Axonal Degeneration in Soft Palate Nerves May Contribute to Obstructive Sleep Apnea
Obstructive sleep apnea (OSA), the intermittent cessation of breathing during sleep, occurs when the upper airway tissues (e.g., tonsils, fatty tissue) repeatedly collapse into the upper airway and partially or fully block airflow. The collapsibility of the upper airway in people with OSA is believed to occur because the upper airway muscles relax excessively during sleep, which allows structures supported by the muscles to collapse into the upper airway. Some research indicates that altered neuronal activation may contribute to the reduced tone of the upper airway muscles. Much of this research has focused on innervation of dilator muscles such as the genioglossus muscle (which forms the bulk of the tongue). However, another structure that contributes to obstruction is the soft palate. In recent years, scientists have begun examining whether neuronal injury in the soft palate muscles could contribute to OSA.
People with OSA often have an elongated uvula, a structure that extends like a pendulum from the soft palate just above the tongue at the back of the throat. The soft palate muscles consist of the uvular muscle (which raises the uvula), the levator veli palatini muscle (which raises the soft palate) and the tensor veli palatini muscle (which aids in raising the soft palate). Whether the elongated uvula results from muscle injury due to stretching of the uvular muscle during OSA episodes or results from abnormal neuronal activation is unclear
During the obstructive phase of an OSA episode, the impeded airflow decreases the amount of oxygen in the blood. As a consequence, a person makes increasingly strong efforts to breathe. When the oxygen level falls to a certain point, the respiratory center in the brain triggers a brief arousal, during which the upper airway muscle tone is restored and a person is able to take some deep, quick breaths to restore the blood oxygen level. During this brief arousal, snoring may occur because the rapid airflow through the upper airway causes soft tissues to flutter, much like the flutter that occurs when air escapes rapidly from a small opening in a balloon. In studies of animal models of OSA and human snorers, the upper airway tissues show signs of damage such as inflammation (e.g., swelling, redness, increased levels of inflammatory substances such as tumor necrosis factor, and increased levels of inflammatory cells). These changes are believed to result from vibration of the upper airway tissues. Whether the vibration occurring with OSA episodes could also damage the axons of nerves that supply the upper airway muscles has been of recent focus.
You can read the whole article in the Q4 issue of A2Zzz.