Case 41 A 51-year-old man was admitted to the hospital with recurrent worsening of a pre-existing dysarthria which he had acquired 4 years earlier due to a left-sided rostral paramedian medullary infarction. The infarct, diagnosed in a different hospital, was assumed to be caused by a proximal basilar artery (BA) occlusion which showed collateralization from the anterior circulation. Furthermore, an asymptomatic left-sided internal carotid artery (ICA) occlusion was reported. Since then he had been treated with aspirin, a statin, and β-blockers. His neurologic examination showed a mild right-sided sensorimotor hemiparesis and dysarthria, the degree of which seemed unchanged. Arterial hypertension was his only known vascular risk factor. On admission, however, his systolic blood pressure was low, at ~100 mm Hg. Acute cerebral MRI was performed because of the posterior circulation pathology mentioned above. Diffusion-weighted images disclosed acute vascular lesions. FLAIR sequences showed a slim left paramedian rostral medullary infarct. On contrast-enhanced MR angiography (ce-MRA) the reported left ICA occlusion was confirmed. The vertebrobasilar arteries showed a left vertebral artery (VA) occlusion distal of the posterior cerebellar artery (PICA) origin, and a right-sided complete PICA-ending VA. The BA was visualized over its entire length with a small vessel lumen. Intracranial time-off-light (TOF) MRA showed reduced brightness of the left middle cerebral artery (MCA), indicative of hemodynamic restrictions and no BA and left V4-VA signal. Furthermore, a left fetal-type (FT) posterior cerebral artery (PCA) and a right posterior communicating artery (PCoA) could be identified (Fig. B41.1, Fig. B41.2, Fig. B41.3, Fig. B41.4). Recurrent brainstem ischemia of possible hemodynamic origin in severely impaired vertebrobasilar circulation and left-sided ICA occlusion. B-mode imaging showed moderate mixed echogenic plaques in both carotid bifurcations. A stenosis was seen in the right external carotid artery (ECA). The right common carotid artery (CCA) was wider than the contralateral CCA. No flow was detected in the left ICA. A markedly increased flow velocity and blood volume flow (BVF) of 630 mL/min was seen in the right ICA. The left V2-VA displayed normal diameter of 3.2 mm and the right VA a smaller diameter of 2.6 mm. Both vessels had a mildly increased pulsatility with a preserved diastolic flow (Figs. B41.5–B41.12). Transtemporal insonation on the right side revealed normal flow parameters in the M1-MCA and markedly increased flow velocities in the A1-ACA. The flow in the left-sided A1-ACA was retrograde and a moderately post-stenotic flow pattern was seen in the left M1-MCA. The anterior communicating artery (ACoA) revealed a functional stenosis. On both sides, a prominent PCoA was detectable with a flow toward the posterior circulation. On the right side, a prominent retrograde P1-PCA flow was detectable, which could be followed up to the reversed perfused distal BA. The right P2-PCA showed a normal flow signal. The left P2-PCA had a poststenotic flow pattern similar to the ipsilateral M1-MCA, so an FT-PCA was considered. Transforaminal insonation confirmed a retrograde BA flow with low flow velocities. Both V4-VA yielded flow signals different from the V2-VA flow signals, which was considered to be an angle-related phenomenon. The right ophthalmic artery (OA) revealed a normal antegrade flow. The left OA was internalized and had a retrograde flow (Figs. B41.13–B41.29; see also Video Fig. B41.1 MR T2-weighted images, axial plane, sagittal plane (top) and axial plane (bottom) revealing left paramedian rostral medullary infarction probably caused by intrinsic distal VA athero-sclerotic large-vessel disease (arrowhead, large arrow). Note that the lumen of the BA appears less affected (arrows). Fig. B41.2 Extracranial ce-MRA, coronal maximal intensity projection (MIP). Proximal left ICA occlusion (arrow), distal (post-PICA) left VA occlusion (large arrowhead) and PICA-ending right VA (small arrowhead). Note the BA is visible over its entire length. No information is given in regard to the flow direction (arrows). Fig. B41.3 Intracranial TOF-MRA, coronal MIP. Missing BA signal (arrows) suggestive of long segmental occlusion or flow reversal. Considering the findings of ce-MRA, a low flow state was assumed. Note the missing left distal VA and prominent right PICA signal (arrowhead). Fig. B41.4 Intracranial TOF-MRA, axial MIP. Left FT-PCA (arrowhead) and prominent right PCoA (large arrow). Note the prominent signals of the right P1-PCA and the BA head (short arrow). The reduced brightness of the left insular MCA branches indicates hemo-dynamic restriction (arrows). Fig. B41.5 Extracranial duplex, longitudinal plane. High-resistance flow pattern in the left CCA (flow velocity 61/14 cm/s, PI = 1.64). Fig. B41.6 Extracranial duplex, longitudinal plane. Pulsatile flow signal in the distal left CCA (flow velocity 15/0 cm/s) and missing flow signal in the left ICA. Note the missing delineation of the ICA intima-media complex, suggestive of old vessel occlusion (arrows). Fig. B41.7 Extracranial duplex, longitudinal plane. Normal flow parameters in the left ECA without indirect signs of collateral flow activation (flow velocity 104/24 cm/s, PI = 1.82). Fig. B41.8 Extracranial duplex, longitudinal plane. Right CCA with “internalized” flow signal including low pulsatility (flow velocity 74/41 cm/s, PI = 0.67). Fig. B41.9 Extracranial duplex, longitudinal plane. Increased flow velocity and BVF in the right ICA (flow velocity 100/56 cm/s, PI = 0.63, BVF 630 mL/min). The BVF nearly equals the normal global cerebral blood flow. Fig. B41.10 Extracranial duplex, longitudinal plane. Right ECA stenosis with turbulence and increased flow velocities (flow velocity 284/45 cm/s).
Right Internal Carotid Artery as the Remaining Patent Brain-supplying Artery
Clinical Presentation
Initial Neuroradiologic Findings
Suspected Diagnosis
Questions to Answer by Ultrasound Techniques
Neurosonologic Findings (Day 2)
Extracranial Duplex Sonography
Transcranial Duplex Sonography
B41.1).
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