Discussion
We describe two cases where Arnold’s nerve ear-cough reflex was a manifestation of a vagal sensory neuropathy and this was identified as the cause of a refractory chronic cough that was successfully treated with gabapentin. In both cases, the cough was triggered by mechanical stimulation of the external auditory meatus and accompanied by other neuropathic features such as throat irritation (laryngeal paresthesia), and cough triggered upon exposure to nontussive triggers such as cold air and eating (termed allotussia). These features suggest a neuropathic origin to the cough (4). We therefore used gabapentin to treat the patients based on its known success in sensory neuropathic disorders (5,6) and recently chronic cough (7,8). These observations strengthen the emerging concept that vagal sensory neuropathy may underlie many cases of refractory or idiopathic chronic cough.
SLN (1) and PVVN (2,3) have been described as potential causes of chronic cough. SLN may occur after viral infections or after mechanical trauma to the vagus or superior laryngeal nerve (1,3,9). It is thought to result in a lowered threshold for sensory laryngeal nerve firing and is consequently perceived as throat irritation and often chronic cough. In 2005, a form of hereditary sensory neuropathy was observed to be associated with chronic cough in a case study of two families (10). Affected individuals had an adult onset of paroxysmal cough, gastroesophageal reflux disease and distal sensory loss. Cough could be triggered by noxious odours or by pressure in the external auditory canal (Arnold’s ear-cough reflex). Other features included throat clearing, hoarse voice, cough syncope and sensorineural hearing loss. This disorder clearly demonstrated how cough could be linked to denervation hypersensitivity of the upper airways and oesophagus. Similarly, PVVN is a condition that occurs following an upper respiratory illness, which represents injury to various branches of the vagus nerve. The pattern of symptoms and findings in this condition are consistent with the hypothesis that viral infection causes or triggers vagal dysfunction (9). These patients may also have airway hyperresponsiveness persisting beyond the acute upper respiratory tract infection that manifests as a decrease in cough threshold in response to irritating chemical or mechanical stimuli.
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There is therefore a body of evidence that links chronic cough to a neuropathic disorder involving the vagus nerve. The cases reported here extend this data by objectively documenting the Arnold nerve cough reflex, and showing that a treatment approach based on a neuropathic disorder can effectively improve cough severity, cough frequency and quality of life. We also observed an association with VCD in the first case. Cough is not uncommon in VCD, and may be a manifestation of upper airway hypersensitivity (11). Further, EAHR was also evident in one of the two cases reported. This may be a physiological example of paradoxical vocal cord closure, and is a more prevalent syndrome than first thought, potentially affecting areas under vagal innervation. In a study by Cho et al. (12) cough sensitivity was found to be closely related with EAHR during capsaicin provocation in some CC subjects. It is therefore possible that EAHR may be one of the mechanisms developing some subtypes of CC. The presence of EAHR is confirmed in this case report by hypertonic saline challenge testing with a greater than 20% fall in mid-inspiratory airflow and/or the identification of associated VCD confirmed by fibre optic laryngoscopy which also presents with extrathoracic obstruction and chronic cough.
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