Abstract
INTRODUCTION: Cerebral arteriovenous malformations (AVM) are an abnormal tangle of blood vessels in the brain that connects arteries to veins directly. This can lead to a variety of symptoms, including headaches, hemorrhages, seizures, and progressive neurological deficits. Effective treatment requires a multidisciplinary, individualized approach to maximize positive outcomes. We present the successful case of an 86‐year‐old male with a complex cardiac history who developed acute‐onset weakness and refractory focal motor seizures due to a large subcortical AVM in an eloquent location, treated with n‐Butyl Cyanoacrylate (nBCA) embolization while awake. RESULTS: 86‐yo male with a significant cardiac history, including hypertension, persistent atrial fibrillation on Xarelto, and heart failure, presented to the emergency department (ED) two hours after developing left facial droop, dysarthria, followed by a left‐sided focal motor seizure. Computerized tomography (CT) scan of the brain revealed a hypodense area in the right fronto‐parietal lobe, associated with vasogenic edema. Magnetic resonance imaging (MRI) indicated a possible AVM, with subtle nodular enhancement along the cortex and evidence of prior microhemorrhages. A diagnostic cerebral angiogram confirmed the presence of a Spetzler‐Martin grade 2 pial AVM in the posterior right frontal region, with a nidus measuring 6.2 mm by 4.29 mm. The AVM was supplied by the distal arterial pedicle from the inferior branch of the middle cerebral artery (MCA) and drained into the vein of Trolard. No aneurysm, varix, or venous congestion was identified. Following optimization of the patient's heart failure and seizure management, a multidisciplinary team discussed treatment options with the patient and his family. Given the AVM's eloquent location, n‐Butyl Cyanoacrylate (nBCA) embolization was performed while the patient was awake to allow for continuous neurological monitoring. Propofol was slowly injected into the arterial pedicle supplying the nidus, followed by a thorough neurological examination, which revealed no deficits. The nBCA embolization was then completed. Post‐procedural angiography showed significant obliteration of the AVM nidus and reduced arteriovenous shunting. The patient did not experience any parenchymal perfusion defects, thromboembolic complications, or vascular injuries. He was monitored in the neurointensive care unit and exhibited only mild left‐sided weakness and facial droop. Repeat CT imaging was stable. At a five‐month follow‐up, a cerebral angiogram demonstrated complete obliteration of the AVM, with no residual shunting. The patient remained neurologically intact and seizure‐free. A follow‐up angiogram is planned for six to twelve months to monitor for ongoing stability. CONCLUSION: The successful treatment of this complex cerebral AVM using n‐BCA embolization in an awake state underscores the importance of a carefully tailored, multidisciplinary approach to managing such cases. Performing the procedure while the patient is awake allowed for continuous neurological monitoring, significantly reducing the risk of inadvertent damage. This case illustrates that, even in patients with significant comorbidities and high procedural risks, a well‐coordinated, individualized treatment strategy can lead to favorable outcomes. Ongoing follow‐up will be essential to maintain long‐term stability and address any potential complications.