Vocal cord paralysis (VCP) occurs when nerve impulses controlling the muscles in the voice box (larynx) are disrupted. This interruption leads to the inability of one or both vocal folds to move properly. The vocal folds produce voice, protect the airway during swallowing, and regulate breathing. When movement is impaired, patients often experience significant changes in voice quality and may face difficulties with breathing and eating.
The Mechanism of Vocal Cord Paralysis
Vocal fold movement is primarily governed by the vagus nerve (the tenth cranial nerve) and its branch, the recurrent laryngeal nerve (RLN). The RLN travels a long, circuitous path from the brainstem down into the chest before looping back up to innervate most laryngeal muscles. Damage to this nerve anywhere along its route prevents the corresponding vocal fold from opening and closing correctly.
The resulting paralysis manifests depending on the position the vocal fold settles into. When a single fold is paralyzed, it typically remains in a fixed, slightly open position, causing air to leak during speech. This results in a hoarse, breathy voice and forces the patient to take frequent breaths. The inability of the paralyzed fold to close tightly also compromises the airway’s protective function, leading to difficulty swallowing and a risk of aspiration.
Primary Causes of Vocal Cord Paralysis
The causes of VCP involve damage to the vagus or recurrent laryngeal nerves. A common cause is iatrogenic injury, which is nerve damage sustained during surgical procedures in the neck or chest. Operations involving the thyroid, parathyroid glands, esophagus, or major chest blood vessels risk inadvertently stretching or severing the RLN.
Tumors are another cause, as a mass can physically compress the nerve. Malignancies originating in the lungs, thyroid, or skull base may exert pressure on the vagus nerve or RLN, blocking nerve signals. Because the left RLN travels deeper into the chest, it is more commonly affected by masses in the mediastinum, such as those caused by lung cancer.
Viral infections can also trigger VCP by causing inflammation that damages nerve fibers, known as post-viral neuropathy. Viruses such as herpes, Epstein-Barr, and COVID-19 have been implicated, often following an upper respiratory illness. In these cases, the nerve damage is often temporary, leading to potential spontaneous recovery over several months.
Systemic neurological disorders are also a factor, as conditions affecting the central nervous system can impair vocal fold muscles. Stroke, Parkinson’s disease, and multiple sclerosis can disrupt the brain signals controlling laryngeal function. Despite thorough investigation, many VCP cases remain classified as idiopathic, meaning no specific underlying cause can be identified.
Diagnostic Procedures
Evaluation for VCP begins with a detailed medical history and a comprehensive voice assessment to gauge symptom severity and pinpoint the onset of voice changes. Physicians specializing in ear, nose, and throat conditions look for associated symptoms, such as recent surgeries, neck trauma, or viral illnesses. This initial assessment determines the patient’s functional limitations, especially regarding breathing and swallowing safety.
Vocal fold immobility is confirmed using laryngoscopy, which involves inserting a thin, flexible tube with a camera through the nose to visualize the larynx. During the examination, the physician observes the vocal folds in real-time while the patient breathes and speaks. Specialized techniques, such as videostroboscopy, use synchronized light flashes to capture the mucosal wave and vibration, distinguishing paralysis from other causes of restricted movement.
Once paralysis is confirmed, imaging studies locate the cause of nerve damage along its length. A computed tomography (CT) scan or magnetic resonance imaging (MRI) scan is ordered to examine the nerve pathway from the skull base, through the neck, and into the chest. These high-resolution images detect masses, tumors, or structural abnormalities that might be compressing the vagus or recurrent laryngeal nerves.
To assess the long-term prognosis and extent of nerve damage, laryngeal electromyography (EMG) may be performed. This test involves inserting small needles into the laryngeal muscles to measure the electrical activity generated by nerve signals. The EMG provides quantifiable data on nerve function and helps predict the likelihood of spontaneous nerve recovery, aiding in therapeutic timing.
Management Options Following Diagnosis
Management of VCP begins with watchful waiting, especially if the cause is unknown or viral, as nerve function may spontaneously return. During this period (six months to a year), the physician monitors vocal fold mobility and symptom progression. Immediate intervention is reserved for patients experiencing severe breathing difficulties or aspiration risk.
Voice therapy, conducted by a speech-language pathologist, is a common initial step to strengthen remaining laryngeal muscles and improve breath support. These specialized exercises teach the patient to use the unaffected vocal fold more efficiently to compensate for the paralyzed one, improving voice quality and reducing vocal effort. Voice therapy serves as a conservative measure while nerve regeneration is assessed.
If paralysis is permanent, surgical intervention may be recommended. One option is a bulk injection, where a filler material like collagen or fat is injected into the paralyzed vocal fold to increase its size. This bulk moves the paralyzed fold closer to the midline, allowing the functioning fold to make better contact and improve voice closure.
Laryngeal framework surgery, such as medialization laryngoplasty, is another option. This procedure involves placing a small implant into the voice box structure to permanently push the paralyzed vocal fold toward the center. Both surgical approaches aim to close the gap between the folds, stabilizing the voice and reducing the risk of aspiration.