Retrograde cricopharyngeus dysfunction (R-CPD), also known as inability to belch syndrome—a narrative review

Introduction

Retrograde cricopharyngeus dysfunction (R-CPD) is an under-recognized disorder wherein the upper esophageal sphincter (UES) fails to open following gaseous reflux from the stomach thereby trapping the refluxed air in the distended esophagus. The result is an inability to belch which can be associated with an array of symptoms including gurgling noises in the chest, bloating, flatulence, and chest pain that can severely impact a patient’s quality of life. First described as a case report in 1987 (1), this was an obscure condition until the description of botulinum toxin (Botox) injection into the cricopharyngeus (CP) as an effective therapy in 2019 (2) and the widespread dissemination of the syndrome’s existence over social media. In parallel with the explosion of R-CPD cases, there has also been an explosion of medical publications related to the disorder as evident in Figure 1. This narrative review will discuss the normal mechanism of belching, clinical and physiological observations made regarding R-CPD, what is known of the epidemiology of R-CPD, diagnostic criteria for R-CPD, the clinical experience in treating R-CPD, and a proposed management strategy when the disorder is suspected. We present this article in accordance with the Narrative Review reporting checklist (available at https://tgh.amegroups.com/article/view/10.21037/tgh-2025-158/rc).

Figure 1 After the publication of the index case in 1987, two other single cases were reported. The publication of the first patient series treated with Botox in 2019 triggered a logarithmic increase in the number of publications. Link to search string used in PubMed accessed on November 15, 2025. Figure used with permission of the Ken Griffin Esophageal Center at Northwestern. Botox, botulinum toxin.

Methods

The search for relevant publications was performed by both authors using the PubMed, Scopus and Cochrane databases, and the time frame was 1987 to November 15, 2025. Only papers with an abstract in English were considered. The keywords used in the database searches and the details of the search process are provided in Table 1 and Table S1.

The normal mechanism of belching

The muscular components of the UES include the inferior pharyngeal constrictor, the CP muscle, and the proximal esophagus. However, the dominant contractile component is the CP muscle which inserts to the lateral aspects of the cricoid cartilage in a C-shaped configuration with the plate of the cricoid cartilage forming the anterior wall of the sphincter and closing the C. Because of this dominance, the terms ‘cricopharyngeal sphincter’ and UES are often considered synonymous and retrograde UES dysfunction was rebranded as R-CPD. The CP is striated muscle but contains about 40% connective tissue, much of which is elastic (3) resulting in a passive residual tone of about 6 mmHg even when the sphincter is devoid of neural excitation (4). That residual tone is eliminated if the sphincter is ‘stretched’ open by anterior traction on the cricoid cartilage by the hyolaryngeal strap muscles as occurs during swallowing (5) or, in the case of belching, either by contraction of the thyrohyoideus muscle (6-8) to ‘pull’ it open or by intraesophageal gas pressure to ‘push’ it open.

Unlike other sphincters that have a constant tone generated by neural input and/or intrinsic contractility of the muscle, the UES does not exhibit a constant neurogenic or myogenic tone. Cricopharyngeal electromyography (EMG) of chronically instrumented awake animals exhibit very low activity when the animal is calm and resting its head (9,10). Similarly in awake humans undergoing prolonged manometric recordings with a miniature recording device to minimize discomfort, UES pressure during long inter-swallow intervals was sufficiently low to suggest that it was mainly attributable to the elastic properties of the CP rather than active contraction (11). However, the UES contracts during a multitude of bodily functions (1° and 2° peristalsis, respiration, coughing, sneezing) and in response to a wide array of extrinsic stimuli (pharyngeal stimulation, proximal esophageal distention, pulmonary distention, head movements, emotional stress) (12). Hence, most manometrically recorded UES pressure is attributable to these reflexive responses [some stimulated by the recording technique itself (9,13)] rather than sphincter ‘tone’. Devoid of these influences UES tone falls to low values consistent with the elastic properties of the CP muscle as seen during anesthesia (9) and sleep (14).

