Non-arteritic anterior ischemic optic neuropathy

Last updated
Non-arteritic anterior ischemic optic neuropathy
Other namesNAION
Specialty Ophthalmology
Symptoms Optic disc swelling, optic atrophy, vision loss

Non-arteritic anterior ischemic optic neuropathy (NAION) is a medical condition characterized by loss of vision caused by damage to the optic nerve as a result of ischemia, or insufficient blood supply. The key symptom of NAION is optic disc swelling, which typically resolves within 2 months, but often leads to optic atrophy. The likelihood of vision improvement after developing this condition is low.

Contents

NAION is characterized by localized disruptions in blood flow to the optic nerve, often linked with broader systemic vascular conditions. Key risk factors include coronary artery disease, cerebrovascular disease, sleep apnea, diabetes, and hypertension. Currently, there is no universally accepted, scientifically proven treatment for NAION. However, there is a general consensus on the importance of managing underlying risk factors to prevent further complications. This includes controlling blood pressure, managing diabetes, and treating sleep apnea. [1] [2]

Etymology

The name non-arteritic anterior ischemic optic neuropathy is derived from several medical terms that describe the condition: [3]

Causes

The underlying causes of NAION are largely unknown. Multiple theories suggest different mechanisms for the reduction in blood flow that triggers this condition, but there is no consensus on the precise cause of optic nerve damage.

"Disc-at-risk"

The term "disc-at-risk" refers to an optic nerve head characterized by a small cup-to-disc ratio and a crowding of optic nerve fibers. This anatomical feature is a significant factor in the development of NAION. [4] [5] Individuals predisposed to this condition typically have smaller optic discs with minimal or no cupping. This anatomical configuration leads to a congestion of nerve fibers, which can contribute to the onset of NAION. This mechanism is somewhat similar to compartment syndrome, where increased pressure within a confined space impairs blood flow and tissue function. [6]

Optic nerve blood supply

The optic nerve head, or prelaminar disc, primarily receives blood from the peripapillary choroidal arterioles, which stem from the elliptical anastomotic annulus connected to the circle of Zinn-Haller. The circle of Zinn-Haller is formed by branches of the lateral and posterior ciliary arteries. [7] [8] Beyond this region, different segments of the optic nerve are supplied by various networks of arteries and capillaries originating from the ophthalmic artery and the central retinal artery. The Zinn-Haller circle also provides blood to the thin, sieve-like section of the eye's outer layer and the optic nerve fibers within it through small, inward-facing arteries. The area just behind this layer in the optic nerve is vascularized by small returning arteries and minute blood vessels that arise from the eye's surrounding circulation and the main ophthalmic artery, interweaving through the nerve's supporting fibers.

The parts of the optic nerve located within the eye socket and the canal it traverses receive blood from small arteries branching off the primary network surrounding the eye, as well as from the central retinal artery. Fluorescein angiographic studies [9] [10] have demonstrated that during the acute phase of NAION, there is a delay in blood flow to the optic disc, suggesting a potential impairment in the arteries directly supplying it. Other research indicates that a drop in blood pressure within specific critical areas of the optic disc's blood supply network may increase its susceptibility to damage. [11]

There are debates over other potential causes such as nighttime drops in blood pressure, as well as the hypothesis that the optic disc's ability to regulate its blood flow may be compromised. [12] Some researchers have even suggested that blockages in the veins could be responsible. [13]

One hypothesis suggests that the underlying cause may be a subtle decrease in blood flow to the optic nerve, which is enough to cause swelling of the nerve fibers but not severe enough to disrupt vision through tissue death and permanent damage to the optic nerve. When considering the possible causes for spontaneous NAION, the list includes other conditions like arteritic anterior ischemic optic neuropathy (associated with inflammation of arteries), optic neuritis (inflammation of the optic nerve), infiltrative and compressive types of optic neuropathy (where the optic nerve is invaded or pressed upon by abnormal substances or structures), diabetic papillopathy (swelling of the optic disc in diabetes), radiation-induced damage to the optic nerve, neuroretinitis (inflammation of the optic nerve and retina), and swelling of the optic disc linked with retinal diseases like central retinal vein occlusion. [14]

Predisposing conditions

While most cases of NAION have no known cause, it has been frequently linked to certain conditions. These include general surgical procedures, cataract surgery, hemorrhagic shock, certain medications, and optic disc drusen. The exact mechanism of optic nerve ischemia in these cases remains unclear, but contributing factors may include hypotension, anemia, hypoxia, and changes in the autoregulation of optic nerve arterial blood flow. The incidence of ischemic optic neuropathy leading to vision loss following general surgeries ranges between 0.1% and 0.002%. [15] [16]

Drug reactions

Certain medications, such as amiodarone [17] and phosphodiesterase type 5 (PDE5) inhibitors like sildenafil, [18] [19] have been associated with optic neuropathy symptoms, including optic disc swelling and hemorrhages. The relationship between these medications and vision loss remains disputed due to anecdotal evidence, the lack of clear dose-response relationship, and co-existing risk factors. Clinical studies suggest a temporal increase in AION risk following PDE5 inhibitor use, leading to recommendations against their use in affected individuals to preserve remaining vision.

