BACKGROUND: Secondary progressive multiple sclerosis (SPMS) is characterized by worsening of postural control and brain atrophy. However, little is known about postural deficits and their neuroanatomical correlates in this population. We aimed to determine the neuroanatomical correlates of postural deficits in people with SPMS and whether posture control deteriorates concomitantly with the brain and spinal cord atrophy in 2 years in SPMS. METHODS: This study is a post hoc analysis of data from 27 people with SPMS (mean ± SE age, 58.6 ± 1.1 years). Participants had magnetic resonance imaging (MRI) of the brain and cervical spinal cord followed by sway testing using inertial sensors during standing with eyes open (EO) and eyes closed without (EC) and with (ECC) a cognitive task. Partial correlations investigated relationships between postural control and MRI measures at baseline and 2 years. RESULTS: At baseline, sway measures were inversely related to cortical thickness and cord cross-sectional area (CSA) during the EO task but only to cord CSA with EC (P < .05). After 2 years, the percentage change in sway amplitude and dispersion during EO tasks significantly related to the percentage decline in cord CSA (P < .01). CONCLUSIONS: Cortical and spinal cord inputs are essential for regulation of postural control during standing with EO in SPMS. Without visual input, people with SPMS preferentially rely on somatosensory inputs from the spinal cord for maintaining postural control. Postural deficits related to cord atrophy over 2 years, suggesting that postural control may be a surrogate marker of disease progression in people with SPMS.
BACKGROUND: Secondary progressive multiple sclerosis (SPMS) is characterized by worsening of postural control and brain atrophy. However, little is known about postural deficits and their neuroanatomical correlates in this population. We aimed to determine the neuroanatomical correlates of postural deficits in people with SPMS and whether posture control deteriorates concomitantly with the brain and spinal cord atrophy in 2 years in SPMS. METHODS: This study is a post hoc analysis of data from 27 people with SPMS (mean ± SE age, 58.6 ± 1.1 years). Participants had magnetic resonance imaging (MRI) of the brain and cervical spinal cord followed by sway testing using inertial sensors during standing with eyes open (EO) and eyes closed without (EC) and with (ECC) a cognitive task. Partial correlations investigated relationships between postural control and MRI measures at baseline and 2 years. RESULTS: At baseline, sway measures were inversely related to cortical thickness and cord cross-sectional area (CSA) during the EO task but only to cord CSA with EC (P < .05). After 2 years, the percentage change in sway amplitude and dispersion during EO tasks significantly related to the percentage decline in cord CSA (P < .01). CONCLUSIONS: Cortical and spinal cord inputs are essential for regulation of postural control during standing with EO in SPMS. Without visual input, people with SPMS preferentially rely on somatosensory inputs from the spinal cord for maintaining postural control. Postural deficits related to cord atrophy over 2 years, suggesting that postural control may be a surrogate marker of disease progression in people with SPMS.
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