25 Progressive Right M1 Middle Cerebral Artery Occlusion Treated with Extracranial–Intracranial Bypass Surgery

Progressive Right M1 Middle Cerebral Artery Occlusion Treated with Extracranial–Intracranial Bypass Surgery

Clinical Presentation

A 31-year-old woman was admitted with a transient mild paresis of the left arm lasting for 6 hours. One year ago she had been admitted to a district general hospital with a left-sided brachiofacial hemiparesis which had completely resolved within 4 weeks. Cerebral MRI at that time showed multiple right-sided ischemic lesions within the middle cerebral artery (MCA) territory (Fig. B25.1). Transcranial duplex sonography at that time revealed a right proximal high-grade MCA stenosis which was then confirmed by digital subtraction angiography (DSA) (Fig. B25.2). She had multiple vascular risk factors including arterial hypertension, heavy smoking, hyperlipidemia, obesity, and use of an estrogen-containing contraceptive. A cardiac embolic source had not been detected and she was given clopidogrel for long-term stroke prevention.

Initial Neuroradiologic Findings

Cerebral MRI on the day of this admission revealed the known old ischemic lesions which were partly territorial MCA infarction and partly internal and external border zone infarctions (Fig. B25.3). There was no evidence of any new ischemic brain lesions. Secondary widening of the anterior horn of the right lateral ventricle was observed.

Suspected Diagnosis

Right hemispheric transient ischemic attack (TIA) of embolic or hemodynamic origin caused by high-grade stenosis of the right M1-MCA segment, which had been detected 1 year before.

Questions to Answer by Ultrasound Techniques

What was the status of the extracranial brain-supplying arteries?
What was the status of the right MCA stenosis?
Were there any potential collateral pathways?

Initial Neurosonologic Findings (Day 2)

Extracranial Duplex Sonography

B-mode imaging did not reveal any atherosclerotic vascular changes. Doppler spectrum analysis showed normal and symmetric flow signals with no difference in the pulsatility of the extracranial internal carotid arteries (ICAs) (Fig. B25.4 and Fig. B25.5).

Transcranial Duplex Sonography

The distal ICA and the carotid siphon showed normal flow signals on both sides. The left proximal M1-MCA segment revealed a mildly stenotic flow signal (flow velocity 181/83 cm/s). Normal signals were observed in the corresponding M2 branches. The complete right M1-MCA segment could well be visualized using the color mode in a low flow pulse repetition frequency (PRF) setting. Doppler flow analysis revealed markedly reduced velocities without turbulence but with a mild poststenotic flow pattern throughout its entire length (flow velocity 17/10 cm/s). Doppler spectrum analysis of the left A1 anterior cerebral artery (ACA) segment was normal (flow velocity 110/68 cm/s). The right A1-ACA segment revealed a mildly increased nonturbulent flow (flow velocity 156/84 cm/s). The flow velocity in the right P2 posterior cerebral artery (PCA) segment was also increased (flow velocity 105/57 cm/s) when compared with the left side (flow velocity 61/25 cm/s). Also, a right-sided fetal-type PCA was seen (Figs. B25.6–B25.11; see also Videos B25.1 and B25.2).

Conclusion

Near-occlusion of the right M1-MCA with leptomeningeal collaterals from the ipsilateral ACA and PCA and mild M1-MCA stenosis on the left side.

Conventional Angiography (Day 4)

DSA was performed to clarify the suspected intracranial pathology. Significant progression was found in comparison with the DSA performed 14 months previously. The near-occlusion of the right M1-MCA segment was confirmed and leptomeningeal collateralization was seen via the right ACA and PCA. No definite caliber variations were described in the left MCA. There were no signs of vasculitis or fibromuscular dysplasia (Fig. B25.12, Fig. B25.13, Fig. B25.14).

Fig. B25.1 MR FLAIR images, axial plane. (A) Multiple right hemispheric signal abnormalities, consistent with a large basal ganglia ischemia and anterior and external border zone infarction (arrow). (B) Internal border zone infarction at the cella media level (arrow) in addition to partial inhomogeneous territorial MCA infarction. (Courtesy of Dr. Schröter, Radiologische Praxis am Krankenhaus Rüdersdorf, Rüdersdorf, Germany.)

Fig. B25.2 DSA, right ICA injection, posteroanterior view. High-grade right M1-MCA stenosis (arrows). Note the concomitant filling of the fetal-type PCA (single arrow). (Courtesy of Dr. Schröter, Radiologische Praxis am Krankenhaus Rüdersdorf, Rüdersdorf, Germany.)

Fig. B25.3 MR FLAIR image, axial plane. (A) Shrunken ischemic lesions in the right hemisphere. Enlarged right frontal horn, secondary to the adjacent ischemic defect. (B) Mildly enlarged ventricles. Note the residual external anterior border zone infarction (arrow).

Fig. B25.4 Extracranial duplex, longitudinal plane. Normal flow signal in the left ICA (flow velocity 45/21 cm/s). Note a normal pulsatility index (PI) of 0.84.

Clinical Course (1)

The new transient ischemic event was thought to be of hemodynamic origin. The pathogenesis of the progressive right M1-MCA stenosis was unclear. A cardiac or artery-to-artery embolism was unlikely. Thrombophilia, vasculitis, and autoimmune disease had been ruled out. The young age of the patient, the rapid progression of the stenosis, and the normal vessel wall findings in the extracranial carotid arteries argued against atherosclerotic stenosis despite the presence of multiple vascular risk factors. Moyamoya disease was discussed but seemed unlikely because of the rapid progression of vessel disease and the spared terminal ICA on both sides.

Xenon CT following acetazolamide infusion revealed diminished cerebrovascular reactivity (CVR) on the effected side. Because of the rapid progression and the recurrent symptoms as well as the limited hemodynamic reserve, an extracranial–intracranial superior temporal artery (STeA)–MCA bypass was performed and long-term stroke prevention with clopidogrel was continued.

Fig. B25.5 Extracranial duplex, longitudinal plane. Normal flow signal in the right ICA (flow velocity 49/34 cm/s). Note a normal PI of 0.76.

Fig. B25.6 TCCS (transtemporal approach), left-sided insonation, midbrain plane. Mildly increased and turbulent flow in the left

Fig. B25.7 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Severely reduced flow without turbulence in the right M1-MCA over all his length (arrows) (flow velocity 17/10).

Fig. B25.8 TCCS (transtemporal approach), left-sided insonation, midbrain plane. Normal flow in the left A1-ACA (flow velocity 110/68 cm/s).

Fig. B25.9 TCCS (transtemporal approach), right-sided insonation, midbrain plane. Strong flow signal in the right A1-ACA, indicating leptomeningeal collateralization (flow velocity: 156/84).

Fig. B25.10 TCCS (transtemporal approach), left-sided insonation, midbrain plane. Normal flow signal in the left proximal P2-PCA (flow velocity 61/25 cm/s).