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Published before final editing as: Dysphagia. 2026 May 23:10.1007/s00455-026-10965-0. doi: 10.1007/s00455-026-10965-0

Pharyngeal dysphagia in cancer: characterizing functional and physiological swallow targets across 12 cancer types

Beatrice Manduchi 1,2, Carla L Warneke 1, Carly EA Barbon 1, Xiaohui Tang 1, Ariana J Sahli 1, Sheila N Buoy 1, Katherine A Hutcheson 1
PMCID: PMC13435115  NIHMSID: NIHMS2196642  PMID: 42177326

Abstract

Background:

Dysphagia is common across cancer populations, yet it remains poorly characterized outside of head and neck (HN) cancer. Defining swallowing profiles in diverse cancer groups is essential to guide targeted supportive care and rehabilitation.

Methods:

We analyzed 10,677 MBSs from 6,423 adult cancer patients referred for dysphagia assessment (2016–2021) across 12 cancer diagnoses, at a designated comprehensive cancer center. Swallowing safety and efficiency were graded using the DIGEST scale. Multivariable mixed-effects ordinal logistic regression assessed differences in DIGEST impairment (≥1) across diagnoses. In a subset of 704 studies, physiologic impairments were examined with the MBSImP and correlated with DIGEST outcomes.

Results:

Dysphagia frequency varied significantly across cancer types for overall, safety, and efficiency domains (all p<0.05). Overall dysphagia (DIGEST≥1) was most frequent in patients with multiple cancers including HN (71%) and gastrointestinal (64%) and lowest in breast and endocrine/thyroid cancers. Safety impairments were highest in patients with multiple cancers including HN (59%), gastrointestinal (52%), and CNS (51%), while efficiency deficits predominated in patients with multiple cancers including HN (54%), HN alone (46%), CNS and multiple non-HN cancers (both 44%). Pharyngeal swallow initiation, anterior hyoid excursion, and laryngeal vestibular closure were the most frequently impaired physiologic components. Correlations between MBSImP and DIGEST varied across cancer types.

Conclusions:

Swallowing impairment profiles differ substantially by cancer type, and link to distinct physiologic targets. These findings support developing cancer-specific dysphagia pathways and integrating physiologic and functional metrics to optimize rehabilitation.

Keywords: Cancer, Deglutition, videofluoroscopy, DIGEST, Neoplasm

INTRODUCTION

Dysphagia is a debilitating consequence of cancer treatment, significantly affecting morbidity, mortality, and quality of life (QoL) across the care continuum. In head and neck cancer (HNC), where the tumor and treatments directly impact the anatomical and physiological mechanisms of swallowing, dysphagia is the leading cause of non-cancer-related death and a major contributor to long-term disability (1–3). Nearly half of HNC patients experience dysphagia within the first two years of diagnosis (4), and for many, its impact on QoL exceeds that of any other cancer-related toxicity (5).

Although much of the literature on cancer-related dysphagia centers on HNC, dysphagia is also common in cancers outside the aerodigestive tract and independently predicts survival (6–8). Causes of cancer-related dysphagia broadly include iatrogenic and treatment toxicities (e.g., surgery, neuropathy, fibrosis, sarcopenia), comorbidities, or disease progression itself (9). Furthermore, cancer patients endure challenges such as immunosuppression, prolonged hospitalization with increased exposure to healthcare-associated infections, malabsorption, constipation, diarrhea, nausea, vomiting, cachexia, general pain, and fatigue, all factors that can affect or exacerbate dysphagia (10). Kenny et al. conducted a multimodal swallowing assessment in 385 patients with solid tumors outside the head, neck, and upper gastrointestinal tract and found a dysphagia prevalence of 19%, with highest risk among individuals receiving palliative or hospice care, or those with poor functional status (11). Similarly, Frowen et al. identified a 54% prevalence of self-reported swallowing problems across patients with one of 14 different cancer types, with 46% reporting dysphagia for solids and 20% for liquids (12). A recent systematic review found that in patients with advanced non-HNC cancers, dysphagia was associated with increased mortality risk (hazard ratios 1.12–1.40), despite published prevalence estimates ranging widely from 4% to 78% (13). Beyond these clinical sequelae, dysphagia also exerts profound psychosocial burdens, with survivors of any solid tumor ranking feeding tube dependence among the most devastating treatment outcomes worse than death (14).