Drusen

NAION in patients with optic disc drusen has unique characteristics: earlier onset, history of transient visual disturbances, and generally better visual outcomes. Mechanical pressure from drusen on blood vessels near the optic nerve may contribute to NAION development in these individuals. [20] [21]

Sleep apnea

Sleep apnea is a condition characterized by repeated interruptions in breathing during sleep, significantly affecting the flow of blood through the brain's blood vessels. These interruptions cause intermittent hypoxia, leading to vascular changes such as the constriction of cerebral blood vessels, thereby impacting overall brain blood flow. Sleep apnea can also result in reduced blood flow in the ciliary artery area, contributing to the development of NAION through various mechanisms.

The results of a retrospective study investigating high altitude (7,000-9,000 feet) as a potential risk factor for NAION suggested that high-altitude-associated NAION might be linked to undiagnosed obstructive sleep apnea. The study concluded that NAION could occur under high-altitude conditions, often in younger individuals with obstructive sleep apnea and "disc-at-risk". [22]

Each apnea episode typically causes temporary increases in blood pressure and heart rate, leading to fluctuations that can result in irregular blood flow to the brain. This may cause long-term changes in the structure and function of cerebral blood vessels. The brain's mechanism for maintaining constant blood flow despite changes in systemic blood pressure, known as cerebral autoregulation, can be impaired by sleep apnea. This impairment results in periods of both reduced and excessive cerebral blood flow. [23] [24]

Repeated airway obstruction during sleep leads to intermittent hypoxia, causing oxidative stress and damaging endothelial cells of blood vessels, including those supplying the optic nerve head. Chronic intermittent hypoxia impairs endothelial function, reducing nitric oxide production, which leads to vasoconstriction and reduced blood flow to the optic nerve head. Additionally, fluctuations in pressure within the thoracic cavity during apnea episodes can alter intraocular pressure, affecting the blood supply to the optic nerve head . Sleep apnea often causes dips in blood pressure during sleep, particularly in the early morning hours, reducing blood supply to the optic nerve head and increasing the risk of ischemia. [25] [26]

Epidemiology

NAION is the most frequently diagnosed sudden optic nerve disease in adults over 50, predominantly affecting Caucasians, [27] with variable rates reported in Asian populations, [28] [29] and affecting males more than females. [30] Presentation can vary, but patients typically report painless visual loss upon waking up in the morning or after a nap. [31] While the exact number of cases is unclear, estimates suggest thousands of new cases occur annually in the United States alone. [32] [33] Associations with other health issues like diabetes and sleep apnea have been observed, though links with arteriosclerosis and cerebrovascular diseases are not typically found with NAION. [34] [35] [36] [37] [38] [39] [40]

Signs and symptoms

NAION usually presents suddenly as painless vision loss in one eye, often noticed upon waking up. The visual field defects can vary, and while some patients may experience immediate maximal vision loss, others may notice a gradual worsening. The optic disc in these cases can appear swollen, sometimes accompanied by hemorrhages. [41] In some cases, there might be a phase where the disc appears swollen without immediate vision loss, potentially indicating a precursor to more severe damage. [42]

NAION may present with color vision deficiency and a relative afferent pupillary defect. In NAION, the severity of color vision deficiency correlates with the level of loss of visual acuity. [43]

Optical coherence tomography angiography effectively illustrates disruptions in microvascular blood flow within the retinal peripapillary capillaries and peripapillary choriocapillaries in individuals diagnosed with NAION. [44] [45] [46] [47] [48] This method aids in visualizing minute vascular changes that are crucial for accurate diagnosis. Concurrently, magnetic resonance imaging (MRI) of the optic nerves plays a pivotal role in distinguishing NAION from optic neuritis, a condition with similar symptoms. Notably, MRI revealed optic nerve abnormalities in only a small fraction (15.6%) of NAION patients, compared to almost all (96.9%) patients with optic neuritis. Additionally, certain symptoms, including elevated swelling, paleness, narrower arteries, and hemorrhages, were more common in NAION than in optic neuritis. [49]

The natural progression of NAION following acute vision loss typically includes an improvement in visual acuity by 3 or more lines on the Early Treatment Diabetic Retinopathy Study (ETDRS) chart in 43% of those not receiving treatment. [50] As the initial swelling of the optic disc subsides, optic atrophy generally develops within one to two months after onset. A retrospective diagnosis of optic atrophy due to previous ischemic optic neuropathy is often possible when a small optic disc is detected in both the affected and the opposite eye, and when other tests for potential causes of optic atrophy yield normal results.

