Reversal of carotid dissection-induced ocular and cerebral ischemia by stenting

Abstract

Purpose: To present an example of how close clinical monitoring of a patient with acute Horner syndrome from carotid artery dissection may be critical in reversing neurologic dysfunction.

Observations: A patient whose initial neuro-ophthalmic manifestation was Horner syndrome, but who evolved over 14 days to display transient monocular vision loss, ipsilateral ocular ischemic syndrome, and episodic contralateral hemiparesis. Digital subtraction angiography demonstrated progressive ipsilateral carotid occlusion with lack of collateral flow. The patient underwent stenting with rapid reversal of transient monocular visual loss and hemiparesis. Follow-up examination several months later confirmed complete resolution of all clinical abnormalities.

Conclusions and importance: This case displayed protracted evolution of ischemic manifestations following carotid artery dissection and their prompt reversal with stenting. This case emphasizes the value of close clinical attention to a patient with acute Horner syndrome because manifestations may appear more than 10 days after event onset that impel intervention for the dissection.

Keywords: Carotid artery dissection; Carotid artery stenting; Hemiparesis; Horner syndrome; Ischemic ocular syndrome.

Fig. 1

Initial computed tomography angiogram (CTA) in axial projection (A) demonstrates a narrowed column of contrast in the high cervical right internal carotid artery (arrow) consistent with dissection. Corresponding maximum intensity projection (MIP) (B) demonstrates the narrowed arterial portion (arrows). Repeat CTA performed 12 days after the initial CTA in the axial projection (C) demonstrates interval worsening of the internal carotid artery dissection (arrow). Corresponding MIP (D) demonstrates apparent occlusion at the cervical-petrous junction (arrows).

Fig. 2

Catheter angiogram (early arterial phase) in the anteroposterior (A) and lateral (B) projections, performed on the same day as the repeat computed tomography angiogram (Fig. 1CD), demonstrates an irregular, narrowed column of contrast in the right internal carotid artery (solid arrows) consistent with dissection. There is normal opacification of right external carotid branches (dashed arrow). Anteroposterior projection in the late arterial phase (C) demonstrates washout of the contrast within the right external carotid artery (dashed arrow) but persistence of contrast within the right internal carotid artery (arrow head), indicating prolonged transit time compared to the right external carotid artery (dashed arrow). Left internal carotid artery angiogram in the anteroposterior projection (D) demonstrates normal left cerebral vascular opacification (solid arrow) but absence of cross filling of the right anterior and middle cerebral arteries. The lack of collateral flow partly explains why a critical stenosis of the right internal carotid artery might have led to enough cerebral ischemia to cause transient contralateral hemiparesis.

Fig. 3

Right internal carotid angiogram in anteroposterior (A) and lateral (B) projections performed after placement of three Neuroform stents within the right internal carotid artery demonstrates substantial improvement in caliber and flow within the carotid artery (arrows).

Fig. 4

Time line of the patient’s clinical and radiologic events.