Despite the established burden of dysphagia outside HNC, our understanding of its clinical presentation across cancer types remains limited. Most studies in non-HNC populations have relied on patient-reported symptoms (15) or clinical (i.e., bedside) swallow examinations (11), which, while useful for screening, frontline assessment, and capturing subjective experience, fail to detail the underlying biomechanical impairments driving dysfunction. For example, Kenny et al. used clinical swallow evaluation to describe dysphagia characteristics in individuals with non-HNC solid tumors and found frequent co-occurrence of oral health issues, cranial nerve dysfunction, and signs of disease progression (16). Yet, gold standard imaging assessments of swallowing function and physiology, particularly using the Modified Barium Swallow Study (MBSs), have been largely absent from cancer investigations outside the HN region.

The absence of such data does not imply that MBSs are not routinely performed outside HNC care. A recent institutional review at a large academic cancer center revealed that among 13,055 MBSs conducted over a 6-year period, slightly over half of examinations were completed in patients with HNC, indicating frequent MBS conduct (over 1,000 annual exams) among other patients with non-HN cancer (17). This has prompted important efforts to expand the evidence base for existing clinical tools for broader oncology use. For instance, the DIGEST (Dynamic Imaging Grade of Swallowing Toxicity) scale (originally developed for HNC) was recently validated for use in non-HNC populations (18). DIGEST validation across all cancer types lays the groundwork for clinical implementation of more standardized, evidence-based approaches to dysphagia measurement across cancer types

Dysphagia care is guided by the specific clinical features of functional swallowing impairments (e.g., safety and efficiency) and underlying physiology, which may help prioritize targets for clinical research agendas surrounding dysphagia outside HN cancer. The present study aims to: i) characterize frequency and profiles of functional swallowing impairment (safety, efficiency) and ii) examine underlying physiology to explore distinct features of dysphagia across diagnoses that might be targeted for novel cancer-related dysphagia algorithms. Importantly, because HNC represents a well-characterized reference population, HNC profiles will also be derived to provide a benchmark for interpreting swallowing impairment patterns across other cancer types.

METHODS

Study design and participants

This study is a retrospective analysis of a large single institution clinical registry of MBS studies conducted between 2016 and 2021 at The University of Texas MD Anderson Cancer Center (institutional protocol PA19–0261) with data queried from the institutional EHR data warehouse. The registry includes all consecutive patients with a diagnosed or suspected cancer who underwent an MBS for any clinical indication, in both inpatient and outpatient settings. The published dataset includes patient demographics, cancer diagnoses, and MBS indication (19). For this study, any diagnosis made before or within 90 days after the MBS was considered the patient’s diagnosis. Patients who, at the time of the MBS, had had more than one primary tumor involving different anatomical regions were categorized as having multiple cancer diagnoses, whereas those with multiple primaries within the same anatomical region were classified according to that regional cancer category (e.g., multiple thoracic tumors were classified as thoracic). Patients with no identified primary tumor but with evidence of metastatic disease were classified as metastatic. Patients were excluded from this analysis if they had missing information on cancer diagnosis, missing dates of diagnosis, or missing data for the primary swallowing outcome measure (DIGEST).

MBS procedure and swallowing outcomes assessment

MBS exams were performed by speech-language pathologists (SLPs) using a standardized protocol (20), including two trials each of: 5 mL and 10 mL thin liquid barium, self-administered cup sips of thin liquid barium, one teaspoon of barium pudding, and a ¼ cracker coated in pudding (all Varibar®; Bracco Diagnostics, Inc.). Imaging was acquired in the lateral plane at 15 to 30 frames per second with audio synchronization (TIMS Medical, Foresight Imaging).

Each study was rated using the DIGEST method (21), which classifies dysphagia severity on a 5-point scale (0 = no dysphagia to 4 profound dysphagia) based on two functional domains: swallowing safety (DIGEST-S) and efficiency (DIGEST-E). DIGEST-S is determined using patterns and frequency of airway invasion (per Penetration-Aspiration Scale [PAS]), and DIGEST-E is based on ordinal estimations of pharyngeal residue. MBS studies were scored by the treating clinician; all raters met DIGEST reliability standards (≥80% exact agreement with gold-standard rater), with inter-rater reliability further established against independent central research lab scoring in a subsample of this registry (DIGEST overall κw = 0.70)(18).