Following the ischemic damage to one optic disc, there exists a notable risk of involvement of the second eye. The recurrence rate of NAION in the same eye is approximately 6.4%. [51] Data from the trial estimate this risk at about 15% over 5 years. In cases where the second eye also experiences NAION, there is no clear consensus regarding the correlation between the final visual outcomes. [52] [53]

Treatment

Proposed treatments include hyperbaric oxygen, [54] levodopa or carbidopa, [55] aspirin, [56] transvitreal optic neurotomy, [57] bevacizumab [58] [59] and vitrectomy. The Ischemic Optic Neuropathy Decompression Trial [60] [61] observed that while spontaneous visual function deterioration occurred in 12% of 125 control eyes, the condition worsened in 24% of 119 eyes that underwent decompressive surgery. [62] The application of corticosteroids in NAION treatment remains a topic of debate. [63] [64]

Research into potential therapies for NAION is ongoing, including studies using animal models to explore neuroprotective treatments for the optic nerve. Despite these efforts, including a clinical trial examining the potential neuroprotective effects of topical brimonidine that was discontinued due to stringent eligibility requirements, effective treatment for idiopathic NAION remains elusive. Further trials have been halted prematurely, and a third trial investigated the intravitreal injection of a small interfering ribonucleic acid targeting caspase 2 as a treatment approach.

Epigenetic reprogramming

Epigenetic reprogramming through a novel gene therapy shows promise in restoring vision loss in a non-human primate model of NAION. This study builds on previous research demonstrating that AAV2-induced transient expression of the reprogramming genes Oct4, Sox2, and Klf4 (OSK) could reverse retinal aging and restore visual function in mice. Given the limitations of mice for modeling human vision, African green monkeys were used as a more accurate model. NAION was induced in these primates, and two groups were treated with either AAV2-OSK gene therapy or a vehicle. The results showed that pre-treated eyes with AAV2-OSK had significantly improved visual function compared to vehicle-treated eyes, as measured by parameters such as pERG response and optic nerve axon count. Post-treatment also resulted in significant recovery, albeit after an initial decline. These findings suggest that AAV2-OSK gene therapy has potential for clinical application in treating human optic nerve diseases. [65]

Related Research Articles

<span class="mw-page-title-main">Optic nerve</span> Second cranial nerve, which connects the eyes to the brain

In neuroanatomy, the optic nerve, also known as the second cranial nerve, cranial nerve II, or simply CN II, is a paired cranial nerve that transmits visual information from the retina to the brain. In humans, the optic nerve is derived from optic stalks during the seventh week of development and is composed of retinal ganglion cell axons and glial cells; it extends from the optic disc to the optic chiasma and continues as the optic tract to the lateral geniculate nucleus, pretectal nuclei, and superior colliculus.

<span class="mw-page-title-main">Papilledema</span> Swelling of the eyes optic disc due to high intracranial pressure

Papilledema or papilloedema is optic disc swelling that is caused by increased intracranial pressure due to any cause. The swelling is usually bilateral and can occur over a period of hours to weeks. Unilateral presentation is extremely rare.

<span class="mw-page-title-main">Amaurosis fugax</span> Medical condition

Amaurosis fugax is a painless temporary loss of vision in one or both eyes.

<span class="mw-page-title-main">Optic disc</span> Optic nerve head, the point of exit for ganglion cell axons leaving the eye

The optic disc or optic nerve head is the point of exit for ganglion cell axons leaving the eye. Because there are no rods or cones overlying the optic disc, it corresponds to a small blind spot in each eye.

Anterior ischemic optic neuropathy (AION) is a medical condition involving loss of vision caused by damage to the optic nerve as a result of insufficient blood supply (ischemia). This form of ischemic optic neuropathy is generally categorized as two types: arteritic AION, in which the loss of vision is the result of an inflammatory disease of arteries in the head called temporal arteritis, and non-arteritic AION, which is due to non-inflammatory disease of small blood vessels.

Posterior ischemic optic neuropathy (PION) is a medical condition characterized by damage to the retrobulbar portion of the optic nerve due to inadequate blood flow (ischemia) to the optic nerve. Despite the term posterior, this form of damage to the eye's optic nerve due to poor blood flow also includes cases where the cause of inadequate blood flow to the nerve is anterior, as the condition describes a particular mechanism of visual loss as much as the location of damage in the optic nerve. In contrast, anterior ischemic optic neuropathy (AION) is distinguished from PION by the fact that AION occurs spontaneously and on one side in affected individuals with predisposing anatomic or cardiovascular risk factors.

<span class="mw-page-title-main">Ophthalmic artery</span> Artery of the head

The ophthalmic artery (OA) is an artery of the head. It is the first branch of the internal carotid artery distal to the cavernous sinus. Branches of the ophthalmic artery supply all the structures in the orbit around the eye, as well as some structures in the nose, face, and meninges. Occlusion of the ophthalmic artery or its branches can produce sight-threatening conditions.

