It’s not uncommon for those with hypermobility to have difficulty with swallowing, voice, reflux, and last but not least, that maddening feeling of a lump in the throat that never seems to have a name. Globus sensation, chronic throat clearing, a voice that gives out by 4pm, food that seems to get stuck halfway down, and reflux that doesn’t behave like normal heartburn. If any of that sounds familiar, you’re not imagining it, and you’re not alone.
When it comes to hypermobility and Ehlers-Danlos syndromes (EDS), most of the conversation understandably goes to joints. Shoulders that come out of socket, knees that give way, fingers that bend the wrong way for a party trick. What gets missed, a lot, is that the throat is basically a stack of small joints, sphincters and finely timed muscle sequences too. It just doesn’t look like a joint, so nobody thinks to treat it like one.
So, here’s what this article is going to do. We’re going to look at why the throat is such a common trouble spot for those with hypermobility, what the actual research says about swallowing (dysphagia), voice problems (dysphonia) and reflux, including a large 2026 study that pours some cold water on assumptions the field has been making for years. We’re going to cover the mechanisms properly, not just list symptoms, and we’re going to be honest about where the evidence is thin, where it’s solid, and where it flatly contradicts the popular narrative.
One thing this article is not: it’s not a diagnostic tool, and it’s not a replacement for an ENT assessment, a speech and language therapy review, or a proper gastroenterology workup if you’re struggling to swallow safely. If you’re choking on food regularly, losing weight without trying, or aspirating (food or liquid going down the wrong way), that needs a face-to-face assessment, not a blog post. What this article will do is help you understand the mechanisms well enough to have a much better conversation with whoever you see next.
So, if you’re ready to actually understand what’s going on in your throat, let’s go!
Why the throat is a hotspot for those with hypermobility in the first place
The throat and the top of the food pipe rely on a surprising number of small joints and sphincters working in a tightly timed sequence. The cricoarytenoid joints rotate and slide to open and close the vocal cords. The cricothyroid joint tilts to tension the vocal folds for pitch. The upper oesophageal sphincter (UES), a muscular sling made up of the cricopharyngeus, thyropharyngeus and proximal cervical oesophageal muscles wrapped around the cricoid cartilage, has to relax in a fraction of a second during a swallow and then snap shut again to stop reflux and air from coming back up. None of that works well if the connective tissue holding those joints and that sphincter in position is looser than it should be, or if the sensory feedback telling the brain where those structures are and what they’re doing is unreliable.
Now, this is where it gets properly multi-system, and it’s why this article can’t just be “collagen is loose, therefore throat breaks”. Three things converge on this small stretch of anatomy in those with hypermobility. First, the connective tissue itself, which affects the mechanical stability of the joints and sphincters we just mentioned. Second, autonomic and vagal nerve regulation, because the vagus nerve does an enormous amount of the unglamorous work of coordinating swallowing, peristalsis (the wave-like muscle contraction that pushes food down) and the reflexes that stop reflux, and autonomic dysfunction is common in hypermobility. Third, mast cell activation, which can drive inflammation in the same tissues that are already mechanically vulnerable. Pull any one of these threads on its own and you get half the picture. That’s the trap most articles on this topic fall into.
The numbers: how common are throat symptoms in hEDS and HSD
The best data we have on how common throat symptoms actually are in hypermobility comes from a 2023 cross-sectional survey of 1,620 people with EDS or hypermobility spectrum disorder (HSD), with 1,405 full completions.[1] The sample was heavily hEDS (75.5%) and HSD (17.8%), with a smaller classical EDS (cEDS) group (3.3%), and, worth flagging honestly, 96.6% female, which means the study can’t really tell us anything about sex differences. If you’re unsure which category you fall into, it’s worth reading up on how hypermobility and EDS are actually diagnosed before assuming the numbers below apply to you directly.
