Optical coherence tomography reflects brain atrophy in multiple sclerosis: A four‐year study. Issue 5 (1st October 2015)

• Record Type: Journal Article
• Authors: Saidha, Shiv; Al‐Louzi, Omar; Ratchford, John N.; Bhargava, Pavan; Oh, Jiwon; Newsome, Scott D.; Prince, Jerry L.; Pham, Dzung; Roy, Snehashis; van Zijl, Peter; Balcer, Laura J.; Frohman, Elliot M.; Reich, Daniel S.; Crainiceanu, Ciprian; Calabresi, Peter A.
• Is Part Of: Annals of neurology. Volume 78:Issue 5(2015:Nov.)
• Page Start: 801
• Page End: 813
• Publication Date: 2015-10-01
• Subjects: Neurology -- Periodicals; Pediatric neurology -- Periodicals; Nervous system -- Surgery -- Periodicals; 616.8
• DOI: 10.1002/ana.24487
• Languages: English
• ISSNs: 0364-5134

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="ana24487-sec-0001" sec-type="section"> <title>Objective</title> <p>The aim of this work was to determine whether atrophy of specific retinal layers and brain substructures are associated over time, in order to further validate the utility of optical coherence tomography (OCT) as an indicator of neuronal tissue damage in patients with multiple sclerosis (MS).</p> </sec> <sec id="ana24487-sec-0002" sec-type="section"> <title>Methods</title> <p>Cirrus high‐definition OCT (including automated macular segmentation) was performed in 107 MS patients biannually (median follow‐up: 46 months). Three‐Tesla magnetic resonance imaging brain scans (including brain‐substructure volumetrics) were performed annually. Individual‐specific rates of change in retinal and brain measures (estimated with linear regression) were correlated, adjusting for age, sex, disease duration, and optic neuritis (ON) history.</p> </sec> <sec id="ana24487-sec-0003" sec-type="section"> <title>Results</title> <p>Rates of ganglion cell + inner plexiform layer (GCIP) and whole‐brain (r = 0.45; <italic>p</italic> < 0.001), gray matter (GM; r = 0.37; <italic>p</italic> < 0.001), white matter (WM; r = 0.28; <italic>p</italic> = 0.007), and thalamic (r = 0.38; <italic>p</italic> < 0.001) atrophy were associated. GCIP and whole‐brain (as well as GM and WM) atrophy rates were more strongly associated in progressive MS (r = 0.67; <italic>p</italic> < 0.001) than relapsing‐remitting MS (RRMS; r = 0.33; <italic>p</italic> = 0.007). However, correlation between rates of GCIP and whole‐brain (and additionally GM and WM) atrophy in RRMS increased incrementally with step‐wise refinement to exclude ON effects; excluding eyes and then patients (to account for a phenotype effect), the correlation increased to 0.45 and 0.60, respectively, consistent with effect modification. In RRMS, lesion accumulation rate was associated with GCIP (r = −0.30; <italic>p</italic> = 0.02) and inner nuclear layer (r = −0.25; <italic>p</italic> = 0.04) atrophy rates.</p> </sec> <sec id="ana24487-sec-0004" sec-type="section"> <title>Interpretation</title> <p>Over time GCIP atrophy appears to mirror whole‐brain, and particularly GM, atrophy, especially in progressive MS, thereby reflecting underlying disease progression. Our findings support OCT for clinical monitoring and as an outcome in investigative trials. Ann Neurol 2015;78:Ann Neurol 2015;78:679–696</p> </sec> </abstract>