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Interactions of optic radiation lesions with retinal and brain atrophy in early multiple sclerosis
Objective Retrograde trans‐synaptic neuroaxonal degeneration is considered a key pathological factor of subclinical retinal neuroaxonal damage in multiple sclerosis (MS). We aim to evaluate the longitudinal association of optic radiation (OR) lesion activity with retinal neuroaxonal damage and its r...
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| Published in: | Annals of clinical and translational neurology 2024-01, Vol.11 (1), p.45-56 |
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| container_title | Annals of clinical and translational neurology |
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| creator | Lin, Ting‐Yi Chien, Claudia Kuchling, Joseph Asseyer, Susanna Motamedi, Seyedamirhosein Bellmann‐Strobl, Judith Schmitz‐Hübsch, Tanja Ruprecht, Klemens Brandt, Alexander U. Zimmermann, Hanna G. Paul, Friedemann |
| description | Objective
Retrograde trans‐synaptic neuroaxonal degeneration is considered a key pathological factor of subclinical retinal neuroaxonal damage in multiple sclerosis (MS). We aim to evaluate the longitudinal association of optic radiation (OR) lesion activity with retinal neuroaxonal damage and its role in correlations between retinal and brain atrophy in people with clinically isolated syndrome and early MS (pweMS).
Methods
Eighty‐five pweMS were retrospectively screened from a prospective cohort (Berlin CIS cohort). Participants underwent 3T magnetic resonance imaging (MRI) for OR lesion volume and brain atrophy measurements and optical coherence tomography (OCT) for retinal layer thickness measurements. All pweMS were followed with serial OCT and MRI over a median follow‐up of 2.9 (interquartile range: 2.6–3.4) years. Eyes with a history of optic neuritis prior to study enrollment were excluded. Linear mixed models were used to analyze the association of retinal layer thinning with changes in OR lesion volume and brain atrophy.
Results
Macular ganglion cell‐inner plexiform layer (GCIPL) thinning was more pronounced in pweMS with OR lesion volume increase during follow‐up compared to those without (Difference: −0.82 μm [95% CI:‐1.49 to −0.15], p = 0.018). Furthermore, GCIPL thinning correlated with both OR lesion volume increase (β [95% CI] = −0.27 [−0.50 to −0.03], p = 0.028) and brain atrophy (β [95% CI] = 0.47 [0.25 to 0.70], p |
| doi_str_mv | 10.1002/acn3.51931 |
| format | article |
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Retrograde trans‐synaptic neuroaxonal degeneration is considered a key pathological factor of subclinical retinal neuroaxonal damage in multiple sclerosis (MS). We aim to evaluate the longitudinal association of optic radiation (OR) lesion activity with retinal neuroaxonal damage and its role in correlations between retinal and brain atrophy in people with clinically isolated syndrome and early MS (pweMS).
Methods
Eighty‐five pweMS were retrospectively screened from a prospective cohort (Berlin CIS cohort). Participants underwent 3T magnetic resonance imaging (MRI) for OR lesion volume and brain atrophy measurements and optical coherence tomography (OCT) for retinal layer thickness measurements. All pweMS were followed with serial OCT and MRI over a median follow‐up of 2.9 (interquartile range: 2.6–3.4) years. Eyes with a history of optic neuritis prior to study enrollment were excluded. Linear mixed models were used to analyze the association of retinal layer thinning with changes in OR lesion volume and brain atrophy.
Results
Macular ganglion cell‐inner plexiform layer (GCIPL) thinning was more pronounced in pweMS with OR lesion volume increase during follow‐up compared to those without (Difference: −0.82 μm [95% CI:‐1.49 to −0.15], p = 0.018). Furthermore, GCIPL thinning correlated with both OR lesion volume increase (β [95% CI] = −0.27 [−0.50 to −0.03], p = 0.028) and brain atrophy (β [95% CI] = 0.47 [0.25 to 0.70], p < 0.001). Correlations of GCIPL changes with brain atrophy did not differ between pweMS with or without OR lesion increase (ηp2 = 5.92e−7, p = 0.762).
