20 Right Internal Carotid Artery Dissection with Fast Recanalization

Right Internal Carotid Artery Dissection with Fast Recanalization

Clinical Presentation

A 56-year-old man presented with progressive paresis of his left arm. Three days prior to presentation, he had experienced some pain on the right side of his neck and headaches while exercising in a gym for the first time. The following day, he observed clumsiness of his left hand and drooping of his right eyelid. The left-sided paresis continued to progress, at which stage he presented to the hospital emergency department. The patient had no known vascular risk factors. The neurologic examination revealed a mild left-sided sensorimotor hemiparesis and Horner’s syndrome on the right side (National Institute of Health Stroke Scale [NIHSS] score: 3).

Initial Neuroradiologic Findings

Cranial CT on the day of admission revealed multiple hypodense areas in the right middle cerebral artery (MCA) territory. MRI confirmed multiple ischemic lesions within the internal border zone region of the right hemisphere. Axial images demonstrated a reduced flow void in the right carotid siphon. Time-of-flight MR angiography (TOF-MRA) depicted an absent signal of the right distal internal carotid artery (ICA) and a bilateral partial fetal-type posterior cerebral artery (FT-PCA) origin (Fig. B20.1 and Fig. B20.2).

Suspected Diagnosis

Right internal border zone infarction (BZI) caused by ICA dissection and secondary ICA occlusion.

Questions to Answer by Ultrasound Techniques

Was there evidence of dissection?
Was there a real occlusion or high-grade stenosis of the ICA?
If so, what were the intracranial collateral pathways?

Initial Neurosonologic Findings (Day 1)

Extracranial Duplex Sonography

B-mode imaging was normal. There were no atherosclerotic changes and no signs of proximal ICA dissection. Doppler spectrum analysis showed a high pulsatility in the right common carotid artery (CCA) and a high-resistance flow signal in the right ICA with a low and short systolic flow and completely absent diastolic flow component, indicative of either near-occlusion or occlusion of the ICA below of the origin of the ophthalmic artery (OA). External carotid artery (ECA) Doppler spectra were normal (Fig. B20.3, Fig. B20.4, Fig. B20.5, Fig. B20.6; see also Video B20.1).

Transcranial Duplex Sonography

The right M1-MCA segment presented a marked poststenotic flow pattern. The A1 segment of the anterior cerebral artery (A1-ACA) yielded a retrograde flow, also with severe poststenotic alterations. The anterior communicating artery (ACoA) was not visualized. Elevated flow velocities were seen in the right P1-PCA segment (125/69 cm/s), here with an obviously turbulent flow pattern, and in the left A1-ACA segment (150/75 cm/s), both indicative of collateral flow to the right anterior circulation via the ACoA and the posterior communicating artery (PCoA). The left MCA and PCA, in addition to the distal right P2-PCA segment, demonstrated normal flow. No flow was detected in the OA on the right side. The flow signal of the left OA was normal (Figs. B20.7–B20.12; see also Video B20.1).

Evaluation of Collateral Function

Cerebrovascular Reactivity Testing

Intravenous administration of 1 g acetazolamide during continuous transcranial Doppler (TCD) monitoring of both M1-MCA segments revealed a 60.6% increase in flow velocity on the left side and a 1.6% increase in flow velocity on the right (Fig. B20.13) (see also Chapter 3, “Acetazolamide Infusion Test” under “Metabolic Coupling”).

Ultrasound Delay Testing

After intravenous administration of a 3-mL sonographic contrast bolus (Levovist, 300 mg/dL) and continuous monitoring of both M1-MCA Doppler spectra, a right-sided, 1-second delay of bolus arrival was observed (Fig. B20.14) (see also Chapter 3, “Ultrasound Delay Test” under “Metabolic Coupling”).

Fig. B20.1 (A) MR T2-weighted image, axial plane. Multiple hyperintense signals within the right internal border zone (arrows), indicative of hemodynamic infarction. (B) MR T2-weighted image, axial plane (magnified view). Absent flow void within the right-sided cavernous ICA segment, suggestive of reduced or absent intraluminal flow (arrow). Note the contralateral normal flow void signal of the ICA and of the BA in front of the pons (arrowheads).

Fig. B20.2 Intracranial 3D TOF-MRA, axial maximal intensity projection (MIP). Signal loss of the right ICA indicating high-grade flow reduction or occlusion. Note the bilateral fetal-type PCA (arrowheads). Both P1-PCA segments are hardly visible. Note also the reduced signal in the right MCA (arrows) and in the right A1-ACA (arrows) indicating compromised postocclusive flow (arrows)

Fig. B20.3 Extracranial duplex, longitudinal plane. Normal left CCA flow (flow velocity 87/28 cm/s).

Fig. B20.4 Extracranial duplex, longitudinal plane. High-resistance flow signal in the right CCA (peak-systolic flow velocity 63 cm/s).

Conclusion

Suspected right distal ICA dissection with near-occlusion or occlusion proximal to the OA origin. Exhausted CVR and insufficient collateral pathways supplying the right MCA territory via the ACoA and the ipsilateral PCoA.

Conventional Angiography

Digital subtraction angiography (DSA) demonstrated a long segmental irregularity in the right ICA with a cone-shaped high-grade stenosis starting 5 cm above the carotid bifurcation and extending to the vertical segment of the petrous C6-ICA segment. Only residual and delayed contrast filling was seen in the distal ICA. Collateralization mainly occurred via the ACoA and partially via a hypoplastic right P1-PCA segment providing retrograde blood flow into the right MCA via the FT-PCA and antegrade blood flow into the distal PCA segments. Filling of the right MCA territory was delayed. These findings were consistent with a near-occlusion of the right ICA due to vessel wall dissection (Figs. B20.15–B20.20).

Fig. B20.21 shows a schematic of the patient’s extra-and intracranial brain-supplying arteries.

Clinical Course (1)

Intravenous heparin, aiming for a twofold increase of partial thromboplastin time (PTT) was started. TOF-MRA 2 weeks later demonstrated a normalized right ICA signal.

Fig. B20.5 Extracranial duplex, longitudinal plane. Normal flow signal in the left ICA (flow velocity 79/40 cm/s).

Fig. B20.6 Extracranial duplex, longitudinal plane. High-resistance flow signal in the right ICA with a low and short systolic, and completely absent diastolic flow component indicative of near-occlusion or occlusion of the ICA below the OA origin.

Fig. B20.7 TCCS (transtemporal approach), left-sided insonation, midbrain plane. Normal left M1-MCA flow (flow velocity 69/31 cm/s). Note the prominent left blue-coded signal indicating flow away from the probe and toward the P2-PCA corresponding to a fetal-type PCA seen in MRA (arrow).

Fig. B20.8 TCCS (transtemporal approach), right-sided insonation. Poststenotic flow pattern in the right M1-MCA (flow velocity 54/38 cm/s).