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Obstructive sleep apnoea prevalence in non-arteritic anterior ischaemic optic neuropathy
  1. Hatice Arda1,
  2. Serife Birer1,
  3. Murat Aksu2,
  4. Sevda Ismailogulları2,
  5. Sarper Karakucuk1,
  6. Ertugrul Mirza1,
  7. Koray Gumus1,
  8. Ayse Oner1
  1. 1Department of Ophthalmology, Erciyes University Faculty of Medicine, Kayseri, Turkey
  2. 2Department of Neurology, Erciyes University Faculty of Medicine, Kayseri, Turkey
  1. Correspondence to H Arda, Department of Ophthalmology, Erciyes University Faculty of Medicine, Kayseri 38039, Turkey; haticearda75{at}


Aims The aim of this study was to show the prevalence of obstructive sleep apnoea (OSA) in non-arteritic anterior ischaemic optic neuropathy (NAION).

Methods 20 patients diagnosed with NAION were included in the study. 20 age and sex matched subjects with similar risk factors for NAION, such as diabetes mellitus (DM) and hypertension (HT), constituted the control group. All cases underwent polysomnography for investigation of the presence of OSA. Cases with an Apnoea–Hypopnoea Index >5 were accepted as having OSA.

Results Mean ages of the patients and controls were 60.90±8.14 and 61.15±7.23 years, respectively. There were no significant differences between the patient and control groups in terms of age, gender, body mass index, smoking/alcohol consumption or systemic diseases. In the patient group, 85% were diagnosed with OSA compared with 65% in the control group (p>0.05).

Conclusions We found a high prevalence of OSA in patients with NAION but it was also high in the control group (p>0.05). This may be due to the fact that the two groups were matched for the same risk factors for NAION. The study indicates that OSA is not a risk factor for NAION in itself but is the contributing factor as it has effects on the vascular endothelium in DM, HT and atherosclerosis.

  • Optic Nerve
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Non-arteritic anterior ischaemic optic neuropathy (NAION) is clinically characterised by acute painless monocular vision loss.1 It is the most common acute optic neuropathy, with an incidence of 2.3–10.2 per 100 000 people aged 50 years and older.2 ,3 Several risk factors have been reported, including advanced age, systemic hypertension (HT), diabetes mellitus (DM), arteriosclerosis, hypercholesterolaemia, nocturnal hypotension and a small optic cup to disc ratio.1 ,4–8 These pathological conditions favour changes in the structure or function of the microcirculation and autoregulation at the level of the optic nerve head.9 Moreover, acute vision loss associated with NAION frequently occurs on awakening, suggesting that a pathological event during sleep may trigger NAION.10

Obstructive sleep apnoea (OSA) is characterised by repeated total (apnoea) or partial (hypopnoea) obstruction of the upper airway with decreasing oxygen saturation during sleep.11 The prevalence of sleep disordered breathing is approximately 2% in women and 4% in men in those aged 30–60 years.12 Kokturk et al found that the prevalence of OSA is 0.9–1.9% in Turkey.13 Several ophthalmic disorders related to OSA were reported recently, including floppy eyelid syndrome, glaucoma, papilloedema, visual field defects, NAION, ptosis, ectropion of the lower eyelid, blepharochalasis, keratoconus, xerophthalmia and recurrent epithelial defect, and progressive endotheliopathy.14 In this prospective study we aimed to show the association between OSA and NAION.

Patients and methods

The study was conducted between December 2010 and March 2012. It was approved by the institutional review board of the university. The research protocol adhered to the tenets of the Declaration of Helsinki for clinical research. Written informed consent was obtained from all participants after explanation of the purpose and possible consequences of the study.

Twenty patients with a newly diagnosed NAION (see criteria below) were included in this study. Twenty age and sex matched subjects with similar risk factors for NAION, such as DM and HT, constituted the control group. All patients underwent a detailed ophthalmological examination, including best corrected visual acuity (VA), evaluation of relative afferent pupillary defect, colour test using pseudo-isochromatic plates, intraocular pressure measurement by the Goldmann applanation tonometer, evaluation of the anterior segment by slit lamp biomicroscopy and fundus examination from dilated pupilla by slit lamp biomicroscopy with +90 D lens, and examination of visual field by Octopus 900 perimetry. Values for erythrocyte sedimentation rate and C reactive protein for all the cases were recorded for the differential diagnosis of arteritic anterior ischaemic optic neuropathy, and patients who had increased values were excluded from the study.

