Anterior Ischemic Optic Neuropathy represents an acute ischaemic disorder of the optic nerve. The source and pattern of blood supply of the anterior a part of the nervusopticus (also called the nervusopticus head, ONH) are hugely different from that of the posterior part.
The ONH is nearly entirely supplied by the posterior arteria ciliaris (PCA) circulation; therefore, the remainder of the nervusopticus posterior to the ONH is supplied from several other sources.
Given that, pathogenetically, as well as clinically, ischaemic optic neuropathy is of two very distinct types: anterior ischemic optic neuropathy (AION) involving the ONH, and posterior ischaemic optic neuropathy (PION) involving a segment of the rest of the optic nerve posteriorly.
The former is way more common than the latter. It is often not appreciated that AION is one of the most prevalent and visually crippling diseases in the middle-aged and elderly, and is potentially bilateral.
To understand the various features of a clinical condition and its management, it is necessary to comprehend the various fundamental scientific issues involved, and the scientific basis of the disease process.
Therefore, before describing the clinical characteristics of the two types of ischaemic optic neuropathy and their management, I will first discuss some of the fundamental issues about the optic nerve circulation, the pathogeneses of AION and PION, and the role of various factors in their development very briefly.
What is anterior ischemic optic neuropathy?
Ischemic optic neuropathy could also be a severe explanation for blindness or significantly impaired vision, and there are few definitive answers regarding its cause, clinical features, and treatment. This is of two types as follows.
Arteritic AION (A-AION): This is almost invariably due to giant cell arteritis (GCA).
Non-arteritic AION (NA-AION): This is due to causes other than GCA.
Additionally, each type has several subtypes. Anterior ION is that the most prevalent form, while posterior ION is rare. Both are often divided into three subtypes: arteritic (usual thanks to giant cell arteritis), nonarteritic (due to non-inflammatory causes), and perioperative.
Patients with both anterior and posterior ischemic optic neuropathy present with acute vision loss in one or both eyes that are not related to pain.”Arteritic anterior and posterior ION are less common than nonarteritic anterior and posterior ION, but they’re ocular emergencies that need early diagnosis and immediate treatment.
Anterior ischemic optic neuropathy symptoms
The classic description of patients with NAION presenting with acute, painless unilateral vision loss that’s often described as a blurring or cloudiness of vision, often inferiorly, has been expanded.
Although the bulk of patients don’t have accompanying pain, headache, or periocular pain is reported in 8-12% of patients, which may make it difficult to differentiate from optic neuritis. Both diabetes and sleep apnea have been associated with NAION, and diabetes has been associated with increased risk of NAION in the fellow eye.
Optimal control of diabetes and treatment of sleep apnea is recommended; however, three patients with sleep apnea developed NAION while being treated with continuous positive airway pressure (CPAP) for four months to 6 years before symptom onset. In this series, CPAP didn’t prevent the event of NAION. More extensive studies are needed to determine the benefit of CPAP in preventing NAION in patients with sleep apnea.
Anterior ischemic optic neuropathy diagnosed
Currently, there’s no generally accepted treatment for NAION, but a variety of medical and surgical therapies are proposed. Because the pathophysiology of NAION remains elusive, most are empirical and include a wide range of agents presumed to act on thrombosis, on the blood vessels, on the disc edema itself, or presumed to have a neuroprotective effect.
Ischemic damage in NAION affects the optic nerve, and therefore the axons of the retinal ganglion cells. Some data from animal models suggest that the therapeutic window for NAION may be as long as two to three weeks.
This is consistent with the typical clinical finding of progressive visual loss over two weeks, and the observation that most cases of NAION do not progress after one month. Visual dysfunction appears to plateau around the same time that disc edema is superseded by optic atrophy, but this does not necessarily mean that this is cause and effect.
The IONDT specified a two-week therapeutic window for surgical decompression, as did another recent study using steroids. The therapeutic window remains unclear; however, it seems reasonable that earlier intervention might lead to less axonal damage.
How is anterior ischemic optic neuropathy treated?
When a patient is diagnosed as having AION, the first crucial step in patients aged 50 and over is to identify immediately whether it is arteritic or non-arteritic. A-AION is due to GCA.” Visual loss is preventable if GCA is diagnosed and treated early.
Therefore, immediate diagnosis of A-AION and the start of high-dose steroid therapy is the key to preventing any further visual loss in the same eye or both eyes. Intravitreal triamcinolone acetonide injection has also shown promising results in a small number of patients.
Recently, it was used to treat a patient with nonarteritic anterior ION in Korea.9 Fundus examination and measurements of the 65-year-old patient’s best-corrected visual acuity and visual field were performed before the injection and after the injection at two weeks and one, three, and six months. BCVA was 0.05 before the injection, 0.16 at two weeks, 0.3 at one month, and 0.4 at three months after the injection.
Controlling the danger factors related to NA-AION is a necessary precaution. Also, people that have risk factors should avoid the utilization of blood pressure-lowering medications or male erecticle dysfunction drugs before bedtime.
The combination of such drugs alongside the traditional drop by vital signs while sleeping might be enough to interrupt blood supply to the nervusopticus.
What is the outlook?
NAION remains frustrating for clinicians and sometimes devastating for patients. The pathophysiology remains unclear, and it’s uncertain whether any treatment are going to be useful for NAION. Many therapies have been inadequately studied. Despite its limitations, the NAION animal model will allow preclinical evaluation of neuroprotective agents and may be necessary for suggesting future approaches to treatment.
The role of oral steroids remains controversial, and the literature regarding the prevention of sequential NAION is contradictory.
Treatment of vascular risk factors and anti-platelet therapy; however, both have an established role in the prevention of cerebral and myocardial infarction and should be considered in NAION despite the lack of class I evidence.
Patients with A-PION, if treated urgently and aggressively with high dose steroid therapy, showed no improvement in vision but also showed no further visual loss. Patients with surgical PION usually suffer severely, often bilateral, and irreversible visual loss; this doesn’t answer steroid therapy.
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