**Figure 1.**

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

**4.1 TCD/TCCS can detect, localize, and grade the severity of ICAS**

In clinical practice, interpretation of TCD data should be individualized, with various parameters (velocities values, spectrum, waveform patterns, flow pulsatility, collateral flows, status of extracranial arteries, systemic conditions: anemia, etc.) (**Tables 1** and **2**) [35]. TCD presents higher precision for identification of ICAS in the MCA and BA than in other intracranial arteries, due to the tortuosity in

> **Stenosis >70% (MFV, SPR)**

MCA >100 cm/s, >2 >120 cm/s, >3 <30 cm/s, <1 ACA >80 cm/s, >2 n.a., >3 <30 cm/s, <1 PCA >80 cm/s, >2 n.a., >3 <30 cm/s, <1 BA >90 cm/s, >2 >110 cm/s, >3 <20 cm/s, <1 VA >90 cm/s, >2 >110 cm/s, >3 <20 cm/s, <1 *MCA, middle cerebral artery; ACA, anterior cerebral artery; PCA, posterior cerebral artery; BA, basilar artery; VA,* 

*vertebral artery; MFV, mean flow velocity; n.a., not available; and SPR, stenotic/prestenotic MFV ratio.*

**Artery Mild stenosis Moderate stenosis Severe stenosis**

MCA >155 cm/s >220 cm/s +Indirect signs ACA >120 cm/s >155 cm/s +Indirect signs PCA >100 cm/s >145 cm/s +Indirect signs BA >100 cm/s >140 cm/s +Indirect signs VA >90 cm/s >120 cm/s +Indirect signs *MCA, middle cerebral artery; ACA, anterior cerebral artery; PCA, posterior cerebral artery; BA, basilar artery; VA,* 

**Stenosis <50% (PSV) Stenosis >50% (PSV) Stenosis >80%**

**Diffuse disease or near occlusion (MFV, SPR)**

blood flow steals.

the latter [33].

**Table 1.**

ICAS criteria are direct and indirect.

**SPR)**

*TCD criteria for intracranial stenosis (ICAS) [33].*

*vertebral artery; and PSV, peak systolic velocity.*

*TCCS criteria for intracranial stenosis (ICAS) [42].*

**Artery Stenosis >50% (MFV,** 

Transcranial ultrasound is used for multiple aims: TCD/TCCS can detect, localize, and grade the severity of ICAS; can detect and localize the intracranial arterial occlusion; can realize the real-time monitoring of recanalization in patients treated with systemic thrombolysis and of rescue reperfusion techniques (identification of reocclusion, hyper-perfusion syndrome, etc.); can detect clinically silent emboli: microembolic signals (MES), which recognizes patients at higher risk of embolic stroke; can recognize patients with extracranial internal carotid artery (ICA) stenosis at a higher stroke risk; can assess both collateral pathways and the vasomotor reactivity (VMR), which detects the risk stratification of hemodynamic stroke [22, 33, 37, 41]; and can identify intracranial arterial

**86**

**Table 2.**

*TCDS, transtemporal approach, axial midbrain plane, color mode (left M1 higher grade stenosis).*

**Figure 2.** *TCDS transtemporal approach, axial, midbrain plane, color mode (left C1 stenosis).*

Baracchini noted that, as a rule for a vessel with straight walls, a 50% diameter reduction double the velocity, and a 70% stenosis may triple the velocity at the end of the stenosis compared with a prestenotic segment or with the contralateral no affected side. The velocity values detected by TCCS are higher than those by TCD (due to angle correction) [35].

	- a.Only observed in very severe stenosis (>80%).
	- b.Are the same as for occlusion—proximal or distal flow alterations: a diastolic velocity drop; high RI in the feeding vessel or in the proximal segment of the stenotic vessel; a delayed systolic flow augmentation and velocity drop downstream; and flow diversion and signs of collateralization [35, 41–43].

TCD criteria for ICAS in anterior as well as posterior circulation have been validated against DSA, MRA, and CTA, and serve as reliable tools for their diagnosis (**Table 1**) [33].

The velocity criteria for ≥50% ICAS were detected by Feldmann and coworkers in (SONIA) trial [39], which standardized the data of TCD, MRA, and DSA. The cut points were the measures of continuous variables such as the percentage of stenosis on MRA or velocity on TCD for each intracranial arterial vessel:


SONIA trial established that both TCD and MRA could reliably exclude the presence of ICAS, rather than identifying them; abnormal findings on TCD or MRA requiring a confirmatory test such as DSA to diagnose ICAS [39].