For belching to occur, both the lower esophageal sphincter (LES) and the UES must not only relax, but they must physically open. Normally, this occurs by the following sequence of events: (I) transient lower esophageal sphincter relaxation (tLESR), a vagovagal reflex that elicits LES relaxation, crural diaphragm inhibition, and distal esophageal longitudinal muscle contraction (15,16); (II) gastroesophageal gas reflux, manometrically evident by slight pan-esophageal pressurization of the esophagus, usually to less than 10 mmHg making it equal to intragastric pressure e.g. ‘common cavity pressure’ (17); (III) UES opening [elimination of all neurally driven UES contractility and contraction of the thyrohyoideus muscle to eliminate the elastic component of UES pressure and open the sphincter (6-8)]; (IV) variably, an abdominal contraction or ‘strain’ (18); (V) esophago-pharyngeal gas reflux evident by esophageal depressurization with or without an audible belch (19); and (VI) restoration of intra-esophageal pressure to baseline by a peristaltic contraction, usually secondary peristalsis (17). The relationship between tLESRs and gastric venting was clearly demonstrated in normal subjects fed a high-fat test meal and then monitored with high-resolution manometry (HRM) and a distal esophageal pH electrode for a 2-hour period (19). More than 200 tLESRs were observed and 79% of these were associated with brief periods of UES relaxation, usually after manometric evidence of gas reflux. These UES relaxations were usually very short, not associated with audible burps, and often subconscious leading the investigators to call them ‘microburps’ (Figure 2). Notably, the pattern of UES response was the same during tLESRs with or without acid reflux as detected by the distal esophageal pH electrode implying that gas venting of the stomach is the physiological ‘purpose’ of tLESRs.

Figure 2 High resolution manometry recording (top panel) of a ‘microburp’ in a normal volunteer. The lower panel shows pressure recordings from representative pressure sensors located in the stomach (green), distal esophagus (blue), and proximal esophagus (red). Note that with the onset of gas reflux, there is rapid pressurization of the distal esophagus to intragastric pressure, an event termed a ‘common cavity’. Within 0.5 s of the common cavity, upper esophageal sphincter pressure drops to 0 mmHg facilitating gas escape into the pharynx and depressurization of the esophagus. Also note that during the microburp, there is a slight increase in intragastric pressure caused by a brief abdominal strain and that the net result of the microburp is for gastric pressure to fall from about 11 to 8 mmHg. Figure used with permission of the Ken Griffin Esophageal Center at Northwestern.

Although both LES and UES opening are a prerequisite for belching, they occur by independent mechanisms. LES opening occurs by tLESRs; UES opening occurs in response to gaseous distention of the esophagus. If air is rapidly injected into the mid esophagus, it triggers UES opening without a tLESR. The larger the volume of air injected, the greater the likelihood of eliciting UES relaxation and the more prolonged the period of relaxation (17). With 5 mL injections UES relaxations occurred <20% of the time averaging 0.34 s whereas with 30 mL injections UES relaxations occurred >80% of the time averaging 0.8 s. Although only 14 subjects were studied in those experiments, the results suggest that there are ‘low threshold belchers’ and ‘higher threshold belchers’. In contrast to the air injections, rapidly injecting saline into the mid esophagus did not elicit UES relaxation but caused either no change in UES pressure or UES contraction.

Animal experiments suggest that the UES opening response is mediated by esophageal mucosal receptors that are sensitive to rapid distention as occurs during gas reflux since the response is eliminated by mucosectomy or lidocaine infusion onto the mucosa (6). UES relaxation is also not observed during rapid esophageal distention with bagged saline as occurs during repetitive antegrade contractions in functional lumen imaging probe (FLIP) panometry studies (albeit not as rapid as occurs with gaseous distention) (20). As for timing, on average UES opening occurred about 0.4 s after gas reflux in the microburp experiments. However, this was widely variable ranging from 0.3 s before proximal esophageal pressurization to 1.3 s after proximal esophageal pressurization. In other words, in some instances UES opening occurred in anticipation of gas reflux. The observed variability in latency between esophageal pressurization and UES opening both within individuals and among individuals as well as the observations that UES opening sometimes anticipates gas and that the threshold gas volume necessary to elicit gas reflux is variable among subjects all imply that the UES belch reflex involves a complex neural pathway subject to some degree of volitional (or subconscious) control. It also suggests that there are likely ‘low threshold belchers’ and ‘high threshold belchers’.

Neuronal control of the belch reflex

Three types of vagal esophageal mechanoreceptors have been described: (I) mucosal intra- or subepithelial free nerve endings (21,22); (II) intramuscular intraganglionic laminar endings sensitive to tension (23); and (III) muscular/mucosal receptors which are sensitive to both mucosal stroking and circumferential tension (24). In healthy individuals, slow distension of the proximal esophagus has no effect or triggers UES contraction (17,25). Rapid distension, on the other hand, can produce relaxation, be uneventful, or stimulate contraction (17,25). Topical anesthesia increased the likelihood of contraction and decreased the probability of relaxation in response to rapid distension (25). In experiments on decerebrate cats, these responses were all abolished by vagotomy, and mucosectomy prevented relaxation but not contraction (26). Collectively, these findings suggest that mucosal mechanoreceptors trigger UES relaxation while muscular receptors produce contraction (25,26). The role of muscular/mucosal mechanoreceptors is unknown. It also appears that there are separate pathways for mucosal and muscular receptors to brainstem UES motoneurons since neurons in the nucleus of the solitary tract activated by mucosal and muscular receptors are differentially distributed as visualized with c-fos immunohistochemistry (27).

