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Otakar R. Hubschmann and David Kornhauser

T he nature of response of the cortical cells to acute subarachnoid hemorrhage (SAH) remains unknown. The ensuing cellular dysfunction is most often assumed to be related to processes within the arterial wall or microvasculature, 1, 8, 13 leading to vascular spasm and ischemia from decreased local blood flow, although a convincing confirmation of this theory has not been obtained. Blood, or its byproducts, injected into the subarachnoid space or directly applied on vessel surfaces can produce vascular spasm, 2, 7, 13, 17, 25 but the causal relationship

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Samuel H. Greenblatt

I n the initial management of acute subarachnoid hemorrhage (SAH), one of the greatest concerns is to know whether there is associated brain tissue damage, especially when aneurysm surgery is anticipated. The common usage of clinical grading systems is based on this premise. Hence, the potential existence of other parameters of the brain's pathophysiological status merits serious consideration. Since mammalian erythrocytes contain only negligible amounts of creatine phosphokinase (CPK), 1, 18 Wolintz, et al. , 19 found cerebrospinal fluid (CSF) CPK levels

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Ciro Ramos-Estebanez, Maryo Kohen, Jonathan Pace, Alireza Bozorgi, Sunil Manjila, Vilakshan Alambyan, Ifeyinwa Nwankwo, Michael DeGeorgia, Nicholas C. Bambakidis, and Faruk Orge

P atients with acute subarachnoid hemorrhage (aSAH) may experience complications from Terson’s syndrome (TS). 18 This entity manifests as ocular bleeds associated with aSAH or other types of intracranial hemorrhages. 18 Estimations of the incidence of TS in aSAH range from 8% to 40%, 18 and are limited by the report’s sample size, varying definitions, and use of different diagnostic methodologies. 21 TS is easily diagnosed by funduscopy and/or ocular ultrasonography/CT in a minority of patients who present with vitreous hemorrhages (approximately 4% of cases

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Alistair Jenkins, Donald M. Hadley, Graham M. Teasdale, Barrie Condon, Peter Macpherson, and James Patterson

fossa: 50 cases. Clin Radiol 34: 173–188, 1983 7. Bydder GM , Steiner RE , Young IR , et al : Clinical NMR imaging of the brain: 140 cases. AJR 139 : 215 – 236 , 1982 Bydder GM, Steiner RE, Young IR, et al: Clinical NMR imaging of the brain: 140 cases. AJR 139: 215–236, 1982 8. Chakeres DW , Bryan RN : Acute subarachnoid hemorrhage: in vitro comparison of magnetic resonance and computed tomography. AJNR 7 : 223 – 228 , 1986 Chakeres DW, Bryan RN: Acute subarachnoid

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Ichiro Yuki, Yuichi Murayama, and Fernando Viñuela

Object. The authors report on a series of 29 patients presenting with acute subarachnoid hemorrhage (SAH) related to the rupture of a vertebrobasilar dissecting aneurysm. Special attention was focused on embolization techniques and immediate and midterm anatomical and clinical outcomes.

Methods. Between March 1994 and January 2003, 29 patients presented with acute SAH caused by the rupture of a vertebrobasilar dissecting aneurysm. Eleven patients (37.9%) had Hunt and Hess Grade I SAH, four (13.8%) Grade II, six (20.7%) Grade III, five (17.2%) Grade IV, and three (10.3%) Grade V. Aneurysms were classified into five groups based on lesion location, and treatment courses were decided. All patients except two were treated by endovascular trapping of the aneurysm with concomitant occlusion of the involved vertebral artery (VA). No technical or clinical complication was observed in 28 patients (97%). Aneurysm perforation occurred during the procedure in one patient (3%). There was evidence of aneurysm recanalization in one patient. One patient with Hunt and Hess Grade IV SAH and two patients with Grade V SAH died. One patient died of respiratory infection 1 year after aneurysm trapping. One patient presented with a recurrent hemorrhage 1 month after treatment and died. Overall morbidity and mortality rates were 13.8 and 17.2%, respectively.