A subset of exams was additionally scored using the Modified Barium Swallow Impairment Profile (MBSImP™©)(22), a standardized tool that evaluates physiologic swallowing impairment across 17 components: oral (items 1–6), pharyngeal (items 7–16), and esophageal (item 17). Each component is rated on an ordinal scale, ranging from 0 (normal) to 2–4. Due to our focused goal of characterizing pharyngeal swallowing impairment, only pharyngeal components were included, with two exceptions: Oral Component 6 (initiation of the pharyngeal swallow) was retained due to its known relevance in the pharyngeal dysphagia profile of HNC survivors (23), while Pharyngeal Component 16 (pharyngeal residue) was excluded because it was not collected systematically in this sample (due to residue rating as a component of the DIGEST grading system that is universally used in the institution). MBSImP scoring was not available for all patients and analyses are therefore restricted to the subset with complete data.

Statistical Analysis

Demographic and clinical characteristics were summarized using descriptive statistics. DIGEST scores were reported for the full sample and stratified by cancer diagnosis. Likelihood ratio tests of nested multilevel logistic regression models assessed differences in dysphagia prevalence (DIGEST ≥1) across cancer types, separately for overall, safety, and efficiency outcomes. To evaluate differences in functional swallowing profiles by diagnosis, mixed-effects ordinal logistic regression models were fit for each DIGEST domain, adjusting for MBS indication and for clustering of observations within subjects among patients with multiple MBS exams. An exploratory model additionally adjusted for age. Results were reported as odds ratios (ORs) with 95% confidence intervals (CIs). The proportional odds assumption was checked using the Brant test, with non-significant p-values (p>0.05) indicating no violation.

For the secondary aim, a subgroup analysis was conducted on MBS studies that were also scored in the EHR using the MBSImP. Only independent observations were included, selecting a single exam per patient based on the fewest missing values for MBSImP Pharyngeal items. Component scores were summarized descriptively overall and by diagnosis, with each included pharyngeal component dichotomized as “no impairment” (score = 0) vs. “any impairment” (score ≥1), except for Component 15 (tongue base retraction), dichotomized as 0–1 vs. ≥2 per previous latent class analysis (24). To examine associations between physiologic and functional impairment, DIGEST-S and DIGEST-E grades were correlated with each MBSImP pharyngeal component using Spearman correlation coefficients, stratified by diagnosis. A minimum of 15 patients per diagnostic group was required to detect a correlation of ρ ≥ 0.6 (α = 0.05, power = 0.8); diagnosis groups with fewer than 15 patients were merged based on DIGEST severity profiles from Aim 1.

All analyses were conducted using R (version 2024.09.0+375) and Stata (version 18.5), with 2-sided tests and statistical significance set at α = 0.05.

RESULTS

The registry initially included 13,055 MBS studies from 7,842 unique patients (Online Resource, eFigure 1). After excluding 918 MBS studies with missing DIGEST data and an additional 1,460 studies with missing diagnosis or diagnosis date, the final analysis included 10,677 MBS studies from 6,423 unique patients (Table 1). The majority were male (70.0%), with a mean age of 62.7 years (SD = 12.8). Most patients had HN (56.9%), followed by multiple cancers including HN (7.2%), endocrine/thyroid (6.4%), and hematologic cancers (4.6%). Most MBSs were performed in outpatient settings (89.8%, Table 1). By diagnosis, symptomatic indications accounted for more than two-thirds of MBSs (66.4–90.8%) across all groups except HN, multiple including HN, and metastatic cancers, where baseline and surveillance indications were also common (Online Resource, eTable 1).

Table 1.

Sample and MBS characteristics.

