The evaluation of UVFP begins with a thorough history and physical examination. The symptoms of UVFP are well known to all otolaryngologists. These symptoms are related to glottic insufficiency resulting from some degree of lateral displacement of the paralyzed vocal fold. The primary symptom of UVFP is dysphonia, or hoarseness. The voice can vary from simple vocal fatigue in mild or well-compensated cases, to almost complete aphonia in severe cases. Much of the quality of the voice is determined by the muscular tone and position of the affected vocal fold and each patient’s unique glottal compensatory strategy during phonation. An atrophic and poorly compensated VFP typically presents with a breathy, weak voice caused by air escape. The voice may also have a “watery” or “wet” quality to it if secretions are retained in the pyriform sinus, as is typical in high vagal injuries. With time, most patients eventually progress to a stronger but not normal voice using various compensatory strategies. Supraglottic hyperfunctional strategies are common. These patients constrict the supraglottic tract either laterally, apposing the false folds, or in an anterior posterior dimension, apposing the epiglottis to the arytenoids or the arytenoid cartilage to the contralateral false fold. This hyperfunctional muscular contraction leads to a characteristic rough, pitch-locked, low-frequency voice. This voice can sound similar to that of a patient with primary muscular tension dysphonia, and the diagnosis of VFP may not be suspected (17). “Unloading” of the voice, as described later in this chapter, is used to help analyze these patients. In contrast, other patients may develop an unnaturally high-pitched voice that is breathy in quality. This has been referred to as a “paralytic falsetto,” and is characterized by a mean increase in fundamental frequency 85 Hz above “natural” pitch. This condition is thought to be caused by compensatory contraction of the ipsilateral CT muscle, which remains innervated in isolated RLN paralysis (18).

Swallowing difficulties are often encountered, specifically aspiration of liquids, along with a weak and ineffective cough. Some dysphagia for solids may also be present, especially in brainstem or high vagal injuries, because of the concomitant denervation of the pharyngeal constrictors. Risk of aspiration is heightened in these instances as well, because of the loss of ipsilateral laryngeal sensation from SLN involvement.

It is important to obtain a vocal inventory of the patient’s voice responsibilities (both work related and social). Vocal professionals rely on a serviceable voice for their livelihood, and these patients should be questioned regarding their upcoming work schedule to help determine the urgency of early surgical intervention (19). Most professional voice users will opt for temporizing vocal augmentation (e.g., Gelfoam, carboxymethylcellulose, and hyaluronic acid) so that they can return to work as soon as possible. Standardized patient-based voice handicap instruments are useful during the initial assessment and for documenting treatment progress (see Chapter 65).

A patient with UVFP can occasionally complain of being “short of breath”; however, careful history will show that the patient is not experiencing airway obstruction, as seen with BVFP. These patients are actually reporting a breathlessness that principally occurs during conversation and is caused by inefficient laryngeal closure. Poor glottal closure impairs the capacity to project the voice because of a “leaky” valve. Many patients increase respiratory effort and laryngeal muscle activity in an attempt to achieve glottal closure and produce a louder voice. These compensatory behaviors are mostly ineffective, placing undue strain on the paralaryngeal musculature, and resulting in vocal fatigue. This leaky laryngeal valve obviously requires increased respiratory drive to function, further contributing to the breathless feeling many patients report. In addition, exertional activity that requires lifting, pushing, and pulling can be difficult for patients with UVFP, because of the lack of an effective valsalva mechanism.

There is little yield from ordering screening laboratory tests such as chemistry panel, complete blood count, urinalysis,
Venereal Disease Research Laboratory, or fluorescent treponemal antibody absorption test, thyroid function tests, autoimmune panels, or erythrocyte sedimentation rate. Terris et al. (27) studied 84 patients with UVFP in which serologic studies had 0% yield in determining the cause. If additional elements of the history and physical examination point toward a systemic process as the cause of UVFP, directed serology tests may be indicated. In general, however, a “shotgun” approach to the workup of uncomplicated UVFP is unnecessary and wasteful.

