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This is manifested by a progressive exophthalmos, a restrictive myopathy that restricts eye movements and an optic neuropathy. With enlargement of the extraocular muscle at the orbital apex, the optic nerve is at risk of compression. The orbital fat or the stretching of the nerve due to increased orbital volume may also lead to optic nerve damage.
The optic nerve can be damaged when exposed to direct or indirect injury. Direct optic nerve injuries are caused by trauma to the head or orbit that crosses normal tissue planes and disrupts the anatomy and function of the optic nerve; e.g., a bullet or forceps that physically injures the optic nerve.
Diagram illustrating the locations of extraocular muscles and ocular cranial nerves. Paresis of the oculomotor nerve (CNIII) reduces the strength of medial rectus, superior rectus, inferior rectus, and inferior oblique muscles, while trochlear nerve (CNIV) and abducens nerve (CNVI) paralysis affect superior oblique muscle and lateral rectus muscle respectively.
It presents with visual loss and signs of optic nerve dysfunction, such as loss of color vision, afferent pupil defect, and sometimes abnormalities of the optic disc. The clinical features of AON can be variable and present in several unilateral or bilateral forms: Acute anterior or retrobulbar optic neuritis sometimes associated with pain.
The exact mechanism of optic nerve ischemia in these cases remains unclear, but contributing factors may include hypotension, anemia, hypoxia, and changes in the autoregulation of optic nerve arterial blood flow. The incidence of ischemic optic neuropathy leading to vision loss following general surgeries ranges between 0.1% and 0.002%.
The anterior optic nerve receives blood primarily from the posterior ciliary arteries. The anterior optic nerve, a.k.a. the optic nerve head, is surrounded by the scleral canal, and is vulnerable to crowding of nerve fibers. The portion of the optic nerve head that is visible by looking into the eye with an ophthalmoscope is called the optic disc.
Chronic relapsing inflammatory optic neuropathy (CRION) is a form of recurrent optic neuritis that is steroid responsive and dependent. [1] Patients typically present with pain associated with visual loss. [1] CRION is a clinical diagnosis of exclusion, and other demyelinating, autoimmune, and systemic causes should be ruled out. [3]
The optic tract is a continuation of the optic nerve that relays information from the optic chiasm to the ipsilateral lateral geniculate nucleus (LGN), pretectal nuclei, and superior colliculus. [14] The optic tract represents the first stage in the visual pathway in which visual information is transferred in a homonymous nature. [ 15 ]
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