18 Traumatic Bilateral Internal Carotid and Vertebral Artery Dissection with Right-sided Embolic Middle Cerebral Artery Occlusion

Traumatic Bilateral Internal Carotid and Vertebral Artery Dissection with Right-sided Embolic Middle Cerebral Artery Occlusion

Clinical Presentation

A 27-year-old left-handed woman without relevant medical history or known vascular risk factors was admitted after a severe motor vehicle accident in which her car turned over several times. The initial neurologic examination was normal. A CT of the head showed a left subgaleal hematoma as the only finding (not shown). A body CT showed a pelvis fracture and foreign particles in the legs, for which the patient was surgically treated. On the following morning a left-sided hemiparesis with gaze palsy, aphasia, and a decreased level of consciousness were noted. The exact onset of symptoms was not clear (National Institute of Health Stroke Scale [NIHSS] score: 9).

Neuroradiologic Findings (Day 2)

A second cranial CT yielded a dense media sign on the right side and a new hypodense area in the right frontal middle cerebral artery (MCA) territory (Fig. B18.1) confirmed by CT perfusion. CT angiography showed right-sided extracranial internal carotid artery (ICA) occlusion starting 2 cm distal of the bifurcation together with an ipsilateral proximal MCA occlusion (Fig. B18.2). Furthermore, irregular vessel lumina were seen extracranially in the left ICA and in both V2 segments of the vertebral arteries (VA) (not shown).

Suspected Diagnosis

Partial territorial right MCA infarction in proximal MCA occlusion caused by extradural traumatic cervical arterial dissection (CAD) of all four brain-supplying arteries with occlusive dissection of the right ICA and artery-to artery embolic occlusion of the right MCA.

Conventional Angiography with Endovascular Thrombectomy (Day 2)

Urgent mechanical thrombectomy was performed within 1 hour after CT. Digital subtraction angiography (DSA) confirmed CAD of both ICA and VA with a submandibular near-occlusion of the right ICA, multisegmental lumen reduction of the left ICA starting 2 cm distal of the bifurcation with a small submandibular dissecting aneurysm without a stenosis, and left-pronounced mild to moderate dissecting stenosis at the entrance of both V2-VA segments. The right proximal M1-MCA remained occluded. There was no opacity of the right A1 anterior cerebral artery (ACA) which was related to the poststenotic low flow state. Leptomeningeal collateralization was assured by the posterior circulation via the right posterior cerebral artery (PCA) (Fig. B18.3, Fig. B18.4, Fig. B.18.5). Using a stent retriever and aspiration device the right MCA was reopened via the occluded ICA under generalized anesthesia (Fig. B18.6). Secondary prevention was started with intravenous partial thromboplastin time (PTT)-guided heparin.

Fig. B18.7 and Fig. B18.8 show schematics of the extra-and intracranial brain-supplying arteries before and after mechanical thrombectomy of right M1-MCA.

Clinical Course (1)

The patient was transferred to the intensive care unit (ICU). Her neurologic status improved slightly during the next day with partial regression of the aphasic syndrome and hemiparesis. Extracranial and intracranial ultrasound was first requested for vessel status analysis. CT on the next day revealed a large frontal MCA infarction but no intracranial bleeding.

Questions to Answer by Ultrasound Techniques

Does ultrasound affirm dissection in all brain-supplying arteries?
Did the right M1-MCA remain open after intervention?
Did the right extracranial ICA remain occluded?
If yes, what were the intracranial collaterals to protect the brain from large hemodynamic ischemic events?
Could the small dissecting aneurysm be detected by duplex sonography?
Was there progress stenosis in the nonoccluded brain-supplying arteries during anticoagulation with heparin?

Fig. B18.1 Unenhanced cranial CT, axial plane. (A) Long-segmented dense media sign on the right side indicating vessel occlusion (arrow). (B) Early parenchymal signs of ischemia can be seen in the right frontal area of the MCA territory (yellow circle).

Fig. B18.2 Intracranial 3D CTA, axial MIP (A) and coronal MIP (B), confirming M1-MCA occlusion starting at its mid part (arrows).

Fig. B18.3 DSA, superimposed right and left selective ICA injection, posteroanterior view. Right ICA injection, showing dissecting high-grade stenosis submandibular at the entrance to the skull base (large arrowhead) and a distal ICA occlusion (arrow), presumably caused by artery-to artery embolism. Left ICA injection, showing also signs of dissection with a small aneurysm (yellow circle) and a suspicion of mild involvement in the distal part of its vertical petrosal segment (small arrowhead). Ipsilateral flow is undisturbed and a collateral flow into the right ACA territory via the left A1-ACA is evident (white arrows).

Fig. B18.4 DSA, superimposed right and left selective VA injection, posteroanterior view. Long-segmented mild right and a moderate left V2-VA stenoses, starting typically at the entrance to V2-VA (arrows).

