Laryngopharyngeal Symptoms and Laryngopharyngeal Reflux Disease: Interdisciplinary Considerations and Management

Abstract

Background:

The San Diego Consensus for Laryngopharyngeal Symptoms (LPS) and Laryngopharyngeal Reflux Disease (LRPD) describes a broad-based multidisciplinary management paradigm that focuses on mechanisms underlying symptoms to improve treatment outcomes.

Purpose:

This review expands on the San Diego Consensus framework to discuss multidisciplinary management of LPS and LPRD. LPS manifest as persistent or disproportionate symptoms despite minimal or inconsistent evidence of reflux exposure. Emerging evidence suggests that hyperresponsiveness, hypervigilance, and symptom-specific anxiety are more strongly associated with LPS than objective reflux metrics and may contribute to symptom persistence through heightened attention to perceived irritation and protective behavioral responses. Repeated peripheral sensory input may further contribute to central sensitization and lower perceptive thresholds. While these behavioral and neurophysiological processes may be partially improved by reducing reflux exposure, behavioral therapies that address the multidimensional nature of LPS may provide additional benefit. Laryngeal Recalibration Therapy addresses LPS by retraining maladaptive laryngeal behaviors, enhancing vagal tone via heart rate variability biofeedback, and cognitive reframing to reduce symptom amplification. Meta-therapy, a clinical dialogue approach used in speech-language pathology to facilitate behavioral change, alongside psychological interventions such as mindfulness meditation, cognitive-behavioral therapy, and gut-directed hypnotherapy, may further target cognitive–affective processes that shape perception. Behavioral interventions can be combined with neuromodulators, particularly delta ligands such as gabapentin in patients with chronic cough, and tricyclic antidepressants or selective serotonin reuptake inhibitors in select cases. Effective management relies on multidisciplinary collaboration, integration of reflux-directed and behavioral therapies, and patient-centered education that supports adaptive symptom interpretation.

1 |. Introduction

The widely used term “laryngopharyngeal reflux” implies reflux-related pathophysiology for throat and upper airway symptoms [1, 2]. However, the likelihood of finding objective reflux, and response to reflux-based therapy is low in these patients, despite high economic burden and impact on quality of life [3–6]. The San Diego consensus was convened with a multinational panel of gastroenterologists, otolaryngologists, speech-language pathologists (SLPs) and a clinical psychologist to develop a modern paradigm for definition of throat and airway symptoms as distinct from settings where reflux is demonstrated on objective testing [7]. The consensus panel unanimously agreed that the term laryngopharyngeal symptoms (LPS) should be used to describe throat and airway symptoms (cough, throat clearing, regurgitation, excessive phlegm in throat, hoarseness/voice changes, throat pain/sore throat), as distinct from laryngopharyngeal reflux disease (LPRD) which requires LPS and objective evidence of reflux on diagnostic testing [7].

The presence or absence of objective reflux evidence plays a key role in planning management. Reflux-directed therapies are less likely to be effective in the absence of abnormal reflux burden, which is relevant to avoid unnecessary escalation of acid suppression therapy or anti-reflux surgery. An early inflection point in the evaluation is determining whether typical esophageal symptoms co-occur with LPS or if LPS is isolated (Figure 1). When typical symptoms are present, the pretest probability of objective reflux has been demonstrated to be higher in a large multicenter study performed to validate San Diego consensus pathways [8], supporting an initial empiric treatment trial. Diagnostic evaluation is reserved for patients with alarm features or failure of empiric therapy. Upfront diagnostic testing is favored in isolated LPS, where non-reflux etiologies are more likely. In both contexts, cognitive-affective and behavioral processes, such as hyperresponsiveness, hypervigilance, and other non-reflux mechanisms, may contribute to symptom perception. Management therefore requires coordinated, multidisciplinary care across evaluation, treatment, and follow-u p to optimize outcomes.

FIGURE 1 |.

An algorithm describing use of behavioral therapy and neuromodulators in patients with laryngopharyngeal symptoms (LPS). Laryngeal hyperresponsiveness, hypervigilance, and overlap with disorders of gut-brain interaction (DGBI) are suspected in patients with isolated LPS especially when testing does not demonstrate laryngopharyngeal reflux disease (LPRD) or when symptoms persist despite optimized management of LPRD in both isolated LPS and LPS with typical symptoms. In these instances, behavioral therapy and/or neuromodulators may be considered.

