Department of Ophthalmology, Mayo Clinic, Rochester, Minnesota, United States.
Department of Neurology, Mayo Clinic, Rochester, Minnesota, United States.
Invest Ophthalmol Vis Sci. 2018 Apr 1;59(5):1964-1968. doi: 10.1167/iovs.18-23780.
Essential infantile esotropia is generated by prenuclear visual pathways that increase esotonus and gradually drive the eyes into a convergent position. Contrary to the prevailing notion that infantile esotropia reflects a primary disturbance within the visual cortex, accumulating evidence suggests that infantile esotropia is generated by lower subcortical centers that subserve nasalward optokinesis. These phylogenetically older visuo-vestibular pathways include the nucleus of the optic tract, accessory optic system, inferior olive, cerebellar flocculus, and vestibular nucleus. In humans, the subcortical visual system is normally turned off after the first few months of infancy but retains its function in children who develop infantile esotropia. Mutations or other perturbations that prolong subcortical neuroplasticity may therefore lead to a persistent simultaneous nasalward optokinetic imbalance in both eyes to generate infantile esotropia. Deficits in cortical motion processing and monocular nasotemporal asymmetry to foveated optokinetic targets are likely the effect, rather than the cause, of infantile esotropia.
内斜视的基本成因是核前视觉通路导致的高斜视度，这些通路逐渐使眼球汇聚。与内斜视主要反映视皮层内原发性障碍的普遍观点相反，越来越多的证据表明，内斜视是由下级皮质下中枢产生的，这些中枢负责鼻侧眼球运动。这些进化上更早的视-前庭通路包括视束核、副视系统、下橄榄核、小脑绒球和前庭核。在人类中，皮质下视觉系统在婴儿出生后的头几个月后通常会关闭，但在发展为内斜视的儿童中仍然保持其功能。因此，延长皮质下神经可塑性的突变或其他干扰可能导致双眼持续出现鼻侧眼球运动不平衡，从而导致内斜视。皮质运动处理缺陷和注视性视动目标的单眼鼻颞侧不对称很可能是内斜视的结果，而不是原因。
