Chronic demyelination exacerbates neuroaxonal loss in patients with MS with unilateral optic neuritis
To examine the effect of chronic demyelination in the optic nerve of patients with MS on progressive loss of retinal ganglion cell (RGC) axons. Progressive retinal nerve fiber layer (RNFL) loss, as measured by optical coherence tomography, was longitudinally examined in 51 patients with MS with a hi...
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| Vydané v: | Neurology : neuroimmunology & neuroinflammation Ročník 7; číslo 3; s. e700 |
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| Hlavní autori: | , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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United States
American Academy of Neurology
01.05.2020
Lippincott Williams & Wilkins |
| ISSN: | 2332-7812, 2332-7812 |
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| Abstract | To examine the effect of chronic demyelination in the optic nerve of patients with MS on progressive loss of retinal ganglion cell (RGC) axons.
Progressive retinal nerve fiber layer (RNFL) loss, as measured by optical coherence tomography, was longitudinally examined in 51 patients with MS with a history of unilateral optic neuritis (ON) and 25 normal controls. Patients were examined annually with a median of 4-year follow-up. Pairwise intereye comparison was performed between ON and fellow non-ON (NON) eyes of patients with MS using the linear mixed-effects model and survival analysis. The latency asymmetry of multifocal visual evoked potential (mfVEP) was used to determine the level of demyelination in the optic nerve.
Although both ON and NON eyes demonstrate significantly faster loss of RGC axons compared with normal subjects, ON eyes with severe chronic demyelination show accelerated thinning in the RNFL in the temporal sector of the optic disc (temporal RNFL [tRNFL]) compared with fellow eyes (evidenced by both the linear mixed-effects model and survival analysis). Furthermore, progressive tRNFL thinning is associated with the degree of optic nerve demyelination and reflects the topography of pathology in the optic nerve. More rapid axonal loss in ON eyes is also functionally evidenced by mfVEP amplitude reduction, which correlates with the level of optic nerve demyelination.
Although the effect of demyelination on axonal survival has been demonstrated in experimental studies, our results provide first clinically meaningful evidence that chronic demyelination is associated with progressive axonal loss in human MS. |
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| AbstractList | To examine the effect of chronic demyelination in the optic nerve of patients with MS on progressive loss of retinal ganglion cell (RGC) axons.
Progressive retinal nerve fiber layer (RNFL) loss, as measured by optical coherence tomography, was longitudinally examined in 51 patients with MS with a history of unilateral optic neuritis (ON) and 25 normal controls. Patients were examined annually with a median of 4-year follow-up. Pairwise intereye comparison was performed between ON and fellow non-ON (NON) eyes of patients with MS using the linear mixed-effects model and survival analysis. The latency asymmetry of multifocal visual evoked potential (mfVEP) was used to determine the level of demyelination in the optic nerve.
Although both ON and NON eyes demonstrate significantly faster loss of RGC axons compared with normal subjects, ON eyes with severe chronic demyelination show accelerated thinning in the RNFL in the temporal sector of the optic disc (temporal RNFL [tRNFL]) compared with fellow eyes (evidenced by both the linear mixed-effects model and survival analysis). Furthermore, progressive tRNFL thinning is associated with the degree of optic nerve demyelination and reflects the topography of pathology in the optic nerve. More rapid axonal loss in ON eyes is also functionally evidenced by mfVEP amplitude reduction, which correlates with the level of optic nerve demyelination.