Interpretation
Faster GCIPL thinning rate is associated with increased OR lesion load. Our results support the value of GCIPL as a sensitive biomarker reflecting both posterior visual pathway pathology and global brain neurodegeneration.</description><identifier>ISSN: 2328-9503</identifier><identifier>EISSN: 2328-9503</identifier><identifier>DOI: 10.1002/acn3.51931</identifier><identifier>PMID: 37903651</identifier><language>eng</language><publisher>United States: John Wiley & Sons, Inc</publisher><subject>Atrophy ; Brain research ; Hypotheses ; Inflammation ; Magnetic resonance imaging ; Multiple sclerosis ; Optic nerve ; Optics ; Pathology ; Radiation ; Tomography</subject><ispartof>Annals of clinical and translational neurology, 2024-01, Vol.11 (1), p.45-56</ispartof><rights>2023 The Authors. published by Wiley Periodicals LLC on behalf of American Neurological Association.</rights><rights>2023 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.</rights><rights>2024. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c5411-185f1c6ac0ab176ed7d59eb9a9d5828f00e9d3c2f46ffb757bd05015c30fcb03</cites><orcidid>0000-0002-0276-8051 ; 0000-0003-4833-5937 ; 0000-0002-6897-5387 ; 0000-0002-9768-014X ; 0000-0002-7981-2073 ; 0000-0003-1962-6014 ; 0000-0002-6378-0070 ; 0000-0001-9605-8095</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2915103717/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2915103717?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,11541,25731,27901,27902,36989,36990,44566,46027,46451,53766,53768,74869</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37903651$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lin, Ting‐Yi</creatorcontrib><creatorcontrib>Chien, Claudia</creatorcontrib><creatorcontrib>Kuchling, Joseph</creatorcontrib><creatorcontrib>Asseyer, Susanna</creatorcontrib><creatorcontrib>Motamedi, Seyedamirhosein</creatorcontrib><creatorcontrib>Bellmann‐Strobl, Judith</creatorcontrib><creatorcontrib>Schmitz‐Hübsch, Tanja</creatorcontrib><creatorcontrib>Ruprecht, Klemens</creatorcontrib><creatorcontrib>Brandt, Alexander U.</creatorcontrib><creatorcontrib>Zimmermann, Hanna G.</creatorcontrib><creatorcontrib>Paul, Friedemann</creatorcontrib><title>Interactions of optic radiation lesions with retinal and brain atrophy in early multiple sclerosis</title><title>Annals of clinical and translational neurology</title><addtitle>Ann Clin Transl Neurol</addtitle><description>Objective
Retrograde trans‐synaptic neuroaxonal degeneration is considered a key pathological factor of subclinical retinal neuroaxonal damage in multiple sclerosis (MS). We aim to evaluate the longitudinal association of optic radiation (OR) lesion activity with retinal neuroaxonal damage and its role in correlations between retinal and brain atrophy in people with clinically isolated syndrome and early MS (pweMS).
Methods
Eighty‐five pweMS were retrospectively screened from a prospective cohort (Berlin CIS cohort). Participants underwent 3T magnetic resonance imaging (MRI) for OR lesion volume and brain atrophy measurements and optical coherence tomography (OCT) for retinal layer thickness measurements. All pweMS were followed with serial OCT and MRI over a median follow‐up of 2.9 (interquartile range: 2.6–3.4) years. Eyes with a history of optic neuritis prior to study enrollment were excluded. Linear mixed models were used to analyze the association of retinal layer thinning with changes in OR lesion volume and brain atrophy.
Results
Macular ganglion cell‐inner plexiform layer (GCIPL) thinning was more pronounced in pweMS with OR lesion volume increase during follow‐up compared to those without (Difference: −0.82 μm [95% CI:‐1.49 to −0.15], p = 0.018). Furthermore, GCIPL thinning correlated with both OR lesion volume increase (β [95% CI] = −0.27 [−0.50 to −0.03], p = 0.028) and brain atrophy (β [95% CI] = 0.47 [0.25 to 0.70], p < 0.001). Correlations of GCIPL changes with brain atrophy did not differ between pweMS with or without OR lesion increase (ηp2 = 5.92e−7, p = 0.762).
