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Paul Klimo Jr., Clinton J. Thompson, James Drake and John R. W. Kestle

Object. Most surgical procedures are associated with a learning curve in which the success rate is lower early in the experience before mistakes have been identified and modifications made to the procedure. Negative results obtained early in a trial's learning curve may be a matter of timing rather than a reflection of the procedure's effectiveness. The recently published results of the Endoscopic Shunt Insertion Trial (ESIT) represent the notion that endoscopically placed shunts were no more likely to survive than conventionally placed shunts. This negative result may be due to inexperience in performing endoscopic surgeries.

Methods. Surgical experience was assessed in two ways. Shunt survival rates were compared between cases treated endoscopically in the 1st and last years of the ESIT. The effect of center volume was evaluated using a Cox proportional hazard model in which the following variables were analyzed: age at registration, the diagnosis of myelomeningocele, head size, method of shunt placement (endoscopic compared with conventional), and center volume.

There was no difference in survival (endurance) of the shunt between patients enrolled in the 1st and last years (log rank = 0.08, p = 0.77). Likewise, no variable in the Cox multivariate model, including center volume, was a significant factor in predicting shunt survival.

Conclusions. The primary result of the ESIT was found to be internally valid. The fact that endoscopic shunt placement did not benefit patients evaluated in the study was not due to early timing of the trial. Any learning curve among the participating surgeons did not adversely affect the results.

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Ron I. Riesenburger, Steven W. Hwang, Clemens M. Schirmer, Vasilios Zerris, Julian K. Wu, Kerry Mahn, Paul Klimo Jr., John Mignano, Clinton J. Thompson and Kevin C. Yao


Gamma Knife surgery (GKS) has been shown to be effective in treating trigeminal neuralgia (TN). Existing studies have demonstrated success rates of 69.1–85% with median follow-up intervals of 19–60 months. However, series with uniform long-term follow-up data for all patients have been lacking. In the present study the authors examined outcomes in a series of patients with TN who underwent a single GKS treatment followed by a minimum follow-up of 36 months. They used a clinical scale that simplifies the reporting of outcome data for patients with TN.


Fifty-three consecutive patients with typical, intractable TN received a median maximum radiation dose of 80 Gy applied with a single 4-mm isocenter to the affected trigeminal nerve. Follow-up data were obtained by clinical examination and questionnaire. Outcome results were categorized into the following classes (in order of decreasing success): Class 1A, complete pain relief without medications; 1B, complete pain relief with either a decrease or no change in medications; 1C, ≥ 50% pain relief without medications; 1D, ≥ 50% pain relief with either a decrease or no change in medications; and Class 2, < 50% pain relief and/or increase in medications. Patients with Class 1A–1D outcome (equivalent to Barrow Neurological Institute Grades I–IIIb) were considered to have a good treatment outcome, whereas in patients with Class 2 outcome (equivalent to Barrow Neurological Institute Grades IV and V) treatment was considered to have failed.


A good treatment outcome from initial GKS was achieved in 31 (58.5%) patients for whom the mean follow-up period was 48 months (range 36–66 months). Outcomes at last follow-up were reflected by class status: Class 1A, 32.1% of patients; 1B, 1.9%; 1C, 3.8%; 1D, 20.8%; and Class 2, 41.5%. Statistical analysis showed no difference in outcomes between patients previously treated with microvascular decompression or rhizotomy compared with patients with no previous surgical treatments. Thirty-six percent of patients reported some degree of posttreatment facial numbness. Anesthesia dolorosa did not develop in any patient.


Despite a time-dependent deterioration in the success rate of GKS for medically intractable TN, the authors' study showed that > 50% of patients can be expected to have a good outcome based on their scoring system, with ~ 33% having an ideal outcome (pain free with no need for medications). Long-term data, as those presented here, are important when counseling patients on their treatment options.

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Oral Presentations

2010 AANS Annual Meeting Philadelphia, Pennsylvania May 1–5, 2010

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Dallas L. Sheinberg, David J. McCarthy, Omar Elwardany, Jean-Paul Bryant, Evan Luther, Stephanie H. Chen, John W. Thompson and Robert M. Starke

Endothelial cell (EC) dysfunction is known to contribute to cerebral aneurysm (CA) pathogenesis. Evidence shows that damage or injury to the EC layer is the first event in CA formation. The mechanisms behind EC dysfunction in CA disease are interrelated and include hemodynamic stress, hazardous nitric oxide synthase (NOS) activity, oxidative stress, estrogen imbalance, and endothelial cell-to-cell junction compromise. Abnormal variations in hemodynamic stress incite pathological EC transformation and inflammatory zone formation, ultimately leading to destruction of the vascular wall and aneurysm dilation. Hemodynamic stress activates key molecular pathways that result in the upregulation of chemotactic cytokines and adhesion molecules, leading to inflammatory cell recruitment and infiltration. Concurrently, oxidative stress damages EC-to-EC junction proteins, resulting in interendothelial gap formation. This further promotes leukocyte traffic into the vessel wall and the release of matrix metalloproteinases, which propagates vascular remodeling and breakdown. Abnormal hemodynamic stress and inflammation also trigger adverse changes in NOS activity, altering proper EC mediation of vascular tone and the local inflammatory environment. Additionally, the vasoprotective hormone estrogen modulates gene expression that often suppresses these harmful processes. Crosstalk between these sophisticated pathways contributes to CA initiation, progression, and rupture. This review aims to outline the complex mechanisms of EC dysfunction in CA pathogenesis.

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John W. Thompson, Omar Elwardany, David J. McCarthy, Dallas L. Sheinberg, Carlos M. Alvarez, Ahmed Nada, Brian M. Snelling, Stephanie H. Chen, Samir Sur and Robert M. Starke

Cerebral aneurysm rupture is a devastating event resulting in subarachnoid hemorrhage and is associated with significant morbidity and death. Up to 50% of individuals do not survive aneurysm rupture, with the majority of survivors suffering some degree of neurological deficit. Therefore, prior to aneurysm rupture, a large number of diagnosed patients are treated either microsurgically via clipping or endovascularly to prevent aneurysm filling. With the advancement of endovascular surgical techniques and devices, endovascular treatment of cerebral aneurysms is becoming the first-line therapy at many hospitals. Despite this fact, a large number of endovascularly treated patients will have aneurysm recanalization and progression and will require retreatment. The lack of approved pharmacological interventions for cerebral aneurysms and the need for retreatment have led to a growing interest in understanding the molecular, cellular, and physiological determinants of cerebral aneurysm pathogenesis, maturation, and rupture. To this end, the use of animal cerebral aneurysm models has contributed significantly to our current understanding of cerebral aneurysm biology and to the development of and training in endovascular devices. This review summarizes the small and large animal models of cerebral aneurysm that are being used to explore the pathophysiology of cerebral aneurysms, as well as the development of novel endovascular devices for aneurysm treatment.