Vascular hypoperfusion in acute optic neuritis

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Vascular hypoperfusion in acute optic neuritis

Postby frodo » Wed Sep 20, 2017 1:25 am

Vascular hypoperfusion in acute optic neuritis is a potentially new neurovascular model for demyelinating diseases.

Source: https://www.ncbi.nlm.nih.gov/pubmed/28926646

Abstract
PURPOSE:

Optic neuritis is highly correlated with multiple sclerosis and is a major cause of acute visual loss and long-term neuronal degeneration. Primary cerebral hypoperfusion has been reported in brain demyelinating diseases. This study investigated whether peripapillary perfusion is changed in patients with acute optic neuritis (AON).
METHODS:

This three-year cohort study was conducted from September 1 2012, to August 31, 2015. Two hundred and forty-one patients with non-glaucomatous acute optic neuropathy were screened, and 42 non-highly myopic patients who had suffered their first episode of unilaterally idiopathic AON were studied. All cases received spectral-domain optical coherence tomography (OCT) examination, general survey, and standard corticosteroid therapy. OCT images were analyzed using a customized MATLAB program for measuring peripapillary choroidal thickness (PCT). Multivariate regression models were constructed to identify factors that are significantly related to peripapillary perfusion.
RESULTS:

Decreased PCT was found in eyes experiencing AON combined with disc swelling (the ratio of lesion eye PCT/fellow eye PCT was 0.87 ± 0.08; range, from 0.75 to 1.00). In comparison to the healthy fellow eyes, approximately every 26% increase in the thickness of the retinal nerve fiber layer due to axonal swelling was associated with a 10% decreased thickness of PCT. Thinner PCT is also correlated with poorer trough vision, which may lead to poorer final vision. These findings were obvious in patients with optic papillitis but not in patients with retrobulbar neuritis.
CONCLUSIONS:

Peripapillary vascular hypoperfusion was found in patients experiencing AON combined with disc swelling. These findings are unlike those for other ocular inflammatory diseases but are consistent with cerebral hypoperfusion, which is found in brain demyelinating diseases; thus, these findings may represent a new neurovascular model in this field.
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