Proposed Section Structure
1. Highlights
2. Clinical Background and Unmet Need
3. Study Design and Patient Cohort
4. Interventions and Outcome Measures
5. Key Results
6. Clinical Interpretation
7. Limitations and Research Gaps
8. Practice Implications
9. Funding, Registration, and Citation
10. References
Highlights
In this retrospective series of seven patients with absent upper esophageal sphincter opening after neurological injury, cricopharyngeus-targeted interventions were associated with better pharyngoesophageal segment opening and improved oral intake.
Functional gains were reflected by improvements in the Functional Oral Intake Scale and Mann Assessment of Swallowing Ability, suggesting that mechanical restoration of bolus passage may translate into meaningful nutritional benefit.
Airway safety improved far less consistently. Penetration-Aspiration Scale scores remained high in most patients, indicating persistent aspiration risk despite better upper esophageal sphincter opening.
Patients treated within 6 months of neurological injury appeared to experience larger improvements in oral intake than those treated later, raising the possibility that timing of intervention is clinically important.
Clinical Background and Unmet Need
Dysphagia after neurological injury is common, clinically consequential, and often multifactorial. Stroke, traumatic brain injury, hypoxic brain injury, and other central or peripheral neurological insults can impair bolus formation, pharyngeal propulsion, laryngeal closure, and relaxation or distension of the upper esophageal sphincter (UES). Among the most challenging phenotypes is absent UES opening during swallowing, a problem that can severely limit bolus transit from the pharynx into the esophagus.
The UES is not simply a static muscular valve. Effective opening depends on coordinated neural control, cricopharyngeus relaxation, anterior-superior hyolaryngeal excursion, intrabolus pressure generation, and compliance of the pharyngoesophageal segment. In neurological injury, failure of this integrated system can lead to profound residue in the pyriform sinuses and hypopharynx, repeated airway contamination, inability to sustain oral nutrition, and prolonged dependence on enteral feeding.
Clinically, absent UES opening presents a therapeutic dilemma. Traditional swallowing therapy may strengthen compensatory mechanisms and improve timing, but if the pharyngoesophageal segment remains mechanically non-opening, functional recovery may be limited. Conversely, interventions directed at the cricopharyngeus muscle, such as balloon dilation, botulinum toxin injection, or surgical myotomy, may improve bolus passage but do not necessarily correct coexisting deficits in airway protection. The present study by Rawat and colleagues addresses this exact tension: can cricopharyngeus-directed treatment meaningfully improve swallowing in patients with absent UES opening after neurological injury, and if so, what aspects of swallowing recover and what risks remain?
Study Design and Patient Cohort
The investigators performed a retrospective review of seven patients treated between September 2021 and July 2024. All patients had absent UES opening confirmed on Modified Barium Swallow Study (MBSS), and all had dysphagia following neurological injury. The article focuses on a rare and severe subgroup rather than the broader population of post-neurological dysphagia, which is both a strength and a limitation: the findings are highly clinically specific, but the small sample size constrains inference.
Each patient underwent swallowing therapy before receiving at least one cricopharyngeus-targeted intervention. These interventions included balloon dilation, botulinum toxin injection, and/or cricopharyngeal myotomy. The sequence reflects real-world escalation of care in complex dysphagia management, where conservative therapy is usually attempted before more invasive procedures are considered.
The study did not include a parallel control group managed with therapy alone, and treatment selection was individualized. As a result, the analysis is best interpreted as hypothesis-generating rather than definitive comparative effectiveness research.
Interventions and Outcome Measures
The study used clinically meaningful and widely recognized swallowing outcome measures.
The Functional Oral Intake Scale (FOIS) assessed the degree of oral intake, ranging from nothing by mouth to a full oral diet without restrictions. This is often the most patient-centered dysphagia endpoint because it reflects real-world nutritional independence.
The Mann Assessment of Swallowing Ability (MASA) provided a broader clinical assessment of swallowing function, incorporating bedside swallowing features and risk domains.
The Penetration-Aspiration Scale (PAS) measured airway invasion during swallowing, with higher scores indicating deeper entry of material into the airway and poorer clearance. Persistent PAS values of 7 or higher typically signify severe impairment in airway protection.
Pharyngoesophageal segment opening scores were derived from the Modified Barium Swallow Impairment Profile, offering a structured fluoroscopic measure of the specific physiological target under treatment.
Together, these endpoints allowed the authors to separate mechanical opening from airway protection and from functional oral intake. That distinction is especially important in neurogenic dysphagia, where improvement in one physiological domain does not guarantee normalization of the entire swallow.
Key Results
The main signal in the study was consistent: cricopharyngeus-targeted surgery or procedural intervention was associated with improved UES-related mechanics and better oral intake. FOIS scores improved after intervention, suggesting that patients were able to resume or advance oral feeding to a clinically meaningful degree. MASA scores also improved, indicating broader gains in swallowing performance. In parallel, pharyngoesophageal segment opening scores improved on MBSS, supporting the biological plausibility of the treatment effect. In simple terms, the procedures appeared to make the UES open better and thereby facilitate bolus passage.
