Median Arcuate Ligament Syndrome Explained: Symptoms, Testing, and Treatment Options

Median arcuate ligament syndrome (MALS)—also called celiac artery compression syndrome or Dunbar syndrome—is a rare condition in which a fibrous band under the diaphragm (the median arcuate ligament) compresses the celiac artery and often irritates the nearby celiac plexus nerves. This can produce post-prandial epigastric pain, early fullness, nausea, and weight loss, most often in slender or thin adults. In many, pain worsens with eating or exercise and eases with fasting. ^[1]

Median Arcuate Ligament Syndrome is under-recognized and easily mistaken for gastritis, gallbladder disease, or functional dyspepsia. Because endoscopy and standard labs may be normal, patients can spend months searching for answers. Early recognition shortens that journey and directs the right imaging tests. ^[2]

The median arcuate ligament can sit lower than usual, bowstringing across the proximal celiac artery. As the diaphragm moves with breathing, compression is typically worst on expiration and less on inspiration. Reduced blood flow (particularly during digestive demand) and stimulation of the celiac plexus together are thought to drive cramping epigastric pain, “food fear,” and weight loss. ^[3]

Imaging often shows a characteristic focal narrowing with a “hooked” appearance of the celiac artery’s superior wall on sagittal reconstructions—an important clue that distinguishes Median Arcuate Ligament Syndrome from atherosclerotic stenosis. ^[4]

Median Arcuate Ligament Syndrome is uncommon, and true prevalence is unknown because many people have asymptomatic celiac artery indentation on imaging. It tends to be reported more often in younger or middle-aged women with low body mass index, but it can occur in men and in older adults as well. The key is the symptom pattern: post-prandial epigastric pain, exercise-induced epigastric pain, nausea, and weight loss that improve with fasting. ^[1]

Important nuance: Imaging compression alone is not Median Arcuate Ligament Syndrome. Many healthy people show some celiac artery indentation without symptoms. Diagnosis requires symptom correlation plus supportive imaging and exclusion of better explanations. ^[2]

• Upper-abdominal (epigastric) pain that peaks after eating or during aerobic exercise
• Early satiety, nausea, bloating, or vomiting
• Unintentional weight loss and food fear (avoiding meals to prevent pain)
• Pain out of proportion to benign endoscopy and normal labs or ultrasound
• Occasionally, an abdominal bruit that varies with respiration (not required)

These features form a common clinical triad: post-prandial pain, weight loss, and radiologic celiac artery compression. ^[2]

Before labeling pain as Median Arcuate Ligament Syndrome, clinicians systematically exclude more common causes of post-prandial epigastric pain and weight loss:

• Gallbladder disease and biliary dyskinesia
• Peptic ulcer disease or gastritis (including bile reflux)
• Chronic pancreatitis and pancreaticobiliary obstruction
• Functional dyspepsia or gastroparesis
• Superior mesenteric artery syndrome in very thin individuals
• Chronic mesenteric ischemia from atherosclerosis (usually in older adults with vascular risk factors)

A careful history, labs, stool testing as indicated, hepatobiliary ultrasound, and upper endoscopy help prune this list before specialized vascular imaging is ordered. ^[2]

CTA with arterial-phase imaging in deep expiration followed by venous-phase imaging in deep inspiration can demonstrate dynamic compression. Radiologists look for:

• Focal superior indentation of the proximal celiac artery on sagittal images with a “hooked” configuration
• Post-stenotic dilatation
• Respiratory variation in the degree of narrowing

These features support Median Arcuate Ligament Syndrome when they mirror symptoms. ^[4]

A skilled sonographer measures peak systolic velocity (PSV) in the celiac artery during expiration and inspiration. In Median Arcuate Ligament Syndrome, PSV rises on expiration (when the ligament compresses more) and falls on inspiration as the stenosis relaxes. Commonly cited thresholds to suggest hemodynamically significant stenosis are PSV greater than or equal to 200-240 cm/s (for >50% stenosis) and greater than or equal to 320 cm/s (for >70% stenosis), interpreted alongside the inspiratory drop and clinical context. Examples in the literature show marked velocity reduction with deep inspiration. ^[5]

Ultrasound is operator-dependent but powerful: a marked expiratory PSV with normalization on inspiration is a classic Median Arcuate Ligament Syndrome signature. ^[6]

Catheter angiography is rarely needed for diagnosis now that CTA/MRA and duplex ultrasound are robust, but it may be used when endovascular therapy is considered or when noninvasive imaging is inconclusive. ^[1]