A series of three technical reviews expand in detail the data underlying San Diego Consensus statements, for which extensive literature searches of available published studies were performed by an interdisciplinary multinational team as part of the original consensus. This review, the third in the series, expands on the San Diego Consensus paradigms to discuss multidisciplinary evaluation and management of LPS and LPRD, the implications of esophageal and laryngeal hyperresponsiveness, disease-specific cognitive-affective processes, and overlap with affective disorders, as well as integrative behavioral and pharmacologic treatment approaches. Two other reviews discuss presentation/terminology [9], and diagnostic testing/clinical approach [10].

2 |. The Role of Multidisciplinary Evaluation and Management of LPS

Effective evaluation and management of patients with LPS requires input from a broad complement of providers that includes primary care, gastroenterology, otolaryngology, respiratory medicine, and SLP among others. Referral pathways vary, with primary care often directing patients to different specialists based on the symptoms they present.

Gastroenterologists play an important role in identifying and managing esophageal contributors to LPS, including determining whether gastroesophageal reflux is involved in the pathogenesis. Pulmonologists evaluate for and exclude respiratory causes, particularly in patients with chronic cough. Otolaryngologists evaluate both non-reflux and reflux mechanisms for upper aerodigestive symptoms and are key to management of laryngeal symptoms such as dysphonia.

SLPs contribute to both assessment and management by quantifying LPS, evaluating respiratory and voice patterns, and delivering behavioral interventions such as Laryngeal Recalibration Therapy [11]. Behavioral interventions may performed alone or be combined with other approaches, such as neuromodulator therapy.

Input from multidisciplinary experts may occur concurrently or sequentially. While integrated teams with all services in one setting are ideal, this is not always possible. In these instances, clear referral pathways, communication, documentation, and coordinated decision-making across providers are essential. Each expert reinforces shared goals—such as medication adherence, understanding the rationale for medical treatments, and consistent practice of lifestyle and behavioral strategies.

Practice varies by region and is often shaped by service availability. Clinicians must balance comprehensive testing with pragmatic treatment. While alarm symptoms need attention and readily treatable conditions require identification, extensive investigations can prolong symptoms, increase cost burden, and contribute to patient frustration and dissatisfaction. Although endoscopy has high specificity for objective esophageal findings of gastroesophageal reflux disease (GERD), the diagnostic yield is overall low, and many patients improve with behavioral treatment even without these studies, especially in the absence of esophageal symptoms or other alarm features. This raises an important question of whether a test finding always indicates a cause-and-effect relationship to symptoms.

Evaluation of LPS should begin with a thorough history and use of validated symptom measures to quantify symptoms (Figure 1). In patients with typical reflux symptoms, a short trial of empiric anti-reflux therapy and lifestyle modification is reasonable, with discontinuation and progression to diagnostic testing if there is no improvement. In patients without overt reflux symptoms, clinicians should consider objective reflux testing and/or therapy targeting other potential drivers of symptoms, such as laryngeal hypersensitivity, maladaptive behaviors (e.g., hyperresponsiveness), laryngeal-specific cognitive and affective processes (e.g., laryngeal hypervigilance and anxiety), and autonomic dysregulation. Objective confirmation of reflux is important before initiating long-term anti-reflux therapy, and treatment response should be monitored to inform ongoing management decisions (Figure 1).

3 |. Concepts of Hypervigilance and Hyperresponsiveness

LPS were recently defined by the San Diego Consensus [7] to include cough, voice change, throat clearing, excess throat phlegm, and throat pain/sore throat. These symptoms are highly prevalent across several voice and upper airway disorders [12–16] making them inherently nonspecific indicators of underlying pathology. Consequently, multidisciplinary evaluation is essential for diagnostic precision in suspected LPRD [7], particularly given evidence that LPS alone have suboptimal accuracy in predicting LPRD [17–20].

LPS vary in occurrence, severity, and treatment response [11, 20–25]. This variability supports a biopsychosocial clinical framework in which physiologic, behavioral, and cognitive-affective factors interact to shape symptom perception and burden [7, 11, 17, 18, 22, 26, 27]. The Psychobiological Model of Disorders of Gut–Brain Interaction identifies key cognitive-affective and behavioral processes, including hypervigilance, symptom-specific anxiety, and maladaptive behaviors, and proposes pathways in which they interact with each other, the autonomic nervous system, and with peripheral physiology in shaping visceral symptom perception [28]. Given the overlap in symptom amplification and perceptual processes, this framework may also help explain symptom perception and persistence in LPS. Within this framework, hyperresponsiveness and hypervigilance have been proposed as potential factors that may contribute to persistent or disproportionate symptoms relative to the degree of reflux exposure—whether minimal, inconsistent, or conclusive [11, 18, 19, 22, 25–27, 29–31]. Importantly, hypervigilance and hyperresponsiveness, while conceptually distinct processes, may interact in a reinforcing loop, whereby increased attention on laryngeal sensations heightens symptom salience and prompts maladaptive protective behaviors, which may in turn perpetuate symptom persistence.