Initial Neurosonologic Findings (Day 3)

Extracranial Duplex Sonography

B-mode imaging revealed no atherosclerotic transformation of carotid vessels. Doppler spectrum analysis in the right common carotid artery (CCA) showed a high resistance flow with increased pulsatility suggestive of an ICA occlusion below the origin of the ophthalmic artery (OA). The right proximal ICA itself revealed a tapering of the vessel with a stump signal. No direct signs of a dissecting lesion could be seen. The ipsilateral external carotid artery (ECA) showed an “internalized” flow signal (Fig. B18.9, Fig. B18.10, Fig. B18.11). In the left ICA a massive and lengthy vessel lumen reduction was seen, caused by a hypoechoic lesion indicating a mural hematoma. Doppler spectrum analysis revealed a turbulent flow with reduced flow velocity (55/9 cm/s) and a markedly increased pulsatility (PI 2.1) indicative of a further distal flow obstruction (Fig. B18.12). The left ECA flow signal also appeared “internalized.” Despite a submandibular access with adequate inclination of the linear probe the small dissecting aneurysm could not be detected. B-mode imaging of both V2-VAs showed multiple segmental vessel diameter differences ranging from 1.5 to 4.2 mm in the left V2-VA and from 1.6 to 3.8 mm in the right V2-VA, also caused by hypoechoic material considered to be mural hematomas. Accordingly, the flow velocities varied widely in different segments of the V2-VAs (right V2-VA between 100/75 cm/s and 294/148 cm/s, left V2-VA between 44/38 cm/s and 408/216 cm/s) primarily suggestive of multiple stenoses (Fig. B18.13). Blood volume flow measurements of the V2-VA revealed high values of 258 mL/min in the right and 152 mL/min in the left V2-VA (Fig. B18.14). Together with a high diastolic flow component the findings were interpreted as an additional compensatory vertebrobasilar hyperperfusion to collateralize the right-sided ICA occlusion and the suspected severe steno-occlusive lesion in the distal left ICA.

Fig. B18.5 DSA, right selective VA injection, posteroanterior view. Undisturbed vertebrobasilar flow. Note the prominent filling of the right MCA and ACA vessels (arrows) indicating leptomeningeal collateral flow via the PCA.

Fig. B18.6 DSA, right selective distal ICA injection, posteroanterior view. (A) Proximal right MCA occlusion but open ipsilateral ACA at this time point. (B) Final result after treatment with stent retriever and suction systems revealing a reopened MCA (arrows).

Fig. B18.7 Schematic of the patient’s extra- and intracranial brain-supplying arteries on day 2 before the first DSA with assumed right M1-MCA occlusion.

Fig. B18.8 Schematic of the patient’s extra- and intracranial brain-supplying arteries directly after mechanical thrombectomy of the right M1-MCA occlusion.

Transcranial Duplex Sonography

The right M1-MCA was open. Doppler spectra of both M1-MCA and A1-ACA segments showed a moderate poststenotic flow pattern (Fig. B18.15). Digital tapping of the ipsilateral ocular bulb led to typical transients on both M1-MCA indicating collateral flow via the OA (see Fig. B18.24). The main collateral pathway was via both posterior communicating arteries (PCoAs) indicated by elevated flow velocities in both P1-PCA segments (right P1-PCA 103/60 cm/s; left P1-PCA 133/82 cm/s) and normal values in both P2-PCA (right P2-PCA 31/17 cm/s; left P2-PCA 46/30 cm/s) as well as a functional stenosis in both PCoAs with a flow direction toward the anterior circulation (right PCoA 112/69 cm/s; left PCoA 143/106 cm/s) (Fig. B18.16, Fig. B18.17, Fig. B18.18). The C6-ICA was undetectable on both sides. Right and left OA showed an internalized and retrograde flow signal with markedly elevated flow velocities (right OA 52/26 cm/s; left OA 89/39 cm/s) (Fig. B18.19 and Fig. B18.20). Elevated flow velocities with low pulsatility were seen also in both V4-VA segments (right V4-VA 120/71 cm/s; left V4-VA 63/47cm/s) and in the basilar artery (BA) (89/58 cm/s) suggestive of hyperperfusion (not shown).

Fig. B18.9 Extracranial duplex, longitudinal plane. Doppler spectrum analysis of the right CCA with reduced flow velocity and increased pulsatility (flow velocity 69/7 cm/s, PI = 3.7).

Fig. B18.10 Extracranial duplex, longitudinal plane. Doppler spectrum analysis of the right ICA revealing a low velocity and increased pulsatility (flow velocity 18/0 cm/s) compatible with an infraophthalmic ICA occlusion. Note the reduced diameter of the ICA without direct signs of dissection at this level (arrows).

Fig. B18.11 Extracranial duplex, longitudinal plane. Doppler spectrum analysis of the right ECA revealing an “internalized” flow signal with a low pulsatility (flow velocity 56/12 cm/s, PI = 2.1).

Fig. B18.12 Extracranial duplex, longitudinal plane. Doppler spectrum analysis of the left ICA demonstrating direct signs of a dissecting lesion with a distal vessel widening (dotted lines) due to an intramural hematoma (arrows), subsequently causing a marked local stenosis. Despite this, only a low flow velocity and a high pulsatility was seen and considered as indirect signs of an additional flow obstruction with further distal location (flow velocity 55/9 cm/s, PI = 2.1)

Conclusion

Traumatic four-vessel dissection with steno-occlusive infraophthalmic lesions of both ICAs and with multisegmental stenoses of both VAs. Additional bilateral VA hyperperfusion due to collateral function via the PCoAs toward the anterior circulation as well as additional collateral flow via both OAs.

Clinical Course (2)

The patient’s condition remained stable with further slight improvement of the hemiparesis and aphasia. Because of the suspected steno-occlusive lesion of the left ICA not seen before, a second DSA was performed.