To study the time course of demineralization and fracture incidence after spinal cord injury (SCI), 100 paraplegic men with complete motor loss were investigated in a cross-sectional study 3 months to 30 years after their traumatic SCI. Fracture history was assessed and verified using patients' files and X-rays. BMD of the lumbar spine (LS), femoral neck (FN), distal forearm (ultradistal part = UDR, 1/3 distal part = 1/3R), distal tibial diaphysis (TDIA), and distal tibial epiphysis (TEPI) was measured using DXA. Stiffness of the calcaneus (QUI.CALC), speed of sound of the tibia (SOS.TIB), and amplitude-dependent SOS across the proximal phalanges (adSOS.PHAL) were measured using QUS. Z-Scores of BMD and quantitative ultrasound (QUS) were plotted against time-since-injury and compared among four groups of paraplegics stratified according to time-since-injury (<1 year, stratum I; 1-9 years, stratum II; 10-19 years, stratum III; 20-29 years, stratum IV). Biochemical markers of bone turnover (deoxypyridinoline/creatinine (D-pyr/Cr), osteocalcin, alkaline phosphatase) and the main parameters of calcium phosphate metabolism were measured. Fifteen out of 98 paraplegics had sustained a total of 39 fragility fractures within 1,010 years of observation. All recorded fractures were fractures of the lower limbs, mean time to first fracture being 8.9 ± 1.4 years. Fracture incidence increased with time-after-SCI, from 1% in the first 12 months to 4.6%/year in paraplegics since >20 years (p<.01). The overall fracture incidence was 2.2%/year. Compared with nonfractured paraplegics, those with a fracture history had been injured for a longer time (p<.01). Furthermore, they had lower Z-scores at FN, TEPI, and TDIA (p<.01 to <.0001), the largest difference being observed at TDIA, compared with the nonfractured. At the lower limbs, BMD decreased with time at all sites (r=.49 to .78, all p<.0001). At FN and TEPI, bone loss followed a log curve which leveled off between 1 to 3 years after injury. In contrast, Z-scores of TDIA continuously decreased even beyond 10 years after injury. LS BMD Z-score increased with time-since-SCI (p<.05). Similarly to DXA, QUS allowed differentiation of early and rapid trabecular bone loss (QUI.CALC) vs slow and continuous cortical bone loss (SOS.TIB). Biochemical markers reflected a disproportion between highly elevated bone resorption and almost normal bone formation early after injury. Turnover declined following a log curve with time-after-SCI, however, D-pyr/Cr remained elevated in 30% of paraplegics injured >10 years. In paraplegic men early (trabecular) and persistent (cortical) bone loss occurs at the lower limbs and leads to an increasing fracture incidence with time-after-SCI.

In humans, the relationships of blood flow changes to structure, function, and shear rate of conducting arteries have not been thoroughly examined. Therefore, the purpose of this study was to investigate these parameters of the elastic-type, common carotid artery (CCA) and the muscular-type, common femoral artery (CFA) in long-term highly active and extremely inactive individuals, assuming that the impact of activity-induced blood flow changes on conduit arteries, if any, should be seen in these subjects. We examined 21 highly endurance-trained athletes (A), 10 paraplegic subjects (P), and 20 sedentary subjects (S) by means of noninvasive ultrasound. As a result, the CFA diameter and compliance were highest in A (9.7+/-0.81 mm; 1.84 +/-0.54 mm(2)/kPa) and lowest in P (5.9+/-0.7 mm; 0.54+/-0.27 mm(2)/kPa) compared with S (8.3+/-1.0 mm; 0.92+/-0.48 mm(2)/kPa) with P <0.01 among the groups. Both parameters correlated with each other (r = 0.62; P<0.01). Compared with A (378+/-84 s(-1); 37+/-15 s(-1)) and S (356+/-113 s(-1); 36+/-20 s(-1)), the peak and mean shear rates of the CFA were almost or more than doubled in P (588+/-120 s(-1); 89+/-26 s(-1)). In the CCA, only the compliance and peak shear rate showed significant differences among the groups (A: 1.28+/-0.47 mm(2)/kPa, 660+/-138 s(-1); S: 1.04+/-0.27 mm(2)/kPa, 588+/-109 s(-1); P: 0.65+/- 0.22 mm(2)/kPa, 490+/-149 s(-1); P<0.05). In conclusion, the results suggest a structural and functional adaptation in the CFA and a predominantly functional adaptation of the arterial wall properties to differences in the physical activity level and associated exercise-induced blood flow changes in the CCA. The results for humans confirm those from animal experiments. Similar shear rate values of S and P in the CFA support the hypothesis of constant shear stress regulation due to local blood flow changes in humans. On the other hand, the increased shear rate in the CFA in P indicates an at least partially nonphysiological response of the arterial wall in long-term chronic sympathectomy due to a change in local blood flow.

