blood pressure dysregulation (ref 39). Treatment pre and post surgery. PT sessions (not standardized), repeated visits, ongoing home exercises, twice-daily lymphatic strategies, and effects lasting from immediate relief to approximately 2 weeks for some techniques. Instrument assisted soft tissue mobilization; stretching and strengthening to reduce lumbar lordosis; diaphragm lift/primal reflex release; manual lymphatic drainage; rib mobilization/repositioning; positional strategies integrated into activities of daily living. Temporary symptom reduction post Rx. Diaphragm lift produced immediate increased diaphragmatic motion with mild relief of postprandial epigastric pain for approx 2 weeks; lymphatic techniques temporarily reduced oedema; symptom recurrence paralleled worsening lordosis, while later reduction in lordosis after hip arthroplasty coincided with resolution of recurrent MALS-related symptoms.
23 y/o female with prior laparoscopic MAL decompression and coeliac nerve removal, and persistent stress-related post-surgical flare-ups of epigastric pain, nausea, and autonomic/viscerosomatic findings (ref 29). Single OMT session delivered during an acute post-surgical flare; reassessment immediately after treatment, symptom check at 2 days, and follow-up over several months. Bilateral rib raising to T5-T9; myofascial release to suboccipital and mid-thoracic musculature; Chapman’s point treatment; collateral ganglia release with respiratory assist directed to restricted coeliac plexus fascia. Immediate softening of tissues on reassessment; significant pain reduction reported at 2 days; complete resolution shortly thereafter; relief persisted for several months according to follow-up.
23 y/o female with MALS, POTS, and gastroparesis; wheelchair-bound because of severe syncopal and pain episodes (ref 41). Four OMT sessions; exact treatment interval not provided. Visceral techniques to increase bowel movements; treatment directed to the origin and insertion of the median arcuate ligament. Substantial symptom reduction, with marked improvement in mobility and quality of life after four treatments.
Rx = treatment, OMT = osteopathic manual therapy.
These reports suggest the approach is feasible and biologically plausible, with efficacy still to be confirmed in larger studies. Although the evidence is limited by single-patient designs, heterogeneous techniques, lack of controls, unclear dosing, short follow-up in some cases, and inconsistent use of validated outcomes, manual therapy may still have a useful role as part of a broader conservative management approach. This may include support in mild, moderate, or equivocal cases, while severe cases should be managed with an integrative medical and manual therapy approach. osteopathy may be beneficial for pre-operative optimisation of breathing, thoracic mobility, posture, symptom regulation, and post-operative rehabilitation for residual viscerosomatic pain, dysautonomia, deconditioning, or recurrent flares. Importantly, it should not delay vascular referral when red flags, severe weight loss, progressive symptoms, or clear haemodynamically significant compression are present.

Rehabilitation Implications: Autonomic-Informed Care Pathways After Intervention

Given that MALS is commonly associated with dysautonomia and deconditioning, a post-operative program that incorporates pacing strategies, monitoring of orthostatic symptoms and heart rate responses, as well as adjustments of exercise prescription to avoid patients’ flares would be in order. Psychological support, including pain-focused cognitive and behavioural strategies to address anxiety and depression, may also be beneficial as chronic pain and diagnostic delay are recognised contributors to psychosocial distress in MALS [12,14].
osteopathic and manual therapy literature describes multimodality rehabilitation approaches that address spinal and rib mobility, diaphragmatic function, postural control, and lymphatic congestion, often in the context of broader interprofessional care [29,39,40,41]. In one detailed case report, instrument assisted soft tissue mobilisation, core and hip strengthening, psoas stretching, diaphragm lift techniques and manual lymphatic drainage were associated with improvements in breathing mechanics, postural alignment, epigastric pain and oedema in a patient with MALS and complex comorbidities [39]. Other autonomically informed non-osteopathic rehabilitation strategies that focus on thoraco-abdominal mechanics, venous-lymphatic return, and graded exposure to activity are conceptually consistent with MALS pathophysiology and should be systematically evaluated in both postsurgical and conservatively managed cohorts [29,39,40,41].