The area postrema, one of the brain’s circumventricular organs belonging to the dorsal vagal complex, is selectively activated by rapid esophageal distension (27) and, importantly, experimental ablation of area postrema in cats blocks the belch reflex (8). The thyrohyoideus contraction is eliminated and the CP relaxation is converted to a contraction. This is identical to what is seen in R-CPD and suggests that area postrema serves an inhibitory function facilitating the belch reflex and inhibiting reflexive contraction of the CP in response to esophageal stimulation. Area postrema also has a central role in emesis suggesting that its dysregulation is not only linked to R-CPD but also to emetophobia, another symptom often reported by R-CPD patients. Indeed, some R-CPD patients claim that they cannot vomit at all (2). Figure 3 summarizes the neural control of the UES in belching (Figure 3A) or reflexive contraction (Figure 3B), ultimately mediated by activation or inhibition of motoneurons in nucleus ambiguus (13).

Figure 3 Neural regulation of the UES. Contraction of the striated muscle of the UES (CP, IPC and PE) is modulated by motoneurons in N. ambiguus. With belching (A), rapid gaseous distention of the esophagus activates vagal mucosal mechanosensitive afferents [1] resulting in stimulation of N. tractus solitarius neurons that project to area postrema [2] and ultimately activate the belch pattern generator [3]. The belch pattern generator, the precise locus of which is unknown, strongly inhibits the N. ambiguus motoneurons projecting to the UES (indicated by the red neuron) [4] causing UES relaxation [5] and stimulates the thyrohyoideus muscle via spinal C1 neurons and the hypoglossal nerve to pull the UES open (green neurons) [6] and facilitate belching. Area postrema is also essential in activation of the vomiting pattern generator (the precise location of which is also unknown) which shares some of the motor outputs of the belch pattern generator. (B) On the other hand, with slow distention of the proximal esophagus such as occurs during balloon distention (pictured) or liquid gastroesophageal reflux, the vagal afferents originating from mechanoreceptors in the esophageal muscularis [1] dominate, activating a different pathway in N. tractus solitarius [2] that stimulates the N. ambiguus motoneurons projecting to the UES resulting in UES contraction [3]. In this case, the inhibitory area postrema pathway is bypassed. This pathway is also activated by numerous other reflexes as well as subconscious/volitional control (detailed in the box). Ultimately, whether the net result of an esophageal stimulus is of UES opening or UES contraction depends on the balance of outputs from pathway A and pathway B. Note that in A and B, no distinction has been made between mono- and polysynaptic circuits. Figure used with permission of the Ken Griffin Esophageal Center at Northwestern. CP, cricopharyngeus; IPC, inferior pharyngeal constrictor; N., nucleus; PE, proximal esophagus; UES, upper esophageal sphincter.

Area postrema probably doesn’t control belching directly but rather coordinates afferent input with the complex motor response; Lang (8) has proposed that it stimulates a ‘belch pattern generator’ analogous to the vomiting pattern generator (Figure 3A). However, based on the above, it can be speculated that the root cause of R-CPD involves area postrema dysregulation, be that the result of short circuiting it or overwhelming it with input from opposing excitatory pathways (Figure 3B). Alternatively, R-CPD may be due to an absent or insufficient signaling from mucosal receptors while muscular receptor function is intact. However, the area postrema hypothesis seems more plausible since it also may explain the emetophobia and inability to vomit.

Clinical and physiological observations regarding R-CPD

The fundamental abnormality in R-CPD is an inability to belch leading some to call the condition ‘abelchia’ (19,28). However, an inability to belch is also a fundamental symptom of the post-fundoplication gas bloat syndrome wherein the barrier occurs at the surgically modified esophagogastric junction (29,30) making the term ‘abelchia’ less specific than R-CPD; in the case of R-CPD, gastric venting into the esophagus is unimpaired. Rather, gas escapes into the esophagus and its entry into the pharynx is blocked by failed opening of the UES. This usually initiates secondary peristalsis which clears the esophagus of the gaseous reflux (Figure 4A). In many cases, this occurs repetitively in an oscillatory fashion until termination of the tLESR that initiated the sequence (Figure 4B) (1,18,31,32). Of note, the repetitive series of secondary peristaltic contractions seen in R-CPD occur at a very similar rate (about 6 per minute) to the repetitive antegrade contractions seen in normal subjects during FLIP panometry studies suggesting that the rate is a consequence of the esophageal refractory period observed after a peristaltic contraction (Figure 4C) (20,33). It is also increasingly evident that peristaltic abnormalities are often associated with R-CPD, primarily ineffective esophageal motility (31% to 63%) or absent contractility (11% to 53%) (18,31,34). Either ineffective esophageal motility or absent contractility were reported in 88% (31), 84% (32), 66% (18), 70% (35), and 64% (34) of R-CPD cases in the five patient series that were studied with HRM. It can be speculated that chronic, repetitive, esophageal distension from trapped gas reflux induces esophageal dysmotility but, ultimately, the cause-and-effect relationship of these findings remains to be determined. Likewise, the reversibility of esophageal dysmotility is not known.

