Inflammatory diseases of the sinuses:anatomy.

Inflammatory sinus disease most commonly results from or is exacerbated by areas of obstruction within the sinuses. Recent revision of our understanding of mucociliary clearance has placed a renewed emphasis on sinus anatomy, particularly in identifying natural sinus ostia. A discussion of paranasal sinus anatomy is presented in this article along with special reference to these areas as well as contiguous sites that may be involved as a complication of inflammatory disease.

Transmucosal electrical stimulation of laryngeal muscles.

A new technique is described that enables discrete activation of individual laryngeal muscles by electrical stimulation across overlying mucosa. In 15 dogs, we defined six distinct motor points by transmucosal stimulation at 3 mA while observing the resulting characteristic position of the arytenoid and true vocal cord. Five dogs were then paralyzed with succinylcholine in order to simulate bilateral vocal cord paralysis. Application of a 3-mA stimulus at each motor point yielded no motion of the cords, but when the current was increased to 20 mA, characteristic responses were elicited. In five other dogs, botulinum toxin was injected directly into laryngeal muscles. Stimulation was used in an attempt to quantify the degree of neuromuscular blockade. In the last group of five dogs, we simulated cricoarytenoid arthritis by scarifying the joint. The extent and nature of the joint's impairment could be demonstrated by stimulation. Transmucosal stimulation appears promising as a clinical technique for correlating particular vocal cord movements and thresholds of activation with specific laryngeal disorders. Additionally, such a technique may be useful in clarifying how each laryngeal muscle acts upon the cricoarytenoid joint.

Overcoming laryngospasm by electrical stimulation of the posterior cricoarytenoid muscle.

The intent of this study was to demonstrate that the technique of transmucosal electrical stimulation of laryngeal muscles may be of clinical use in airway management. Specifically, its ability to overcome laryngospasm was evaluated. Laryngospasm was induced in eight tracheotomized dogs by hyperventilating each dog, and then applying 0.1 M ammonia to the laryngeal mucosa while administering continuous positive airway pressure (CPAP). Laryngospasm was defined by steady apposition of the vocal cords, massive electromyographic activity in the laryngeal adductor muscles, absence of such activity in the posterior cricoarytenoid muscle (PCA), and intraglottic pressure greater than 80 mm Hg. Upon transmucosal application of 10 mAmp current to the PCA bilaterally, the vocal cords abducted for the duration of the stimulus. We theorize that overcoming laryngospasm by electrostimulation involves a reflexive inhibition of the laryngeal adductors. This study provides an objective model for laryngospasm, and demonstrates that electrical manipulation of the vocal cords may have clinical relevance.

Laryngeal electrode platform: an indwelling device for mobilizing the vocal cords.

By passing electrical current across the laryngeal mucosa and esophageal wall, the recurrent laryngeal nerve can be stimulated, thereby mobilizing the vocal cords. In designing a device that would utilize this phenomenon, we theorized that stability, targeting, and mucosal contact could be maximized by an indwelling device that would conform precisely to the topography of the posterior larynx. In five dogs, molds of the hypopharynx and proximal esophagus were fashioned in vivo by injection of an alginate compound. From each mold was constructed a vinyl platform blanketed with electrodes. Each platform fit snugly in place, and could activate the nerve consistently in any of the dogs. With as little as 3 mA pulsatile current, use of specific electrodes enabled bilateral abduction, more than doubling the resting glottic aperture. Bilateral adduction was sometimes attainable. Such a platform may have use in visualizing subglottic lesions, diagnosing laryngeal movement disorders, and facilitating intubation and extubation.

Transtracheal/transesophageal stimulation of the recurrent laryngeal nerve.

A new technique is described which allows stimulation of the recurrent laryngeal nerve (RLN) through intact tracheal and esophageal mucosa. In ten anesthetized dogs, the posterior-lateral tracheal wall and the anterior-lateral esophageal wall were stimulated by a 1 to 2 mA current with a probe placed just distal to the edge of the cricoid cartilage. The tracheal mucosa was approached through a tracheostomy stoma and the esophageal mucosa through the mouth. The resultant vocal cord motion was frequency dependent, with graded abduction occurring below 30 Hz and adduction above 40 Hz. By stimulating the posterior laryngeal mucosa proximal to the cricoid edge, the RLN branch to the posterior cricoarytenoid muscle was activated, causing ipsilateral vocal cord abduction independent of frequency. Monitoring of cardiopulmonary parameters demonstrated no alterations at these amperages. There were no mucosal abrasions noted. The transtracheal and transesophageal approaches to RLN stimulation appear promising as diagnostic techniques for evaluating vocal cord function during laryngoscopy and, possibly, as methods of glottic airway control.

Transcutaneous electrical stimulation of the recurrent laryngeal nerve in monkeys.

The recurrent laryngeal nerve (RLN) of four anesthetized adult Macaca fascicularis monkeys was stimulated by applying current with blunt electrodes placed unilaterally and bilaterally on the intact neck skin along the tracheoesophageal groove. The stimulus consisted of 2.5- to 4.0-mA cathodal pulses, each of 1-ms duration, beginning at a frequency of 10 Hz and increasing by 10-Hz increments to 100 Hz. Unilateral stimulation from 10 to 30 Hz resulted in a graded vocal cord abduction, with the maximal glottic aperture occurring at 30 Hz. Stimulation above 30 Hz produced a graded cord adduction, with nearly complete glottic closure at 100 Hz; bilateral stimulation yielded similar results, with total glottic closure at 100 Hz. Confirmation of the RLN as mediator of this frequency-dependent cord motion was achieved by surgically isolating it and attaining identical results with direct stimulation. No cardiopulmonary alterations were observed in any trial. Transcutaneous electrical stimulation of the RLN seems to be a relatively safe, reliable, and noninvasive method of controlling vocal cord position and thereby the glottic airway in monkeys.