Sample characteristics (n=6,423)
Age 62.7 (12.8)
Sex
 Female 1,926 (30.0%)
 Male 4,497 (70.0%)
Diagnosis
 HN 3,653 (56.9%)
 Multiple w/HN 461 (7.2%)
 Endocrine/Thyroid 409 (6.4%)
 Thoracic 396 (6.2%)
 Hematologic 296 (4.6%)
 Multiple no HN 265 (4.1%)
 CNS 183 (2.8%)
 Metastatic 163 (2.5%)
 Gastrointestinal 137 (2.1%)
 Skin 93 (1.4%)
 Breast 80 (1.2%)
 Other solid tumors 287 (4.5%)
N of MBSs per patient
 1 3,913 (60.9%)
 2 1,358 (21.1%)
 3 760 (11.8%)
 4 257 (4.0 %)
 5 94 (1.5 %)
 6–10 41 (0.6%)
MBSs characteristics (n=10,677)
MBS indication
 Symptomatic 5,595 (52.4%)
 Surveillance pathway 2,250 (21.1%)
 Baseline 1,789 (16.8%)
 Rule out leak 881 (8.3%)
 Missing indication 162 (1.5%)
Setting
 Outpatient 8,067 (89.8%)
 Inpatient 914 (10.2%)
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CNS = Central Nervous System; HN= Head and Neck; MBS = Modified Barium Swallow

Aim 1: Functional swallow profiles per DIGEST

The distribution of DIGEST grades by cancer diagnosis is illustrated in Figure 1A–C and eTable 2. Overall swallow impairment frequency (DIGEST ≥1) differed significantly across cancer types (LR χ2(11) = 87.01, p<0.001); DIGEST ≥1 was most prevalent among patients with multiple cancers including HN and not (70.9% and 62.7%, respectively) and CNS (61.1%). Severe-to-profound overall impairment (DIGEST ≥3) was highest in patients with multiple including HN (37.0%, Figure 1A).

Fig. 1.

Fig. 1

Fig. 1

Fig. 1

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Distribution of DIGEST Overall (A), Safety (B), and Efficiency (C) impairment grades across n = 10,686 MBS studies, by cancer diagnosis. Only impairment grades ≥1 are displayed for each DIGEST domain. Dysphagia frequency differed significantly by cancer type for all domains (Overall: LR χ2(11) = 87.01, p < 0.001; Safety: LR χ2(11) = 91.30, p < 0.001; Efficiency: LR χ2(11) = 116.31, p < 0.001).

CNS = Central Nervous System; DIGEST = Dynamic Imaging Grade of Swallowing Toxicity; HN= Head and Neck

Prevalence of safety impairments (DIGEST-S ≥1) also varied significantly by cancer type (LR χ2(11) = 91.30, p < 0.001). Any safety impairment (≥1) was most common in multiple cancers including HN (58.8%), CNS cancers (51.0%) and gastrointestinal (50.4%). Severe-to-profound safety impairments (DIGEST-S ≥3) were again most frequent in multiple including HN (27.2%, Figure 1B).

Similarly, efficiency impairments (DIGEST-E ≥1) also varied significantly across cancer types (LR χ2(11) = 116.31, p < 0.001). DIGEST-E ≥1 was most frequently observed in multiple including HN (54.3%) and HN alone (46.2%). Severe-to-profound efficiency impairments (DIGEST-E ≥3) were highest in patients with multiple tumors including HN (28.1%, Figure 1C).

Table 2 and Figure 2 summarize cancer-specific odds of higher DIGEST Overall, DIGEST-S, and DIGEST-E grades (Ref: HN). Patients with multiple cancers including HN had the highest odds of increased DIGEST scores across all domains (ORs range: 1.87–2.88, p<0.05). All other cancer types had lower odds of higher DIGEST compared to HN, with breast cancer showing the lowest odds across all domains, followed by endocrine/thyroid and other solid tumors. Several cancer types (including gastrointestinal, hematologic, CNS, and patients with multiple non-HNC cancers) had lower odds compared to HN but did not reach statistical significance for Overall and DIGEST-S grades (ORs 0.61–1.05, p>0.05). In exploratory age-adjusted models (eTable 3), the pattern of cancer-type differences was largely preserved in direction and magnitude.

Table 2.