Figure 4 Illustrative HRM recordings of R-CPD. Pressure scale applies to Panels A, B, and C. (A) HRM recording of the entire sequence beginning with transient LES relaxation and gas reflux. Gas reflux pressurizes the esophagus to the UES which fails to relax, trapping the pressurized air in the esophagus until cleared by secondary peristalsis which also terminates the transient LES relaxation in this case. (B) Gas reflux oscillations. Repetitive gas reflux events are the genesis of the gurgling sounds in the chest experienced by many afflicted patients. Note how gas reflux causes a common cavity, equalizing esophageal pressure with gastric pressure and increasing it abruptly by 11 mmHg. (C) Concurrent FLIP panometry and HRM study in a normal volunteer with normal motility. The FLIP panometry study shows RACs occurring at about 6 per minute as the saline contained in the FLIP bag is repeatedly pushed distally only to reflux back, triggering another contraction. The concomitant HRM recording shows the associated contractile pressures (black rectangle) with no associated UES relaxation as this is not gaseous distention. Note that the RAC frequency is very similar to the frequency of oscillations shown in panel B suggesting that this frequency of about 6 per minute is a function of the refractory period of the esophageal muscularis after passage of a peristaltic contraction. Figure used with permission of the Ken Griffin Esophageal Center at Northwestern. FLIP, functional lumen imaging probe; HRM, high-resolution manometry; LES, lower esophageal sphincter; RAC, repetitive antegrade contraction; R-CPD, retrograde cricopharyngeus dysfunction dysfunction; UES, upper esophageal sphincter.

Along with complete inability (or great difficulty) in belching, there are a number of other symptoms associated with or attributed to R-CPD. In the three case series that verified R-CPD manometrically totaling 122 cases (18,31,32), the most common additional symptoms were gurgling noises in the chest resultant from the oscillatory episodes of gas reflux (46% to 100%), bloating (92% to 100%) and flatulence (38% to 98%) attributable to gas retention, and chest pain related to esophageal distention (67% to 90%). Variably reported associated symptoms include an inability to vomit, emetophobia, hiccups, nausea, and dysphagia. Broadening the R-CPD population to include individuals diagnosed based only on their symptom complex the array of associated symptoms was similar. A systematic review conducted in 2024 (36) reported on 637 R-CPD patients in 17 case series inclusive of only 9 patients with a manometrically verified diagnosis [it predated Sanagapalli 2024 (32) and Raymenants 2025 (18)]. Among these 637 patients the dominant presenting symptoms were an inability to belch (100%), abdominal bloating (83%), gurgling noises (75%), and excessive flatulence (71%) with hiccups, dysphagia, globus sensation, throat tightness, difficulty vomiting, excessive vomiting, chest pain, and nausea variably reported as ‘other’ in 14%. With the exception of gurgling noises in the chest, these symptoms are commonly encountered in a gastroenterology practice and often attributed to disorders of gut brain interaction (specifically irritable bowel syndrome and dyspepsia). It is, however, noteworthy that chest pain was a dominant symptom in the cases series reported by gastroenterologists but not in those reported by otolaryngologists. This likely reflects referral bias as the esophagus has a long history of being implicated in non-cardiac chest pain (NCCP) which is generally in the clinical domain of gastroenterologists.

R-CPD and chest pain

The subject in the original report describing R-CPD had incapacitating chest pain along with chest gurgling as a presenting symptom (1). Following provocation with swallowed gas forming crystals during fluoroscopy, she experienced chest pain along with gastroesophageal gas reflux and esophageal distention up to a 3.5 cm diameter leading the authors to conclude that the patient’s perception of chest pain was likely attributable to the esophageal distention (Figure 5). Hence, R-CPD offered a plausible mechanistic explanation for the observation by Richter et al. that 60% (18 of 30) of NCCP patients but only 20% (6 of 30) of control subjects (P<0.005) exhibited hypersensitivity to esophageal balloon distention (37).