<span class="mw-page-title-main">Ischemic optic neuropathy</span> Medical condition

Ischemic optic neuropathy (ION) is the loss of structure and function of a portion of the optic nerve due to obstruction of blood flow to the nerve. Ischemic forms of optic neuropathy are typically classified as either anterior ischemic optic neuropathy or posterior ischemic optic neuropathy according to the part of the optic nerve that is affected. People affected will often complain of a loss of visual acuity and a visual field, the latter of which is usually in the superior or inferior field.

Arteritic anterior ischemic optic neuropathy is the cause of vision loss that occurs in temporal arteritis. Temporal arteritis is an inflammatory disease of medium-sized blood vessels that happens especially with advancing age. AAION occurs in about 15-20 percent of patients with temporal arteritis. Damage to the blood vessels supplying the optic nerves leads to insufficient blood supply (ischemia) to the nerve and subsequent optic nerve fiber death. Most cases of AAION result in nearly complete vision loss first to one eye. If the temporal arteritis is left untreated, the fellow eye will likely suffer vision loss as well within 1–2 weeks. Arteritic AION falls under the general category of anterior ischemic optic neuropathy, which also includes non-arteritic AION. AION is considered an eye emergency, immediate treatment is essential to rescue remaining vision.

Optic neuropathy is damage to the optic nerve from any cause. The optic nerve is a bundle of millions of fibers in the retina that sends visual signals to the brain.

Ocular ischemic syndrome is the constellation of ocular signs and symptoms secondary to severe, chronic arterial hypoperfusion to the eye. Amaurosis fugax is a form of acute vision loss caused by reduced blood flow to the eye; it may be a warning sign of an impending stroke, as both stroke and retinal artery occlusion can be caused by thromboembolism due to atherosclerosis elsewhere in the body. Consequently, those with transient blurring of vision are advised to urgently seek medical attention for a thorough evaluation of the carotid artery. Anterior segment ischemic syndrome is a similar ischemic condition of anterior segment usually seen in post-surgical cases. Retinal artery occlusion leads to rapid death of retinal cells, thereby resulting in severe loss of vision.

<span class="mw-page-title-main">Optic disc drusen</span> Medical condition

Optic disc drusen (ODD) are globules of mucoproteins and mucopolysaccharides that progressively calcify in the optic disc. They are thought to be the remnants of the axonal transport system of degenerated retinal ganglion cells. ODD have also been referred to as congenitally elevated or anomalous discs, pseudopapilledema, pseudoneuritis, buried disc drusen, and disc hyaline bodies.

Central retinal artery occlusion (CRAO) is a disease of the eye where the flow of blood through the central retinal artery is blocked (occluded). There are several different causes of this occlusion; the most common is carotid artery atherosclerosis.

<span class="mw-page-title-main">Central retinal vein occlusion</span> Medical condition

Central retinal vein occlusion, also CRVO, is when the central retinal vein becomes occluded, usually through thrombosis. The central retinal vein is the venous equivalent of the central retinal artery and both may become occluded. Since the central retinal artery and vein are the sole source of blood supply and drainage for the retina, such occlusion can lead to severe damage to the retina and blindness, due to ischemia and edema (swelling).

Pseudoexfoliation syndrome, often abbreviated as PEX and sometimes as PES or PXS, is an aging-related systemic disease manifesting itself primarily in the eyes which is characterized by the accumulation of microscopic granular amyloid-like protein fibers. Its cause is unknown, although there is speculation that there may be a genetic basis. It is more prevalent in women than men, and in persons past the age of seventy. Its prevalence in different human populations varies; for example, it is prevalent in Scandinavia. The buildup of protein clumps can block normal drainage of the eye fluid called the aqueous humor and can cause, in turn, a buildup of pressure leading to glaucoma and loss of vision. As worldwide populations become older because of shifts in demography, PEX may become a matter of greater concern.

Sohan Singh Hayreh was an ophthalmologist, clinical scientist, and professor emeritus of ophthalmology at the University of Iowa. As one of the pioneers in the field of fluorescein angiography, he was generally acknowledged to be a leading authority in vascular diseases of the eye and the optic nerve. For over 60 years, Hayreh was actively involved in basic, experimental, and clinical research in ophthalmology, publishing over 400 original peer-reviewed articles in various international ophthalmic journals, six classical monographs and books in his field of research, and more than 50 chapters in ophthalmic books. He made many seminal observations dealing with the ocular circulation in health and disease, the optic disc and the optic nerve, retinal and choroidal vascular disorders, glaucomatous optic neuropathy, fundus changes in malignant arterial hypertension, ocular neovascularization, rheumatologic disorders of the eye, and nocturnal arterial hypotension. He was an elected fellow of the National Academy of Medical Sciences.

