Snorers and Apnea Patients Show Upper Airway Sensory Impairment

August 6, 2001

Canadian investigators found that snorers and individuals with obstructive sleep apnea demonstrated upper airway sensory impairment, revealing a problem that could predispose them to upper airway obstruction during sleep.

Writing in the second of two July issues of the American Thoracic Society's peer-reviewed American Journal of Respiratory and Critical Care Medicine, R. John Kimoff, M.D., along with four associates, measured individual two-point probe discrimination and vibratory thresholds in the lip, hand, and margin of the soft palate in 37 patients with obstructive sleep apnea (OSA), 12 non-apneic snorers, and 15 control subjects. The researchers were from the Respiratory Division and Department of Neurology, McGill University Health Center, Montreal, Quebec, Canada.

The premise of this research was based on the concept that upper airway mechanical sensory detection is impaired in OSA. Interfering with sensory function in the mucous membrane increases the tendency of airway collapse, causing obstructive episodes such as apneas. The selective impairment appears to be partly reversible after treatment of these patients with nasal continuous positive airway pressure.

Apnea occurs when a person repeatedly stops breathing during sleep long enough to decrease oxygen in the blood and increase carbon dioxide. This stoppage of respiration is caused by the collapse of the upper airway during sleep. After a brief arousal, the patient starts to breathe again, but usually suffers 10 or more of these apneic events per hour of sleep.

Physicians treat OSA patients with continuous positive airway pressure (CPAP). This therapeutic approach involves a mask worn during sleep that delivers pressurized air through the nose. CPAP partially reversed the sensory impairment of the OSA patients.

The sensory values for the two-point probe and the vibratory sensation test on the lips and hands of each individual were essentially the same for the OSA patients, the snorers, and the control patients. However, the levels for the soft palate test detected significantly reduced sensory ability in the upper airways of the OSA patients and snorers.

"We conclude that these findings demonstrate the presence of selective impairment in the upper airway mucosal sensory function in patients who have OSA or who are snorers," said Dr. Kimoff. "We also find evidence of partial reversibility of the sensory changes after CPAP treatment in patients with OSA, although a significant impairment persisted."

Overall, the researchers believe that nerve or sensory receptor damage to the upper airway are related to mucosal edema (fluid) present in OSA patients. Although the factors responsible are unknown, they presumably relate to repeated trauma to the upper airway tissues from snoring-associated vibrations and from forceful suction collapse of the airway during apneas. Accumulation of fluids due to mechanical effects, vascular changes, or release of inflammatory mediators could potentially interfere with function of nerve endings in the mucous membrane.

The investigators say that further studies are needed to more clearly establish the mechanisms of impairment and to evaluate its contribution to the pathophysiology of OSA.

Editorial by Expert Claims Motor Neuron Lesions Could Cause Airway Collapse

In an editorial in the same issue of the American Journal of Respiratory and Critical Care Medicine, Eva Svanborg, M.D., Ph.D., postulates that the sensory dysfunction found in the airways of the obstructive sleep apnea (OSA) patients who were studied by the Canadian researchers could be caused by motor neuron lesions. Such lesions could produce partial paralysis of the dilating muscles of the upper airway, according to Dr. Svanborg of the Department of Neuroscience and Locomotion, Division of Clinical Neurophysiology, University of Linköping, Linköping, Sweden.

She notes, for example, that long-term employment of workers who use vibrating tools can cause local nerve lesions in the hands. Why then could not vibrations from heavy snoring night after night cause neuronal lesions in the upper airway? These lesions could, in turn, produce a gradual collapse of the airway due to muscular weakness and/or impaired reflex mechanisms.

When an individual breathes in, the patency-- or openness of the upper airway-- is maintained by dilating muscles. These are activated by a reflex mechanism resulting from negative intra-pharyngeal pressure in the airway. In discussing another pertinent demonstration of sensory dysfunction, she points out that patients with OSA have exhibited a marked reduction in reactivity to electrical stimulation which normally would cause dilation of the airway.

In addition, Dr. Svanborg points out that in an electron microscopy study; researchers found degenerative changes in neurons from the soft palate and uvula of OAS patients. Also, other investigators claim muscle pathology increases in parallel with the proportion of obstructive breathing during sleep.

She believes these studies and others support the hypothesis that upper airway lesions are present in some snorers and in most patients with OSA.

She notes that Dr. Kimoff and his coworkers have shown that the patient's neuronal dysfunction can be ameliorated by treatment with continuous positive airway pressure. She would like to see these studies replicated in persons with mild sleep apnea and habitual snorers who normally do not get this treatment. Since these types of cases usually develop full-blown OSA later, the further positive results might serve as an argument for early preventive therapy.