Ronda Alexander, MD
Assistant Professor
The past decade has seen vocal fold paresis gain a foothold in the diagnostic algorithm of otorhinolaryngologists. It is now accepted that neurologic impairments of vocal fold motion exist along a continuum and can range from obvious dysphonia and full immobility to subtle physical findings and somewhat ambiguous symptoms. Identification of this condition requires a careful ear and eye during the patient encounter and special diagnostic techniques to gain a global understanding of the individual patient’s disorder.
Weakness of one or more laryngeal nerves results in uneven tension on the suspensory and motor apparatus of the larynx. Even with apparently full motion of the arytenoids complex, a gentle listing of the superstructure can bring the vocal folds out of a uniform axial plane, resulting in glottal incompetence as the phonatory margins no longer approximate each other exactly. Alternately, the slackened tone of one, or both, vocal folds can result in mid-fold bowing. Not surprisingly, the list of the causes of paresis is similar to that of paralysis and includes trauma, iatrogenic injury, post-viral neuropathy, various medical conditions and ‘idiopathic’ or unknown factors.1
The natural history of paresis has yet to be established but it is believed that spontaneous return of function is possible; that recovery may be incomplete or full. The true incidence is not known but studies in tertiary care laryngology practices show that the practitioner accumulates anywhere from 12-29 cases over the course of a year. It is expected to be significantly lower in a practice offering comprehensive general otorhinolaryngology care.
As always, careful attention to the patient’s description of their symptom is integral to recognizing paresis. Commonly reported symptoms include breathiness, diplophonia, odynophonia, vocal fatigue and narrowed pitch range. The complaint may, however, be as vague as a sensation of mildly increased phonatory effort. It is common for the patient to report a specific time frame in days or weeks over which the change in voice developed. Despite the fact that sensory nerves may also be involved dysphagia is generally absent.
Physical diagnosis relies heavily on videolaryngoscopy with stroboscopy. Rigid peroral and flexible transnasal examinations may be combined to obtain sufficient information. Abnormalities in arytenoid abduction or adduction may or may not be obvious at the outset so it is helpful to record the patient’s performance of several vocal tasks in order to unmask subtle asymmetries.2 At rest and under steady illumination, you may note uneven vocal process height, one vocal fold appearing shorter or mid-fold bowing. During phonatory tasks one may see tilting of the larynx at high pitches and weakened or poorly coordinated abduction of the arytenoids.3 During stroboscopy, the mucosal wave may demonstrate a ‘chasing’ pattern of asymmetry which the mucosal wave appears to begin on one fold and then propagate to the other as a result of uneven tension on the components of the phonatory glottis.
A significant confounding factor is the fact that patients often have developed abnormal muscle tension patterns to compensate for the underlying glottal insufficiency. These patients may appear hyperfunctional upon initial exam with bulging ventricular folds and excessive tension within the larynx. Voice therapy aids in separating paresis from muscle tension dysphonia since the patients with underlying neurologic derangements do not improve with vocal retraining alone while those with functional voice disorders generally will. Once the patient had been ‘unloaded’ of the compensatory postures, the true pathology can then be seen on exam.
If the history is classic or abnormal physical findings are present, laryngeal EMG (LEMG) can then examine the integrity of the neural circuit. Although LEMG cannot make comparisons to an absolute standard of ‘normal,’, it does allow us to describe the relative activity of each muscle to its contralateral counterpart. Cricothyroid muscle activity reflects the function of the superior laryngeal nerve and the thyroarytenoid muscle reflects that of the anterior division of the recurrent laryngeal nerve (RLN); some practitioners test the posterior cricoarytenoid muscle to interrogate the posterior division of the RLN as well. The LEMG may show frank evidence of neural dysfunction such as fibrillations, polyphasic potentials and positive sharp waves or more understated findings like decreased amplitude of the motor unit action potentials (MUAPs), increased duration of waveform and decreased recruitment of MUAPs during a sustained task. This last sign is the most consistent among patients with paresis.4
Patients have been reported to respond to a number of different treatment strategies. Some have recovered after oral steroids and anti-viral agents while other mild cases have improved with voice therapy alone. Practically, we focus on relieving the glottal incompetence. This can be achieved by vocal fold medialization using injection techniques as well as structural laryngoplasty. Recently paretic larynges are more appropriate for temporary injectables since they will allow for continued observation as the paresis evolves. However, if the patient remains dysfunctional for several months or longer, the experienced practitioner may employ either long-term injectables or open thyroplasty as appropriate to the clinical circumstance.
Voice complaints can be difficult to parse and the often subtle abnormalities in vocal fold paresis can be easily missed. Even so, an index of suspicion along with thorough examination and testing can lead to the right diagnosis and better outcomes in satisfied patients.