• No relation of pain to meals or exercise
• Diffuse pain with predominant bowel changes pointing to irritable bowel syndrome
• Clear atherosclerosis with multivessel mesenteric disease (a different problem)
• Imaging showing no respiratory variation and a fixed stenosis from plaque rather than ligament indentation

In such cases, pursue other diagnoses and vascular pathways. ^[2]

Because the root issue is extrinsic compression plus probable plexus irritation, treatment aims to divide the median arcuate ligament and free the celiac artery, often with celiac ganglionectomy to reduce neurogenic pain. This is typically done using a laparoscopic or robot-assisted approach; open surgery is reserved for complex anatomy or reoperations. Many centers confirm adequacy of release intra-operatively with intraoperative duplex or post-operative imaging. ^[7]

Endovascular stenting is not a stand-alone solution for classic Median Arcuate Ligament Syndrome because the stenosis is external and dynamic; stents risk fracture or restenosis from ongoing diaphragmatic motion. Stents may be considered after surgical release if a fixed residual narrowing persists, but decompression is the mainstay. ^[2]

Across adult series and systematic reviews, most carefully selected patients report meaningful symptom relief after decompression. Pooled literature suggests >70% sustained improvement after treatment in many adult cohorts; single-center experiences range from approximately 60% to 80% relief, with variation tied to selection and follow-up length. Quality-of-life measures also tend to improve when symptoms match the radiology and other causes have been excluded. ^[8]

However, outcomes are not uniform:

• Some patients need additional procedures (for example, endovascular touch-up of a fixed residual stenosis).
• A minority have persistent pain despite technically adequate release; coexisting conditions such as mast cell activation syndrome have been associated with poorer response in small series. ^[9]

Bottom line: when symptoms are classic, other causes are excluded, and dynamic imaging matches the story, the odds of improvement are good—but not guaranteed. Shared decision-making is essential. ^[10]

Complications are uncommon but can include bleeding, pancreatitis, infection, and, rarely, injury to nearby vessels. Transient symptom recurrence during healing is possible. As with any operation, outcomes improve with experienced teams familiar with both laparoscopic and open techniques and with vascular backup available. ^[11]

• Track meals and symptoms. A simple diary clarifies the post-prandial pattern and helps gauge improvement after therapy.
• Optimize nutrition. Work with a clinician or dietitian to prevent further weight loss while evaluation is in progress.
• Ease into activity. Many report exercise-induced epigastric pain; gradual return to activity after treatment is common as tolerance improves.
• Follow-up imaging. Your team may order duplex ultrasound after surgery to document reduced velocities and to screen for residual stenosis. ^[7]

Not every person with celiac artery indentation needs an operation. The best outcomes typically occur when all three pillars align:

• Classic symptoms: post-meal epigastric pain, early satiety, food avoidance, weight loss; sometimes exercise-induced pain.
• Supportive dynamic imaging: a “hooked” celiac narrowing on sagittal computed tomography or magnetic resonance angiography with respiratory variation, plus duplex ultrasound showing high expiratory velocities that fall on inspiration.
• Exclusion of better explanations: normal or non-explanatory endoscopy, gallbladder evaluation, pancreatic assessment, and nutrition review.

People who improve the most often describe a clear link between eating and pain, show dynamic compression (not a fixed plaque), and lack competing gastrointestinal drivers of symptoms.

• Laparoscopic or robot-assisted release: small incisions; the surgeon divides the median arcuate ligament and removes fibrous tissue tethering the celiac artery. Many teams add celiac plexus neurolysis to quiet nerve irritation. Short hospital stays and faster recovery are typical.
• Open release: a traditional incision provides wide exposure and is reserved for complex anatomy, reoperations, or when vascular reconstruction is anticipated.
• Adjunct endovascular work: if a fixed residual stenosis remains after release, a balloon or stent may be considered—but only after external compression is removed because the lesion is otherwise dynamic.

• Most laparoscopic patients go home within 24-48 hours.
• Diet advances as tolerated; some need a low-fat, small-frequent-meals strategy while the plexus settles.
• Incisional soreness is expected; deep-breathing and gentle walking are encouraged.

• Progressive return to usual activities; aerobic exercise is reintroduced gradually.
• Many report steadier appetite and less “food fear”; weight stabilizes, then climbs.
• Your team may order post-op duplex ultrasound to document improved celiac velocities and support symptom tracking.

