Abstract

Spinal cord injury (SCI) leads to severe chronic disability, but also to secondary adaptive changes upstream to the injury in the brain which are most likely induced due to the lack of afferent information. These neuroplastic changes are a potential target for innovative therapies such as neuroprostheses, e.g., by stimulation in order to evoke sensation or in order to suppress phantom limb pain. Diverging results on gray matter atrophy have been reported in patients with SCI. Detectability of atrophy seems to depend on the selection of the regions of interest, while whole-brain approaches are not sensitive enough. In this study, we discussed previous research approaches and analyzed differential atrophic changes in incomplete SCI using manual segmentation of the somatosensory cortex. Patients with incomplete SCI (ASIA C-D), with cervical (N = 5) and thoracic (N = 6) injury were included. Time since injury was ≤12 months in 7 patients, and 144, 152, 216, and 312 months in the other patients. Age at the injury was ≤26 years in 4 patients and ≥50 years in 7 patients. A sample of 12 healthy controls was included in the study. In contrast to all previous studies that used voxel-based morphometry, we performed manual segmentation of the somatosensory cortex in the postcentral gyrus from structural magnetic resonance images and normalized the calculated volumes against the sum of volumes of an automated whole-head segmentation. Volumes were smaller in patients than in controls (p = 0.011), and as a tendency, female patients had smaller volumes than male patients (p = 0.017, uncorrected). No effects of duration (subacute vs. chronic), level of lesion (cervical vs. thoracic), region (left vs. right S1), and age at onset (≤26 vs. ≥50 years) was found. Our results demonstrate volume loss of S1 in incomplete SCI and encourage further research with larger sample sizes on volumetric changes in the acute and chronic stage of SCI, in order to document the moderating effect of type and location of injury on neuroplastic changes. A better understanding of neuroplastic changes in the sensorimotor cortex after SCI and its interaction with sex is needed in order to develop efficient rehabilitative interventions and neuroprosthetic technologies.

Highlights

  • Spinal cord injury (SCI) induces a loss of both motor and sensory function below the level of injury [1]

  • We found a lower volume of S1 in patients with incomplete SCI compared to controls, and a lower volume of the somatosensory cortex in females than in males, and an interaction between the factors age, level of injury, and region, as well as duration, level of injury, and region

  • It was repeatedly claimed that SCI leads to atrophy of the sensorimotor cortex

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Summary

Introduction

Spinal cord injury (SCI) induces a loss of both motor and sensory function below the level of injury [1]. This leads to a degenerative development along the descending and ascending pathways transferring information between the spinal cord and the brain [2,3,4,5,6,7]. Spinal cord atrophy is the result of a combination of pathophysiological processes, including loss of neurons as well as axonal demyelination, degeneration, and dieback [8]. Several studies reported atrophy of the cortex and the spinal cord in patients with SCI, to a loss of axonal integrity [1,2,3, 5, 6, 8, 10,11,12,13,14,15,16,17,18]

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