Gray Matter Atrophy to Explain Subclinical Oculomotor Deficit in Multiple Sclerosis
Eye movement deficits are frequently noted in multiple sclerosis during bedside clinical examination, but subtle dysfunction may remain undetected and might only be identified with advanced approaches. While classical neurology provides insight into the complex functional anatomy of oculomotor funct...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2019-06-01
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| Series: | Frontiers in Neurology |
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| Online Access: | https://www.frontiersin.org/article/10.3389/fneur.2019.00589/full |
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| author | Bálint Kincses Benjámin J. Hérák Nikoletta Szabó Bence Bozsik Péter Faragó András Király Dániel Veréb Eszter Tóth Krisztián Kocsis Krisztina Bencsik László Vécsei László Vécsei Zsigmond Tamás Kincses Zsigmond Tamás Kincses |
| author_facet | Bálint Kincses Benjámin J. Hérák Nikoletta Szabó Bence Bozsik Péter Faragó András Király Dániel Veréb Eszter Tóth Krisztián Kocsis Krisztina Bencsik László Vécsei László Vécsei Zsigmond Tamás Kincses Zsigmond Tamás Kincses |
| author_sort | Bálint Kincses |
| collection | DOAJ |
| description | Eye movement deficits are frequently noted in multiple sclerosis during bedside clinical examination, but subtle dysfunction may remain undetected and might only be identified with advanced approaches. While classical neurology provides insight into the complex functional anatomy of oculomotor functions, little is known about the structural background of this dysfunction in MS. Thirty four clinically stable, treated relapsing-remitting MS patients with mild disability and 34 healthy controls were included in our study. Group difference and correlation with clinical parameters were analyzed in case of the latency, peak-velocity, gain, dysconjugacy index, and performance during a saccade and anti-saccade task. High-resolution T1 weighted, T2 FLAIR, and double inversion recovery images were acquired on 3T to evaluate the correlation between behavioral and MRI parameters, such as T2 lesion and T1 black-hole burden, global brain, gray, and white matter atrophy. VBM style analysis was used to identify the focal gray matter atrophy responsible for oculomotor dysfunction. Significantly increased latency in the prosaccade task and significantly worse performance in the anti-saccade task were found in MS patients. The detailed examination of conjugated eye movements revealed five subclinical internuclear ophthalmoparesis cases. The peak velocity and latency of the anti-saccade movement correlated with the number of black holes, but none of the eye movement parameters were associated with the T2 lesion burden or location. Global gray matter volume correlated with saccade and anti-saccade latency, whereas white matter and total brain volume did not. Local gray matter atrophy in the left inferio-parietal lobule and temporo-occipital junction correlated with anti-saccade peak velocity. Our results show that neurodegeneration-like features of the MRI (black-hole, gray matter atrophy) are the best predictors of eye movement deficit in MS. Concurring with the clinico-radiological paradox, T2 lesion burden cannot explain the behavioral results. Importantly, anti-saccade peak velocity correlates with gray matter atrophy in the left parietal regions, which are frequently implicated in attention tasks. |
| first_indexed | 2024-12-14T09:59:14Z |
| format | Article |
| id | doaj.art-0c625db296c84f23b6e6d4f97e20ba9e |
| institution | Directory Open Access Journal |
| issn | 1664-2295 |
| language | English |
| last_indexed | 2024-12-14T09:59:14Z |
| publishDate | 2019-06-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Neurology |