3.1 |. Hyperresponsiveness

Laryngopharyngeal hyperresponsiveness is defined as heightened sensorimotor reactivity of the laryngeal and upper airway systems, characterized by lowered thresholds for triggering protective or compensatory behaviors such as throat clearing, coughing, breath holding, inducible laryngeal obstruction (paradoxical vocal fold movement) during breathing, or increased biomechanical strain during phonation [16, 31, 32]. These responses may arise from chronic or intermittent mucosal exposure, including exposure to refluxate constituents such as pepsin, bile acids, and trypsin [2, 33–36]. Repeated irritation may contribute to altered sensory processing and motor responses, contributing to symptom persistence even when reflux burden appears limited. The San Diego Consensus Group [7] proposed hyperresponsiveness as a potential mechanism in both LPS and confirmed LPRD, noting that these behaviors may persist independently of reflux activity and may be amenable to behavioral therapies [7, 11, 22]. The concept of hyperresponsiveness has informed emerging interventions such as Laryngeal Recalibration Therapy [11], which aims to desensitize laryngeal reflexes and retrain maladaptive response patterns (Table 1).

TABLE 1 |.

Core components of Laryngeal recalibration therapy (LRT).

Domain	Target	Mechanism	Clinical focus
Laryngeal mechanics	Maladaptive motor patterns	Retraining of voice, breathing and swallowing; suppression of cough and throat clearing	Reduce laryngeal tension and reflexive behaviors
Autonomic regulation	Vagal tone/autonomic balance	Heart rate variability biofeedback	Address physiologic drivers of hyperresponsiveness
Cognitive alignment	Symptom interpretation and response patterns	Enhancement of cognitive flexibility; cognitive reframing; values-based strategies	Reduce hypervigilance and maladaptive responses

3.2 |. Hypervigilance

Laryngeal hypervigilance reflects heightened interoceptive attention, characterized by increased monitoring of throat and airway sensations in response to the perception of threat [22, 29]. Consistent with the Psychobiological Model of Disorders of Gut-Brain Interaction (DGBI) [28], individuals may misinterpret benign sensations as evidence of ongoing reflux or tissue injury, increasing symptom-focused attention and anxiety while reinforcing maladaptive LPS behaviors such as throat clearing and repeated swallowing [22, 37, 38]. Laryngeal hypervigilance and symptom-specific anxiety are significantly associated with greater symptom severity [22, 26, 29]. Consistent with this, Krause et al. [22] reported that these cognitive-affective factors show stronger associations with LPS than objective reflux metrics. While these processes remain relatively understudied in LPS, they are well characterized in esophageal disorders. Esophageal hypervigilance and symptom-specific anxiety are consistently associated with greater symptom severity across conditions, including GERD, achalasia, and eosinophilic esophagitis [29]. Given their central cognitive-affective nature and relative independence from specific peripheral pathology, similar mechanisms may plausibly contribute to symptom perception in laryngeal disorders.

3.3 |. Central and Autonomic Mechanisms Associated With Hypervigilance and Hyperresponsiveness

Symptom severity in LPRD and laryngeal pain syndromes is often disproportionate to objective reflux burden and mucosal findings. This dissociation likely reflects interactions between peripheral mechanisms and centrally mediated processes, including hypervigilance and hyperresponsiveness, as described above. These cognitive-affective and behavioral processes may, in turn, interact with central neurophysiological systems, such as altered sensory processing and autonomic regulation, contributing bidirectionally to symptom perception and persistence [28].

Central sensitization is a proposed mechanism in esophageal DGBI (e.g., functional heartburn, reflux hypersensitivity, and functional chest pain) [39, 40] and chronic cough syndromes [41, 42]. These conditions are characterized by altered central sensory processing, including increased excitability and reduced inhibitory modulation, resulting in amplification of otherwise benign sensory input [43]. This framework supports shared pathways of symptom amplification across disorders of visceral hypersensitivity, including LPS.

