Emanuele Pravatà1, Paola Valsasina2, Claudio Gobbi3, Chiara Zecca3, Gianna C Riccitelli4, Massimo Filippi5, Maria A Rocca6. 1. Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy/Department of Neuroradiology, Neurocenter of Southern Switzerland, Civic Hospital, Lugano, Switzerland. 2. Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy. 3. Department of Neurology, Neurocenter of Southern Switzerland, Civic Hospital, Lugano, Switzerland. 4. Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy/Department of Neurology, Neurocenter of Southern Switzerland, Civic Hospital, Lugano, Switzerland. 5. Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy/Neurology Unit, IRCCS San Raffaele Scientific Institute, Milan, Italy/Vita-Salute San Raffaele University, Milan, Italy. 6. Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, IRCCS San Raffaele Scientific Institute, Milan, Italy/Department of Neurology, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Abstract
BACKGROUND: Mechanisms associated with cervical spinal cord (CSC) and upper thoracic spinal cord (TSC) atrophy in multiple sclerosis (MS) are poorly understood. OBJECTIVE: To assess the influence of brain, CSC and TSC T2-hyperintense lesions on cord atrophy and disability in MS. METHODS: Thirty-four MS patients underwent 3T brain, cervical and thoracic cord magnetic resonance imaging (MRI) and Expanded Disability Status Scale (EDSS) score assessment. CSC/TSC lesion number and volume (LV), whole-brain and cortico-spinal tract (CST) LVs were obtained. Normalized whole CSC and upper TSC cross-sectional areas (CSAn) were also derived. Age- and sex-adjusted regression models assessed associations of brain/cord lesions with CSAn and EDSS and identified variables independently associated with CSAn and EDSS with a stepwise variable selection. RESULTS: CSC CSAn (β = -0.36, p = 0.03) and TSC CSAn (β = -0.60, p < 0.001) were associated with CSC T2 LV. EDSS (median = 3.0) was correlated with CSC T2 LV (β = 0.42, p = 0.01), brain (β = 0.34, p = 0.04) and CST LV (β = 0.35, p = 0.03). The multivariate analysis retained CSC LV as significant predictor of CSC CSAn (R2 = 0.20, p = 0.023) and TSC CSAn (R2 = 0.51, p < 0.001) and retained CSC and CST LVs as significant predictors of EDSS (R2 = 0.55, p = 0.001). CONCLUSIONS: CSC LV is an independent predictor of cord atrophy. When neurological impairment is relatively mild, central nervous system (CNS) lesion burden is a better correlate of disability than atrophy.
BACKGROUND: Mechanisms associated with cervical spinal cord (CSC) and upper thoracic spinal cord (TSC) atrophy in multiple sclerosis (MS) are poorly understood. OBJECTIVE: To assess the influence of brain, CSC and TSC T2-hyperintense lesions on cord atrophy and disability in MS. METHODS: Thirty-four MS patients underwent 3T brain, cervical and thoracic cord magnetic resonance imaging (MRI) and Expanded Disability Status Scale (EDSS) score assessment. CSC/TSC lesion number and volume (LV), whole-brain and cortico-spinal tract (CST) LVs were obtained. Normalized whole CSC and upper TSC cross-sectional areas (CSAn) were also derived. Age- and sex-adjusted regression models assessed associations of brain/cord lesions with CSAn and EDSS and identified variables independently associated with CSAn and EDSS with a stepwise variable selection. RESULTS: CSC CSAn (β = -0.36, p = 0.03) and TSC CSAn (β = -0.60, p < 0.001) were associated with CSC T2 LV. EDSS (median = 3.0) was correlated with CSC T2 LV (β = 0.42, p = 0.01), brain (β = 0.34, p = 0.04) and CST LV (β = 0.35, p = 0.03). The multivariate analysis retained CSC LV as significant predictor of CSC CSAn (R2 = 0.20, p = 0.023) and TSC CSAn (R2 = 0.51, p < 0.001) and retained CSC and CST LVs as significant predictors of EDSS (R2 = 0.55, p = 0.001). CONCLUSIONS: CSC LV is an independent predictor of cord atrophy. When neurological impairment is relatively mild, central nervous system (CNS) lesion burden is a better correlate of disability than atrophy.
Authors: Jyothsna Chitturi; Basavaraju G Sanganahalli; Peter Herman; Fahmeed Hyder; Li Ni; Stella Elkabes; Robert Heary; Sridhar S Kannurpatti Journal: Brain Connect Date: 2020-10-29
Authors: Matthias Bussas; Malek El Husseini; Laura Harabacz; Viktor Pineker; Sophia Grahl; Viola Pongratz; Achim Berthele; Isabelle Riederer; Claus Zimmer; Bernhard Hemmer; Jan S Kirschke; Mark Mühlau Journal: Neuroimage Clin Date: 2022-04-13 Impact factor: 4.891