Case 12 A 79-year-old man, who had never sought medical attention before, was admitted with unusual dizziness that had occurred intermittently over the past 3 days. The patient had no vascular risk factors apart from a history of heavy smoking and alcohol abuse. The neurologic examination on admission revealed mild gait ataxia (National Institutes of Health Stroke Scale [NIHSS] score: 1). Unenhanced cranial CT was unremarkable. Diffusion-weighted (DW) MRI showed a small subacute right posterior inferior cerebellar artery (PICA) infarction at the cortical–subcortical border (Fig. B12.1). Intracranial time-of-flight MR angiography (TOF-MRA) showed bilateral internal carotid artery (ICA) and right-sided vertebral artery (VA) occlusion. No further intracranial pathology was observed. Contrast-enhanced (ce) MRA of the brain-supplying arteries revealed bilateral proximal ICA occlusions, a moderate distal stenosis of the left common carotid artery (CCA), and a high-grade stenosis of the left VA origin. The right VA signal was missing over the entire length of the artery (Fig. B12.2 and Fig. B12.3). Right-sided cerebellar ischemic infarction likely caused by a periocclusional artery-to-artery embolism in right distal VA occlusion. Clinically asymptomatic bilateral ICA occlusion and high-grade left proximal VA stenosis, likely caused by severe generalized extracranial atherosclerosis. B-mode sonography revealed generalized atherosclerosis in both carotid arteries. Both CCAs had a high-resistance flow signal with increased pulsatility. The left distal CCA showed a 40% local lumen reduction in the cross-sectional plane caused by a largely hypoechoic plaque. Despite this lumen reduction, no flow disturbances or increased flow velocities were observed. Flow was absent in both ICAs. The left ICA had a roughly 5 mm residual small-vessel lumen (“blind sack”). No residual lumen was observed in the right ICA. Both external carotid arteries (ECAs) had mildly internalized flow signals. The dominant left V2-VA (diameter 5.4 mm) had a mild poststenotic flow pattern. Nevertheless, flow velocities were high and the blood volume flow measured 580 mL/min. At the V1-VA segment, the flow was turbulent and had a flow velocity similar to the V2-VA. The origin was not detected. Only minimal systolic spikes were registered in the right V1- and V2-VA segments, which otherwise had a normal diameter (3.9 mm). No cervical spinal collaterals were observed throughout the entire V2-VA length (Figs. B12.4–B12.9). All intracranial vessels had mild poststenotic flow patterns. Blood flow in both anterior cerebral arteries (ACAs) was antegrade. Increased and turbulent flow velocities were seen in both P1-PCAs and posterior communicating arteries (PCoAs). This, in combination with the normal flow velocities in both P2-PCAs, was considered indicative of collateral flow function from the posterior toward the anterior circulation. Transforaminal insonation revealed a marked flow signal in the left V4-VA and basilar artery. On the right side, no proximal or distal V4-VA signals were observed. Transorbital insonation revealed a retrograde flow in both ophthalmic arteries (OAs) (Figs. B12.10–B12.18). Bilateral proximal extracranial ICA occlusion and distal right VA occlusion proximal to the PICA origin. Left proximal VA stenosis sonographically assumed to be of beginning hemodynamic relevance or a collateral flow due to the mild poststenotic downstream flow pattern. Considering the ce-MRA findings, the final diagnosis was determined to be a high-grade VA stenosis of incipient hemodynamic relevance. Intracranial collateral blood flow to both the middle cerebral artery (MCA) and ACA territories occurred primarily via both PCoAs, and to a lesser extent via both OAs. Fig. B12.19 shows a schematic of the patient’s extra-and intracranial brain-supplying arteries. Fig. B12.1 Diffusion-weighted MRI, axial plane, revealing a small fresh infarct in the right PICA territory (arrow). The patient was send to rehabilitation with aspirin and statin medication. There, his unsteadiness remitted but the dizziness remained. The etiology of the three and a half-vessel disease was severe atherosclerosis caused by severe, long-standing, combined heavy smoking and alcohol misuse. Stenting of the left VA stenosis was discussed but refused by the patient. Regular 6-month follow-ups revealed no further clinical events, and the neurosonologic findings remained unchanged over an observational period of 2 years. Fig. B12.2 3D MRA, coronal maximal intensity projection (MIP), TOFMRA (A) and contrast-enhanced (ce) MRA (B). Missing bilateral ICA signals. Prominent PCoA on both sides (arrowheads). Small right distal V4-VA filling, indicating a possible retrograde flow toward the PICA or to relevant V4-VA perforator arteries (arrow). Note that ce-MRA is superior to TOF-MRA in visualizing the right distal V4-VA lumen. Fig. B12.3 Extracranial 3D ce-MRA, coronal MIP, different views (A–C). Bilateral ICA occlusion with large residual lumen on the left ICA (A, arrowhead). Residual lumen of the distal right V4-VA (A, small arrow). Moderate CCA stenosis, best identified in B (large arrow). (C) Proximal left VA stenosis (arrow) and right ICA occlusion (arrowhead). Fig. B12.4 Extracranial duplex, longitudinal plane (left), and cross-sectional plane (right). Left CCA with 40% lumen reduction (arrows). Fig. B12.5 Extracranial duplex, longitudinal plane. Left ICA with a large “blind sack” several centimeters long and a weak, almost retrograde flow signal. Fig. B12.6 Extracranial duplex, longitudinal plane. Right ICA filled with homogeneous hypoechoic material (arrow). Fig. B12.7 Extracranial duplex, longitudinal plane. Mild poststenotic flow pattern in the dominant left V2-VA with marked increased blood volume flow (580 mL/min, diameter 5.4 mm).
Extracranial Bilateral Internal Carotid Artery and Right Vertebral Artery Occlusion, and Left Vertebral Artery Stenosis
Clinical Presentation
Initial Neuroradiologic Findings
Suspected Diagnosis
Questions to Answer by Ultrasound Techniques
Initial Neurosonologic Findings
Extracranial Duplex Sonography
Transcranial Duplex Sonography
Conclusion
Clinical Course

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