Compressive Optic Neuropathy

Excerpt

Any intrinsic or extrinsic compression anywhere along the optic nerve can produce compressive optic neuropathy (CON). Other than damage by compression, optic nerve damage can occur as a result of demyelination, ischemia, metabolic, and traumatic insult. The most common sign is a slow progressive monocular visual loss, sometimes associated with headaches. Bilateral visual loss can result from midline lesions (pituitary adenoma, craniopharyngioma, meningioma, giant aneurysms) or bilateral orbital lesions (thyroid disease, sarcoidosis). It is essential to correctly identify the cause of the CON as the differential diagnosis is broad, and management varies accordingly.

The optic nerve has over 1 million nerve fibers. This quantity of fibers demonstrates the complexity and importance that the visual system has had in our evolution. The visual pathway starts in the retina and ends in the visual cortex at the occipital lobe. The retina consists of two functional parts: the optic part and the non-visual retina. The optic part of the retina consists of the neural and pigmented layer. In contrast, the non-visual retina is an extension of the pigmented layer and ends in the ciliary and iridial parts of the retina.

The optic nerve begins in the lamina cribrosa of the sclera and exits the orbit through the optic canal. As it leaves the orbit, it is engulfed with an extension of the cranial dura and subarachnoid layer, which forms the optic nerve sheath. The axons of the ganglion cells project as the optic nerve and decussate in the optic chiasm and continue as the optic tract which courses to the lateral geniculate ganglion, which then projects to the primary visual cortex as the optic radiations. The optic nerve averages 50 mm in length (1 mm intraocular segment, 25 mm intraorbital segment, 9 mm intracanalicular segment, and 16 mm intracranial segment).