3 Left Common Carotid Artery Occlusion

Left Common Carotid Artery Occlusion

A 64-year-old man was admitted with a transient right-sided facial paresis that had lasted a few minutes. At the same time he experienced some slurring of his speech as well as difficulty finding appropriate words. The symptoms started while he was standing in his kitchen, preparing breakfast. Six years earlier, he had had an ischemic brain infarction with right-sided hemiparesis. An artery-to-artery embolism was suspected due to symptomatic internal carotid artery (ICA) stenosis, and a carotid endarterectomy (CEA) was performed. At this time, long-term secondary stroke prevention was started with daily aspirin. Follow-up several weeks after the surgery revealed complete occlusion of the common carotid artery (CCA) and ICA on the operated side. The patient had no history of vascular risk factors, particularly no arterial hypertension, and he was not taking any other medication.

Initial Neuroradiologic Findings

Cerebral MRI showed old ischemic brain lesions in the left middle cerebral artery (MCA) and anterior cerebral artery (ACA) territories. In addition, multiple small focal lesions were found in the right hemisphere. However, there were no signs of acute cerebral ischemia in the diffusion-weighted MR images. The cervical contrast-enhanced magnetic resonance angiogram (MRA) showed no contrast in the left CCA, ICA, and external carotid artery (ECA). Regular signal intensities were present within the right carotid arteries and the vertebral arteries (VAs) (Fig. B3.1 and Fig. B3.2).

Suspected Diagnosis

Left hemispheric transient ischemic attack (TIA) of hemodynamic origin.

Questions to Answer by Ultrasound Techniques

Was there evidence of occlusion or near occlusion of the left CCA or ICA?
If so, was there evidence of collateral blood flow via the anterior communicating artery (ACoA) and posterior communicating artery (PCoA) or leptomeningeal vessels via the posterior cerebral artery (PCA)?

Initial Neurosonologic Findings

Extracranial Duplex Sonography

B-mode sonography revealed distinct atherosclerotic vascular changes, particularly in the right carotid bifurcation. The right CCA revealed a mildly increased velocity of 128/33 cm/s. Doppler spectrum analysis showed no signal in the left CCA, ICA, and ECA. The lumen of the left CCA was small and completely filled with moderate hyperechoic material, consistent with an old occlusion. Assessment of the VAs was normal (Fig. B3.3, Fig. B3.4, Fig. B3.5).

Transcranial Duplex Sonography

A poststenotic flow pattern was seen in the left M1 segment of the MCA with an oscillation effect following digital tapping of the contralateral ICA at the submandibular level. No flow signal was seen in the intracranial segment of the left distal ICA. The left A1 segment of the anterior cerebral artery (ACA) flow direction was retrograde due to cross-flow from the contralateral ICA. In the ACoA (depth 72 mm) an increased flow velocity and turbulence was detected, indicative of a functional stenosis. Flow in the right A1-ACA segment was slightly increased (flow velocity 135/65 cm/s) but not turbulent. Comparing both P1- and P2-PCA segments, a mild increased flow velocity was seen on the left side. The left ophthalmic artery (OA) could not be detected transorbitally (Figs. B3.6–B3.12; see also Videos B3.1 and B3.2).

Conclusion

Extracranial occlusion of the left common, internal, and external carotid arteries.
Intracranial collateral blood flow into the left MCA and ACA territory via ACoA and via leptomeningeal collaterals of the PCA.

Fig. B3.13 and Fig. B3.14 show schematics of the extra- and intracranial brain-supplying arteries of a healthy subject and of the patient, respectively.

Clinical Course

The acute clinical symptoms in our patient suggested a TIA in the left cerebral hemisphere. Neurosonologic findings confirmed the already known left CCA and ICA occlusion which excluded an embolic event and argued in favor of a hemodynamic event. The 24-hour blood pressure recordings did not demonstrate hypotensive episodes. To assess the risk for further hemodynamically induced ischemic episodes, an acetazolamide test (see also Chapter 3, “Acetazolamide Infusion Test” under “Metabolic Coupling”) was performed. Intravenous administration of 1 g acetazolamide led to a 23.4% increase of right MCA flow velocity and a less prominent flow velocity increase in the left MCA of 10.2%, but this was still within the normal range. As a result of these findings and in the absence of recent cerebral ischemia on MRI, it was decided to keep the patient under regular follow-up and no medication changes were made. He remained stable with no further ischemic attacks over a follow-up period of 4 years.

Fig. B3.1 MR FLAIR image, axial plane. Old MCA infarction in the left central region (arrow).

Fig. B3.2 Contrast-enhanced 3D MRA, coronal MIP. No signals in the left common, internal, and external carotid arteries.

Fig. B3.3 Extracranial duplex, longitudinal plane. Mild increase of flow velocity in the right CCA (flow velocity 128/33 cm/s) which can be interpreted as sign of collateral flow.

Fig. B3.4 Extracranial duplex, longitudinal plane (B-mode image): The narrowed lumen of the left CCA is completely filled with moderate echogenic material indicating a nonacute occlusion (arrows).