Faculty Bibliography

BACKGROUND:Subarachnoid hemorrhage resulting from spontaneous perforation of a small intracranial vessel, with resultant pseudoaneurysm formation, has not been widely reported in the literature. CASE DESCRIPTION/METHODS:We present the case of a 71-year-old patient with rupture of a small aneurysm of a duplicated left anterior choroidal artery causing an acute third nerve palsy. The aneurysm was not able to be treated endovascularly without sacrifice of the parent vessel. At surgery, a pseudoaneurysm was seen completely separate from the parent vessel, which was actively bleeding through a hole in the vessel. The pseudoaneurysm was indenting the oculomotor nerve. After confirmation of adequate collateral flow, the abnormal segment of vessel was trapped and the pseudoaneurysm removed with surrounding clot. The patient's cranial nerve palsy resolved. CONCLUSIONS:This case illustrates an unusual sequela of subarachnoid hemorrhage presenting a unique challenge in surgical management.

A 39-year-old man presented with a large left paramedian frontal lobe intracerebral hemorrhage. Computed tomography angiography and magnetic resonance imaging revealed a tangle of vessels arising from the anterior cerebral arteries (ACAs) and dilated draining veins entering the superior sagittal sinus. Angiography confirmed a Spetzler-Martin grade 3, supplemented 2 arteriovenous malformation (AVM) with predominant supply from branches of the left ACA with superficial and deep drainage (Video 1). The case illustrates an unusual cerebrovascular pathology involving the entire A2 ACA segment. The AVM extended from the A1/2 junction along the entire A2 segment past the genu of the corpus callosum (A3 segment). A combined pterional transsylvian and bifrontal interhemispheric approach was performed. The proximal sylvian fissure and opticocarotid cistern were opened to expose the A1/2 junction. Once proximal control was obtained, the hematoma was evacuated to define the lateral border of the AVM. The interhemispheric fissure was then opened to identify the draining vein and the distal pericallosal arteries. The interhemispheric approach also defined the medial border of the AVM. The A2 ACAs were then skeletonized from the AVM from the A1/2 junction to the pericallosal arteries. Aneurysm clips were used to interrupt large AVM feeders from the A2 arteries, which avoids cautery and heat transmission to the parent vessel. Once the AVM was disconnected and skeletonized from the A2s, the draining vein was clipped and the nidus was removed. Indocyanine green angiography confirmed patency of the A2s and pericallosal arteries. Postoperative angiography demonstrated no residual shunting, and the patient was discharged in good condition.

INTRODUCTION:There is little data on the cost of treating brain arteriovenous malformations (AVMs). The goal of this study then is to identify cost determinants in multimodal management of brain AVMs. METHODS:One hundred forty patients with brain AVMs prospectively enrolled in the UCSF brain AVM registry and treated between 2012 and 2015 were included in the study. Patient and AVM characteristics, treatment type, and length of stay and radiographic evidence of obliteration were collected from the registry. We then calculated the cost of all inpatient and outpatient encounters, interventions, and imaging attributable to the AVM. We used generalized linear models to test whether there was an association between patient and AVM characteristics, treatment type, and cost and length of stay. We tested whether the proportion of patients with radiographic evidence of obliteration differed between treatment modalities using Fisher's exact test. RESULTS:The overall median cost of treatment and interquartile range was $77,865 (49,566-107,448). Surgery with preoperative embolization was the costliest treatment at $91,948 (79,914-140,600), while radiosurgery was the least at $20,917 (13,915-35,583). In multi-predictor analyses, hemorrhage, Spetzler-Martin grade, and treatment type were significant predictors of cost. Patients who had surgery had significantly higher rates of obliteration compared with radiosurgery patients. CONCLUSIONS:Hemorrhage, AVM grade, and treatment modality are significant cost determinants in AVM management. Surgery with preoperative embolization was the costliest treatment and radiosurgery the least; however, surgical cases had significantly higher rates of obliteration.

BACKGROUND:Despite a variety of technologies that are available for treatment of complex intracranial aneurysms, certain anatomic configurations remain challenging to address endovascularly. CASE DESCRIPTION/METHODS:A patient was found to have an incidental 12 mm × 11 mm × 10 mm, wide-necked right posterior communicating artery aneurysm with a fetal origin of the posterior cerebral artery arising directly from the aneurysm dome. After multidisciplinary discussion, a staged endovascular treatment approach was undertaken in 2 stages. First, a Y-stent construct using 2 overlapping Neuroform Atlas stents was placed into the M1 and fetal posterior cerebral artery segments. Two months later, after endothelialization of the stent construct, coil embolization of the aneurysm was performed. The patient tolerated both stages of the procedure well and was discharged the following day in each case. She remained neurologically intact, and at follow-up 5 months later had no evidence of residual or recurrent aneurysm. CONCLUSIONS:This case illustrates a number of important considerations in the management approach for wide-necked intracranial aneurysms.