A new system of operative fixation of thoracolumbar and lumbar spine fractures is presented: the 'fixateur interne' (F.I.). From a posterior approach long Schanz screws are inserted through the pedicles into the body of the two vertebrae just adjacent to the lesion and connected by th threaded F.I. rods. By tightening the nuts the Schanz screws are fixed in all directions. The advantages of the F.I. system are: excellent reposition by the long lever-arm of the Schanz screws, immobilization of only two segments and therefore good mobility of the residual spine, stability against flexion forces better than is obtained with Harrington distraction rods, additional rotational stability, and fixation in lordosis or kyphosis as is desired. The F.I. does not act as a four point bending system like all other dorsal spine instrumentation systems, but provides stability in flexion by itself. Therefore it can be Used independently of the condition of all ligaments (including the anterior longitudinal ligament) and of the posterior wall of the fractured vertebrae, and there is no need to fix more than the two immediately adjacent vertebrae, thus avoiding the often painful and cumbersome iatrogenic loss of lumbar lordosis and of mobility and permitting early mobilization of the patient. Experience with the first 45 patients is very promising.

To assess the effects of long-term treatment of bone loss with alendronate in a group of paraplegic men, 55 patients were evaluated in a prospective randomized controlled open label study that was 2 years in duration comparing alendronate and calcium with calcium alone. Bone loss was stopped at all cortical and trabecular infralesional sites (distal tibial epiphysis, tibial diaphysis, total hip) with alendronate 10 mg daily. Introduction: Bone loss after spinal cord injury (SCI) leads to increased fracture risk in the lower limbs of paraplegics. The aim of this study was to document long-term treatment of bone loss with alendronate in a group of paraplegic men with complete motor lesion after SCI. Materials and Methods: Sixty-five men with complete motor post-traumatic medullary lesion between T 1 and L 3 with total motor and sensory loss (Frankel classification, stage A) or with total motor and partial sensory loss (Frankel classification, stage B) after SCI were included in this prospective randomized controlled open label study that was 2 years in duration. The patients were randomized to either the treatment group with alendronate 10 mg daily and elemental calcium 500 mg daily or to the control group with elemental calcium 500 mg daily alone. The primary endpoint was defined as the effect over 24 months of alendronate and calcium compared with calcium alone on the BMD values at the distal tibial epiphysis (as a surrogate for trabecular bone in the paralyzed zone). The secondary endpoints were changes in BMD at supra-and infralesional sites of measurement. Biochemical markers of bone turnover were assessed. Results: Fifty-five subjects, 0.1-29.5 years post-SCI, completed the study over 24 months. BMD at the distal tibial epiphysis significantly decreased from baseline in the calcium group (Ϫ10.8 Ϯ 2.7% at 24 months, p Ͻ 0.001), whereas it remained stable in the alendronate plus calcium group (Ϫ2.0 Ϯ 2.9% at 24 months, p ϭ not significant versus baseline), leading to a significant intergroup difference over time (p ϭ 0.017). At the tibial diaphysis, similar significant results were observed. At the ultradistal radius and the radial shaft, BMD did not change significantly from baseline in either treatment group. At the total hip, BMD decreased significantly in the calcium group (Ϫ4.1 Ϯ 1.6%, p ϭ 0.038) but remained stable in the alendronate plus calcium group (ϩ0.43 Ϯ 1.2%), with a significant intergroup difference (p ϭ 0.037). At the lumbar spine, BMD increased significantly (p Ͻ 0.0001) from baseline in both groups. Biochemical markers of bone resorption were significantly decreased with alendronate versus baseline and control. Alendronate and calcium were generally safe and well tolerated. Conclusions: In paraplegic men, SCI bone loss was stopped at all measured cortical and trabecular infralesional sites over 24 months with alendronate 10 mg daily.

Incidence of SAS is high in tetraplegia, particularly in older male patients with large neck circumference, long standing spinal cord injury and under cardiac medication. As tetraplegics with RDI between 15 and 40 reported no daytime complaints and often have normal BMI, these tetraplegics are not clinically suspicious for SAS. The increased use of cardiac medication in tetraplegics with SAS may implicate a link between SAS and cardiovascular morbidity, one of the leading causes of death in tetraplegia.