Horton J C
Beckman Vision Center, University of California, San Francisco 94143-0730, USA.
Trans Am Ophthalmol Soc. 1997;95:579-609.
The anterior chiasmal syndrome consists of a temporal hemianopia or complete visual field loss in one eye, plus a superior temporal hemianopia in the other eye. The superior temporal hemianopia in the other eye is thought to result from injury to Wilbrand's Knee of the optic chiasm. Wilbrand's Knee is a loop of decussating fibers which detours into the contralateral optic nerve before entering the optic tract. I studied the organization of fibers in the optic chiasm of monkeys and humans to verify the existence of Wilbrand's Knee and to elucidate further the pattern of visual field loss seen from lesions of the sellar region.
The primary optic pathway was labelled in monkeys by injection of [3H] proline into one eye, followed by autoradiography. There were 8 intact Rhesus monkeys and 3 intact squirrel monkeys. In addition, the optic pathway was studied in the Rhesus monkey 6 months and 4 years after monocular enucleation. The optic chiasm was also examined using myelin stains in specimens obtained post-mortem from 3 patients. The patients had lost 1 eye 5 months, 2 years, and 28 years prior to their deaths. Finally, clinical observations were recorded in 3 patients with the anterior chiasmal syndrome.
In normal Rhesus and squirrel monkeys, optic nerve fibers crossed the optic chiasm without entering the contralateral optic nerve. After short-term monocular enucleation, fibers from the normal optic nerve were drawn closer to the entry zone of the degenerating optic nerve, but Wilbrand's Knee was still absent. After long-term enucleation, a typical Wilbrand's Knee was induced to form. In the human, Wilbrand's Knee was absent 5 months after monocular enucleation, but emerged in the two cases involving long-term enucleation, in a fashion analogous to the monkey. The case reports describe 3 patients with variants of the anterior chiasmal syndrome from parasellar tumors.
Wilbrand's Knee does not exist in the normal primate optic chiasm. It forms gradually over a period of years following monocular enucleation, presumably from shrinkage of the optic chiasm caused by atrophy of fibers from the enucleated eye. Therefore, the superior temporal hemianopia in the "other eye" seen in the anterior chiasmal syndrome cannot be due to compression of Wilbrand's Knee. I propose that it occurs from combined compression of the optic chiasm and one (or both) optic nerves.
视交叉前综合征表现为一只眼颞侧偏盲或完全视野缺损，另一只眼颞上象限偏盲。另一只眼的颞上象限偏盲被认为是由于视交叉的威尔布兰德膝部受损所致。威尔布兰德膝部是交叉纤维的一个环，在进入视束之前绕入对侧视神经。我研究了猴子和人类视交叉中纤维的组织结构，以验证威尔布兰德膝部的存在，并进一步阐明鞍区病变导致的视野缺损模式。
通过向一只眼睛注射[3H]脯氨酸，然后进行放射自显影，对猴子的主要视觉通路进行标记。共有8只完整的恒河猴和3只完整的松鼠猴。此外，还对单眼摘除术后6个月和4年的恒河猴的视觉通路进行了研究。还使用髓鞘染色法对3例死后获得的标本中的视交叉进行了检查。这些患者在死亡前分别有1只眼失明5个月、2年和28年。最后，记录了3例视交叉前综合征患者的临床观察结果。
在正常的恒河猴和松鼠猴中，视神经纤维穿过视交叉而不进入对侧视神经。短期单眼摘除后，来自正常视神经的纤维被拉向变性视神经的进入区，但威尔布兰德膝部仍然不存在。长期摘除后，诱导形成了典型的威尔布兰德膝部。在人类中，单眼摘除后5个月威尔布兰德膝部不存在，但在两例长期摘除的病例中出现，其方式与猴子类似。病例报告描述了3例因鞍旁肿瘤导致的视交叉前综合征变体患者。
正常灵长类动物的视交叉中不存在威尔布兰德膝部。它在单眼摘除后的几年内逐渐形成，可能是由于摘除眼的纤维萎缩导致视交叉收缩所致。因此，视交叉前综合征中“另一只眼”出现的颞上象限偏盲不能归因于威尔布兰德膝部受压。我认为它是由于视交叉和一条（或两条）视神经的联合受压所致。