Conclusions. Twenty-nine patients with acute SAH due to rupturing of vertebrobasilar dissecting aneurysms were treated using endovascular techniques. In most cases, endovascular trapping of the aneurysm and concomitant occlusion of the VA was technically and clinically successful.

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Stephan A. Mayer, Giuseppe Limandri, David Sherman, Laura Lennihan, Matthew E. Fink, Robert A. Solomon, Marco Ditullio, Louise M. Klebanoff, Avis R. Beckford, and Shunichi Homma

treatment of cardiac injury in patients with acute SAH. Fig. 2. Suggested clinical algorithm for the detection of left ventricular dysfunction in patients with acute subarachnoid hemorrhage (SAH). Refer to text for details. ECG = electrocardiogram; CK = creatine kinase. * = Q waves, ST segment elevation, or other abnormalities diagnostic of acute ischemia. Acknowledgments The authors thank Mohammed Gasser, R.D.C.S., Catherine York, R.D.C.S., and Steve Nadelberg for assistance in performing the echocardiograms, and Steven Albert, Ph.D., for

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Kazuo Tsutsumi, Yoshiaki Shiokawa, Tatsuo Sakai, Nobuhiko Aoki, Masaru Kubota, and Isamu Saito

✓ Postoperative venous infarction following aneurysm surgery was studied in 48 patients with anterior communicating artery aneurysms operated on through the interhemispheric approach at the acute stage of subarachnoid hemorrhage (SAH). Of 23 patients whose bridging veins were sacrificed during surgery, 11 (47.8%) showed venous infarction in the frontal lobes. In contrast, only one (5.9%) of 17 patients whose bridging veins were preserved developed cerebral edema. None of eight patients who were operated on after Day 11 (the day of SAH was defined as Day 0) showed this complication, although bridging veins were sacrificed in six of them. Venous infarction following acute aneurysm surgery tended to occur more frequently in patients of higher SAH grade and/or more advanced age, but these correlations were not significant. However, the correlation between the sacrifice of veins and venous infarction was significant (p < 0.025). Because this potential complication may compromise the benefit of acute aneurysm surgery and cause damage, it is important to preserve the venous system and in some instances to select another surgical approach based on the pattern of venous drainage in the frontal lobe.

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Kevin McCoyd, Kevin D. Barron, and Robert J. Cassidy

intracranial and intraspinous neoplasms with acute subarachnoid hemorrhage is well known. Stehbens 6 recently referred to both malignant and benign neoplasms, but included no proven acoustic neurinomas, as sources of subarachnoid hemorrhage. Most reported cases involved tumors that had become symptomatic before bleeding but had not been approached surgically. An early review by Glass and Abbott 4 contained one case of cerebellopontine angle neoplasm, but it was not established histologically. Various benign tumors have been reported as causes of subarachnoid hemorrhage

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Fernando Viñuela, Gary Duckwiler, and Michel Mawad

✓ From December 1990 to July 1995, the investigators participated in a prospective clinical study to evaluate the safety of the Guglielmi detachable coil (GDC) system for the treatment of aneurysms. This report summarizes the perioperative results from eight initial interventional neuroradiology centers in the United States. The report focuses on 403 patients who presented with acute subarachnoid hemorrhage from a ruptured intracranial aneurysm. These patients were treated within 15 days of the primary intracranial hemorrhage and were followed until they were discharged from the hospital or died.

Seventy percent of the patients were female and 30% were male. The patients' mean age was 58 years old. Aneurysm size was categorized as small (60.8%), large (34.7%), and giant (4.5%); and neck size was categorized as small (53.6%), wide (36.2%), fusiform (6%), and undetermined (4.2%). Fifty-seven percent of the aneurysms were located in the posterior circulation and 43% in the anterior circulation.

