Dilek Top Karti1, Omer Karti2, Gulsum Saruhan Durmaz3, Figen Gokcay3, Nese Celebisoy3. 1. Department of Neurology, Bozyaka Training and Research Hospital, Izmir, Turkey. 2. Department of Ophthalmology, İzmir Democracy Univesity, Güzelyalı Konak /İZMİR, Mehmet Ali Akman Mahallesi, 13. Sokak No:2, Izmir, Turkey. kartiomer@gmail.com. 3. Department of Neurology, Ege University Medical Faculty, Izmir, Turkey.
Abstract
PURPOSE: We aimed to demonstrate the patient demographics, etiologies and apraclonidine test results in adult Horner's syndrome. METHODS: This retrospective study was performed by the analysis of medical data of patients who were given 0.5% apraclonidine test. Patients' past medical history, demographic data, etiologies, accompanying neurological findings and pharmacological test results were assessed. RESULTS: Forty patients (21 females and 19 males) with a mean age of 50.3 ± 11.6 years were evaluated. Apraclonidine 0.5% test was positive in 37 patients (92.5%). An etiology could be identified in 20 patients (central [9 patients, 45%], preganglionic [9 patients, 45%] and postganglionic [2 patients, 10%]). Neurological findings accompanying Horner's syndrome were present in 8 patients. CONCLUSION: Despite detailed investigations, in a significant number of patients with Horner's syndrome an underlying cause may not be detected. Among the identifiable lesions, central and preganglionic involvements are still the first leading causes of Horner's syndrome. In addition, apraclonidine test may not be positive in all patients and a negative response does not exclude Horner's syndrome.
PURPOSE: We aimed to demonstrate the patient demographics, etiologies and apraclonidine test results in adult Horner's syndrome. METHODS: This retrospective study was performed by the analysis of medical data of patients who were given 0.5% apraclonidine test. Patients' past medical history, demographic data, etiologies, accompanying neurological findings and pharmacological test results were assessed. RESULTS: Forty patients (21 females and 19 males) with a mean age of 50.3 ± 11.6 years were evaluated. Apraclonidine 0.5% test was positive in 37 patients (92.5%). An etiology could be identified in 20 patients (central [9 patients, 45%], preganglionic [9 patients, 45%] and postganglionic [2 patients, 10%]). Neurological findings accompanying Horner's syndrome were present in 8 patients. CONCLUSION: Despite detailed investigations, in a significant number of patients with Horner's syndrome an underlying cause may not be detected. Among the identifiable lesions, central and preganglionic involvements are still the first leading causes of Horner's syndrome. In addition, apraclonidine test may not be positive in all patients and a negative response does not exclude Horner's syndrome.