Oscillopsia after lateral wall orbital decompression.

PURPOSE: To assess the incidence, duration, and severity of oscillopsia after lateral wall orbital decompression for thyroid eye disease. DESIGN: Retrospective telephone interview. PARTICIPANTS: A consecutive group of patients who had undergone lateral wall orbital decompression for thyroid eye disease performed by 2 consultants at Moorfields Eye Hospital between January 2008 and December 2010. METHODS: Patients were telephoned and a standardized interview related to postoperative oscillopsia was performed. The degree of preoperative and late postoperative exophthalmometry was assessed from clinical records. MAIN OUTCOME MEASURES: The presence, severity, and duration of postoperative oscillopsia and its impact on daily activities. RESULTS: Ninety-eight patients were interviewed successfully, of which 34 (35%) had noted postoperative oscillopsia that occurred upon chewing in 29 of 34 patients (85%) and upon walking in 8 of 34 patients (24%). The oscillopsia resolved within 1 year in 15 of 34 patients (44%), and 16 of 34 (47%) still had mild symptoms at 2 years or more after surgery. Fourteen patients (41% of affected patients; 14% of the entire group) initially were troubled by the symptom, but at the time of interview, only 1 person found it troublesome and 7 reported it as a minimal problem. The reduction in proptosis was similar among those with and without oscillopsia. CONCLUSIONS: The incidence of oscillopsia after lateral wall orbital decompression was 35% when patients were questioned directly, and was much higher than anticipated from extensive clinical experience (where very few patients mention the symptom). In almost all cases, the oscillopsia resolved or was not troublesome, and only 1 patient found it bothersome more than 2 years after surgery. FINANCIAL DISCLOSURE(S): The author(s) have no proprietary or commercial interest in any materials discussed in this article.

Bilateral presumed ischemic optic neuropathy secondary to cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.

PURPOSE: To report a case of bilateral ischemic optic neuropathy (ION) secondary to hypoperfusion of the optic nerve because of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy, an uncommon condition causing stepwise subcortical small vessel infarcts because of arterial wall rigidity, loss of autoregulation, and hypoperfusion. METHODS: We describe the ophthalmological presentation of this case including fluorescein angiography and kinetic perimetry. RESULTS: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy is an increasingly recognized condition with significant neurological sequelae. This case demonstrates the potential for secondary visual loss because of optic nerve hypoperfusion, and the literature confirms this mechanism of injury for both the optic nerve and retina. Retinal screening may add evidence toward the diagnosis in visually asymptomatic patients. Because there is no treatment for the condition, management is symptomatic only but involves psychological support and genetic counseling. CONCLUSION: We propose that cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy be added to the list of potential differential diagnoses for ION in young patients.