• Continued improvement in meal tolerance and exercise capacity is common.
• If symptoms persist, clinicians reassess for residual fixed stenosis, adjacent diagnoses (for example, gastroparesis, functional dyspepsia), or rare nerve-pain persistence requiring targeted management.

• Meal pacing: small, frequent meals; avoid very large, high-fat loads that increase splanchnic demand.
• Hydration and electrolytes: especially around activity; some patients find gentle, isotonic fluids easier to tolerate with meals.
• Activity timing: avoid intense cardio immediately after eating until evaluated; many feel better separating meals and workouts.
• Nausea strategies: ginger tea, prescription antiemetics as advised.
• Nutrition support: if weight loss is ongoing, involve a dietitian early to prevent malnutrition.

These measures are bridges—not cures—while you complete testing.

• Incidental imaging finding: a celiac “hook” on computed tomography without post-prandial pain is not median arcuate ligament syndrome. Incidental compression is surprisingly common.
• Atherosclerotic chronic mesenteric ischemia: usually an older population, risk factors present, fixed multivessel stenoses (often superior mesenteric artery), no respiratory variation. Management and prognosis are different.
• Functional dyspepsia or gastroparesis: bloating and early fullness dominate; gastric emptying or symptom patterns point away from median arcuate ligament syndrome.
• Biliary disease: right-upper-quadrant pain or abnormal ultrasound and labs tell a different story.

Clear documentation of the symptom-imaging relationship prevents mislabeling and unnecessary surgery.

A 29-year-old distance runner with body mass index of 19 develops sharp epigastric pain 15-30 minutes after meals and during tempo runs. Endoscopy, laboratory tests, and gallbladder ultrasound are normal. Computed tomographic angiography shows a hooked narrowing of the proximal celiac artery with post-stenotic dilatation; dynamic duplex reveals expiratory peak systolic velocity of 340 cm/s that falls to 140 cm/s on deep inspiration. After laparoscopic ligament release and celiac plexus neurolysis, she advances diet over two weeks. At three months, she reports meal tolerance without pain and resumes running with gradual mileage increases; follow-up ultrasound shows normalized velocities.

“Any celiac stenosis means median arcuate ligament syndrome.

” Myth: Many people have asymptomatic indentation. Symptoms plus dynamic imaging and exclusion of other causes define the syndrome.

“A stent will fix it”

Myth for classic cases.The compression is external and respiratory-dependent; release is the cornerstone. Stents are considered only after adequate decompression, if a fixed residual narrowing persists.

“Median arcuate ligament syndrome is just for young women.”

Myth: It is more often reported in slender adult women but occurs across ages and sexes. The pattern, not the demographic, is decisive.

• Do my symptoms clearly relate to eating or exercise, and have we ruled out more common causes?
• Will we obtain CTA with sagittal reconstructions in expiration and inspiration, and a dynamic duplex ultrasound?
• If imaging confirms median arcuate ligament syndrome, which approach (laparoscopic, robot-assisted, open) do you recommend, and what is your center’s success rate?
• How will we monitor improvement—symptom diary, weight, and post-op duplex?
• If pain persists after release, what are our next steps?

These questions anchor a productive, evidence-based discussion.

Some patients feel early relief, especially from food fear; others improve over weeks to months as nerve irritation settles and nutrition normalizes. Persistent or recurrent pain triggers reassessment for residual stenosis or alternative diagnoses.

Light aerobic activity typically resumes in 2-4 weeks, progressing as tolerated. High-intensity intervals and heavy lifting are usually delayed until your surgeon clears you, often 6-8+ weeks, depending on individual recovery.

True re-compression is uncommon after a complete release. When symptoms recur, clinicians check for incomplete decompression, scar tethering, or unrelated gastrointestinal causes; occasionally, endovascular touch-up treats a residual fixed narrowing.

Median arcuate ligament syndrome turns eating—one of life’s basics—into a trigger for upper-abdominal pain and weight loss in a subset of mostly slender adults. The diagnosis is clinical first, supported by dynamic imaging (the “hooked” celiac narrowing and respiratory-dependent velocities), and confirmed by excluding more common explanations. When these pieces align, surgical release with celiac plexus neurolysis helps the majority of appropriately selected patients reclaim normal meals, weight, and activity. If your story fits, ask for CTA with sagittal reconstructions and a dynamic duplex ultrasound, then decide next steps with a team that treats median arcuate ligament syndrome regularly.

Educational information only; not a substitute for personalized medical care.