Figure 5 R-CPD imaged fluoroscopically after a test meal and ingestion of gas forming crystals. Tracings are of selected fluoroscopic images. Note how rapid gaseous distention completely distends the esophagus in <0.03 s (the temporal resolution of the fluoroscopy recording) after LES relaxation. However, there is no UES opening. This is followed by secondary peristalsis (2° P) which clears the air from the esophagus only to reflux again. Gas reflux was accompanied by gurgling and chest discomfort, but no belching. Redrawn from Kahrilas et al. (1) and Figure used with permission of Elsevier. LES, lower esophageal sphincter; R-CPD, retrograde cricopharyngeus dysfunction; UES, upper esophageal sphincter.

The relationship between esophageal balloon distention, belching, and NCCP was further explored by Gignoux et al. in a study comparing 54 consecutive NCCP patients to 33 asymptomatic controls (38). All subjects were studied with the balloon distention protocol of Richter et al. (37) and a modified version of the air distention protocol of Kahrilas et al. (17) to elicit belching with 20, 30, 40, 50, and 60 mL rapid air injections to the mid esophagus. The NCCP patients were then grouped as hypersensitive using a cutoff defined by the 95^th percentile of the control group (pain at 7 mL balloon distention) and as ‘low-threshold belchers’ or ‘high-threshold belchers’ using the cutoff of whether belching was elicited by at least two of three 40-mL air injections into the mid esophagus, again the 95^th percentile of the control group. Their findings, summarized in Table 2, are consistent with the hypothesis that gaseous distension of the esophagus attributable to a high threshold for eliciting belching is the mechanism producing NCCP in patients with a positive balloon distension test. Although the paper did not comment on whether any of these NCCP patients described difficulty belching, it seems highly likely that being a ‘high-threshold belcher’ was the mechanism of chest pain in almost half of that group.

Epidemiology of R-CPD

The epidemiology of R-CPD is difficult to assess reliably because of the unusual way that cases come to light. The first case was reported in 1987, diagnosed by confirmatory manometry and videofluoroscopy, and prior to 2019 there were only 3 cases in the literature (1,39,40), all diagnosed physiologically. Then, in 2015, an otolaryngologist and founder a tertiary care clinic focused on oropharyngeal swallowing disorders, Dr Robert Bastian, encountered a young man afflicted with the disorder and empirically treated him with Botox injection into the CP reasoning that he suffered from ‘R-CPD’, entirely based on the man’s symptom complex. The Botox injection resolved the patient’s inability to belch, gurgling noises, bloating, excess flatulence, and inability to vomit; a symptom complex that had gone undiagnosed despite numerous previous physician consultations. The patient then posted his most-satisfactory experience on Reddit, a large, community-based discussion website, which rapidly spread the word to others with symptoms like his and, by the time of Bastian’s initial report in 2019, he had encountered 121 similar patients from far and wide, all of whom he treated with Botox injection, and all diagnosed based on their symptom complex. Since then, social media has become even more effective in spreading awareness of R-CPD among patients (41). There have now been several large retrospective series of R-CPD cases from around the world [summarized in Malhotra 2024 (36)], all comprised of patients who self-diagnosed themselves after reading postings on Reddit or TikTok (18,28,32,42-44). Consequently, more than 750 cases have been reported since 2019.

In recent decades, social media has been increasingly utilized by the public to educate themselves about health concerns from patient forums and to share their own health journey experiences (45). Among the social media platforms, TikTok has the largest user base inclusive of more than 1 billion people worldwide including 62% of Americans between ages 18 and 29 years (46). This has had a remarkable impact on the detection of R-CPD evident both by the explosion of reported cases since 2019 and the mirroring of the demographic of reported R-CPD cases [mean age 29 years (range 7–68 years), 50% male] (36) with that of TikTok users (dominant ages 18-34, years, 57% male) (47). Furthermore, although essentially all patients in published series reported either life-long symptoms or symptoms for as long as they could remember (43), nearly all of them ended up being self-diagnosed based on social media research. Reflective of this, a recent analysis of TikTok content related to R-CPD found that there were 32.2 million views and 3.1 million likes across 103 posted videos pertaining to “#noburp”, “#noburpsyndrome”, and “#retrogradecricopharyngealdysfunction” with 94% of the 103 posts created by patients or the public; only 84,500 of views (0.3%) were of content generated by otolaryngologists (46).

Most R-CPD patients in the Botox-treated published series report having life-long symptoms. A recent systematic review summarized the published experience as 84% reporting life-long symptoms, 11% dating the onset to adolescence, and 3% to post-adolescence. Among the 84% with life-long symptoms, childhood problems such as gassiness, colic, incessant crying from pain, projectile vomiting, and difficulty burping were confirmed by parental recollection in 33% (48). This suggests that in most cases, where an individual lies on the low-threshold belcher—high-threshold belcher—R-CPD spectrum is established by the time of birth. Maturation for UES contractile reflexes is also demonstrable at birth (49). On the other hand, in a minority of cases R-CPD is acquired, sometimes in response to a traumatic experience involving vomiting that the patient either experienced themselves or witnessed in a loved one. Hence, in all likelihood, there can be either a genetic predisposition or a learned etiology to individual R-CPD cases. In two large case series, a positive family history was present in 21% (50) and 29% (51) of cases.

