Recent literature points to postviral sensory neuropathy as a possible cause for refractory chronic cough. Vagal neuropathy may affect the sensory branches, inducing chronic cough or laryngospasm. Although the clinical presentation is fairly well described, there is little in the way of diagnostic criteria to establish this diagnosis. This article highlights the clinical picture of this disease and the efficacy, side-effect profiles of the currently used pharmacological interventions.
Postnasal drip, cough-variant asthma, and gastroesophageal reflux disease are the cause of chronic cough in 86% of adult patients. This percentage increases to over 99% when evaluating immunocompetent nonsmokers with normal chest radiograph findings and no history of angiotensin-converting enzyme-inhibitor use. Despite this, a significant number of patients continue to have unexplained cough after an exhaustive workup and failed empiric treatments. Recently, a body of literature has emerged supporting a sensory or motor neuropathy responsible for many of the previously refractory cases of chronic cough. First introduced by Morrison and colleagues in 1999, the idea of the irritable larynx has been redefined throughout the years, holding various titles for the same suspected cause: postviral vagal neuropathy (PVVN), sensory neuropathic cough and laryngeal sensory neuropathy (LSN). Many recent studies not only identify the at-risk population, but the common presenting symptoms, potential pathophysiology behind vagal neuropathy, and several promising medical interventions. The purpose of this article is to emphasize that postviral vagal neuropathy may be a distinct and treatable cause of chronic idiopathic cough while reviewing common clinical presentations and potential treatments. See the article by Irwin elsewhere in this issue for another perspective of the role of sensory neuropathy in the unexplained chronic cough.
The idea of postviral neuropathies has been well studied in various other disease processes, such as Bell palsy, Guillain-Barré syndrome, and postherpetic neuralgias. Of interest to otolaryngologists is the small, but significant, subset of patients with treatment-resistant chronic cough that have been identified with clinical or objective evidence suggesting an underlying vagal neuropathy. PVVN is a condition of vagal nerve injury or dysfunction following an antecedent viral illness. Vagal neuropathy may affect the motor branches of the vagus nerve, resulting in vocal fold paralysis or paresis, or it may affect the sensory branches, inducing a throat tickle, globus sensation, excessive throat mucous, odynophonia, chronic cough, or laryngospasm. These symptoms may be aggravated by sensory stimuli such as laughing, prolonged phonation, and noxious stimuli, and has been described being elicited clinically by palpation at the cricoid level.
In 2001, Amin and Koufman first described the association of neuropathic cough and previous upper respiratory tract infection. They described a case report of five patients presenting over 5 years with similar symptoms consisting of chronic cough, globus, dysphagia, vocal fatigue, and effortful phonation, persisting long after resolution of their acute viral illness. Subsequent investigation through videostroboscopy and laryngeal electromyography (LEMG) revealed varied presentations: (1) vocal fold paresis, (2) neuropathy-induced laryngopharyngeal reflux disease, (3) dysphagia, and (4) neuropathic pain.
Two potential mechanisms by which viral infection may cause nerve injury have been described: (1) direct infection and inflammation of the nerve or (2) induction of a nonspecific inflammatory response that secondarily involves a nerve. In either situation, viral involvement lowers the threshold of both the efferent and afferent arms, sensitizing the nerves to previously ignored stimuli. In 2009, Rees and colleagues made clinical distinction between the motor and sensory components of vagal neuropathy. In a prospective cross-sectional series of 44 patients presenting with persistent cough, throat clearing, dysphonia, and vocal fatigue following a previous upper respiratory infection, 45% with motor and sensory neuronal involvement, 41% with isolated sensory nerve involvement, and 14% with isolated motor nerve involvement. Rees and colleagues concluded “cough, throat clearing, and globus are considered primarily sensory symptoms while loss of voice and vocal fatigue are considered primarily motor symptoms,” which all may be attributed to vagal nerve dysfunction. Unfortunately, it may never be possible to definitely establish this causal relationship, as vagal nerve biopsy remains the only means of definitive diagnosis. As more case studies and prospective analysis emerge, greater support appears for a clinical diagnosis of PVVN.
Clinical evaluation
In diagnosing PVVN, the clinician must maintain a high level of suspicion. As with all clinical diagnoses, a thorough history is essential in providing clues to this potential cause. Many algorithms, such as the anatomic diagnostic protocol, are available to help guide the clinician in assessing the patient. Once the most common causes of chronic cough have been ruled out, further inquiry into potential viral illness surrounding the initial presentation of symptoms should be investigated. PVVN is usually associated with an acute onset of cough that persists long after the resolution of the concomitant viral symptoms. The majority of patients presenting with PVVN have previously been misdiagnosed. An average of 83 weeks from onset to diagnosis has been sited; therefore, patients may show significant frustration in the persistence of their symptoms. Many of these patients have been treated with multiple rounds of antibiotics, proton pump inhibitors, and antihistamines well before presenting to the otolaryngologist. Although not all the literature agrees, the majority of recent studies suggest PVVN is more common in women, occurring most often in the fifth and sixth decade of life. The vagus, supplying both the superior laryngeal nerve (SLN) and recurrent laryngeal nerve (RLN), allows for a multitude of presentations, many of which can be classified according the their primary symptoms: motor, sensory, or mixed motor-sensory dysfunction.
Motor Symptoms
Acute onset of “breathy dysphonia, vocal fatigue, effortful phonation, odynophagia, cough, globus, or dysphagia lasting long after the resolution of the acute viral illness” may represent the initial presentation of PVVN involving the efferent branches. Whereas routine nasolaryngoscopy can appear both anatomically and functionally normal, videostroboscopy and LEMG may provide the only objective evidence of RLN or SLN dysfunction. With primary motor branch involvement, stroboscopy may reveal reduced diadochokinesis of the vocal folds or axis deviation of the glottis. LEMG may also reveal the presence of polyphasic units, rapid-firing units, and reduced recruitment in the cricothyroid and thyroarytenoid muscles, providing further objective evidence for RLN or SLN paresis.
Sensory Symptoms
When the sensory branches are mainly affected, the patient may not necessarily present with sharp pain or the classic burning ache associated with many of the other neuropathies, but may instead describe a tickle, dry patch, or globus most commonly found at the level of the cricoid. This sensation often precipitates a 20- to 30-second coughing spell. Bastian and colleagues describe this phenomenon as a “bogus tickle that leads to uncontrollable coughing.” Excessive throat clearing is another well-recognized symptom within the literature. Tussive-like spells and laryngospasm have been reported, usually following exposure to specific aromatics such as perfume or household cleaning agents.
Viral-induced Laryngopharyngeal Reflux
Several studies have recognized symptoms consistent with laryngopharyngeal reflux (LPR) beginning with the onset of a previous viral illness. Rees and colleagues propose postviral LPR may be secondary to altered esophageal peristalsis and esophageal clearing or alternately an increase in symptoms through altered sensation in the throat due in part to preexisting reflux.
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
