RETINAL VENOUS SHEATHING AND THE BLOOD-RETINAL BARRIER IN MULTIPLE-SCLEROSIS

Citation
Mk. Birch et al., RETINAL VENOUS SHEATHING AND THE BLOOD-RETINAL BARRIER IN MULTIPLE-SCLEROSIS, Archives of ophthalmology, 114(1), 1996, pp. 34-39
Citations number
24
Categorie Soggetti
Ophthalmology
Journal title
ISSN journal
00039950
Volume
114
Issue
1
Year of publication
1996
Pages
34 - 39
Database
ISI
SICI code
0003-9950(1996)114:1<34:RVSATB>2.0.ZU;2-7
Abstract
Objective: To assess the temporal relations among retinal appearance, disruption of the blood-retinal barrier, clinical subgroup, disease co urse, and disruption of the blood-brain barrier in multiple sclerosis. Design: A 6-month prospective study involving monthly clinical ocular examinations, color fundus photography, fundus fluorescein angiograms , and magnetic resonance brain scans wi th gadolinium-diethylenetriami ne-pentaacetic acid (Gd-DPTA) enhancement. Setting: University-based o phthalmology and neurology departments. Patients: Twenty-three patient s with relapsing-remitting, primary-progressive, or secondary-progress ive multiple sclerosis. Results: Retinal venous sheathing was seen in six patients. The appearances observed included focal venous sheathing , diffuse venous sheathing sheathing centered on sites of arteriovenou s crossover, and focal perivenous hemorrhage. Arteriolar sheathing was also observed in one patient. Venous leakage on fundus fluorescein an giogram was detected in three patients, all of whom also had sheathing . The following three patterns of disruption of the blood-retinal barr ier were seen on fundus fluorescein angiogram: focal leakage, extensiv e leakage, and very late wall staining. In one patient, the leakage wa s transitory. No correlations were observed between ophthalmologic fea tures and multiple sclerosis clinical subgroup, disease course, or the number of new (Gd-DTPA-enhancing) lesions on magnetic resonance imagi ng. Conclusions: Disruption of the blood-retinal barrier, like the mor e frequent disruption of the blood-brain barrier seen on magnetic reso nance imaging, is often unrelated to clinical neurologic relapses and occurs with apparently similar frequency in different patients indepen dent of clinical disease course.