The correlation between TCD and DSA for the identification of ≥50% ICAS at laboratories with (SONIA) TCD scanning protocol was established by Limin Zhao and coworkers [40]. Stenosis ≥50% on TCD was detected using an MFV >100 cm/s in the MCA, >90 cm/s in the intracranial ICA, or >80 cm/s in the VAs/BA. For ≥70% ICAS, they used expanded criteria (MFV-MCA >120 cm/s, MFV-VAs/BA >110 cm/s, stenotic/ prestenotic velocity/ratio-SPR ≥3, and low velocity). These criteria demonstrated excellent-to-good sensitivity of TCD and indicated good agreement with DSA [40].

Baumgartner and coworkers conducted a TCCS study that evaluated PSV cutoff values for the assessment of >50 and <50% stenosis of the intracranial arteries (**Table 2**) [42].

#### **4.2 TCD/TCCS can detect and localize the intracranial arterial occlusion**

Intracranial occlusion can be directly or indirectly detected by ultrasound examination.

**89**

**Figure 3.**

*Diagnosis of Symptomatic Intracranial Atherosclerotic Disease*

criteria of intracranial arterial occlusion) [35, 36, 43, 44].

a.Direct criteria for intracranial arterial proximal occlusion are diagnosed using the thrombolysis in brain ischemia (TIBI) flow-grading system. They include: no flow signal (TIBI 0) and minimal flow signal (TIBI 1), while blunted flow signal (TIBI 2) and dampened flow signal (TIBI 3) are criteria for distal occlusion (**Figure 3**). A missing flow signal could be occlusion or hypoplasia/aplasia (it is essential to use ultrasound contrast agents and to verify for indirect

b.Indirect criteria for intracranial arterial occlusion comprise proximal or distal flow alterations: a diastolic velocity drop; high RI in the feeding vessel or in the proximal segment of the stenotic vessel; a delayed systolic flow augmentation and velocity drop downstream; and flow diversion and signs of collateraliza-

**4.3 TCD/TCCS can realize the real-time monitoring of recanalization in acute ischemic stroke patients treated with systemic thrombolysis and of rescue reperfusion techniques (identification of reocclusion, hyperperfusion** 

Absent flow (TIBI 0): no flow signals; or lack of regular pulsatile flow signals (using lowest pulse repetition frequency-PRF and increased color-gain settings). Minimal (TIBI I): systolic spikes of variable velocity and duration; and absent

Blunted (TIBI II): flattened or delayed systolic flow acceleration compared with control side; positive end-diastolic velocity (EDV); and pulsatility index

Dampened (TIBI III): normal systolic flow acceleration; positive EDV; and

>30% decrease in mean flow volume (MFV) compared with control side.

TCD/TCCS can detect the residual flow at thrombus-blood interface. The TIBI flow grading system, TIBI: 0–5, was elaborated to identify residual

flow and to monitor thrombus dissolution in real time [37, 43–45].

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

tion (**Figure 4**) [33–38].

diastolic flow during all cardiac cycles.

*Thrombolysis in brain ischemia (TIBI) flow-grading system.*

**syndrome, etc.)**

(PI) <1.2.

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

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

vessel segments after angle correction) [35].

**B.** Indirect criteria (changes observed in other arteries):

a.Only observed in very severe stenosis (>80%).

(due to angle correction) [35].

sis (**Table 1**) [33].

and VA 130 [39].

vessel:

Baracchini noted that, as a rule for a vessel with straight walls, a 50% diameter reduction double the velocity, and a 70% stenosis may triple the velocity at the end of the stenosis compared with a prestenotic segment or with the contralateral no affected side. The velocity values detected by TCCS are higher than those by TCD

c.A significant (>30%) side-to-side difference of velocity (for symmetrical

b.Are the same as for occlusion—proximal or distal flow alterations: a diastolic velocity drop; high RI in the feeding vessel or in the proximal segment of the stenotic vessel; a delayed systolic flow augmentation and velocity drop downstream; and flow diversion and signs of collateralization [35, 41–43].

TCD criteria for ICAS in anterior as well as posterior circulation have been validated against DSA, MRA, and CTA, and serve as reliable tools for their diagno-

ers in (SONIA) trial [39], which standardized the data of TCD, MRA, and DSA. The cut points were the measures of continuous variables such as the percentage of stenosis on MRA or velocity on TCD for each intracranial arterial

The velocity criteria for ≥50% ICAS were detected by Feldmann and cowork-

a.MRA ≥50% stenosis, without occlusion, or the presence of a flow gap defined a positive test. Stenosis ≥50% on TCD was identified using an MFV >100 cm/s in MCA, >90 cm/s in the intracranial ICA, or >80 cm/s in the BA or VAs [39].