Criteria for NAION diagnosis

NAION was diagnosed when the following items were present:

  1. A history of sudden painless visual loss that affect VA and/or visual field.

  2. Diffuse or sectoral optic disc oedema, sometimes with focal microhaemorrhages around the head of the optic nerve.

  3. Lack of findings on physical or ophthalmological examination, suggesting another disorder could be causing the symptoms.

Criteria for exclusion

  1. A diagnosis of arteritic anterior ischaemic optic neuropathy by clinical presentation, erythrocyte sedimentation rate and C reactive protein.

  2. Subjects who had toxic or nutritional optic neuropathy, optic neuritis or glaucoma.

  3. Subjects who had any neurological diseases which can affect sleep.

All patients underwent an overnight polysomnography (PSG)—details are given below.


All participants underwent an overnight PSG recording. The full night PSG recordings were performed using a computerised system (Grass-Telefactor, West Warwick, Rhode Island, USA) consisting of: (1) sleep monitoring through six channel electroencephalography, two channel electrooculography and one channel electromyography; (2) respiratory monitoring through a thermistor as well as a nasal pressure sensor for apnoea–hypopnoea detection, piezo crystal effort belts for thoraco-abdominal movement detection and a pulse oximeter; (3) two lead electrocardiogram; and (4) bilateral tibial electromyography and a body position detector. All recordings were scored based on 30 s epochs according to the criteria of the American Academy of Sleep Medicine.15 Sleep stages were scored as W (wake), N1 (stage 1 sleep), N2 (stage 2 sleep), N3 (slow wave sleep) and R (rapid eye movement sleep). An obstructive apnoea was defined as a drop in the peak thermal sensor excursion by ≥90% of baseline, lasting at least 10 s, accompanied by respiratory effort movement. An obstructive hypopnoea was defined as a drop in nasal pressure signal excursion by at least 30% of baseline with at least 4% desaturation from the pre-event baseline, or at least 50% of baseline with ≥3% desaturation from the pre-event baseline and/or the event is associated with an arousal. The Apnoea–Hypopnoea Index was defined as ‘total number of apnoeas and hypopnoeas×60/total sleep time (in minutes). All PSG data were scored after completion of the whole study by a sleep medicine specialist who was blinded to the status of the subjects (patients vs controls). Cases with an Apnoea-Hypopnoea Index >5 were regarded as having OSA.

Statistical analysis

In our study, ‘mean’, ‘SD’, ‘frequency’ and ‘ratio’ were used for descriptive statistics. The distribution of variables was evaluated by the Kolmogrov–Simirnov test. The Student's t test was used for analysis of parametric variables and the Mann-Whitney U test for non-parametric variables. The χ2 test was used for proportional analysis; Fisher's exact test was used where necessary. The Statistical Package for the Social Sciences (SPSS) V.20.0, on a Windows based PC, was used for the statistical analysis; p<0.05 was accepted as statistically significant.


Mean ages of the patients and controls were 60.90±8.14 and 61.15±7.23 years, respectively. There were no significant difference between the patient and control groups with regard to age, gender, waist circumference, smoking or alcohol consumption (p>0.05); neck circumference in patients was significantly different from the control group (p=0.003). Demographic data are shown in table 1.

Table 1

Demographic data for the patient and control groups

There were no significant differences between the groups with regard to systemic diseases or drug usage (p>0.05, table 2). In the patients group, 85% (17 of 20 patients) were diagnosed with OSA whereas in the control group 65% (13 of 20 controls) were diagnosed with OSA (p>0.05, table 3). Mean VA of the affected eyes in the patient group was 0.29±0.38, significantly lower than the fellow eyes of the patient group (0.69±0.41) and the control group (0.62±0.30) (p<0.05; p<0.05, respectively).

