11 Secondary Occlusion in Left-sided Extracranial Internal Carotid Artery Dissection

Case 11

Secondary Occlusion in Left-sided Extracranial Internal Carotid Artery Dissection

Clinical Presentation

A 43-year-old man complained of transient right-sided weakness, amnesic aphasia, and decreased visual acuity in his left eye that started while he was undertaking exercise in a gym. The symptoms gradually faded over 15 minutes. The patient had no vascular risk factors except for a known migraine with aura. On admission to our hospital he was free of symptoms. Headaches were not reported. The neurologic examination revealed a mild left-sided Horner’s syndrome. There were no other focal neurologic deficits.

Initial Neuroradiologic Findings

Cerebral MRI on the day of admission showed no ischemic parenchymal lesion but perfusion imaging revealed a pronounced hypoperfusion within the left middle cerebral artery (MCA) territory and both anterior cerebral artery (ACA) territories. Time-of-flight MR angiography (TOF-MRA) showed reduced signal intensity in the left distal internal carotid artery (ICA), left MCA, and both ACAs, as well as an aplasia or severer hypoplasia of the right A1-ACA segment and both posterior communicating arteries (PCoAs) (Fig. B11.1 and Fig. B11.2). The cervical vessels were not examined, yet axial T2-weighted images at the level of the skull base suggested an intramural hematoma of the left ICA.

Suspected Diagnosis

Dissection of the left ICA.

Questions to Answer by Ultrasound Techniques

  • Was there evidence of dissection, high-grade stenosis, or occlusion of the ICA?
  • If so, was there evidence of collateral blood flow via the ACA, PCoA, ophthalmic artery (OA), or leptomeningeal vessels via the posterior cerebral artery (PCA)?

Initial Neurosonologic Findings (Day 1)

Extracranial Duplex Sonography

B-mode ultrasound did not show atherosclerosis or other structural vessel abnormalities and no direct signs of vessel dissection. Color-mode imaging of the left ICA demonstrated a tapering lumen and reduced color signal intensity. Doppler spectrum analysis revealed a pronounced reduction of flow velocity (28/8 cm/s) in contrast with the contralateral side (78/26 cm/s) (Fig. B11.3 and Fig. B11.4; see also Video images B11.1). The external carotid artery (ECA) had an increased diastolic, i.e., an “internalized,” blood flow pattern. Assessment of the vertebral arteries (VAs) was normal.

Transcranial Duplex Sonography

A poststenotic flow pattern was observed in the left carotid siphon, the left M1-MCA segment, and the left A1-ACA segment. No right A1-ACA segment and no flow signal in the presumed area of both PCoAs were detected. The flow direction in the left OA was reversed and showed a high diastolic flow component similar to that of a brain-supplying artery. The right OA was normal. Assessment of the posterior circulation was unremarkable and without evidence of collateral leptomeningeal flow (Figs. B11.5B11.10; see also Videos images B11.2 and B11.3).


Suspected dissection of the left ICA with high-grade stenosis of hemodynamic relevance below the OA origin. Insufficient intracranial collateral blood flow toward the left MCA and both ACA territories solely via the left OA.

Clinical Course (1)

Intravenous heparin was started, aiming for a doubling of partial thromboplastin time (PTT). During the patient’s first night in hospital, he developed a severe right-sided brachiofacial paresis and a global aphasia. Laboratory monitoring revealed a fourfold increase in PTT. Intracranial bleeding was ruled out by a CT scan.

Questions to Answer by Ultrasound Techniques

  • Was the clinical worsening caused by a thromboembolic event with secondary occlusion of distal MCA branches or by hemodynamic impairment due to stenosis progression or occlusion of the ICA?
  • If an occlusion of the ICA was present, which collateral pathways were activated in comparison with the initial investigation?

Follow-up Neurosonologic Findings (Day 2)

Extracranial Duplex Sonography

B-mode imaging of the left ICA remained unchanged. However, Doppler spectrum analysis now demonstrated a high-resistance flow signal with a low and short systolic flow and completely absent diastolic flow component indicating distal ICA occlusion proximal to the OA origin (Fig. B11.11).

Transcranial Duplex Sonography

A worsened poststenotic flow pattern was observed in the left M1-MCA and A1-ACA segments. Furthermore, there was an increase of retrograde flow in the left OA. Raised flow velocity in the left P2/3-PCA segments, previously not observed, indicated leptomeningeal collateral flow from the PCA to the left anterior territory (Fig. B11.12, Fig. B11.13, Fig. B11.14, Fig. B11.15).


Secondary distal occlusion of the left ICA. Further worsening of the pre-existing insufficient blood flow in the left MCA and both ACA territories. Collateralization via the left OA and in addition via leptomeningeal collaterals from the left PCA.

Fig. B11.16 shows a schematic drawing of the extra-and intracranial brain-supplying arteries.

Clinical Course (2)

CT angiography (CTA) demonstrated a left intracranial ICA occlusion in its petrosal part. The beginning of the dissection was assumed to be located in the midcervical extracranial ICA (Fig. B11.17). None of the studied intraand extracranial arteries showed evidence of fibromuscular dysplasia. Under hypervolemic treatment the aphasia and the hemiparesis improved slowly over subsequent days. Six days after admission, cerebral MRI revealed a large internal border zone infarction (BZI) between the left ACA and MCA territories (Fig. B11.18).

Follow-up Neurosonologic Findings (Day 7)

Extracranial Duplex Sonography

Partial reopening of the left ICA was seen, now demonstrating a flow signal similar to that on day 1 (Fig. B11.19; see also Video images B11.4).

Transcranial Duplex Sonography

A continuing poststenotic flow pattern was seen within the left M1-MCA and A1-ACA segments. However, flow velocities had slightly increased. The OA flow was still reversed indicating a persisting hemodynamically relevant ICA obstruction below the origin of the OA (Fig. B11.20; see also Video images B11.5 and B11.6).


Partial reopening of the distal ICA with a remaining hemodynamically relevant high-grade stenosis. The result is equivalent to the neurosonologic findings on admission.

Clinical Course (3)

Treatment was changed from heparin to continuous oral anticoagulation with phenprocoumon. Three weeks after admission the patient was clinically stable and was discharged with a moderate right-sided paresis and motor aphasia.

Follow-up Neurosonologic Findings (6 Months)

Extracranial Duplex Sonography

The left ICA had normalized (Fig. B11.21; see also Video images B11.7).

Transcranial Duplex Sonography

The left MCA and ACA as well as the PCAs demonstrated normalized flow velocities and pulsatility. The flow direction of the left OA was now antegrade (Fig. B11.22, Fig. B11.23, Fig. B11.24, Fig. B11.25; see also Video images B11.8).


Flow normalization in the left ICA without signs of intracranial collateral blood flow, indicating hemodynamic normalization.

Final Diagnosis

Spontaneous dissection of the left ICA in a patient with unfavorable cerebral arterial circle (circle of Willis) due to a nonfunctional right A1-ACA and nonfunctional bilateral PCoAs. Secondary transient occlusion, presumably triggered by anticoagulation with intravenous heparin, leading to internal BZI.

Jun 20, 2018 | Posted by in NEUROSURGERY | Comments Off on 11 Secondary Occlusion in Left-sided Extracranial Internal Carotid Artery Dissection
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