Optic Chiasm

Optic Chiasm

The optic nerves elevate, and move medially as they extend intracranially to form the optic chiasm. The optic chiasm, which is the confluence of the optic nerves, sits approximately 10 mm above the dorsum sellae. At the chiasm, the nasal fibers of each optic nerve that represent the temporal visual field cross to the contralateral optic tract. Temporal optic nerve fibers which represent the nasal visual fields proceed posteriorly along the ipsilateral portion of the optic chiasm to join the crossing nasal fibers to form the ipsilateral optic tract. Posterior to the optic chiasm, the optic tracts are comprised of ipsilateral temporal fibers and contralateral nasal fibers.

Several anatomic features of the chiasm contribute to the specific types and patterns of visual field defects that occur with lesions in this region. Given that optic chiasm lies 10 mm above the roof of the pituitary fossa pituitary microadenomas do not produce visual field defects. The macular fibers, which comprise 90% of the optic fibers, cross in the posterior aspect of the chiasm. Inferior retinal fibers which represent the superior visual field are located in the inferior portion of the optic chiasm.

The position of the chiasm influences the pattern of visual field loss produced by lesions in the parachiasmal area. The most common position (approximately 80%) for the chiasm is on the diaphragm sellae projecting onto the dorsum sellae. In a prefixed chiasm (15%), the chiasm lies upon the tuberculum sellae or diaphragma sella, while in a postfixed chiasm (5%), the chiasm lies on the dorsum sella posterior to the fossa. The other important structure in the parachiasmal area is the cavernous sinus. The cavernous sinus is comprised of the venous space situated between the meningeal and periosteal layers of the dura mater on either side of the sphenoid bone. It extends from the end of the superior orbital fissure to the apex of the petrous bone. The cavernous sinus contains the carotid artery and the cranial nerves (CN) III, IV, and VI. Parachiasmal tumors may cause visual field defects as well as ocular motility disturbances.

Disorders of the optic chiasm initially may present with visual acuity loss. The clinical demonstration of a chiasmal pattern of visual loss enables the physician to order the appropriate tests and to establish the correct
diagnosis. The single most important nonradiologic test in determining if the optic chiasm is the involved site producing visual loss is the visual field. The confluence of the optic nerves and the crossing of the nasal fibers at the chiasm, combined with the 90-degree rotation that the visual fibers undergo en route to the chiasm from the retina, orient the nerve fibers along the vertical meridian. Therefore, visual field defects at the optic chiasm and posteriorly will characteristically respect the vertical meridian on perimetric testing.


Junction Scotoma

Classically, this is a combination of a central scotoma in one eye and a temporal hemianopic defect in the other (Fig. 6-1). The localization of this visual field defect is the junction of the optic nerve, on the side of the central scotoma, and the optic chiasm. The classically accepted cause for this pattern of visual loss is the existence of Wilbrand’s knee, which is the anterior extension of the inferior nasal crossing fibers from one eye into the opposite optic nerve. Therefore, a lesion of the right optic nerve will produce a right central scotoma and a left superior temporal defect. However, modern studies in monkeys have failed to show the anatomic existence of Wilbrand’s knee, despite the fact that the junctional scotoma still is a valid sign that localizes lesions to the junction of the optic nerve and chiasm.

A lesion may involve only the crossing visual fibers at the anterior angle of the optic chiasm. This produces a monocular temporal hemianopic defect with no visual field loss in the contralateral eye (Fig. 6-2).

Bitemporal Hemianopia

It is described in textbooks as the classic visual field abnormality produced by lesions of the body of the optic chiasm. The visual field defects may be complete (Fig. 6-3A) or incomplete (Fig. 6-3B), but they always obey the vertical meridian. In most cases, however, pure bitemporal hemianopic defects are infrequent. Usually, there is decreased acuity in one or both eyes. A central bitemporal defect may occur in patients with prefixed chiasm or posterior growing tumors because the macular fibers are located posteriorly in the chiasm.

Homonymous Hemianopia

A parasellar lesion may produce an incongruous homonymous hemianopia by involving the optic tracts. This may occur with mass lesions that are directed posteriorly or because the optic chiasm is prefixed. The homonymous hemianopia often is associated with a central scotoma and a relative afferent pupillary defect (RAPD) on the side of the mass lesion. This is known as the optic tract syndrome (page 194).

Binasal Visual Field Defect

This is said to occur in a patient with a postfixed chiasm in which the lesion is located between both optic nerves along the anterior aspect of the chiasm displacing the optic nerves laterally against the supraclinoid internal carotid arteries or A1 segments of the anterior cerebral arteries. This is such an extraordinarily uncommon visual field defect that we have never encountered it.

Any patient with decreased vision of unknown etiology requires a visual field. When the visual field shows one of the defects associated with chiasmal involvement, the next test to perform is an MRI scan.

FIGURE 6-1. A. Temporal hemianopic defect in the right eye and central scotoma in the left. B. Causal lesion is perichiasmal mass (arrow).

FIGURE 6-2. Patient with a large suprasellar meningioma presented with a temporal hemianopic defect and decreased vision in the left eye with no defect in the right.

FIGURE 6-3. A. Complete bitemporal hemianopia. B. Incomplete bitemporal hemianopia.


  • Approximately 90% of the disorders that produce chiasmal syndromes are mass lesions. The most frequent of these are listed in Table 6-1.