Wilbrand's knee of the primate optic chiasm is an artefact of monocular enucleation

Abstract

Purpose: 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.

Methods: 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.

Results: 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.

Conclusions: 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.