| spelling | doaj.art-0c625db296c84f23b6e6d4f97e20ba9e2022-12-21T23:07:19ZengFrontiers Media S.A.Frontiers in Neurology1664-22952019-06-011010.3389/fneur.2019.00589444948Gray Matter Atrophy to Explain Subclinical Oculomotor Deficit in Multiple SclerosisBálint Kincses0Benjámin J. Hérák1Nikoletta Szabó2Bence Bozsik3Péter Faragó4András Király5Dániel Veréb6Eszter Tóth7Krisztián Kocsis8Krisztina Bencsik9László Vécsei10László Vécsei11Zsigmond Tamás Kincses12Zsigmond Tamás Kincses13Department of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, HungaryDepartment of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, HungaryDepartment of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, HungaryDepartment of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, HungaryDepartment of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, HungaryDepartment of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, HungaryDepartment of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, HungaryDepartment of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, HungaryDepartment of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, HungaryDepartment of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, HungaryDepartment of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, HungaryMTA-SZTE Neuroscience Research Group, Szeged, HungaryDepartment of Neurology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, HungaryDepartment of Radiology, Albert Szent-Györgyi Clinical Center, University of Szeged, Szeged, HungaryEye movement deficits are frequently noted in multiple sclerosis during bedside clinical examination, but subtle dysfunction may remain undetected and might only be identified with advanced approaches. While classical neurology provides insight into the complex functional anatomy of oculomotor functions, little is known about the structural background of this dysfunction in MS. Thirty four clinically stable, treated relapsing-remitting MS patients with mild disability and 34 healthy controls were included in our study. Group difference and correlation with clinical parameters were analyzed in case of the latency, peak-velocity, gain, dysconjugacy index, and performance during a saccade and anti-saccade task. High-resolution T1 weighted, T2 FLAIR, and double inversion recovery images were acquired on 3T to evaluate the correlation between behavioral and MRI parameters, such as T2 lesion and T1 black-hole burden, global brain, gray, and white matter atrophy. VBM style analysis was used to identify the focal gray matter atrophy responsible for oculomotor dysfunction. Significantly increased latency in the prosaccade task and significantly worse performance in the anti-saccade task were found in MS patients. The detailed examination of conjugated eye movements revealed five subclinical internuclear ophthalmoparesis cases. The peak velocity and latency of the anti-saccade movement correlated with the number of black holes, but none of the eye movement parameters were associated with the T2 lesion burden or location. Global gray matter volume correlated with saccade and anti-saccade latency, whereas white matter and total brain volume did not. Local gray matter atrophy in the left inferio-parietal lobule and temporo-occipital junction correlated with anti-saccade peak velocity. Our results show that neurodegeneration-like features of the MRI (black-hole, gray matter atrophy) are the best predictors of eye movement deficit in MS. Concurring with the clinico-radiological paradox, T2 lesion burden cannot explain the behavioral results. Importantly, anti-saccade peak velocity correlates with gray matter atrophy in the left parietal regions, which are frequently implicated in attention tasks.https://www.frontiersin.org/article/10.3389/fneur.2019.00589/fullmultiple sclerosisprosaccadeanti-saccadeatrophyblack hole |
| spellingShingle | Bálint Kincses Benjámin J. Hérák Nikoletta Szabó Bence Bozsik Péter Faragó András Király Dániel Veréb Eszter Tóth Krisztián Kocsis Krisztina Bencsik László Vécsei László Vécsei Zsigmond Tamás Kincses Zsigmond Tamás Kincses Gray Matter Atrophy to Explain Subclinical Oculomotor Deficit in Multiple Sclerosis Frontiers in Neurology multiple sclerosis prosaccade anti-saccade atrophy black hole |
| title | Gray Matter Atrophy to Explain Subclinical Oculomotor Deficit in Multiple Sclerosis |
| title_full | Gray Matter Atrophy to Explain Subclinical Oculomotor Deficit in Multiple Sclerosis |
| title_fullStr | Gray Matter Atrophy to Explain Subclinical Oculomotor Deficit in Multiple Sclerosis |
| title_full_unstemmed | Gray Matter Atrophy to Explain Subclinical Oculomotor Deficit in Multiple Sclerosis |
| title_short | Gray Matter Atrophy to Explain Subclinical Oculomotor Deficit in Multiple Sclerosis |
| title_sort | gray matter atrophy to explain subclinical oculomotor deficit in multiple sclerosis |
| topic | multiple sclerosis prosaccade anti-saccade atrophy black hole |
| url | https://www.frontiersin.org/article/10.3389/fneur.2019.00589/full |
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