Introduction: Heather Moss, MD, PhD (Attending) - University of ...

Compressive Optic Neuropathy: (Continued)
DISCUSSION Thyroid eye disease (TED) is an autoimmune disease which is usually self-limited but can be progressive. It is most commonly
associated with Graves’ disease and hyperthyroidism, but can occur in patients who are euthyroid or hypothyroid. TED incidence is
four times higher in women than men. Diagnosis is usually made clinically but imaging with CT or MRI can be done. Classically this shows
enlargement of the EOMs with sparing of the tendons. Common clinical characteristics consist of inflammation and congestion of EOMs,
proptosis, eyelid retraction, lid lag, diplopia, lid edema, chemosis, exposure keratopathy, and possible optic neuropathy. Treatment starts
with establishing a euthyroid state. The literature has shown that corticosteroids are the most effective initial treatment. There is no additional
benefit from early surgical decompression. Intraorbital steroid injections are another possible form of treatment which has shown to be effective.
Radiation therapy is another effective treatment option, especially in patients who have failed treatment with steroids.
REFERENCES:
Phillips ME, Marzban MM, Kathuria SS. Treatment of thyroid eye disease. Current Treatment Options in Neurology. 2010 Jan;12(1):64-9.
Modjtahedi SP, Modjtahedi BS, Mansury AM, Selva D, Douglas RS, Goldberg RA, Leibovitch I. Pharmacological treatments for thyroid eye
disease. Drugs. 2006;66(13):1685-700.
Alkawas AA, Hussein AM, Shahien EA. Orbital steroid injection versus oral steroid therapy in management of thyroid-related ophthalmopathy.
Clinical and Experimental Ophthalmology. 2010 Oct;38(7):692-7.
Abboud M, Arabi A, Salti I, Geara F. Outcome of thyroid associated ophthalmopathy treated by radiation therapy. Radiation Oncology. 2011
May;6:46.
Acute Altitudinal Visual Field Defect with Optic Disc Edema: Sara Huh, MD (Resident)
A 68 year old male presents with the chief complaint of left eye vision loss. His medical history includes shingles affecting
V1, V2, and V3 branches of his left face 9 months prior to presentation at UIC. His shingles started with a rash on
his skin, foreign body sensation in the left eye with photophobia. He was treated with oral valacyclovir for 30 days and
Lotemax for the ocular involvement. With the resolution of the rash, he developed severe left sided facial pain and was
treated for post-herpetic neuralgia with improvement of his symptoms. CTA and MRI of the brain were performed at
the time showing non-specific periventricular T2 signaling, likely due to small vessel ischemic disease. 2 weeks prior to
presentation, he noted a grey shade being pulled down over the superior portion of his left eye visual field, without ocular
pain. He went to his local ophthalmologist where his visual acuity was 20/100 and examination showed a swollen left
optic nerve. Visual field testing showed a dense superior altitudinal loss in the left eye (see Figure 1). His ophthalmologist
ordered a few laboratory tests, including ESR, CRP and platelets which were normal, presumed to rule out giant cell
arteritis. He was started on Valtrex 1 g daily. 1 week later his vision improved to 20/30 in the left eye.
He has no known drug allergies, is currently on valacyclovir, gabapentin, and Lotemax eye drops to his left eye. He has a 20 pack year smoking
history; however he quit 30 years ago and he consumes alcohol socially.
On presentation to the neuro-ophthalmology clinic, his left eye visual acuity was 20/30 with full color plates. He had a Relative Afferent Pupillary
Defect (rAPD) on the left and superior field defect on confrontational visual field testing. His intraocular pressures were within normal limits.
His anterior segment examination was significant for blepharitis bilaterally, some conjunctival injection in the left eye with dense inferior punctate
staining with fain subepithelial infiltrates. There was no evidence of corneal pseudodendrites.
On dilated fundus examination, the vitreous was clear with small cup to disc ratio bilaterally. The left optic nerve was diffusely hyperemic and
edematous. Otherwise his fundus examination was within normal limits.
The question at this point becomes – was this an idiopathic non-arteritic anterior ischemic optic neuropathy or a zoster related optic neuropathy?
The plan was to rule out potential vasculopathy due to Varicella zoster virus (VZV) as an etiology of ischemic optic nerve injury – MRI of the brain
and orbits were ordered and a lumbar puncture performed for IgG and IgM antibodies and VZV DNA by PCR. He was treated with IV acyclovir for
10 days followed by oral acyclovir and IV solumedrol.
THE ILLINOIS EYE AND EAR INFIRMARY: Treating the most serious and complicated ophthalmology cases for over 150 years