**1. Introduction**

Ischemic optic neuropathies (IONs) are a major cause of blindness or seriously impaired vision in the middle-aged and elderly population, although they can occur at any age. ION is of two types: anterior (AION) and posterior (PION), the first involving the anterior part of the optic nerve (also called the optic nerve head, ONH) and the second, the rest of the optic nerve. Pathogenetically AION and PION are very different diseases. AION represents an acute ischemic disorder (a segmental infarction) of the ONH supplied by the posterior ciliary arteries (PCAs), while PION has no specific location in the posterior part of the optic nerve and does not represent ischemia in a specific artery [1].

Blood supply blockage can occur with or without arterial inflammation. For this reason, AION is of two types: non-arteritic AION (NA-AION) and arteritic AION (A-AION). The former is far more common than the latter, and they are distinct entities etiologically, pathogenetically, clinically and from the management point of view [1, 2].

A-AION is an ocular emergency and requires immediate treatment with systemic corticoste‐ roids to prevent further visual loss. This is almost invariably due to giant cell arteritis (GCA), which is a primary vasculitis that affects extracranial medium (especially external carotid artery-ECA-branches) and sometimes large arteries (aorta and its major branches)-large-vessel GCA [3, 4]. The diagnosis of GCA requires age more than 50 years at disease onset, new headache in the temporal area, temporal artery tenderness, and/or reduced pulse, jaw claudication, systemic symptoms, erythrocyte sedimentation rate (ESR) exceeding 50 mm/hr, and typical histologic findings (granulomatous involvement) in temporal artery biopsy (TAB) [5]. Approximately 40-50% of patients with GCA have ophthalmologic complications, including visual loss secondary to A-AION, central retinal artery occlusion, homonymous hemianopsia or cortical blindness (uni- or bilateral occipital infarction) [6].

© 2013 Jianu and Jianu; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

NA-AION is a multifactorial disease with multiple risk factors that contribute to its develop‐ ment: the nocturnal arterial hypotension is the most important risk factor. Often, NA-AION patients have an anatomical predisposition: small discs, where structural crowding of nerve fibers (crowded disk), and reduction of the vascular supply, which may combine to impair perfusion to a critical degree [1, 2].

**3. Pathophysiology of factors controlling blood flow in the optic nerve head**

Giant Cell Arteritis and Arteritic Anterior Ischemic Optic Neuropathies

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The blood flow in the ONH depends upon: a). resistance to blood flow, b). arterial blood

**a.** resistance to blood flow. It depends upon the state and calibre of the vessels supplying the ONH, which in turn are influenced by: the efficiency of autoregulation of the ONH blood flow, the vascular changes in the arteries feeding the ONH circulation, and the

**b.** arterial blood pressure (BP). Both arterial hypertension and hypotension can influence the ONH blood flow in a number of ways. In an ONH, a fall of blood pressure below a critical level of autoregulation would decrease its blood flow. Fall of BP in the ONH may be due to systemic (nocturnal arterial hypotension during sleep, intensive antihypertensive

**c.** intraocular pressure (IOP). There is an inverse relationship between IOP and perfusion

Perfusion pressure = Mean BP minus intraocular pressure (IOP). Mean BP = Diastolic BP + 1/3

**1.** AION due to thrombotic or embolic lesions of the arteries/arterioles feeding the ONH:

**a.** thrombotic lesions: Occlusion of the PCAs is most commonly caused by GCA (resulting in infarction of the ONH and A-AION) and less commonly by other types

**b.** embolic lesions: Multiple emboli in the vessels of the ONH have been demonstrated

**2.** AION due to transient non-perfusion or hypoperfusion of the nutrient vessels in the ONH (paraoptic branches of PCAs). A transient non-perfusion or hypo-perfusion of the ONH can occur due to a transient fall of perfusion pressure in its vessels, which in turn in susceptible persons would produce NA-AION. Almost all NA-AION cases belong to this

**4. The major features of arteritic-anterior ischemic optic neuropathies and**

For the comparison of major features of A-AION and NA-AION we use a *complex protocol:*

The blood flow in the ONH is calculated by using the following formula [1]:

AION cases can be broadly classified into two groups [1, 2]:

histopathologically in NA-AION.

**nonarteritic-anterior ischemic optic neuropathies**

pressure (BP), and c). intraocular pressure (IOP) [1, 2].

rheological properties of the blood.

medication, etc.) or local hypotension.

pressure in the ONH.

(systolic BP- diastolic BP).

of vasculitis.

group.
