**3.2 DSA allows an excellent localization and evaluation of the degree and length of intracranial arterial stenosis (ICAS)**

Angiographic measurement methods are routinely used nowadays in clinical practice to identify patients who may benefit from carotid endarterectomy [29]. Samuels affirmed that the established methods for measuring extracranial ICA stenosis are unsuitable for measuring the stenosis of a major intracranial artery because the intracranial arteries are often tortuous, have several branches, and are narrowing gradually in their distal portions [29].

If the prognosis of ICAS and the choice of therapy for these patients was clearly shown by WASID trial [2] to be based on the severity of ICAS, a repeatable method for measuring percent stenosis of the major intracranial arteries was required: standard WASID criteria for grading of ICAS [29].

All patients enrolled in the WASID trial have been subjected to DSA, to confirm a symptomatic ICAS (50–99%) of the ICA, MCA, VA, or BA. All major intracranial vessels were screened for stenosis stratified into three categories of lumen reduction (30–50, 50–70, and >70%). The percentage of stenosis of an intracranial artery was defined by Samuels [29].

$$\text{WASID method [1 - (D\_{\text{stensis}}/D\_{\text{normal}})] } \times 100 = \text{\%} \text{ Stensis.} \tag{1}$$

Rules applied for measuring a stenosis of the carotid siphon and basilar artery. Dstenosis is the residual diameter of the artery at the site of the most severe stenosis, and Dnormal is the diameter of the proximal normal artery.


When a "gap sign" is present (i.e., the lumen of the vessel cannot be visualized at the site of severe stenosis), D stenosis cannot be measured with calipers. In these cases, percent stenosis is defined as 99% luminal stenosis [29].

#### **3.3 DSA is an excellent assessor of collateral intracranial arterial circulation**

Cerebral collateral circulation is a supplementary vascular channels network that plays an important role in stabilizing the cerebral blood flow when the main arterial supplying systems fail (Liebeskind and coworkers) [30, 31]. Arterial insufficiency due to thromboembolism, hemodynamic compromise, or a combination of these factors may lead to the recruitment of collaterals [30, 31].

Impaired cerebral hemodynamics is a well-established predictor in large artery stroke [32]. Cerebral perfusion pressure distal to a high-grade stenosis or occlusion depends on collateral sources of blood flow. The anterior and posterior communicating arteries (ACoA, PCoA) provide most collateral flow in ICA and BA stenosis (primary collaterals), while distal pial and leptomeningeal anastomoses (secondary collaterals) are important in MCA stenosis [32]. DSA is the most valuable investigation that provides the assessment of collateral cerebral flow; Liebeskind and coworkers reporting that collateral flow on DSA was found to be absent in 69% of patients with symptomatic ICAS and it was also considered an independent predictor of recurrent ipsilateral stroke [30, 31].

Stroke risk, due to ICAD, increases with the arterial stenosis degree. Liebeskind and coworkers conducted a retrospective analysis of the baseline DSA acquired in the WASID trial, and they provided the first comprehensive evaluation of collaterals in modifying stroke risk in patients diagnosed with ICAD and its impact on subsequent stroke characteristics. They observed that the collateral circulation was adequately available for analysis in 287/569 patients from WASID (50%) subjects with proximal arterial stenoses ranging from 50 to 99% [30, 31].

According to Liebeskind, collateral brain circulation is one of the most significant factors that mediates the potentially devastating effects of cerebral ischemia. He asserted that patho-physiological recruitment of these collateral vessels (potential anastomotic connections) depends on the temporal course of numerous compensatory (hemodynamic, metabolic, and neural) mechanisms and on the caliber and patency of primary pathways that may rapidly compensate for decreased

**85**

*Diagnosis of Symptomatic Intracranial Atherosclerotic Disease*

blood flow and the adequacy of secondary collateral routes [30, 31]. He asserted that collaterals maintain perfusion downstream from arterial occlusions in acute stroke, determining the hemodynamic characteristics of the ischemic penumbra, the evolution of infarct, and susceptibility for hemorrhagic transformation [30]. He suggested that focal neurologic symptoms manifest only when collaterals fail. Regarding the therapeutic point of view, robust collaterals are an effective predictor of arterial recanalization and good clinical outcomes in acute stroke [31]. It is also well known that arterial occlusion secondary to progressive atherosclerotic stenosis of an intracranial segment allows the development of robust collaterals over time, unlike the cardioembolic or abrupt thrombotic occlusion. Collaterals and functional demonstration of flow impairment may be more informative than isolated anatomic

Liebeskind concluded that collateral circulation is a powerful determinant of stroke risk in ICAD, demonstrating a protective role with severe stenoses and perhaps distinguishing milder stenoses that are relatively unstable [30, 31].

Intracranial circulation can be examined by transcranial Doppler ultrasonography (TCD) or transcranial color-coded duplex sonography (TCCS) through different bone windows (transtemporal, transforaminal, and transorbital). The signal can be enhanced by using ultrasound contrast agents [33–38]. TCD combines in real-time intracranial blood flow patterns and velocities modifications with arterial diameter in the stenotic vessels. The most important data are: depth, blood flow direction, different velocities (peak systolic-PSV, end diastolic-EDV, and mean blood flow velocity-MFV), pulsatility index-PI, and resistance index-RI. The physiological data assessed from TCD are complementary to the anatomical data analyzed from other neuroimaging techniques (DSA, CTA, and MRA)