Measurement and Outcomes: Autonomic Markers and Patient-Reported Outcome Measures Relevant to MALS

Existing MALS outcome data are predominantly based on symptom regression, weight gain and return to activities, leaving a gap where ANS regulation is not definitively assessed [4]. Many reports rely on non-standardised descriptions of pain, nausea and food fear, without validated gastrointestinal or quality-of-life scales. Vascular outcomes are assessed by duplex ultrasound or CT angiography and stenosis grading, which does not capture neurogenic contributions or dysautonomia. Adopting an ANS-focused approach, where there is a clear rationale to incorporate structured autonomic testing, such as the NASA lean test and heart rate variability measures in both pre and post-intervention assessment, especially in patients with suspected or confirmed POTS or orthostatic intolerance, has merit. Complementary use of generic and disease-specific Patient Reported Outcome Measures (PROMs), covering abdominal pain, gastrointestinal function, orthostatic symptoms, fatigue, psychological distress and role functioning (for example, instruments used in dysautonomia and functional GI research) would permit more nuanced evaluation of treatment effects that matter to patients. In rehabilitation and manual-therapy studies, combining symptom scales with objective autonomic markers and imaging follow-up would strengthen mechanistic reasoning and move the field beyond descriptive single cases.

Knowledge Gaps and Future Directions for ANS-Focused MALS Research

Despite growing recognition of MALS as a mixed vascular-neurogenic syndrome, substantial knowledge gaps remain regarding its autonomic pathophysiology, natural history and response to both surgical and conservative interventions. Few studies systematically characterise dysautonomia using standardised testing, and even fewer correlate autonomic markers with imaging metrics, symptom severity or surgical outcomes [4]. This limits the ability to distinguish phenotypes such as vascular or neuropathically dominant or a combined presentation, which may require different management strategies.
Second, there is minimal prospective work tracking patients from initial presentation through diagnostic work-up, decision-making and post-intervention recovery, so the impact of diagnostic delay, misdiagnosis and variable access to high-risk vascular surgery on autonomic and psychosocial outcomes remains poorly defined. Third, the role of connective tissue and extracellular matrix factors in predisposing to multiple compression syndromes, autonomic instability and nociplastic pain is hypothesised but not well quantified, particularly in relation to hypermobile EDS and overlapping vascular compressions. Finally, evidence for osteopathic and manual therapy remains confined to isolated case reports and small series, with heterogeneous techniques, low treatment fidelity and limited autonomic or imaging outcomes, preventing firm conclusions about efficacy, optimal dosing or patient selection.

Clinical Implications

MALS should be considered in patients, especially younger women who present with postprandial epigastric pain, weight loss, nausea, upper abdominal bloating and “IBS-like” or functional dyspepsia symptoms, despite normal routine investigations. Clinicians should be aware of specific vascular imaging (mesenteric Doppler ultrasound, CTA or MRA) with inspiratory-expiratory assessment of the coeliac axis and careful attention to the characteristic “hooked” configuration of the proximal coeliac artery. As a part of a thorough patient workup, practitioners should increase their understanding of the rising proliferation of dysautonomia conditions, along with their common comorbidities such as POTS, MCAS, EDS, MALS and their high prevalence in women. This will help develop a more in-depth and up to date given diagnostic process. Within this framework, osteopathic and other manual approaches can be utilised with three main focal points: (1) as conservative management in patients with mild to moderate compression and prominent autonomic or musculoskeletal symptoms; (2) as pre-operative optimisation to improve diaphragmatic mechanics, venous and lymphatic drainage, and autonomic balance; and (3) as post-operative rehabilitation to address residual viscerosomatic reflexes, dysautonomia, and biomechanical contributors to symptom recurrence.

Future Directions

Future research on MALS could be developed to clarify associated mechanisms, refine diagnosis, and test multimodality treatment pathways, including osteopathic care. Reviews would benefit from correlating symptom severity with imaging-based metrics, such as coeliac artery compression angle ratios and heart rate variability, to identify potential subgroups with comorbidities (e.g., severe arterial compression with significant dysautonomia and EDS versus mild compression with predominantly functional pain). These subgroups could then be analysed for likely surgical success rates, durability of benefit, and the impact of associated conditions such as connective tissue disorders, POTS, MCAS, and EDS rather than treating MALS as a single homogeneous syndrome. These subcategories can then be assessed for potential success rates with structured non-surgical options. Future reviews could also examine protocols that integrate manual therapy into pre- and post-operative care, using validated patient-reported outcome measures to evaluate pain, quality of life, autonomic symptoms, and function. Qualitative research exploring how patients understand and prioritise different interventions, ranging from surgery to manual therapies, could clarify intervention preferences, risk/benefit analysis, and non-invasive options for mild to moderate cases of MALS.