Within this model, repeated peripheral sensory input from reflux, inflammation, or phonotrauma may be associated with sustained alterations in central sensory processing, lowering perceptual thresholds, and expanding the range of stimuli perceived as noxious [40]. However, direct evidence for such processes in LPS/LPRD remains limited. These centrally mediated changes may interact with attentional and behavioral processes, such as hypervigilance and hyperresponsiveness, which may amplify symptom salience and contribute to reinforcing cycles of symptom-focused attention and protective behaviors (e.g., throat clearing and repeated swallowing) [28].

Evidence suggests that autonomic dysregulation contributes to LPRD and is characterized by reduced parasympathetic activity and relative sympathetic dominance [44, 45]. This pattern may be associated with esophageal dysmotility and transient sphincter relaxations, leading to pharyngeal reflux events [30, 44–46], although causal directionality remains uncertain. Psychological stressors including symptom-specific and more general affective disorders (e.g., anxiety and depression) may amplify autonomic dysfunction through sustained sympathetic activation and vagal inhibition, establishing a bidirectional relationship between mental health disorders and LPRD symptomatology.

Recognition of processes that are potentially associated with hypervigilance and hyperresponsiveness has significant implications for interdisciplinary management. Treatment of refractory LPRD and LPS is most effective with a combined approach that includes reflux-directed therapy, behavioral strategies to optimize laryngeal function and reduce vagal hypersensitivity, and cognitive interventions that modify symptom perception [2, 7, 11].

4 |. Primary Hypervigilance and Hyperresponsiveness vs. Overlap With LPRD

In conditions such as LPRD and the broader category of LPS, both peripheral and central contributors shape symptom experience. Cognitive-affective processes—including symptom-specific anxiety and hypervigilance—are observed across patients with LPS, regardless of the presence of objective pathological reflux [22, 47]. Research in esophageal disorders supports this framework, demonstrating that psychological factors, including hypervigilance and anxiety, correlate more strongly with symptom burden than objective measures of reflux, histologic activity, or motility disturbances [48–51]. Collectively, these findings may help explain the variable response of laryngeal symptoms to standard reflux-directed therapies targeting GERD. Although proton pump inhibitors (PPIs) reduce peripheral acid exposure, symptom persistence may reflect ongoing hypervigilance and hyperresponsiveness, suggesting a role for centrally mediated processes that may persist despite adequate acid control.

Assessing hypervigilance requires validated instruments that distinguish physiological triggers from perceived symptom salience. The Laryngeal Cognitive-Affective Tool (LCAT) [52] is a validated patient-reported outcome measure that assesses laryngeal-specific hypervigilance and symptom-related anxiety, capturing cognitive-affective and behavioral processes that can guide targeted treatment. Narrative prompts (e.g., “Do you find yourself checking in on your body often?”) can further clarify the degree of internal focus. It is important to note that laryngeal hypervigilance and hyperresponsiveness are disease-specific cognitive-affective and behavioral processes that can influence symptom perception independent of diagnosable mental health disorders. Although these processes may coexist with mood and anxiety disorders, they represent distinct constructs. Recognizing this distinction helps avoid mislabeling symptoms as purely psychiatric and supports precise, mechanism-based care.

Effective patient education involves conversations that clarify underlying mechanisms rather than dismissing lived experience. Clinicians in primary care, gastroenterology, and otolaryngology can support patients by acknowledging their symptoms and framing hypervigilance as a perceptual process that can change symptom experience, rather than as a sign of psychopathology. A biopsychosocial framework [28] recognizes that peripheral and perceptual factors interact to shape symptom burden without implying that all patients require the same range of treatment modalities. For example, when symptoms resolve with appropriate peripheral therapy, additional behavioral intervention may not be necessary. In contrast, persistent symptoms associated with heightened cognitive-affective or behavioral factors (e.g., high LCAT score) may benefit from strategies that target attentional processes and symptom interpretation.

5 |. Overlap With Affective Disorders

Beyond symptom-specific psychological processes, prior research has examined associations among broader affective symptomatology, most commonly anxiety and depressive symptoms, and LPS/LPRD. Importantly, most studies have relied on self-report symptom measures rather than formal psychiatric diagnoses. Several studies have found that patients with LPS report higher anxiety and depressive symptoms compared to healthy controls [30, 46, 53–55]. However, research suggests only clinically significant anxiety is more prevalent in LPS, while rates of clinically significant depression are similar to controls [53]. Conversely, other studies report no differences in psychological symptoms between LPS patients and controls [54, 56, 57]. These discrepancies may reflect differences in how studies define and measure both LPS/LPRD and psychological symptoms, limiting comparability.

