Case 24 A 34-year-old woman presented with a 1-year history of severe headaches that were thought to be caused by repeated hypertensive episodes. She also reported a single episode of left-sided facial pain and ipsilateral conjunctival injection lasting for several hours ~1 year ago. After the initiation of antihypertensive treatment the headaches subsided. However, ambulatory examination of the optic fundi revealed retinal vessel narrowing. This finding prompted an ultrasound examination of the brain-supplying arteries. Transcranial Doppler (TCD) revealed a left M1 middle cerebral artery (MCA) stenosis. In addition to having hypertension, the patient was a smoker and used an oral contraceptive. An ambulatory cerebral CT scan had been unremarkable. She was now admitted to our department for elective catheter angiography to search for extended intracranial vascular pathology. Digital subtraction angiography (DSA) demonstrated mild bilateral extracranial internal carotid artery (ICA) elongations and wide carotid bulbs, but there was no evidence of stenosis or atherosclerosis. Intracranially a left long-segmented high-grade stenosis of the proximal M1-MCA segment could be confirmed. Distal to the stenosis, the residual M1 segment was mildly dilated. Also, a delayed contrast filling of the distal MCA segments in relation to the distal anterior cerebral artery (ACA) segments was seen indicating a high-grade stenosis of hemodynamic relevance. There were no signs of vasculitis (Fig. B24.1 and Fig. B24.2). Asymptomatic left high-grade M1-MCA stenosis. In the absence of atherosclerotic vessel changes, and the presence of a history of left-sided facial pain with associated conjunctival injection and headache 1 year previously, an MCA dissection was suspected. Two weeks later, the patient was readmitted to our hospital for further evaluation. On admission she reported a continuing right-sided neck pain that started during the catheter angiography 2 weeks before and a sore throat on the day following it. The neurologic examination was normal; in particular, she did not have Horner’s syndrome. No parenchymal lesions were seen on MRI. On T2-weighted axial MRI images, a distinctly reduced flow void could be seen in the distal ICA on axial and coronal images. 3D time-of-flight MR angiography (TOF-MRA) of the cerebral arterial circle (circle of Willis, CW) demonstrated the known left high-grade M1-MCA stenosis. A reduced signal was observed within the right terminal ICA. Cervical MRI and MRA of the extracranial vessels were not performed (Fig. B24.3 and Fig. B24.4). There were no atherosclerotic vascular changes. The right ICA revealed a long-segmented lumen reduction that started 2 cm above the carotid bifurcation and continued over the whole visible distal vessel segment. There were no typical signs of a dissection. Flow velocity in the right ICA reached a systolic maximum of 200 cm/s. The right common carotid artery (CCA) showed a high-resistance flow signal with a reduced diastolic flow component. The left ICA, both external carotid arteries (ECAs), and the vertebral arteries (VAs) presented normal flow signals (all images not shown). Within the left M1-MCA, transcranial color-coded sonography (TCCS) detected a turbulent stenotic flow (flow velocity 383/267 cm/s). A poststenotic flow pattern was observed in the left M2-MCA branches. The flow signal of the right M1-MCA segment appeared normal. The right A1-ACA segment showed reversed flow while the left-sided A1-ACA segment demonstrated increased flow velocities without turbulence (flow velocity 225/140 cm/s). Assessment of the posterior cerebral arteries, VAs, the basilar artery (BA), and the ophthalmic arteries (OAs) revealed overall normal antegrade flow signals without signs of leptomeningeal or ophthalmic collateral support. There was a positive oscillation effect in the right M1-MCA segment with slight submandibular tapping of the left ICA and the dominant left VA at the atlas loop. This indicated collateral flow through the anterior communicating artery (ACoA) and right posterior communicating artery (PCoA) (Fig. B24.5, Fig. B24.6, Fig. B24.7, Fig. B24.8, B24.9; see also Videos B24.1 and