However, improvement in airway safety was much less evident. PAS scores did not change substantially, and six of the seven patients continued to demonstrate PAS values of 7 or greater. This finding is arguably the most important clinical caution in the study. It indicates that even when the bolus can pass more effectively into the esophagus, substantial aspiration or near-aspiration risk may remain. For clinicians, that means procedural success at the pharyngoesophageal segment should not be misinterpreted as complete swallowing recovery.
The study also reported a notable timing signal. Patients who underwent cricopharyngeus-directed intervention within 6 months of neurological injury had greater FOIS improvement than those treated later, with mean improvement of 3.25 points versus 0.33 points. Although based on very few patients, this difference is clinically striking. It raises the possibility that earlier intervention may prevent maladaptive disuse, prolonged tube dependence, or fibrosis-related loss of segment compliance, while capitalizing on the period of greatest neuroplastic recovery.
Because the cohort was small and treatment strategies varied, the study was not positioned to determine which intervention among dilation, botulinum toxin, or myotomy is superior. Nonetheless, the aggregate message is that a CP-directed approach can be useful when absent UES opening is clearly documented and conservative therapy alone is insufficient.
Clinical Interpretation
This study highlights a clinically important principle: dysphagia physiology should be decomposed into its component failures. In patients with neurological injury and absent UES opening, a purely compensatory therapy strategy may be inadequate if the cricopharyngeus remains a major outflow obstruction. By targeting the obstruction directly, clinicians may improve bolus clearance and oral intake even when the neurological injury itself is not reversible.
At the same time, the persistent PAS abnormalities underscore that swallowing is more than a conduit problem. Airway protection requires timely laryngeal vestibule closure, glottic competence, sensory responsiveness, pharyngeal contraction, and post-swallow clearance. These functions may remain severely compromised after neurological injury even if the UES opens better. In fact, improved bolus flow into and through the hypopharynx could still coexist with aspiration if supraglottic and glottic defenses are weak or delayed.
For this reason, the article appropriately emphasizes continued swallowing therapy after intervention. Therapy remains necessary to address hyolaryngeal excursion, pharyngeal constriction, timing, secretion management, compensatory strategies, and diet modification. Procedural intervention should therefore be seen as part of a multimodal dysphagia program rather than a standalone cure.
The apparent benefit of earlier intervention is also biologically plausible. Neurogenic swallowing disorders evolve over time. Early in the course, there may be reversible neural dysfunction and preserved tissue compliance. With prolonged dysfunction, patients may develop severe deconditioning, persistent nonuse, altered sensorimotor patterns, and greater nutritional compromise. Delayed intervention may therefore be less effective, not because the procedure is inferior, but because the overall swallowing system has become less recoverable.
How This Fits With Existing Literature
The findings align with prior literature suggesting that impaired UES opening can respond to targeted treatment in selected patients. The mechanisms may differ among interventions. Balloon dilation increases segment compliance; botulinum toxin can temporarily reduce cricopharyngeal hypertonicity; myotomy provides a more definitive reduction in outflow resistance. Earlier studies in neurogenic and structural cricopharyngeal dysfunction have shown that treatment can improve transit and symptoms, but outcomes are heterogeneous and strongly influenced by the integrity of the rest of the swallowing mechanism.
One of the foundational concepts in this field is that UES opening depends not only on cricopharyngeus relaxation but also on traction generated by hyolaryngeal excursion. Shaker and colleagues previously demonstrated that exercise-based rehabilitation can improve UES opening in selected patients with pharyngeal dysphagia. The present study addresses the subset in whom opening is absent despite therapy, effectively identifying patients in whom a direct intervention on the pharyngoesophageal segment may be necessary.
The study’s cautionary message on aspiration also fits long-standing clinical experience. Patients may report easier swallowing or improved oral intake after CP intervention yet remain vulnerable to silent aspiration, recurrent pneumonia, or chronic airway contamination. This reinforces the need for objective reassessment with instrumental studies rather than relying on symptom improvement alone.
Limitations and Research Gaps
The central limitation is sample size. With only seven patients, effect estimates are unstable, subgroup comparisons are fragile, and treatment heterogeneity is unavoidable. The retrospective design further introduces selection bias, variable follow-up, and uncertainty about how decisions were made to escalate to one intervention versus another.
Another limitation is the absence of a control group treated with swallowing therapy alone. Some degree of recovery may have occurred because of spontaneous neurological improvement, concurrent therapy, or time. This issue is especially relevant when interpreting the apparent advantage of earlier intervention, because those treated sooner may also differ systematically in injury type, baseline reserve, or access to specialized care.
