Laryngeal paralysis (laryngeal paresis) - Causes and pathogenesis

Causes of laryngeal paralysis (laryngeal paresis)

Laryngeal paralysis is a polyetiological disease. It can be caused by compression of the structures that innervate it or by the involvement of nerves in the pathological process developing in these organs, their traumatic damage, including during surgical interventions on the neck, chest or skull.

Depending on the topography of the lesion in relation to the nucleus ambiguus, paralysis of central genesis is conventionally divided into supranuclear (cortical and corticobulbar) and bulbar. Cortical palsy is always bilateral in accordance with the innervation from the motor nucleus; possible causes are contusion, congenital cerebral palsy, encephalitis, bilirubin encephalopathy, diffuse atherosclerosis of the cerebral vessels. Corticobulbar palsy may occur as a result of damage to the area of the crossing of the corticobulbar tract, for example, with insufficiency of blood circulation in the basin of the vertebral artery, occlusion of the latter. Bulbar palsy may be a consequence of impaired blood circulation in the basins of the vertebral, posterior and anterior inferior cerebellar, upper, middle, lower lateral branches of the cerebellar arteries; as well as polysclerosis, syringobulbia, syphilis, rabies, encephalitis, poliomyelitis, intracerebellar tumors. Partial damage to the nucleus is sufficient for the development of symptoms of laryngeal paralysis. Central laryngeal paralysis accounts for approximately 10% of cases. The main causes of peripheral laryngeal paralysis:

• medical trauma during surgery on the neck and chest;
• compression of the nerve trunk along its length due to a tumor or metastatic process in the neck and chest area, diverticulum of the trachea or esophagus, hematoma or infiltrate during trauma and inflammatory processes, with an increase in the size of the heart and aortic arch (tetralogy of Fallot), mitral valve disease, aortic aneurysm, ventricular hypertrophy, dilation of the pulmonary artery);
• neuritis of inflammatory, toxic or metabolic origin (viral, toxic (poisoning with barbiturates, organophosphates and alkaloids), hypocalcemic, hypokalemic, diabetic, thyrotoxic).

The most common cause of paralysis is thyroid pathology and medical trauma during thyroid surgery. The complication rate during primary intervention is 3%, during repeated intervention - 9%; during surgical treatment of thyroid cancer - 5.7%. In 2.1% of patients, paralysis is diagnosed at the preoperative stage.

Pathogenesis of laryngeal paralysis (laryngeal paresis)

In laryngeal paralysis, all three functions of the larynx suffer. The severity of clinical symptoms and morphofunctional changes in the larynx depend on the degree of denervation and the nature of compensatory-adaptive changes, the position of the paralyzed vocal fold, the development of atrophic processes in the muscular apparatus of the larynx, and the state of the crico-cranial joint. The severity of the disease in unilateral paralysis is due to the failure of the glottis to close, and in bilateral paralysis, on the contrary, to the median position of the vocal folds, leading to stenosis of the larynx.

The timing of the onset of laryngeal muscle atrophy is not precisely defined, is individual and depends on the degree of denervation and the distance of the vocal fold from the midline. Vocal fold atrophy worsens the course of unilateral laryngeal paralysis, as it leads to its additional lateralization and decreased tone. The arytenoid cartilages on the side of paralysis are often displaced toward the healthy side, rotated forward. The results of electromyographic studies prove that complete denervation of the vocal fold with muscle atrophy in laryngeal paralysis develops infrequently; in most cases, some level of synkinesis and reinnervation is diagnosed. With long-term paralysis, ankylosis of the arytenoid joint occurs, detected by probing.

The airways are protected from aspiration during swallowing by several reflex mechanisms, including the upward movement of the larynx and its forward tilt, adduction of the vocal folds, and coordination of breathing and swallowing. Such protection is impaired in laryngeal paralysis, especially in the early stages of its development, and normally the elevation of the larynx during swallowing is accompanied by closure of the glottis. In patients with laryngeal paralysis, this does not occur; the intact vocal fold occupies a more elevated position. Compensation for lost functions in unilateral laryngeal paralysis is achieved by changing the tension of the adductors, forcing the voice to increase the subglottic pressure, and changing the configuration of the supraglottic space. Clinically, this is expressed in the displacement of the glottis during phonation towards the paralysis due to the movement of the healthy vocal fold to the opposite side, and hypertrophy of the vestibular folds. In bilateral laryngeal paralysis with an intermedian position of the vocal folds, over time they often shift toward the midline with the development of laryngeal stenosis.

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