Multiple evanescent white dot syndrome (MEWDS) is an uncommon inflammatory condition of the retina that typically affects otherwise healthy young females in the second to fourth decades of life.

Autoimmune optic neuropathy (AON), sometimes called autoimmune optic neuritis, may be a forme fruste of systemic lupus erythematosus (SLE) associated optic neuropathy. AON is more than the presence of any optic neuritis in a patient with an autoimmune process, as it describes a relatively specific clinical syndrome. AON is characterized by chronically progressive or recurrent vision loss associated with serological evidence of autoimmunity. Specifically, this term has been suggested for cases of optic neuritis with serological evidence of vasculitis by positive ANA, despite the lack of meeting criteria for SLE. The clinical manifestations include progressive vision loss that tends to be steroid-responsive and steroid dependent.

<span class="mw-page-title-main">Helen Danesh-Meyer</span> New Zealand ophthalmology academic

Helen Victoria Danesh-Meyer is a New Zealand ophthalmology academic, and as of 2008 is a full professor at the University of Auckland.

Diabetic papillopathy is an ocular complication of diabetes mellitus characterized by optic disc swelling and edema of optic nerve head. The condition may affect both type 1 and type 2 diabetic patients.

References

  1. ↑ Wilhelm H, Beisse F, Rüther K (2015-11-01). "Non-Arteritic Ischemic Optic Neuropathy (NAION)". Klin Monbl Augenheilkd. 232 (11): 306–209. doi:10.1055/s-0035-1558170. PMC   9885744 . PMID   36715340.
  2. ↑ Hayreh, Sohan Singh; Jonas, Jost B.; Zimmerman, M. Bridget (April 2007). "Nonarteritic Anterior Ischemic Optic Neuropathy and Tobacco Smoking". Ophthalmology. 114 (4): 804–809. doi:10.1016/j.ophtha.2006.07.062.
  3. ↑ "Non-Arteritic Anterior Ischemic Optic Neuropathy (NAION)". Brigham and Women's Hospital.
  4. ↑ Beck RW, Servais GE, Hayreh SS (1987). "Anterior ischemic optic neuropathy. IX: Cup-to-disc ratio and its role in pathogenesis". Ophthalmology. 94 (1503). doi:10.1016/S0161-6420(87)33263-4. PMID   3684223.
  5. ↑ Mansour AM, Shoch D, Logani S (1988). "Optic disc size in ischemic optic neuropathy". Am J Ophthalmol. 106 (587): 587–589. doi:10.1016/0002-9394(88)90591-0. PMID   3189474.
  6. ↑ Tesser RA, Niendorf ER, Levin LA (2003). "The morphology of an infarct in nonarteritic anterior ischemic optic neuropathy". Ophthalmology. 2031.
  7. ↑ Hayreh SS (1995). "The optic nerve head circulation in health and disease". Exp Eye Res. 61 (259).
  8. ↑ Onda E, Ciofi GA, Bacon DR, van Buskirk EM (1995). "Microvasculature of the human optic nerve". Am J Ophthalmol. 120 (92): 92–102. doi:10.1016/S0002-9394(14)73763-8. PMID   7611333.
  9. ↑ Arnold AC, Hepler BS (1994). "Fluorescein angiography in acute nonarteritic anterior ischemic optic neuropathy". Am J Ophthalmol. 117 (222): 222–230. doi:10.1016/S0002-9394(14)73080-6. PMID   8116751.
  10. ↑ Arnold AC (2003). "Pathogenesis of nonarteritic anterior ischemic optic neuropathy". J Neuroophthalmol. 23 (2): 157–163. doi:10.1097/00041327-200306000-00012. PMID   12782932.
  11. ↑ Hayreh SS (1974). "Anterior ischemic optic neuropathy. I: terminology and pathogenesis". Br J Ophthalmol. 158 (955).
  12. ↑ Hayreh SS, Podhajsky PA, Zimmerman B (2001). "Ipsilateral recurrence of nonarteritic anterior ischemic optic neuropathy". Arch Ophthalmol. 132 (734).
  13. ↑ Levin LA, Danesh-Meyer HV (2008). "Hypothesis: a venous etiology for nonarteritic anterior ischemic optic neuropathy". Arch Ophthalmol. 26 (1582).
  14. ↑ Wu, Kevin Yang; Evoy, François (2022-08-01). "NAION: Diagnosis and management". EyeNet Magazine. Archived from the original on 2024-07-04. Retrieved 2024-06-30.
  15. ↑ Williams E, Hart W, Tempelhoff R (1995). "Postoperative ischemic optic neuropathy". Anesth Analg. 80 (1018): 1018–1029. doi:10.1097/00000539-199505000-00029. PMID   7726399.
