Neurological Institute, University Hospitals Health System, Cleveland, OH, United States; Department of Neurology, School of Medicine, Case Western Reserve University, Cleveland, OH, United States.
Neurological Institute, University Hospitals Health System, Cleveland, OH, United States; Department of Neurology, School of Medicine, Case Western Reserve University, Cleveland, OH, United States; Daroff-Dell'Osso Ocular Motility Laboratory, Louis Stokes Cleveland VA Medical Center, Cleveland, OH, United States; Neurology Service, Louis Stokes Cleveland VA Medical Center, Cleveland, OH, United States.
J Neurol Sci. 2018 Jul 15;390:239-245. doi: 10.1016/j.jns.2018.05.002. Epub 2018 May 3.
Seesaw nystagmus is characterized by the rhythmic combination of vertical and torsional dysconjugate oscillations where one eye moves up and inward while the other moves down and outward. Common association of seesaw nystagmus with accessory optic track lesions lead to traditional hypothesis that it is due to the mismatch in the vision and vestibular systems. Here we propose a novel mechanism for seesaw nystagmus. We hypothesize that reverberations due to abnormal increases in the excitability of the reciprocally innervating circuit of excitatory burst neuron in the midbrain interstitial nucleus of Cajal causes the seesaw nystagmus. Analogous oscillations of the brainstem burst generators may be responsible for generation of saccadic oscillations or opsoclonus. The key difference is that the interstitial nucleus of Cajal lacks inhibitory burst neurons, hence the lack of post-inhibitory rebound, and relatively lower frequency of the oscillatory cycles causing pendular seesaw nystagmus. In contrast the brainstem burst generator, with reciprocally innervating excitatory and inhibitory burst neurons, and further inhibitory influence of the omnipause neurons results in the post-inhibitory rebound at the burst neurons, hence high oscillation frequency. This novel concept is supported by a unique observation in a patient with antineuronal nuclear autoantibody type 2 due to breast cancer who had combined seesaw nystagmus and superimposed saccadic oscillations. The patient neither had cerebellar deficits typically thought to cause paraneoplastic opsoclonus nor visual deficits that are known cause of seesaw nystagmus. We propose that hyperexcitability of the burst neurons in the interstitial nucleus of Cajal due to paraneoplastic antibody caused pendular seesaw nystagmus. On the other hand, increased excitability of brainstem burst generators and reduced efficacy of the omnipause neurons caused saccadic oscillations.
跷跷板眼球震颤的特征是垂直和扭转的非共轭摆动的有节奏组合，一只眼睛向上向内移动，而另一只眼睛向下向外移动。跷跷板眼球震颤与辅助视束病变的常见关联导致了传统假说，即它是由于视觉和前庭系统之间的不匹配引起的。在这里，我们提出了一种新的跷跷板眼球震颤机制。我们假设，由于中脑间质核兴奋性爆发神经元的相互支配回路的兴奋性异常增加而引起的回波，导致了跷跷板眼球震颤。类似的脑干爆发发生器的振荡可能是引起扫视性振荡或眼震的原因。关键区别在于 Cajal 间质核缺乏抑制性爆发神经元，因此缺乏后抑制性反弹，并且振荡周期的相对较低频率导致摆动性跷跷板眼球震颤。相比之下，脑干爆发发生器具有相互支配的兴奋性和抑制性爆发神经元，以及来自普遍抑制神经元的进一步抑制影响，导致爆发神经元的后抑制性反弹，因此具有较高的振荡频率。这一新概念得到了一位因乳腺癌而患有神经元核自身抗体 2 型的患者的独特观察结果的支持，该患者同时患有跷跷板眼球震颤和叠加性扫视性眼球震颤。该患者既没有通常被认为会引起副肿瘤性眼震的小脑缺陷，也没有已知会引起跷跷板眼球震颤的视觉缺陷。我们提出，由于副肿瘤抗体导致 Cajal 间质核中的爆发神经元过度兴奋，引起摆动性跷跷板眼球震颤。另一方面，脑干爆发发生器的兴奋性增加和普遍抑制神经元的效能降低导致扫视性眼球震颤。
