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.

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.

Study design: Assessment of spasticity before and after hippotherapy treatment. Objective: To evaluate the short-term effect of hippotherapy on spasticity of spinal cord injured patients (SCIs). Setting: Swiss Paraplegic Centre, Nottwil. Methods: 32 patients with spinal cord injury with various degrees of spasticity had repeated sessions (mean 11) of Hippotherapy-K s . Spasticity of the lower extremities was scored according to the Ashworth Scale. Results: In primary rehabilitation patients Ashworth values after hippotherapy were significantly lower than before (Wilcoxon's signed-rank test: Po0.001). Highest improvements were observed in SCIs with very high spasticity. No significant difference between short-term effect in paraplegic and short-term effect in tetraplegic subjects was found. Conclusions: Hippotherapy significantly reduces spasticity of lower extremities in SCIs.

Study design: A series of 94 urinary bladder biopsies in spinal cord injured (SCI) patients were histopathologically and statistically analysed. Objectives: The following hypotheses were examined: (1) The number of clinical bladder infections per year in each patient does not in¯uence the histopathological type of in¯ammation of the urinary bladder; (2) The duration of the spinal cord lesion does not have a strong eect on the type of in¯ammation; (3) The dierent neurological levels (upper and lower motor neuron lesions) do not relate to a speci®c histopathology. Settings: All patients received their treatment at the Swiss Paraplegic Centre in Nottwil, near Lucerne (Switzerland). Methods: The samples were taken from the bladder fundus during endoscopic urologic operations. Histopathological standard procedures were carried out. Statistical analysis including Kruskal ± Wallis and Chi-square tests were performed. Results: Histopathological analysis showed abnormal alterations of the urinary bladder mucosa in 86 SCI-patients: (91.5%). 63 cases (67.0%) showed a chronic type and 23 cases (24.5%) showed a subacute type of in¯ammation. A normal urinary bladder was found in eight cases (8.5%). The three hypotheses were statistically not rejected. Conclusion: Results demonstrated no correlation between the number of bladder infections per year, the period since injury, the neurologic level of the spinal cord lesion and the histopathology of the urinary bladder mucosa.

Our findings indicate that for a reliable and comparable measurement of spasticity, an exact description of test position and procedure is essential.