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  • Author or Editor: Christopher J. Moran x
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James M. Milburn, Christopher J. Moran, DeWitte T. Cross III, Michael N. Diringer, Thomas K. Pilgram and Ralph G. Dacey Jr.

Object. This study was conducted to determine if there is a change in intracranial arterial diameters after papaverine infusion for vasospasm and to determine whether the change occurs in proximal, intermediate, and distal arteries.

Methods. The authors measured arterial diameters retrospectively in all patients who received intraarterial papaverine for treatment of vasospasm between November 1992 and August 1995. Patients who received papaverine in the same session with or following angioplasty were excluded. Measurements were made in a blinded manner with the aid of a magnification loupe at 12 predetermined sites on each angiogram before and after papaverine infusion. Eighty-one treatments in 34 patients were included. Angiograms obtained at the time of presentation with subarachnoid hemorrhage (SAH) were examined in 26 of the 34 patients. Nine carotid territories visualized by repeated angiography on the day after infusion were examined to determine the duration of the papaverine effect.

Conclusions. In all treatment groups an increase was found in the average arterial diameters ranging from 2.8 to 73.9%, with a mean increase of 26.5%. Increases in diameter were observed in proximal, intermediate, and distal arteries. The timing of treatments ranged from Day 3 to Day 19 post-SAH, and there was no relationship between timing and arterial responsiveness (r = −0.06). There was a moderately good correlation between the degree of vasospasm in an artery and its responsiveness to papaverine (r = −0.54, −0.66, and −0.66, for proximal, intermediate, and distal arteries, respectively). The effect of papaverine did not persist until the following day in patients in whom repeated angiography was performed.

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Manish N. Shah, James A. Botros, Thomas K. Pilgram, Christopher J. Moran, DeWitte T. Cross III, Michael R. Chicoine, Keith M. Rich, Ralph G. Dacey Jr., Colin P. Derdeyn and Gregory J. Zipfel


The goal of this study was to determine the clinical course of Borden-Shucart Type I cranial dural arteriovenous fistulas (DAVFs) and to calculate the annual rate of conversion of these lesions to more aggressive fistulas that have cortical venous drainage (CVD).


A retrospective chart review was conducted of all patients harboring DAVFs who were seen at the authors' institution between 1997 and 2009. Twenty-three patients with Type I DAVFs who had available clinical follow-up were identified. Angiographic and clinical data from these patients were reviewed. Neurological outcome and status of presenting symptoms were assessed during long-term follow-up.


Of the 23 patients, 13 underwent endovascular treatment for intolerable tinnitus or ophthalmological symptoms, and 10 did not undergo treatment. Three untreated patients died of unrelated causes. In those who were treated, complete DAVF obliteration was achieved in 4 patients, and palliative reduction in DAVF flow was achieved in 9 patients. Of the 19 patients without radiographic cure, no patient developed intracranial hemorrhage or nonhemorrhagic neurological deficits (NHNDs), and no patient died of DAVF-related causes over a mean follow-up of 5.6 years. One patient experienced a spontaneous, asymptomatic obliteration of a partially treated DAVF in late follow-up, and 2 patients experienced a symptomatic conversion of their DAVF to a higher-grade fistula with CVD in late follow-up. The annual rate of conversion to a higher-grade DAVF based on Kaplan-Meier cumulative event-free survival analysis was 1.0%. The annual rate of intracranial hemorrhage, NHND, and DAVF-related death was 0.0%.


A small number of Type I DAVFs will convert to more aggressive DAVFs with CVD over time. This conversion to a higher-grade DAVF is typically heralded by a change in patient symptoms. Follow-up vascular imaging is important, particularly in the setting of recurrent or new symptoms.

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Colin P. Derdeyn, DeWitte T. Cross III, Christopher J. Moran, George W. Brown, Thomas K. Pilgram, Michael N. Diringer, Robert L. Grubb Jr., Keith M. Rich, Michael R. Chicoine and Ralph G. Dacey Jr.

Object. Ischemic stroke or transient ischemic attack (TIA) may occur after the treatment of intracranial aneurysms with Guglielmi detachable coils (GDCs). The purpose of the present study is to investigate possible risk factors for thromboembolic events and to determine their frequency and time course.

Methods. The records of 178 consecutive patients with 193 treated intracranial saccular aneurysms were reviewed. A total of 159 GDC procedures were performed to treat 143 aneurysms in 133 of those patients who were in good neurological condition, allowing clinical detection of postprocedure ischemic events (TIA or stroke). The association of clinical, anatomical, and pharmacological factors with intraprocedure intraarterial thrombus and with postprocedure ischemic events was investigated by using uni- and multivariate analyses.

Thrombus protruding into the parent artery was noted during six of 159 GDC procedures, resulting in a clinical deficit in one patient. No factor was associated with intraprocedure intraarterial thrombus. Ten postprocedure ischemic events occurred in nine patients. Seven events occurred within 24 hours, and three events occurred between 24 hours and 58 days. Aneurysm diameter and protruding coils were significant independent predictors of postprocedure ischemic events in multivariate analysis (both p = 0.02). The actuarial risk of stroke was 3.8%.

Conclusions. Larger aneurysm diameter and protruding loops of coils are associated with postprocedure ischemic events after GDC placement. It is unlikely that GDC-treated aneurysms retain thromboembolic potential beyond 2 months.

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Ayman A. Elsayed, Christopher J. Moran, DeWitte T. Cross III, Colin P. Derdeyn, Thomas K. Pilgram, James M. Milburn, Ralph G. Dacey Jr. and Michael N. Diringer Jr.


The goal in this study was to determine if there was a change in intracranial venous diameters after endo-vascular treatment of carotid distribution vasospasm caused by subarachnoid hemorrhage.


The venous diameters were measured in all patients who received intraarterial papaverine and/or balloon angioplasty for treatment of vasospasm during the study period of 3 years. To evaluate the veins of Labbé and Trolard, the straight sinus, and the superior sagittal sinus (SSS), measurements were performed in a blinded manner with the aid of a magnification loupe. Predetermined sites were evaluated on angiograms obtained before and after endovascular treatment. Forty-three treatments in 26 patients were included: 18 patients (33 territories) were treated with intraarterial papaverine alone, four (four territories) were treated with balloon angioplasty alone, and four (six territories) were treated with both papaverine infusion and angioplasty.

The mean measured venous diameters increased significantly after addition of papaverine (10.9%), and also after combined papaverine and angioplasty (4.2%). There was no statistically significant increase in the mean venous diameters after angioplasty alone. If the initial intracranial pressure (ICP) was less than 15 mm Hg before treatment, the veins showed a greater tendency to dilate than if the initial ICP measurements were greater than 15 mm Hg. The straight sinus and the SSS increased more in diameter than the veins of Labbé and Trolard. There was no statistically significant correlation between the change in venous diameters with treatment and ICP.


Endovascular treatment produces measurable increases in intracranial venous diameters. However, these changes do not correlate with changes in ICP.