Nakada T, Kwee I L, Lee H
J Clin Neuroophthalmol. 1984 Mar;4(1):35-7.
Sustained upgaze is a rare phenomenon that is observed primarily in those patients with coma secondary to cardiac arrest or prolonged hypotension. Because of "selective vulnerability" of the brain, cardiac arrest or prolonged hypotension may produce both cerebral and cerebellar cortical damage sparing the brain stem vestibulo-ocular reflex (VOR) pathways. This selective damage may be responsible for the generation of sustained upgaze. The VORs receive their selective inhibition from the cerebellar flocculus. This inhibition is exerted on only one of the two VOR pathways converging on each extra-ocular muscle, so that total disinhibition of the VOR pathway activities will result in a tonic upward bias. The underlying neuronal mechanism of sustained upgaze appears to be due to total floccular disinhibition resulting in upward drift produced by the biased VOR and the lack of correcting saccades due to cerebral dysfunction releasing the brain stem ocular motor systems from their control.
持续上视是一种罕见现象，主要见于继发于心搏骤停或长时间低血压的昏迷患者。由于大脑的“选择性易损性”，心搏骤停或长时间低血压可能导致大脑和小脑皮质受损，而脑干前庭眼反射（VOR）通路得以保留。这种选择性损伤可能是持续上视产生的原因。VOR受到来自小脑绒球的选择性抑制。这种抑制仅作用于汇聚到每条眼外肌的两条VOR通路中的一条，因此VOR通路活动的完全去抑制将导致强直性向上偏斜。持续上视的潜在神经元机制似乎是由于绒球完全去抑制，导致由偏向性VOR产生向上漂移，以及由于脑功能障碍使脑干眼动系统失去控制而缺乏纠正性扫视。
