Optic Chiasmal Disorders

Andrew G. Lee, MD

Anatomy

The optic nerves exit the globe posteriorly and converge at the optic chiasm (Greek Χ chi). The visual fibers then diverge from the chiasm to form the optic tracts (Slide 1). The temporal fibers remain uncrossed and the nasal fibers cross in the chiasm. Clinically, chiasmal syndromes may be divided into those affecting the anterior portion of the optic chiasm (i.e., the junction of the optic nerve and chiasm); the body of the optic chiasm; and the posterior portion of the optic chiasm. This tutorial reviews each of the chiasmal syndromes, with an emphasis on the afferent presentations of chiasmal disease.

Slide 2

Slide 1

Anterior Chiasmal Syndrome

The retinal nerve fibers form the ipsilateral optic nerve, exit the eye, and travel to the optic chiasm. Patients with sellar or suprasellar lesions can thus present with a unilateral or bilateral optic neuropathy (Slide 2). These visual fibers follow a specific topographical pathway from the optic nerve to the chiasm and optic tracts, and then posteriorly to the geniculate body. The intracranial optic nerves join at the optic chiasm with the nasal fibers crossing into the contralateral optic tract and the temporal fibers remaining uncrossed in the ipsilateral optic tract. These crossed (nasal retinal) and uncrossed (temporal retinal) nerve fibers are anatomically separated at the junction of the optic nerve and chiasm. In the past, it was postulated that inferior nasal crossing fibers looped anteriorly for a short distance into the contralateral optic nerve and were called the anterior knee or the Wilbrand knee. The anatomic existence of the Wilbrand knee has come into question by Horton. Wilbrand's experience was restricted to examining eyes that were the product of enucleation. In the enucleated eye, the nerve fibers had become atrophic and were mistakenly interpreted as being distinct from the nerve fibers of the normal eye on myelin staining. Horton, using axon labeling techniques in a monkey with both eyes intact, showed that no inferonasal crossing fibers loop into the contralateral optic nerve (i.e., the Wilbrand's knee was not seen). A different monkey that had undergone enucleation 4 years previously, however, demonstrated the Wilbrand knee and Horton believes that it was artifact of enucleation and not a normal anatomic finding.¹

Slide 3

Regardless of whether the Wilbrand knee exists anatomically, the localizing clinical value of junctional visual field loss remains important. A lesion at the junction of the intracranial optic nerve and the optic chiasm can produce characteristic "junctional" visual field defects. For example, a junctional lesion can produce an ipsilateral optic neuropathy with loss of visual acuity and of color vision, and a relative afferent pupillary defect. If the fibers from the inferonasal retina of the contralateral eye in the chiasm (the presumed Wilbrand knee) are involved, then contralateral superotemporal visual field loss occurs in addition to the ipsilateral optic neuropathy. This contralateral visual field loss has been termed the junctional scotoma (Slide 3).²

Slide 4

Another type of junctional visual field loss can occur due to selective ipsilateral compression of the crossing (nasal) or non-crossing (temporal) visual fibers as they approach the junction. A lesion in this location may rarely result in a monocular temporal or nasal hemianopic field defect. Although Traquair had originally used the term junction scotoma to refer to this unilateral temporal hemicentral field defect due to compression of the nasal fibers crossing in the intracranial optic nerve at the junction of the optic nerve and chiasm,³ Miller emphasized that this junctional scotoma described by Traquair referred to a strictly unilateral temporal scotoma (Slide 4). A monocular hemianopic (nasal or temporal) visual field defect localizes to the junction of the optic nerve and chiasm and is therefore a form of junctional visual field defect.⁴ Because of the confusion with the term junctional scotoma (describing the contralateral superotemporal field loss with an ipsilateral optic neuropathy) and the junctional scotoma of Traquair, it is recommended that different terms be used for these two forms of junctional visual field loss (Table 1).

Trobe and Glaser reported that junctional visual field loss was due to a compressive lesion in 98 of 100 cases.⁵ The differential diagnosis of a junctional syndrome is listed in Table 2. Neuroimaging (preferably contrast head magnetic resonance imaging [MRI]) should be directed to the junction in patients with junctional visual field loss. The clinical importance of detecting the junctional scotoma is that a small superotemporal visual field defect may be unnoticed by a patient presenting with unilateral visual complaints. An ipsilateral retrobulbar optic neuritis can easily be misdiagnosed without checking the contralateral visual field. This is especially important if the clinician has elected not to image a presumed retrobulbar optic neuritis.

Body of the Chiasm Lesions

The body of the chiasm contains the crossing nasal fibers that represent the temporal visual field. Lesions of the body of the chiasm thus produce bitemporal hemianopic field loss (Slide 5A and Slide 5B) that may be peripheral, paracentral, or central, and may either "split" or "spare" the central visual field. Like junctional visual field loss, bitemporal hemianopsias are often the result of a compressive mass lesion of the optic chiasm.^4,6 Table 3 lists the multiple causes for a chiasmal syndrome. Neuroimaging (preferably MRI with contrast directed to the chiasm) should be performed.

Slide 5a

Slide 5b

It is important for ophthalmologists to perform formal perimetry in patients with unexplained visual loss. The detection of a bitemporal hemianopsia should prompt further evaluation and neuroimaging. In the acute setting, especially if accompanied by severe headache, pituitary apoplexy (rapid expansion, hemorrhage, or necrosis in a pituitary adenoma) must be urgently evaluated. Panhypopituitarism in these patients may be life threatening and emergent surgery may be required.

Lateral Extension of Tumor into the Cavernous Sinus

Sellar and suprasellar lesions may extend laterally to involve the cavernous sinus rather than extend upward to the chiasm. The clinician should be aware that ophthalmoplegia (from a 3rd, 4th, 6th nerve palsy or combination nerve palsies), ptosis (e.g., 3rd nerve palsy, Horner syndrome), pupil involvement (mydriasis or miosis), and facial pain or numbness (trigeminal) may be presenting signs of a sellar lesion. Chiasmal lesions may also produce nystagmus (see-saw nystagmus).⁷

Slide 6

Posterior Chiasm Syndrome

Posterior chiasmal lesions may produce paracentral bitemporal hemianopic field defects that may be mistaken for cecocentral field loss (Slide 6). Unlike true cecocentral scotomas from a bilateral optic neuropathy, the color vision and visual acuity are usually spared in these patients. The optic tracts are the continuation of the nasal crossed and temporal uncrossed fibers as they exit the chiasm. A contralateral homonymous hemianopsia may occur due to involvement of the optic tract. Patients with suprasellar lesions may have combination deficits, however, due to involvement of one or both optic nerves, the chiasm, or the optic tract.

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