Mixed-effects models of odds of worse DIGEST grades by cancer diagnosis, adjusted for repeated measures and MBS indication (MBSs n=10,677)

Diagnosis ORs (95% CI) of ↑ DIGEST grade ORs (95% CI) of ↑ Safety grade ORs (95% CI) of ↑ Efficiency grade
HN (reference) – – –
Multiple w/HN 2.64 (1.91–3.64)* 2.88 (1.96–4.23)* 1.87 (1.28–2.74)*
Multiple no HN 0.79 (0.51–1.22) 0.84 (0.50–1.40) 0.46 (0.28–0.78)*
CNS 0.61 (0.36–1.03) 0.99 (0.54–1.83) 0.47 (0.26–0.88)*
Thoracic 0.57 (0.40–0.83)* 0.90 (0.58–1.40) 0.30 (0.19–0.47)*
Gastrointestinal 0.61 (0.33–1.12) 0.98 (0.49–1.96) 0.40 (0.18–0.75)*
Hematologic 0.68 (0.45–1.04) 0.86 (0.53–1.39) 0.56 (0.35–0.91)*
Skin 0.43 (0.21–0.88)* 0.38 (0.17–0.89)* 0.57 (0.25–1.28)
Endocrine/Thyroid 0.32 (0.22–0.46)* 0.38 (0.24–0.58)* 0.18 (0.11–0.27)*
Other solid tumors 0.37 (0.24–0.57)* 0.35 (0.21–0.58)* 0.34 (0.20–0.56)*
Metastatic 0.46 (0.26–0.79)* 0.40 (0.21–0.78)* 0.36 (0.19–0.69)*
Breast 0.08 (0.03–0.19)* 0.14 (0.05–0.35)* 0.05 (0.02–0.13)*
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*

p<0.05.

CNS = Central Nervous System; DIGEST = Dynamic Imaging Grade of Swallowing Toxicity; HN= Head and Neck

Fig. 2.

Fig. 2

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Forest plots of odds ratios for worse DIGEST overall, safety, and efficiency grades across cancer diagnoses, relative to head and neck cancer (MBSs n=10,677)

*p<0.05.

CNS = Central Nervous System; DIGEST = Dynamic Imaging Grade of Swallowing Toxicity; HN= Head and Neck

Aim 2: Physiological swallow profiles per MBSImP

MBSImP scores were available for 704 unique patients. Figure 3 and eTable 4 summarize the distribution of impaired components across cancer groups. The highest impairment rates were observed in patients with multiple diagnoses including HN and not, HN alone, and gastroinstestinal, while the lowest rates in those with other solid tumors, endocrine/thyroid and metastatic/skin/breast cancers. Impairment of pharyngeal swallow initiation was most prevalent (95.2% and 93.8% in multiple no HN and in CNS, respectively). Anterior hyoid excursion impairment was also high (multiple without/HN: 84.2%, multiple w/HN: 80.0%), followed by laryngeal vestibular closure (multiple w/HN: 68.0%, hematologic and gastrointestinal both: 66.7%). Tongue base retraction impairment was highest in multiple without/HN (71.4%) and hematologic cancers (61.9%).

Fig. 3.

Fig. 3

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Proportion of patients with impaired MBSImP pharyngeal components (score ≥1 for all but ≥2 for tongue base retraction) across cancer groups (n = 704 MBSs).

CNS = Central Nervous System; HN = Head and Neck; PES = Pharyngoesophageal Segment; MBSImP = Modified Barium Swallow Impairment Profile.

Across cancer types, distinct Spearman correlation patterns emerged between MBSImP components and DIGEST-S and DIGEST-E (Figure 4). In multiple cancer including HN, safety impairments correlated most strongly with pharyngeal stripping wave, laryngeal vestibular closure, and elevation (r = 0.65–0.69), while efficiency impairments were driven by tongue base retraction, pharyngeal contraction and epiglottic movement (r = 0.65–0.75). Gastrointestinal cancers showed strong safety associations with airway protection components (r = 0.69–0.83), with efficiency dominated by pharyngeal contraction and stripping wave (r = 0.73–75). Hematologic cancers showed strong safety correlations with vestibular closure, tongue base retraction, and PES opening (r = 0.72–0.86), while efficiency correlations were broad yet high (r = 0.78–0.95). Endocrine cancers demonstrated high correlations for safety with vestibular closure, tongue base, and stripping wave (r = 0.72–0.86), and strong efficiency correlations with tongue base retraction, pharyngeal contraction, stripping wave, and epiglottic movement (r = 0.85–0.91, Figure 4).

