Case 11 A 43-year-old man complained of transient right-sided weakness, amnesic aphasia, and decreased visual acuity in his left eye that started while he was undertaking exercise in a gym. The symptoms gradually faded over 15 minutes. The patient had no vascular risk factors except for a known migraine with aura. On admission to our hospital he was free of symptoms. Headaches were not reported. The neurologic examination revealed a mild left-sided Horner’s syndrome. There were no other focal neurologic deficits. Cerebral MRI on the day of admission showed no ischemic parenchymal lesion but perfusion imaging revealed a pronounced hypoperfusion within the left middle cerebral artery (MCA) territory and both anterior cerebral artery (ACA) territories. Time-of-flight MR angiography (TOF-MRA) showed reduced signal intensity in the left distal internal carotid artery (ICA), left MCA, and both ACAs, as well as an aplasia or severer hypoplasia of the right A1-ACA segment and both posterior communicating arteries (PCoAs) (Fig. B11.1 and Fig. B11.2). The cervical vessels were not examined, yet axial T2-weighted images at the level of the skull base suggested an intramural hematoma of the left ICA. Dissection of the left ICA. B-mode ultrasound did not show atherosclerosis or other structural vessel abnormalities and no direct signs of vessel dissection. Color-mode imaging of the left ICA demonstrated a tapering lumen and reduced color signal intensity. Doppler spectrum analysis revealed a pronounced reduction of flow velocity (28/8 cm/s) in contrast with the contralateral side (78/26 cm/s) (Fig. B11.3 and Fig. B11.4; see also Video A poststenotic flow pattern was observed in the left carotid siphon, the left M1-MCA segment, and the left A1-ACA segment. No right A1-ACA segment and no flow signal in the presumed area of both PCoAs were detected. The flow direction in the left OA was reversed and showed a high diastolic flow component similar to that of a brain-supplying artery. The right OA was normal. Assessment of the posterior circulation was unremarkable and without evidence of collateral leptomeningeal flow (Figs. B11.5– B11.10; see also Videos Suspected dissection of the left ICA with high-grade stenosis of hemodynamic relevance below the OA origin. Insufficient intracranial collateral blood flow toward the left MCA and both ACA territories solely via the left OA. Intravenous heparin was started, aiming for a doubling of partial thromboplastin time (PTT). During the patient’s first night in hospital, he developed a severe right-sided brachiofacial paresis and a global aphasia. Laboratory monitoring revealed a fourfold increase in PTT. Intracranial bleeding was ruled out by a CT scan. B-mode imaging of the left ICA remained unchanged. However, Doppler spectrum analysis now demonstrated a high-resistance flow signal with a low and short systolic flow and completely absent diastolic flow component indicating distal ICA occlusion proximal to the OA origin (Fig. B11.11). A worsened poststenotic flow pattern was observed in the left M1-MCA and A1-ACA segments. Furthermore, there was an increase of retrograde flow in the left OA. Raised flow velocity in the left P2/3-PCA segments, previously not observed, indicated leptomeningeal collateral flow from the PCA to the left anterior territory (Fig. B11.12, Fig. B11.13, Fig. B11.14, Fig. B11.15). Secondary distal occlusion of the left ICA. Further worsening of the pre-existing insufficient blood flow in the left MCA and both ACA territories. Collateralization via the left OA and in addition via leptomeningeal collaterals from the left PCA. Fig. B11.16 shows a schematic drawing of the extra-and intracranial brain-supplying arteries. CT angiography (CTA) demonstrated a left intracranial ICA occlusion in its petrosal part. The beginning of the dissection was assumed to be located in the midcervical extracranial ICA (Fig. B11.17). None of the studied intraand extracranial arteries showed evidence of fibromuscular dysplasia. Under hypervolemic treatment the aphasia and the hemiparesis improved slowly over subsequent days. Six days after admission, cerebral MRI revealed a large internal border zone infarction (BZI) between the left ACA and MCA territories (Fig. B11.18). Partial reopening of the left ICA was seen, now demonstrating a flow signal similar to that on day 1 (Fig. B11.19; see also Video A continuing poststenotic flow pattern was seen within the left M1-MCA and A1-ACA segments. However, flow velocities had slightly increased. The OA flow was still reversed indicating a persisting hemodynamically relevant ICA obstruction below the origin of the OA (Fig. B11.20; see also Video Partial reopening of the distal ICA with a remaining hemodynamically relevant high-grade stenosis. The result is equivalent to the neurosonologic findings on admission. Treatment was changed from heparin to continuous oral anticoagulation with phenprocoumon. Three weeks after admission the patient was clinically stable and was discharged with a moderate right-sided paresis and motor aphasia. The