TY - JOUR
T1 - Tuberothalamic artery infarctions following coil embolization of ruptured posterior communicating artery aneurysms with posterior communicating artery sacrifice
AU - Endo, Hidenori
AU - Sato, K.
AU - Kondo, R.
AU - Matsumoto, Y.
AU - Takahashi, A.
AU - Tominaga, T.
PY - 2012/3
Y1 - 2012/3
N2 - BACKGROUND AND PURPOSE: Ischemic complications after coil embolization of the PcomA aneurysms are not thoroughly understood, especially in cases in which the PcomA is sacrificed. Our purpose was to examine the preoperative angiographic features and pattern of postoperative cerebral infarctions exhibited by patients who underwent embolization of ruptured PcomA aneurysms with PcomA sacrifice. MATERIALS AND METHODS: A retrospective review identified 14 patients with ruptured PcomA aneurysms who underwent embolization of the aneurysms in combination with PcomA sacrifice. Preoperative angiographic data, including the Allcock test, postoperative DWI, and neurologic status, were examined. RESULTS: Elimination of the aneurysm was complete in all cases. Postoperative DWI indicated 7 cases with infarctions (infarction group) and 7 cases without infarctions (noninfarction group). All patients in the infarction group developed infarctions in the vicinity of the tuberothalamic artery. In all 14 cases, a preoperative Allcock test demonstrated a retrograde filling of the PcomA through the P1 segment. The incidence of negative visualizations of the P1 segment on vertebral angiograms was significantly higher in the infarction group (100%) than in the noninfarction group (0%; P = .00058). The mean PcomA diameters, PcomA/P1 ratios, and aneurysm sizes observed in the infarction group were significantly greater than those in the noninfarction group (P < .05, P < .01, and P < .02, respectively). Tuberothalamic artery infarction caused hemiparesis and memory disturbance, which were associated with unfavorable outcomes. CONCLUSIONS: After the coil occlusion of ruptured PcomA aneurysms with PcomA sacrifice, tuberothalamic artery infarctions tended to occur in cases exhibiting negative visualization of the P1 segment, even when collateral flow was observed with the Allcock test.
AB - BACKGROUND AND PURPOSE: Ischemic complications after coil embolization of the PcomA aneurysms are not thoroughly understood, especially in cases in which the PcomA is sacrificed. Our purpose was to examine the preoperative angiographic features and pattern of postoperative cerebral infarctions exhibited by patients who underwent embolization of ruptured PcomA aneurysms with PcomA sacrifice. MATERIALS AND METHODS: A retrospective review identified 14 patients with ruptured PcomA aneurysms who underwent embolization of the aneurysms in combination with PcomA sacrifice. Preoperative angiographic data, including the Allcock test, postoperative DWI, and neurologic status, were examined. RESULTS: Elimination of the aneurysm was complete in all cases. Postoperative DWI indicated 7 cases with infarctions (infarction group) and 7 cases without infarctions (noninfarction group). All patients in the infarction group developed infarctions in the vicinity of the tuberothalamic artery. In all 14 cases, a preoperative Allcock test demonstrated a retrograde filling of the PcomA through the P1 segment. The incidence of negative visualizations of the P1 segment on vertebral angiograms was significantly higher in the infarction group (100%) than in the noninfarction group (0%; P = .00058). The mean PcomA diameters, PcomA/P1 ratios, and aneurysm sizes observed in the infarction group were significantly greater than those in the noninfarction group (P < .05, P < .01, and P < .02, respectively). Tuberothalamic artery infarction caused hemiparesis and memory disturbance, which were associated with unfavorable outcomes. CONCLUSIONS: After the coil occlusion of ruptured PcomA aneurysms with PcomA sacrifice, tuberothalamic artery infarctions tended to occur in cases exhibiting negative visualization of the P1 segment, even when collateral flow was observed with the Allcock test.
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U2 - 10.3174/ajnr.A2828
DO - 10.3174/ajnr.A2828
M3 - Article
C2 - 22194388
AN - SCOPUS:84863380623
SN - 0195-6108
VL - 33
SP - 500
EP - 506
JO - American Journal of Neuroradiology
JF - American Journal of Neuroradiology
IS - 3
ER -