Abstract
Next to gray and white matter atrophy, cerebrospinal fluid (CSF) volume and ventricular dilation may be surrogate biomarkers for brain atrophy in spinal cord injury (SCI). We therefore aimed to track brain atrophy by means of CSF volume changes and ventricular enlargements over two years after SCI. Fifteen patients with SCI and 18 healthy controls underwent a series of T1-weighted scans during five time points over two years. Changes of CSF/intracranial volume (CSF/ICV) ratio, CSF volume, and ventricular enlargement rate over time were determined. Sample sizes with 80% power and 5% significance were calculated to detect a range of treatment effects for a two-armed trial. There was a significant cross-sectional increased CSF/ICV ratio in patients compared with controls at each time point (p < 0.02). The rate of CSF/ICV changes, however, was not significantly different between groups over time. CSF volume increased linearly over bilateral sensorimotor cortices (left: p = 0.002, right: p = 0.042) and in the supracerebellar space (p < 0.001) within two years. An acceleration of the enlargement within the third (p = 0.017) and the fourth (p = 0.006) ventricles was observed in patients over time. Sample size estimation for six-month trials with CSF volume requires 25 patients per treatment arm to detect a hypothetical treatment effect in terms of slowing of atrophy rate of 30%. This study shows that SCI-induced changes in CSF/ICV ratio and ventricular expansion rate provide additional information on the neurodegenerative processes after injury. The sensitivity to scoring treatment effects speaks to its potential to serve as a sensitive biomarker in addition to local atrophy measures.
Highlights
Traumatic spinal cord injury (SCI) leads in most patients to profound neurological dysfunction and paralysis below the level of lesion[1] as information flow between supraspinal and spinal neuronal networks is impaired.[2]
The aim of this study was to investigate the trajectory of progressive global brain atrophy (i.e., cerebrospinal fluid (CSF)/intracranial volume (ICV) ratios, volumetric CSF changes) and local brain atrophy over two years in the same SCI patient cohort that previously showed enduring neurodegenerative changes in the cortical gray matter (GM) and white matter (WM) after SCI.[7]
At baseline, CSF/intracranial volume (CSF/ICV) ratio was significantly increased in patients compared with controls
Summary
Traumatic spinal cord injury (SCI) leads in most patients to profound neurological dysfunction and paralysis below the level of lesion[1] as information flow between supraspinal and spinal neuronal networks is impaired.[2] Functional recovery after human SCI is restricted but can be fostered by intensive neurorehabilitation. The neuronal mechanisms underlying neurological and functional recovery, are still not well understood because of the complex relationship between neurodegeneration and plasticity. A follow-up study in the same patient cohort revealed that these changes continued for at least two years post-SCI.[7] Crucially, the magnitude of neurodegeneration at the level of the spinal cord, brainstem, and cortex over the first six months predicted clinical outcome at two years, independent of early clinical changes.[7]
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