Other / Other / MRI

Vocal fold paralysis

Vocal fold paralysis (VCP) presents clinically with dysphonia (hoarseness), dysphagia, or dyspnea depending on unilateral vs bilateral involvement, and can be diagnosed incidentally on laryngoscopy or imaging. Imaging is essential to identify the underlying etiology along the recurrent laryngeal nerve course from brainstem to superior mediastinum.
Look For First
  • Abducted/paramedian position of the paralyzed vocal fold at rest with failure to adduct during phonation on US or CT
  • Asymmetric vocal fold atrophy, particularly of the thyroarytenoid muscle bulk on the affected side
  • Unilateral absence of vocal fold and arytenoid cartilage motion on dynamic ultrasound during breathing and phonation
  • Enlarged pyriform sinus and medialized aryepiglottic fold on the paralyzed side
Key Image Findings
  • On ultrasound: unilateral absence of true and false vocal fold motion during quiet inspiration, apneic pause, and phonation with preserved motion of contralateral structures; the true vocal folds appear hyperechoic and more superficial relative to false folds and arytenoid cartilages
  • On CT/MRI: atrophy of the thyroarytenoid muscle (which comprises the bulk of the true vocal cord) on the paralyzed side with anteromedial deviation of the arytenoid cartilage
  • On CT/MRI: enlarged ipsilateral pyriform sinus and medialized/thickened aryepiglottic fold due to lack of muscular tone
  • On CT/MRI: enlarged laryngeal ventricle (sail sign) on the affected side
  • On CT/MRI: atrophy of the posterior cricoarytenoid muscle, one of the key intrinsic laryngeal muscles affected by recurrent laryngeal nerve injury
  • During breath-hold CT imaging: abducted positioning of the paralyzed vocal fold with compensatory hyperadduction of the contralateral vocal cord
  • Ultrasound allows real-time dynamic assessment during inspiration, apnea, and phonation with patient in supine position and neck slightly extended; transducer positioned transversely over thyroid cartilage
  • Findings correlate well with flexible endoscopy, making ultrasound a practical bedside imaging modality for diagnosis confirmation
Differential Diagnosis
  • Vocal fold paresis or partial paralysis showing reduced but present motion on dynamic imaging, distinguished from complete paralysis by residual movement during phonation on ultrasound
  • Laryngospasm or vocal fold immobility from psychological causes, which typically normalizes with different phonatory tasks or during sleep
  • Cricoarytenoid joint fixation from ankylosis or arthritis, showing mechanical constraint without neurologic denervation atrophy patterns
  • Unilateral vocal fold scar contracture from prior trauma or surgery, appearing as focal thickening without the diffuse muscle atrophy pattern of paralysis
Discussion

Recurrent laryngeal nerve injury is the most common cause of vocal fold paralysis due to its long course through the neck and mediastinum, with the left side more frequently affected due to the longer path of the left recurrent laryngeal nerve

Superior laryngeal nerve injury causes subtle voice changes affecting only the cricothyroid muscle and is less clinically significant than recurrent laryngeal nerve injury

Unilateral involvement is much more common than bilateral; bilateral paralysis with folds near midline causes dyspnea by severely limiting the glottic airway, while unilateral causes breathy dysphonia and aspiration risk

Common etiologies include lung cancer (most frequent), thyroid/laryngeal cancer, thoracic aortic aneurysm, thyroid surgery, and idiopathic causes; traumatic injury can occur from blunt/penetrating trauma

Congenital causes include meningomyelocele, Chiari malformation, and hydrocephalus; neurologic diseases like adult-onset Alexander disease and multiple system atrophy also cause VCP

Up to one-third of patients with vocal cord impairment are asymptomatic, highlighting the importance of imaging recognition and investigation when VCP is suspected

Reporting Pearls

Describe the specific location and laterality of the paralyzed fold (e.g., 'left vocal fold fixed in paramedian abduction'), note the absence of motion during dynamic imaging maneuvers (inspiration/phonation), identify associated structural changes (thyroarytenoid atrophy, arytenoid deviation), and conclude with a recommendation to evaluate the entire recurrent laryngeal nerve course from brainstem through superior mediastinum for an underlying etiology.

Pitfalls
  • Mistaking passive motion of a paralyzed fold due to contralateral hyperadduction or cricothyroid movement for true vocal fold adduction; dynamic ultrasound assessment is critical to confirm unilateral absence of intrinsic fold motion
  • Failing to investigate the full course of the recurrent laryngeal nerve from brainstem to mediastinum; lung cancer is the most common etiology and may not be appreciated if only laryngeal imaging is performed
  • Assuming idiopathic paralysis without thorough imaging workup; always exclude malignancy, vascular pathology, and surgical complications along the nerve course
  • Overlooking compensatory hyperadduction of the contralateral vocal fold, which may initially suggest bilateral involvement or obscure the true findings on limited imaging