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Permanent Cerebral Vessel Occlusion via Double Ligature and Transection
Published on: July 21, 2013
Perforating artery injury as a critical factor besides cortical dysfunction in motor deficit after peri-rolandic
Atsuhiko Ninomiya1, Shin-Ichiro Osawa1, Kyoko Suzuki2
1Departments of1Neurosurgery.
Objective:
Surgery for peri-rolandic epilepsy requires appropriate consideration to balance the functional risk of postoperative motor deficit and seizure outcome. Based on voxel-based morphometric analysis, the authors hypothesized that cortical damage and ischemic subcortical damage related to surgery could affect postoperative motor deterioration.
Methods:
Sixteen patients with peri-rolandic epilepsy who underwent resective surgery at a single institution were retrospectively investigated. Their imaging findings, postoperative seizure outcomes, and postoperative neurological deteriorations in motor function, as well as duration, were analyzed. Using the standardized MRI data of each case, the authors examined the surgically resected area on high-resolution 3D MR images and the high-intensity area on diffusion-weighted images, which were converted to voxel data. These voxel data were superimposed on a standard brain image for neuroimaging assessment. Postoperative motor deterioration of the orofacial region, upper limb, or lower limb was noted as no, transient, or permanent deterioration and analyzed in relation to the surgically resected area and subcortical damage. Univariate analysis of the clinical factors was conducted between cases with permanent upper- and/or lower-limb motor deterioration and those with no or transient deterioration.
Results:
The mean follow-up period was 28 months. Ten patients (62.5%) achieved Engel class I. Fourteen patients (87.5%) experienced postoperative motor deteriorations in the following areas (no/transient/permanent): orofacial (11/5/0), upper limb (9/5/2), and lower limb (9/3/4). All cases with orofacial motor deterioration underwent cortical resection of the inferior third of the peri-rolandic cortex. Cortical resection of the precentral gyrus only, in contrast to both the precentral and postcentral gyri, was not associated with permanent upper- and/or lower-limb motor deterioration. Cortical resection involving the postcentral gyrus was significantly associated with permanent upper- and/or lower-limb motor deterioration in 4 cases (25.0%). Surgically related perforating artery injury caused ischemic subcortical damage, which was significantly associated with postoperative transient or permanent motor deterioration by extending to the corticospinal tract (CST).
Conclusions:
Postoperative motor deterioration for peri-rolandic epilepsy was related to both the resected cortex and ischemic subcortical damage. In peri-rolandic epilepsy, cortical resection of the precentral gyrus might not necessarily cause permanent upper- and/or lower-limb motor deterioration because of the functional reserve in other peri-rolandic areas outside the epileptic focus. On the other hand, cortical resection of the postcentral gyrus could cause permanent upper- and/or lower-limb motor deterioration because of injury to the vasculature, which is crucial for the descending motor pathway in the CST.
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