Anthony C. Arnold, M.D., UCLA Department of Ophthalmology
Postoperative visual function relates to preoperative duration of symptoms, visual acuity and fields, and degree of optic atrophy (including retinal nerve fiber layer loss). Visual acuity improves in 46-65% and visual fields in 67-92%; decrease in visual function occurs in 2%. Neuro-ophthalmologic followup is recommended within the first month, at 6 months, and then yearly postoperatively with quantitative perimetry unless problems occur. Late visual loss may be divided into three major categories:
Postoperative Tumor Recurrence
Tumor recurrence is the most common cause of late visual deterioration; such change in visual function may be the first manifestation. of regrowth. Rate of tumor recurrence varies with tumor type, initial size, and mode of therapy (including use of radiation), but figures from 4 to 12% have been reported, most often within 5 years. Visual loss from tumor recurrence is typically slowly progressive, affecting one or both eyes, and involving either central or peripheral field. Clinical neuro-ophthatmic examination with quantitative perimetry is a sensitive indicator of compressive neuropathy; however, early detection may be more difficult in patients with more severe visual loss and optic atrophy, and regular neuroimaging is essential. Tumor regrowth must be differentiated from radiation changes on MR scanning.
Secondary Empty Sella Syndrome
While primary empty sella syndrome is not associated with visual loss, the secondary form may result in bilateral visual loss. This rare syndrome, which arises after either surgery or radiation, is characterized by downward herniation of the chiasm into the empty sella, either from lack of support or from traction related to arachnoidal adhesions. The chiasmal distortion results in progressive visual loss which may be quite severe. It typically begins months to years after treatment, shows features of chiasmal or optic nerve dysfunction, and is gradually progressive over weeks to months. Displacement and distortion of the chiasm and intracranial optic nerves is well visualized on MR imaging. Surgical repair with lysis of adhesions and packing of the sella has been reported to improve visual prognosis.
Delayed radionecrosis of chiasm and optic nerves
Late delayed radiation effect on the central nervous system is well known. It may occurs from 4 months to 15 years after initial exposure, but most frequently presents within several years post-treatment. In the visual system, it typically produces an acute syndrome of bilateral visual loss. Both central and peripheral fields are usually affected, and degree of loss is severe, with no light perception not uncommon. The optic nerve heads may be swollen, but are more typically unchanged from their prior postoperative appearance initially, with increasing atrophy developing within 4-8 weeks. Radiation retinopathy may occasionally be associated. Individual tolerance to radiation varies, dependent on degree of prior tissue damage, status of vascular system, total dose, fractionation, and volume of tissue treated; no absolute criteria for safety in radiation therapy can be applied. In general, however, radionecrosis is rarely seen with total dose under 50 Gy in fractions under 2.5 Gy. MR imaging demonstrates tissue swelling and enhancement acutely, and typically clearly differentiates this syndrome from tumor recurrence. There is not proven therapy, though high dose corticosteroids have been used. The results of hyperbaric oxygen have been controversial.
Cranial nerve palsies
Postoperative dysfunction of cranial nerves 3, 4, and 6 has been infrequently reported after intracranial or trans-sphenoidal techniques. In large reviews of trans-sphenoidal surgeries,.4-2% of cases demonstrated these findings, the majority of which showed significant improvement or resolution within 6 months.
Radiation may also produce cranial nerve palsies as a late manifestation. The oculomotor nerve is most frequently affected, probably due to its proximity to the tumor laterally, followed by the abducens and trochlear nerves. Onset is typically within one year after therapy. In contrast to damage to the afferent visual pathways, impairment is often at least partially reversible. Involvement of the cranial nerves at doses under 5000 rad is extremely unusual by current techniques.
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