15 Near-occlusion of the Right and High-grade Stenosis of the Left Extracranial Internal Carotid Artery

Near-occlusion of the Right and High-grade Stenosis of the Left Extracranial Internal Carotid Artery

Clinical Presentation

A 58-year-old man was admitted after suffering a transient left-sided weakness and confusion 3 hours before presentation. The symptoms had already completely resolved. The patient was a smoker and suffered from arterial hypertension, which had been treated for 15 years. The neurologic examination revealed no deficits.

Initial Neuroradiologic Findings

Cerebral MRI on the day of admission demonstrated a large anterior territorial infarction in the right middle cerebral artery (MCA) territory. Contrast-enhanced magnetic resonance angiography (ce-MRA) was consistent with a near-occlusion of the right internal carotid artery (ICA) with a marked poststenotic vessel collapse and a high-grade stenosis of the contralateral ICA. Intracranial time-of-flight (TOF) MRA showed only a weak signal in the right ICA and right MCA corresponding to the extracranial ICA near-occlusion. A small ipsilateral posterior communicating artery (PCoA) was seen. The nevertheless weak MCA signal indicated a compromised collateral pathway. The lower signal intensity of the left M1-MCA, compared with the ipsilateral posterior cerebral artery (PCA), also indicated impaired left-sided perfusion (Fig. B15.1 and Fig. B15.2).

Suspected Diagnosis

Right hemispheric transient ischemic attack (TIA) and large right MCA territorial infarction, probably caused by artery-to-artery embolism from right-sided near-occlusion of the ICA. Asymptomatic high-grade stenosis of the left ICA.

Questions to Answer by Ultrasound Techniques

Could the right ICA near-occlusion and the left high-grade ICA stenosis be confirmed?
What was the underlying vascular pathology?
What was the resulting intracranial collateral flow pattern?

Initial Neurosonologic Findings

Extracranial Duplex Sonography (Day 2)

B-mode imaging demonstrated bilateral atherosclerotic changes, predominantly with homogeneous hypoechoic plaques in both carotid bifurcations. There were no signs of arteritis. The right common carotid artery (CCA) displayed a mildly increased pulsatility. Both external carotid arteries (ECAs) had flow signals considered to be “internalized.” The right ICA showed a stump signal at the bulb. However, after adjusting the settings for low flow signals, i.e., reduced pulse repetition frequency (PRF) and increased gain, a severe turbulent flow with a flow velocity of 121/38 cm/s was detected slightly distal to the ICA bulb. Distal to that, the ICA was partly collapsed (diameter 3.1 mm) showing a marked poststenotic flow pattern and low velocities (14/5 cm/s). The left ICA revealed a stenotic flow signal with turbulence and a marked increased flow velocity (394/231 cm/s). The distal vessel segments displayed a spiculated flow signal but otherwise no signs of a hemodynamic restriction. Normal findings were seen in the vertebral arteries (VAs) (Fig. B15.3–Fig. B15.11; see also Video B15.1).

Transcranial Duplex Sonography

The right MCA and anterior cerebral artery (ACA) were antegrade perfused and presented a moderate post-stenotic flow pattern. A residual flow was seen in the C6-ICA. The ophthalmic artery (OA) had a marked retrograde flow (62/26 cm/s). Flow velocity in the right P1 segment of the PCA was higher than in the ipsilateral P2-PCA (79/35 cm/s versus 43/17 cm/s) indicating collateral flow via the PCoA. Accordingly, the PCoA was detected with a mild turbulent flow. On the left side, a more compromised anterior circulation was observed. The poststenotic flow pattern of the antegrade perfused M1-MCA and A1-ACA was more obvious. The A1-ACA revealed a high velocity indicating collateral flow (98/53 cm/s). The C6-ICA was markedly reduced in flow and revealing a severe poststenotic flow pattern. As on the right side, a marked retrograde flow was seen in the OA. Unlike the right side, no PCoA was seen and the P1- and P2-PCA segments had continuously increased systolic flow velocities ~80–90 cm/s, indicating leptomeningeal collateral flow. Accordingly, elevated flow velocities were seen in cortical PCA branches, the anterior temporal artery (ATA), and occipitotemporal artery (OTA). Normal flow patterns were seen in the vertebrobasilar arteries (Fig. B15.12–Fig. B15.27; see also Video B15.2).

Conclusion

Bilateral severe atherosclerotic macroangiopathy with near-occlusion of the right ICA and high-grade stenosis (>80% according to NASCET criteria, >90% according to ECST). Collateral blood flow to the right anterior circulation from the PCA via the PCoA and retrograde OA and to the left anterior circulation leptomeningeal via the ACA and PCA as well as via a retrograde OA.

Conventional Angiography (Day 3)

Because of the bilateral impaired anterior circulation perfusion we decided to treat the symptomatic right ICA by stenting without delay. Digital subtraction angiography (DSA) confirmed the near-occlusion of the right ICA. In the early arterial phase the ICA appeared occluded (similar to the initial duplex examination analyzing the carotid bulb). In the subsequent images (late arterial phase) the residual flow and the collapsed vessel were detected. DSA also confirmed the left high-grade ICA stenosis (Fig. B15.28).

Fig. B15.29 shows a schematic of the patient’s extra-and intracranial brain-supplying arteries before stenting of the right ICA.

Clinical Course (1)

The stenting proceeded uneventfully and the patient was started on aspirin and clopidogrel for 6 weeks. No ischemic events occurred. Notably, the patient and his wife reported that his neuropsychologic status, alertness, drive, and concentration had increased and had ameliorated even when compared with his status before stroke.

