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瞳孔不等大——海马病变的瞳孔征象:在猫身上使用神经毒素的实验研究

Anisocoria--a pupillary sign of hippocampal lesions: an experimental study in the cat by using neurotoxins.

作者信息

Hashida N, Shoumura K, Ichinohe N, Hirama J, Amayasu H

机构信息

Department of Anatomy, Hirosaki University School of Medicine, Japan.

出版信息

J Hirnforsch. 1997;38(1):9-26.

PMID:9059914
Abstract

Pupillary inequality developed after unilateral lesions of the hippocampal formation (HF) of the cat. Lesions were made by an injection of a small amount of colchicine, ibotenic acid or kainic acid. In all anisoric cats, the pupil on the side of the lesions was invariably smaller than its partner. Evident pupillary inequality developed in the cats with dorsal HF lesions. Although there was a considerable variation in the extent and the location of lesions among these cats, the involvement of the giganto-pyramidal CA 3-2 appeared very responsible for the development of the pupillary sign. However, an evidently anisoric cat hat a lesion affecting only the prosubiculum and the subiculum in the posterior part of the dorsal HF. Despite a large involvement of CA 3-2 with or without coincident injuries to CA1, the prosubiculum and the subiculum, only slight pupillary inequality developed following ventral HF lesions. Evident anisocoria in the cats with large dorsal HF lesions disappeared after bilateral cervical sympathectomy, implying that the asymmetry of sympathetic nervous activity might be critically involved in the development of the pupillary sign. The hippocampo-spinal pathway relayed by the lateral septal nucleus and, then, by the lateral hypothalamic area to terminate in the intermedio-lateral cell column of the spinal cord was considered to be most concerned with anisocoria caused by HF lesions.

摘要

猫海马结构(HF)单侧损伤后出现瞳孔不等大。通过注射少量秋水仙碱、鹅膏蕈氨酸或 kainic 酸造成损伤。在所有出现瞳孔不等大的猫中,损伤侧的瞳孔始终小于对侧瞳孔。背侧 HF 损伤的猫出现明显的瞳孔不等大。尽管这些猫的损伤范围和位置存在相当大的差异,但巨大锥体细胞 CA 3-2 的受累似乎是瞳孔体征出现的主要原因。然而,一只明显瞳孔不等大的猫的损伤仅累及背侧 HF 后部的前下托和下托。尽管 CA 3-2 大量受累,无论是否伴有 CA1、前下托和下托的合并损伤,腹侧 HF 损伤后仅出现轻微的瞳孔不等大。双侧颈交感神经切除术后,背侧 HF 大损伤的猫明显的瞳孔不等大消失,这意味着交感神经活动的不对称可能在瞳孔体征的出现中起关键作用。由外侧隔核中继,然后通过外侧下丘脑区域传递至脊髓中间外侧细胞柱的海马-脊髓通路被认为与 HF 损伤引起的瞳孔不等大关系最为密切。

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