Endovascular Treatment of an Acute Embolic Anterior Cerebral Artery Occlusion and a Pseudoaneurysm Resulting from Chronic Dissection of an Extracranial Segment of the Internal Carotid Artery

A 58-year-old male was admitted to our hospital in July 2008 with right-sided hemiparesis affecting the leg primarily and aphasia since awakening and a National Institute of Health Stroke Scale (NIHSS) score of 12 points. He had a history of arterial hypertension and underwent mitral valve reconstruction 9 years before presentation. A magnetic resonance imaging study revealed acute infarction in the vascular territory supplied by the left anterior cerebral artery. Because the patient’s condition was unclear at the time of onset, intravenous thrombolysis was not performed. Digital subtraction angiography (DSA) revealed a dissecting pseudoaneurysm and stenosis of the left internal carotid artery (ICA) and embolic occlusion of the left pericallosal artery. The left pericallosal artery was recanalized using a self-expanding nickel-titanium stent (Enterprise, Cerenovus) with no procedural complications. The patient was discharged with mild neurological deficits (NIHSS score of 2 points) on acetylsalicylic acid (100 mg/day) and clopidogrel (Plavix, 75 mg/day) for secondary prevention. A follow-up DSA performed 10 weeks after discharge revealed patency of the left A2 segment and no evidence of in-stent thrombosis. The DSA confirmed chronic dissection of the left cervical ICA with a fusiform extension and high distal stenosis. The neurology, neurointerventional, and cardiovascular surgical teams reviewed the case. These groups concluded that, given the overall likelihood of another infarction, the potential benefits of combined surgery and endovascular treatment outweighed the potential risks. One month later, a surgical shortening of the left ICA was performed to eliminate the kinked segment. The fusiform aneurysm was covered, and the distal ICA stenosis was removed by stent-mediated percutaneous transluminal angioplasty at that time. The patient’s hospital course was otherwise uneventful, with no neurologic complications and continued aspirin and clopidogrel. One month later, the patient developed a fatal intracerebral hemorrhage, most likely due to arterial hypertension complicated to some extent by the dual antiplatelet regimen. This chapter discusses the risks associated with dissecting ICA aneurysms and strategies used to minimize the development of distal emboli and associated hemodynamic events.