Case 28 A 50-year-old woman was admitted to the emergency department with acute weakness of her left arm, left drooping lip, and slurred speech. She had woken up with these symptoms that morning. One year previously, she had had two transient episodes of left-sided hemihypesthesia, each lasting about 20 minutes. She had multiple vascular risk factors including arterial hypertension, hypercholesterolemia, and heavy smoking. On admission, the neurologic examination revealed left-sided supranuclear facial palsy, mild left-sided sensorimotor hemiparesis, and dysarthria (National Institute of Health Stroke Scale [NIHSS] score: 6). Cranial CT demonstrated early signs of extended right-sided territorial middle cerebral artery (MCA) infarction, which was confirmed by MRI. Time-of-flight MR angiography (TOF-MRA) depicted absent signals of the right internal carotid artery (ICA) and right MCA and a prominent right posterior communicating artery (PCoA) (Fig. B28.1 and Fig. B28.2). Ischemic right-sided MCA infarction in ICA and M1-MCA occlusion. Thrombolysis was not performed because the unknown time of stroke onset (wake-up stroke) and because of the CT findings visualizing ischemia in more than one-third of the MCA territory. B-mode imaging revealed severe atherosclerotic changes in extracranial vessels with distinct accentuation in the right carotid bifurcation. A high-resistance flow signal with reduced flow velocity and increased pulsatility was seen in the right common carotid artery (CCA). The right external carotid artery (ECA) was normal. No flow signal was seen in the right ICA. Both vertebral arteries (VAs) were of normal caliber in the V2 segment (left, 4.1 mm; right, 3.9 mm). Flow assessment of the left VA demonstrated an almost retrograde flow with only a minimal diastolic flow component. Upper arm compression test with a blood pressure cuff (pressure above the systolic blood pressure) led to a bidirectional flow signal with retrograde systolic and antegrade diastolic flow component. Release of the pressure cuff (reactive hyperemia of the arm) led to completely retrograde flow. Increased flow velocities but otherwise normal flow signals were seen in all detectable segments of the right VA. Both V0-VA segments and the subclavian arteries (SAs) could not be visualized (Figs. B28.3–B28.9; see also Video The right M1-MCA and A1-ACA segments revealed an obvious poststenotic flow pattern with antegrade A1-ACA flow. A positive oscillation effect in the right MCA was seen during slight tapping of the right VA at the level of the atlas loop. Marked turbulence including a musical murmur was observed in the right PCoA at its junction with the PCA. On the left side a strong antegrade A1-ACA segment was seen (flow velocity 142/74 cm/s). The anterior communicating artery (ACoA) was not visible. The left M1-MCA segment was normal (flow velocity 110/60 cm/s). The right P1-PCA had a markedly increased flow velocity (160/100 cm/s). Both P2- and P3-PCA segments had flow velocities at normal ranges with a post-stenotic flow pattern. Transforaminal insonation revealed a nearly complete retrograde systolic flow component in the left V4-VA segment similar to the extracranial findings and a normal antegrade flow in the right V4-VA segment. The basilar artery (BA) showed a poststenotic flow pattern. On transorbital insonation, the right OA could not be seen (Fig. B28.10–B28.19; see also Video Intravenous administration of 1 g acetazolamide induced a 31% increase of mean flow velocity above baseline levels in the left M1-MCA and an 8% decrease in the right M1-MCA, indicative of a steal phenomenon (Fig. B28.20). Severe atherosclerotic vascular changes with proximal occlusion of the right extracranial ICA but with a patent right MCA. Insufficient intracranial collateral blood flow toward the right MCA and ACA via the right PCoA. Additional collateral flow toward the right ACA via the left ACA (double filling). Furthermore, indirect signs of left proximal SA occlusion or high-grade stenosis with asymptomatic subclavian steal phenomenon grade III. Notably, the right VA was the only patent vessel providing blood flow, not only to the total posterior circulation but also to the right anterior circulation and to the left arm. Digital subtraction angiography (DSA) confirmed the proximal occlusion of the right ICA and the collateralization of the right MCA territory via the right PCoA. On selective left ICA injection, double filling of both A2-ACA segments via the left A1-ACA segment was observed. In addition, a left SA occlusion was detected and the subclavian steal phenomenon was confirmed (Figs. B28.21–B28.26). A periocclusional embolism on the basis of severe atherosclerosis originating from the right ICA with spontaneous recanalization was thought to be the cause of the MCA infarction. Subsequently, long-term secondary stroke prevention