Decisions regarding intervention in cases of vocal fold paralysis are made on the basis of the laryngeal function that is most compromised. In the case of unilateral paralysis, the voice is breathy and the patient is at risk for aspiration due to compromised adduction. Inspiratory capacity is minimally impaired, as abduction of the opposite vocal fold provides adequate ventilation. In bilateral paralysis, the gravest concern is total loss of abduction. Because the vocal folds are paralyzed in proximity to one another, voice tends to be functional but airway embarrassment is often severe enough to warrant emergency intubation or tracheotomy to relieve inspiratory stridor and dyspnea [25, 32].
In unilateral paralysis, the objective of treatment is to medialize the paralyzed vocal fold to improve glottal closure. Despite the improvement in voice and aspiration that thyroplasty or injectable materials provide, the static nature of these types of implants ignore the long-term effects of atrophy on vocal fold mass and position. In some patients, voice undergoes a gradual deterioration over time, such that a larger implant or repeat injection is required.
The aim of treatment for bilateral paralysis is to restore adequate ventilation. Tracheotomy is a simple procedure for establishing an emergency airway in case of acute bilateral paralysis. Unfortunately, permanent tracheostomy is known to have the complications of tracheal stenosis, chronic infection, and psychosocial impairment. Procedures such as arytenoidec-tomy and cordotomy, while regarded as the standard of care for enlarging the glottis, also have inherent complications. Specifically, these procedures irreversibly destroy voice and may compromise airway protection during swallowing.
The limitations associated with current therapy for both unilateral and bilateral paralysis have prompted investigation into more physiological, dynamic approaches to rehabilitation: reanimation of laryngeal muscles by functional electrical stimulation or selective reinnervation. Electrical stimulation of the PCA muscle, when paced with inspiration, offers an innovative method for restored ventilation in case of bilateral vocal fold paralysis, with none of the disadvantages associated with conventional surgical treatment. Paced muscle stimulation has been studied in animals and explored more recently in preliminary clinical trials using an implantable commercial stimulator [33,34]. Of six patients successfully implanted, five demonstrated stimulated abduction sufficient to restore mouth breathing. Three patients were subsequently decannulated. Unlike conventional treatment, pacing had no negative effect on voice quality . Laryngeal pacing is covered in depth elsewhere in this text.
While electrical reanimation of the paralyzed larynx appears promising, the more natural approach to treatment would be to manipulate the process of nerve regeneration and muscle reinnervation. Since Horseley's original report of successful restoration of vocal fold mobility following RLN anastomosis , many investigators have attempted to reinnervate the paralyzed larynx using a variety of approaches in both animal experiments and limited clinical trials. Despite early favorable reports, the present consensus is that end-to-end RLN anastomosis results in crossed innervation of abductor and adductor muscles [15,17, 25, 37]. Attempts to prevent synkinesis have looked to extrinsic sources for reinnervation of the larynx.
With respect to bilateral paralysis, phrenic nerve to RLN anastomosis has been performed to restore abduction, but with poor results . Other approaches have focused on reinnervation of individual muscles. Tucker transposed a nerve-muscle pedicle, composed of a branch of the ansa hypoglossi and a pedicle of the omohyoid muscle, into the denervated PCA of dogs and humans, and reported return of vocal fold abduction [42-44]; however, failure of reinnervation with this procedure has been observed histochemically and electromyographi-cally [37, 45]. Furthermore, other investigators have been unable to replicate good return of abduction. In animal experiments and limited clinical trials, Crumley et al. attempted to rein-nervate the PCA by grafting the phrenic nerve to the abductor branch of the RLN and cutting the adductor branch . Although this approach remains experimental, fair results were obtained in his study.
At present, it would appear that there has been more progress made toward reinnervation of adductor muscles in case of unilateral laryngeal paralysis. Despite failure to restore unilateral mobility, a new generation of reinnervation experiments has found success in using an extrinsic nerve to give the muscles bulk and tonus. One of the most pursued approaches, introduced in 1924 by Fraser , is an ansa cervicalis to RLN transfer. A purported advantage of the approach is that the nerve subserves only tonic, postural function, and therefore causes no extraneous twitching of the vocal fold or voice disturbance after transfer [48-50]; however, failure to restore adduction during vocalization requires that a medializa-tion procedure still be used in combination with reinnervation . Another promising new approach is that introduced by Paniello  and Paniello et al. , a hypoglossal nerve to RLN transfer. In animal and human experiments, they showed strong indication that the CXII can serve as a suitable donor for not only maintenance of vocal fold bulk, but also reanimation for deglutition and voice. In the animal studies, all animals showed strong return of adduction, particularly during swallowing. In the preliminary clinical study, 5 patients were reported to have excellent voice quality with no aspiration îyear after surgery. The return of motion with this strategy could supersede ansa cervicalis transfer, as it obviates the need for a primary thyroplasty, however, this approach has its own inherent disadvantages: a longer distal RLN segment is needed for anastomosis, and the procedure creates a lingual deficit.
These novel trends in clinical research attempt to address laryngeal paralysis through reinnervation of individual muscles using an extrinsic, non-native source. There are two fundamental problems with this strategy. Firstly, stealing another muscle's nerve supply compromises that muscle's function. In case of bilateral paralysis, splitting the phrenic nerve for PCA reinnervation will result in hemidia-phragm paresis. The second problem arises from the differences between the host and donor muscle functions. Clearly, all complex voluntary and involuntary functions cannot be accommodated by the external nerve source. Indeed, because of this problem, the strategy for reinnervating the adductor muscles in case of unilateral paralysis is to identify a nerve source that performs minimal, only tonic function such as the ansa cervicalis. The goal is to maintain or restore bulk to the vocal fold without inducing extraneous motion. Ideally, a means could be found to selectively control reinnervation of laryngeal muscles by their original motoneurons in the RLN.
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