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Neuro-Ophthalmology Newsletter October 2012

Optic nerve gliomas in children present a significant problem in management. The best form of treatment and the appropriate modalities for measuring the effectiveness of therapy are still under review. Kelly, et al (Ophthalmology 2012; 119:1231-1237, monitored visual acuity, tumor volume, and visual evoked potentials over time in children with optic nerve gliomas. The authors identified 21 patients between the ages of 0.7 and 9 years who had undergone treatment. 18 patients had undergone chemotherapy, 3 radiation therapy. All patients had serial MRI, visual acuity measurements in logMAR units, and pattern VEP. Patients were followed for an average of 9 years. The authors had available estimated tumor volumes before and after treatment in 15 patients. 81% had reduced visual acuity and optic nerve pallor prior to treatment. All had abnormal visual evoked potentials in one or both eyes. After initial treatment, there was a 53% decrease in tumor volume while 20% continued to progress. Visual acuity tended to stabilize visual acuity for four to five years. Patients often held constant visual acuities even without shrinkage of the tumor. 62% needed addition treatment with chemotherapy or radiation when the tumor continued to grow or growth recurred. The final visual acuity was stable or improved in 33% but overall declined 0.4 logMAR units on average. Initial visual acuity and tumor volume estimates were the best factors for predicting final visual outcome. The authors concluded that chemotherapy was successful in stabilizing visual function for 5 years on average. VEP was the most sensitive parameter for estimating the amount of visual pathway damage. Unfortunately, the final visual outcome tended to be limited by the amount of damage that preceded the initiation of therapy.

 

Ophthalmic or retinal artery occlusion may occur with the injection of cosmetic filler materials to the face. Park, et al (Am J Ophthalmol 2012; 154:653-662), performed a retrospective analysis on twelve consecutive patients with this complication.  Seven had ophthalmic artery occlusion, two central retinal artery occlusion, and three branch retinal artery occlusion. Parameters examined included the type of filler, injection sites, visual acuity, fluorescein angiography, OCT, and any associated ocular and systemic symptoms. Injected materials included autologous fat, hyaluronic acid, and collagen. Injection sites were the glabellar region in seven patients, nasolabial fold in four patients, and both sites in one patient. Fat injection led to the greatest drops in final visual acuity. All patients with ophthalmic artery occlusion suffered pain and did not regain any vision. Patients with ophthalmic artery occlusion also showed significant damage to the choroid. Two patients with central retinal artery occlusion and two patients with ophthalmic artery occlusion suffered cerebral infarction as well. Ophthalmic artery occlusion led to phthisis in one patient. The authors wished to alert practitioners regarding the risk for this severe complication and recommended that any patient with ocular pain after injection should be evaluated immediately.

 

 

Neuro-Ophthalmology Newsletter

Volume IX, Number 10 – October 2012

Case Study

 

Patient IX10 is a 65-year-old man who suffered a heart attack six days before this examination. He had some periods of significant hypotension. For the past two days he has noted horizontal, constant, binocular double vision worse looking to his left. His vision seems blurred. His medical history was significant for sinus congestion, myocardial infarcts in 1996 and recently, shoulder surgery, neck surgery, and cutaneous actinic keratosis. His ocular history was significant for the problems listed above. A social history indicated cessation of smoking cigarettes in 2010 and social alcohol consumption. His family history was non-contributory. Current medications included Plavix, Aspirin, Zocor, Allegra, Zyrtec, and over the counter dietary supplements. He reported allergies to Morphine and ACE inhibitors.

 

At exam, his visual acuity with correction was 20/30 in each eye. He had normal pupillary function without a relative afferent pupillary defect. Confrontation testing was full in both eyes. There was a normal appearance of his eyelids, orbits, lacrimal glands, lacrimal drainage system, and regional lymph nodes. His right eye showed a slight decrease in adduction and delayed adduction saccades. His left eye showed abduction nystagmus. He demonstrated a low amplitude, high frequency up-beating nystagmus in neutral position. He had a 5 diopter right hypertropia in neutral position, right gaze, and down gaze that increased slightly in left gaze and up gaze. His right eye did not converge to an approaching target. His anterior segments were healthy. His optic discs were pink and flat. He was alert and oriented time four.

 

What are his diagnoses and where is the lesion?

Discussion of Case IX9 from September 2012 Newsletter

 

This patient has a right junctional scotoma. All practitioners should recognize this pattern since it pinpoints the site of the problem. A junctional scotoma consists of a central defect in one eye with a superior temporal defect in the opposite eye. This pattern is noted in patients with lesions at the anterior aspect of the optic chiasm. The usual culprits are at fault, including pituitary adenomas, meningiomas, and craniopharyngiomas.

 

A couple of hypotheses have been presented to explain the combination of visual changes seen. Traditionally, the central scotoma in one eye, in this case the right eye, results from compression of the optic nerve just anterior to the optic chiasm. Anatomical studies have shown the presence of Wilbrand’s knee related to optic nerve fibers crossing in the chiasm from the contralateral eye. The optic nerve fibers from the inferior nasal retina of the contralateral eye corresponding to the superior temporal field in that eye (in this case the left eye) swing forward for a short distance into the optic nerve as they cross. As a result, these crossing fibers are affected simultaneously with the optic nerve fibers when the nerve is compressed.

 

Dr. Jonathan Horton, however, performed studies on the visual pathways of primates that indicated that Wilbrand’s knee was an artifact of tissue preparation and really does not exist. His suspicions were based on the fact that patients who have surgical resection of the optic nerve just anterior to the optic chiasm did not develop junctional scotomas. Her used MRIs from patients with junctional scotomas and demonstrated that they had both optic nerve and anterior chiasmal compression.

 

Horton’s arguments certainly are convincing. No matter which hypothesis you believe, however, this defect always locates to the junction of an optic nerve and the anterior optic chiasm.