The results are stark. Using the Reflux Symptom Index (RSI), a validated 9-item questionnaire used clinically to flag laryngopharyngeal reflux, 86.1% of respondents scored 13 or above, which is the threshold generally taken to indicate significant reflux symptoms reaching the throat. The mean score was 22.95, well over double that threshold. On the EAT-10, a validated screening tool for swallowing difficulty, 79.4% scored 3 or above (the cutoff for concern), with a mean of 11.91. On the Voice Handicap Index (VHI), which measures how much a voice problem affects daily life, 53.4% reported mild handicap, 32.6% moderate, and 14.6% severe.
Those with hEDS scored significantly higher than those with HSD on both the RSI and EAT-10 totals, though the effect sizes were small to moderate (Hedge’s g of 0.29 and 0.37 respectively), and interestingly, total VHI didn’t differ significantly between hEDS and HSD at all, only one individual item did (a creaky, dry-sounding voice). So there’s a real hEDS versus HSD gradient for reflux and swallowing symptoms, but not really one for overall voice handicap. That’s a nuance worth sitting with rather than skating past.
The honest caveats matter here too. This was a convenience and snowball sample, recruited online, which almost certainly means people with more severe or more troubling symptoms were more likely to take part in the first place. It’s self-report, with no laryngoscopy, no manometry, nothing objective behind the numbers. And the RSI, useful as it is, isn’t specific to laryngopharyngeal reflux alone, it can pick up throat symptoms with other causes too. So take the scale of the numbers seriously as a signal that something real and common is going on, but don’t treat an 86% figure as a clinical prevalence rate carved in stone.
Reflux that reaches the throat: laryngopharyngeal reflux explained
Ordinary heartburn and laryngopharyngeal reflux (LPR) are not quite the same animal, and the difference matters for hypermobility. Normal gastro-oesophageal reflux disease (GERD) happens when the lower oesophageal sphincter (LES) lets stomach contents back up into the oesophagus. LPR happens when that same material gets past the upper oesophageal sphincter too, and ends up in the throat, larynx and sometimes even the back of the nose, tissue that is a lot less tolerant of acid exposure than the oesophagus is. Reflux problems rarely travel alone either, plenty of those with hypermobility also deal with gut motility issues further down the digestive tract, which points to the same underlying connective tissue and vagal story playing out at both ends of the gut.
The mechanism, laid out in a 2024 narrative review of LPR pathophysiology, comes down to four protective barriers: the lower oesophageal sphincter, the upper oesophageal sphincter, oesophageal peristalsis (the muscular wave that clears refluxate back down), and epithelial resistance factors like saliva.[9] When any of those fail, refluxate reaches tissue that sits at a pH of roughly 6.8 to 7.0, while the refluxate itself is sitting at a pH of around 1.5 to 2.0. That’s a big mismatch, and it does real damage: hydrochloric acid injures the tight-junction proteins that hold laryngeal epithelial cells together, pepsin (a gastric enzyme that’s mostly inactive above pH 4) gets taken up into cells and can be reactivated in more acidic pockets inside them, like the Golgi bodies, causing cellular damage from the inside out, and bile acids can injure tissue even at a much less acidic pH than you’d expect. On top of the direct chemical injury, there’s a vagally mediated reflex, acid touching the lower oesophagus can trigger throat clearing, coughing and a globus sensation even without acid physically reaching the throat itself.[9]
Here’s where hypermobility plausibly plugs into that mechanism. If the connective tissue supporting the upper and lower oesophageal sphincters is looser than typical, and there’s decent reason to think it might be given how much of the sphincter’s resting tone depends on structural, not just muscular, support, then two of those four protective barriers are already working from a weaker starting position. A small 2017 study looking specifically at joint hypermobility syndrome (the older name that mostly maps onto today’s HSD and hEDS) and reflux found that of 30 patients with reflux symptoms, 53% had genuinely pathological acid reflux on testing, 21% had reflux hypersensitivity (normal acid levels but heightened symptom perception), and 25% had functional heartburn (symptoms with no measurable acid correlation at all).[4] A hypotensive (weak) lower oesophageal sphincter was found in a third of patients, and acid exposure was more likely when lying down than upright, both consistent with a mechanical weak point rather than pure overproduction of acid.