Diagnostic criteria for R-CPD

Other than the first three case reports (1,39,40) and the first case deduced by Bastian (2), almost all cases of R-CPD to date have ‘diagnosed’ themselves based on internet research. They then presented themselves to a specialist (also identified on the internet) who ‘confirmed’ the diagnosis, again based on the symptom complex (can’t burp, gurgling noises, bloating, flatulence) and subsequent response to Botox injection into the CP. None of these reported case series indicate any instances wherein the diagnosis of R-CPD was refuted by the evaluating specialist. That implies that the positive predictive value of self-diagnosed R-CPD is 100%. Although the 100% positive predictive value is seemingly unlikely, one explanation could be that this avenue of case identification finds only the most severe R-CPD patients. It is also possible that some of the observed therapeutic failures (average of about 10% among series) were attributable to misdiagnosis. Another limitation with self-diagnosis is that not all individuals, be they R-CPD patients or not, accurately report their ability to belch. In support of this notion, among a group of achalasia patients with ‘abelchia’ or ‘dysbelchia’, some only acknowledged this disability after being specifically questioned about it (52).

The above observations argue for the need of a diagnostic test for R-CPD. Having objective criteria for defining R-CPD would not only solidify the diagnosis in less obvious cases, but it would also be invaluable as an outcome measure for clinical trials. Objective criteria for stratifying retrograde UES function would also test the hypothesis that this is not a dichotomous situation of ‘yes R-CPD’ vs. ‘no R-CPD’; rather, individuals likely exist along a spectrum consistent with the concept of Gignoux et al. that there are ‘high-threshold belchers’ and ‘low-threshold belchers’ (38) with the self-identified R-CPD cases being extreme ‘high-threshold belchers’. Furthermore, threshold aside, patients who swallow less and don’t drink carbonated beverages may have less frequent symptoms. It has been calculated that the daily volume of air swallow varies enormously among subjects: 320–47,000 mL (53). This must have an impact on symptom severity in R-CPD patients.

Among potential technologies to objectively diagnose R-CPD the most attractive are HRM or high-resolution impedance manometry (HRIM) with carbonated beverage provocation. HRM easily visualizes UES tone, esophagogastric junction tone, gas reflux, and UES relaxation (Figure 4). Provocative testing with 200 mL (or more if necessary) carbonated water is very effective both in eliciting symptoms and providing confirmatory manometric/impedance findings (18,31,32,54). A repetitive oscillatory pattern of gas reflux, secondary peristaltic contractions clearing the refluxed gas, but without UES relaxation or gas venting (belching) such as illustrated in Figure 4B is also typical, but not necessarily a uniform finding given that a substantial fraction of R-CPD patients have impaired or absent peristalsis.

Additionally, to fully explore one’s (in)ability to belch the threshold air volume necessary to trigger UES relaxation can be quantified as described by Gignoux et al. (38). This would be unnecessary with a positive carbonated water challenge but would be helpful in instances when the carbonated water challenge was non-diagnostic or when individuals were being evaluated for difficulty but not necessarily a complete inability to belch. Testing would involve having a second tube alongside the HRM probe through which the operator could rapidly inject air boluses starting at 20 mL and progressing upward to 30, 40, 50, or 60 mL until defining the volume at which 2 of 3 test injections were effective in eliciting complete UES relaxation and gas venting; reproducing the patient’s symptoms with air injections would also support the R-CPD diagnosis.

Treatment for R-CPD

Botox

Practically all R-CPD cases in the published literature have been treated with Botox injection to the CP as summarized in a 2024 systematic review inclusive of 637 patients (36). In that review the initial Botox dose ranged from 25 to 100 units with most patients receiving 50 units (n=204, 37.3%) and 554/637 (87%) reporting an improvement in symptoms following the first treatment. Seventy-nine percent of injections were done with rigid endoscopy under general anesthesia and 20% were injected with transcutaneous EMG-guided injection (55,56). Table 3 summarizes the findings from the larger series included in the 2024 systematic review and two case series (32,42) not included in that review. Overall, the initial treatment was judged to be successful in about 90% of cases with only minor and transient reported side effects, predominantly solid food dysphagia. Social media posts support the transient nature (several weeks) of Botox side effects, embellishing them to include ‘slow swallowing with food sticking in the throat’, acid regurgitation, heartburn, and uncontrollable burping. The solid food dysphagia is consistent with loss of the UES contractile reflex wherein it reflexively contracts on a solid bolus during and after passage of the pharyngeal contraction. This occurs in conjunction with the laryngeal descent after a swallow to assure transfer of luminal contents to a position 2–3.5 cm below the level of the laryngeal vestibule thereby providing protection against aspiration when the airway reopens (58).