Research has also linked psychological symptoms to LPS severity. For example, in patients without esophagitis, anxiety, and depressive symptoms were associated with increased chronic cough, whereas in patients with esophagitis, positive correlations were observed for chronic cough, throat clearing, and heartburn [53]. Studies by Tseng et al. and Kang et al. [54, 55] report that greater psychological symptom scores are associated with more severe overall symptoms. Some studies indicate that increased reflux burden may influence psychological symptoms. In one cohort of individuals with LPS defined by both symptom-and laryngoscopy-based criteria, patients with LPRD reported higher depressive and anxiety symptom scores than those without LPRD [58]. Moreover, clinically significant depressive symptoms, but not anxiety, were more prevalent in the LPRD group, suggesting that depressive symptoms may be particularly associated with reflux burden [58]. Similarly, individuals with overlapping GERD and LPS demonstrated greater psychological distress compared to those with GERD alone [59]. There is also evidence that psychological distress may decrease after PPI therapy [53].

Laryngeal providers may find it useful to assess elevated affective symptoms in patients presenting with LPS/LPRD. One efficient approach is the use of brief, validated self-report screening tools, such as the PHQ-9 [60], and GAD-7 [61], which assess depressive and anxiety symptoms, respectively, and include established cutoffs to distinguish symptom severity. Additionally, providers may use brief “foot-in-the-door” questions to assess current mental health symptoms and patients' openness to discussing them or accepting referral. For example, providers might ask, “Many patients with ongoing GI symptoms notice that stress, anxiety, or low mood can make symptoms harder to manage—have you noticed anything like that for yourself?” or more simply, “How have these symptoms been affecting your mood or stress levels day-to-day?” Patients who endorse significant symptoms can then be referred for further mental health evaluation and care.

LPS/LPRD patients with comorbid mental health disorders (e.g., generalized anxiety disorder and major depressive disorder) should be referred to a mental health practitioner for appropriate evaluation and treatment. This differs from referral to a GI-specific mental health provider, such as a GI psychologist. Referral to a GI psychologist may be more appropriate when symptom-specific processes—such as hypervigilance, symptom-related anxiety, or maladaptive illness behaviors—are prominent. In contrast, referral to a general mental health practitioner focuses on the broader mental health condition and its associated symptoms rather than their specific relationship with LPS/LPRD. Although GI symptoms may still be discussed, they would not be the central treatment target and are instead addressed within broader behavioral interventions.

6 |. Diet and Lifestyle

The current literature supports the role of specific dietary patterns as potential triggering factors for pharyngeal reflux events [62]. From a physiological standpoint, foods and beverages influence gastroesophageal function, transient sphincter relaxations, and resultant reflux risk according to their chemical composition, nutrient profile, and physical properties [63, 64]. High-fat foods, caffeine, alcohol, carbonated beverages, and high-glycemic index items have been identified as particularly refluxogenic, promoting lower and upper esophageal sphincter (UES) relaxations that facilitate gastroduodenal content backflow into the upper aerodigestive tract [63, 64]. Dietary modifications emphasizing low-fat, high-protein, alkaline, plant based and low-glycemic foods benefit symptoms in certain clinical settings [62, 65]. For patients with persistent symptoms, targeted approaches such as a gluten-free diet may be worth considering in select populations; still, further study is needed to clarify the relationship between gluten, lactose intolerance, and LPRD [62].

Studies combining dietary modifications with medications consistently demonstrate superior outcomes compared to medication alone [66]. However, it is important to note that current evidence remains limited by methodological heterogeneity, reliance on suspected rather than objectively confirmed LPRD diagnoses (notably with ambulatory reflux monitoring), and insufficient consideration of LPRD-specific pathophysiology distinct from GERD. Future randomized controlled trials comparing dietary interventions to several pharmacotherapies (PPIs, alginate, and magaldrate) in objectively diagnosed LPRD populations, with extended follow-up periods and consideration of confounding factors including chronic rhinosinusitis and allergic conditions, are important to establish evidence-based management protocols.

Lifestyle modifications including stress management, smoking cessation, portion size reduction, and avoiding late-evening meals complement dietary interventions.