Table 2

Systemic diseases and drug usage in the patient and control groups

Table 3

Percentage of obstructive sleep apnoea cases in both groups


The pathogenesis of NAION is not fully understood; however, it is believed that NAION is caused by vascular insufficiency resulting from disturbed small vessel autoregulation of the posterior ciliary circulation that leads to optic nerve head ischaemia.16

OSA is characterised by intermittent upper airway obstruction during sleep, with concurrent hypoxia, hypercapnic acidosis and sympathetic activation in parallel with arterial HT.17

Several mechanisms previously reported on the relation between NAION and OSA include impaired optic nerve head blood flow autoregulation secondary to repeated apnoeas, optic nerve vascular dysregulation secondary to OSA induced arterial blood flow variations (episodic nocturnal HT or hypotension), arteriosclerosis, imbalance between nitric oxide (a vasodilator) and endothelin (a vasoconstrictor), and direct optic nerve damage due to prolonged hypoxia or increased intracranial pressure during apnoea.6 ,17–19

A recent study by Mojon et al17 reported a 71% prevalence of sleep apnoea syndrome in 17 patients diagnosed with NAION who were compared with 17 age and sex matched control subjects with restless leg syndrome. In this study, the controls were only age and sex matched; other risk factors such as DM, HT, atherosclerosis and smoking were not matched, in contrast with our study. Palombi et al9 found that the prevalence of OSA was five times higher in NAION than in the normal population. They also found that OSA was observed 1.5–2 times more than other risk factors, such as DM or HT. Li et al20 used the survey of Sleep Apnoea Scale of Disorders Questionnaire for the diagnosis of OSA, instead of PSG. In their study, they found that the prevalence of OSA was 30% in 73 newly diagnosed NAION patients and 17.8% in 73 age and sex matched controls.

In our study, there was no statistically significant difference between the patient and control groups regarding age, sex, body mass index (BMI), smoking, alcohol consumption, DM, HT or any other systemic diseases which can lead to OSA. The most important difference in our study was that the control group consisted of not only age and sex matched cases, but also cases matched for DM and HT. This is the first study to do this. The prevalence of OSA was found to be 85% and 65% in the patient and control groups, respectively. Although this rate is much higher than in the normal population, there were no significant differences between the patient and control groups. This may be due to the fact that the two groups were matched for the same risk factors for NAION (DM and HT), which are known to develop as a complication of OSA. The prevalence of OSA is very high in some diseases, such as DM, HT, obesity, coronary artery disease, cerebrovascular disease and cardiac insufficiency, in which endothelial dysfunction plays an important role in the physiopathology.21 The desaturation–reoxygenation episodes lead to oxidative stress chronically, with production of oxygen species, and cause vascular endothelium damage.22–25 This endothelial dysfunction can damage autoregulation of blood flow of the optic nerve head.

Obesity is defined by calculating BMI, and central obesity is evaluated by measuring waist circumference.26 Compared with age, sex and systemic disease matched controls, we did not find a significant difference in BMI or waist circumference in patients and controls, although waist circumference are slightly higher in the NAION group (103.75±12.58 vs 99.70±10.26). However, neck circumference was significantly higher in the NAION group (37.95±4.94 vs 33.85±2.92). The cut-off point that determines neck circumference as a risk factor for OSA was found to be >40 cm for men and >38 cm for women in the Turkish adult population, and an increase in neck circumference was found to be a higher risk for the development OSA compared with BMI or waist circumference.27 Martimore et al28 also found that lipid deposition in the neck region, shown by MRI, was greater in OSA patients compared with controls. The higher neck circumference in the NAION group in our study could be related to the relatively higher numbers of OSA patients in this group (17/20 vs 13/20; p>0.05).

In conclusion, due to the effects of OSA on vascular structures, OSA should be considered in NAION patients, and PSG should be performed. Although there is no satisfactory treatment for NAION, regulation of risk factors such as DM, HT and hypercholesterolaemia, and OSA is advisable. For this reason, specific investigation for the presence of OSA should be performed in every newly diagnosed NAION patient.


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  • Contributors Design and conduct of the study: HA, SB, MA and SI. Collection of the data: SB. Management: HA, MA, SI, SK and EM. Analysis: HA, MA, SI, SK, EM, KG and AO. Interpretation of the data: HA, MA, SI, SK and EM. Preparation, review and approval of the manuscript: HA, SB, MA, SI, SK, EM, KG and AO.

  • Funding This work was supported by a research grant from Erciyes University, Scientific Research Project Unit (project No: TSU-11–3717).

  • Competing interests None.

  • Ethics approval The study was approved by the institutional review board of Erciyes University.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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