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

Case 18


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?





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.






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).






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.


Second Conventional Angiography (Day 4)


The second DSA confirmed a right-sided submandibular rat-tail-like ICA occlusion with collateral supply of the still open MCA and ACA territory via the PCoA and retrograde right OA. The left ICA now revealed a long-segmented extracranial stenosis beneath the known small dissecting aneurysm. However, the major finding was a new circumscribed high-grade left ICA stenosis in the petrosal part at the junction between the vertical and horizontal segment. There was also a progressed lumen reduction in the left VA, which was important as the main collateral flow into both anterior circulations was ensured by the vertebrobasilar circulation (Fig. B18.21, Fig. B18.22, Fig. B18.23).


Jun 20, 2018 | Posted by in NEUROSURGERY | Comments Off on 18 Traumatic Bilateral Internal Carotid and Vertebral Artery Dissection with Right-sided Embolic Middle Cerebral Artery Occlusion
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