Draft:Non-Arteriitic Anterior Ischemic Optic Neuropathy

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"NAION" redirects here. For other uses, see Naion (disambiguation).
Non-arteriitic anterior ischemic optic neuropathy
Other namesNAION
SpecialtyOphthalmology
SymptomsOptic disc swelling, optic atrophy, vision loss

Non-arteriitic anterior ischemic optic neuropathy (NAION) is a medical condition involving loss of vision caused by damage to the optic nerve as a result of ischemia (insufficient blood supply). The key symptom of NAION is optic disc swelling, which typically resolves within two months, but often leads to optic atrophy. Unfortunately, the likelihood of vision improvement following this condition is low. NAION is associated with both localized abnormalities in the vascular supply to the optic nerve and systemic vascular risk factors. Major risk factors include diabetes, hypertension, and sleep apnea, with sleep apnea being particularly significant. As of now, there is no definitive treatment for NAION that is universally supported by robust scientific evidence. 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]

Pathogenesis[edit]

The underlying causes of NAION are largely unknown, as it is difficult to gather enough tissue samples from the optic nerve during the initial occurrence of vision loss to study them effectively. Several theories have been proposed to explain the reduction in blood flow that leads to this condition, but they often contradict each other, leading to no agreed-upon explanation for the onset of this type of optic nerve damage.

The optic nerve head, or prelaminar disc, mainly receives blood from peripapillary choroidal arterioles from the elliptical anastomotic annulus that are linked to the circle of Zinn-Haller, which is formed by branches of the lateral and posterior ciliary arteries [2][3]. Beyond this region, different parts 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 sends blood to the thin, sieve-like section of the eye's outer layer and the optic nerve fibers inside it through tiny, inward-facing arteries. The area just behind this layer in the optic nerve gets blood from small returning arteries and tiny blood vessels that come from the eye's surrounding circulation and the main eye artery, weaving through the nerve's supporting fibers. Further along, the parts of the optic nerve inside the eye socket and the canal it passes through receive blood from small arteries that branch off the main network surrounding the eye, and also from the central artery of the eye itself. Fluorescein angiographic studies [4][5] have shown that during the acute phase of NAION, there is a delay in blood flow to the optic disc, indicating a possible impairment in the arteries directly feeding it. Other studies suggest that a drop in blood pressure within certain critical areas of the optic disc's blood supply network might make it more vulnerable to damage on [6].

The structure of the optic disc itself may also contribute to the risk of developing NAION. Typically, affected individuals have smaller optic discs with little to no cupping, which may lead to a crowding of nerve fibers and contribute to the condition [7][8], somewhat similar to compartment syndrome.[9]

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.[10] Some researchers have even suggested that blockages in the veins could be responsible.[11]

While most cases of NAION are idiopathic, it has been frequently linked to certain conditions, enough to suggest an association. 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 perfusion. The incidence of ischemic optic neuropathy leading to vision loss following general surgeries ranges between 0.1% and 0.002%.[12][13] This condition, encompassing both anterior and posterior types, has been noted after cardiopulmonary bypass [14], spine [15], and other surgical interventions.[16][17] Key risk factors include anemia during surgery, hypotension, hypoxemia, and pre-existing conditions such as hypertension, diabetes, or renal failure. There remains no consensus on the optimal management of blood pressure or hematocrit levels under anesthesia during these procedures.

Vision loss following cataract surgery, termed anterior ischemic optic neuropathy (AION), may arise from compromised optic nerve blood supply due to increased intraocular pressure or residual surgical materials. Despite diligent monitoring, AION may still manifest, with cases reported in both eyes sequentially after uneventful initial surgeries.[18] The onset of vision loss can range from hours to weeks after surgery, with ongoing debates regarding the causative factors, particularly in sequential bilateral surgeries.[19][20]

Both anterior and posterior ischemic optic neuropathy have been documented following significant blood loss and resultant shock [21], often due to trauma or surgical complications. Vision loss may develop days after the event, persisting even after stabilization of blood pressure and anemia.[22][23][24] Diagnosis is frequently delayed, particularly in sedated patients, with a generally poor prognosis for vision recovery.

The link between certain medications, such as amiodarone [25] and phosphodiesterase type 5 (PDE5) inhibitors like sildenafil [26][27], and the onset of AION is contentious. These drugs 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.

NAION in patients with optic disc drusen is characterized by distinct features such as younger patient age, prior transient visual disturbances, and generally better visual outcomes. It is hypothesized that mechanical stress on the blood vessels near the optic nerve, induced by the presence of drusen, may trigger AION in these patients.).[28][29]

Incidence[edit]

NAION is the most frequently diagnosed sudden optic nerve disease in adults over 50, predominantly affecting Caucasians.[30]

While the exact number of cases is unclear, estimates suggest thousands of new cases occur annually in the United States alone [31][32], with variable rates reported in Asian populations.[33][34] 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.[35][36][37][38][39][40][41]

Clinical features[edit]

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.[42] 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.[43]

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.

Optical coherence tomography angiography effectively illustrates disruptions in microvascular blood flow within the retinal peripapillary capillaries and peripapillary choriocapillaris 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, Rizzo and colleagues found that 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 findings from the Ischemic Optic Neuropathy Decompression Trial indicate that 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. 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.[51][52]

Hayreh has reported that the recurrence rate of NAION in the same eye is approximately 6.4%. [53]

Treatment[edit]

To date, no medical interventions have successfully restored vision in cases of NAION. 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 conducted a thorough examination on the effectiveness of optic nerve sheath fenestration, which involves draining cerebrospinal fluid from around the optic nerve, in a large number of patients.[60][61] This trial 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] In a study by Hayreh, patients with NAION who opted for treatment with oral prednisone were compared to those who received no treatment.[65] The findings indicated that steroid treatment significantly increased the likelihood of improving both visual acuity and visual field. However, other studies did not demonstrate any improvement in visual outcomes between steroid-treated patients and those without treatment.[66] 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. Overall, there is currently no effective treatment established for idiopathic NAION. Emphasis is placed on identifying modifiable vascular risk factors that could influence the risk of the condition affecting the other eye.

References[edit]

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External links[edit]


Category:Disorders of optic nerve and visual pathways

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