left ICA had normalized (Fig. B11.21; see also Video The left MCA and ACA as well as the PCAs demonstrated normalized flow velocities and pulsatility. The flow direction of the left OA was now antegrade (Fig. B11.22, Fig. B11.23, Fig. B11.24, Fig. B11.25; see also Video Flow normalization in the left ICA without signs of intracranial collateral blood flow, indicating hemodynamic normalization. Spontaneous dissection of the left ICA in a patient with unfavorable cerebral arterial circle (circle of Willis) due to a nonfunctional right A1-ACA and nonfunctional bilateral PCoAs. Secondary transient occlusion, presumably triggered by anticoagulation with intravenous heparin, leading to internal BZI. Fig. B11.1 (A) MRI, apparent diffusion coefficient (ADC) map, axial plane. No signs of cytotoxic edema. (B) MR T2* perfusion image (time-to-peak map), axial plane. Pronounced hypoperfusion indicated by a brighter signal within the left MCA and both ACA territories. Fig. B11.2 3D TOF-MRA, axial maximal intensity projection (MIP). Reduced signal intensity in the left intracranial ICA (arrows), left MCA (large arrowhead), and ACA (small arrowhead) indicating reduced flow in these vessels. Note the missing signals in the right A1-ACA (arrow) and the PCoAs, suggesting aplasia or severe hypoplasia. Fig. B11.3 Extracranial duplex, longitudinal plane. Tapering vessel size and pronounced reduction of blood flow in the left ICA distal of the bifurcation (flow velocity 28/8 cm/s). Fig. B11.4 Extracranial duplex, longitudinal plane. Right ICA with normal flow signal (flow velocity 78/26 cm/s). Fig. B11.5 TCCS (transtemporal approach), left-sided insonation midbrain/thalamic plane. Poststenotic flow pattern in the left M1-MCA (flow velocity 31/20 cm/s). Fig. B11.6 TCCS (transtemporal approach), left-sided insonation, midbrain plane. Poststenotic flow pattern in the left A1-ACA (flow velocity 32/20 cm/s). Note that the correct PI is 0.5. Fig. B11.7 TCCS (transtemporal approach), right-sided insonation midbrain plane. Normal flow in the right M1-MCA (flow velocity 94/46 cm/s). Fig. B11.8 TCCS (transorbital approach), left-sided insonation. Reversed flow direction and increased flow velocity in the left OA (flow velocity 70/40 cm/s). Fig. B11.9 TCCS (transorbital approach), right-sided insonation. Normal flow direction in the right OA (flow velocity 65/20 cm/s). Fig. B11.10 TCCS (transtemporal approach), left-sided insonation, thalamic plane. Normal flow velocity in the distal left P2-PCA (flow velocity 46/28 cm/s). Fig. B11.11 Extracranial duplex, longitudinal plane. High-resistance flow signal with a low and short systolic flow and completely absent diastolic flow component considered to correspond to distal left ICA occlusion proximal to the OA origin. Fig. B11.12 TCCS (transtemporal approach), left-sided insonation, midbrain plane. Further worsening of the pre-existing marked compromised poststenotic flow pattern in the left M1-MCA (flow velocity 25/14 cm/s). Note the positive oscillation effect caused by slight digital tapping of the left optic bulb (arrows). Fig. B11.13 TCCS (transtemporal approach), left-sided insonation, midbrain plane. Similar worsened poststenotic flow pattern in the left A1-ACA (flow velocity 25/10 cm/s). Fig. B11.14 TCCS (transtemporal approach), left-sided insonation, midbrain/thalamic plane. Increased flow velocity in the left distal P2-PCA indicating leptomeningeal collateral flow (flow velocity 122/53 cm/s). Fig. B11.15 TCCS (transorbital approach), left-sided insonation. Further increase of the reversed flow in the left OA (flow velocity 97/54 cm/s). Fig. B11.16 Schematic of this patient’s extra- and intracranial brain-supplying arteries. Note the left distal ICA occlusion (circle). Collateral blood flow is via the left ECA and retrograde OA toward the left MCA and ACA as well as to the right ACA territory. There is additional leptomeningeal collateralization of the left MCA territory after secondary occlusion via the left PCA (green arrow).
Secondary Occlusion in Left-sided Extracranial Internal Carotid Artery Dissection
Clinical Presentation
Initial Neuroradiologic Findings
Suspected Diagnosis
Questions to Answer by Ultrasound Techniques
Initial Neurosonologic Findings (Day 1)
Extracranial Duplex Sonography
B11.1). The external carotid artery (ECA) had an increased diastolic, i.e., an “internalized,” blood flow pattern. Assessment of the vertebral arteries (VAs) was normal.
Transcranial Duplex Sonography
B11.2 and B11.3).
Conclusion
Clinical Course (1)
Questions to Answer by Ultrasound Techniques
Follow-up Neurosonologic Findings (Day 2)
Extracranial Duplex Sonography
Transcranial Duplex Sonography
Conclusion
Clinical Course (2)
Follow-up Neurosonologic Findings (Day 7)
Extracranial Duplex Sonography
B11.4).
Transcranial Duplex Sonography
B11.5 and B11.6).
Conclusion
Clinical Course (3)
Follow-up Neurosonologic Findings (6 Months)
Extracranial Duplex Sonography
B11.7).
Transcranial Duplex Sonography
B11.8).
Conclusion
Final Diagnosis
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