Isolated abducens nerve palsy associated with subarachnoid hemorrhage: A localizing sign of ruptured posterior inferior cerebellar artery aneurysms

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Objective: Compressive cranial nerve syndromes can be useful bedside clues to the diagnosis of an enlarging intracranial aneurysm and can also guide subsequent evaluation, as with an acute oculomotor nerve (cranial nerve [CN] III) palsy that is presumed to be a posterior communicating artery aneurysm and a surgical emergency until proven otherwise. The CN VI has a short cisternal segment from the pontomedullary sulcus to Dorello's canal, remote from most PICA aneurysms but in the hemodynamic pathway of a rupturing PICA aneurysm that projects toward Dorello's canal. The authors describe a cranial nerve syndrome for posterior inferior cerebellar artery (PICA) aneurysms that associates subarachnoid hemorrhage (SAH) and an isolated abducens nerve (CN VI) palsy. Methods: Clinical and radiological data from 106 surgical patients with PICA aneurysms (66 ruptured and 40 unruptured) were retrospectively reviewed. Data from a group of 174 patients with other aneurysmal SAH (aSAH) were analyzed in a similar manner to control for nonspecific effects of SAH. Univariate statistical analysis compared incidence and risk factors associated with CN VI palsy in subarachnoid hemorrhage. Results: Overall, 13 (4.6%) of 280 patients had CN VI palsy at presentation, and all of them had ruptured aneurysms (representing 13 [5.4%] of the 240 cases of ruptured aneurysms). CN VI palsies were observed in 12 patients with ruptured PICA aneurysms (12/66 [18.1%]) and 1 patient with other aSAH (1/174 [0.1%], p < 0.0001). PICA aneurysm location in ruptured aneurysms was an independent predictor for CN VI palsy on multivariate analysis (p = 0.001). PICA aneurysm size was not significantly different in patients with or without CN VI palsy (average size 4.4 mm and 5.2 mm, respectively). Within the PICA aneurysm cohort, modified Fisher grade (p = 0.011) and presence of a thick cisternal SAH (modified Fisher Grades 3 and 4) (p = 0.003) were predictors of CN VI palsy. In all patients with ruptured PICA aneurysms and CN VI palsy, dome projection and presumed direction of rupture were directed toward the ipsilateral and/ or contralateral Dorello's canal, in agreement with laterality of the CN palsy. In patients with bilateral CN VI palsies, a medial projection with extensive subarachnoid blood was observed near bilateral canals. Conclusions: This study establishes a localizing connection between an isolated CN VI palsy, SAH, and an underlying ruptured PICA aneurysm. CN VI palsy is an important clinical sign in aSAH and when present on initial clinical presentation may be assumed to be due to ruptured PICA aneurysms until proven otherwise. The deficit may be ipsilateral, contralateral, or bilateral and is determined by the direction of the aneurysm dome projection and extent of subarachnoid bleeding toward Dorello's canal, rather than by direct compression.

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Journal of Neurosurgery









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