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January 1996

Retinal Venous Sheathing and the Blood-Retinal Barrier in Multiple Sclerosis

Author Affiliations

From St Paul's Eye Unit, Royal Liverpool (England) University Hospital (Drs Birch, O'Brien, and Harding) and the Department of Neurological Sciences, University of Liverpool (Dr Barbosa); and the Division of Clinical Neurology, University Hospital Nottingham (England) (Dr Blumhardt).

Arch Ophthalmol. 1996;114(1):34-39. doi:10.1001/archopht.1996.01100130032005

Objective:  To assess the temporal relations among retinal appearance, disruption of the blood-retinal barrier, clinical subgroup, disease course, 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 with gadolinium-diethylenetriaminepentaacetic acid (Gd-DPTA) enhancement.

Setting:  University-based ophthalmology and neurology departments.

Patients:  Twenty-three patients with relapsing-remitting, primary-progressive, or secondary-progressive 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 arteriovenous crossover, and focal perivenous hemorrhage. Arteriolar sheathing was also observed in one patient. Venous leakage on fundus fluorescein angiogram was detected in three patients, all of whom also had sheathing. The following three patterns of disruption of the blood-retinal barrier were seen on fundus fluorescein angiogram: focal leakage, extensive leakage, and very late wall staining. In one patient, the leakage was transitory. No correlations were observed between ophthalmologic features and multiple sclerosis clinical subgroup, disease course, or the number of new (Gd-DTPA—enhancing) lesions on magnetic resonance imaging.

Conclusions:  Disruption of the blood-retinal barrier, like the more frequent disruption of the blood-brain barrier seen on magnetic resonance imaging, is often unrelated to clinical neurologic relapses and occurs with apparently similar frequency in different patients independent of clinical disease course.

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