Cerebral hyperperfusion syndrome after endovascular reperfusion therapy for medium vessel occlusion: A case report.

Cerebral hyperperfusion syndrome is a rare but serious complication after revascularization procedures for cerebrovascular diseases. Cerebral hyperperfusion syndrome can develop after treatment of acute ischemic stroke, including intravenous thrombolysis and endovascular treatment of large vessel occlusion. However, to the best of our knowledge, there are no previous reports describing cerebral hyperperfusion syndrome after endovascular treatment of medium vessel occlusion (eg, anterior cerebral artery A2/3 segment). We report a case of cerebral hyperperfusion syndrome after endovascular reperfusion therapy for medium vessel occlusion. A 70-year-old woman with a history of hypertension and dyslipidemia was transferred by ambulance to our hospital because of immobility and slurred speech. She had mild right lower extremity paralysis, and her symptoms appeared improved compared with onset. She was diagnosed with cerebral infarction in the left frontal lobe. After hospitalization, her neurological symptoms worsened and she was referred to our department. We performed endovascular reperfusion therapy for left anterior cerebral artery A2 occlusion. Recanalization was achieved with residual stenosis. Despite the lack of complications associated with the procedure, the patient had prolonged disorientation, severe hemiplegia, and aphasia. Arterial spin labeling demonstrated hyperperfusion in the left anterior cerebral artery area. The symptoms gradually improved under strict blood pressure control. This report provides evidence that cerebral hyperperfusion syndrome can occur even after endovascular treatment for medium vessel occlusion. Arterial spin labeling was useful in detecting hyperperfusion.

Acute reperfusion therapy via occluded vertebral artery using a guiding sheath for posterior circulation tandem occlusion: illustrative case.

BACKGROUND: Vertebral artery (VA) size, anatomy, and occlusion status should be considered when selecting endovascular access for basilar artery mechanical thrombectomy. In a patient with concomitant basilar artery and VA occlusion and a patent but hypoplastic contralateral VA, the occluded VA should be selected. The authors report a technique that utilizes advancing a guiding sheath with attached dilator via an occluded VA. OBSERVATIONS: A 65-year-old male presented with disturbed consciousness because of an acute infarction of the brainstem and cerebellum caused by a basilar artery occlusion. Cerebral angiography showed a hypoplastic right VA and occlusion of the left VA at the origin. A regular wire was easily advanced through the occlusion and a 4-Fr diagnostic catheter was advanced into the distal left VA. A 6-Fr guiding sheath with attached dilator was placed in the left VA beyond the occlusion by exchanging it over a long wire. After removing the basilar artery thrombus, balloon angioplasty was performed at the left VA origin. Complete revascularization of the posterior circulation was achieved. LESSONS: A guiding sheath with dilator can advance across and dilate a VA occlusion at the origin to provide rapid access to the basilar artery.

Large vessel occlusions requiring repeated mechanical thrombectomy caused by silent myocardial infarction in a young adult.

OBJECTIVES: Silent myocardial ischemia, defined as objective evidence of myocardial ischemia without symptoms, is associated with ischemic stroke. Nevertheless, silent myocardial infarction is a rare cause of ischemic stroke, especially in young adults with no medical history. MATERIALS AND METHODS: Herein, we report a young adult patient with acute ischemic stroke treated with repeated mechanical thrombectomy for recurrent large vessel occlusions caused by left ventricular thrombus following a silent myocardial infarction. RESULTS: A 40-year-old man was transferred by ambulance to our hospital because of a generalized seizure. He was diagnosed with cerebral infarction and left middle cerebral artery occlusion. We performed intravenous thrombolysis and mechanical thrombectomy. Recanalization was achieved and his symptoms gradually improved. However, the day after treatment he developed bilateral cerebellar infarction and basilar artery occlusion. We performed a second mechanical thrombectomy and recanalization was achieved. Transthoracic echocardiography revealed a mobile left ventricular thrombus. Although he had no previous chest symptomatic episodes, cardiac examination confirmed myocardial infarction of unknown onset. He was diagnosed with acute ischemic stroke with large vessel occlusions caused by left ventricular thrombus following a silent myocardial infarction. Anticoagulation therapy reduced the amount of thrombus. At 1-year follow-up, he had not experienced any recurrences or symptoms. CONCLUSIONS: Silent myocardial infarction should be considered a cause of ischemic stroke in young adults, even without any vascular risk factors. Recurrent large vessel occlusion may occur in patients with left ventricular thrombus, and repeated mechanical thrombectomy should be considered for treatment.

Target Embolization of Dilated Post-PICA Segment for Ruptured PICA-Involved Type Vertebral Artery Dissecting Aneurysm.

Objective: In parent artery occlusion (PAO) for ruptured vertebral artery dissecting aneurysms (RVADA), target embolization using coils in a short segment to occlude only the vasodilated area containing the rupture point is selected as a first-choice procedure at our institute. We focused on RVADA involving the posterior inferior cerebellar artery (PICA) and evaluated the treatment results. Methods: This study consisted of eight cases with RVADA involving the PICA which were treated between October 2007 and January 2020. Based on radiological findings such as the bleb, the rupture points were located at the affected vertebral artery (VA) distal to PICA in all cases. Target embolization, by which only coiling at the dilated segment distal to the VA was performed. We aimed to preserve blood flow to the PICA. The incidence and extent of medullary infarctions, and neurological outcome were retrospectively assessed. Results: Regarding the diameter of bilateral VA, there were no differences in six cases while the affected VA with RVADA were larger in the remaining two cases. PICA was preserved in all cases but one in which occlusion of complementary PICA was observed. Postoperative medullary infarction was not noted. There was no rebleeding during the follow-up period. However, recanalization of the VA was observed in four cases and additional coil embolization was performed. All patients were discharged with a good outcome (modified Rankin Scale [mRS] 0; seven patients, mRS 2; one patient). Conclusion: Target embolization preserving the PICA in PICA-involved type RVADA was considered to be an effective treatment method for cases whose rupture point was located in the VA distal to PICA orifice.