Follow-up Neurosonologic Findings (6 Weeks)

Extracranial Duplex Sonography

Doppler spectrum analysis showed a normalized flow in the right stented ICA segment without evidence of restenosis. The left high-grade ICA stenosis remained unchanged (Fig. B15.30 and Fig. B15.31).

Transcranial Duplex Sonography

The right ICA, MCA, ACA, and PCA segments as well as the right OA demonstrated normalized flow signals indicating adequate flow and remission of the PCoA activation. Interestingly, flow velocity of the right A1-ACA increased markedly. The left M1-MCA as well as A1-ACA and the PCA signals remained unchanged. The increased flow velocity in the right A1-ACA was therefore assumed to indicate leptomeningeal collateral flow to the left anterior circulation (Fig. B15.32, Fig. B15.33, Fig. B15.34, Fig. B15.35, Fig. B15.36).

Conclusion

Right ICA after stent insertion without residual stenosis and normalized right intracranial circulation. Unchanged left high-grade ICA. The left collateral circulation ameliorated slightly via the activation of the right A1-ACA.

Fig. B15.37 shows a schematic of the extra- and intracranial brain-supplying arteries after successful stenting of the right ICA.

Clinical Course (2)

Because of the patient’s relatively young age and the hypoechoic plaques, considered to increase the risk of further strokes, a stent was also inserted in the left ICA 2 months later. Since then, the patient has had no further ischemic attacks. Neuropsychologic testing revealed a significant improvement of his cognitive function, especially of his alertness, response time, and capability of readjustment.

Follow-up Neuroradiologic Findings (2 Months)

MRI showed no new ischemic or other lesion after the second intervention. TOF-MRA presented normalized findings with bright signals of both MCA and ACA now similar to the PCA signals. The right PCoA was no longer visible, indicating the abolished PCoA flow (Fig. B15.38).

Follow-up Neurosonologic Findings (3 Months)

Extracranial Duplex Sonography

Doppler spectrum analysis within the left ICA stent showed a normalized flow, and the pulsatility index (PI) of the left ECA had increased. The contralateral carotid artery remained unchanged (not shown).

Transcranial Duplex Sonography

Intracranial findings in the left ICA, MCA, ACA, PCA, and OA had normalized. Interestingly, flow velocities in the right C6-ICA and A1-ACA were lower than before, indicating the disappearance of the previous leptomeningeal collateral flow from the right A1-ACA to the left anterior circulation. Also, the proximal cortical branches of the left PCA (ATA and OTA) were no longer detected (Fig. B15.39–Fig. B15.47).

Fig. B15.1 (A) MR diffusion-weighted image, axial plane. Large, right-sided anterior territorial MCA infarction mostly sparing the basal ganglia and internal capsule. (B) Ce-MRA, left anterior oblique MIP. Signal gap in the right proximal ICA (arrow) and collapsed vessel up to the carotid siphon (small arrows) compatible with a near-occlusion. The left ICA shows a small signal gap (arrowhead) without distal vessel collapse (small arrowheads).

Fig. B15.2 Intracranial 3D TOF-MRA, axial MIP. Markedly reduced signal in the right A1-ACA and M1-MCA (small arrows). Note the right PCoA (arrow). The left A1-ACA and M1-MCA (arrowhead) presented a less reduced signal intensity compared with the right side but were also clearly affected if compared with the two bright PCA signals.

Fig. B15.3 Extracranial duplex, longitudinal plane. Doppler spectrum analysis revealed only a mild resistance flow signal in the right CCA (flow velocity 101/23 cm/s, PI = 1.6).

Fig. B15.4 Extracranial duplex, longitudinal plane. Right ECA shows a mildly increased diastolic, i.e., “internalized” blood flow signal (flow velocity: 128/29 cm/s, PI = 1.8).

Fig. B15.5 Extracranial duplex, longitudinal plane. Right ICA showing a stump signal in the bulb, suggestive of ICA occlusion.

Fig. B15.6 Extracranial duplex, longitudinal plane. Slightly more distal and after adjusting PRF to visualize low flow signals a stenotic flow signal with marked turbulence but not really high velocities can be detected in the right proximal ICA (flow velocity 121/38 cm/s).

Fig. B15.7 Extracranial duplex, longitudinal plane. Right midpart ICA showing a severe poststenotic flow pattern with reduced flow velocities (14/5 cm/s) in an almost collapsed vessel (diameter 3.1 mm).

Fig. B15.8 Extracranial duplex, longitudinal plane. Left CCA Doppler spectrum without any relevant prestenotic flow pattern (flow velocity 126/38 cm/s, PI = 1.3).

Fig. B15.9 Extracranial duplex, longitudinal plane. Left ECA shows a mildly increased diastolic, i.e., “internalized” blood flow signal (flow velocity 175/52 cm/s, PI = 1.5).

Fig. B15.10 Extracranial duplex, longitudinal plane. Left ICA demonstrating a severe stenotic flow signal with marked turbulences and increased flow velocities (394/231 cm/s).

Fig. B15.11 Extracranial duplex, longitudinal plane. Left ICA showing a spiculated flow signal shortly after the focal stenosis additionally indicating a high grade of stenosis (flow velocities 95/20 cm/s).

Fig. B15.12 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Mildly poststenotic flow pattern in the right M1-MCA (flow velocity 77/42 cm/s).