Eighty-two patients were classified as Hunt and Hess Grade I (20.3%), 105 Grade II (26.1%), 121 Grade III (30%), 69 Grade IV (17.1%), and 26 Grade V (6.5%). All patients in this study were excluded from surgical treatment either because of anticipated surgical difficulty (69.2%), attempted and failed surgery (12.7%), the patient's poor neurological (12.2%) or medical (4.7%) status, and/or refusal of surgery (1.2%).

The GDC embolization was performed within 48 hours of primary hemorrhage in 147 patients (36.5%), within 3 to 6 days in 156 patients (38.7%), 7 to 10 days in 71 patients (17.6%), and 11 to 15 days in 29 patients (7.2%). Complete aneurysm occlusion was observed in 70.8% of small aneurysms with a small neck, 35% of large aneurysms, and 50% of giant aneurysms. A small neck remnant was observed in 21.4% of small aneurysms with a small neck, 57.1% of large aneurysms, and 50% of giant aneurysms. Technical complications included aneurysm perforation (2.7%), unintentional parent artery occlusion (3%), and untoward cerebral embolization (2.48%). There was a 8.9% immediate morbidity rate related to the GDC technique. Seven deaths were related to technical complications (1.74%) and 18 (4.47%) to the severity of the primary hemorrhage.

The findings of this study demonstrate the safety of the GDC system for the treatment of ruptured intracranial aneurysms in anterior and posterior circulations. The authors believe additional randomized studies will further identify the role of this technique in the management of acutely ruptured incranial aneurysms.

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Fernando Viñuela, Gary Duckwiler, and Michel Mawad

✓From December 1990 to July 1995, the investigators participated in a prospective clinical study to evaluate the safety of the Guglielmi detachable coil (GDC) system for the treatment of aneurysms. This report summarizes the perioperative results from eight initial interventional neuroradiology centers in the United States. The report focuses on 403 patients who presented with acute subarachnoid hemorrhage from a ruptured intracranial aneurysm. These patients were treated within 15 days of the primary intracranial hemorrhage and were followed until they were discharged from the hospital or died.

Seventy percent of the patients were female and 30% were male. The patients' mean age was 58 years old. Aneurysm size was categorized as small (60.8%), large (34.7%), and giant (4.5%); and neck size was categorized as small (53.6%), wide (36.2%), fusiform (6%), and undetermined (4.2%). Fifty-seven percent of the aueurysms were located in the posterior circulation and 43% in the anterior circulation.

Eighty-two patients were classified as Hunt and Hess Grade I (20.3%), 105 Grade II (26.1%), 121 Grade III (30%), 69 Grade IV (17.1%), and 26 Grade V (6.5%). All patients in this study were excluded from surgical treatment either because of anticipated surgical difficulty (69.2%), attempted and failed surgery (12.7%), the patient's poor neurological (12.2%) or medical (4.7%) status, and/or refusal of surgery (1.2%).

The GDC embolization was performed within 48 hours of primary hemorrhage in 147 patients (36.5%), within 3 to 6 days in 156 patients (38.7%), 7 to 10 days in 71 patients (17.6%), and 11 to 15 days in 29 patients (7.2%). Complete aneurysm occlusion was observed in 70.8% of small aneurysms with a small neck, 35% of large aneurysms, and 50% of giant aneurysms. A small neck remnant was observed in 21.4% of small aneurysms with a small neck, 57.1% of large aneurysms, and 50% of giant aneurysms. Technical complications included aneurysm perforation (2.7%), unintentional parent artery occlusion (3%), and untoward cerebral embolization (2.48%). There was a 8.9% immediate morbidity rate related to the GDC technique. Seven deaths were related lo technical complications (1.74%) and 18 (4.47%) to the severity of the primary hemorrhage.

The findings of this study demonstrate the safety of the GDC system for the treatment of ruptured intracranial aneurysms in anterior and posterior circulations. The authors believe additional randomized studies will further identify the role of this technique in the management of acutely ruptured incranial aneurysms.