Interpretation
Faster GCIPL thinning rate is associated with increased OR lesion load. Our results support the value of GCIPL as a sensitive biomarker reflecting both posterior visual pathway pathology and global brain neurodegeneration.</description><subject>Atrophy</subject><subject>Brain research</subject><subject>Hypotheses</subject><subject>Inflammation</subject><subject>Magnetic resonance imaging</subject><subject>Multiple sclerosis</subject><subject>Optic nerve</subject><subject>Optics</subject><subject>Pathology</subject><subject>Radiation</subject><subject>Tomography</subject><issn>2328-9503</issn><issn>2328-9503</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNp9kktrGzEQgJfS0oQ0l_6AIuilFJxqJGu1OpVg-jCE9pK7mNUjlpFXrrTb4H9f2ZuGpIeeNMx8fMyMpmneAr0CStknNAO_EqA4vGjOGWfdQgnKXz6Jz5rLUraUUgAmuGSvmzMuFeWtgPOmXw-jy2jGkIZCkidpPwZDMtqAxxyJrpxK92HckOzGMGAkOFjSZwwDwTGn_eZAaugwxwPZTXEM--hIMdHlVEJ507zyGIu7fHgvmtuvX25X3xc3P7-tV9c3CyOWAAvohAfToqHYg2ydlVYo1ytUVnSs85Q6Zblhftl630she0sFBWE49aan_KJZz1qbcKv3OewwH3TCoE-JlO805jpbdLpXjlFUiIKbpTfYGQ5oOgCpWs6tqa7Ps2s_9TtnjRvGjPGZ9HllCBt9l35roFIBZaoaPjwYcvo1uTLqXSjGxYiDS1PRrOuWrWyBtRV9_w-6TVOua66UAgGUS5CV-jhTpi61ZOcfuwGqj5egj5egT5dQ4XdP-39E__57BWAG7kN0h_-o9PXqB5-lfwAXMb8k</recordid><startdate>202401</startdate><enddate>202401</enddate><creator>Lin, Ting‐Yi</creator><creator>Chien, Claudia</creator><creator>Kuchling, Joseph</creator><creator>Asseyer, Susanna</creator><creator>Motamedi, Seyedamirhosein</creator><creator>Bellmann‐Strobl, Judith</creator><creator>Schmitz‐Hübsch, Tanja</creator><creator>Ruprecht, Klemens</creator><creator>Brandt, Alexander U.</creator><creator>Zimmermann, Hanna G.</creator><creator>Paul, Friedemann</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><general>Wiley</general><scope>24P</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88G</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>M0S</scope><scope>M2M</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-0276-8051</orcidid><orcidid>https://orcid.org/0000-0003-4833-5937</orcidid><orcidid>https://orcid.org/0000-0002-6897-5387</orcidid><orcidid>https://orcid.org/0000-0002-9768-014X</orcidid><orcidid>https://orcid.org/0000-0002-7981-2073</orcidid><orcidid>https://orcid.org/0000-0003-1962-6014</orcidid><orcidid>https://orcid.org/0000-0002-6378-0070</orcidid><orcidid>https://orcid.org/0000-0001-9605-8095</orcidid></search><sort><creationdate>202401</creationdate><title>Interactions of optic radiation lesions with retinal and brain atrophy in early multiple sclerosis</title><author>Lin, Ting‐Yi ; Chien, Claudia ; Kuchling, Joseph ; Asseyer, Susanna ; Motamedi, Seyedamirhosein ; Bellmann‐Strobl, Judith ; Schmitz‐Hübsch, Tanja ; Ruprecht, Klemens ; Brandt, Alexander U. ; Zimmermann, Hanna G. ; Paul, Friedemann</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5411-185f1c6ac0ab176ed7d59eb9a9d5828f00e9d3c2f46ffb757bd05015c30fcb03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Atrophy</topic><topic>Brain research</topic><topic>Hypotheses</topic><topic>Inflammation</topic><topic>Magnetic resonance imaging</topic><topic>Multiple sclerosis</topic><topic>Optic nerve</topic><topic>Optics</topic><topic>Pathology</topic><topic>Radiation</topic><topic>Tomography</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lin, Ting‐Yi</creatorcontrib><creatorcontrib>Chien, Claudia</creatorcontrib><creatorcontrib>Kuchling, Joseph</creatorcontrib><creatorcontrib>Asseyer, Susanna</creatorcontrib><creatorcontrib>Motamedi, Seyedamirhosein</creatorcontrib><creatorcontrib>Bellmann‐Strobl, Judith</creatorcontrib><creatorcontrib>Schmitz‐Hübsch, Tanja</creatorcontrib><creatorcontrib>Ruprecht, Klemens</creatorcontrib><creatorcontrib>Brandt, Alexander U.</creatorcontrib><creatorcontrib>Zimmermann, Hanna G.