7 |. Adjunctive Measures and Supportive Data

Gastroesophageal reflux into the proximal esophagus leads to an increase in intraesophageal pressure. Therefore, the functional integrity of the UES plays a crucial role in the prevention of reflux from the proximal esophagus to pharynx [67]. It has been reported that patients with suspected supraesophageal reflux disease have impaired UES contractile reflexes in response to esophageal acid infusion when compared with controls and patients with GERD [68]. Augmentation of UES pressure implies therapeutic potential for LPRD. Shaker et al. [69] reported that sustained cricoid pressure between 20 and 30 mmHg significantly reduced esophagopharyngeal reflux events in patients with LPRD. An external UES augmentation device demonstrated safety and tolerability in phase II studies and was initially cleared by the US FDA. The basis for this device is that cricopharyngeal pressure has been demonstrated to reduce both LPS burden and salivary pepsin concentrations as monotherapy or in combination with PPI therapy [70, 71]. In a recent double-blinded, randomized controlled trial of patients with LPRD refractory to acid suppression, low pressure UES compression (4–11 mmHg) achieved comparable improvement in LPS and salivary pepsin concentrations compared to the device applying higher therapeutic pressure (20–30 mmHg). This study suggested that application of low external cricoid pressure remains a potential therapy for LPRD, particularly as an adjunct to acid suppression [72]. However, the external UES augmentation device is not commercially available at present.

8 |. Neuromodulation and Supportive Data

Pharmacologic neuromodulation targets the neural pathways that mediate LPS. Neuromodulators attenuate laryngeal hypersensitivity related to aberrant central modulation of visceral sensation and heightened laryngeal and esophageal sensory circuits. LPS related to laryngeal hypersensitivity may present with overlapping symptoms such as refractory chronic cough, globus, paradoxical vocal fold movement, inducible laryngeal obstruction, and muscle tension dysphonia. Neuromodulators may be considered as add-on or alternative medical therapy in LPRD patients with suboptimal response to anti-secretory therapy or SLP intervention, and in isolated LPS with negative esophageal testing.

Current clinical evidence for neuromodulators, notably gabapentin and pregabalin, focuses primarily on the treatment of neurogenic chronic cough through mediation of vagal hypersensitivity. A randomized controlled trial showed a significant reduction in cough severity and improvement in cough-related quality of life with gabapentin at doses up to 1800 mg/day compared to placebo. The number needed to treat for a response was 3.58 [73]. It has been reported in a retrospective study that pregabalin improved symptom severity for patients with laryngeal sensory neuropathy (odynophagia, globus, and cough) [74]. Tricyclic antidepressants (TCA), such as amitriptyline, have also been shown to reduce chronic cough and globus in a prospective cohort study [75, 76]. However, TCA should be used with caution because of anticholinergic effects which may cause dry mouth and aggravate LPS. While there is a paucity of data for selective serotonin reuptake inhibitors and serotonin norepinephrine reuptake inhibitors, they can be considered in individuals who have concomitant anxiety and depression.

9 |. Behavioral Management Approaches

Complementary and alternative medicine is increasingly used for aerodigestive disorders [11, 77], as research demonstrates that patients with LPS need therapies targeting cognitive-affective and behavioral processes [52]. Non-pharmacologic therapy can target specific LPS such as cough and dysphonia. The strongest evidence comes from randomized, placebo-controlled trials supporting SLP interventions for chronic cough [78, 79]. Traditional recommendations such as prolonged absolute voice rest have been shown to offer limited benefit and may paradoxically increase symptom awareness and anxiety. Studies comparing absolute voice rest with relative voice rest or early voice therapy demonstrate superior functional outcomes and patient satisfaction with graded voice use and behavioral retraining [80, 81]. These findings underscore the importance of recalibrating sensory perception and vocal behaviors rather than reinforcing avoidance. Reflux lifestyle modifications [62, 82, 83] and traditional mechanistic voice therapies (e.g., flow phonation and resonant voice) reduce LPS in patients unresponsive to PPI [84], and Behavioral Cough Suppression Therapy decreases cough burden [15], but additional interventions may optimize treatment precision.

Therapies targeting central processes may better address the multidimensional nature of LPS (Table 2). Non-pharmacological interventions such as Meta-Therapy (MT), mindfulness-based interventions, and CBT aim to modify maladaptive cognitive-affective and behavioral processes that influence symptom perception and persistence. Behavioral interventions can be integrated with neuromodulators, dietary modification, and reflux-directed pharmacological treatments, supporting a multidisciplinary treatment approach. These evidence-based modalities can be integrated into counseling, a recognized domain of service delivery within the practice of SLP as outlined by the American Speech-Language-Hearing Association.

