Guilleminault and colleagues presented data that proved the latter assertion in a 1993 publication. They prospectively evaluated all of the patients referred for EDS to their sleep disorders clinic over a 6-month period, and they found 15 patients who met the strict criteria for UARS based on brief arousals, esophageal manometry, and pneumota-chography. Two of the 15 qualifying patients never snored, and 3 of the 15 had only light, intermittent snoring. The researchers concluded that snoring was neither sufficient nor necessary for the diagnosis of UARS. It is interesting that in all 15 patients, cephalometry showed a narrow posterior pharynx at the base of the tongue.
In 1994, Braver and Block showed that positional therapy and nasal decongestants had no effect on snoring, but they did find a significant decrease in the AHI of asymptomatic snorers. Woodson published a case report of a patient who developed UARS 3 years after uvulopalatopharyngoplasty (UPPP) for OSAS. The author substantiated the diagnosis of UARS with esophageal manometry, showing 89 arousals/h associated with increased negative Pes nadirs. Although anecdotal, this report supports the contiguity of UARS and OSAS on a continuum of severity because it is likely that UPPP only partially ameliorated the patient’s upper airway pathology. online antibiotics
Despite these data, the notion that snoring occupies the mildest end of the pathophysiologic spectrum of sleep-disordered breathing has persisted in the literature. In 1998, for example, Friberg et al studied the histologic specimens of palatopharyngeal muscles from 10 asymptomatic nonsnorers, from 10 OSAS patients who snored, and from 11 snorers who did not meet the criteria for OSAS. All 21 of the snorers had various degrees of EDS. The biopsies showed findings that were consistent with a primary neurogenic lesion (including muscle fiber hypertrophy, atrophy, and type grouping), the severity of which varied with the percent of periodic obstructive breathing. The researchers postulated that a progressive, local neurogenic lesion resulting from the trauma of snoring was the cause of these findings. However, they failed to define the extent of the upper airway pathophysiology present in the snoring patients who did not have OSAS. Because EDS was present in this entire group, it is possible that a substantial proportion of these patients had UARS rather than simple snoring; therefore, the speculation that snoring, per se, produces neurogenic lesions is poorly substantiated.