Fig.4.

Fig.4

Fig.4

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Spearman rho correlation between MBSImP pharyngeal components scores and DIGEST Safety (A) and Efficiency (B) across cancer groups (n = 704 MBSs).

*p < 0.05. Note that perfect association (1.00) in GI is due to event rate (no pts with impaired soft palate elevation).

CNS = Central Nervous System; HN = Head and Neck; PES = Pharyngoesophageal Segment; MBSImP = Modified Barium Swallow Impairment Profile

DISCUSSION

Dysphagia is a prevalent and debilitating consequence of cancer and its treatment, long recognized in HNC but increasingly reported across a broader range of malignancies. As cancer care evolves, with improved survival, earlier detection, and multimodal treatment paradigms (25–27), understanding how dysphagia manifests across different diagnoses is essential for timely, personalized care. Our study offers one of the most comprehensive examinations to date of swallowing dysfunction across multiple cancer diagnoses, integrating standardized image-graded functional (DIGEST) and physiologic (MBSImP) assessments. Findings provide robust evidence that dysphagia is not a uniform phenomenon in cancer but instead exhibits diagnosis-specific severity and physiologic patterns.

Across the cohort, DIGEST outcomes showed a clear diagnosis-dependent gradient. Patients with multiple cancers (with or without HN) showed the highest rates of impairment, likely reflecting cumulative anatomic and treatment-related burden. Despite variability, most diagnostic groups exhibited dysphagia in at least half of patients (except metastatic and breast cancer), and roughly one-third of the entire cohort demonstrated high-grade dysphagia (DIGEST ≥2). Regression analyses further supported these patterns: only individuals with multiple cancers including HN had significantly higher odds of severe dysphagia relative to HN alone, whereas GI, hematologic, CNS, and multiple-cancer (non-HN) groups exhibited comparable frequency. These results highlight a substantial burden of dysphagia in non-HN cancers and suggest that these under-recognized groups may be under-served by current dysphagia care pathways. Established models for HNC, including, for instance, early swallowing intervention during radiotherapy (28), multidisciplinary pathways (29), or structured high-intensity rehabilitation programs (30), demonstrate the value of systematic surveillance and targeted therapy, yet similar frameworks remain limited for other cancer groups. These findings underscore the opportunity to consider proactive screening and timely referral to speech–language pathology across a broader range of oncology settings.

Understanding the physiologic drivers of dysphagia is crucial for designing effective, diagnosis-specific interventions. Correlations between DIGEST and MBSImP revealed both shared and distinct mechanisms of impairment in cancer subgroups. Across diagnoses, safety impairments were most strongly associated with reduced epiglottic inversion and incomplete laryngeal vestibular closure, while efficiency deficits were predominantly linked to pharyngeal stripping wave, pharyngeal contraction, and tongue base retraction. Notably, across all diagnostic groups, impairments were most consistently observed in swallowing components that rely heavily on effective force generation and endurance across the swallowing musculature, which may signal a broader phenomenon of sarcopenic dysphagia. Sarcopenia, characterized by generalized skeletal muscle loss, is well recognized as a contributor to dysphagia in cancer populations (31–33). Reduced muscle mass and function affect multiple structures involved in swallowing, including the tongue, suprahyoid muscles, pharyngeal walls, and masticatory system, with imaging studies showing a link between skeletal muscle atrophy with dysphagia severity (32). In cancer, progressive muscle loss is often driven by poor intake and abnormal metabolism. Given that exercise can improve metabolic function, reduce inflammation, and promote muscle maintenance (34), targeted exercise may offer a promising approach to mitigate dysphagia in patients with advanced cancer. Exploratory age-adjusted models confirmed that cancer-type differences relative to HN were largely preserved after adjustment, supporting the interpretation that diagnosis-specific swallowing profiles reflect disease-related mechanisms beyond age-driven muscle loss alone. Other cancer-wide toxicities, including mucositis and oral complications from chemotherapy, likely contribute additional layers of impairment not fully captured here given this study’s focus on pharyngeal physiology. Diagnosis-specific distinctions were evident and are outlined below.