70–99% DSA stenosis of different arteries were: MCA 240, ICA 130, BA 130,

b.For 80% stenosis on MRA, the SONIA TCD-MFV (cm/s) cut points for

SONIA trial established that both TCD and MRA could reliably exclude the presence of ICAS, rather than identifying them; abnormal findings on TCD or MRA

The correlation between TCD and DSA for the identification of ≥50% ICAS at laboratories with (SONIA) TCD scanning protocol was established by Limin Zhao and coworkers [40]. Stenosis ≥50% on TCD was detected using an MFV >100 cm/s in the MCA, >90 cm/s in the intracranial ICA, or >80 cm/s in the VAs/BA. For ≥70% ICAS, they used expanded criteria (MFV-MCA >120 cm/s, MFV-VAs/BA >110 cm/s, stenotic/ prestenotic velocity/ratio-SPR ≥3, and low velocity). These criteria demonstrated excellent-to-good sensitivity of TCD and indicated good agreement with DSA [40]. Baumgartner and coworkers conducted a TCCS study that evaluated PSV cutoff

values for the assessment of >50 and <50% stenosis of the intracranial arteries

**4.2 TCD/TCCS can detect and localize the intracranial arterial occlusion**

Intracranial occlusion can be directly or indirectly detected by ultrasound

requiring a confirmatory test such as DSA to diagnose ICAS [39].

**88**

(**Table 2**) [42].

examination.


TCD/TCCS can detect the residual flow at thrombus-blood interface.

The TIBI flow grading system, TIBI: 0–5, was elaborated to identify residual flow and to monitor thrombus dissolution in real time [37, 43–45].

Absent flow (TIBI 0): no flow signals; or lack of regular pulsatile flow signals (using lowest pulse repetition frequency-PRF and increased color-gain settings).

Minimal (TIBI I): systolic spikes of variable velocity and duration; and absent diastolic flow during all cardiac cycles.

Blunted (TIBI II): flattened or delayed systolic flow acceleration compared with control side; positive end-diastolic velocity (EDV); and pulsatility index (PI) <1.2.

Dampened (TIBI III): normal systolic flow acceleration; positive EDV; and >30% decrease in mean flow volume (MFV) compared with control side.

**Figure 3.** *Thrombolysis in brain ischemia (TIBI) flow-grading system.*

**Figure 4.**

*TCDS, transtemporal approach, axial midbrain plane, color mode (right proximal ICA occlusion, with right M1-MCA poststenotic flow pattern).*

Stenotic (TIBI IV): MFV >80 cm/s and velocity difference >30% compared with control side; if the velocity difference is <30%, look for additional signs of stenosis; and affected and comparison sides have MFV <80cm/s.

Normal (TIBI V): <30% MFV difference compared with control side; and similar wave form shapes compared with control side [37, 43–45].

TIBI flow grades I–III correspond to acute proximal intracranial artery occlusion, while a TIBI flow grade of IV is an indicative of proximal artery hemodynamically significant (>50%) stenosis.

The assessment of the diagnostic value of transcranial power motion-mode Doppler (PMD-TCD) against computed tomography angiography (CTA) in patients with acute ischemic stroke was evaluated by Tsivgoulis and coworkers. They asserted that PMD-TCD detected a substantial proportion of ICAS or occlusions, in concordance with CTA in patients with acute ischemic stroke. PMD-TCD identified data supplementary to the CTA: collateralization of flow with extracranial ICA stenosis/occlusion; real-time embolization-MES; and arterial blood flow steal [45].

The evaluation of the diagnostic value of PMD-TCD against DSA in the detection of acute posterior circulation steno-occlusive disease was realized by Tsivgoulis and coworkers. They showed that the higher value of PMD-TCD compared with single-gate TCD may be associated with its ability to observe flow on the PMD display along tortuous and long arterial segments that may not be readily identified by sonographers during a single-gate TCD exam. In conclusion, PMD-TCD can exclude vertebro-basilar artery occlusion and can select patients for DSA and endovascular interventions if the sonographers are confirmed by DSA [46].

An acute arterial occlusion differs from chronic as it is often partial and incomplete and exhibits dynamic processes (partial obstruction to flow, thrombus propagation, reocclusion, and sometimes spontaneous recanalization). TCD can rapidly identify patients with these lesions and detect not only the flow-limiting lesion but also the ongoing embolization, the collateralization, and the failure of the vasomotor reserve [37].

**91**

syndrome).

distal vessels) [33–35].

*Diagnosis of Symptomatic Intracranial Atherosclerotic Disease*

bilateral arteries indicates a cardiac origin [33, 41, 47].

CTA, MRA, or DSA [33, 36, 38].