</creatorcontrib><creatorcontrib>Paul, Friedemann</creatorcontrib><collection>Wiley-Blackwell Open Access Collection</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Psychology Database (Alumni)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Psychology Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Annals of clinical and translational neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lin, Ting‐Yi</au><au>Chien, Claudia</au><au>Kuchling, Joseph</au><au>Asseyer, Susanna</au><au>Motamedi, Seyedamirhosein</au><au>Bellmann‐Strobl, Judith</au><au>Schmitz‐Hübsch, Tanja</au><au>Ruprecht, Klemens</au><au>Brandt, Alexander U.</au><au>Zimmermann, Hanna G.</au><au>Paul, Friedemann</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interactions of optic radiation lesions with retinal and brain atrophy in early multiple sclerosis</atitle><jtitle>Annals of clinical and translational neurology</jtitle><addtitle>Ann Clin Transl Neurol</addtitle><date>2024-01</date><risdate>2024</risdate><volume>11</volume><issue>1</issue><spage>45</spage><epage>56</epage><pages>45-56</pages><issn>2328-9503</issn><eissn>2328-9503</eissn><abstract>Objective
Retrograde trans‐synaptic neuroaxonal degeneration is considered a key pathological factor of subclinical retinal neuroaxonal damage in multiple sclerosis (MS). We aim to evaluate the longitudinal association of optic radiation (OR) lesion activity with retinal neuroaxonal damage and its role in correlations between retinal and brain atrophy in people with clinically isolated syndrome and early MS (pweMS).
Methods
Eighty‐five pweMS were retrospectively screened from a prospective cohort (Berlin CIS cohort). Participants underwent 3T magnetic resonance imaging (MRI) for OR lesion volume and brain atrophy measurements and optical coherence tomography (OCT) for retinal layer thickness measurements. All pweMS were followed with serial OCT and MRI over a median follow‐up of 2.9 (interquartile range: 2.6–3.4) years. Eyes with a history of optic neuritis prior to study enrollment were excluded. Linear mixed models were used to analyze the association of retinal layer thinning with changes in OR lesion volume and brain atrophy.
Results
Macular ganglion cell‐inner plexiform layer (GCIPL) thinning was more pronounced in pweMS with OR lesion volume increase during follow‐up compared to those without (Difference: −0.82 μm [95% CI:‐1.49 to −0.15], p = 0.018). Furthermore, GCIPL thinning correlated with both OR lesion volume increase (β [95% CI] = −0.27 [−0.50 to −0.03], p = 0.028) and brain atrophy (β [95% CI] = 0.47 [0.25 to 0.70], p < 0.001). Correlations of GCIPL changes with brain atrophy did not differ between pweMS with or without OR lesion increase (ηp2 = 5.92e−7, p = 0.762).
Interpretation
Faster GCIPL thinning rate is associated with increased OR lesion load. Our results support the value of GCIPL as a sensitive biomarker reflecting both posterior visual pathway pathology and global brain neurodegeneration.</abstract><cop>United States</cop><pub>John Wiley & Sons, Inc</pub><pmid>37903651</pmid><doi>10.1002/acn3.51931</doi><tpages>56</tpages><orcidid>https://orcid.org/0000-0002-0276-8051</orcidid><orcidid>https://orcid.org/0000-0003-4833-5937</orcidid><orcidid>https://orcid.org/0000-0002-6897-5387</orcidid><orcidid>https://orcid.org/0000-0002-9768-014X</orcidid><orcidid>https://orcid.org/0000-0002-7981-2073</orcidid><orcidid>https://orcid.org/0000-0003-1962-6014</orcidid><orcidid>https://orcid.org/0000-0002-6378-0070</orcidid><orcidid>https://orcid.org/0000-0001-9605-8095</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Annals of clinical and translational neurology, 2024-01, Vol.11 (1), p.45-56 |
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| source | Wiley-Blackwell Open Access Collection; Publicly Available Content Database; PubMed Central |
| subjects | Atrophy Brain research Hypotheses Inflammation Magnetic resonance imaging Multiple sclerosis Optic nerve Optics Pathology Radiation Tomography |
| title | Interactions of optic radiation lesions with retinal and brain atrophy in early multiple sclerosis |
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