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Background: Vertebral artery stump syndrome (VASS) develops into recurrent posterior circulation ischemic stroke after ipsilateral vertebral artery (VA) occlusion at its origin. Case Description: The patient was a 46-year-old man with the right posterior cerebral artery occlusion. We used a recombinant tissue plasminogen activator (rt-PA) and then performed mechanical thrombectomy using a stent retriever. Angiography revealed left VA occlusion and stagnant flow to the left VA from the right deep cervical artery; therefore, we diagnosed VASS. Within 24 h of the rt-PA injection, the symptoms had dramatically improved, and so we avoided additional antithrombotic agents. Only 13 h later, the patient developed a basilar artery occlusion and died in spite of a repeated mechanical thrombectomy. Conclusion: Vigilance against early (and sometimes fatal) recurrent stroke induced by VASS is required.

A 56-year-old man noted sudden onset of headache, fever, right pupil-spared oculomotor nerve palsy and consciousness disturbance. Swelling of pituitary with T1 high intensity on brain MRI suggested the diagnosis of pituitary apoplexy. Considering significant decrease of pituitary anterior lobe hormone and central diabetes insipidus, high dose of hydrocortisone was administered. Eight days after onset, consciousness level and headache improved. On day 30, brain MRI revealed the reduction of mass size, and on day 46, photophobia and double vision disappeared. Following the rapid response to steroid and disappearance of pituitary lesion, pituitary apoplexy was probably caused by panhypophisitis. Thin-slice brain MRI confirmed the compression of oculomotor nerve at inlet zone of cavernous sinus, suggesting the mechanism of oculomotor palsy was perfusion impairment of feeding artery.

Background: Carotid endarterectomy (CEA) has been the standard preventive procedure for cerebral infarction due to cervical internal carotid artery stenosis, and internal shunt insertion during CEA is widely accepted. However, troubleshooting knowledge is essential because potentially life-threatening complications can occur. Herein, we report a case of cervical internal carotid artery injury caused by the insertion of a shunt device during CEA. Case Description: A 78-year-old man with a history of hypertension, diabetes, and hyperuricemia developed temporary left hemiplegia. A former physician had diagnosed the patient with a transient cerebral ischemic attack. The patient’s medical history was significant for the right internal carotid artery stenosis, which was severe due to a vulnerable plaque. We performed CEA to remove the plaque; however, there was active bleeding in the distal carotid artery of the cervical region after we removed the shunt tube. Hemostasis was achieved through compression using a cotton piece. Intraoperative digital subtraction angiography (DSA) revealed severe stenosis at the internal carotid artery distal to the injury site due to hematoma compression. The patient underwent urgent carotid artery stenting and had two carotid artery stents superimposed on the injury site. On DSA, extravascular pooling of contrast media decreased on postoperative day (POD) 1 and then disappeared on POD 14. The patient was discharged home without sequela on POD 21. Conclusion: In the case of cervical internal carotid artery injury during CEA, hemostasis can be achieved by superimposing a carotid artery stent on the injury site, which is considered an acceptable troubleshooting technique.