The report also cannot resolve procedural sequencing. In clinical practice, balloon dilation, botulinum toxin, and myotomy are often considered along an invasiveness spectrum, but which patients should receive which procedure first remains uncertain. Future studies would ideally stratify patients by mechanism of UES dysfunction, such as hypertonic nonrelaxation versus reduced traction versus fibrotic noncompliance, because response is likely mechanism-specific.
Finally, the study focuses on surrogate and functional swallowing outcomes but offers limited information on hard clinical endpoints such as pneumonia, hospitalization, feeding tube removal rates, nutritional status, or quality of life. These outcomes matter greatly for patients and health systems and should be incorporated into future prospective work.
Practice Implications
For clinicians managing severe neurogenic dysphagia, this study supports several practical points.
First, absent UES opening on MBSS should prompt careful physiological analysis rather than therapeutic nihilism. In selected patients, the pharyngoesophageal segment may represent a treatable bottleneck.
Second, CP-targeted intervention may improve oral intake, particularly when paired with expert swallowing therapy. This can be meaningful even if swallowing does not normalize, because small gains in oral intake may reduce tube dependence, improve patient morale, and expand rehabilitation possibilities.
Third, aspiration risk should be assumed to persist until proven otherwise. High PAS scores after intervention mean diet liberalization must be cautious and guided by repeat instrumental assessment and speech-language pathology expertise.
Fourth, earlier referral to a multidisciplinary dysphagia team may matter. Patients with prolonged severe dysphagia after neurological injury should not wait indefinitely for spontaneous recovery if instrumental studies show a persistent non-opening UES and poor oral intake.
A practical care pathway emerging from this report would include early MBSS characterization, intensive swallowing therapy, multidisciplinary review, and timely consideration of balloon dilation, botulinum toxin, or myotomy when absent UES opening remains a dominant abnormality. Reassessment after intervention should include both swallowing efficiency and airway safety.
Conclusion
Rawat and colleagues present an important early signal in a rare but clinically significant dysphagia phenotype. In patients with absent UES opening after neurological injury, cricopharyngeus-targeted intervention appears capable of improving pharyngoesophageal segment opening and advancing oral intake. Yet the study also makes clear that restoring mechanical opening does not reliably restore airway protection. Most patients remained at high aspiration risk, reinforcing the central role of ongoing swallowing therapy and repeat instrumental reassessment.
The most provocative finding is the suggestion that treatment within 6 months of injury may yield greater functional benefit. Although this observation requires confirmation in larger prospective studies, it supports earlier multidisciplinary evaluation rather than prolonged passive observation. Future research should define which physiological subtypes respond best to which procedures, determine optimal timing, and evaluate patient-centered outcomes such as feeding tube independence, pneumonia, and quality of life.
For now, the key takeaway is balanced and clinically useful: CP intervention can be an important tool in severe neurogenic dysphagia with absent UES opening, but it should be deployed as part of a comprehensive rehabilitation strategy, not as a substitute for it.
Funding and ClinicalTrials.gov
Funding information was not provided in the abstract. No ClinicalTrials.gov registration was reported; the study was a retrospective review.
Citation
Rawat R, Abrahamson CW, Rogers K, Langenstein J, Bromfield J, Seth A, Burns JA, Stein AP. Management of Absent Upper Esophageal Sphincter Opening After Neurological Injury. The Laryngoscope. 2026-05-18. PMID: 42152494. URL: https://pubmed.ncbi.nlm.nih.gov/42152494/
References
1. Rawat R, Abrahamson CW, Rogers K, Langenstein J, Bromfield J, Seth A, Burns JA, Stein AP. Management of Absent Upper Esophageal Sphincter Opening After Neurological Injury. The Laryngoscope. 2026-05-18. PMID: 42152494.
2. Shaker R, Easterling C, Kern M, Nitschke T, Massey B, Daniels S, Grande B, Kazandjian M, Dikeman K. Rehabilitation of swallowing by exercise in tube-fed patients with pharyngeal dysphagia secondary to abnormal UES opening. Gastroenterology. 2002;122(5):1314-1321.
3. Cook IJ, Kahrilas PJ. AGA technical review on management of oropharyngeal dysphagia. Gastroenterology. 1999;116(2):455-478.
4. Logemann JA. Evaluation and Treatment of Swallowing Disorders. 2nd ed. Austin, TX: Pro-Ed; 1998.
5. Martin-Harris B, Brodsky MB, Michel Y, Ford CL, Walters B, Heffner J, Breeding K, Blair J, Wallace KL, Rosenbek JC. MBS measurement tool for swallow impairment—MBSImP: establishing a standard. Dysphagia. 2008;23(4):392-405.
6. Rosenbek JC, Robbins JA, Roecker EB, Coyle JL, Wood JL. A penetration-aspiration scale. Dysphagia. 1996;11(2):93-98.
7. Crary MA, Mann GD, Groher ME. Initial psychometric assessment of a functional oral intake scale for dysphagia in stroke patients. Arch Phys Med Rehabil. 2005;86(8):1516-1520.