  16. ↑ Roth S, Thisted R, Erickson J (1996). "Eye injuries after nonocular surgery: a study of 60,965 anesthetics from 1988 to 199". Anesthesiology. 85 (1020): 1020–1027. doi:10.1097/00000542-199611000-00009. PMID   8916818.
  17. ↑ Macaluso DC, Shults WT, Fraunfelder FT (1999). "Features of amiodarone-induced optic neuropathy". Am J Ophthalmol. 127 (610): 610–612. doi:10.1016/S0002-9394(99)00016-1. PMID   10334361.
  18. ↑ Pomeranz HD, Smith KH, Hart WM, Egan RA (2002). "Sildenafil-associated nonarteritic anterior ischemic optic neuropathy". Ophthalmology. 109 (584): 584–587. doi:10.1016/S0161-6420(01)00976-9. PMID   11874765.
  19. ↑ Bollinger K, Lee ML (2005). "Recurrent visual field defect and ischemic optic neuropathy associated with tadalafil rechallenge". Arch Ophthalmol. 123 (400): 400–401. doi:10.1001/archopht.123.3.400. PMID   15767488.
  20. ↑ Gittinger JW, Lessell S, Bondar RL (1984). "Ischemic optic neuropathy associated with optic disc drusen". J Clin Neuroophthalmol. 4 (79). PMID   6233327.
  21. ↑ Purvin V, King R, Kawasaki A, Yee R (2004). "Anterior ischemic optic neuropathy in eyes with optic disc drusen". Arch Ophthalmol. 122 (48): 48–53. doi:10.1001/archopht.122.1.48. PMID   14718294.
  22. ↑ Liu YA, Mesentier-Louro LA, Shariati MA, Moss HE, Beres SJ, Liao YJ (2023). "High Altitude as a Risk Factor for the Development of Nonarteritic Anterior Ischemic Optic Neuropathy". J Neuroophthalmol. 43 (1): 69–75. doi:10.1097/WNO.0000000000001629. PMC   10870828 . PMID   36166787.
  23. ↑ Baril A et al. Regional Cerebral Blood Flow during Wakeful Rest in Older Subjects with Mild to Severe Obstructive Sleep Apnea. Sleep, Volume 38, Issue 9, September 2015, Pages 1439–1449.
  24. ↑ How does obstructive sleep apnea alter cerebral hemodynamics? Sleep, Volume 46, Issue 8, August 2023, zsad122.
  25. ↑ Buckley R et al. Cerebral blood flow is not impaired in persons with moderate obstructive sleep apnoea when awake. Sleep Breathing Physiology and Disorders • Original Article. Published: 08 May 2024.
  26. ↑ Gregori-Pla C et al. How does obstructive sleep apnea alter cerebral hemodynamics? Sleep, Volume 46, Issue 8, August 2023, zsad12.
  27. ↑ IONDT Study Group (1996). "Characteristics of patients with nonarteritic anterior ischemic neuropathy eligible for the ischemic optic neuropathy decompression trial". Arch Ophthalmol. 114 (1366).
  28. ↑ Xu L, Wang Y, Jonas JB (2007). "Incidence of nonarteritic anterior ischemic optic neuropathy in adult Chinese: the Beijing Eye Study". Eur J Ophthalmol. 17 (459): 459–460. doi:10.1177/112067210701700335. PMID   17534837.
  29. ↑ Lee JY, Park KA, Oh SY (2018). "Prevalence and incidence of non-arteritic anterior ischaemic optic neuropathy in South Korea: a nationwide population-based Study". Br J Ophthalmol. 102 (936): 936–941. doi:10.1136/bjophthalmol-2017-311140. PMID   28972024.
  30. ↑ Hayreh, Sohan Singh; Jonas, Jost B.; Zimmerman, M. Bridget (April 2007). "Nonarteritic Anterior Ischemic Optic Neuropathy and Tobacco Smoking". Ophthalmology. 114 (4): 804–809. doi:10.1016/j.ophtha.2006.07.062.
  31. ↑ Hayreh, Sohan Singh; Podhajsky, Patricia A.; Zimmerman, Bridget (November 1997). "Nonarteritic Anterior Ischemic Optic Neuropathy: Time of Onset of Visual Loss". American Journal of Ophthalmology. 124 (5): 641–647. doi:10.1016/S0002-9394(14)70902-X.
  32. ↑ Johnson LN, Arnold AC (1994). "Incidence of nonarteritic and arteritic anterior ischemic optic neuropathy". J Neuroophthalmol. 114 (38).
  33. ↑ Hattenhauer MG, Leavitt JA, Hodge DO (1997). "Incidence of nonarteritic anterior ischemic optic neuropathy". Am J Ophthalmol. 123 (103): 103–107. doi:10.1016/S0002-9394(14)70999-7. PMID   9186104.
