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• W2057121685 abstract "Horner syndrome, manifested by ipsilateral miosis, upper lid ptosis, and sometimes facial anhidrosis, is caused by disruption of sympathetic innervation to the eye and face (1). Lack of pupil dilation after instillation of cocaine, an indirect sympathomimetic (2), has been traditionally used to support a clinical diagnosis of Horner syndrome (1). However, cocaine has the disadvantages of high cost, poor dilating capability, and lack of ready availability (3). Topical 0.5% or 1% apraclonidine (Iopidine; Alcon, Fort Worth, TX) has recently been proposed as a substitute for cocaine in testing for Horner syndrome (4-12). Although apraclonidine is primarily an α2 agonist, it also has weak affinity for α1, the predominant receptor in the iris dilator muscle (13). Sympathetic denervation in Horner syndrome results in upregulation or increased sensitivity of α1 receptors (14). Topical apraclonidine dilates a sympathetically denervated iris but not a normally innervated iris. However, the latency between sympathetic damage and development of upregulated adrenergic iris receptors is uncertain. In previous reports, patients had long-standing Horner syndrome before the application of the apraclonidine test (4-9,11,12). The shortest documented latency from occurrence of the lesion to a positive apraclonidine test is 1 month in a patient with “carotid stenosis” (5). We report a patient who developed a Horner syndrome acutely from carotid artery dissection who had a positive apraclonidine test within 2 weeks of symptom onset. A 36-year-old man was “cracking his neck” as a customary practice when he heard a loud popping sound in his neck. He immediately developed right-sided headache and right posterior neck pain. A coworker noted that the patient's right upper eyelid was droopy and that the right pupil was relatively small. Ten days after onset, he presented to a hospital emergency room and was transferred to our care with a clinical presumption of right Horner syndrome. Head and neck computed tomographic angiography (CTA) and catheter-based carotid angiography (Fig. 1) showed tapered narrowing of the right internal carotid artery of 2.5 cm extending from the carotid artery bifurcation to the skull base in a configuration typical of dissection.FIG. 1: Right carotid catheter angiography shows tapered narrowing (arrow) of the right internal carotid artery consistent with dissection.We examined the patient 14 days after symptom onset. Visual acuity was 20/20 in both eyes. There was 1 mm of right upper lid ptosis with good levator function. In dim illumination, the pupils measured 2 mm on the right and 3 mm on the left with both pupils constricting adequately to direct light (Fig. 2). The anisocoria was more apparent in dim illumination. There was no relative afferent pupillary defect. Results for the remainder of the ophthalmic and neurologic examinations were normal.FIG. 2: Our patient at 14 days after onset of right neck pain. A. Before instillation of 0.5% apraclonidine, the right pupil measures 2 mm and the left pupil measures 3 mm. B. Thirty minutes after instillation of 0.5% apraclonidine, the right pupil measures 5 mm and the left pupil measures 3 mm.Thirty minutes after instillation of one drop of apraclonidine 0.5% in both eyes, the right pupil measured 5 mm and the left pupil measured 3 mm in dim illumination (Fig. 2). The right upper lid ptosis disappeared. Because our patient's manifestations of carotid artery dissection had such abrupt onset, we can accurately date the latency from the time of sympathetic damage to the performance of the apraclonidine test as being no more than 14 days. Apraclonidine testing in Horner syndrome has been reported to have been administered in 65 patients. The documented latency of a positive test after sympathetic damage ranges between 1 month and 10 years (4-12). The sensitivity of the apraclonidine test for Horner syndrome is still unknown. Among the patients tested with apraclonidine (using cocaine as the pharmacologic gold standard), two false-negative results have been reported (5,8), and an additional three patients have shown reversal of the anisocoria only in bright illumination (6). One explanation for false-negative test results has been the unknown latency required for up-regulation of α1 receptors. The false-negative results occurred, however, in patients who had had clinical evidence of Horner syndrome for a minimum of 6 months. Wider studies will need to be performed to determine the shortest latency and the reliability of the apraclonidine test in the diagnosis of Horner syndrome. Brenda L. Bohnsack, MD, PhD Jared W. Parker, MD Kellogg Eye Center University of Michigan Ann Arbor, Michigan [email protected]" @default.
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• W2057121685 title "Positive Apraclonidine Test Within Two Weeks of Onset of Horner Syndrome Caused by Carotid Artery Dissection" @default.
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