TCD has some advantages: inexpensive, noninvasive, portable test than can be performed bedside, serial examination, emboli detection, and vasomotor reactivity testing. TCD has high specificity, sensitivity, and negative predictive value (NPV) [33–38]. In the same time, TCD has some disadvantages: low reliability, technical limits (inadequate or absent windows, the tortuous course of the basilar artery, etc.), and operator-dependent results. TCD presents a modest positive predictive value (PPV) (36–75%). Therefore, it is useful to exclude significant ICAS with high certainty but requires confirmation by other imaging methods when stenosis is suggested [33–41]. The circle of Willis is complete in only 20% of cases; in other cases, one or several vascular segments may be hypoplastic or aplastic. Visualization of the intracranial vessels and assessment of cerebral hemodynamics are only possible with TCCS, but this technique still requires further certification

Prabhakaran and coworkers suggested that TCD can specify the mechanisms of stroke in symptomatic ICAS by using surrogate imaging markers of stroke risk: for the mechanism of decreased antegrade flow—the surrogate imaging marker of flow velocity; for the progression of stenosis—the flow velocity; for the poor collateral flow—the circle of Willis collaterals; for the artery-to-artery embolism—the microembolic signal; and for the impaired vasomotor reactivity—the cerebrovascular reactivity [33–41]. Serial monitoring of flow velocities by TCD can detect the

**4. Transcranian Doppler (TCD) and transcranian color—coded sonography (TCCS)—diagnostic tests for intracranial arterial** 

*DOI: http://dx.doi.org/10.5772/intechopen.90250*

measures of maximal stenosis or length [30].

**stenosis (ICAS)**

in larger studies [33–41].

evolution of ICAS and therapeutic effects [22, 41].

[33–38].

#### *Diagnosis of Symptomatic Intracranial Atherosclerotic Disease DOI: http://dx.doi.org/10.5772/intechopen.90250*

*New Insight into Cerebrovascular Diseases - An Updated Comprehensive Review*

sis, and Dnormal is the diameter of the proximal normal artery.

cases, percent stenosis is defined as 99% luminal stenosis [29].

these factors may lead to the recruitment of collaterals [30, 31].

with proximal arterial stenoses ranging from 50 to 99% [30, 31].

tor of recurrent ipsilateral stroke [30, 31].

defined by Samuels [29].

is selected.

All patients enrolled in the WASID trial have been subjected to DSA, to confirm a symptomatic ICAS (50–99%) of the ICA, MCA, VA, or BA. All major intracranial vessels were screened for stenosis stratified into three categories of lumen reduction (30–50, 50–70, and >70%). The percentage of stenosis of an intracranial artery was

WASID method [1 − (Dstenosis/Dnormal)] × 100 = % Stenosis. (1)

Rules applied for measuring a stenosis of the carotid siphon and basilar artery. Dstenosis is the residual diameter of the artery at the site of the most severe steno-

• If the proximal segment is diseased, contingency sites are chosen to measure D normal: distal artery (second choice) or feeding artery (third choice).

basilar), percent stenosis of both sites is measured and the more severe stenosis

When a "gap sign" is present (i.e., the lumen of the vessel cannot be visualized at the site of severe stenosis), D stenosis cannot be measured with calipers. In these

• If tandem intracranial lesions are present (e.g., distal vertebral and mid-

**3.3 DSA is an excellent assessor of collateral intracranial arterial circulation**

Cerebral collateral circulation is a supplementary vascular channels network that plays an important role in stabilizing the cerebral blood flow when the main arterial supplying systems fail (Liebeskind and coworkers) [30, 31]. Arterial insufficiency due to thromboembolism, hemodynamic compromise, or a combination of

Impaired cerebral hemodynamics is a well-established predictor in large artery stroke [32]. Cerebral perfusion pressure distal to a high-grade stenosis or occlusion depends on collateral sources of blood flow. The anterior and posterior communicating arteries (ACoA, PCoA) provide most collateral flow in ICA and BA stenosis (primary collaterals), while distal pial and leptomeningeal anastomoses (secondary collaterals) are important in MCA stenosis [32]. DSA is the most valuable investigation that provides the assessment of collateral cerebral flow; Liebeskind and coworkers reporting that collateral flow on DSA was found to be absent in 69% of patients with symptomatic ICAS and it was also considered an independent predic-

Stroke risk, due to ICAD, increases with the arterial stenosis degree. Liebeskind and coworkers conducted a retrospective analysis of the baseline DSA acquired in the WASID trial, and they provided the first comprehensive evaluation of collaterals in modifying stroke risk in patients diagnosed with ICAD and its impact on subsequent stroke characteristics. They observed that the collateral circulation was adequately available for analysis in 287/569 patients from WASID (50%) subjects

According to Liebeskind, collateral brain circulation is one of the most significant factors that mediates the potentially devastating effects of cerebral ischemia. He asserted that patho-physiological recruitment of these collateral vessels (potential anastomotic connections) depends on the temporal course of numerous compensatory (hemodynamic, metabolic, and neural) mechanisms and on the caliber and patency of primary pathways that may rapidly compensate for decreased

**84**

blood flow and the adequacy of secondary collateral routes [30, 31]. He asserted that collaterals maintain perfusion downstream from arterial occlusions in acute stroke, determining the hemodynamic characteristics of the ischemic penumbra, the evolution of infarct, and susceptibility for hemorrhagic transformation [30]. He suggested that focal neurologic symptoms manifest only when collaterals fail. Regarding the therapeutic point of view, robust collaterals are an effective predictor of arterial recanalization and good clinical outcomes in acute stroke [31]. It is also well known that arterial occlusion secondary to progressive atherosclerotic stenosis of an intracranial segment allows the development of robust collaterals over time, unlike the cardioembolic or abrupt thrombotic occlusion. Collaterals and functional demonstration of flow impairment may be more informative than isolated anatomic measures of maximal stenosis or length [30].

Liebeskind concluded that collateral circulation is a powerful determinant of stroke risk in ICAD, demonstrating a protective role with severe stenoses and perhaps distinguishing milder stenoses that are relatively unstable [30, 31].
