Vocal cord paralysis is loss of vocal cord abduction and/or adduction movement due to recurrent laryngeal nerve (RLN) damage. Unilateral paralysis is much more common, with the left side (60-70%) significantly more frequently affected than the right; this is because the left RLN follows a much longer course, looping under the aortic arch. Thyroid surgery is the most common iatrogenic cause (30-40%), idiopathic cases account for 20-30%. Mediastinal mass (lung carcinoma, lymphoma), aortic aneurysm, esophageal carcinoma, and skull base lesions are other causes. Imaging shows characteristic findings of vocal cord fixation in paramedian position, ipsilateral arytenoid anteromedial rotation, piriform sinus dilatation, and laryngeal ventricle enlargement. CT or MRI scanning along the entire RLN course from skull base to mediastinum is mandatory for cause investigation.
Age Range
20-80
Peak Age
55
Gender
Equal
Prevalence
Common
Vocal cord paralysis results from damage at any point along the recurrent laryngeal nerve (branch of the vagus nerve). The left RLN loops under the aortic arch at the level of the ligamentum arteriosum, with a total course of approximately 12 cm; the right RLN loops under the subclavian artery with only 5-6 cm course — this length difference makes the left side more susceptible to injury. Nerve damage regardless of cause leads to motor denervation: in the acute phase (0-6 months), muscle tone is preserved but active movement is lost (neuropraxia/axonotmesis); in the chronic phase (>6 months), denervated muscles undergo atrophy and fatty degeneration. On imaging, the paralytic vocal cord remaining in paramedian position reflects denervation of the posterior cricoarytenoid muscle that provides active movement of the cricoarytenoid joint. Ipsilateral piriform sinus and vallecula dilatation is due to pharyngeal phase swallowing dysfunction — bolus accumulation and stasis develop on the paralytic side. In chronic paralysis, fatty infiltration (T1 hyperintensity) and volume loss in the vocal cord muscle on T1 MRI reflects denervation atrophy.
Vocal cord fixation in paramedian position combined with ipsilateral piriform sinus and vallecula dilatation — most reliable CT finding combination for paralysis diagnosis, confirms denervation finding regardless of cause.
On axial CT, the paralyzed vocal cord is fixed in paramedian position and is asymmetric with the contralateral side. The airway at glottic level is asymmetric. The ipsilateral arytenoid is displaced anteriorly and medially (anteromedial rotation). The vocal cord effectively remains fixed at or near midline while the contralateral side shows normal abduction.
Report Sentence
The left vocal cord is fixed in paramedian position with anteromedial rotation of the left arytenoid, consistent with left vocal cord paralysis.
Ipsilateral piriform sinus widening is one of the most reliable findings of vocal cord paralysis. The piriform sinus on the paralytic side is significantly wider than the contralateral side and filled with fluid/secretion accumulation. The ipsilateral vallecula may also be dilated. This finding reflects pharyngeal phase swallowing dysfunction.
Report Sentence
The left piriform sinus is significantly dilated compared to the contralateral side with secretion accumulation, a finding consistent with left vocal cord paralysis.
In chronic vocal cord paralysis (>6 months), fatty degeneration develops in the denervated vocal cord muscle (thyroarytenoid muscle) on T1-weighted MRI. Normal muscle signal is replaced by T1 hyperintense fat signal, accompanied by volume loss (atrophy). This finding indicates chronicity of denervation and suggests low likelihood of spontaneous recovery.
Report Sentence
T1 hyperintense fatty degeneration and volume loss in the left vocal cord muscle (thyroarytenoid muscle) is seen, consistent with chronic denervation atrophy.
Contrast-enhanced CT scanning along the entire RLN course from skull base to mediastinum is performed to investigate the cause of vocal cord paralysis. Left side: jugular foramen → carotid sheath → aortopulmonary window → below aortic arch → return to tracheoesophageal groove. Right side: jugular foramen → carotid sheath → below subclavian artery → tracheoesophageal groove. Thyroid pathology, mediastinal mass, lung apex mass, aortic aneurysm, esophageal mass, and skull base lesions are investigated.
Report Sentence
The RLN course from skull base to mediastinum was evaluated for left vocal cord paralysis, and conglomerate lymphadenopathy was identified in the aortopulmonary window.
Laryngeal ultrasonography allows real-time assessment of vocal cord movement. Absence of abduction movement during inspiration and phonation is observed in the paralyzed cord. US is a non-invasive, radiation-free method and serves as an alternative screening method to laryngoscopy. Additionally, associated thyroid pathology and cervical lymphadenopathy can be assessed during the same examination.
Report Sentence
On laryngeal US, no movement is seen in the left vocal cord during inspiration and phonation, consistent with left vocal cord paralysis.
Criteria
Left vocal cord paralysis (60-70% of cases)
Distinct Features
Left RLN long course (under aortic arch), susceptible to mediastinal pathologies, aortopulmonary window LAP and lung apex tumor common causes
Criteria
Both vocal cord paralysis (rare)
Distinct Features
Emergency airway obstruction risk, most common after thyroid surgery, stridor and respiratory distress, tracheotomy may be required
Criteria
Cases with no identifiable cause on imaging (20-30%)
Distinct Features
Possibility of spontaneous recovery in 6-12 months, viral neuritis probable mechanism, follow-up required
Distinguishing Feature
SCC enhancing mass present; paralysis no mass, atrophy and piriform sinus dilatation dominant
Distinguishing Feature
Laryngocele cystic/air-filled structure; paralysis ventricle enlargement from dilatation (not cystic mass)
Distinguishing Feature
Chondrosarcoma expansile calcified mass; paralysis no mass, normal cartilage, functional disorder
Urgency
urgentManagement
conservativeBiopsy
Not NeededFollow-up
specialist-referralPriority in vocal cord paralysis is cause investigation — skull base-neck-mediastinum CT/MRI is mandatory. Spontaneous recovery is expected in 6-12 months for idiopathic cases. For permanent unilateral paralysis, medialization thyroplasty or vocal cord injection improves voice quality. Bilateral paralysis may require emergency airway management (tracheotomy).
The most important step in vocal cord paralysis is cause investigation. CT or MRI should scan for all pathologies along the RLN course from skull base to mediastinum. In idiopathic cases (20-30%), spontaneous recovery may be expected within 6-12 months. For permanent paralysis, medialization thyroplasty or vocal cord injection improves voice quality. Bilateral paralysis may require emergency airway management.