๐”– Bobbio Scriptorium
โœฆ   LIBER   โœฆ

Osteoporosis after spinal cord injury

โœ Scribed by Dr. Douglas E. Garland; Charles A. Stewart; Rodney H. Adkins; Serena S. Hu; Charles Rosen; Ferdinand J. Liotta; David A. Weinstein


Publisher
Elsevier Science
Year
1992
Tongue
English
Weight
735 KB
Volume
10
Category
Article
ISSN
0736-0266

No coin nor oath required. For personal study only.

โœฆ Synopsis


Abstract

Dualโ€photon absorptiometry characterized bone loss in males aged <40 years after complete traumatic paraplegic and quadriplegic spinal cord injury. Total bone mass of various regions and bone mineral density (BMD) of the knee were measured in 55 subjects. Three different populations were partitioned into four groups: 10 controls (healthy, age matched); 25 acutely injured (114 days after injury), with 12 reexamined 16 months after injury; and 20 chronic (>5 years after injury). Significant differences (p < 0.0001) in bone mass mineral between groups at the arms, pelvis, legs, distal femur, and proximal tibia were found, with no differences for the head or trunk. Post hoc analyses indicated no differences between the acutely injured at 16 months and the chronically injured. Paraplegic and quadriplegic subjects were significantly different only at the arms and trunk, but were highly similar at the pelvis and below. In the acutely injured, a slight but statistically insignificant rebound was noted above the pelvis. Regression techniques demonstrated early, rapid, linear (p < 0.0001) decline of bone below the pelvis. Bone mineral loss occurs throughout the entire skeleton, except the skull. Most bone loss occurs rapidly and below the pelvis. Homeostasis is reached by 16 months at two thirds of original bone mass, near fracture threshold.


๐Ÿ“œ SIMILAR VOLUMES


Muscle after spinal cord injury
โœ Bo Biering-Sรธrensen; Ida Bruun Kristensen; Michael Kjรฆr; Fin Biering-Sรธrensen ๐Ÿ“‚ Article ๐Ÿ“… 2009 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 227 KB
Changes in afferent activity after spina
โœ William C. de Groat; Naoki Yoshimura ๐Ÿ“‚ Article ๐Ÿ“… 2010 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 551 KB

## Abstract ## Aims To summarize the changes that occur in the properties of bladder afferent neurons following spinal cord injury. ## Methods Literature review of anatomical, immunohistochemical, and pharmacologic studies of normal and dysfunctional bladder afferent pathways. ## Results Studi

Blood-spinal cord barrier after spinal c
โœ William D. Whetstone; Jung-Yu C. Hsu; Manuel Eisenberg; Zena Werb; Linda J. Nobl ๐Ÿ“‚ Article ๐Ÿ“… 2003 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 773 KB

## Abstract Spinal cord injury produces prominent disruption of the bloodโ€spinal cord barrier. We have defined the bloodโ€spinal cord barrier breakdown to the protein luciferase (61 kDa) in the acutely injured murine spinal cord and during revascularization. We show that newly formed and regeneratin

Increase of oligodendrocyte progenitor c
โœ Ken Ishii; Masahiro Toda; Yoko Nakai; Hiroaki Asou; Masahiko Watanabe; Masaya Na ๐Ÿ“‚ Article ๐Ÿ“… 2001 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 1019 KB

## Abstract The reaction of oligodendrocyte progenitor cells (OPCs) after spinal cord injury (SCI) is poorly understood. In this study, we examined oligodendroglial reactions after contusion SCI in adult rats by immunohistochemistry. OPCs were identified by staining with monoclonal antibodies (mAbs

Neurobiology of spinal cord injury
โœ Gihan Tennekoon ๐Ÿ“‚ Article ๐Ÿ“… 2001 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 97 KB ๐Ÿ‘ 2 views
Neurotrophic factors expressed in both c
โœ Lijun Zhou; H. David Shine ๐Ÿ“‚ Article ๐Ÿ“… 2003 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 265 KB

## Abstract We reported recently that overexpression of neurotrophinโ€3 (NTโ€3) by motoneurons in the spinal cord of rats will induce sprouting of corticospinal tract (CST) axons (Zhou et al. [2003] J. Neurosci. 23:1424โ€“1431). We now report that overexpression of brainโ€derived neurotrophic factor (BD