Comparative Analysis of Anterior Petrosectomy and Transcavernous Approaches to Retrosellar and Upper Clival Basilar Artery Aneurysms

2006 ◽  
Vol 58 (suppl_1) ◽  
pp. ONS-13-ONS-21 ◽  
Author(s):  
Eberval Gadelha Figueiredo ◽  
Joseph M. Zabramski ◽  
Puspha Deshmukh ◽  
Neil R. Crawford ◽  
Robert F. Spetzler ◽  
...  

Abstract OBJECTIVE: To compare two techniques, transcavernous approach (TcA) and anterior petrosectomy (AP), used to manage retrosellar and upper clival basilar artery (BA) aneurysms. METHODS: AP and TcA were carried out on nine sides of cadaver heads. With use of a computerized tracking system, the area of surgical exposure in the ventral surface of the brain stem, the superficial area of exposure, and the linear exposure of the BA were evaluated. The angles of approach in the horizontal and vertical axes were measured using a robotic microscope. The caudal extent of exposure was determined by an aneurysm clip applied to proximal BA, and the distance between the clip and the floor of the sella was quantified after performing TcA. RESULTS: TcA (1127.3 ± 438.4 mm2) provided a greater superficial exposure than AP (697.7 ± 219.1 mm2) (P = 0.01). There were no statistical differences in the deep working exposure (P = 0.303) between TcA (206.9 ± 40.7 mm2) and AP (260.2 ± 137.1 mm2). The linear exposure of the BA was greater for AP (22.7 ± 6.2 mm2) than for the TcA (12.8 ± 2.9 mm2) (P = 0.004). The caudal extent of exposure averaged 6.1 mm from the floor of the sella. No differences were found in horizontal angles (P = 0.596); however, vertical angles were significantly greater for the TcA than AP (15.2 ± 3.4) (P = 0.004). CONCLUSION: From an anatomic standpoint, the TcA offers more advantages than the AP, when approaching retrosellar BA aneurysms, except for those cases in which proximal control is the principal issue and the neck of the aneurysm is located more than 6.0 mm below the floor of the sella.

1997 ◽  
Vol 17 (10) ◽  
pp. 1089-1096 ◽  
Author(s):  
Kazunori Toyoda ◽  
Kenichiro Fujii ◽  
Setsuro Ibayashi ◽  
Tetsuhiko Nagao ◽  
Takanari Kitazono ◽  
...  

We tested the hypothesis that nitric oxide (NO) plays a role in CBF autoregulation in the brain stem during hypotension. In anesthetized rats, local CBF to the brain stem was determined with laser-Doppler flowmetry, and diameters of the basilar artery and its branches were measured through an open cranial window during stepwise hemorrhagic hypotension. During topical application of 10−5 mol/L and 10−4 mol/L Nω-nitro-L-arginine (L-NNA), a nonselective inhibitor of nitric oxide synthase (NOS), CBF started to decrease at higher steps of mean arterial blood pressure in proportion to the concentration of L-NNA in stepwise hypotension (45 to 60 mm Hg in the 10−5 mol/L and 60 to 75 mm Hg in the 10−4 mol/L L-NNA group versus 30 to 45 mm Hg in the control group). Dilator response of the basilar artery to severe hypotension was significantly attenuated by topical application of L-NNA (maximum dilatation at 30 mm Hg: 16 ± 8% in the 10−5 mol/L and 12 ± 5% in the 10−4 mol/L L-NNA group versus 34 ± 4% in the control group), but that of the branches was similar between the control and L-NNA groups. Topical application of 10−5 mol/L 7-nitro indazole, a selective inhibitor of neuronal NOS, did not affect changes in CBF or vessel diameter through the entire pressure range. Thus, endothelial but not neuronal NO seems to take part in the regulation of CBF to the the brain stem during hypotension around the lower limits of CBF autoregulation. The role of NO in mediating dilatation in response to hypotension appears to be greater in large arteries than in small ones.


1966 ◽  
Vol 24 (2) ◽  
pp. 544-551 ◽  
Author(s):  
George C. Stevenson ◽  
Ronald J. Stoney ◽  
Roland K. Perkins ◽  
John E. Adams

1975 ◽  
Vol 34 (1) ◽  
pp. 151-156 ◽  
Author(s):  
Pascal Bousquet ◽  
Josiane Feldman ◽  
Jeanne Velly ◽  
Roger Bloch

1999 ◽  
Vol 23 (1) ◽  
pp. 59-66
Author(s):  
Khalid Kamil Kadhum

The brain of the sheep receives its blood supply through the carotid rete and the basilar artery. The carotid rete formed of contribution of internal carotid artery and branches from maxillary artery. The internal carotid artery courses on the ventral surface of the cerebal crus to give the rostral cerebal artery and the caudal communicating artery . Thus , arteries excepted the middle cerebal artery forming with the same arteries of the opposite side , the cerebal arterial circle or circle of Willis. The internal caroted artery also gives off hypophysialartery to the  1999 ind, (1) swell, ügymielly wel dati', il pellilendiambell ileti  hypophysis. The caudal communicating artery give off the caudal cerebal artery and the rostral cerebellar artery and unite with the corresponding artery of the opposite side to form the basilar artery rostral to the pone . The basilar artery gives off the pontine artery , caudal cerebellar artery and the medullary branch. 


Stroke ◽  
1991 ◽  
Vol 22 (6) ◽  
pp. 763-767 ◽  
Author(s):  
K Fujii ◽  
D D Heistad ◽  
F M Faraci

Author(s):  
Ljubisa Borota ◽  
Sylvia Libard ◽  
Markus Fahlström ◽  
Francesco Latini ◽  
Erik Lundström

AbstractStroke caused by dissection of arteries of the vertebrobasilar system in children is still poorly investigated in terms of etiology, means of treatment, course of disease, and prognosis. The aim of this report was to describe the unusual course of a spontaneous dissection of the basilar artery (BA) in a child treated with endovascular techniques and to point out that the plasticity of the brain stem can fully compensate for structural damage caused by stroke. We report the case of a 15-year-old boy who suffered a wake-up stroke with BA occlusion caused by spontaneous dissection. A blood clot was aspirated from the false lumen and the true lumen re-opened, but the patient deteriorated a few hours later, and repeated angiography revealed that the intimal flap was detached, occluding the BA again. The lumen of BA was then reconstructed by a stent. Despite a large pons infarction, the patient was completely recovered 11 months after the onset. The case was analyzed with angiograms and magnetic resonance imaging, macroscopic and microscopic pathological analysis, computed tomographic angiography, magnetic resonance-based angiography, and diffusion tensor imaging. This case illustrates that applied endovascular techniques and intensive care measures can alter the course of potentially fatal brain stem infarction. Our multimodal analysis gives new insight into the anatomical basis for the plasticity mechanism of the brain stem.


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