As screening tools, barium swallow and thyroid scans have virtually no yield in determining the cause of VFP and are not advocated in the diagnostic workup (28). In contrast, a modified barium swallow or functional endoscopic evaluation of swallowing to evaluate swallowing and aspiration risk (29) is frequently helpful in managing cases of dysphagia in the workup of VFP.

In cases where a clear-cut temporal relation exists between surgical iatrogenic trauma and VFP, no additional radiologic workup is necessary. In cases where no cause can be found for the VFP, imaging studies are essential. Some disagreement exists to what constitutes an “adequate” radiologic assessment for unexplained VFP. Most investigators agree that a CT scan (with contrast) or magnetic resonance imaging (MRI) encompassing the base of the skull through the upper chest is adequate. The radiologist should be informed that the entire course of the vagus down to the take-off point of the RLN in the thoracic cavity needs to be included in the study. Benninger et al. (1) have argued that CT or MRI of the neck combined with chest radiography constitutes an adequate workup. They noted that 100% of pulmonary or mediastinal malignancies associated with VFP were detected on routine chest radiography, and that imaging of the chest by CT was unnecessary. Others disagree with this approach. Glazer et al. (28) demonstrated that of 18 metastatic mediastinal masses seen on CT, only 5 were visualized on routine chest radiographic study. Koufman et al. (30) advocate the addition of MRI of the brainstem in cases of obvious “high vagal” lesion (palatal paralysis + VFP), because this is a difficult area to image and small lesions can be missed.

The utility of imaging studies in the setting of vocal fold paresis is less well defined, as the presence of partial vocal fold motion is considered by many to be indicative of a lower likelihood of a radiographically identifiable compressive lesion of the RLN. These authors do not routinely perform radiologic evaluation of patients with vocal fold paresis.

LEMG has an increasingly crucial role in the workup of unilateral vocal fold immobility. The findings of LEMG are important in determining prognosis, differentiating UVFP and CA joint pathology, diagnosing suspected vocal fold paresis, and directing treatment decision making (31,32,33,34,35,36).

Useful information from LEMG is obtained between 1 and 6 months after the onset of VFP. Evaluation outside of these parameters can render the information misleading (too early), or of limited usefulness (too late) (37). Munin et al. (37) have shown that serial LEMG provide better prognostic information in the determination of UVFP recovery.

Qualitative LEMG has been a long-time tool in the evaluation of VFP. More recent reports describe quantitative aspects of LEMG that provide additional information regarding prognosis (38,39). The term “spontaneous activity” refers to fibrillation potentials (spontaneous discharges during rest). This finding is consistent with active nerve denervation (Fig. 69.7B). “Recruitment” is the finding of increase in the number and rate of motor unit discharges as contraction is increased (as the patient increases the loudness of the vocalization); this can be reduced or absent with nerve injury. Normal motor unit potentials (MUP) are biphasic or triphasic, whereas polyphasic MUP indicate early reinnervation (Fig. 69.7C). Clear-cut cases of normal (class I) and grossly abnormal (class V) give good prognostic information. Statham et al. (38) have recently demonstrated that motor unit recruitment can be quantitatively measured within the TA muscle complex by a “turns analysis,” evaluating the number of “turns,” or peaks of the measured MUP signal. Their report evaluated both control and UVFP patients and revealed that a mean decrease in turns below 400 at maximal effort is reflective of a neurogenic lesion (Fig. 69.8).

Additionally, synkinesis reflects a misdirected reinnervation following RLN injury and/or reinnervation from nonnative nerves and is demonstrated by MUP in the TA muscle complex during vocal fold abduction tasks (such as a sniff) (Fig. 69.9A and B). The presence of synkinesis has been shown to be a poor prognostic indicator (34). Smith et al. (39) demonstrated that use of quantitative LEMG improves the ability to predict return of vocal fold motion, with 100% positive and 89.5% negative predictive values in their study utilizing this technique. Clearly, LEMG in general, and quantitative LEMG specifically, represent a clinically useful tool in the management of patients with VFP.