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SYMPTOMS
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Vision loss, Headache, Diplopia, Loss of stereopsis, Bitemporal hemianopia
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SIGNS
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Optic disc may show pallor, especially in a “bow tie” configurationOptic disc may show pallor, especially in a “bow tie” configuration
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Papilledema is an unusual sign but can be seen with craniopharyngiomas
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WORK-UP
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Pupils (An APD is typically present especially if unilateral or asymmetric vision loss is present)
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EOMs (Cranial nerve III, IV, or VI involvement may be present. See-saw nystagmus may also be present)
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Cover test
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Color vision (Dyschromatopsia may be present)
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Complete eye exam with dilation
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Cranial nerve testing
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Ptosis testing
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OCT of the optic nerve (Temporal RNFL thinning)
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OCT of the macula (Binasal ganglion cell thinning)
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VEP
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Visual field threshold 30-2
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Junctional scotoma: Central scotoma in one eye and temporal hemianopia defect in the other eye. This indicates that the lesion is closer to the optic nerve on the side with the central scotoma at the anterior knee of von Willebrand
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Bitemporal hemianopia (Classic presentation): Complete or incomplete bilateral hemianopia. Predominantly superior temporal hemianopia defects that eventually progress to a complete hemianopia are due to pituitary adenomas. Predominantly inferior temporal hemianopia defects that eventually progress to a complete hemianopia are due to craniopharyngiomas
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Homonymous hemianopia: Incongruent homonymous hemianopia due to a parasellar lesion. Associated with a central scotoma on the same side as the location of the lesion. Also called optic tract syndrome
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TREATMENT
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Refer to neuro-ophthalmologist/neurology for further evaluation and treatment
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After treatment, about 40% of patients will fully recover (Most visual recovery is noted in 1-4 months). Visual recovery after 6 months is unlikely. If visual symptoms are still present, patient should undergo vision rehabilitation and vision restorative training (glasses, prism, tint, etc)
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FOLLOW-UP
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Patient will likely be monitored by neurology/neuro-ophthalmology on a regular basis. Patient should be seen back once underlying neurological etiology is in control or stable.
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Monitor every 3 months for the first year and then every 6-12 months thereafter
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ADDITIONAL LAB | TESTS
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MRI with and without contrast of the brain (concentration on the chiasm) | Neurological evaluation | Endocrine workup
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ETIOLOGY
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Optic chiasm lesions are secondary to tumors 90% of the time. These tumors can include pituitary adenomas (most common), craniopharyngiomas, meningiomas, and gliomas
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DIFFERENTIAL DX
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Parietal lobe lesion, Temporal lobe lesion, Occipital lobe lesion
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NOTES
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Macroadenomas: > 10mm | Microadenomas: < 10mm
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Systemic signs associated with optic chiasm include hypopituitarism, hypothyroidism, amenorrhea, galactorrhea, diabetes insipidus, impotence, and acromegaly
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Meningiomas are grow slowly that are less likely to present with endocrine abnormalities
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A glioblastoma is an aggressive form of a glioma and has a very high mortality rate within 1 year
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Diplopia associated with optic chiasm lesions without evidence of cranial nerve III, IV, or VI involvement is referred to as a hemifield slide
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Pituitary apoplexy occurs when there is hemorrhaging in a preexisting pituitary tumor which causes it to get larger very quickly. This causes a severe thunderclap headache, sudden changes in peripheral vision, sudden vision loss, sudden EOM palsies and diplopia, altered mental status, nausea, vomiting, and loss of appetite. This is considered an emergency and needs to be referred to the ER STAT
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Reasons for progression in visual field loss even with treatment: · Regrowth of tumor · Damage to the optic chiasm from radiation · Chiasmal prolapse into an empty sella · Arachnoiditis
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