5 11 12 7 3 18 22 27 22 2 14 20 14 21 24 23 15 The study’s aim was to investigate the ocular blood flow in patients with OSAS since pathological ocular blood flow has been suggested as a major mechanism in the etiology of glaucoma and also to detect the glaucoma prevalence in the study group. Patients and methods Patients were recruited from those who were referred for suspected OSAS to the “Sleep Unit” of the Neurology Clinic (Erciyes University Faculty of Medicine, Kayseri, Turkey) between December 2003 and July 2004. These were consecutively all patients referred to the Sleep Unit during the 7-month period. A total of 42 patients were evaluated during this period. Among these, 31 patients fulfilled the inclusion criteria. The remaining 11 patients were excluded from the study because they had at least one of the exclusion criteria (such as those who had previous eye surgery or laser treatment, who had any anterior or posterior segment disease or a history of ocular trauma, those with secondary glaucoma, history of chronic steroid use, history of shock, and diabetes mellitus). The study included 31 patients with OSAS and 25 healthy controls. Diagnosis of OSAS was made by the Sleep Unit of the Neurology Clinic. p A cup to disc ratio (c/d) over 0.5 or difference of c/d between two eyes >0.2 with thinning of the neuroretinal rim; a careful search was made to detect the presence of any disc hemorrhages to strongly support the diagnosis. The c/d ratio and the optic disc evaluation were derived with a +90 diopter aspherical Volk lens by two independent examiners who were masked to the condition of the patient. Any of the detected visual field defects such as localized defects, paracentral scotoma, Bjerrum scotoma, nasal step, temporal sector defect, and diffuse defect which cannot be explained by any neurologic or fundus lesion. Open iridocorneal angle. An intraocular pressure (IOP) >21 mmHg without treatment. Diagnosis of normotensive glaucoma was made with criteria similar to those stated for POAG except for the fact that IOP was <21 mmHg without treatment. No IOP elevation over 21 mmHg No evidence of glaucomatous optic nerve appearance (no disc hemorrhages) and a c/d ratio less than 0.5 Normal anterior chamber angle on slit lamp and gonioscopic examination Normal visual field test results No previous history of antiglaucomatous drug usage, ocular trauma, ocular surgery, or laser therapy Patients underwent orbital color Doppler ultrasonography (Toshiba Power Vision 6000, Osaka, Japan) at the Radiology Unit of the University. An 11-MHz linear surface probe was used and the measurements were performed between 12:00 a.m. and 13:00 p.m. The patient was supine; eyes were closed and aimed at the ceiling under the closed eyelids. Systolic blood velocity (PSV) and end-diastolic blood velocity (EDV) were calculated in the ophthalmic artery and central retinal artery; resistivity index (RI) was calculated for the central retinal artery (CRARI) and ophthalmic artery (OARI; RI=PSV-EDV/PSV). Polysomnography was performed at the Sleep Research Unit of the University; it was constituted by two EEG channels, two EOG channels, one EMG channel recording from the submental muscle, one nasal current channel, one thoracic motion channel, one abdominal motion channel, one oximeter channel, a microphone, two leg movement channels from the right and left anterior tibialis muscles, and video recordings made between 2300 and 0700 hours. The parameter used was the apnea-hypopnea index (AHI). Diagnosis of OSAS was made when the AHI was over 5. When the AHI was between 5 and 15, OSAS was regarded as “mild,” between 16 and 30 as “moderate,” and when it was over 30, it was regarded as “severe.” All the subjects in the study underwent a complete ophthalmological examination including visual acuity, slit lamp biomicroscopy, IOP measurement, gonioscopy, and fundus examination. Perimetric examination was made with the Octopus 500 EZ perimeter (Interzeag AG, Schlieren, Switzerland); stimulus size: white, III, full threshold strategy was used. Only phases 1 and phase 3 of the G1 program were used. The Octopus perimeter has a prior education (preparation) program for possibly naive patients, which was used for all patients who were naive to the examination. A factor based on the number of false-positive and false-negative replies to the stimuli, and their ratio (<13%), was used to determine reliability. Unreliable results were retested on another day. Disc analysis was made with the Heidelberg Retinal Tomograph II (Heidelberg Engineering GmbH 2001, software version 3.0, Heidelberg, Germany). Mean nerve fiber layer thickness, rim area, rim volume, and linear c/d ratio were noted. p t The study was conducted in accordance with the Declaration of Helsinki and was approved by an Institutional Ethics Committee. Results p p t p The prevalence of glaucoma was 4 of 31 OSAS patients (12.9%). In two of these four patients, both eyes were affected. One of these patients had normotensive glaucoma and one had POAG. The other two patients had normotensive glaucoma only in one eye. The other eyes had large cupping without any visual field defect. All of these four patients belonged to the severe OSAS group (AHI > 30). p p p 1 Table 1 Comparison of patients and controls with respect to intraocular pressure (IOP), ophthalmic artery resistivity index (OARI), and central retinal artery resistivity index (CRARI) Parameters n n t p IOP (mmHg) 13.37 ± 4.37 14.00 ± 4.31 −1.00 0.32 OARI 0.72 ± 0.06 0.71 ± 0.06 0.769 0.44 CRARI 0.69 ± 0.06 0.70 ± 0.05 −0.803 0.42 p r p 1 r p 2 r p 3 r p 4 Fig. 1 r p  Fig. 2 r p  Fig. 3 r p  Fig. 4 r p  Discussion 8 21 r p 27 27 27 18 24 24 17 23 9 Similar to most of the above-mentioned studies, the authors of the present study also found a high prevalence of glaucoma (12.9%) in the study group of 31 patients suggesting that OSAS in conjunction with a vessel disease is an important risk factor for glaucoma. 8 8 21 29 25 4 6 25 26 1 10 16 28 30 13 13 19 In conclusion, in our group of patients with OSAS, a high prevalence was found (12.9% = 4 glaucoma patients of 31 OSAS patients) and it is interesting to note that all four of the glaucoma patients were in the severe OSAS group. The positive correlation detected between OARI and MD, and also between CRARI and MD as well as LV, suggests that visual field defects may be due to optic nerve perfusion defects and that these field defects also increase as the RI increases. The presence and progression of glaucoma should be investigated particularly in patients with severe OSAS in the long-term follow-up, and changes in retinal nerve fiber layer thickness and ocular Doppler ultrasonographic findings should also be monitored in such patients.