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

Case 25

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. B25.6B25.11; see also Videos Images B25.1 and B25.2).


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).

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. B25.12 DSA, right ICA injection, posteroanterior view. Near-oclusion of the right M1-MCA corresponding to the site of stenosis seen 1 year before in Fig. B25.2 (arrow). Note the residual flow signal in the distal M1-MCA and M2-MCA (arrows). Note also the leptomeningeal collaterals from the ACA and PCA (arrowheads).

Jun 20, 2018 | Posted by in NEUROSURGERY | Comments Off on 25 Progressive Right M1 Middle Cerebral Artery Occlusion Treated with Extracranial–Intracranial Bypass Surgery
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