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T.F. Freddo, S. Patz, Y. Arshanskiy; Aqueous Flare Is Not Always Pathological . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3666.
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To determine whether clinical flare, resulting from administration of topical pilocarpine, is the result of increased ciliary epithelial permeability.
Four normal human volunteers, of both sexes, ranging in age from 23–40 years. Studies were IRB–approved. Pupil size was recorded and baseline measurements of flare were obtained with a KOWA 1000 Flare Cell meter. A standard drop of 3% pilocarpine was topically instilled in one eye and pupil size and flare measurements were recorded every 15 minutes for 45 minutes. The eye to be examined by MRI was taped closed, covered with gauze and a TMJ surface coil was fixed over the eye. A baseline, T1–weighted, spin–echo MR image was obtained (TR/TE=1400/15ms–image acquisition time 4 min 45 sec/image). The subject then received a bolus injection of 0.4 mg/kg Gadolinium dimeglumine i.v., and serial images were obtained every 10 min for at least 60 min. Mean and SD of signal intensity (SI) in regions of interest (ROI) in the anterior (AC) and posterior chambers (PC) were obtained and percent enhancement in the mean SI of these two ROIs were calculated.
Initial pupil size in mm (mean/SD) was 6/1.4, decreasing to 2.4/0.5, by 45 min after pilocarpine. During this period, average flare/SD (photons/ms) increased from 3.4/1.0 to 13.4/4.9. MRI showed a rapid increase in SI in the ciliary body in all cases. Mean/SD enhancement of the AC and PC respectively were 27%/19% and –1.7%/12%. Representative image in Figure below (60 min post–gado) shows enhancement of AC but not PC.
Prior studies have generally attributed the flare following pilocarpine to breakdown of the ciliary epithelial barrier but these studies were done using either cell–flare readings only, or in conjunction with fluorophotometry, neither of which can directly assess dynamics behind the iris plane. Despite the small N, the lack of enhancement in the PC clearly indicates that the flare after pilocarpine (SI enhancement of the AC) does not result from breakdown of the ciliary epithelial barrier. More likely the added protein originates from the reservoir known to exist in the iris stroma and is released as the stroma thins during miosis.
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