B24.2). Fig. B24.2 (A) DSA, left ICA injection, posteroanterior view. Long high-grade stenosis of the proximal left M1-MCA (arrow). Note the dilation of the MCA distal of the stenosis. Also note the delayed filling of the distal MCA segments in comparison to distal ACA segments. (B) DSA, left ICA injection, posteroanterior view. Magnified view of A demonstrating a filiform MCA stenosis considered as dissection (arrows) and poststenotic vessel dilation Fig. B24.3 (A) MRI T2-weighted image, axial plane, magnified view. Note the prominent right PCoA already visible (arrow). (B) MR T2-weighted image, axial plane, magnified view. Attenuated flow void in the right ICA (arrowhead) indicating a significantly reduced blood flow. Note the normal signal voids in the opposite ICA and BA. Fig. B24.4 3D TOF-MRA, axial maximal intensity projection (MIP). Reduced signal in the left M1-MCA (single arrow), indicating high-grade stenosis. Note that the right-sided distinct PCoA seen in T2-weighted images is not visualized. Note also a reduced signal in the intracranial right ICA indicating severely compromised ICA flow (arrows). Hemodynamically relevant left high-grade M1-MCA stenosis. High-grade stenosis of the right extracranial ICA of hemodynamic relevance, suspicious for dissection, induced by the diagnostic DSA 2 weeks previously. Excellent collateral flow to the right MCA and ACA via the ACoA as well as the right PCoA. DSA performed on the same day demonstrated a conical lumen reduction of the right ICA directly above the carotid bifurcation with a filiform stenosis up to the base of the skull which was suggestive of ICA dissection. Collateralization toward the right MCA and ACA territory was via the left ICA and ACoA. Selective VA angiography showed that the right MCA was also perfused by the ipsilateral PCoA. There was no evidence of ophthalmic collaterals. The known high-grade M1-MCA stenosis remained unchanged (Fig. B24.10, Fig. B24.11, Fig. B24.12). In addition, renal angiography was performed, which excluded signs of fibromuscular dysplasia. Fig. B24.6 TCCS, transtemporal approach, midbrain plane. Normal flow pattern in the right M1-MCA (flow velocity 92/41 cm/s) despite the proximal extracranial high-grade ICA stenosis. Fig. B24.7 TCCS, transtemporal approach, midbrain plane, left-sided insonation. Increased flow velocity in the left A1-ACA without turbulence, suggesting collateralization of the contralateral anterior circulation via the ACoA but also for the ipsilateral MCA territory (flow velocity 225/140 cm/s). Fig. B24.8 TCCS, transtemporal approach, midbrain plane, right-sided insonation. The right A1-ACA presented with reversed flow direction (flow velocity 83/30 cm/s). Note the effect of contralateral ICA tapping on the flow signal of the right A1-ACA assuring the cross-flow via ACoA. Fig. B24.9 TCCS, transtemporal approach, midbrain plane, left-sided insonation. Turbulent flow and increased flow velocity within the ACoA (functional stenosis) caused by intracranial cross-flow from the left ICA. Note also the prominent blue-coded right PCoA (arrow). The dissection of the right ICA was considered to be of iatrogenic origin caused by the catheter during the initial DSA. Intravenous heparin treatment was started, aiming for a twofold rise in partial thromboplastin time (PTT). The patient was then switched to oral anticoagulation with phenprocoumon for 6 months. The etiology of the left M1-MCA stenosis remained unclear. After exclusion of all other differential diagnoses, particularly vasculitis, a dissection was assumed to be most likely. After 6 months the patient was re-examined to evaluate the requirement for long-term secondary stroke prevention.
Dissection of the Right Extracranial Internal Carotid Artery and Left M1 Middle Cerebral Artery
Clinical Presentation
Initial Neuroradiologic Findings
Suspected Diagnosis
Clinical Course (1)
MRI and MR Angiography (10:00 Hours)
Questions to Answer by Ultrasound Techniques
Neurosonologic Findings (12:00 Hours)
Extracranial Duplex Sonography
Transcranial Duplex Sonography
Conclusion
Conventional Angiography (16:00 Hours)
Clinical Course (2)
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