Morecraft R J, Binneboese A, Stilwell-Morecraft K S, Ge J
Laboratory of Neurological Sciences, Division of Basic Biomedical Sciences, Sanford School of Medicine, University of South Dakota, Vermillion, South Dakota.
J Comp Neurol. 2017 Nov 1;525(16):3429-3457. doi: 10.1002/cne.24275. Epub 2017 Aug 2.
Subcortical white matter injury is often accompanied by orofacial motor dysfunction, but little is known about the structural substrates accounting for these common neurological deficits. We studied the trajectory of the corticobulbar projection from the orofacial region of the primary (M1), ventrolateral (LPMCv), supplementary (M2), rostral cingulate (M3) and caudal cingulate (M4) motor regions through the corona radiata (CR), internal capsule (IC) and crus cerebri of the cerebral peduncle (ccCP). In the CR each pathway was segregated. Medial motor area fibers (M2/M3/M4) arched over the caudate and lateral motor area fibers (M1/LPMCv) curved over the putamen. At superior IC levels, the pathways were widespread, involving the anterior limb, genu and posterior limb with the M3 projection located anteriorly, followed posteriorly by projections from M2, LPMCv, M4 and M1, respectively. Inferiorly, all pathways maintained this orientation but shifted posteriorly, with adjacent fiber bundles overlapping minimally. In the ccCP, M3 fibers were located medially and M1 fibers centromedially, with M2, LPMCv, and M4 pathways overlapping in between. Finally, at inferior ccCP levels, all pathways overlapped. Following CR and superior IC lesions, the dispersed pathway distribution may correlate with acute orofacial dysfunction with spared pathways contributing to orofacial motor recovery. In contrast, the gradually commixed nature of pathway representation inferiorly may enhance fiber vulnerability and correlate with severe, prolonged deficits following lower subcortical and midbrain injury. Additionally, in humans these findings may assist in interpreting orofacial movements evoked during deep brain stimulation, and neuroimaging tractography efforts to localize descending orofacial motor pathways.
皮质下白质损伤常伴有口面部运动功能障碍,但对于导致这些常见神经功能缺损的结构基础却知之甚少。我们研究了从初级运动区(M1)、腹外侧运动区(LPMCv)、辅助运动区(M2)、扣带回前部(M3)和扣带回后部(M4)的口面部区域发出的皮质延髓投射纤维束,经放射冠(CR)、内囊(IC)和大脑脚的大脑脚底(ccCP)的走行轨迹。在放射冠中,各条纤维束相互分离。内侧运动区纤维(M2/M3/M4)呈弓形跨过尾状核,外侧运动区纤维(M1/LPMCv)呈弧形跨过壳核。在内囊上部水平,纤维束分布广泛,涉及内囊前肢、膝部和后肢,M3投射位于前方,其后依次为M2、LPMCv、M4和M1的投射。在下部,所有纤维束均保持这种排列方向,但向后移位,相邻纤维束的重叠最小。在大脑脚底,M3纤维位于内侧,M1纤维位于中央内侧,M2、LPMCv和M4的纤维束在其间重叠。最后,在大脑脚底下部水平,所有纤维束相互重叠。在放射冠和内囊上部损伤后,纤维束分散的分布可能与急性口面部功能障碍相关,而未受损的纤维束有助于口面部运动功能的恢复。相反,下部纤维束逐渐混合的特性可能会增加纤维的易损性,并与皮质下和中脑下部损伤后严重且持久的功能缺损相关。此外,在人类中,这些发现可能有助于解释在深部脑刺激过程中诱发的口面部运动,以及用于定位下行口面部运动纤维束的神经影像学纤维束成像研究结果。