Diagnosis-specific patterns

Patients with CNS tumors exhibited frequent and often severe functional impairments, particularly in safety. Physiologic profiles mirrored classic neurogenic patterns. As described in patients with brain tumors (especially infratentorial lesions) (35), our cohort exhibited hallmark impairments such as delayed swallow initiation, vallecular and pyriform residue, reduced pharyngeal stripping wave, and diminished laryngeal elevation, paralleling stroke-derived MBSImP profiles (36). This reinforces the interpretation of CNS-related dysphagia as a neurogenic phenotype, with important implications for considering the development and testing of stroke-based rehabilitation approaches.

In thoracic cancers, including lung and esophageal malignancies, functional impairment was moderate but frequent, with focal deficits in swallow initiation, hyolaryngeal mechanics, and vestibular closure. These findings are consistent with prior reports on lung and mediastinal tumors, where dysphagia may arise from neuromuscular discoordination due to paraneoplastic syndromes, recurrent laryngeal nerve compression (37–39), as well as generalized weakness or cachexia (37). In esophageal cancers, oropharyngeal impairment may also reflect postsurgical changes due to RLN injury or reduced laryngeal elevation, which are frequently transient (40), but can persist in a subset (41), contributing to aspiration risk (40,42). Together, these observations indicate that thoracic cancer dysphagia may arise from a combination of mechanical, neurogenic and systemic factors, highlighting potential physiologic targets for intervention and suggesting that rehabilitative approaches should extend beyond traditional surgical or palliative options such as vocal fold medialization (43–45).

In gastrointestinal cancers, functional impairment was common but typically mild, while physiologic impairments were diffuse and correlated with both safety and efficiency outcomes. This pattern suggests a non-focal mechanism, in which swallowing function is broadly affected without a single dominant driver. This pattern suggests that dysphagia may arise from broad systemic vulnerability, such as reduced neuromuscular reserve, sarcopenia, or treatment-related fatigue, rather than focal structural lesions. Given the limited literature characterizing swallowing physiology in this population, these findings highlight an important area for further mechanistic investigation.

In hematologic cancers, patients exhibited moderate-to-severe functional impairment and physiologic burden, with deficits in swallow initiation, epiglottic movement, laryngeal vestibular closure, and pharyngeal contraction. These deficits likely reflect generalized deconditioning and a sarcopenic pattern rather than isolated structural injury. Treatment-related factors commonly associated with dysphagia, such as graft-versus-host disease (GVHD)-associated fibrosis (46,47) may contribute. The observed common PES opening impairment might correspond to esophageal strictures, submucosal fibrosis, or physiologic reduction, also common post-GVHD (47), or with extrinsic compression from lymphadenopathy or direct disease involvement (9). These multifactorial impairments might reflect generalized debility or indicate combined sensory, muscular, and/or structural dysfunction contributing to dysphagia in this population.

In endocrine/thyroid cancers, physiologic impairments were relatively focal and mild. Pharyngeal stripping wave and PES opening were generally preserved, whereas hyolaryngeal impairments were most frequent consistent with literature indicating that dysphagia in thyroid cancer is most often caused by mechanical factors (e.g., tumor mass effect or postoperative changes tethering the larynx, including injury to the external branch of the RLN or SLN) rather than diffuse neuromuscular dysfunction (48–50). In contrast, dysphagia in non-malignant endocrine disorders like diabetes or hypothyroidism is often neuromuscular or metabolic in nature, involving neuropathy, myopathy, or dysmotility (51). These distinctions offer data to support that dysphagia arising in endocrine malignancies follows different physiologic pathways than dysphagia in non-malignant endocrine disease, highlighting the need for management frameworks that account for these divergent mechanisms.

Taken together, these hypothesis-generating findings highlight the need for diagnosis-specific evaluation and management paradigms in cancer related dysphagia. The frequent involvement of strength-based physiologic impairment across multiple cancer diagnoses also suggests a potential role for exercise-based interventions aimed at mitigating sarcopenia. Given evidence that exercise can improve muscle mass, metabolic function, and inflammatory profiles, further investigation of exercise-oriented dysphagia rehabilitation in different oncology settings is warranted.

