Case 22 A 41-year-old woman was admitted to the emergency department with acute weakness of her left arm and leg. The symptoms had commenced 1 hour prior to presentation while she had been walking. No headaches were reported. The patient had no vascular risk factors except that she experienced about two migraine attacks with visual aura per month. On neurologic examination, the woman had left-sided supranuclear facial palsy, gaze deviation to the right side, and marked left sensorimotor hemiparesis (National Institute of Health Stroke Scale [NIHSS] score: 12). Emergency unenhanced cranial CT revealed mild early signs of infarction comprising less than one-third of the right middle cerebral artery (MCA) territory and a dense media sign. Perfusion CT showed a pronounced perfusion deficit within the right hemisphere. CT angiography (CTA) depicted a right proximal M1-MCA occlusion. On the basis of these findings and after considering exclusion criteria, intravenous thrombolysis with recombinant tissue plasminogen activator (IV rt-PA) was performed (Fig. B22.1, Fig. B22.2, Fig. B22.3). Right M1-MCA occlusion of unknown origin. There was no evidence of atherosclerotic vascular changes or dissection (Fig. B22.4 and Fig. B22.5). Doppler spectrum analysis of the right ICA showed a discrete increase in pulsatility and a mildly reduced flow velocity when compared with the left side (flow velocity: right ICA 54/22 cm/s, PI = 1.0; left ICA 67/32 cm/s, PI = 0.8). Normal findings were seen in the other extracranial vessels. Color-mode imaging revealed a discontinuous image of the presumed right M1-MCA segment only. Doppler spectrum analysis showed reduced flow velocity in the right proximal M1-MCA segment (flow velocity 60/30 cm/s). The middle M1-MCA segment signal was absent. However, signals from the distal M1-MCA segment at a depth of 40 mm demonstrated a flow pattern similar to the proximal segment. The right A1 segment of the anterior cerebral artery (ACA) revealed a mildly increased flow velocity with a high diastolic flow component (flow velocity 159/77 cm/s). A lower flow velocity was seen in the left A1-ACA segment (flow velocity 125/53 cm/s). The right posterior cerebral artery (PCA) showed higher flow velocities in the P2-PCA segment compared with the left P2-PCA segment (flow velocity: right, 87/30 cm/s; left, 50/20 cm/s) (Figs. B22.6–B22.12; see also Video Reopening of the right M1-MCA segment after thrombolysis but indirect signs of relevant distal flow occlusion at the M2-MCA level corresponding to TIBI (Thrombolysis In Brain Ischemia) grade 3 and COGIF (Consensus on Grading Intracranial Flow obstruction) grade 3. Leptomeningeal collateralization via the right ACA and PCA. Despite thrombolysis, the patient did not improve clinically. Follow-up cranial CT 1 day later showed subcortical infarction, predominantly in the right putamen and a persisting hyperdense media sign (Fig. B22.13). Transesophageal echocardiography (TEE) revealed a patent foramen ovale (PFO) with spontaneous right-to-left shunt but no atrial septum aneurysm. Deep vein thrombosis could have been a potential source for such a paradoxical embolic event but no signs were found by duplex ultrasound, and blood tests excluded thrombophilia. Fig. B22.2 CTA, coronal maximal intensity projection (MIP). Proximal occlusion of the right M1-MCA segment (single arrow). The faint signal beneath the presumed M1-MCA segment was afterwards interpreted as an early temporal branch (short arrows). Note also the strong signals of the sylvian MCA branches (large arrows). Fig. B22.3 Perfusion CT, rCBF, rCBV, and mean transit time (MTT) maps axial planes: cerebral blood flow/volume (CBF/CBV) mismatch indicating tissue at risk within the right MCA territory. (A) Decreased CBF (arrows). (B) Mildly reduced CBV. (C) Delayed MTT. Fig. B22.4 Extracranial duplex, longitudinal plane. Mildly reduced flow and increased pulsatility in the right ICA (flow velocity 54/22 cm/s, PI = 1.0). The reduced flow velocity persisted in the proximal MCA (flow velocity 66/31 cm/s). Again, there was impaired signal continuity in the mid M1-MCA segment despite the visualization of the lateral fissure and the assumed M1-MCA and, in contrast with the contralateral side the vessel seemed to turn down toward the base of the skull. This segment was therefore thought to be an early prominent temporal branch of the M1-MCA and not the M1-MCA segment itself, of which occlusion had initially been suspected. Unchanged, mildly increased flow velocities were seen in the