45 Bilateral Proximal Vertebral Artery Stenosis and Bilateral Middle Cerebral Artery Aneurysm

Bilateral Proximal Vertebral Artery Stenosis and Bilateral Middle Cerebral Artery Aneurysm

Clinical Presentation

A 49-year-old man presented with mild left-sided weakness. The patient was a heavy smoker and drinker but no other vascular risk factors were known. Neurologic examination revealed a left-sided mild brachiofacial hemiparesis and left-sided homonymous hemianopia (National Institutes of Health Stroke Scale [NIHSS] score: 4).

Initial Neuroradiologic Findings

Unenhanced cranial CT was normal. CT angiography (CTA) revealed bilateral stenoses of the vertebral artery (VA) origin; the dominant left side was more severely affected than the right side. The left-sided stenosis was caused by a marked cuff-like calcified plaque. Along the vessel course, small collaterals were detected that originated from neck muscle branches and connected to the left VA (Fig. B45.1 and Fig. B45.2). The carotid arteries revealed generalized atherosclerotic plaques without major narrowing. Intra cranially, no steno-occlusive processes were seen. However, a left middle cerebral artery (MCA) bifurcation aneurysm was detected.

Suspected Diagnosis

Right posterior cerebral artery (PCA) territory ischemia caused by one of the proximal VA stenoses, incidental left MCA aneurysm.

Questions to Answer by Ultrasound Techniques

What was the grade of the reported proximal VA stenoses?
Was the underlying vessel pathology of atherosclerotic origin?
If the stenoses were hemodynamically relevant, what kind of collateral flow could be seen?
Could the left-sided MCA aneurysm be detected?

Initial Neurosonologic Findings (Day 1)

Extracranial Duplex Sonography

B-mode sonography revealed predominantly hypoechoic atherosclerotic plaques that were most pronounced in the left internal carotid artery (ICA) and in the left proximal VA. ICA flow signals were normal. The dominant left VA (diameter 5.0 mm) revealed highly increased flow velocities at the vessel origin. A marked poststenotic, pseudovenous, flow pattern beginning in the distal V1-VA and intensifying throughout the course of the V2-VA segment up to the C3–4 level was seen distal to the stenosis. Though the flow pattern improved due to contributing small collaterals from cervical muscle branches more distally, i.e., from the C2–3 level up to the V3-VA, the flow pattern remained poststenotic (see also Video B45.1). The origin of the right VA (diameter 3.1 mm) also showed an intrastenotic flow velocity increase, but flow signals distal to the stenosis were normal without indication of a hemodynamic restriction (Fig. B45.3–Fig. B45.11).

Transcranial Duplex Sonography

Transtemporal insonation showed a vessel widening of the left distal MCA at a depth of 52 mm which was considered to present the reported aneurysm (see also Video B45.2). Doppler spectra within the widened vessel revealed a moderately turbulent flow and mildly increased flow velocities compared with the homologous right MCA segment. The remaining anterior circulation vessels showed normal flow parameters. Both PCAs showed poststenotic flow patterns. No steno-occlusive lesions could be detected, especially regarding the clinically affected right PCA. No posterior communicating arteries (PCoAs) were seen. Similar poststenotic flow patterns like in the left V2-VA were seen transforaminally in the basilar artery (BA) and the anterior inferior cerebellar artery (AICA), as well as in the left V4-VA and the left posterior inferior cerebellar artery (PICA). The right V4-VA showed a normal flow signal corresponding to the extracranial findings. No vertebrobasilar confluence could be visualized (Fig. B45.12–Fig. B45.20; see also Video B45.3).

Conclusion

Bilateral proximal VA stenosis presumably of atherosclerotic origin with hemodynamic relevance in the dominant left VA. Suspected PICA ending of the right VA. Left MCA bifurcation aneurysm.

Clinical Course (1)

Clinical symptoms improved and subsided completely within 2 hours. Therefore, a transient ischemic attack (TIA) was diagnosed and no thrombolysis was performed. No cardiac embolic source was found and artery-to-artery embolism, presumably originating from the left proximal VA stenosis, was postulated. Further hemodynamic assessment and aneurysm evaluation was declined by the patient although it was recommended by the treating physicians. Subsequently, he was discharged with the recommendation not to drink alcohol and to stop smoking. For secondary stroke prevention, he was put on a combined medication of aspirin and a statin.

Fig. B45.1 Extracranial CTA, coronal maximal intensity projection (MIP). Left dominant VA. High-grade stenosis on the right VA (arrowhead) and left VA (arrow). Note the calcified “cuff” at the left VA origin.

Fig. B45.2 Extracranial CTA. Left: Coronal MIP. Small cervical collateral anastomoses connecting muscle branches of the ECA with the VA, most evident at the transverse processes C2 and C3 (arrows). Right: Axial MIP demonstrating the small collaterals in the cross-sectional planes (arrows).

Fig. B45.3 Extracranial duplex, longitudinal plane. (A) B-mode indicating a predominantly hypoechoic plaque at the left VA origin (arrowheads). (B) Color mode showing the vessel tailoring and a marked aliasing indicating VA stenosis.

Fig. B45.4 Extracranial duplex, longitudinal plane. Increased flow velocities at the origin of the dominant left VA indicating severe stenosis (flow velocity 325/172 cm/s).

Fig. B45.5 Extracranial duplex, longitudinal plane. Severe post-stenotic flow pattern and reduced flow velocity in the distal left V1-VA (flow velocity: 18/11 cm/s, vessel diameter 5.0 mm).

Fig. B45.6 Extracranial duplex, longitudinal plane. Intensified post-stenotic flow pattern in the proximal left V2-VA at the C3-C4 transverse process level (flow velocity 18/13 cm/s).

Fig. B45.7 Extracranial duplex, longitudinal plane. Prominent collateral vessel with an “internalized” flow signal at the level of the C2-C3 transverse processes (flow velocity 48/23 cm/s).

Fig. B45.8 Extracranial duplex, longitudinal plane. Improved V2-VA flow at the level of the C2-C3 transverse processes caused by the additional collateral influx (flow velocity 47/21 cm/s).

Fig. B45.9 Extracranial duplex, longitudinal plane. Persisting ameliorated, but markedly poststenotic flow in the left V3-VA segment. Note the inadequate insonation angle leading to artificial low flow velocity (flow velocity 19/12 cm/s).

Fig. B45.10 Extracranial duplex, longitudinal plane. Intrastenotic flow at the right VA origin (flow velocity 180/25 cm/s).

Fig. B45.11 Extracranial duplex, longitudinal plane. Normal flow pattern in the right V2-VA excluding hemodynamic relevance of the proximal stenosis (flow velocity 38/11 cm/s, diameter 3.1 mm).

Fig. B45.12 TCCS (transtemporal approach), left-sided insonation, midbrain plane. Widening of the left MCA at a depth of 52 mm suspected to be an aneurysm.

Fig. B45.13 TCCS (transtemporal approach), left-sided insonation, midbrain plane. Turbulent flow and mild increased flow velocity in the assumed aneurysm (flow velocity 128/62 cm/s).

Fig. B45.14 TCCS (transtemporal approach), left-sided insonation, midbrain plane. Normal flow signal and parameters in a proximal M2-MCA branch (flow velocity 69/38 cm/s).

Fig. B45.15 TCCS (transtemporal approach), left-sided insonation, midbrain plane. Moderate poststenotic flow pattern in the left P1/P2-PCA (flow velocity 85/49 cm/s).