Neurogenic heterotopic ossi®cation (NHO) is a frequent complication in spinal cord injury (SCI) that is often di cult to treat. This review emphasizes the incidence, risk factors and clinical signs of NHO in SCI patients. Although the exact pathophysiology underlying NHO in neurologic patients is not yet understood, di erent pathogenic mechanisms have been proposed in the literature. A selection of the most important theories will be given and discussed. Moreover the di erent diagnostic, therapeutic, and preventive methods currently used in NHO management after SCI will be reviewed.
Flow-mediated dilatation (FMD) of the brachial and radial arteries is an important research tool for assessment of endothelial function in vivo, and is nitric oxide (NO) dependent. The leg skeletal muscle vascular bed is an important territory for studies in exercise physiology. However, the role of endothelial NO in the FMD response of lower limb arteries has never been investigated. The purpose of this study was to examine the contribution of NO to FMD in the superficial femoral artery in healthy subjects. Since physical inactivity may affect endothelial function, and therefore NO availability, spinal cord-injured (SCI) individuals were included as a model of extreme deconditioning. In eight healthy men (34 ± 13 years) and six SCI individuals (37 ± 10 years), the 5 min FMD response in the superficial femoral artery was assessed by echo-Doppler, both during infusion of saline and during infusion of the NO synthase blocker N G -monomethyl-L-arginine (L-NMMA). In a subset of the controls (n = 6), the 10 min FMD response was also examined using the same procedure. The 5 min FMD response in controls (4.2 ± 0.3%) was significantly diminished during L-NMMA infusion (1.0 ± 0.2%, P < 0.001). In SCI, L-NMMA also significantly decreased the FMD response (from 8.2 ± 0.4% during saline to 2.4 ± 0.5% during L-NMMA infusion). The hyperaemic flow response during the first 45 s after cuff deflation was lower in both groups during infusion of L-NMMA, but the effect of L-NMMA on FMD persisted in both groups after correction for the shear stress stimulus. The 10 min FMD was not affected by L-NMMA (saline: 5.4 ± 1.6%, L-NMMA: 5.6 ± 1.5%). Superficial femoral artery FMD in response to distal arterial occlusion for a period of 5 min is predominantly mediated by NO in healthy men and in the extremely deconditioned legs of SCI individuals.
The purpose of the present study was to determine the effect of a 4-week training program on a newly developed hybrid functional electrical stimulation (FES)-cycle on physical fitness in spinal cord-injured (SCI) individuals. Ten SCI individuals (age 23-53 years, lesion level range T3-T11) participated and trained 8-12 times in 4 weeks on the hybrid FES-cycle (voluntary arm-contractions and stimulation of leg muscles). Leg volume was measured. During a graded hybrid exercise test, peak oxygen consumption (VO2peak), peak power output (POpeak) and power of the legs (dP) were measured pre and post training. Upper leg volume increased significantly (8.5% (p = 0.047) and 8.3% (p = 0.018) for the right and left leg, respectively). POpeak and VO2peak increased 11.7% (p = 0.012) and 9.3% (p = 0.015), respectively. There was no significant difference in dP between pre and post training. After only 4 weeks of training, considerable training effects were observed, which are comparable to longer training studies in literature. The results of this study indicate that hybrid training on the new hybrid FES-cycle is an appropriate training method for individuals with a spinal cord injury to increase physical fitness.
The impact of health problems after SCI is considerable and hardly diminishes over time. These results emphasize the need for structured long-term care for people with SCI.
Effective alpha-adrenergic blockade did not reduce HUT-induced vasoconstriction, regardless of intact baroreflex control of the leg vasculature. Apparently, redundant mechanisms compensate for the absence of sympathetic alpha-adrenoceptor leg vasoconstriction in response to postural stress.
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