The honest evidence problem: what the newest research actually shows
Right, this is the section where we have to be straight with you, because the research has actually moved since a lot of the older articles on this topic were written, and it’s moved in a direction that complicates the tidy story.
The Fikree study we just quoted was small: 30 patients, one centre, from 2017. Since then, the same research group has done something a lot more convincing. A study published in Clinical Gastroenterology and Hepatology in 2026 looked at consecutive outpatients at two tertiary neurogastroenterology centres between 2010 and 2022, comparing hEDS/HSD patients against non-hypermobile patient controls using the same gold-standard objective tests: high-resolution manometry for dysphagia (300 patients total, 134 with hEDS/HSD) and 24-hour pH-impedance monitoring for reflux (229 patients total, 114 with hEDS/HSD).[5]
The result: on a multivariable logistic regression, hEDS/HSD was not associated with oesophageal dysmotility (P=.12). Chicago v4.0 normal motility was actually the most common finding in the hEDS/HSD group (61.9%), not some dramatic dysmotility pattern. On the reflux side, the proportion diagnosed with actual gastro-oesophageal reflux disease under the Lyon consensus criteria was 26.3% in hEDS/HSD versus 33.0% in controls, again not significantly different (P=.27). What was the most common diagnosis in hEDS/HSD patients with reflux symptoms? Rome IV functional heartburn, in 62.5% of cases, meaning symptoms without the objective acid burden to match.
So, what do we do with two studies from overlapping research groups that seem to disagree? We don’t just pick the one that fits the narrative we’d prefer. The honest read is this: the newer, larger, controlled study is the stronger piece of evidence by a wide margin, ten times the sample size, two centres, proper patient controls rather than population assumptions, and objective testing throughout. What it tells us is that people with hEDS and HSD really do have a lot of throat and reflux symptoms (that part isn’t in dispute, the survey data backs it up too), but on gold-standard testing, most of those symptoms don’t correspond to measurable structural sphincter failure or true excess acid exposure. A lot of it looks like visceral hypersensitivity, a nervous system that reports pain and discomfort from stimuli that wouldn’t bother someone else’s throat or gut nearly as much, layered over occasional genuine mechanical weakness in a subset of people.
To be fair to the other side of this, it isn’t a clean, one-study answer. A separate 2025 exploratory study out of a tertiary care centre looked specifically at people with hypermobility spectrum disorders and gut symptoms, and found oesophageal dysmotility in 36% of them, a fair bit higher than the Butt paper’s figures.[12] When it comes to squaring that with the larger study, two things matter. First, it was an HSD cohort rather than an hEDS-specific one, so it isn’t measuring quite the same group. Second, and more importantly, it was a referral sample at a specialist centre, which is exactly the kind of setting where the more complicated cases end up. Send only the people whose symptoms are bad enough to reach a tertiary clinic and you’ll naturally find more measurable pathology than you would in the wider hypermobile population. So it doesn’t overturn the bigger, controlled study. But it’s a useful reminder that a real subset of people do have genuine motility problems, and “most symptoms are functional” is a statement about the average, not about every individual sitting in front of you.
That’s not a dismissal. Functional symptoms are not imaginary and they are not “just anxiety“, the discomfort is entirely real and can be just as disruptive as structural disease. But it does change what “treatment” should sensibly look like. If you’re throwing maximum-dose proton pump inhibitors at someone whose reflux testing is actually normal, you’re not addressing the mechanism that’s actually driving their symptoms, and you’re not going to get the results either of you are hoping for.