was started with aspirin. Because of the impaired intracranial collateralization, mildly hypertensive blood pressure values were tolerated. A right EC–IC bypass was discussed but the decision was postponed until re-examination of cerebrovascular reactivity (CVR) and evaluation of the clinical course 4 weeks later. During the hospital stay, the left-sided hemiparesis improved markedly. Assessment of the extracranial arteries remained unchanged demonstrating the right-sided ICA occlusion and left-sided subclavian steal phenomenon (not shown). Unchanged intracranial findings (not shown). A 52% acetazolamide induced flow increase was seen in the left M1-MCA. The right M1-MCA demonstrated a 16% flow decrease (not shown). Right extracranial ICA occlusion with unchanged intracranial collateralization mainly via the right PCoA. Unchanged asymptomatic subclavian steal phenomenon grade III on the left side. Worsened CVR implicating an increased risk of developing hemodynamic ischemia. Fig. B28.27 shows a schematic of the patient’s extra-and intracranial brain-supplying arteries. A right-sided STeA–MCA bypass was performed. The intervention was uneventful and the angiographic control immediately after surgery showed a patent collateral vessel (not shown). CT revealed no intracranial bleeding and no new ischemic brain damage. Long-term stroke prevention with clopidogrel was recommended. Follow-up over a 4-year period revealed no further ischemic events. Periocclusional right territorial MCA infarction caused by an occlusion of the right ICA. Impaired intracranial collateralization with cross-flow via the ACoA only to the contralateral ACA territory and insufficient collateral flow to the MCA via the ipsilateral PCoA, complicated by a left subclavian steal phenomenon. Successful insertion of an STeA–MCA bypass on the right side. Fig. B28.1 Cerebral MR T2-weighted image, axial plane. Right partial territorial MCA infarction sparing the basal ganglia. Fig. B28.2 3D TOF-MRA, axial maximal intensity projection (MIP). Absent right ICA signal and large signal gap in the course of the right MCA (arrows) suggestive of distal M1-MCA and ICA occlusion. Note the prominent distal ICA perfused by the right PCoA (arrowhead). Fig. B28.3 Extracranial duplex, longitudinal plane. Normal left CCA flow (flow velocity 76/35 cm/s, PI = 1.25). Fig. B28.4 Extracranial duplex, longitudinal plane. Resistance flow signal with reduced velocity and increased pulsatility in the right CCA (flow velocity 33/15 cm/s, PI = 1.39). Fig. B28.6 Extracranial duplex, longitudinal plane. Retrograde systolic flow with at best minimal antegrade diastolic flow in the normally developed left V2-VA (diameter 4.1 mm, flow velocity 84/0 cm/s). Fig. B28.7 Extracranial duplex, longitudinal plane. Increased antegrade flow in the normally developed right V2-VA (diameter 3.9 mm, flow velocity 160/88 cm/s). Fig. B28.8 Extracranial duplex, longitudinal plane. Left V2-VA during upper arm compression, induced by a blood pressure cuff inflated to more than the systolic blood pressure (arrow), leading to a bidirectional flow signal with antegrade diastolic flow. Fig. B28.9 Extracranial duplex, longitudinal plane. Left V2-VA after the release of upper arm compression (arrow) leading to reactive hyperemia and completely retrograde flow. Fig. B28.10 TCCS (transtemporal approach), left-sided insonation, midbrain plane. Almost normal flow signal in the left M1-MCA (flow velocity 110/60 cm/s). Fig. B28.11 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Distinct poststenotic flow pattern in the right M1-MCA (flow velocity 55/35 cm/s). Fig. B28.12 TCCS (transtemporal approach), left-sided insonation, midbrain plane. Marked but otherwise normal flow in the left A1-ACA indicating collateral flow (flow velocity 142/74 cm/s). Fig. B28.13 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Antegrade flow with a poststenotic flow pattern in the right A1-ACA identical to the pattern of the right M1-MCA (flow velocity 52/33 cm/s). Fig. B28.14 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Musical murmurs in the right PCoA at the junction with the PCA indicating functional stenosis.
Subclavian Steal in Left Subclavian Artery and Right Internal Carotid Artery Occlusion Leading to Extracranial–Intracranial Bypass Surgery
Clinical Presentation
Initial Neuroradiologic Findings
Suspected Diagnosis
Questions to Answer by Ultrasound Techniques
Initial Neurosonologic Findings (Day 1)
Extracranial Duplex Sonography
B28.1).
Transcranial Duplex Sonography
B28.2).
Cerebrovascular Reactivity Testing
Conclusion
Conventional Angiography (Day 2)
Clinical Course (1)
Follow-up Neurosonologic Findings (4 Weeks)
Extracranial Duplex Sonography
Transcranial Duplex Sonography
Cerebrovascular Reactivity Testing
Conclusion
Clinical Course (2)
Final Diagnosis
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