Laryngeal dystonia in multiple system atrophy.
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Biomedical subjects
Publications and source records attributed to I Sanders.
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Botulinum toxin was recently approved for treating several head and neck dystonias. Paralysis of neighboring muscles is the major complication of its use. Spread of toxin from the injected muscle has been suggested as an etiology. This study examines how botulinum toxin crosses muscle fascia by a novel method of quantifying muscular paralysis. Botulinum toxin (0.2 to 10 U) was placed onto the fascia of rat tibialis anterior (TA) muscles (n = 6). Toxin was also placed on dose-matched muscles that had their fascia surgically removed (n = 6). Twenty-four hours later, the nerve to the tibialis anterior was electrically stimulated to deplete the muscle fibers of glycogen. Toxin-paralyzed fibers retained their glycogen and appeared purple on periodic acid-Schiff (PAS) stain. Botulinum toxin easily passed through muscle fascia even at subclinical doses. The presence of fascia reduced the spread of botulinum toxin by 23%. These results suggest that spread of botulinum toxin can be prevented only by delivering small doses to the center of a target muscle.
Most functional electrical stimulation (FES) research has focused on the spinal cord-injured patient whose muscles are paralyzed but still maintain their innervation. This article details the investigation of FES of the laryngeal muscles. In time, FES may become a useful treatment for bilateral vocal cord paralysis (BVCP) and for some laryngeal movement disorders.
The purpose of this study is twofold. First, to introduce a new phenomenon--abductor vocal cord spasm, or abductor laryngospasm. Second, to reconcile a longstanding discrepancy involving the effect of lung inflation on vocal cord position. Abductor laryngospasm was induced in six anesthetized, tracheotomized dogs by the administration of continuous positive airway pressure (CPAP) after occlusion of the trachea for 60 seconds. Abductor laryngospasm was characterized by sustained vocal cord abduction with concomitant massive, continuous posterior cricoarytenoid muscle (PCA) electromyography (EMG) activity and little or no laryngeal adductor muscle EMG activity. Vocal cord opening was sustained for up to 90 seconds. In the same dogs, administration of CPAP, after hyperventilation of the animal, resulted in adductor laryngospasm. Adductor laryngospasm was characterized by steady apposition of the vocal cords, massive laryngeal adductor muscle EMG activity, and silent PCA EMG activity. Abductor laryngospasm appears to be the physiologic converse of adductor laryngospasm. The results of this study show that lung inflation can produce either vocal cord abduction or adduction, depending on whether the dog is hypoventilated or hyperventilated before administration of CPAP.
This experiment investigated the reinnervation of the canine posterior cricoarytenoid (PCA) muscle with preganglionic neurons of the sympathetic nervous system. Six dogs had their right recurrent laryngeal nerve (RLN) sectioned. Four of these dogs had the sympathetic cervical trunk (SCT) implanted into the right PCA muscle, and the two remaining dogs served as denervated controls. Four months later all dogs underwent videolaryngoscopy, electromyography, and electrical stimulation of the SCT. The PCA muscles were excised, sectioned, and stained for glycogen and ATPase. All four experimental PCA muscles demonstrated electrically evoked abduction and tonic electromyographic activity. In two of the specimens, staining (ATPase and PAS) revealed areas of reinnervation with fiber type grouping and glycogen depletion. These results are consistent with the successful reinnervation of the PCA muscle. Further refinement of this technique could be of benefit to patients with bilateral vocal cord paralysis.
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.
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.
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.
This study was designed to examine the feasibility of transcutaneous stimulation of the recurrent laryngeal nerve. Electrical activation of the recurrent laryngeal nerve was achieved by applying a blunt electrode to the intact neck skin at specific points along the tracheoesophageal groove in anesthetized adult dogs. The stimulus consisted of 10 mA cathodal pulses, each of 1 msec duration, delivered at a frequency of 10 Hz and increased by 10 Hz increments up to 100 Hz. Vocal cord excursion was directly related to the frequency of applied current. In all six dogs studies, stimulation at 30 Hz resulted in maximal ipsilateral vocal cord abduction, while stimulation at frequencies greater than 40 Hz resulted in ipsilateral vocal cord adduction up to or across the midline. Vocal cord movement was immediate and persisted for the duration of the stimulus train. Surrounding neck muscles were not visibly activated. We propose that the observed frequency-dependent movement of the vocal cords occurred because of the difference between the contraction times of the intrinsic abductor and adductor muscles of the larynx. Transcutaneous recurrent laryngeal nerve stimulation appears promising, both as a diagnostic aid in laryngoscopy and as a therapeutic tool in controlling the glottic aperture.
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In our modern era, the radiologist is no longer content merely to discern abnormal shadows; he must correlate the radiologic finding with clinical and physiologic findings. With this in mind, the radiologist must be familiar with pertinent data from the patient's history, physical examination and laboratory studies to aid not only in structuring the examination of the patient but also in interpreting the radiologic findings.
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