  34. ↑ Lee MS, Grossman D, Arnold AC, Sloan FA (2011). "Incidence of nonarteritic anterior ischemic optic neuropathy: increased risk among diabetic patients". Ophthalmology. 118 (959): 959–963. doi:10.1016/j.ophtha.2011.01.054. PMC   3087834 . PMID   21439645.
  35. ↑ Cestari DM, Gaier ED, Bouzika P (2016). "Demographic, systemic, and ocular factors associated with nonarteritic anterior ischemic optic neuropathy". Ophthalmology. 123 (2446): 2446–2455. doi:10.1016/j.ophtha.2016.08.017. PMID   27659545.
  36. ↑ Hayreh SS, Joos KM, Podhajsky PA (1994). "Systemic diseases associated with nonarteritic anterior ischemic optic neuropathy". Am J Ophthalmol. 118 (766): 766–780. doi:10.1016/S0002-9394(14)72557-7. PMID   7977604.
  37. ↑ Bilgin G, Koban Y, Arnold AC (2013). "Nonarteritic anterior ischemic optic neuropathy and obstructive sleep apnea". J Ophthalmol. 33 (232). PMID   23719289.
  38. ↑ Wu Y, Zhou LM, Lou H (2016). "The association between obstructive sleep apnea and nonarteritic anterior ischemic optic neuropathy: a systematic review and meta-analysis". Curr Eye Res. 41 (987): 987–992. doi:10.3109/02713683.2015.1075221. PMID   26443989.
  39. ↑ Aptel F, Khayi H, Pepin JL (2015). "Association of nonarteritic ischemic optic neuropathy with obstructive sleep apnea syndrome: consequences for obstructive sleep apnea screening and treatment". JAMA Ophthalmol. 33 (797).
  40. ↑ Sun MH, Lee CY, Liao YJ, Sun CC (2019). "Nonarteritic anterior ischaemic optic neuropathy and its association with obstructive sleep apnoea: a health insurance database study". Acta Ophthalmol. 97 (e64). doi:10.1111/aos.13832. PMID   30171667.
  41. ↑ Warner JE, Lessell S, Rizzo JF, Newman NJ (1997). "Does optic disc appearance distinguish ischemic optic neuropathy from optic neuritis?". Arch Ophthalmol. 115 (1408): 1408–1410. doi:10.1001/archopht.1997.01100160578009. PMID   9366671.
  42. ↑ Subramanian PS, Gordon LK, Bonelli L, Arnold AC (2017). "Progression of asymptomatic optic disc swelling to non-arteritic anterior ischaemic optic neuropathy". Br J Ophthalmol. 101 (671): 671–675. doi:10.1136/bjophthalmol-2016-309250. PMID   27565987.
  43. ↑ Wu KW, Evoy F. NAION: Diagnosis and Management. EyeNet Magazine. August 2022.
  44. ↑ Wright Mayes E, Cole ED, Novais EA (2017). "Optical coherence tomography angiography in nonarteritic anterior ischemic optic neuropathy". J Neuroophthalmol. 37 (358).
  45. ↑ Sharma S, Ang M, Najjar RP (2017). "Optical coherence tomography in acute non-arteritic anterior ischaemic optic neuropathy". Br J Ophthalmol. 101 (1045): 1045–1051. doi:10.1136/bjophthalmol-2016-309245. PMID   28057645.
  46. ↑ Song Y, Min JY, Mao L, Gong YY (2018). "Microvasculature dropout detected by optical coherence tomography angiography in nonarteritic anterior ischemic optic neuropathy". Lasers Surg Med. 50 (194): 194–201. doi:10.1002/lsm.22712. PMID   28986994.
  47. ↑ Hata M, Oishi A, Muraoka Y, Miyamoto K (2017). "Structural and functional analyses in nonarteritic anterior ischemic optic neuropathy: optical coherence tomography angiography study". J Neuroophthalmol. 37 (140): 140–148. doi:10.1097/WNO.0000000000000470. PMID   27984351.
  48. ↑ Gaier ED, Wang M, Gilbert AL (2018). "Quantitative analysis of optical coherence tomographic angiography in patients with non-arteritic anterior ischemic optic neuropathy corresponds to visual function". PLOS ONE. 13. e0199793. doi: 10.1371/journal.pone.0199793 . PMID   29953490.
  49. ↑ Warner JE, Lessell S, Rizzo JF, Newman NJ (1997). "Does optic disc appearance distinguish ischemic optic neuropathy from optic neuritis?". Arch Ophthalmol. 115 (1408): 1408–1410. doi:10.1001/archopht.1997.01100160578009. PMID   9366671.
  50. ↑ Newman NJ, Scherer R, Langenberg P (2002). "Ischemic Optic Neuropathy Decompression Trial Research Group. The fellow eye in NAION: report from the ischemic optic neuropathy decompression trial follow-up". Am J Ophthalmol. 134 (1317). doi:10.1016/S0002-9394(02)01639-2. PMID   12208242.