TABLE 2 |.

Interdisciplinary management modalities for laryngopharyngeal reflux disease (LPRD) and laryngopharyngeal symptoms (LPS).

Management modality	Primary mechanism(s) targeted	Clinical indications
Dietary and lifestyle modification (e.g., low-fat, low-acid, plantbased diet; meal timing; stress reduction)	Reduction of reflux burden; modulation of autonomic nervous system activity	First-line therapy for suspected or confirmed LPRD; adjunctive therapy in LPS to reduce peripheral sensory input and refluxogenic triggers
Laryngeal recalibration therapy (LRT)	Reduction of maladaptive laryngeal behaviors; enhance vagal tone; alter symptom perception	Prominent laryngeal hyperresponsiveness (chronic cough, throat clearing, dysphonia); symptoms disproportionate to reflux burden; persistent LPS despite reflux-directed therapy
Traditional speech-language pathology intervention (behavioral cough/throat clearing suppression; adjusting breathing, voice and swallowing patterns)	Reduction of phonotraumatic behaviors; optimization of respiratory–phonatory coordination	Chronic cough, throat clearing, muscle tension dysphonia, muscle tension dysphagia, dyspnea; refractory LPS with absent or inconclusive evidence of reflux
Meta-therapy (therapeutic educational dialogue)	Modification of symptom interpretation, beliefs, and affective responses	Elevated symptom distress; poor understanding of symptom mechanisms; adjunct to enhance engagement and response to other therapies
Mindfulness-based interventions	Reduction of hypervigilance and improvement of attentional control; regulation of autonomic nervous system activity	Stress-responsive LPS; heightened symptom monitoring or vigilance; adjunct therapy in refractory presentations
Cognitive behavioral therapy (CBT)	Reduction of symptom-specific anxiety, catastrophic symptom appraisal, hypervigilance, and maladaptive behavioral responses	Marked cognitive-affective amplification of symptoms and/ or maladaptive protective behaviors; limited response to peripheral or behavioral laryngeal therapies
Acid suppression therapy (PPIs, H2 receptor antagonists)	Reduction of gastric acid exposure	Patients with typical reflux symptoms and LPS; patients with objectively confirmed reflux (LPRD)
Alginate/barrier therapy	Mechanical barrier to limit proximal refluxate	Breakthrough symptoms despite acid suppression; non-acid or mixed reflux patterns; adjunctive therapy in documented LPRD
Neuromodulator therapy (gabapentin, pregabalin, tricyclic antidepressants; SSRIs/SNRIs in select cases)	Attenuation of central sensory hypersensitivity	Neurogenic or refractory chronic cough; globus or laryngeal pain syndromes with negative reflux testing; adjunct when behavioral therapy alone is insufficient
Upper esophageal sphincter assist device (UESAD)	Augmentation of the UES barrier to reduce esophagopharyngeal reflux	Documented or refractory LPRD; persistent LPS despite acid suppression; adjunct or alternative to pharmacologic therapy

Note: Management of LPS and LPRD benefit from a mechanism-based, interdisciplinary approach. Selection of therapy is guided by the presence or absence of objective reflux, degree of laryngeal hyperresponsiveness, and contribution of cognitive-affective factors. Integration of reflux-directed, behavioral, and neuromodulatory therapies is often required for optimal symptom control.

Related behavioral approaches have also been developed within psychogastroenterology, a field at the intersection of psychology, neuroscience, and gastroenterology. In this context, brain-gut behavior therapies (BGBTs) are designed to target maladaptive cognitive-affective, attentional, and behavioral processes contributing to symptom amplification and distress [85]. BGBTs commonly applied in esophageal disorders include GI-focused cognitive and behavioral therapy (CBT), gut-directed hypnotherapy, and mindfulness-based interventions, several of which may also have relevance for LPS/LPRD management (See Keefer et al. [85] for review of specific BGBTs, therapeutic targets, and associated behavioral skills).

The following are examples of behavioral therapies relevant to LPS/LPRD management and commonly delivered by SLPs and/or GI psychologists.

