Failure to distinguish uveitis from other ocular diseases may result in insufficient or inappropriate therapy with the most disastrous sequelae being continued ocular pain, blindness, or progression of undiagnosed systemic disease. Inflammation of the entire uveal tract is called panuveitis. Inflammation of the anterior uvea is termed anterior uveitis or iridocyclitis, and inflammation of the posterior uvea is termed posterior uveitis or choroiditis. The posterior uvea, or choroid, supplies nourishment to the outer layers of the retina. Also, contraction of the ciliary body and subsequent changes in lens zonular tension are necessary for accommodation (change in shape) of the lens. It is responsible for production of aqueous humor vital for nourishment of the anterior segment of the eye. The ciliary body has two primary functions. Normal pupillary function (and retinal integrity) are evaluated through assessment of the pupillary light reflexes (PLRs). The iris and ciliary body together comprise the anterior uvea. Because of its rich blood supply and proximity to other vital intraocular structures, the uvea is involved in most intraocular disease processes. The uvea is the vascular and muscular tunic of the eye composed of the iris, ciliary body, and choroid. These findings stress the necessity to instill the unaffected eye in diagnosing a suspected Horner's pupil.Uveitis specifically refers to inflammation of the middle layer of the eye (the uveal tract) but more commonly, it may refer to any inflammatory process involving the interior of the eye, with inflammation specifically of the uvea termed iridocyclitis. In patients with Horner's syndrome, the α-1 agonistic effect will dominate because of the supersensitivity of the α-1 receptors, resulting in relative mydriasis. The relative miotic effect of apraclonidine could be explained by the α-2 receptor agonistic effect which is more pronounced than the α-1 agonistic effect in healthy subjects. The amplitude of constriction to light also differs significantly. Instillation of apraclonidine 1% in healthy subjects causes relative miosis, which is most pronounced after 30-60 min. No significant influence was found on the latency, the constriction velocity and redilation velocity. The eye with apraclonidine drops showed relative miosis and an increased amplitude of constriction to light. The anisocoria after dark adaptation and at minimum pupil diameter differed significantly for the measurements obtained 30 and 60 min after instillation with apraclonidine. Measurements were retaken 30, 60, 90, 120, 180, 240, 300 and 360 min after random instillation of one eye with one drop of 1% apraclonidine. The first measurements were performed prior to instillation of apraclonidine. Infrared pupillography was used to measure the scotopic pupil diameter and the dynamic pupil responses to light. Therefore, the effect of apraclonidine on pupillary parameters was investigated in 14 healthy volunteers. By measuring the effect on the pupil intermittently over a few hours, we tried to determine the best moment for evaluation after instillation with apraclonidine. Since the comparison of both the pathologic and the non-pathologic eye is important, we wanted to further investigate the effect of apraclonidine on the healthy eye. Recent literature suggests that in healthy volunteers, apraclonidine provokes a mild miotic effect. Used in the diagnosis of Horner's syndrome, apraclonidine 1% dilatates the involved eye due to denervation supersensitivity.
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