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Background: Delayed ipsilateral intraparenchymal hemorrhage (IPH) has been reported following technically successful treatment of intracranial aneurysms using flow-diverting stents (Pipeline embolization device) in 8.5% of patients and does not appear to be related entirely to dual antiplatelet therapy. We report a similar phenomenon in Neuroform-assisted coiling. Methods: Neuroform-assisted coiling patients were entered into a prospective registry at our institution. Procedural and 30 day complications were recorded. Delayed ipsilateral IPH cases within 30 days were reviewed. Results: Between 11/2002 and 7/2012, 98 patients had Neuroform-assisted coiling of 100 cerebral aneurysms, 8 acutely ruptured. Intra-procedurally, there were 3 thromboembolic events and 4 hemorrhages due to vessel or aneurysm perforation (not necessarily symptomatic). After the procedure but within 30 days follow-up (available for 92 patients), there were 6 TIA’s, 2 minor strokes and 1 SAH. There were 2 cases of ipsilateral IPH (2%). One was a 60-year-old man who had stent-assisted coiling of an ACOM aneurysm (Neuroform from right A1 into left A2). He was on aspirin 81 mg and clopidogrel 75 mg daily with a PRU (P2Y12 reaction units) of 72 on day of procedure. Despite decreasing clopidogrel dosing to every other day, he had a frontal lobe IPH 7 days later (Figure 1) with a PRU of 59. The other IPH (Figure 2) occurred in a 70-year-old man 14 days after Y-stent assisted coiling of an MCA aneurysm. He was on clopidogrel 75 mg and warfarin (INR 2.0) for prior pulmonary embolism and dural venous sinus thrombosis. Both patients recovered without neurological deficit. Conclusion: Recently described in flow diversion, delayed ipsilateral IPH is not limited to flow-diverting stents. Though less frequent, a potential for this may exist following any intracranial stenting procedure, possibly related to hemorrhagic conversion of microembolic phenomenon while on dual antiplatelets or anticoagulation.

Purpose: To determine the number of clopidogrel or prasugrel dose adjustments needed and final DAT regimen used to maintain patients undergoing Pipeline Embolization Device (PED) procedures within a target P2Y12 inhibition range. Methods: We recorded the number of clopidogrel or prasugrel dose adjustments, final DAT regimen and thromboembolic and hemorrhagic complications in patients undergoing PED procedures at our institution over an 8-month period. P2Y12 inhibition was measured with VerifyNow 10 and 30 days after dose adjustments (target range 80-200 P2Y12 reaction units). Patients received 325mg aspirin daily. Results: Forty-four patients underwent PED procedures at our institution during the study period, 36 female and 8 male, mean age 59 years (median 63 years, range 31-81 years). Thirteen patients did not require dose adjustments to remain within the target P2Y12 inhibition range (30%). Thirty-one patients required dose adjustments to remain within the target P2Y12 inhibition range (70%), with a mean of 2.1 dose adjustments per patient (median 2, range 1-5), and a mean time from initiation of DAT to last dose adjustment of 47.5 days (median 42 days, range 8-149 days). Four patients exceeded the target P2Y12 inhibition range after a dose adjustment (13%, 3 prasugrel, 1 clopidogrel), without complications. The table summarizes the final DAT regimen and associated major thromboembolic and hemorrhagic complications leading to death or a permanent neurological deficit in our cohort. Most major complications (80%) occurred in patients who were outside the target P2Y12 inhibition range shortly before or at the time of the complication. Conclusion: The majority of patients undergoing PED procedures in our cohort (70%) required an average of 2 clopidogrel or prasugrel dose adjustments to remain within a target P2Y12 inhibition range. Future research is needed to determine if active management of DAT may decrease the risk of major complications after PED procedures.

Purpose: To determine the medium-term angiographic outcome and packing density threshold for complete aneurysm occlusion at follow-up in a series of cerebral aneurysms treated with a single coil. Methods: We retrospectively identified all cerebral aneurysms treated with a single coil at our institution from July 1997 until September 2011. We recorded aneurysm dimensions, neck size, packing density, and follow-up catheter or MR angiograms to determine the angiographic outcome at last follow-up according to the Raymond scale. We then performed receiver operating characteristic (ROC) analysis of the likelihood of complete aneurysm occlusion at follow-up to determine the packing density maximum operating point (MOP). Results: Eighty-one aneurysms in 79 patients were treated with a single coil at our institution during the study period. Sixty-four patients were female (81%) and mean age was 53 years (range 23-87 years). Mean maximum aneurysm dimension was 2.8mm (range 1.6-4.8mm), and mean dome-to-neck ratio was 1.3 (median 1.3, range 0.8-1.9). Mean aneurysm packing density was 35.3% (median 32.8%, range 10.2-94.3%). Three patients with ruptured aneurysms died during the hospitalization (7.7%), and follow-up angiographic examinations were performed in 65 patients with 67 aneurysms (85.9%). Mean time to last angiographic follow-up was 26.4 months (range 4-102 months). Complete aneurysm occlusion at last follow-up was present in 46 aneurysms (68.7%), a neck remnant in 16 aneurysms (23.9%) and sac recanalization in 5 aneurysms (7.4%). ROC analysis of the likelihood of complete aneurysm occlusion at last follow-up yielded a packing density MOP of >36.3%, with a specificity of 85.7%, sensitivity of 47.8%, and an area under the curve of 0.61 (95%CI 0.49-0.73). There was a statistically-significant difference in the likelihood of complete aneurysm occlusion at last follow-up between the 25 aneurysms with a packing density >36.3% (88%), and the 42 aneurysms with a packing density ≤36.3% (57.1%, OR 5.5 [95%CI 1.4-21.3], p-value 0.009). Conclusion: Achieving a packing density >36.3% predicts a significantly higher likelihood (88%) of complete aneurysm occlusion at medium-term angiographic follow-up in cerebral aneurysms treated with a single coil.

