Nerve lesions in pharynx : an aetiology of obstructive sleep apnoea

Abstract: "Heavy snorers disease" is defined as the progression from habitual snoring to obstructive sleep apnoea (OSA). Apart from a significant weight gain, the aetiology underlying progression to a collapse of the upper airways during inspiration and sleep remains unclear. Previous studies have shown that nocturnal respiratory disturbances became worse even in some OSA patients who did not gain weight. Chronic vibration of a tissue may cause neuronal damage. Therefore, our hypothesis is that the snoring vibration, may cause a progressive pharyngeal nerve lesion. To study whether uvulopalatopharyngoplasty (UPPP) prevents progression in habitual snorers without OSA, we performed a five-year follow-up in 56 such patients. In the patients' estimation, the postoperative results were good. However, sleep recordings before and five years after surgery in 53 of them showed a slight but significant increase in respiratory disturbances, significantly correlated to weight gain. Six patients developed OSA postoperatively, one of them despite a weight loss of 10 kg. The patency of the upper airways depends on the balance between the negative intrapharyngeal pressure developed during inspiration and its counteraction by dilating muscles. The reflexogenic dilation is probably mediated by afferent nerve endings in the pharyngeal mucosa. To investigate whether there are signs of a local nerve lesion, three methods were used in patients with habitual snoring and various degrees of respiratory disturbances and in non-snoring controls: I) Biopsies of m. palatopharyngeus from 21 patients (10 with OSA) and 10 controls were investigated. The severity of the morphological abnormalities, including signs of efferent nerve lesions (e.g., type-grouping), was significantly greater in patients than in controls. The individual abnormality score correlated significantly to the amount of obstructive breatbing, but not to the oxygen desaturation index. 2) The vascular reaction in the soft palatal mucosa after afferent nerve stimulation was recorded by a laser Doppler perfusion monitoring method in 35 patients (24 with OSA) and in 13 controls Electrical stimulation activates nerve endings of C-fibre type, which release vasoactive agents- e.g., substance P (SP) and calcitonin gene-related peptide (CGRP)- resulting in vasodilation. The snorers and some mild OSA patients showed significantly more vasodilation after stimulation, than did controls, indicating sensitized nerves, e.g., due to sprouting. Patients with moderate-to-severe OSA demonstrated significantly less vasodilation than in controls, indicating degenerated nerves. 3) Biopsies of the soft palatal mucosa from 21 patients (10 with OSA) and 11 controls were immunohistochemically stained with PGP 9.5 (specific nerve-protein), SP and CGRP. All three substances showed an increase in the number of varicose nerve endings, in and below the epithelium in nine of 10 patients with rnild-to-moderate OSA and in four of 11 habitual snorers, compared to controls. This indicates a nerve lesion, e.g., nervous sprouting. CONCLUSIONS: UPPP does not completely prevent the development of OSA, especially if the patients gain weight postoperatively. The histological and physiological methods used indicate a progressive local nerve lesion. This lesion may be an aetiology to the collapse of upper airways in OSA.