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INFORMATION PRIMARILY FOR PHYSICIANS

ANTERIOR ISCHEMIC OPTIC NEUROPATHY (AION)

By S. S. Hayreh

INTRODUCTION

Anterior ischemic optic neuropathy (AION) is one of the most prevalent and visually crippling diseases in the middle-aged and elderly population, although no age is immune, and is potentially bilateral, a fact not fully appreciated by most physicians.

The following brief summary is based on our multiple basic, experimental and clinical studies on AION over the years.2-4,8-11,14-18,21-26,28-36,38-40,42-58,62

CLINICAL CLASSIFICATION OF AION

Clinically, based on its cause, AION is of two types:23,30,36

    1. Arteritic AION: This is the most serious type and is due to giant cell arteritis.
    2. Non-arteritic AION: This is the usual and the most common one, and consists of all cases other than those due to giant cell arteritis; in this type of AION usually there is no one cause.

Before discussing the symptoms and signs and how to manage the two types of AION, it is essential to understand the basic mechanism of development of AION as a whole and the various factors that play a role in its development.

MECHANISM OF DEVELOPMENT OF AION

This account is based essentially on my basic, experimental and clinical studies (in more than 1,000 patients) on this disorder. AION is due to acute ischemia of the anterior part of the optic nerve (the optic nerve head).8,11,15,18,30,42 The main source of blood supply to the optic nerve head is from the posterior ciliary artery circulation (Fig. 1).7,8,11,14,20,25,27,30,37 Therefore, AION represents an ischemic disorder of posterior ciliary artery circulation in the optic nerve head. The blood supply and blood flow patterns in the optic nerve head have a marked inter-individual variation20,25,27,37 which exercises a profound influence on the mechanism of development and clinical features of AION.30

From the mechanism of development point of view, AION cases can be broadly classified into two groups:18,30

  1. Due to Thrombosis or Embolisms of the posterior ciliary arteries or their Subdivisions Feeding the optic nerve head
    2.

    (i) Caused by Thrombosis: Most common cause here is giant cell arteritis (temporal arteritis), and less commonly other types of vasculitis.

    (ii) Caused by Embolism: These seem to occur much less frequently than those due to thrombosis.

    In the thrombotic/embolic group, there is usually massive, severe, and permanent damage to the optic nerve head, the extent of which depends on the size of the artery involved and the area of the optic nerve head supplied by the blocked artery.

  2. Due to Transient Poor Circulation or No Circulation in the Blood Vessels of the Optic Nerve Head

This is by far the most common cause of AION , indeed almost all AION cases which are not due to inflammation of the arteries (i.e. non-arteritic AION). The blood flow in the optic nerve head depends upon several factors, the most important of which is the blood pressure in its vessels.27,30,38 Transient poor circulation or loss of circulation in the optic nerve head can occur due to a transient fall of blood pressure below a critical level in its vessels, which in turn, in susceptible persons, would produce AION. It is extremely important to remember that in this mode of development of AION there is no actual blockage of the posterior ciliary arteries. A fall of the blood pressure below the critical level in the capillaries of the optic nerve head may be caused either by a marked fall in blood pressure (e.g., in shock, fall of blood pressure during sleep at night or a nap during the day,28,30,33,47,50,51,58 blockage or severe narrowing of the internal carotid artery and/or ophthalmic artery,62 and other causes) or by a rise in the eye pressure,16 or a combination of these factors.62 The optic nerve head damage, which may be mild to marked, depends upon the severity and the duration of the transient ischemia, but is usually less extensive and less severe than that due to thrombosis or embolism.

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© text and images, 2003, Sohan Singh Hayreh.
Reproduction of any part of this material is not permitted without express permission from Dr. Hayreh.
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