Alterations of resting-state regional and network-level neural function after acute spinal cord injury.

OBJECT: The purpose of this study was to investigate functional alterations of the brain in the early stage of spinal cord injury (SCI) and further investigate how these functional alterations relate to SCI patients' sensorimotor functions. METHODS: Twenty-five patients with SCI and 25 matched healthy controls underwent imaging by using resting-state functional magnetic resonance imaging (fMRI). The amplitude of low-frequency fluctuations (ALFF) were used to characterize regional neural function, and the seed-based functional connectivity (FC) was used to evaluate the functional integration of the brain network. RESULTS: Compared to healthy controls, patients with SCI showed decreased ALFF in the bilateral primary sensorimotor cortex, and increased ALFF in the bilateral cerebellum and right orbitofrontal cortex (OFC). The ALFF value in the left cerebellum was negatively correlated with the clinical total motor score in patients with SCI. Furthermore, SCI patients mainly showed decreased inter-hemispheric FC between the bilateral primary sensorimotor cortex, as well as increased intra-hemispheric FC within the motor network, including the primary sensorimotor cortex, premotor cortex, supplementary motor area (SMA), thalamus and cerebellum. Subsequent correlation analyses revealed that increased FC within the primary sensorimotor cortex, SMA, and cerebellum negatively correlated with the total American Spinal Cord Injury Association (ASIA) motor score. CONCLUSIONS: Our findings provide evidence that SCI can induce significant regional and network-level functional alterations in the early stage of the disease. We hypothesized these alterations may be an adaptive phenomenon following SCI, reflecting a compensatory mechanism during the early stage of SCI.

Brain sensorimotor system atrophy during the early stage of spinal cord injury in humans.

Spinal cord injury (SCI) usually leads to severe sensory and motor deficits below the spinal lesion. Previous animal models have shown significant atrophic changes in the neural sensorimotor system following SCI. However, specific anatomical changes in the human brain following SCI remain poorly understood. The purpose of the present study was to investigate structural changes during the early stage of SCI, and to investigate further the association between the structural changes and patients' sensorimotor functions. The study participants included 20 patients with SCI and 30 matched healthy controls. The mean period post-SCI was 8.9±2.7weeks (range 4-12weeks). Voxel-based morphometry was used to investigate the regions with gray and white matter volume changes. Compared to healthy controls, patients with SCI showed significant gray matter atrophy in the primary motor cortex (M1), primary somatosensory cortex (S1), supplementary motor area (SMA), and thalamus, as well as white matter atrophy in the corticospinal tracts at the level of the bilateral cerebral peduncles. In addition, gray matter volume in the primary motor cortex was positively correlated with the total American Spinal Injury Association motor score in patients with SCI. In conclusion, our findings suggest that SCI causes significant anatomical changes in the human sensorimotor system, and that these anatomical changes may occur in the early phase of SCI. Future treatments that aim to restore sensorimotor functions following SCI need to attend to these anatomical changes in the brain.