Extrapolating from the experience of treating other disorders such as torticollis and blepharospasm, the anticipated duration of effect from a Botox injection is 12–18 weeks with a mean of 14 weeks (59,60). Hence, the benefit with respect to R-CPD should dissipate by 4 months. However, as evident in Table 4, this has not been the clinical experience. At longer-term follow-up without retreatment, 53–96% of patients were still clinical successes. Also supportive on benefit beyond the period of Botox effect was that Botox related side effects, particularly solid food dysphagia, resolved in all the reports.

Since Botox has not been convincingly shown to cure any medical condition, let alone R-CPD, it must help facilitate a cure that is then sustained beyond the expected duration of the Botox effect. Given the multitude of UES contractile responses (Figure 3B), this raises the issue of whether Botox allows treated individuals to learn to burp in the absence of UES reflexive contraction. A hint of this is found in the Oude Nijhuis et al. (31) series which commented that although 5 of the 8 R-CPD patients could belch spontaneously after Botox treatment, “three patients still needed an extra maneuver to vent air, for example, contraction of the abdominal muscles to increase abdominal pressure or tilting of the head to the side”. Head turning is known to reduce UES pressure and has been utilized as a treatment for oropharyngeal dysphagia (61). There is also one published series of seven R-CPD patients who had failed Botox (average of 2.2 treatments) and were referred to Speech Language Pathology for Behavioral Eructation Retraining Protocol (BERP) training (62). Patients were trained on the four steps of BERP (laryngeal lowering, jaw protrusion, head turn and tuck, torso anchoring). Each step was taught in isolation, followed by the integration of the steps into a coordinated movement. After an average of 3.7 BERP sessions 6 patients achieved durable relief, although 2 of these required additional Botox in the process. Another suggestion that R-CPD can be a functional disorder amenable to behavioral therapy is found in a case report of resolving the disorder with hypnosis (63). In that report of a 19-year-old lifelong R-CPD sufferer, the effective hypnotic suggestions were to “imagine applying a numbing cream to his throat when he attempts to burp, so that his gag reflex would not be elicited” and to “ask his subconscious to relax his throat muscles while he numbed his gag reflex”.

Biofeedback and cognitive behavioral therapy

Apart from the case report of resolving R-CPD with hypnosis, there are no published case reports or series of resolving R-CPD other than with Botox injection or cricopharyngeal myotomy (64). However, this disorder is the object of intense social media traffic, including testimonials of effective biofeedback, exercises, and/or cognitive behavioral therapy techniques. Surveying a sampling of these postings, there are some repetitive themes. With respect to causation, although some individuals relay a lifelong history of R-CPD, including parents telling them that they were impossible to burp as infants, more commonly the disorder started early in life often related to developing a fear of vomiting (emetophobia) either because of a personal or a witnessed traumatic vomiting experience.

With respect to therapy, the principles of ‘burp training’ are to perform a physical exercise to open the UES through exercise of the anterior strap muscles, to learn to coordinate that opening with either spontaneous gurgling indicative of gas reflux or gas reflux induced by drinking a carbonated beverage, and to enhance gas venting with contraction of abdominal wall musculature. Among postings, the greatest variability was in the description of the technique to open the UES and achieve the first burps. Some patient-generated descriptions of how to accomplish this are detailed in Table 5. These exercises are described as being beneficial both in patients without Botox treatment and in patients with an imperfect response to Botox.

Proposed management for suspected retrograde cricopharyngeus dysfunction (R-CPD)

Although physician and patient/public awareness of R-CPD have improved tremendously since 2019, it still has a way to go. The first step in managing R-CPD is to consider it when confronted with a patient who has difficulty or complete inability to burp and some symptom(s) consistent with the disorder (chest gurgling, NCCP, bloating, excess flatulence). As suggested by Sanagapalli et al. (54), “do you burp, ever?” should be a routine question asked of patients with these symptoms. Next, ideally, the disorder should be physiologically confirmed, preferably by HRM (or HRIM), with a carbonated beverage provocative test. As the reported case numbers explode and to explore the possibility that the disorder exists on a spectrum (low-threshold belcher—high-threshold belcher—R-CPD), it no longer seems reasonable to manage the condition without physiological confirmation. Should the HRM with provocation be negative or equivocal despite a high index of suspicion, we would advocate determining the belch reflex threshold during HRM with air injections to the mid esophagus. This would identify ‘high-threshold belchers’ who may be prone to the same symptoms as non-belchers. With respect to therapy, the potential for behavioral therapy is largely unexplored, especially in the less severely afflicted patients. Obviously, the current experience with behavioral therapy is minimal, but the observed prolonged Botox effect in the majority of patients suggests that some fraction of those patients could have been ‘taught to burp’ without Botox, using guidance such as that detailed in Table 5. Of course, should behavioral therapy fail, there is always the Botox option. As for Botox, although the technique utilized in the majority of publications has been rigid endoscopy and general anesthesia with 50–100 U injected into the CP, it is increasingly apparent that 50–100 U can be safely injected into the CP during flexible endoscopy and monitored anesthesia care (32).