  51. ↑ Nuttall GA, Garrity JA, Dearani JA (2001). "Risk factors for ischemic optic neuropathy after cardiopulmonary bypass: a matched case/control study". Anesth Analg. 93 (1410): 1410–6, table of contents. doi:10.1097/00000539-200112000-00012. PMID   11726415.
  52. ↑ Boone MI, Massry GG, Frankel RA (1996). "Visual outcome in bilateral nonarteritic anterior ischemic optic neuropathy". Ophthalmology. 103 (1223): 1223–1228. doi:10.1016/S0161-6420(96)30519-8. PMID   8764790.
  53. ↑ WuDunn D, Zimmerman K, Sadun AA, Feldon SE (1997). "Comparison of visual function in fellow eyes after bilateral nonarteritic anterior ischemic optic neuropathy". Ophthalmology. 104 (104): 104–111. doi:10.1016/S0161-6420(97)30354-6. PMID   9022112.
  54. ↑ Arnold AC, Hepler RS, Lieber M, Alexander JM (1996). "Hyperbaric oxygen therapy for nonarteritic anterior ischemic optic neuropathy". Am J Ophthalmol. 122 (535): 535–541. doi:10.1016/S0002-9394(14)72114-2. PMID   8862051.
  55. ↑ Johnson LN, Gould TJ, Krohel GB (1996). "Effect of levodopa and carbidopa on recovery of visual function in patients with nonarteritic anterior ischemic optic neuropathy of longer than six months' duration". Am J Ophthalmol. 121 (77): 77–83. doi:10.1016/S0002-9394(14)70536-7. PMID   8554083.
  56. ↑ Botelho PJ, Johnson LN, Arnold AC (1996). "The effect of aspirin on the visual outcome of nonarteritic anterior ischemic optic neuropathy". Am J Ophthalmol. 121 (450): 450–451. doi:10.1016/S0002-9394(14)70448-9. PMID   8604744.
  57. ↑ Soheilian M, Koochek A, Yazdani S, Peyman GA (2003). "Transvitreal optic neurotomy for nonarteritic anterior ischemic optic neuropathy". Retina. 23 (692): 692–697. doi:10.1097/00006982-200310000-00015. PMID   14574257.
  58. ↑ Bennett JL, Thomas S, Olson JL, Mandava N (2007). "Treatment of nonarteritic anterior ischemic optic neuropathy with intravitreal bevacizumab". J Neuroophthalmol. 27 (238): 238–240. doi:10.1097/WNO.0b013e31814b273d. PMID   17895825.
  59. ↑ Rootman DB, Gill HS, Margolin EA (2013). "Intravitreal bevacizumab for the treatment of nonarteritic anterior ischemic optic neuropathy: a prospective trial". Eye. 27 (538): 538–544. doi:10.1038/eye.2012.296. PMC   3626001 . PMID   23370417.
  60. ↑ Movsas T, Kelman SE, Elman MJ (1991). "The natural course of non-arteritic ischemic optic neuropathy". Invest Ophthalmol Vis Sci. 42 (951).
  61. ↑ The Ischemic Optic Neuropathy Decompression Trial Research Group (1995). "Optic nerve decompression surgery for nonarteritic anterior ischemic optic neuropathy (NAION) is not effective and may be harmful". JAMA. 273 (625).
  62. ↑ Hayreh SS Zimmerman MB (2008). "Non-arteritic anterior ischemic optic neuropathy: role of systemic corticosteroid therapy". Graefes Arch Clin Exp Ophthalmol. 246 (1029): 1029–1046. doi:10.1007/s00417-008-0805-8. PMC   2712323 . PMID   18404273.
  63. ↑ Rebolleda G, Perez-Lopez M, Casas-Llera P (2013). "Visual and anatomical outcomes of non-arteritic anterior ischemic optic neuropathy with high-dose systemic corticosteroids". Graefes Arch Clin Exp Ophthalmol. 251 (255): 255–260. doi:10.1007/s00417-012-1995-7. PMID   22441810.
  64. ↑ Saxena R, Singh D, Sharma M (2018). "Steroids versus no steroids in nonarteritic anterior ischemic optic neuropathy: a randomized clinical trial". Ophthalmology. 125 (1623): 1623–1627. doi:10.1016/j.ophtha.2018.03.032. PMID   29705054.
  65. ↑ Ksander B, Shah M, Krasniqi D, Gregory-Ksander MS, Rosenzweig-Lipson S, Broniowska K, Wathier M, Mannick J, Cermak J, Karg M, Shirahama S, Refaian N, Lu Y, Lawrence M, Rizzo JF, Sinclair D (2023). "Epigenetic reprogramming- A novel gene therapy that restores vision loss in a nonhuman primate model of NAION". Investigative Ophthalmology & Visual Science. 64 (8).
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