RESUMO
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.
RESUMO
BACKGROUND/AIMS: To determine the effect of arterial blood pressure (BP) reduction on endocan and soluble cell adhesion molecules' (sCAM) plasma concentration and expression of their ligands on circulatory leukocyte subpopulations. METHODS: 24 hypertensive subjects of both sexes (age: 53±8 yrs) were treated with Ca-channel blocker, amlodipin (5-10 mg/day for 8 weeks; to reach BP≤139/89mmHg). The serum sCAMs and endocan concentrations were determined by ELISA kits. Level of ICAM/VCAM ligands on leukocytes was assessed by flow cytometry. Paired t-test, or t-test were used as appropriate, with Pearson's correlation calculated; p<0.05 was considered significant (SigmaPlot v.11). RESULTS: sICAM-1 and sVCAM-1 were decreased (p≤0.001 and p=0.002, respectively), while E-selectin concentration was increased after amlodipin treatment (P=0.014). CD11a/LFA-1 (ICAM-1 and endocan ligand) was significantly increased in all three cell types with BP decrease. CD15 and CD49d/VLA-4 (VCAM-1 ligand) did not change after the treatment. There was significant positive correlation of systolic and diastolic BP with ICAM-1 and VCAM-1, and significant negative correlation of systolic BP with CD11a/LFA-1. Endocan significantly positively correlated with ICAM-1. CONCLUSIONS: The increased expression of ICAM/VACM ligands, together with decrease of sCAMs and endocan suggests the de-activation of endothelium with reduction in BP, decreasing the adherence of circulatory leukocytes to endothelium; subsequently decreasing the risk for development of atherosclerosis.