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Spinal Cord Atrophy Predicts Progressive Disease in Relapsing Multiple Sclerosis.
Bischof, Antje; Papinutto, Nico; Keshavan, Anisha; Rajesh, Anand; Kirkish, Gina; Zhang, Xinheng; Mallott, Jacob M; Asteggiano, Carlo; Sacco, Simone; Gundel, Tristan J; Zhao, Chao; Stern, William A; Caverzasi, Eduardo; Zhou, Yifan; Gomez, Refujia; Ragan, Nicholas R; Santaniello, Adam; Zhu, Alyssa H; Juwono, Jeremy; Bevan, Carolyn J; Bove, Riley M; Crabtree, Elizabeth; Gelfand, Jeffrey M; Goodin, Douglas S; Graves, Jennifer S; Green, Ari J; Oksenberg, Jorge R; Waubant, Emmanuelle; Wilson, Michael R; Zamvil, Scott S; Cree, Bruce A C; Hauser, Stephen L; Henry, Roland G.
Afiliação
  • Bischof A; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Papinutto N; Department of Neurology with Institute for Translational Neurology, University Hospital Münster, Albert-Schweitzer-Campus 1, Münster, Germany.
  • Keshavan A; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Rajesh A; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Kirkish G; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Zhang X; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Mallott JM; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Asteggiano C; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Sacco S; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Gundel TJ; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Zhao C; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Stern WA; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Caverzasi E; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Zhou Y; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Gomez R; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Ragan NR; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Santaniello A; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Zhu AH; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Juwono J; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Bevan CJ; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Bove RM; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Crabtree E; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Gelfand JM; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Goodin DS; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Graves JS; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Green AJ; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Oksenberg JR; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Waubant E; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Wilson MR; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Zamvil SS; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Cree BAC; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Hauser SL; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
  • Henry RG; Weill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA.
Ann Neurol ; 91(2): 268-281, 2022 02.
Article em En | MEDLINE | ID: mdl-34878197
ABSTRACT

OBJECTIVE:

A major challenge in multiple sclerosis (MS) research is the understanding of silent progression and Progressive MS. Using a novel method to accurately capture upper cervical cord area from legacy brain MRI scans we aimed to study the role of spinal cord and brain atrophy for silent progression and conversion to secondary progressive disease (SPMS).

METHODS:

From a single-center observational study, all RRMS (n = 360) and SPMS (n = 47) patients and 80 matched controls were evaluated. RRMS patient subsets who converted to SPMS (n = 54) or silently progressed (n = 159), respectively, during the 12-year observation period were compared to clinically matched RRMS patients remaining RRMS (n = 54) or stable (n = 147), respectively. From brain MRI, we assessed the value of brain and spinal cord measures to predict silent progression and SPMS conversion.

RESULTS:

Patients who developed SPMS showed faster cord atrophy rates (-2.19%/yr) at least 4 years before conversion compared to their RRMS matches (-0.88%/yr, p < 0.001). Spinal cord atrophy rates decelerated after conversion (-1.63%/yr, p = 0.010) towards those of SPMS patients from study entry (-1.04%). Each 1% faster spinal cord atrophy rate was associated with 69% (p < 0.0001) and 53% (p < 0.0001) shorter time to silent progression and SPMS conversion, respectively.

INTERPRETATION:

Silent progression and conversion to secondary progressive disease are predominantly related to cervical cord atrophy. This atrophy is often present from the earliest disease stages and predicts the speed of silent progression and conversion to Progressive MS. Diagnosis of SPMS is rather a late recognition of this neurodegenerative process than a distinct disease phase. ANN NEUROL 2022;91268-281.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Medula Espinal / Esclerose Múltipla Recidivante-Remitente Tipo de estudo: Observational_studies / Prognostic_studies / Risk_factors_studies Limite: Adult / Female / Humans / Male / Middle aged Idioma: En Revista: Ann Neurol Ano de publicação: 2022 Tipo de documento: Article País de afiliação: Canadá
Texto completo
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Medula Espinal / Esclerose Múltipla Recidivante-Remitente Tipo de estudo: Observational_studies / Prognostic_studies / Risk_factors_studies Limite: Adult / Female / Humans / Male / Middle aged Idioma: En Revista: Ann Neurol Ano de publicação: 2022 Tipo de documento: Article País de afiliação: Canadá