Vocal cord palsy/ Vocal cord paralysis
Vocal fold palsy
All the intrinsic muscles of the larynx, except the posterior cricoarytenoid, bring together (adduct) the vocal folds. The posterior cricoarytenoid muscles abduct the vocal folds. Paralysis of the vocal folds may selectively affect the adductors and cause the vocal fold to lie in a lateral position (adductor palsy). Alternatively, the posterior cricoarytenoid may be weaker than the adductors, leaving the vocal fold in the paramedian position (abductor palsy).
The epidemiology of vocal fold palsy is variable, as it is related to the underlying cause.
Vocal fold palsies are most commonly the result of damage to the nerve supply to the intrinsic muscles of the larynx. Specifically, this may be due to damage in the brainstemor anywhere along the length of the vagus nerve or the recurrent laryngeal nerve . Rarely, myopathies of the intrinsic muscles of the larynx or arthritis affecting the synovial cricoarytenoid joints may produce 'vocal fold palsy'. When no cause is found, the palsy is describedas idiopathic in nature. It is postulated that the majority of these cases are actually due to infection by a neuropathic virus.
Scope of disease
Vocal fold palsies can lead to dysphonia, and aspirationis likely to be problematic in patients with bilateral palsies. As the cough reflex is likely to be ineffective, chronic aspiration may lead to recurrent pneumonias. Acute airways obstruction can also occur as a complication of bilateral palsies.
Causes of vocal palsy includes - peripheral lesion ( 85% ) of cases such as malignant neoplasm - lung cancer, thyroid cancer, layrnx cancer and esophageal cancer, trauma to the neck , surgery such as thyrodectomy , lung surgery or surgery to the aorta, . Central lesion ( 15 % ) - such as poliomyelitis , pseudobulbar palsy, bulbar palsy, multiple sclerosis,and infacrtion of the posterior inferior cerebellar artery ( Wallennberg syndrome )
In adductor palsy, the vocal fold lies in an abducted, or lateral, position. In these cases, the voice is often weak and breathy. The cough in adductor palsies is sometimes likened to that of a cow ('bovine' cough).
In abductor palsy, the paralyzed vocal fold lies in the paramedian position. Voice production is often not a problem but voice frequently tires easily. In bilateral cases, where both vocal folds lie adducted, breathing is surprisingly not compromised until an upper airway infection causes oedema and narrows the airway further. Stridor may then herald acute airway obstruction.
Indirect and flexible fibreoptic laryngoscopy
A thorough evaluation of the airway is critical in the management of patients with vocal fold palsy. Indirect laryngoscopy or flexible fibreoptic laryngoscopy offers a good view of the vocal folds at rest and in phonation. The paralyzed fold often appears atrophic and shorter than its normal fellow. The apparent shortening is due to the arytenoid cartilage prolapsing forwards. The paralyzed fold also appears to lie at a higher level .Upon phonation, compensation by the normal fold may be seen.
CT or MRI of the neck and upper mediastinum
A search for a cause is mandatory. This invariably involves imaging of the brainstem and the length of the recurrent laryngeal nerve by CT or MRI.
Where there is a need to exclude a possible myopathy, laryngeal electromyography is useful.
Examination under anaesthesia
Cricoarytenoid joint fixation may be excluded by direct laryngoscopy under general anaesthesia and joint palpation to assess mobility.
In cases where there are no voice problems, aspiration or breathing difficulties, conservative measures may be employed. Speech therapists often teach patients vocal fold adduction exercises to keep muscle tone from deteriorating and to facilitate compensation.
The indications for surgery include protection of the airway (tracheostomy), improvement of symptoms of upper airways obstruction (laser arytenoidectomy), management of chronic aspiration (laryngeal diversion) and improving phonation (vocal fold medialization procedures
Surgical tracheostomy (more correctly termed a tracheotomy) is the only solution to providing a safe airway in patients with acute breathing difficulties. Tracheostomy may be performed surgically or percutaneously using the Seldinger technique. Mini-tracheostomy may be performed if the main indication is bronchial toilet.
General anaesthesia is required for a surgical tracheostomy.The patient is positioned supine with a roll under the shoulders and the neck extended. The cricoid cartilage is identified, and an incision line falling in a skin crease halfway between this and the suprasternal notch is marked . The incision is made through skin, subcutaneous tissue and platysma , and the strap muscles are separated in the midline to reveal the trachea .A fenestration is made below the first tracheal ring and a cuffed tracheostomy tube is inserted as the endotracheal tube is withdrawn from the trachea.
In cases where breathing limits normal activity, a laser arytenoidectomy with partial resection of one arytenoid creates a large posterior glottic space to improve breathing. The anterior segments of both vocal folds, which are necessary for phonation, remain unaffected.
Chronic aspiration is difficult to manage. Changing the consistency of fluids ingested may minimize aspiration. In some cases, a laryngeal diversion procedure or a laryngectomy is the only solution. Tracheostomy is often a poor solution for aspiration; the presence of a tracheostomy may actually perpetuate aspiration.
Vocal fold medialization
When voice is a problem, a variety of vocal fold medialization procedures are available. The best established procedure is a 'medialization thyroplasty' in which a piece of Silastic is implanted through a window cut in the thyroid cartilage (Isshiki's type I thyroplasty). This effectively pushes a paralyzed vocal fold medially towards its normal fellow.
Advances in endolaryngeal surgery have facilitated the injection of biologically inert materials into the paralyzed vocal fold to effect medialization.
Recovery of a vocal fold palsy, where no cause or a reversible cause is found, may occur up to one year following onset. Any irreversible treatment should therefore not be performed until this period of time has elapsed.
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