Kesserwani Hassan
Neurology, Flowers Medical Group, Dothan, USA.
Cureus. 2021 Jan 28;13(1):e12962. doi: 10.7759/cureus.12962.
All reported cases of cerebral polyopia in the literature are associated solely with occipital lobe disease, as seen with ischemic infarcts, migraine, trauma, and epilepsy. To our knowledge, this is the first case of polyopia associated with posterior parietal cortex (PPC) ischemic infarct to be reported in the literature. Previous hypotheses about mechanisms of polyopia have included cortical spreading depression, the vague idea of abnormal visual synthesis, and the holographic or holonomic brain theory. We propose a new mechanism due to dysfunction of the network from the PPC [Formula: see text] frontal eye field (FEF) [Formula: see text] paramedian midbrain and pontine reticular formation leading to convergence insufficiency, which leads to horizontal diplopia. The evidence ranging from tracer studies in macaque monkeys to functional MRI (fMRI) studies in patients with convergence insufficiency is presented to bolster our hypothesis. In the process, we also briefly review the neural pathways of convergence.
文献中报道的所有脑性复视病例均仅与枕叶疾病相关,如缺血性梗死、偏头痛、创伤和癫痫。据我们所知,这是文献中首次报道的与顶叶后皮质(PPC)缺血性梗死相关的复视病例。先前关于复视机制的假说包括皮质扩散抑制、异常视觉合成的模糊概念以及全息或整体大脑理论。我们提出了一种新机制,即由于从PPC [公式:见正文] 额叶眼区(FEF) [公式:见正文] 脑桥中脑旁正中网状结构的网络功能障碍导致集合不足,进而导致水平性复视。我们展示了从猕猴的示踪研究到集合不足患者的功能磁共振成像(fMRI)研究等一系列证据来支持我们的假说。在此过程中,我们还简要回顾了集合的神经通路。