Wong A M, Musallam S, Tomlinson R D, Shannon P, Sharpe J A
Division of Neurology, University Health Network, Toronto Western Hospital, Toronto, Ontario, Canada.
J Neurol Sci. 2001 Aug 15;189(1-2):71-81. doi: 10.1016/s0022-510x(01)00564-0.
Opsoclonus is a dyskinesia consisting of involuntary, arrhythmic, chaotic, multidirectional saccades, without intersaccadic intervals. We used a magnetic scleral search coil technique to study opsoclonus in two patients with paraneoplastic complications of lung carcinoma. Eye movement recordings provided evidence that opsoclonus is a three-dimensional oscillation, consisting of torsional, horizontal, and vertical components. Torsional nystagmus was also present in one patient. Antineuronal antibody study revealed the presence of anti-Ta (Ma2 onco-neuronal antigen) antibodies in one patient, which had previously been associated only with paraneoplastic limbic encephalitis and brainstem dysfunction, but not opsoclonus, and only in patients with testicular or breast cancer. Neuropathologic examination revealed mild paraneoplastic encephalitis. Normal neurons identified in the nucleus raphe interpositus (rip) do not support postulated dysfunction of omnipause cells in the pathogenesis of opsoclonus. Computer simulation of a model of the saccadic system indicated that disinhibition of the oculomotor region of the fastigial nucleus (FOR) in the cerebellum can generate opsoclonus. Histopathological examination revealed inflammation and gliosis in the fastigial nucleus. This morphological finding is consistent with, but not necessary to confirm, damage to afferent projections to the FOR, as determined by the model. Malfunction of Purkinje cells in the dorsal vermis, which inhibit the FOR, may cause opsoclonus by disinhibiting it.
眼阵挛是一种运动障碍，表现为不自主、无节律、混乱的多方向扫视，且无扫视间歇期。我们使用磁性巩膜搜索线圈技术对两名患有肺癌副肿瘤并发症的患者的眼阵挛进行了研究。眼动记录提供了证据表明眼阵挛是一种三维振荡，由扭转、水平和垂直成分组成。其中一名患者还存在扭转性眼球震颤。抗神经元抗体研究显示一名患者存在抗Ta（Ma2肿瘤神经元抗原）抗体，该抗体此前仅与副肿瘤性边缘叶脑炎和脑干功能障碍相关，而与眼阵挛无关，且仅在睾丸癌或乳腺癌患者中出现。神经病理学检查显示有轻度副肿瘤性脑炎。在中间缝际核（rip）中发现的正常神经元并不支持关于眼阵挛发病机制中全暂停细胞功能障碍的假设。对扫视系统模型的计算机模拟表明，小脑顶核动眼区（FOR）的去抑制可产生眼阵挛。组织病理学检查显示顶核有炎症和胶质细胞增生。这一形态学发现与模型所确定的对FOR传入投射的损伤相符，但并非确认该损伤所必需。抑制FOR的小脑蚓部背侧浦肯野细胞功能障碍可能通过去抑制FOR而导致眼阵挛。
