Kato I, Okada T, Akao I, Shintani T, Kamo T, Sugihara H
Department of Otolaryngology, St. Marianna University School of Medicine, Kawasaki, Japan.
Auris Nasus Larynx. 1998 Dec;25(4):339-47. doi: 10.1016/s0385-8146(98)00026-1.
We experienced four cases of vertical gaze palsy induced by midbrain lesions. Lesions commonly covered the rostral midbrain, including the rostral interstitial nucleus, dorsomedial to the red nucleus. Two of the four cases resulted from vascular insult, in which a single, unpaired perforator is supposed to innervate the rostral midbrain and medial thalamus bilaterally. One case showed vertical gaze palsy accompanied by bilateral ptosis. The findings agree with recent experimental evidence that a neural substrate in eyelid control lies in the supraoculomotor area immediately dorsal to the oculomotor nucleus. The remaining two cases, a brain hemorrhage and an inflammatory tumor, showed unilateral lesions of the rostral midbrain. In these cases, vertical gazes were not abolished, but were limited in an incomplete way. This may be explained by partial damages of the descending fibers, some of which decussate through the posterior commissure before it reaches the oculomotor nucleus. Thus, clinical signs and symptoms were clarified based on anatomical and physiological points of view.
我们遇到了4例由中脑病变引起的垂直凝视麻痹病例。病变通常累及中脑嘴侧，包括嘴侧间质核，位于红核背内侧。4例中有2例由血管损伤导致，推测单一不成对的穿通动脉双侧支配中脑嘴侧和丘脑内侧。1例垂直凝视麻痹伴有双侧上睑下垂。这些发现与最近的实验证据相符，即眼睑控制的神经基质位于动眼神经核背侧的动眼上区。其余2例，1例脑出血和1例炎性肿瘤，表现为中脑嘴侧单侧病变。在这些病例中，垂直凝视并未完全消失，而是以不完全的方式受限。这可能是由于下行纤维部分受损，其中一些纤维在到达动眼神经核之前通过后连合交叉。因此，从解剖学和生理学角度阐明了临床体征和症状。