BACKGROUND:Aneurysms of the anterior choroidal artery (AChA) have been associated with high treatment-associated morbidity due to ischemic complications. OBJECTIVE:To report a large clinical experience of microsurgically treated AChA aneurysms and describe a systematic approach to reduce ischemic complications. METHODS:One hundred forty-six patients with AChA aneurysms were retrospectively reviewed from a prospectively maintained database. Clinical characteristics, surgical techniques, clinical outcomes, arterial infarction, and use of intraoperative adjuncts (ie, ultrasonography, indocyanine green videoangiography, and neuromonitoring) were analyzed. RESULTS:In total, one hundred forty-three aneurysms (97.9%) were clipped. Temporary clipping was utilized in 47 cases (32.2%) with mean occlusion time of 5.6 min. Arterial infarction occurred in 12 patients (8.2%). In clipped aneurysms, 90.5% were completely obliterated, 8.8% had minimal residual (<5% of original), and 0.7% were incompletely occluded (>5% of original). Mortality (2.7%) was limited to patients with high-grade subarachnoid hemorrhage. Indocyanine green videoangiography and neuromonitoring altered operative technique in ∼20% of cases. Multivariate logistic regression identified intraoperative rupture as the sole predictor for arterial infarction. CONCLUSION:Open microsurgical clipping remains a safe, effective treatment for AChA aneurysms. Microsurgical technique is paramount in preserving AChA patency and reducing ischemic complications. Despite increasing reliance on qualitative measures of AChA blood flow (videoangiography and ultrasonography) and neurophysiological monitoring, these technologies aid us infrequently. However, these adjuncts provide important safety checks for AChA patency. Temporary clipping must be used judiciously to lower the risk of intraoperative rupture while limiting possible ischemia in the AChA territory.

INTRODUCTION/BACKGROUND:Anterior inferior cerebellar artery (AICA) aneurysms are rare, accounting for 0.2%-1.3% of all intracranial aneurysms. The standard treatment is often endovascular embolization or neck clipping; however, sacrifice of the parent vessel is sometimes necessary. Addition of revascularization procedures is a subject of controversy. The occipital artery (OA) has been used as a donor for bypass, but recently there has been a trend toward intracranial-intracranial approaches. The posterior inferior cerebellar artery (PICA)-AICA side-to-side bypass may serve as a safe alternative. OBJECTIVE:To characterize the PICA-AICA side-to-side bypass and the OA-AICA end-to-side bypass and review the literature relevant to AICA revascularization. METHODS:We performed a far-lateral approach on 12 cadaveric specimens and analyzed the regional anatomy. On this basis, we performed either an OA-AICA or a PICA-AICA bypass and took morphometric measurements relevant to the technique. RESULTS:PICA-AICA bypass was successful in 6/12 specimens. The length of the flocculopeduncular segment was 42.6 ± 15.8 mm in the specimens in which the bypass was feasible and 26.2 ± 7.2 mm in those in which the bypass was not feasible (P = 0.04). Mean distance between AICA and PICA was 5.3 ± 4 mm in the specimens in which side-to-side bypass was feasible and 11.6 ± 4.2 mm in the specimens in which it was not (P = 0.02). OA-AICA end-to-side bypass was feasible in all the specimens (75% in the flocculopeduncular segment; 25% in the cortical segment). CONCLUSIONS:This is the first cadaveric study analyzing the PICA-AICA side-to-side bypass for AICA revascularization. Our analyses provide evidence for the feasibility of this bypass and document the anatomic variations that may indicate its use.

The neurovascular unit is composed of endothelial cells, vascular smooth muscle cells, pericytes, astrocytes and neurons. Through tightly regulated multi-directional cell signaling, the neurovascular unit is responsible for the numerous functionalities of the cerebrovasculature - including the regulation of molecular and cellular transport across the blood-brain barrier, angiogenesis, blood flow responses to brain activation and neuroinflammation. Historically, the study of the brain vasculature focused on endothelial cells; however, recent work has demonstrated that pericytes and vascular smooth muscle cells - collectively known as mural cells - play critical roles in many of these functions. Given this emerging data, a more complete mechanistic understanding of the cellular basis of brain vascular malformations is needed. In this review, we examine the integrated functions and signaling within the neurovascular unit necessary for normal cerebrovascular structure and function. We then describe the role of aberrant cell signaling within the neurovascular unit in brain arteriovenous malformations and identify how these pathways may be targeted therapeutically to eradicate or stabilize these lesions.

Dural arteriovenous fistulas (DAVFs) represent 10%-15% of all intracranial arteriovenous malformations.¹ DAVFs located in the posterior cranial fossa are rare and often present with intracranial hemorrhage and myelopathy.² Arterial supply could be provided by the meningeal branches of the vertebral artery and external and internal carotid arteries.³ A 68-year-old man presented with progressive lower-extremity weakness (Video 1). Magnetic resonance imaging revealed a patchy longitudinal cord signal abnormality extending from the cervicomedullary junction to C7. A tentorial DAVF supplied by the right posterior meningeal artery with drainage via dorsal and ventral perimedullary veins was identified on angiography. According to the Cognard classification, the patient's DAVF was determined to be high risk as a type V lesion with spinal venous drainage and progressive myelopathy.⁴ The fistula was embolized with 50% ethanol resulting in near-complete occlusion. However, follow-up angiography revealed a persistent arteriovenous shunt and slightly worsening symptoms for the patient. He underwent a sitting supracerebellar approach with a torcular craniotomy for successful clip ligation of the dural arteriovenous fistula. The patient was discharged with improvements in lower-extremity strength and no residual arteriovenous shunting in postoperative imaging.