Association of asymptomatic spinal cord lesions and atrophy with disability 5 years after a clinically isolated syndrome

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  • WJ Brownlee
    Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Institute of Neurology, London, UK
  • DR Altmann
    Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Institute of Neurology, London, UK/Department of Medical Statistics, London School of Hygiene & Tropical Medicine, London, UK
  • P Alves Da Mota
    Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Institute of Neurology, London, UK
  • JK Swanton
    Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Institute of Neurology, London, UK
  • KA Miszkiel
    Lysholm Department of Neuroradiology, National Hospital for Neurology and Neurosurgery, London, UK
  • CAM Gandini Wheeler-Kingshott
    Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Institute of Neurology, London, UK/Brain Connectivity Center, C. Mondino National Neurological Institute, Pavia, Italy
  • O Ciccarelli
    Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Institute of Neurology, London, UK/Biomedical Research Centre, NIHR University College London Hospitals, London, UK
  • DH Miller
    Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Institute of Neurology, London, UK/Biomedical Research Centre, NIHR University College London Hospitals, London, UK

Abstract

<jats:sec><jats:title>Background:</jats:title><jats:p> Spinal cord pathology is an important substrate for long-term disability in multiple sclerosis (MS). </jats:p></jats:sec><jats:sec><jats:title>Objective:</jats:title><jats:p> To investigate longitudinal changes in spinal cord lesions and atrophy in patients with a non-spinal clinically isolated syndrome (CIS), and how they relate to the development of disability. </jats:p></jats:sec><jats:sec><jats:title>Methods:</jats:title><jats:p> In all, 131 patients with a non-spinal CIS had brain and spinal cord imaging at the time of CIS and approximately 5 years later (median: 5.2 years, range: 3.0–7.9 years). Brain magnetic resonance imaging (MRI) measures consisted of T2-hyperintense and T1-hypointense lesion loads plus brain atrophy. Spinal cord MRI measures consisted of lesion number and the upper cervical cord cross-sectional area (UCCA). Disability was measured using the Expanded Disability Status Scale (EDSS). Multiple linear regression was used to identify independent predictors of disability after 5 years. </jats:p></jats:sec><jats:sec><jats:title>Results:</jats:title><jats:p> During follow-up, 93 (71%) patients were diagnosed with MS. Baseline spinal cord lesion number, change in cord lesion number and change in UCCA were independently associated with EDSS ( R<jats:sup>2</jats:sup> = 0.53) at follow-up. Including brain T2 lesion load and brain atrophy only modestly increased the predictive power of the model ( R<jats:sup>2</jats:sup> = 0.64). </jats:p></jats:sec><jats:sec><jats:title>Conclusion:</jats:title><jats:p> Asymptomatic spinal cord lesions and spinal cord atrophy contribute to the development of MS-related disability over the first 5 years after a non-spinal CIS. </jats:p></jats:sec>

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