Vocal Cord Paralysis — Cord Positions, RLN vs SLN Palsy and Management

Vocal cord paralysis means complete immobility of a vocal cord; paresis means reduced movement. The cords have two jobs: phonation and airway protection (closing the glottis during swallowing and coughing) while remaining open for breathing. Which job fails depends on where the paralysed cord comes to rest, so the position of the cord on laryngoscopy predicts the symptoms.

Examiners use cord position to test two things: which nerve is injured (recurrent versus superior laryngeal) and whether the patient will present with a poor voice or with stridor. The diagnosis is made by flexible fibreoptic laryngoscopy, in which the cord is seen to be immobile and its position is noted.

The vagus gives off the superior laryngeal nerve (SLN) and the recurrent laryngeal nerve (RLN). The SLN supplies sensation to the supraglottic larynx and motor supply to the cricothyroid (the pitch-raising muscle). The RLN supplies sensation below the cords and all other intrinsic laryngeal muscles: posterior cricoarytenoid, interarytenoid, lateral cricoarytenoid and thyroarytenoid.

The RLN loops around the subclavian artery on the right and the aortic arch on the left, then ascends in the tracheo-oesophageal groove and enters the larynx posteriorly near the cricothyroid joint. This long course is why mediastinal, thyroid and oesophageal disease and surgery injure it. A small proportion of people have a non-recurrent laryngeal nerve that reaches the larynx directly without passing through the thorax.

Distances below are measured from the midline, as described in a review of abductor paralysis. The cord moves between full abduction (deep breathing) and the midline (phonation).

Why does RLN injury leave the cord near the midline rather than in the neutral position? StatPearls explains that the RLN carries both abductor and adductor fibres, and the adductor fibres outnumber the abductor fibres by about 4:1; after injury the cord therefore tends to sit in a paramedian position. Classic teaching: RLN injury gives a paramedian cord in unilateral cases and a median cord in bilateral cases.

• Flexible fibreoptic laryngoscopy (awake, even in small children) is the diagnostic test; the cord is seen to be immobile and its position is recorded.
• Video stroboscopy and bronchoscopy give extra information when the diagnosis is uncertain.
• Direct laryngoscopy lets the surgeon palpate the arytenoids to rule out mechanical fixation (for example cricoarytenoid joint ankylosis or dislocation) as opposed to true nerve paralysis.
• Laryngeal electromyography assesses innervation of the intrinsic muscles, the duration of paralysis and the potential for recovery.
• Imaging from skull base to aortic arch looks for a lesion along the vagus or RLN.

Hoarseness is the commonest presenting complaint. Others: coughing, choking, aspiration, dyspnoea, dysphagia and globus. A laterally placed cord gives a breathy voice and a poor cough because air escapes through the gap; the inability to close the glottis also causes dysphagia, and severe cases can lead to recurrent aspiration and pneumonia.

• Iatrogenic: thyroid and parathyroid surgery are the traditional cause. Risk rises with aberrant nerve anatomy, thyroid malignancy and revision surgery. Anterior cervical spine surgery, oesophagectomy and cardiothoracic surgery also carry risk.
• Intubation: any endotracheal intubation can injure the cord by cuff pressure or mechanical trauma; arytenoid joint dislocation is the commonest mechanism, but intubation-related palsy occurs in under 1% of intubations.
• Malignancy: large series from 1985 to 1995 found cancer the commonest cause (36%), followed by idiopathic (26%) and surgical injury (25%); later series show surgery has overtaken cancer.
• Idiopathic: 29–67% of cases in published series; possibly post-viral. It is a diagnosis of exclusion.
• Central or neurological: stroke, brainstem or skull-base tumour; isolated neurological cause is under 5%.

Bilateral paralysis is dominated by the airway. With both cords fixed near the midline there is significant obstruction and inspiratory stridor, while the voice stays relatively normal and aspiration is minimal. If both cords sit laterally the glottis is wide open, but the patient has a breathy voice and a high aspiration risk. Presentation after surgery may be acute respiratory distress needing urgent airway intervention.

• Airway first: treatment is guided by the severity of airway compromise, the cause and the chance of recovery. Reversible measures are preferred if recovery is expected.
• Tracheostomy gives the most reliable airway and is reversible, but carries a long-term care burden.
• Endoscopic airway-enlarging procedures: arytenoidectomy and posterior cordotomy (incision through the vocal fold, ligament and thyroarytenoid muscle at the arytenoid) widen the glottic chink but may worsen voice and cause scarring or granulomas.
• Botulinum toxin is used to block aberrant reinnervation of adductors by inspiratory motor neurons.
• Medical treatment of causes: steroids for sarcoidosis, polychondritis or granulomatosis with polyangiitis; control of diabetes.

Management focuses on treating the cause, preventing aspiration and improving the voice. If the work-up finds neither aspiration nor sinister pathology, the standard approach is 12 months of observation plus speech therapy, since many idiopathic cases recover spontaneously. Patients who aspirate need prompt augmentation.