Although the effect of demyelination on axonal survival has been demonstrated in experimental studies, our results provide first clinically meaningful evidence that chronic demyelination is associated with progressive axonal loss in human MS. To examine the effect of chronic demyelination in the optic nerve of patients with MS on progressive loss of retinal ganglion cell (RGC) axons.OBJECTIVETo examine the effect of chronic demyelination in the optic nerve of patients with MS on progressive loss of retinal ganglion cell (RGC) axons.Progressive retinal nerve fiber layer (RNFL) loss, as measured by optical coherence tomography, was longitudinally examined in 51 patients with MS with a history of unilateral optic neuritis (ON) and 25 normal controls. Patients were examined annually with a median of 4-year follow-up. Pairwise intereye comparison was performed between ON and fellow non-ON (NON) eyes of patients with MS using the linear mixed-effects model and survival analysis. The latency asymmetry of multifocal visual evoked potential (mfVEP) was used to determine the level of demyelination in the optic nerve.METHODSProgressive retinal nerve fiber layer (RNFL) loss, as measured by optical coherence tomography, was longitudinally examined in 51 patients with MS with a history of unilateral optic neuritis (ON) and 25 normal controls. Patients were examined annually with a median of 4-year follow-up. Pairwise intereye comparison was performed between ON and fellow non-ON (NON) eyes of patients with MS using the linear mixed-effects model and survival analysis. The latency asymmetry of multifocal visual evoked potential (mfVEP) was used to determine the level of demyelination in the optic nerve.Although both ON and NON eyes demonstrate significantly faster loss of RGC axons compared with normal subjects, ON eyes with severe chronic demyelination show accelerated thinning in the RNFL in the temporal sector of the optic disc (temporal RNFL [tRNFL]) compared with fellow eyes (evidenced by both the linear mixed-effects model and survival analysis). Furthermore, progressive tRNFL thinning is associated with the degree of optic nerve demyelination and reflects the topography of pathology in the optic nerve. More rapid axonal loss in ON eyes is also functionally evidenced by mfVEP amplitude reduction, which correlates with the level of optic nerve demyelination.RESULTSAlthough both ON and NON eyes demonstrate significantly faster loss of RGC axons compared with normal subjects, ON eyes with severe chronic demyelination show accelerated thinning in the RNFL in the temporal sector of the optic disc (temporal RNFL [tRNFL]) compared with fellow eyes (evidenced by both the linear mixed-effects model and survival analysis). Furthermore, progressive tRNFL thinning is associated with the degree of optic nerve demyelination and reflects the topography of pathology in the optic nerve. More rapid axonal loss in ON eyes is also functionally evidenced by mfVEP amplitude reduction, which correlates with the level of optic nerve demyelination.Although the effect of demyelination on axonal survival has been demonstrated in experimental studies, our results provide first clinically meaningful evidence that chronic demyelination is associated with progressive axonal loss in human MS.CONCLUSIONSAlthough the effect of demyelination on axonal survival has been demonstrated in experimental studies, our results provide first clinically meaningful evidence that chronic demyelination is associated with progressive axonal loss in human MS. |
| Author | Barnett, Michael H. Graham, Stuart L. You, Yuyi Yiannikas, Con Klistorner, Alexander Parratt, John Matthews, Jim |
| AuthorAffiliation | From the Save Sight Institute (Y.Y., A.K.), The University of Sydney; Faculty of Medicine and Health Sciences (Y.Y., S.L.G., A.K.), Macquarie University; Brain and Mind Centre (M.H.B.), The University of Sydney; Sydney Neuroimaging Analysis Centre (M.H.B., A.K.); Department of Neurology (C.Y., J.P.), Royal North Shore Hospital; and Sydney Informatics and Data Science Hub (J.M.), The University of Sydney, NSW, Australia |
| AuthorAffiliation_xml | – name: From the Save Sight Institute (Y.Y., A.K.), The University of Sydney; Faculty of Medicine and Health Sciences (Y.Y., S.L.G., A.K.), Macquarie University; Brain and Mind Centre (M.H.B.), The University of Sydney; Sydney Neuroimaging Analysis Centre (M.H.B., A.K.); Department of Neurology (C.Y., J.P.), Royal North Shore Hospital; and Sydney Informatics and Data Science Hub (J.M.), The University of Sydney, NSW, Australia |
| Author_xml | – sequence: 1 givenname: Yuyi surname: You fullname: You, Yuyi organization: From the Save Sight Institute (Y.Y., A.K.), The University of Sydney; Faculty of Medicine and Health Sciences (Y.Y., S.L.G., A.K.), Macquarie University; Brain and Mind Centre (M.H.B.), The University of Sydney; Sydney Neuroimaging Analysis Centre (M.H.B., A.K.); Department of Neurology (C.Y., J.P.), Royal North Shore Hospital; and Sydney Informatics and Data Science Hub (J.M.), The University of Sydney, NSW, Australia – sequence: 2 givenname: Michael surname: Barnett middlename: H. fullname: Barnett, Michael H. – sequence: 3 givenname: Con surname: Yiannikas fullname: Yiannikas, Con – sequence: 4 givenname: John surname: Parratt fullname: Parratt, John – sequence: 5 givenname: Jim surname: Matthews fullname: Matthews, Jim – sequence: 6 givenname: Stuart surname: Graham middlename: L. fullname: Graham, Stuart L. – sequence: 7 givenname: Alexander surname: Klistorner fullname: Klistorner, Alexander |
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