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Tarek Abuelem, David Dornbos III and Adam Arthur

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Benjamin L. Brown, Demetrius Lopes, David A. Miller, Rabih G. Tawk, Leonardo B. C. Brasiliense, Andrew Ringer, Eric Sauvageau, Ciarán J. Powers, Adam Arthur, Daniel Hoit, Kenneth Snyder, Adnan Siddiqui, Elad Levy, L. Nelson Hopkins, Hugo Cuellar, Rafael Rodriguez-Mercado, Erol Veznedaroglu, Mandy Binning, J Mocco, Pedro Aguilar-Salinas, Alan Boulos, Junichi Yamamoto and Ricardo A. Hanel

OBJECT

The authors sought to determine whether flow diversion with the Pipeline Embolization Device (PED) can approximate microsurgical decompression in restoring function after cranial neuropathy following carotid artery aneurysms.

METHODS

This multiinstitutional retrospective study involved 45 patients treated with PED across the United States. All patients included presented between November 2009 and October 2013 with cranial neuropathy (cranial nerves [CNs] II, III, IV, and VI) due to intracranial aneurysm. Outcome analysis included clinical and procedural variables at the time of treatment as well as at the latest clinical and radiographic follow-up.

RESULTS

Twenty-six aneurysms (57.8%) were located in the cavernous segment, while 6 (13.3%) were in the clinoid segment, and 13 (28.9%) were in the ophthalmic segment of the internal carotid artery. The average aneurysm size was 18.6 mm (range 4–35 mm), and the average number of flow diverters placed per patient was 1.2. Thirty-eight patients had available information regarding duration of cranial neuropathy prior to treatment. Eleven patients (28.9%) were treated within 1 month of symptom onset, while 27 (71.1%) were treated after 1 month of symptoms. The overall rate of cranial neuropathy improvement for all patients was 66.7%. The CN deficits resolved in 19 patients (42.2%), improved in 11 (24.4%), were unchanged in 14 (31.1%), and worsened in 1 (2.2%). Overtime, the rate of cranial neuropathy improvement was 33.3% (15/45), 68.8% (22/32), and 81.0% (17/21) at less than 6, 6, and 12 months, respectively. At last follow-up, 60% of patients in the isolated CN II group had improvement, while in the CN III, IV, or VI group, 85.7% had improved. Moreover, 100% (11/11) of patients experienced improvement if they were treated within 1 month of symptom onset, whereas 44.4% (12/27) experienced improvement if they treated after 1 month of symptom onset; 70.4% (19/27) of those with partial deficits improved compared with 30% (3/10) of those with complete deficits.

CONCLUSIONS

Cranial neuropathy caused by cerebral aneurysm responds similarly when the aneurysm is treated with the PED compared with open surgery and coil embolization. Lower morbidity and higher occlusion rates obtained with the PED may suggest it as treatment of choice for some of these lesions. Time to treatment is an important consideration regardless of treatment modality.

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Emad Aboud, Ghaith Aboud, Ossama Al-Mefty, Talal Aboud, Stylianos Rammos, Mohammad Abolfotoh, Sanford P. C. Hsu, Sebastian Koga, Adam Arthur and Ali Krisht

OBJECT

Intraoperative rupture occurs in approximately 9.2% of all cranial aneurysm surgeries. This event is not merely a surgical complication, it is also a real surgical crisis that requires swift and decisive action. Neurosurgical residents may have little exposure to this event, but they may face it in their practice. Laboratory training would be invaluable for developing competency in addressing this crisis. In this study, the authors present the “live cadaver” model, which allows repetitive training under lifelike conditions for residents and other trainees to practice managing this crisis.

METHODS

The authors have used the live cadaver model in 13 training courses from 2009 to 2014 to train residents and neurosurgeons in the management of intraoperative aneurysmal rupture. Twenty-three cadaveric head specimens harboring 57 artificial and 2 real aneurysms were used in these courses. Specimens were specially prepared for this technique and connected to a pump that sent artificial blood into the vessels. This setting created a lifelike situation in the cadaver that simulates live surgery in terms of bleeding, pulsation, and softness of tissue.

