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  • Author or Editor: Yukihiko Fujii x
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Kazuhiko Nishino, Hitoshi Hasegawa, Kenichi Morita, Masafumi Fukuda, Yasushi Ito, Yukihiko Fujii and Mitsuya Sato

OBJECTIVE

Arteriovenous malformations (AVMs) in the cerebellopontine angle cistern (CPAC) are specific lesions that can cause neurovascular compression syndromes as well as intracranial hemorrhage. Although case reports describing the CPAC AVMs, especially those presenting with trigeminal neuralgia (TN), have been accumulating by degrees, the pathophysiology of CPAC AVMs remains obscure. The authors' purpose in the present study was to evaluate the clinical and radiographic features of CPAC AVMs as well as the treatment options.

METHODS

This study defined a CPAC AVM as a small AVM predominantly located in the CPAC with minimal extension into the pial surface of the brainstem and closely associated with cranial nerves. All patients with CPAC AVMs treated in the authors' affiliated hospitals over a 16-year period were retrospectively identified. Clinical charts, imaging studies, and treatment options were evaluated.

RESULTS

Ten patients (6 men and 4 women), ranging in age from 56 to 77 years (mean 65.6 years), were diagnosed with CPAC AVMs according to the authors' definition. Six patients presented with hemorrhage, 3 with TN, and the remaining patient developed a hemorrhage subsequent to TN. Seven AVMs were associated with the trigeminal nerve (Group V), and 3 with the facial-vestibulocochlear nerve complex (Group VII–VIII). All patients in Group VII–VIII presented with the hemorrhage instead of hemifacial spasm. Regarding angioarchitecture, the intrinsic pontine arteries provided the blood supply for all CPAC AVMs in Group V. In addition, 5 of 7 AVMs with hemorrhagic episodes accompanied flow-related aneurysms, although no aneurysm was detected in patients with TN alone. With respect to treatment, all patients with hemorrhagic presentation underwent Gamma Knife surgery (GKS), resulting in favorable outcomes except for 1 patient who experienced rebleeding after GKS, which was caused by the repeated rupture of a feeder aneurysm. The AVMs causing TN were managed with surgery, GKS, or a combination, according to the nidus-nerve relationship. All patients eventually obtained pain relief.

CONCLUSIONS

Clinical symptoms caused by CPAC AVMs occur at an older age compared with AVMs in other locations; CPAC AVMs also have distinctive angioarchitectures according to their location in the CPAC. Although GKS is likely to be an effective treatment option for the CPAC AVMs with hemorrhagic presentations, it seems ideal to obliterate the flow-related aneurysms before performing GKS, although this is frequently challenging. For CPAC AVMs with TN, it is important to evaluate the nidus-nerve relationship before treatment, and GKS is especially useful for patients who do not require urgent pain relief.

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Tomoaki Suzuki, Christopher J. Stapleton, Matthew J. Koch, Kazutoshi Tanaka, Soichiro Fujimura, Takashi Suzuki, Takeshi Yanagisawa, Makoto Yamamoto, Yukihiko Fujii, Yuichi Murayama and Aman B. Patel

OBJECTIVE

Degenerative cerebral aneurysm walls are associated with aneurysm rupture and subarachnoid hemorrhage. Thin-walled regions (TWRs) represent fragile areas that may eventually lead to aneurysm rupture. Previous computational fluid dynamics (CFD) studies reported the correlation of maximum pressure (Pmax) areas and TWRs; however, the correlation with aneurysm rupture has not been established. This study aims to investigate this hemodynamic correlation.

METHODS

The aneurysmal wall surface at the Pmax areas was intraoperatively evaluated using a fluid flow formula under pulsatile blood flow conditions in 23 patients with 23 saccular middle cerebral artery (MCA) bifurcation aneurysms (16 unruptured and 7 ruptured). The pressure difference (Pd) at the Pmax areas was calculated by subtracting the average pressure (Pave) from the Pmax and normalized by dividing this by the dynamic pressure at the aneurysm inlet side. The wall shear stress (WSS) was also calculated at the Pmax areas, aneurysm dome, and parent artery. These hemodynamic parameters were used to validate the correlation with TWRs in unruptured MCA aneurysms. The characteristic hemodynamic parameters at the rupture points in ruptured MCA aneurysms were then determined.

RESULTS

In 13 of 16 unruptured aneurysms (81.2%), Pmax areas were identified that corresponded to TWRs. In 5 of the 7 ruptured cerebral aneurysms, the Pmax areas coincided with the rupture point. At these areas, the Pd values were not higher than those of the TWRs in unruptured cerebral aneurysms; however, minimum WSS, time-averaged WSS, and normalized WSS at the rupture point were significantly lower than those of the TWRs in unruptured aneurysms (p < 0.01).

CONCLUSIONS

At the Pmax area of TWRs, decreased WSS appears to be the crucial hemodynamic parameter that indicates the risk of aneurysm rupture.