Publikation

[Nocturnal measurements of intraocular pressure in patients with normal-tension glaucoma and sleep apnea syndrome]

Wissenschaftlicher Artikel/Review - 01.05.2000

Bereiche
PubMed

Zitation
Goldblum D, Mathis J, Böhnke M, Bassetti C, Hess C, Gugger M, Mojon D. [Nocturnal measurements of intraocular pressure in patients with normal-tension glaucoma and sleep apnea syndrome]. Klinische Monatsblätter für Augenheilkunde 2000; 216:246-9.
Art
Wissenschaftlicher Artikel/Review (Deutsch)
Zeitschrift
Klinische Monatsblätter für Augenheilkunde 2000; 216
Veröffentlichungsdatum
01.05.2000
ISSN (Druck)
0023-2165
Seiten
246-9
Kurzbeschreibung/Zielsetzung

BACKGROUND: About half of all normal-tension glaucoma patients and about one third of all primary open-angle glaucoma patients have sleep apnea syndrome. If sleep apnea syndrome causes some cases of glaucoma, the optic nerve damage could result from repetitive nocturnal hypoxias or from repetitive intraocular pressure elevations at the end of the apneas. In this study, we determined the intraocular pressure at the end of long apneas. PATIENTS AND METHODS: In three patients having sleep apnea syndrome and normal-tension glaucoma we recorded in a sleep laboratory during at least six hours of sleep the respiration (oxymetry, nasal and oral air flow, and inductive plethysmography). The intraocular pressure was measured with a pneumatonometer at predetermined times and compared to the values measured at the end of prolonged apneas. RESULTS: The intraocular pressure during normal respiration was in the first patient 19.5 +/- 1.0 mm Hg OD and 19.3 +/- 1.7 mm Hg OS, in the second patient 25.0 +/- 4.2 respectively 25.5 +/- 4.9 mm Hg and in the third one 22 +/- 1.0 respectively 21.3 +/- 1.3 mm Hg. At the end of prolonged apneas the intraocular pressure was in the first patient 19.0 +/- 0.0 mm Hg OD and 19.5 +/- 0.7 mm Hg OS, in the second patient 26.5 +/- 0.6 and 26.8 +/- 0.1 mm Hg and in the third one 20.0 +/- 0.0 respectively 21.0 +/- 0.0 mm Hg. The difference between intraocular pressures during normal respiration and at the end of prolonged apneas was not significant (p > 0.1 for each comparison, paired t-test). CONCLUSIONS: We did not find an increase of intraocular pressure at the end of prolonged apneas compared to periods of normal respiration in patients with sleep apnea syndrome and normal-tension glaucoma. If sleep apnea syndrome causes some cases of glaucoma, it seems more probable that the the optic nerve is damaged by the repetitive hypoxias. Alternatively, an unknown factor might induce both, sleep apnea syndrome and normal-tension glaucoma.