Swallowing problems: dysphagia, cricopharyngeal dysfunction and globus
Swallowing is a genuinely complicated, highly sequenced motor act, and it’s not surprising it goes wrong more often in a population where motor sequencing and proprioception are already less reliable. Going back to the 2023 survey, 79.4% of respondents scored above the EAT-10 threshold for dysphagia concern, with a mean score of 11.91, well above the cutoff of 3.[1] That’s a big number for a symptom that rarely gets asked about at a standard hypermobility appointment.
One specific and under-discussed swallowing problem worth knowing about is retrograde cricopharyngeus dysfunction, where the upper oesophageal sphincter fails to relax properly in the other direction, meaning people physically cannot burp. A 2024 case series of 50 consecutive patients with this condition found inability to belch in 100% of cases, gurgling throat noises in 98%, and abdominal or chest pain in 96%.[3] Three of the 50 patients (6%) had a diagnosed connective tissue disorder, two with EDS and one with Marfan syndrome, and the authors explicitly flagged that this was clearly higher than you’d expect in the general population. That’s a small, hypothesis-generating observation rather than proof of a strong link, the study wasn’t designed to test that association properly, but it’s an interesting thread, and it maps onto exactly the kind of sphincter-timing failure you’d predict from lax connective tissue around a muscular sling that has to relax and contract with split-second precision.
Then there’s globus, the sensation of a lump in the throat that isn’t actually there. It’s one of those symptoms that gets dismissed fast, often chalked up entirely to anxiety. The truth is more nuanced: some cases do track with emotional state, but elevated cricopharyngeal pressure and abnormal hypopharyngeal motility are also implicated, meaning there can be a genuine, measurable mechanical component sitting alongside or instead of any psychological one.[11] For someone with hypermobility, where the muscles and sphincter around that exact spot may already be working with less structural support, it’s not a stretch to see why globus turns up so often. It doesn’t mean every case of globus is EDS-related, plenty of people without hypermobility get it too, but it’s one more piece of the throat that depends on precise muscular coordination, and precise muscular coordination is exactly what connective tissue laxity tends to disrupt.
Voice problems: dysphonia, vocal fatigue and vocal cord hypermobility
Voice symptoms showed up in just over half of respondents at a mild level and in almost 15% at a severe level in the 2023 survey, using the Voice Handicap Index.[1] The authors proposed three plausible mechanisms, and it’s worth understanding all three because they point to quite different practical fixes. First, incoordination or outright hypermobility of the vocal cords themselves, meaning the folds don’t come together as precisely or consistently as they should for clear phonation. Second, reduced mobility of the cricoarytenoid joint, the small joint that rotates the vocal cords into position, which, if it’s affected by the same joint laxity or instability seen elsewhere in the body, would directly limit how well the voice box can fine-tune itself. Third, loss of the mucosal wave, the fine, fast ripple of the vocal fold’s surface layer during vibration that gives a voice its clarity, potentially altered by collagen changes affecting the tissue’s elasticity.[1]
Here’s the nuance that’s easy to miss: hEDS and HSD did not differ significantly on overall voice handicap in that survey, only on a single specific item (a voice described as “creaky and dry”). So while reflux and swallowing symptoms tracked more strongly with a formal hEDS diagnosis than with HSD, voice problems seem to be more evenly spread across the hypermobility spectrum, which fits with a mechanism that’s more about the shared feature of joint and soft tissue laxity, the same laxity behind how a Beighton score gets measured in the first place, than about anything unique to the more severe end of the spectrum.
The autonomic and vagal piece: why PoTS and dysautonomia matter here
The vagus nerve does a huge amount of unseen work in the throat and gut: it coordinates oesophageal peristalsis, helps trigger the cough and clearance reflexes that protect the airway from reflux, and regulates a good chunk of lower oesophageal sphincter tone. Autonomic dysfunction, including postural tachycardia syndrome (PoTS), is well recognised as common in hypermobility, and it’s not a coincidence that it shows up again here.