**4.4 TCD can identify clinically silent emboli: microembolic signals (MES),** 

MES detection in different interventional procedures (cerebral and coronary angiography, angioplasty, carotid endarterectomy, etc.) and in patients with extra and intracranial large artery atherosclerotic stenosis is useful in risk stratification, thus enabling to select those patients who could benefit from a more aggressive treatment [33, 41, 47]. MES detection requires continuous monitoring (at least 1 hour) of the major intracranial arteries. Most MES can be detected several days after the embolic event. The origin of emboli is important; the detection of an embolic signal in the distal MCA might represent an atherosclerotic plaque in the ipsilateral MCA or ICA. On the other hand, the identification of MES in multiple

**4.5 TCD can recognize patients with extracranial ICA stenosis at a higher stroke risk, can assess both collateral pathways, and the vasomotor reactivity (VMR), which detects patients at higher risk of hemodynamic stroke**

Severe extracranial ICA stenosis may produce embolic or hemodynamic hemispheric infarct [48]. While the risk of an embolic ischemic stroke increases with the severity of ICA's stenosis, the hemodynamic risk correlates less well with the degree of stenosis because of the functional capacity of the collateral pathways [48]. A complete circle of Willis and the possibility to activate primary collaterals (anterior communicating artery-ACoA, posterior communicating artery-PCoA) or secondary collaterals (ophthalmic artery-OA, lepto-meningeal arteries) reduce the risk of hemodynamic infarct ipsilateral to the extracranial ICA disease [33, 36, 38]. In patients with collateral flow signals (reversed OA, anterior cross-filling, and PCoA flow) identified by TCD, proximal ICA occlusion is confirmed by subsequent neck

Vasomotor reactivity (VMR) defines the autoregulatory vasodilation of cerebral vessels in response to a vasodilatory challenge, such as hypercapnia or acetazolamide (apnea test, breath-holding test, and Diamox test). VMR represents a measure of dynamic cerebrovascular reserve capacity. Its study recognizes patients at higher risk of hemodynamic stroke, in both intra and extracranial large vessel disease, thus allowing to select those patients who could benefit from a more aggressive treatment [38, 48]. According to Prabhakaran, the presence of MES, poor collateral flow, and impaired VMR predict the high risk of recurrence in intracranial atherosclerosis [41]. TCD can identify intracranial arterial blood flow steals (reversed Robin Hood

Intracranial arterial blood flow steals can be detected in chronic disease (e.g., subclavian artery stenoses, arterio-venous malformations, and fistulas) but also in patients with acute ischemic stroke. Flow diversion is the hallmark of a steal and can appear at any level of the intracranial arteries (large proximal vessels and small

ICAD includes two major features: (a) atherosis caused by lipid deposits in the intima of the arteries and inflammation; and (b) sclerosis, as a result of endothelial

**5. Magnetic resonance angiography (MRA) and high-resolution magnetic resonance imaging (HR-MRI) for the diagnosis of** 

**intracranial atherosclerotic disease (ICAD)**

dysfunction, leading to arterial stiffness [49].

**which recognizes patients at higher risk of embolic stroke**

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

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

Stenotic (TIBI IV): MFV >80 cm/s and velocity difference >30% compared with control side; if the velocity difference is <30%, look for additional signs of stenosis;

*TCDS, transtemporal approach, axial midbrain plane, color mode (right proximal ICA occlusion, with right* 

Normal (TIBI V): <30% MFV difference compared with control side; and

TIBI flow grades I–III correspond to acute proximal intracranial artery occlusion, while a TIBI flow grade of IV is an indicative of proximal artery hemodynami-

The assessment of the diagnostic value of transcranial power motion-mode Doppler (PMD-TCD) against computed tomography angiography (CTA) in patients with acute ischemic stroke was evaluated by Tsivgoulis and coworkers. They asserted that PMD-TCD detected a substantial proportion of ICAS or occlusions, in concordance with CTA in patients with acute ischemic stroke. PMD-TCD identified data supplementary to the CTA: collateralization of flow with extracranial ICA stenosis/occlusion; real-time embolization-MES; and arterial blood flow

The evaluation of the diagnostic value of PMD-TCD against DSA in the detection of acute posterior circulation steno-occlusive disease was realized by Tsivgoulis and coworkers. They showed that the higher value of PMD-TCD compared with single-gate TCD may be associated with its ability to observe flow on the PMD display along tortuous and long arterial segments that may not be readily identified by sonographers during a single-gate TCD exam. In conclusion, PMD-TCD can exclude vertebro-basilar artery occlusion and can select patients for DSA and endovascular

An acute arterial occlusion differs from chronic as it is often partial and incomplete and exhibits dynamic processes (partial obstruction to flow, thrombus propagation, reocclusion, and sometimes spontaneous recanalization). TCD can rapidly identify patients with these lesions and detect not only the flow-limiting lesion but also the ongoing embolization, the collateralization, and the failure of the

and affected and comparison sides have MFV <80cm/s.

cally significant (>50%) stenosis.

*M1-MCA poststenotic flow pattern).*

similar wave form shapes compared with control side [37, 43–45].

interventions if the sonographers are confirmed by DSA [46].

**90**

vasomotor reserve [37].

steal [45].

**Figure 4.**
