Diabolical Coughing-Prima Facie Protocols for Diagnosis and Treatment of Medically Jaded Patients.

Abstract

The use of botulinum toxin injection as a new treatment for chronic (neurogenic) cough is new and novel. In an article by Sasieta and colleagues1 in this issue of JAMAOtolaryngology— Head & Neck Surgery, 22 patients whose chronic coughing had been repeatedly evaluated and treated for many years without benefit received 31 distinct injections of very large doses of botulinum toxin type A (BtxA) into each thyroarytenoid muscle. In this retrospective study, response to treatment was assessed via telephone follow-up using patient self-reportingofpercent improvementofcoughat 1and 2months. Theprimary outcomeof treatment successwasdefined as a 50%or greater reduction in the patient’s subjective perception or assessment of their cough severity. Theauthors report that theprimaryoutcomewasachieved in 11 of the 22 participants (50%) and after 16 of the 31 (52%) treatment sessions. There were no immediate complications observedafter treatment following theadministrationofBtxA. Transient dysphonia (n = 19 [86%]), and liquid dysphagia (n = 14 [64%]) occurred frequently after the first BtxA injection and was well tolerated. A median time of 3.5 weeks was observed before an unspecified decline of therapeutic benefitwas perceived. The studyprovides some support for BtxA vocal cord injections, though itwould seemfornowtobea last resort treatment option owing to its limitations. The specific cough syndrome being treated in this study was likely neurogenic, but the authors did not declare a diagnosis of sensory neuropathic cough (SNC) outright, preferring to diagnose their patients with refractory chronic cough. By reviewing the literatureonchronic coughand theuseof the neurotoxinproteinbotulinumtoxin, theauthorsbelieve in the neurogenicityof thechronic cough in their studysubjects. Still they appear to consider neurogenic cough as a diagnosis of exclusion to be applied only after exhaustive workup and empirical treatment of other etiologies. Rather than viewing SNC as a diagnosis of exclusion, it is helpful in the clinical setting to vigorously make or rule out SNC as a prima facie diagnosis by using previously proposed syndromiccriteria for thisdisorder.2Thesyndromeis fairlyeasy to recognize. In fact, patients are able to diagnose themselves withstartlingaccuracywhenexposed toavideoonYouTube3,4 or other internetdescription thatdetails SNC.Consider aswell that a local Chicago television news segment on sensory neuropathic coughing (in approximately 2005) to a viewership of 300000 yielded more than 200 correctly self-diagnosed patients tomypractice in the subsequent 2months.Most selfdiagnosed patients with SNC had significant and durable response to amitriptyline or gabapentin. Arguably,when a clear syndromic diagnosis is made during an initial consultation, only an upper aerodigestive tract examination, auscultation of the lungs, andpossiblyaduediligencechest radiographmay be needed. In thisway, the diagnostic process for SNC can become as straightforward as it is for its cousin syndromic diagnoses of postherpetic or trigeminal neuralgia. The criteria for SNC diagnosis can be summarized as follows5: 1. A somewhat stereotyped and abrupt sensory disturbance (suchas tickle,drypatch, sandpaper,pinprick,drippingsensation,mostcommonatsternalnotch, then larynx,andthen mouth/ throat or central—usually upper—chest). It is key to understand that dripping canbe a sensorydisturbance that tricks patients and their doctors into believingmucus is the culprit. Much energy can be spared with this understanding. It is also important toknowthatoccasionalpatientswith thisdisorderhavesuchsubtle sensorydisturbance that they have not really identified it until questioned carefully by a persistent physician. 2. Trigger phenomena. While many attacks occur spontaneously, most patients have 1 or more of the following triggers: talking, laughing, singing (especially in upper voice), inhalingeither coldorwarmair, touchingaspoton theneck, change of position, eating, and/or strong odors. The latter trigger of strong odor may occasionally suggest a possible psychosomatic origin if secondary gain is obvious or suspected. 3. Characteristic cough phenomenology. The majority of patients with SNC experience at least a few of their dozens to hundreds of attacks per day as violent, lasting 10 seconds to several minutes, and associated with some or many of the following: rhinorrhea, tearing, retching (sometimes to the point of vomiting), or stress incontinence. Occasionally, they experience syncope or near-syncope, laryngospasm, and rib fracture. The sheer magnitude of these paroxysms that are indeed impressive towitness,wouldbe quite atypical of coughing associated with pneumonia, asthma, allergy, postnasal drip, and chronic obstructive pulmonary disease. 4. Nonproductive cough, or if productivity is described, always at the endof a severe attack (ie, bronchorrhea as the result rather than the cause of coughing).6 When there is a clearprima facie syndromicmatch, itmay bearguedthat initial empirical treatment forother less strongly matcheddiagnoses is unnecessary. Instead, itwould seemappropriate to begin SNC treatments first rather than last. Empirical, protocol-driven treatment for SNCmeans moving from one neuralgia medication to the next and even to additionalmedications directed at abolishing aberrant sensations that initiate coughing. Thegoal is to identify amedication that works best.5 This is similar to the process for finding best management of persons with neuralgia. Related article page 881 Thyroarytenoid Botulinum Toxin Type A Injection for Refractory Chronic Cough Original Investigation Research