RESULTS

A total of 203 neurosurgical residents and 89 neurosurgeons and faculty members have practiced and experienced the live cadaver model. Clipping of the aneurysm and management of an intraoperative rupture was first demonstrated by an instructor. Then, trainees worked for 20- to 30-minute sessions each, during which they practiced clipping and reconstruction techniques and managed intraoperative ruptures. Ninety-one of the participants (27 faculty members and 64 participants) completed a questionnaire to rate their personal experience with the model. Most either agreed or strongly agreed that the model was a valid simulation of the conditions of live surgery on cerebral aneurysms and represents a realistic simulation of aneurysmal clipping and intraoperative rupture. Actual performance improvement with this model will require detailed measurement for validating its effectiveness. The model lends itself to evaluation using precise performance measurements.

CONCLUSIONS

The live cadaver model presents a useful simulation of the conditions of live surgery for clipping cerebral aneurysms and managing intraoperative rupture. This model provides a means of practice and promotes team management of intraoperative cerebrovascular critical events. Precise metric measurement for evaluation of training performance improvement can be applied.

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Bernhard Sutter, Adam Arthur, Jeffrey Laurent, James Chadduck, Gerhard Friehs, Georg Clarici and Gerhard Pendl

Surgical treatment of intrameduallary spinal cord metastases (ISCM) has become increasingly effective in recent years. The advent of new imaging techniques combined with an enhanced understanding of the natural history of these tumors has improved the effectiveness of the available treatment options. The authors present three new cases of ISCM successfully treated with surgery. A review of 129 cases found in the literature is also discussed. Characteristic symptomology and presentation are reviewed with an eye toward improving diagnostic methodology. The natural history of ISCM is divided into three phases. Surgical intervention should be used early in phase 2.

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Hakan H. Caner, Aij-Lie Kwan, Adam Arthur, Arco Y. Jeng, Rodney W. Lappe, Neal F. Kassell and Kevin S. Lee

✓ The potent vasoconstrictor peptide, endothelin-1 (ET-1), has been implicated in the pathophysiology of cerebral vasospasm that occurs after subarachnoid hemorrhage (SAH). This peptide is synthesized as a large prepropeptide that requires a series of modifying steps for its activation. The last of these steps involves the proteolytic conversion of a relatively inactive propeptide, Big ET-1, to its active, 21—amino acid peptide form. The enzyme responsible for converting Big ET-1 to ET-1 is a metalloprotease called endothelin-converting enzyme (ECE). In the present study the authors examined the effects of a newly developed inhibitor of ECE on responses to ET peptides in the normal basilar artery and on pathophysiological constriction in the spastic basilar artery after SAH.

In the first series of experiments the authors examined normal basilar arteries in the rabbit, which were exposed transclivally and measured on-line using videomicroscopy. Intravenous administration or topical application of an active inhibitor of ECE, CGS 26303, blocked vasoconstrictor responses to topically applied Big ET-1 but not to ET-1. In contrast, topical application of a structurally related compound that does not inhibit ECE, CGS 24592, was ineffective in blocking vasoconstriction that was elicited by a topical application of Big ET-1. These findings indicate that CGS 26303 when administered systemically is capable of blocking the conversion of Big ET-1 to ET-1 in the basilar artery without affecting the ability of the vessel to respond to ET-1. In the second series of experiments the authors examined the effects of the ECE inhibitor on cerebral vasospasm after experimental SAH. Intraperitoneal administration of CGS 26303 via osmotic minipumps significantly attenuated the delayed spastic response of the basilar artery to an intracisternal injection of autologous blood.

This study provides the first evidence that systemic administration of an inhibitor of ECE is capable of preventing cerebral vasospasm after SAH. The results reinforce a growing body of evidence that ETs play a critical role in the development of spastic constriction after SAH. Moreover, the findings indicate that blocking the conversion of Big ET-1 to its active ET-1 form using CGS 26303 may represent a feasible strategy for ameliorating cerebral vasospasm.