A lthough in Rochester, Minnesota, the fatality rate in cases of aneurysmal subarachnoid hemorrhage (SAH) may have decreased in the last decade, 12 overall mortality and physical as well as psychological morbidity rates associated with SAH remain inordinately high. 6, 15, 16, 23, 30, 33 Knowledge about the etiology and pathogenesis of intracranial aneurysms is fragmentary, and prevention of the development of aneurysms is unlikely to be an obtainable goal in the foreseeable future. In contrast to the dismal prognosis of aneurysmal SAH, the morbidity and
Report of three cases
Wouter I. Schievink, David G. Piepgras, and Fremont P. Wirth
Vini G. Khurana, David G. Piepgras, and Jack P. Whisnant
A pproximately 5% of all aneurysms are giant aneurysms, which by definition measure 25 mm or more in diameter. 27 Approximately 25% of giant aneurysms present clinically with subarachnoid hemorhage (SAH). 18, 19 Wiebers, et al., 30 suggested that unruptured giant and near-giant aneurysms have a higher probability of subsequent rupture than smaller ones. Thrombosis of the lesion, which may be extensive in giant aneurysms, does not preclude rupture. 12, 22 Although the incidence of rebleeding from smaller aneurysms has been studied extensively, 5, 8, 9, 14, 15
David G. Piepgras
I appreciate the invitation to participate in the discussion concerning the International Study of Unruptured Intracranial Aneurysms (ISUIA) and to comment additionally on the recent articles of Juvela, et al., 3 Tsutsumi, et al., 5 and the accompanying analysis and synthesis of Drs. Dumont, Lanzino, and Kassell in this issue. As a member of the Steering Committee of the ISUIA and indeed a contributor to the January 2, 2001, ISUIA Letter of Response, I am in general agreement with the points made by Wiebers, et al. Also, as a contributor to the American Heart
Thoralf M. Sundt Jr., Bruce W. Pearson, David G. Piepgras, O. Wayne Houser, and Bahram Mokri
A neurysms of the extracranial internal carotid artery (ICA) are uncommon lesions. Much of the relatively restricted literature on the subject has referred to single cases, 1, 8, 13, 16, 17, 19, 30, 31, 38, 39 dealt with aneurysms primarily involving the carotid bifurcation, 25 or discussed false aneurysms resulting from trauma 10 or a previous carotid endarterectomy. 11, 25 Only a few reports include aneurysms of the distal ICA. 5, 7, 14, 15, 25, 28, 37 The surgical approaches to false aneurysms 10, 11, 20 and aneurysms of the carotid bifurcation 23, 25
Jonathan A. Friedman, Mark A. Pichelmann, David G. Piepgras, John L. D. Atkinson, Cormac O. Maher, Fredric B. Meyer, and Kristine K. Hansen
A neurysms of the AChA account for 2 to 5% of all intracranial aneurysms. 5, 9, 20 The surgical approach and method are typically similar to those used for other supraclinoid carotid artery lesions. 13, 18, 20 However, the important parenchymal territory supplied by the AChA may make surgical clipping of this aneurysm more likely to produce debilitating postoperative ischemic complications. More than 30 years ago, Drake, et al., 4 reported results from the surgical clipping of seven carotid—choroidal artery aneurysms via a subfrontal approach. In 1978
Operative experience with 80 cases
Thoralf M. Sundt Jr. and David G. Piepgras
A neurysms greater than 2.5 cm in diameter are, by convention, classified as giant aneurysms. The review of Morley and Barr 9 includes early major references, and the report by Sonntag, et al. , 16 summarizes more recent work. Drake 3 and Yaşargil and Smith 19 have reported their experience. These studies, and a number of other well documented case reports, 1, 4, 14, 15 illustrate the individual characteristics of giant aneurysms. It seemed appropriate to review the techniques, results, and complications of the surgical management of giant aneurysms in
Vini G. Khurana, David G. Piepgras, and Jack P. Whisnant
The present study was conducted to estimate the frequency and timing of rebleeding after initial subarachnoid hemorrhage (SAH) from ruptured giant aneurysms.
The authors reviewed records of 109 patients who suffered an initial SAH from a giant aneurysm and were treated at the Mayo Clinic between 1973 and 1996. They represented 25% of patients with giant intracranial aneurysms seen at this institution during that 23-year period. Seven of the patients were residents of Rochester, Minnesota, and the rest were referred from other institutions. The aneurysms ranged from 25 to 60 mm in diameter, and 74% were located on arteries of the anterior intracranial circulation. The cumulative frequency of rebleeding at 14 days after admission was 18.4%. Cerebrospinal fluid drainage, cerebral angiography, and delayed aneurysm recurrence were implicated in rebleeding in some of the patients. Rebleeding was not precluded by intraaneurysm thrombosis. Among those who suffered recurrent SAH at the Mayo Clinic, 33% died in the hospital.
Rebleeding from giant aneurysms occurs at a rate comparable to that associated with smaller aneurysms, a finding that should be considered in management strategies.
Neurosurgical Forum: Letters to the Editor To The Editor Kiyoshi Takagi , M.D. Takamitsu Fujimaki , M.D. Teikyo University Tokyo, Japan 1325 1326 Abstract Object. The goal of this study was to determine the frequency of enlargement of unruptured intracranial aneurysms by using serial magnetic resonance (MR) angiography and to investigate whether aneurysm characteristics and demographic factors predict changes in aneurysm size. Methods. A retrospective review of MR angiograms obtained in 57
Frederic P. Collignon, Jonathan A. Friedman, David G. Piepgras, Douglas A. Nichols, and Harry Cloft
years later a cervical CA aneurysm developed. Because of poor tissue quality, we believed that a repeated operation for direct repair of this aneurysm would carry increased risks related to arterial fragility and poor wound healing, and increased chances of infection. Therefore, the aneurysm was treated by placement of two 10 × 20—mm stents (SMART Stents; Cordis, Miami Lakes, FL) within the ICA across the aneurysm neck, and detachment of a 40-cm length of Guglielmi Detachable Coils (GDCs; Target/Boston Scientific, Natick, MA) within the sac of the lesion. An angiogram
Bahram Mokri, David G. Piepgras, and O. Wayne Houser
S pontaneous or traumatic mural arterial dissections are caused by penetration of circulating blood into the arterial wall. Intramural hematoma creates a false lumen that dissects the vessel wall for varying distances along the artery. 3 An aneurysmal dilatation (a “dissecting aneurysm”) may result if the hematoma expands toward the adventitia of the weakened arterial wall. Some dissections occur spontaneously; others occur after a definite head or neck injury. Occasionally, the anamnesis reveals only minimal or trivial trauma that may not be significant. For