Purpose To quantify optic nerve head circulatory abnormalities in patients wit h unilateral non arteritic anterior ischemic optic neuropathy (NAION) or optic n euritis (ON), and to assess the potential of such measurements to differentiate NAION from ON. Design Prospective, cross-sectional, observational study. Partic ipants Thirty consecutive patients with unilateral NAION, 22 consecutive patient s with unilateral ON, and 50 healthy control subjects. Methods All subjects unde rwent a complete neuro-ophthalmologic evaluation. The widths of Dopplerbroadene d frequency spectra, which are directly proportional to the speed of blood cells flowing through the capillaries of the optic nerve head, were measured at multi ple sites in both eyes of each subject. The variation of Doppler broadening(DB) with age was determined in the control subjects. Doppler broadening values in th e patients were compared between similar sites in affected and contralateral eye s, and between both affected and contralateral eyes and the age-adjusted values determined in the control subjects. Main outcome measures The differences in DB between (1) the affected and contralateral eyes of the patients, (2) the patien ts and the control subjects, and (3) the patients with NAION and those with ON. Results In NAION, DB was decreased at both temporal (-20.2%and -18.5%) and n asal (-12.8%and -12.4%) sites of the nerve head in affected eyes compared wi th contralateral eyes or eyes of control subjects. In ON, DB was also decreased at temporal sites (-11.3%and -9.2%) in affected eyes compared with contralat eral or control eyes. At nasal sites, there were no significant differences in D B in affected eyes of ON patients compared with contralateral or control eyes. T he DB decreases were significantly greater in NAION patients than in ON patients . Conclusions Optic nerve head circulatory abnormalities are present in patients with NAION or ON. This is the first demonstration of such abnormalities in ON, a finding consistent with the recent attention given to the phenomenon of axonal loss in this disease. Although there are differences in the circulatory abnorma lities between the 2 diseases that provide insights into the pathophysiological mechanisms at play, they are not large enough to enable the clinician to disting uish between ON and NAION in an individual patient.
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