In the Fikree 2017 study, patients with coexisting PoTS (60% of the sample) had significantly higher dysphagia scores (21 vs 11.5, P=.04) and reflux scores (24.5 vs 16.5, P=.05) than those without PoTS, and there was a trend, not statistically significant but notable, toward double the rate of pathological acid reflux (64% vs 36%) and oesophageal dysmotility (50% vs 25%) in the PoTS group.[4] That’s consistent with a vagal or wider autonomic contribution stacking on top of whatever mechanical vulnerability already exists from joint laxity, rather than either factor working entirely alone. It also lines up with why some people find their throat symptoms fluctuate with the same triggers that worsen their PoTS: poor sleep, dehydration, being upright for long periods, hormonal shifts.
Mast cells, inflammation and the throat
Mast cell activation is the third thread, and it’s the one most likely to get missed entirely in a standard consultation, mostly because mast cell activation syndrome (MCAS) as a concept is still relatively new to mainstream clinical practice. A 2022 review looking at mast-cell-related conditions across hypermobile syndromes proposed that mast cell mediators, histamine and tryptase in particular, can drive chronic inflammation that disrupts connective tissue integrity across multiple organ systems, potentially including the tissues of the throat and upper airway.[8] The same review is refreshingly honest about the limits of what’s actually known, stating plainly that evidence is still needed to properly establish the pathophysiology linking hEDS and mast cell dysfunction, this is a plausible and increasingly discussed mechanism, not a settled one.
The GeneReviews clinical reference chapter on hEDS states it more simply: gastro-oesophageal reflux and mast cell activation disorders both contribute to pharyngeal and throat inflammation in those with hEDS.[2] In practice, that means someone with persistent throat irritation, a chronic tickly cough, or a throat that feels raw with no obvious cause on endoscopy might be dealing with a mast cell component layered on top of, or instead of, classic reflux, and it’s worth that being on the list of things ruled in or out rather than left unconsidered.
The jaw and neck connection: TMJ disorders and craniocervical instability
The jaw and throat share muscles, nerves and, frankly, a lot of referred pain pathways, so it’s worth covering temporomandibular joint (TMJ) disorders here too. The 2023 survey found TMJ disorder in 57.3% of the hEDS group, 40.3% of the HSD group, and 45.1% of the classical EDS group, a significant difference across subtypes.[1] A small French case-control study found an even starker gap: 92.9% of 14 EDS-HT patients had TMD compared to 6.9% of 58 controls, and the disorders in the EDS-HT group were consistently multi-mechanism rather than the single, simpler mechanism typically seen in controls.[6] A larger 2024 Nordic cohort of 185 women with confirmed hEDS found TMD symptoms in a remarkable 98%, with jaw clicking in 90% and jaw fatigue in 80%.[7] A jaw that clicks, locks, or fatigues easily can directly interfere with chewing efficiency and the initiation of a safe swallow, so this isn’t a separate problem sitting next to the throat story, it’s part of the same mechanical chain.
Craniocervical instability (CCI), excess movement at the junction between the skull and the upper cervical spine, is the more serious and considerably less common end of this picture. A 2022 systematic review of CCI in EDS found only 16 usable studies covering 695 patients in total, of whom 78 had been diagnosed with CCI and treated surgically.[10] Swallowing difficulty is mentioned as one feature of the broader cervico-medullary syndrome that can accompany significant CCI, alongside things like dizziness, tinnitus and sensory changes similar to those seen in brain fog and other neurological symptoms in hypermobility, but the review is honest that the evidence quality here is genuinely low, rated level III to V on the standard evidence hierarchy, with a real risk of selection bias since several of the included studies came from overlapping author groups. So, when it comes to CCI, the swallowing connection is real for the small number of people with significant instability, but it should not be presented as a common or well-quantified cause of everyday throat symptoms in the wider hypermobile population. Most people with a scratchy throat and occasional trouble swallowing do not have CCI, and it’s worth being clear about that rather than letting the more dramatic diagnosis crowd out the much more likely explanations covered earlier in this article.
