Laryngeal sensory neuropathy (LSN) is a relatively uncommon peripheral neuropathy thought to affect the superior or recurrent laryngeal nerves. The precise mechanism of LSN has not been fully elucidated but is thought to be similar to that of other peripheral neuropathies: a combination of metabolic abnormalities, mechanical disruption of nerves (ie, trauma or compression), and/or viral infection. LSN typically presents with nonspecific symptoms, most commonly chronic nonproductive cough, throat clearing, throat discomfort or abnormal sensation, or dysphonia. Other symptoms that may be seen include laryngospasm, dyspnea, globus sensation, and hoarseness. This condition is typically an acute process that begins suddenly following viral infection or surgery, although patients may have had chronic cough for several years prior to their diagnosis.

Given that the pathogenesis of LSN is not precisely understood, the risk factors and predisposing conditions are also not fully defined. However, it is known that patients with type 2 diabetes mellitus are at an increased risk of developing LSN, most attributed to metabolic abnormalities. Patients with goiter due to thyroid disease are also shown to have an increased risk. The most common risk factors to developing LSN are antecedent viral infection or trauma, most often related to surgery or instrumentation of the upper aerodigestive tract via endoscopy, intubation, or other surgery.

Patients with LSN often undergo considerable workup before their eventual diagnosis is made, including but not limited to pulmonology, gastroenterology, and otolaryngology. This condition represents a diagnosis of exclusion and is most often made based on history and clinical features. As with other sensory neuropathies, patients may experience relief of symptoms with the use of neuromodulator agents such as gabapentin and/or low-dose tricyclic antidepressants such as amitriptyline.