TY - JOUR
T1 - The clinical neuro-ophthalmologic spectrum of temporal arteritis
AU - Mehler, Mark F.
AU - Rabinowich, Lydia
N1 - Funding Information:
From the Saul R. Korey Department of Neurology, Albert Einstein College of Medicine, Bronx, New York. Preliminary results were presented at the ! lOth Annual Meeting of the American Neurological Association, San Francisco, California, October 4-6, 1987. Dr. Mehler was supported by Teacher-lnvestigator Award NS00856 from the National Institute of Neurological and Communicative Diseases and Stroke, National Institutes of Health. Requests for reprints should be addressed to Dr. Mark F. Mehler, Department of Neurology (F G-9), Albert Einstein College of Medicine, [300 Morris Park Avenue, Bronx, New York 10461. Manuscript submitted June 3, 1988, and accepted October 19, 1988.
PY - 1988/12
Y1 - 1988/12
N2 - The range of neuro-ophthalmologic signs in temporal arteritis is broad and includes diverse presentations of ischemic optic neuropathy, retinal infarction, transient ischemic phenomena, ophthalmoparesis, pupillary autonomic and anterior ocular segment dysfunction, cortical blindness and associated post-chiasmal field defects, and complex visual hallucinations. Neurovascular compromise can follow arteritic lesions at multiple neuroanatomic sites, and reflects different pathogenetic mechanisms and displays distinctive clinical features. A variety of temporal clinical profiles and differential responses to corticosteroids occur. This article reviews the broad range of neuroanatomic pathways affected by diverse and potentially interactive etiologic factors in this systemic arteritis.
AB - The range of neuro-ophthalmologic signs in temporal arteritis is broad and includes diverse presentations of ischemic optic neuropathy, retinal infarction, transient ischemic phenomena, ophthalmoparesis, pupillary autonomic and anterior ocular segment dysfunction, cortical blindness and associated post-chiasmal field defects, and complex visual hallucinations. Neurovascular compromise can follow arteritic lesions at multiple neuroanatomic sites, and reflects different pathogenetic mechanisms and displays distinctive clinical features. A variety of temporal clinical profiles and differential responses to corticosteroids occur. This article reviews the broad range of neuroanatomic pathways affected by diverse and potentially interactive etiologic factors in this systemic arteritis.
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U2 - 10.1016/S0002-9343(88)80031-7
DO - 10.1016/S0002-9343(88)80031-7
M3 - Article
C2 - 3057903
AN - SCOPUS:0024208528
SN - 0002-9343
VL - 85
SP - 839
EP - 844
JO - The American Journal of Medicine
JF - The American Journal of Medicine
IS - 6
ER -