Subtype differences: hEDS, HSD, classical EDS and vascular EDS
Terminology in this space gets used pretty loosely, hEDS, HSD, cEDS, EDS in general, often interchangeably, so it’s worth being precise about what the data actually shows by subtype, because the differences aren’t trivial, and it’s the same reason getting the right diagnosis among all 13 EDS types matters in the first place. In the 2023 survey, hEDS scored significantly higher than HSD on reflux and swallowing measures, though the actual effect sizes were modest.[1] TMJ disorder followed a different pattern again: highest in hEDS (57.3%), then classical EDS (45.1%), then HSD (40.3%). Atlanto-axial subluxation (excess movement between the top two neck vertebrae) showed yet another pattern, highest in classical EDS (19.6%), then hEDS (10%), then HSD (5%), a reminder that “worse in hEDS” is not a rule that applies uniformly across every throat and neck related measure.
Vascular EDS (vEDS) deserves a brief, separate mention, mostly to say what this article is not covering. vEDS carries a distinct and considerably more serious risk profile, arterial fragility and organ rupture risk, driven by a different underlying collagen defect to hEDS. If vEDS is part of your picture, or you suspect it might be, the throat and swallowing mechanisms discussed here may still apply to some degree, but the overall risk management priorities are different and need specialist input well beyond the scope of a blog post about swallowing and reflux. This is also worth bearing in mind if pregnancy is part of your planning, since subtype changes how much of this general throat picture actually applies to you.
What actually helps: a practical, honest read
So, given all of that, what’s actually worth doing? The honest answer is that a proper workup beats guessing every time, and given how often the newest evidence shows symptoms without matching objective pathology, guessing is genuinely more likely to lead you down the wrong treatment path than it would for most other conditions.
If swallowing is the main issue, a speech and language therapy assessment alongside ENT input is the sensible starting point, not because your swallow is necessarily unsafe, but because they can actually see what’s happening mechanically rather than everyone guessing from symptoms alone. If reflux is dominant, ask whether objective testing (pH-impedance monitoring, not just a trial of medication) has actually been done before committing to long-term high-dose acid suppression that may not be targeting the right mechanism. If PoTS or broader dysautonomia is part of your picture, addressing that directly, through the standard autonomic strategies of fluid and salt intake, compression, graded activity and where appropriate medication, may improve throat and reflux symptoms as a knock-on effect, per the pattern we saw in the data above. And if mast cell involvement is suspected, a structured trial of antihistamines under medical guidance is a reasonable, low-risk way to test that hypothesis rather than living with the uncertainty indefinitely.
None of this is about chasing every possible diagnosis at once. It’s about matching the investigation to the mechanism that’s actually most plausible for your specific pattern of symptoms, rather than defaulting to whichever explanation happens to be most fashionable this year. It’s the same principle behind proper pacing for any chronic symptom picture, work with the mechanism you actually have, not the one that’s easiest to Google. The throat is small, but it’s genuinely complicated, and it deserves better than a one-size-fits-all answer.
Frequently Asked Questions
If you’ve read this far, you’ve now got a better grip on throat, voice and reflux problems in hypermobility than most people get from a ten-minute GP appointment, and that includes some of the genuinely inconvenient nuance that gets left out of the tidier versions of this story. Your throat is a small, densely packed piece of anatomy doing an enormous, largely invisible job, several times a minute, every single day, not unlike the rest of the soft tissue systems that quietly do more work than they get credit for in hypermobility. When it comes to hypermobility, it’s not surprising that job gets harder. What matters now is using what you’ve learned here to ask better questions of whoever you see next, and to push, gently but firmly, for the objective testing that actually tells you what’s going on rather than what everyone assumes is going on.