Limitations

This narrative review has several important limitations that should be considered when interpreting the findings. Much of the evidence base for MALS treatment is dominated by small retrospective series, case reports and single-centre cohorts, many of which lack control groups, standardised diagnostic criteria or long-term follow-up. These limitations limit the strength and generalisability of any conclusions drawn. Publication bias towards positive surgical outcomes and technically successful hybrid procedures is likely, particularly given the under-reporting of negative, equivocal or non-operative cases.
Other limitations within the existing literature further constrain the implications of this review. For example, there is a noticeable lack of research examining osteopathic or other manual therapy approaches in MALS, with the available evidence largely confined to isolated case reports and small series lacking standardised protocols or robust patient-reported outcome measures. Very few studies stratify MALS by severity or provide clear criteria to distinguish patients who may benefit from conservative management versus those requiring surgical intervention, making it difficult to propose evidence-based thresholds for referral or operative care. Clear reporting of autonomic nervous system assessment is infrequent and inconsistent, with limited detail on how ANS function was measured, at what time points, and how changes related to symptoms or imaging findings. Similarly, there is little prospective work following patients from initial diagnosis through to surgical decision-making and beyond, so the impact of diagnostic delay, underdiagnosis, and variable access to what is often considered high-risk vascular surgery remains poorly understood. Details of post-surgical care and rehabilitation are rarely described, and long-term follow-up beyond 24 months is uncommon, leaving uncertainties around delayed recurrence, persistent dysautonomia, and optimal post-operative or adjunctive manual therapy treatment options. These limitations emphasise the need for more rigorous, ANS-focused and manual therapy inclusive research to better inform practice and the management of less severe symptomatic patients with MALS.

Conclusion

MALS is an intra-abdominal vascular compression syndrome, associated with psychiatric, autonomic dysregulation, and musculoskeletal and visceral symptomatology. The current standard treatment is surgically focused, with interventions such as laparoscopic, open and robotic decompression of the median arcuate ligament being effective approaches to managing moderate to severely symptomatic patients. Osteopathic manipulative therapy has been shown to have beneficial effects for patients with MALS, either standalone or as part of a multidisciplinary approach post-surgery, though the depth of this research is limited. This narrative review highlights the need for further research into the use of manual therapy intervention as a non-invasive treatment option across all levels of symptom severity in the management of MALS.
Table 2. The search strategy summary. 
Table 2. The search strategy summary. 
Date of search 01/07/2025
Databases and other sources searched PubMed, Cochrane, EBSCOhost, PEDro, ScienceDirect, SpringerLink, Wiley Online Library, BMJ and SAGE.
Search terms used (including MeSH and free text search terms and filters) (“Median Arcuate Ligament Syndrome”[MeSH] OR “median arcuate ligament syndrome” OR MALS OR “coeliac artery compression”) AND (manual therapy OR treatment OR osteopathic)
Timeframe All existing/suitable data from 1963 up until 01/07/2026
Inclusion and exclusion criteria Exclusions: papers written in a language other than English. Inclusions: case studies, case series, narrative reviews, systematic reviews, journal articles, and medical book chapters.
Selection process Erin Barnes conducted all selection, research, and editing.

Ethics statement

This narrative review included published literature only. The authors declare there are no conflicts of interest and have adhered to accepted standards of ethical conduct throughout the review process.

Supplementary Materials

The following supporting information can be downloaded at the website of this paper posted on Preprints.org.

Author Contributions

Erin Barnes is the primary investigator and guarantor; conceived the project, contributed to study design, screening, data charting and drafting and revising the manuscript. Roger Engel, Azharuddin Fazalbhoy and Kesava Kovanur Sampath contributed to revising the manuscript. This statement certifies that all authors have seen and approved the manuscript being submitted. We warrant that the article is the authors’ original work. We warrant that the article has not received prior publication and is not under consideration for publication elsewhere. All authors contributed to the final version of the manuscript. .

Funding

None.

Data availability statement

No new data were generated or analysed in this review; all data discussed are available in the cited publications.

Acknowledgments

None.
Competing interests: The authors declare no competing interests.
Patient and public involvement: No patients or members of the public were involved in the design, conduct, reporting or dissemination plans of this narrative review.

References

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