Meta-therapy (MT) is the nuanced clinical dialogue used by SLPs to facilitate effective and efficient behavioral change [86–89]. Helou et al. [86] mapped MT within the Rehabilitation Treatment Specification System, outlining its goal to modify cognitions, knowledge, beliefs, attitudes, intentions, and awareness of how affective states influence symptoms. Recognizing how stress, fatigue, or emotion can alter LPS encourages self-compassion. For example, educating patients that ~27% of the general population are “laryngoresponders” [89] normalizes variability in symptoms. Research shows the larynx functions as a “posture of protection,” responding to stress through muscular tension [90–92]. Knowledge that some individuals “valve stress” through their larynx can be liberating and reduce fear.

Mindfulness-based interventions emphasize intentional, non-judgmental awareness of the present moment [93]. Techniques such as focused breathing, emotion labeling, and grounding exercises (e.g., 5–4-3–2-1 technique), are hypothesized to improve ANS balance and heart rate variability [94, 95], while also reducing symptom-focused vigilance, processes that are associated with LPRD/GERD/LPS [11]. Experimental evidence further supports this framework, with one study finding that a brief, 15-min mindfulness exercise prior to a cough challenge improved cough sensitivity in health volunteers [96]. Among mindfulness-based approaches, Mindfulness-Based Stress Reduction (MBSR) [97] has shown to be effective in a range of laryngeal and esophageal conditions [98]. In GERD, MBSR is associated with reductions in anxiety and depressive symptoms while improving quality of life [99, 100]. In voice disorders, MBSR showed improvements in perceived stress, voice handicap, and quality of life [101]. Additionally, combined MBSR and CBT interventions demonstrate improvement in laryngeal symptom severity among patients with LPS [102].

Cognitive Behavioral Therapy targets maladaptive cognitive, emotional, and behavioral processes that may contribute to symptom amplification and persistence. A core principle of CBT is that these processes interact bidirectionally and can reinforce one another. Within the context of LPS/LPRD, this may include maladaptive cognitive appraisals of symptoms (e.g., “Something is seriously wrong; I feel a lump in my throat”), emotional responses (e.g., fear and sadness), physiological arousal (e.g., stress activation), and behavioral responses (e.g., avoidance behaviors and excessive throat clearing). Through techniques such as cognitive restructuring, adaptive coping skills, relaxation training, and behavioral exposure, individuals learn strategies to modify these interacting processes and respond to symptoms flexibly. For example, catastrophic interpretations such as “Something is seriously wrong; I feel a lump in my throat,” may be reframed as “This sensation could be stress or muscle tension and does not necessarily indicate something is wrong.” CBT also emphasizes psychoeducation regarding brain–body interactions and how cognitive, emotional, physiological, and behavioral processes may influence symptom perception and distress. Although research specifically examining CBT in LPS remains limited, a systematic review found benefits to pairing CBT with traditional voice therapy for voice disorders [103]. Research supports the use of GI-focused CBT across a range of gastrointestinal disorders, including esophageal conditions [98, 104, 105]. Recommendations from an expert panel encourage CBT and gut-directed hypnotherapy as first-line behavioral treatments for patients with functional heartburn [106].

Clinicians specializing in LPS can offer a range of adjunctive therapies targeting healthful cognitive and affective factors that may further address the multidimensional nature of LPS.

10 |. Conclusions

LPS and LPRD reflect a complex interplay of physiologic, behavioral, and cognitive-affective factors that extend beyond reflux alone. Recognition of hyperresponsiveness and hypervigilance as potential processes influencing symptom burden reframes management toward a more targeted, mechanism-based approach. Effective care relies on multidisciplinary collaboration, integration of reflux-directed and behavioral therapies, and patient-centered education that supports adaptive symptom interpretation. As the field evolves, future work should focus on refining phenotypic classification, optimizing treatment delivery, and continued research to augment evidence for targeted interventions to improve management outcomes.

Key Points.

• While the term “laryngopharyngeal reflux” implies reflux-related pathophysiology, the likelihood of finding objective reflux evidence is low in patients with laryngopharyngeal symptoms (LPS).

• Cognitive–affective and behavioral processes—including hyperresponsiveness, hypervigilance, and symptom-specific anxiety—may contribute to symptom perception, regardless of whether objective reflux evidence is demonstrated on testing.

• A multispecialty approach that includes not just measures to reduce reflux exposure, but also behavioral therapies to address the multidimensional nature of LPS may provide benefit to patients.

• Behavioral interventions can be combined with neuromodulators such as delta ligands, tricyclic antidepressants, or selective serotonin reuptake inhibitors when clinically appropriate.

Data Availability Statement

Data sharing was not applicable to this article as no datasets were generated or analysed during this study.