Causes of Hypopharyngeal Globus Sensation in Laryngopharyngeal Reflux
The globus sensation in LPR arises from three primary mechanisms: direct chemical injury from refluxed gastric contents (particularly pepsin), neurogenic inflammation triggering laryngeal hypersensitivity, and pharyngolaryngeal muscle tension as an aberrant learned behavior—with ongoing controversy about whether acidic refluxate or pepsin-containing non-acid reflux is the primary culprit. 1
Primary Pathophysiologic Mechanisms
Direct Chemical Injury
- Pepsin exposure appears to be a main causative factor, with refluxed gastric contents causing localized damage to laryngeal tissues even in small amounts 2, 3
- The refluxate may be acidic or non-acidic, as controversy exists about whether fluid needs to be acidic or merely contain pepsin to cause symptoms 1
- Unlike classic GERD, LPR typically results from small amounts of refluxate occurring while upright during daytime, producing localized laryngeal symptoms without esophagitis 4
Neurogenic Signaling and Inflammation
- Neurogenic signaling leads to inflammation and subsequent symptoms, representing an alternative or complementary mechanism to direct chemical injury 1
- This mechanism contributes to laryngeal hypersensitivity syndrome, where the larynx becomes hyperresponsive to normal stimuli 5, 6
- The condition involves both reflux and reflex mechanisms, though clear understanding of molecular pathways remains incomplete 3
Pharyngolaryngeal Tension
- Aberrant learned behaviors create pharyngolaryngeal tension that manifests as globus sensation 5, 7
- This represents a functional component rather than true structural pathology, linked to psychological stress with symptom exacerbation during high emotional intensity 5, 8
- The sensation is sensory rather than contractile, not representing true muscle spasm 7
Clinical Implications for Diagnosis
Distinguishing Features
- Globus in LPR presents as a recurrent, non-painful sensation of a lump in the throat that characteristically improves during eating rather than worsening with swallowing 5, 8
- The sensation is more obvious between meals and often resolves during food intake 5, 8
- Patients may not complain of heartburn or regurgitation, placing the diagnostic burden on clinicians to determine if reflux contributes to symptoms 1
Diagnostic Challenges
- No gold standard diagnostic test exists for LPR, creating significant healthcare burden 1, 6
- Variable responses to PPI therapy complicate confirming causal association between reflux and symptoms 1
- Laryngoscopic findings have poor inter-rater reliability, with erythema and edema noted even in healthy volunteers, limiting their diagnostic utility 1
Common Pitfalls to Avoid
- Do not mistake globus for dysphagia—the key distinction is that globus improves with eating while dysphagia worsens with swallowing 5, 8
- Avoid assuming a simple PPI trial provides accurate diagnostic information, as the multifactorial nature of LPR (acid, pepsin, neurogenic mechanisms) means acid suppression alone may not address all pathways 1
- Do not rely solely on laryngoscopic findings for diagnosis, as findings like posterior commissure erythema and arytenoid edema lack specificity and have poor reliability 1
- Recognize the functional component—approximately 20% of patients have coexisting functional dysphagia, and many have pharyngolaryngeal tension requiring behavioral interventions rather than solely medical therapy 5, 8