Third nerve palsy following carotid artery dissection and posterior cerebral artery thrombectomy: Case report and review of the literature

Abstract

Background: Common causes of oculomotor nerve palsy are diabetes, aneurysmal compression, and uncal herniation. A lesser-known cause of third nerve dysfunction is ischemia, often due to carotid artery dissection.

Case description: An 80-year-old man presented with an acute ischemic stroke with a National Institutes of Health Stroke Scale score of >20 from a high cervical internal carotid artery (ICA) dissection and a tandem ICA terminus embolic occlusion with extension of clot into the adjacent fetal posterior cerebral artery (PCA). We used a stentriever to perform selective PCA thrombectomy, with immediate postthrombectomy development of ipsilateral anisocoria. The anisocoria progressed into complete oculomotor nerve palsy over 8 h after the procedure.

Conclusions: The clinical course described in this case is consistent with injury to the third nerve due to mechanical injury or occlusion of perforator supply to the nerve during thrombectomy. Oculomotor nerve palsy is a rare but known complication after ischemia; however, to our knowledge, this is the first case after thrombectomy for a PCA embolus.

Keywords: Carotid artery dissection; mechanical thrombectomy; oculomotor nerve palsy; stroke; third cranial nerve palsy.

Figure 1

(a) Cerebral blood volume scan from a CT perfusion study obtained at the time of admission. A small area of volume deficit is visible in the left PCA territory. (b) Time-to-peak map from the CT perfusion study showing a large area of reduced perfusion in the left PCA, consistent with salvageable penumbra. (c) CT angiogram of the common carotid artery. Proximal occlusion consistent with a dissection flap is seen (arrow). (d) CT angiogram of cerebral vessels showing an early filling defect in the terminal ICA (arrow)

Figure 2

Angiograms preceding and following endovascular intervention. (a) Right ICA injection showing contralateral filling of the MCA with a defect suggestive of a dissection in the ICA terminus on the left (arrow). (b) Left vertebral injection showing filling of the right but not the left PCA. There is retrograde filling of the distal left P2 by superior cerebellar artery collaterals (arrow on far right). (c) Left carotid artery angiogram showing progressive narrowing of the ICA lumen (arrow), consistent with artery dissection. (d) Left ICA injection showing late filling of the left ophthalmic artery due to collateral circulation (arrow). No back filling of the ICA terminus was observed. (e) Left ICA injection is shown. The Penumbra catheter (Penumbra, Inc., Alameda, California, USA) visibly cleared the proximal ICA occlusion; however, a dissection flap is visible distally (arrow). (f) Angiogram obtained immediately after Solitaire (ev3-Covidien, Irvine, California, USA) thrombectomy shows good filling of the distal ICA; however, an occlusion persists in the left P2 segment of the PCA (arrow)

Figure 3

Picture taken on hospital day 4 of patient's right and left eyes, respectively. Mydriasis of the left eye is visible with deviation laterally and inferiorly

Figure 4

(a) CT scan of the head on hospital day 1, after left pupillary dilation was first observed. Hypodensity in the left PCA territory is seen; no effacement of cisterns was evident. (b) Axial T2 fluid-attenuated inversion recovery (FLAIR) magnetic resonance image on hospital day 5 showing evolving left PCA infarct. (c) Coronal T2 magnetic resonance image of head. A left-sided hyperintensity is visible in the retroglobar area (arrow), consistent with congestion of the superior ophthalmic vein