*2.3.2 Probe selection*

Standard neurovascular ultrasound machines equipped with linear-array transducers emitting 6-12 MHz (up to 15 MHz) are adequate for identifying (by Color Doppler sonography), and measuring (by spectral analysis pulsed Doppler sonography) the blood flow in the orbital vessels: the OA, the CRA and central retinal vein (CRV), PCAs, and the superior ophthalmic vein (SOV) [28, 31, 32].

#### **Figure 8.**

*Color Doppler imaging (CDI) of orbital (retro-bulbar) vessels: (A). central retinal artery (CRA); (B). posterior ciliary arteries (PCAs) [15].*


*Note: These are the normal flow velocities and resistances index in orbital vessels which are generally accepted by the specialists.*

#### **Table 1.**

*Normal flow velocities and Resistance Index in orbital vessels [15, 31, 32].*

The CRA, a distal branch of the OA, enters the optic nerve (ON) approximately 1-1.5 cm distal from the bulbus coming from the dorsolateral direction. Parallel to this is the CRV.

The PCAs are located near the optic nerve (ON) (the nasal-nPCA and the temporal-tPCA branches) [28, 31, 32].

If the vessels are difficult to display, the power should be elevated for a short time if the clinical question is important [28, 31, 32].

*2.3.3 Arterial blood supply of the anterior part of the optic nerve*

The optic nerve head (ONH) consists of (from anterior to posterior):


*An Integrated Approach to the Role of Neurosonology in the Diagnosis of Giant Cell Arteritis DOI: http://dx.doi.org/10.5772/intechopen.96379*

or the PCAs instead). In addition, pial branches from the central retinal artery (CRA) also supply this part. The latter is not present in all eyes. When present, it is formed by inconstant branches arising from the intraneural part of the CRA.

From the description of the arterial supply of the ONH given above, it is obvious that the PCAs are the main source of blood supply to the ONH [36–40].

*2.3.4 Pathophysiology of factors controlling blood flow in the optic nerve head (ONH)*

The blood flow in the ONH depends upon [36–40]:


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

Perfusion pressure = Mean BP minus intraocular pressure (IOP). Mean BP = Diastolic BP + 1/3 (systolic - diastolic BP) [6, 13].

#### **3. Anterior ischemic optic neuropathies (AIONs)**

AION is the consequence of an acute ischemic disorder (a segmental infarction) of the ONH supplied by the PCAs. Blood supply interruption can occur with or without arterial inflammation. Therefore, AION is of two types: non-arteritic AION (NA-AION) and arteritic AION (A-AION). The prior is far more common than the last, and they are distinct entities etiologically, pathogenically, clinically and from the management point of view [36–40].

A history of amaurosis fugax before an abrupt, painless, and severe loss of vision of the involved eye, with concomitant diffuse pale optic disc edema is extremely suggestive of A-AION. None of these symptoms are found in NA-AION patients [36–40].

#### **3.1 Spectral Doppler analysis of the orbital (retro-bulbar) vessels in A-AION**

In acute stage, blood flow cannot be detected in the PCAs in the clinically affected eye of any of the GCA patients with A-AION. Low end diastolic velocities (EDV) and high resistance index (RI) are identified in all other orbital vessels (including the PCAs in the opposite eye) of all A-AION patients [9–14, 41].

**Figure 9.**

*CDI of the PCAs in A-AION: (A). Decreased EDV in the nasal PCAs of the clinically affected right eye, and (B) of the clinically unaffected left eye.*

Over 7 days, Spectral Doppler analysis of the orbital vessels highlights blood flow alterations in all A-AION patients even with a high-dose corticosteroids therapy. Severely reduced blood flow velocities (especially EDV) in the PCAs of the affected eye (both nasal and temporal branches), compared to the unaffected eye, are observed. An increased RI in the PCAs is noted (the RI is higher on the clinically affected eye as compared to the unaffected eye) [9–14, 41] (**Figure 9A,B**).

Fewer abnormalities are detected in the CRAs: high RI are measured in both sides, with decreased peak systolic velocities (PSV) in the CRA of the clinically affected eye [9–14, 41].

Similar abnormalities are noted in the OAs: high RI are measured in both sides [9–14, 41].

At 1 month, after treatment with high-dose corticosteroids, CDI examinations of orbital blood vessels reveals that blood flow normalization is slow in all A-AION patients [9–14, 41].

In conclusion, the Spectral Doppler Analysis of the orbital vessels in A-AION indicates (after several days of corticosteroid treatment) low blood velocities, especially EDV, and high RI in all orbital vessels, in both orbits. These signs represent characteristic signs of the CDI of the orbital vessels in A-AION [9–14, 41].
