39 Combined Chronic Right-sided Extracranial Internal Carotid Artery and Middle Cerebral Artery Occlusion

Combined Chronic Right-sided Extracranial Internal Carotid Artery and Middle Cerebral Artery Occlusion

Clinical Presentation

A 62-year-old man was admitted to the emergency department because of a reoccurring transient left-sided hemiparesis, each episode lasting ~20–30 minutes. The symptoms had been noted by the patient’s wife although the patient himself had not perceived them at all. Earlier transient deficits were denied by the patient. The past medical history revealed an ischemic heart disease for which he had been treated with coronary artery stenting 2 years earlier. In addition, he was a smoker and suffered from hypertension, treated with diuretics, β-blockers, and an angiotensin converting enzyme (ACE) inhibitor. No antiplatelet drugs were taken. The neurologic examination revealed a slight left-sided facial weakness (National Institute of Health Stroke Scale [NIHSS] score: 1). Secondary prevention with aspirin was started.

Initial Neuroradiologic Findings

Cranial CT on admission demonstrated no hemorrhage or territorial ischemia. CT angiography (CTA) revealed extracranial occlusion of the right internal carotid artery (ICA) and a contralateral ICA stenosis of ~50% (NASCET criteria). Intracranially, a long-segmented occlusion of the M1 segment of the right middle cerebral artery (MCA) was seen, considered to be caused by embolic material. Prominent insular arteries and a marked posterior cerebral artery (PCA) diameter were seen and an adequate leptomeningeal collateral flow via the PCA considered (Fig. B39.1, Fig. B39.2, Fig. B39.3, Fig. B39.4). Cerebral MRI on the following day demonstrated acute right-sided striatal infarction on diffusion-weighted images. MR angiography was not performed.

Suspected Diagnosis

Pure motor stroke in embolic right-sided M1-MCA occlusion caused by right extracranial ICA occlusion. Asymptomatic left extracranial 50% ICA stenosis (NASCET criteria).

Questions to Answer by Ultrasound Techniques

Was there true occlusion of the right extracranial ICA?
Was there true proximal occlusion of the right proximal M1-MCA segment?
If so, was there evidence of collateral blood flow?
What was the grade of the left-sided ICA stenosis assessed by ultrasound?

Neurosonologic Findings (Day 2)

Extracranial Duplex Sonography

B-mode imaging demonstrated bilateral severe mixed hypo- and hyperechoic plaques in both carotid bifurcations. On the right side, the common carotid artery (CCA) displayed an increased pulsatility, the external carotid artery (ECA) a decreased pulsatility, and the ICA a stump signal within a small blind sack. The left ICA revealed a raised flow velocity of 225/68 cm/s without pre- or post-stenotic flow alterations. The left-sided CCA, ECA, and both vertebral arteries (VAs) had normal flow signals (Fig. B39.5 and Fig. B39.6).

Transcranial Duplex Sonography

The left M1-MCA and A1 segment of the anterior cerebral artery (ACA) presented normal flow signals, the A1-ACA flow velocity being slightly higher than the M1 velocity. Normal flow parameters were seen in the left P1- and P2-PCA segments. On the right side, despite adjusting the settings for low flow, i.e., reducing pulse repetition frequency (PRF) and increasing gain, no color signal of the M1-MCA was detectable over a length >10 mm. Instead, a venous signal of the deep middle cerebral vein (DMCV) was seen, long-segmental in the lateral fissure (see Video A39.1). In projection of the very distal M1-MCA, arterial signals appeared, considered to belong to an M2-MCA branch which revealed a reduced flow velocity of 19/11 cm/s. In projection of the carotid-T only the right proximal right A1-ACA was seen with a mildly reduced flow velocity (42/23 cm/s) but an obviously poststenotic flow pattern. In projection of the anterior communicating artery (ACoA) a turbulent flow with increased flow velocities was detected (functional stenosis). Both right P1- and P2-PCA segments displayed increased flow velocities of ~110/50 cm/s. The left ophthalmic artery (OA) had a normal antegrade flow, but the right OA flow was retrograde (Fig. B39.7–Fig. B39.19).

Fig. B39.1 MR diffusion-weighted image, axial plane. Nonlacunar right-sided striatal infarction.

Fig. B39.2 Intracranial CTA, coronal maximal intensity projection (MIP). Note the presence of the right distal ICA, the missing contrast of the right proximal M1-MCA (short arrow), and the partly visible right A1-ACA segment (long arrow). Distally, the right M2-MCA and dilated insular branches can be seen (arrowheads). The vessel anatomy on the contralateral side appears normal.

Fig. B39.3 Intracranial CTA, axial MIP. No contrast in the main stem of the right M1-MCA (arrows), initially considered to be caused by an embolic occlusion. Note the distal MCA branches (arrowheads) and the prominent PCA signal (arrow).

Fig. B39.4 Intracranial CTA, 3D reconstruction. Note the absence of contrast of the right ICA at the supposed junction with the MCA (short arrow), the slim but otherwise detectable right A1-ACA (large arrow), and parts of the M2-MCA (arrowhead). A vessel seen in the projection of the M1-MCA main stem was considered to be a residual MCA flow (arrows).