– Adam –
References
- Williams HR, Wood G, Hakim AJ, Birchall M, Hirani SP. Self-reported throat symptoms in Ehlers-Danlos syndromes and hypermobility spectrum disorders: A cross-sectional survey study. Laryngoscope Investig Otolaryngol. 2023 Oct, 8(5):1259-1264. doi: 10.1002/lio2.1120
- Hakim A. Hypermobile Ehlers-Danlos Syndrome. GeneReviews [Internet]. Seattle: University of Washington, Seattle. Bookshelf ID: NBK1279. Last updated 22 Feb 2024.
- Arnaert S, Arts J, Raymenants K, Baert F, Delsupehe K. Retrograde Cricopharyngeus Dysfunction, a New Motility Disorder: Single Center Case Series and Treatment Results. J Neurogastroenterol Motil. 2024 Apr 30, 30(2):177-183. doi: 10.5056/jnm23099
- Fikree A, Aziz Q, Sifrim D. Mechanisms underlying reflux symptoms and dysphagia in patients with joint hypermobility syndrome, with and without postural tachycardia syndrome. Neurogastroenterol Motil. 2017 Jun, 29(6). doi: 10.1111/nmo.13029
- Butt MF, Dervin H, Hoshino S, Yazaki E, Gerard P, Sweis R, Sifrim D, Aziz Q, Zárate-López N, Fikree A. Esophageal Dysmotility and Gastroesophageal Reflux Disease Risk in Hypermobile Ehlers-Danlos Syndrome. Clin Gastroenterol Hepatol. 2026 May 11. doi: 10.1016/j.cgh.2026.04.019
- Diep D, Fau V, Wdowik S, Bienvenu B, Bénateau H, Veyssière A. Dysfonction de l’appareil manducateur et syndrome d’Ehlers-Danlos de type hypermobile: étude cas-témoin. Rev Stomatol Chir Maxillofac Chir Orale. 2016 Sep, 117(4):228-233. doi: 10.1016/j.revsto.2016.07.009
- Yekkalam N, Novo M, Tyrberg MJ, Sipilä K. Risk factors associated with symptoms of temporomandibular disorders among women with hypermobile Ehlers-Danlos syndrome: Questionnaire-based study in Finland and Sweden. J Oral Rehabil. 2024 Aug, 51(8):1390-1400. doi: 10.1111/joor.13706
- Monaco A, Choi D, Uzun S, Maitland A, Riley B. Association of mast-cell-related conditions with hypermobile syndromes: a review of the literature. Immunol Res. 2022 Aug, 70(4):419-431. doi: 10.1007/s12026-022-09280-1
- Barham WT, Alvarez-Amado AV, Dillman KM, Thibodeaux E, Nguyen ID, Varrassi G, Armstrong CJ, Howard J, Ahmadzadeh S, Mosieri CN, Kaye AM, Shekoohi S, Kaye AD. Laryngopharyngeal Reflux Pathophysiology, Clinical Presentation, and Management: A Narrative Review. Cureus. 2024 Aug 20, 16(8):e67305. doi: 10.7759/cureus.67305
- Lohkamp LN, Marathe N, Fehlings MG. Craniocervical Instability in Ehlers-Danlos Syndrome: A Systematic Review of Diagnostic and Surgical Treatment Criteria. Global Spine J. 2022 Oct, 12(8):1862-1871. doi: 10.1177/21925682211068520
- Selleslagh M, van Oudenhove L, Pauwels A, Tack J, Rommel N. The complexity of globus: a multidisciplinary perspective. Nat Rev Gastroenterol Hepatol. 2014, 11(4):220-233. doi: 10.1038/nrgastro.2013.221
- Sweerts KWE, Vork L, Mujagic Z, Conchillo JM, Keszthelyi D. Comprehensive Motility Analysis in Patients with Hypermobility Spectrum Disorders and Gastrointestinal Symptoms: An Exploratory Tertiary Care Study. Dig Dis Sci. 2025, 70(10):3443-3452. doi: 10.1007/s10620-025-09206-5
