Cough is one of the most common reasons that patients seek medical care, accounting for approximately 30 million physician visits in the United States each year. A chronic cough persists longer than 8 weeks and has an estimated worldwide prevalence of 9.5% in the adult population. Patients presenting with chronic cough typically undergo workup or empiric treatment for the three most common etiologies of persistent cough in adults: upper airway cough syndrome (UACS), gastroesophageal reflux disease (GERD), and cough variant asthma (CVA). A diagnosis of neurogenic cough is considered when cough persists after the common causes have been ruled out. Neurogenic cough is thought to be due to laryngeal hypersensitivity resulting from postviral neural damage to the superior laryngeal nerve (SLN) and has traditionally been considered a diagnosis of exclusion. However, patients with neurogenic cough have a characteristic set of presenting symptoms and exacerbating factors, and the diagnosis may be considered in some cases before ruling out all other potential causes. Patients typically describe an irritative focus in the paralaryngeal region that triggers their cough, and may describe this as a “tickle,” “drainage/mucus,” or “dry spot.” The sensation may be localized to a specific “trigger point” in the neck, commonly at the site of entry of the internal branch of the SLN (iSLN) through the posterior thyrohyoid (TH) membrane. The iSLN is a branch of the vagus nerve that provides general sensation (pain, touch, and temperature) to the endolarynx and is a commonly affected sensory nerve in patients with neurogenic cough. After its entry through the TH membrane, it divides into an upper and lower branch: the upper branch innervates the inferior pharynx, epiglottis, vallecula, and the laryngeal vestibule; the lower branch supplies the aryepiglottic folds and the false vocal folds. In patients with neurogenic cough, the cough is typically triggered by actions or activities that stimulate the larynx, such as voice use (talking, laughing, and singing), swallowing, temperature changes (typically exposure to cold and dry air), strong smells (chemicals, perfumes, and smoke), position changes (bending or rolling over), or external stimulation of the neck.

The mainstays of treatment for neurogenic cough have traditionally been behavioral cough suppression therapy (BCST) and neuromodulating medications such as amitriptyline, γ-aminobutyric acid (GABA) analogs (gabapentin and pregabalin), and the GABA agonist baclofen. While these are well-established and effective treatments, they both have limitations. Patients may not have access to a speech language pathologist trained in BCST, and cost, time constraints, and travel distance may be prohibitive. Neuromodulators require titration and may be sedating or have other intolerable side effects. The SLN block is a treatment for neurogenic cough that directly targets iSLN and was first described by Simpson et al . in 2018. A mixture of a long-acting corticosteroid and a local anesthetic is injected at the location of the iSLN’s entry site through the TH membrane. Localized nerve blocks are a well-established treatment for peripheral neuropathies, and the iSLN’s superficial location and readily identified landmarks make it an ideal target for percutaneous blockade. Given that pain and cough share a common receptor, transient receptor potential vanilloid 1 (TRPV1), the SLN block may suppress nociceptive discharge and disrupt the sensory feedback loop promoting cough.

While most patients with neurogenic cough are candidates for SLN, those most likely to respond have an irritative focus localized to the posterior TH membrane unilaterally that precedes their cough. Palpation of this area will typically elicit discomfort or cough, and this “trigger point” is the target for the injection. The SLN block may be used as the primary treatment for chronic cough or as an adjunct to other modalities such as BCST and/or neuromodulating medications. In addition, the SLN block is effective in the management of paralaryngeal pain, particularly in the setting of muscle tension dysphonia (MTD). The SLN block may also be a treatment option for other symptoms of the irritable larynx syndrome (ILS), such as recurrent laryngospasm and paradoxical vocal fold motion (PVFM). While therapy with an SLP is the mainstay of treatment for ILS, the SLN block may be a helpful adjunct in refractory cases.

The procedure is performed without sedation in the clinic setting with the patient seated upright in the examination chair. If the patient reports lateralization of their symptoms or is found to have a “trigger point” that elicits cough and/or discomfort, that side is targeted with the initial injection. If no lateralization, either side may be targeted. One milliliter (mL) of a particulate steroid (such as triamcinolone acetonide 200 mg/5 mL or methylprednisolone 80 mg/1 mL) and one mL of a local anesthetic (such as 0.5% bupivacaine or 1% lidocaine with 1:100,000 epinephrine) are then drawn up into separate three mL syringes. The syringes are connected using a female-to-female luer lock adaptor and mixed ( Fig. 48.1 ). Alternatively, the solutions can be drawn up sequentially into the same three mL syringe, taking care to avoid contaminating the second vial if it is multiuse. Particulate steroids precipitate out of solution quickly, so the materials should be drawn up immediately before injection. A 1 ¼ inch 27-gauge needle is then used for the injection.

Use of a female-to-female luer lock adaptor to aid in mixing of the anesthetic and steroid components of the superior laryngeal nerve (SLN) block. After mixing, the solution is transferred to one syringe for the injection.

The injection targets the iSLN at its entry point into the larynx through the posterior aspect of the TH membrane. The posterior TH space may be located by first palpating the thyroid notch and following the superior border of the thyroid cartilage posteriorly. Just anterior to the superior cornu, the cartilage dips inferiorly and creates an enlarged space over the posterior TH membrane. This is a landmark for the entry point of the iSLN into the larynx. Once the target for the injection is located, the fingers of the nondominant hand are used to displace the larynx slightly toward the side of the injection. The thumb of the nondominant hand is placed over the planned injection site to confirm its location and act to stabilize the needle during the injection. The needle is then passed either above or below the thumb and directed toward the TH membrane ( Fig. 48.2 ). Tactile feedback is used to direct the needle—if cartilage is encountered, the needle is pulled back slightly and redirected. There is a slight soft tissue resistance encountered once the location of injection over the TH membrane is reached. Before injecting, the plunger of the syringe is drawn back to ensure the needle is not intravascular or in the airway. The steroid/anesthetic solution is then injected slowly over about 10 seconds, and the needle is withdrawn. The patient is then discharged without restrictions on diet, voice use, or activity. Most patients experience improvement in their cough within 2–3 days.

Injection technique for a left-sided superior laryngeal nerve (SLN) block. The fingers of the nondominant hand are used to displace the larynx toward the side of the injection, and the thumb is used to stabilize and guide the needle toward the posterior thyrohyoid (TH) space.

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