Evidence for Laryngeal Paralysis in Cricoarytenoid Joint Arthritis

Objective/Hypothesis : To demonstrate denervation atrophy of laryngeal muscles in a case of gout involving the cricoarytenoid joint. Methods : The posterior cricoarytenoid (PCA) and arytenoideus (A) muscles from a 72‐year‐old man with extensive gout were compared with those from a normal adult larynx (age and sex unknown) using stereologic techniques for changes in muscle composition and fiber diameter. Results : The PCA and A muscles in the gout specimen contained changes Indicative of muscle degeneration. In the PCA the volume fraction (VF) of intact muscle was 0.30, of degenerating muscle 0.13, and of fat 0.16. A normal PCA had a VF for intact muscle of 0.64 and 0 for degenerating muscle and fat. Similar changes were seen in the gout A muscle but were not measured. Muscle fiber diameters in the gout PCA (1,024 fibers) showed a significantly higher atrophy and hypertrophy factor than the normal PCA (1,255 fibers). The variability coefficient in the gout PCA (487) was almost double that in the normal PCA (290). Although muscle fiber diameters were not measured in the A muscle in gout, variability in fiber size was seen. Conclusions : The pattern and magnitude of muscle fiber degeneration in the PCA and A muscles from a larynx with gout fixation of the cricoarytenoid joint indicate neural degeneration. Since similar changes were not found in the thyroarytenoid (TA) and lateral cricoarytenoid (LCA), the neuropathy is selective for the posterior branch of the recurrent laryngeal nerve. This neuropathy is likely responsible for vocal cord adduction (stridor) and incomplete closure of the posterior commissure (aspiration) associated with acute cricoarytenoid arthritis. In chronic cricoarytenoid joint arthritis, ankylosis of the joint space maintains the adducted cord position.