right-sided A1-ACA and P2-PCA segments. In addition, a right-sided fetal-type PCA was found (not shown). At rest, three high-intensity transient signals were observed in the simultaneously insonated proximal MCAs after antecubital injection of ultrasound contrast agent (Echovist). Sixteen further such signals were seen after a controlled Valsalva maneuver (Fig. B22.14). Fig. B22.6 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Reduced flow velocity but otherwise normal flow signal in projection of the right proximal M1-MCA at a depth of 53 mm (flow velocity 60/30 cm/s). Note that there is poor color imaging throughout the total length of the M1-MCA and a flow gap in its mid part (arrows). Fig. B22.7 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Distal artery at a depth of 40 mm initially considered to be the right distal M1-MCA revealing a reduced velocity (flow velocity 45/21 cm/s). Fig. B22.8 TCCS (transtemporal approach), left-sided insonation, midbrain plane. Normal flow in the left M1-MCA (flow velocity 133/52 cm/s). Right-sided mid-part M1-MCA occlusion. A patent early temporal M1-MCA branch was confused with the main stem in the initial ultrasound examination. Marked leptomeningeal collateralization via ACA and PCA. Small spontaneous right-to-left shunt and moderate right-to-left shunt during Valsalva maneuver in correlation with the echocardiographic findings. Cerebral MRI revealed hemorrhagic transformation in the area of infarction and mild local swelling. The infarct area itself extended to the right insula and temporal lobe. Time-of-flight MR angiography (TOF-MRA) showed a right proximal M1-MCA occlusion. No temporal MCA branch was visualized (Fig. B22.15 and Fig. B22.16). Digital subtraction angiography (DSA) was performed on the same day to resolve the conflicting evaluations. It confirmed the presence of a mid-part M1-MCA occlusion, a prominent temporal MCA branch, and leptomeningeal collaterals from the ACA and PCA as well as the fetal-type PCA (Fig. B22.17, Fig. B22.18, Fig. B22.19). Fig. B22.19 shows a schematic of the patient’s extra-and intracranial brain-supplying arteries. Paradoxical embolism was suspected as a potential cause of stroke on the basis of the PFO. As a differential diagnosis, an in-situ thrombus was also considered because of the persisting M1-MCA occlusion after 11 days of stroke, which seems long for typical cardiac embolism, particularly following systemic thrombolysis. However, the definitive etiology remained unclear. The patient was referred to a neurologic rehabilitation unit. After 3 months, no further clinical events had occurred during anticoagulation therapy but the neurologic deficit had decreased. At this time an endovascular device occlusion of the PFO was performed without our involvement. Long-term stroke prevention was switched to antiplatelet therapy with aspirin. The patient was then lost to follow-up. Fig. B22.10 TCCS (transtemporal approach), left-sided insonation, midbrain plane. Normal findings in the left A1-ACA (flow velocity 125/53 cm/s). Fig. B22.11 TCCS (transtemporal approach), right-sided insonation, thalamic plane. Right distal P2-PCA with mildly raised flow velocities in comparison with the contralateral side indicating leptomeningeal collateral flow (flow velocity 87/30 cm/s). Fig. B22.12 TCCS, (transtemporal approach), left-sided insonation, midbrain plane. Normal flow in the left P2-PCA (flow velocity 50/20 cm/s). Large ischemic stroke in the right MCA territory caused by a right mid-part M1-MCA occlusion. Suspected cardiac embolism due to the presence of a PFO. Collateralization via a patent early temporal MCA branch originating proximal to the occlusion as well as via leptomeningeal pathways from the ACA and PCA. Fig. B22.13 Unenhanced follow-up cranial CT (1 day later), axial plane. Left: Persisting hyperdense media sign (arrow). Right: Demarcation of a large putaminal infarction.
Right Mid-part M1 Middle Cerebral Artery Occlusion with Prominent Early Temporal Branch and Patent Foramen Ovale
Clinical Presentation
Initial Neuroradiologic Findings
Suspected Diagnosis
Questions to Answer by Ultrasound Techniques
Initial Neurosonologic Findings (Day 1)
Extracranial Duplex Sonography
Transcranial Duplex Sonography
B22.1).
Conclusion
Clinical Course (1)
Questions to Answer by Ultrasound Techniques
Neurosonologic Findings (Day 10)
Transcranial Duplex Sonography
PFO Testing
Conclusion
Neuroradiologic Findings (Day 11)
Clinical Course (2)
Final Diagnosis
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