Contextual considerations are important. At our tertiary cancer center, MBS referrals typically arise from overt clinical concern (such as coughing, choking, or suspected aspiration) leading to a sample enriched for more severe impairment. As such, there is referral bias inherent in estimated event rates, and the reported frequency of impairments should not be confused with prevalence of dysphagia in these cancer diagnosis groups. This may also help explain discrepancies in our observed event rates with studies relying on patient-reported outcomes, which often show mild symptoms in non-HNC populations (12). Although such divergences between PROs and instrumental findings are well documented in HNC (52–56), our data suggest that similar mismatches may extend to other diagnoses. Further limitations include the absence of treatment data, preventing definitive attribution of mechanisms, variability in illness acuity. MBSImP data were available for only a subset of patients and were not double-rated, which may introduce scoring variability in physiologic outcome analyses. Additionally, data on BMI, nutritional indices, and physical function were unavailable, precluding formal adjustment for sarcopenia severity beyond age; future studies incorporating these measures would further clarify the relative contribution of systemic muscle loss to diagnosis-specific dysphagia profiles.

CONCLUSION

In conclusion, this study adds to growing evidence that dysphagia in cancer is a complex, multifactorial complication with substantial variation in severity, physiology, and clinical implications across cancer diagnoses. By applying standardized image-graded physiologic and functional assessments (MBSImP and DIGEST) in a large, diverse oncology cohort, we identified shared and diagnosis-specific swallowing patterns. These results offer novel evidence for prioritizing physiologic rehabilitation targets based on cancer type and suggest the potential for diagnosis-specific exercise protocols. These findings reinforce the need for early, tailored assessment and intervention strategies, and lay the foundation for future efforts in personalized care, predictive modeling, and longitudinal monitoring to optimize outcomes and quality of life.

Supplementary Material

Online resource

Funding statement:

Research reported in this publication was partially supported by the National Institutes of Health (NIH), National Cancer Institute (NCI) under award R01CA271223. The Cancer Center Support Grant (NCI Grant P30 CA016672) provided partial support of this work. Dr. Manduchi is supported by the UTHealth Houston Innovation for Cancer Prevention Research Training Program Postdoctoral Fellowship (Cancer Prevention and Research Institute of Texas grant #RP210042). The content is solely the responsibility of the authors and does not necessarily represent the official views of the Cancer Prevention and Research Institute of Texas or NIH.

Footnotes

Conflict of interest: The authors have no relevant financial or non-financial interests to disclose.

Ethical approval: The study was approved by the Institutional Review Board at The University of Texas MD Anderson Cancer Center (protocol PA19–0261); a waiver of informed consent was obtained for retrospective data-review.

CRediT statement: In accordance with the Contributor Roles Taxonomy (CRediT, https://credit.niso.org/), the contributing authors have designated responsibilities and individual author attribution. The corresponding authors (KAH) assume responsibility for role assignment, and all contributors have been given the opportunity to review and confirm assigned roles. Conceptualization: BM, KAH. Methodology: BM, CW, KAH. Formal analysis: BM, CW. Data curation: BM, CEA, CW, XT, AS, SB. Writing – original draft: BM. Writing – review & editing: All authors. Supervision: KAH. Funding acquisition: KAH.

Data availability:

The dataset supporting this study is publicly available through Figshare. All materials were deposited as part of Data Deposition for the MD Anderson Dynamic Imaging of Swallowing Toxicity (DIGEST™) Clinical Implementation Protocol. The dataset can be accessed at the following DOI: https://doi.org/10.6084/m9.figshare.28544234.v1. All data have been de-identified prior to public release to protect participant privacy.

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Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Supplementary Materials

Online resource
NIHMS2196642-supplement-Online_resource.docx (100.2KB, docx)

Data Availability Statement

The dataset supporting this study is publicly available through Figshare. All materials were deposited as part of Data Deposition for the MD Anderson Dynamic Imaging of Swallowing Toxicity (DIGEST™) Clinical Implementation Protocol. The dataset can be accessed at the following DOI: https://doi.org/10.6084/m9.figshare.28544234.v1. All data have been de-identified prior to public release to protect participant privacy.

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