Purpose: To determine the yield of catheter angiography for the detection of causative vascular lesions in patients with subarachnoid hemorrhage (SAH) who have a negative initial non-invasive neurovascular examination. Methods: Between January 1st, 2006 and August 1st, 2011, we instituted a prospective protocol by which patients who presented to our institution with SAH and had a negative initial non-invasive neurovascular examination (CT or MR angiogram [CTA, MRA]) were examined with catheter angiography to detect causative vascular lesions. Two experienced neuroradiologists evaluated the NCCTs to determine the pattern of SAH (diffuse, perimesencephalic or peripheral) and the catheter angiograms to assess for the presence of a causative vascular lesion. All differences in reader interpretation were resolved by consensus. Results: Forty-eight patients were included in our study, with a mean age of 58 years (median 59 years, range 25-84 years). Twenty-six patients were male (54.2%) and 22 female (45.8%). Twenty-eight patients had diffuse SAH (58.3%), 11 peripheral SAH (22.9%) and 9 perimesencephalic SAH (18.8%). The initial non-invasive neurovascular examination was a CTA in 41 patients (85.4%) and an MRA in 7 patients (14.6%). A second catheter angiogram was performed in 30 patients (62.5%). Mean time interval between the initial non-invasive neurovascular examination and the first catheter angiogram was 0.9 days (median 1 day, range 0-7 days) and the second catheter angiogram was 12.2 days (median 8.5 days, range 4-69 days). Catheter angiography demonstrated a causative vascular lesion in 4 patients (8.3%), 3 of which had diffuse SAH (yield of 10.7%) and 1 had peripheral SAH (yield of 9.1%). Of note, 1 of the causative vascular lesions was identified in a second catheter angiogram performed 8 days after the CTA in a patient with diffuse SAH. The vascular lesions identified were 2 dural arteriovenous fistulas, 1 pial cerebellopontine angle arteriovenous malformation with a 2-mm feeding artery aneurysm located in the internal auditory canal ( Figure ), and a 3-mm anterior communicating artery aneurysm. Two of the vascular lesions underwent endovascular embolization, 1 radiosurgery and 1 endovascular embolization followed by radiosurgery. In retrospect, the vascular lesion could be seen in the initial examination in 2 patients. Conclusion: Catheter angiography is a valuable tool in the evaluation of patients with diffuse and peripheral SAH who have a negative initial non-invasive neurovascular examination, demonstrating a causative vascular lesion in 10.7% and 9.1% of patients, respectively.

Purpose: To determine the yield of repeat CT angiography for the detection of causative vascular lesions in patients with subarachnoid hemorrhage (SAH) who have negative initial CT and catheter angiograms. Methods: We conducted a retrospective review of patients who presented to our institution between January 1st, 2008 and August 1st, 2011 with SAH and negative initial CT and catheter angiograms who were examined with repeat CT angiography in order to determine the yield of this imaging modality for the detection of causative vascular lesions. Two experienced neuroradiologists evaluated the NCCTs to determine the pattern of SAH (diffuse, perimesencephalic or peripheral) and the CT angiograms (CTA) to assess for the presence of a causative vascular lesion. All differences in reader interpretation were resolved by consensus. Results: Twenty-two patients were included in our study, with a mean age of 78 years (median 59 years, range 28-78 years). Sixteen patients were male (72.7%) and 6 female (27.3%). Seventeen patients had diffuse SAH (77.3%), 4 perimesencephalic SAH (18.2%) and 1 peripheral SAH (4.5%). Mean time interval between the initial neurovascular examination and the repeat CTA was 26.5 days (median 20.5 days, range 2-150 days). The repeat CTA demonstrated a causative vascular lesion in 2 patients (9.1%), all of which had diffuse SAH (yield of 11.8%). The vascular lesions identified were 1 small pontine arteriovenous malformation and a 2-mm supraclinoid internal carotid artery aneurysm ( Figure ). The pontine arteriovenous malformation underwent radiosurgery and the internal carotid artery aneurysm underwent surgical clipping. In retrospect, none of these vascular lesions were evident in the initial CT or catheter angiograms. Conclusion: Repeat CT angiography is valuable in the evaluation of patients with diffuse SAH who have negative initial CT and catheter angiograms, demonstrating a causative vascular lesion in 11.8% of patients.