Strengths and limitations of this review

The strength of this review is the deep familiarity of both authors with R-CPD either by initially describing the disorder and extensively studying the relevant physiology throughout his career in the case of P.J.K. or by both his own physiological and pharmacological research on belching and by intensively interrogating medical, social media, and professional contacts about the disorder in pursuit of treatment for an affected family member in the case of AL. The major weakness of the review is the nature of the clinical evidence. It is inherently unsatisfying that most diagnoses are, in fact, assumed based only on a symptom assessment. Similarly, the benefit of Botox treatment is generally subjectively assessed and uncontrolled. This is especially troubling since thousands of patients beyond those reported in case series have been treated with Botox (66) including two seen by P.J.K. who had no symptomatic response and no demonstrable R-CPD on physiological testing. Hopefully, this situation will improve with the development and implementation of validated questionnaires (67,68), validated HRM protocols (18,32), and controlled clinical trials such as one currently underway (69).

Conclusions

R-CPD, also known as ‘inability to belch syndrome’, ‘abelchia’, and ‘R-UESD’ is a rare disorder wherein the UES fails to open following gaseous reflux from the stomach resulting in an inability to belch and an array of potential symptoms including gurgling noises in the chest, bloating, flatulence, and chest pain. Although first described in 1987, the disorder was rediscovered in 2019 along with the first effective treatment, Botox injection into the CP. The ultimate cause of R-CPD is dysregulation of the vago-vagal reflex that mediates UES opening in response to gaseous distention of the esophagus which can be easily demonstrated clinically during an HRM study by provoking the need to belch with ingestion of a carbonated beverage. However, most R-CPD cases come to light via internet forums and to date most cases have been treated without any physiological confirmation. The reported success rate of Botox treatment is about 90% with most treated patients having a durable response, well beyond the transient Botox side-effects and the expected 4-month duration of action of the Botox. This raises the possibility that many cases of R-CPD may be amenable to behavioral/biofeedback therapy as a primary or secondary treatment as has shown in a case report (63), described as a salvage therapy for Botox failures (62), and claimed in several internet forums (Table 5). The authors suggest that it is time to objectify the management of R-CPD utilizing HRM studies with carbonated beverage provocation prior to treatment and in instances of treatment failure. We also see considerable potential for behavioral/biofeedback therapy prior to Botox injection to the CP and in instances of Botox failure. Furthermore, when Botox injection is necessary, this can be done safely and effectively with flexible endoscopy and monitored anesthesia care rather than rigid endoscopy and general anesthesia.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the Narrative Review reporting checklist. Available at https://tgh.amegroups.com/article/view/10.21037/tgh-2025-158/rc

Peer Review File: Available at https://tgh.amegroups.com/article/view/10.21037/tgh-2025-158/prf

Funding: None.

Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://tgh.amegroups.com/article/view/10.21037/tgh-2025-158/coif). P.J.K. serves as an unpaid editorial board member of Translational Gastroenterology and Hepatology from August 2025 to June 2027. P.J.K. received consulting fees from Reckitt and Implantica. He has a shared patent on FLIP Panometry with John E Pandolfino and Zhiyue Lin and received patent royalties on the FLIP device. He serves on the speakers bureau for Phathom Pharmaceuticals. He has given multiple lectures related to reflux disease and esophageal motility disorders at national and international meetings including Orlando Health, the American College of Allergy, Asthma and Immunology, a Reckitt sponsored symposium, and the American Foregut Society, and received travel support to attend these meetings. He serves on the data safety monitoring board for the National Institute of Health grant R01 DK138047 (Mechanistic and clinical outcomes of a surgical innovation aimed at minimizing GERD associated with vertical sleeve gastrectomy). He maintains several pages on UpToDate (an on-line medical resource) related to esophageal disorders and has written about the treatment for reflux disease for Reckitt. He is a board member and executive committee member of American Foregut Society. He has also consulted on about 6 medicolegal cases a year since 1990. The other author has no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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