Osteoporosis after spinal cord injury

Dual‐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.

[1]  S. N. Eichenholtz Management of Long-Bone Fractures in Paraplegic Patients , 1963 .

[2]  R. H. Hutchinson,et al.  Extremity fractures of patients with spinal cord injuries. , 1962, American journal of surgery.

[3]  K.,et al.  Differential changes in bone mineral density of the appendicular and axial skeleton with aging: relationship to spinal osteoporosis. , 1981, The Journal of clinical investigation.

[4]  R. Zimmerman,et al.  Investigation of the loss of bone mineral in patients with spinal cord injury , 1976, Paraplegia.

[5]  L. Halstead,et al.  Metabolic and endocrine changes in spinal cord injury: IV. Compounded neurologic dysfunctions. , 1982, Archives of physical medicine and rehabilitation.

[6]  P. Rambaut,et al.  SKELETAL CHANGES DURING SPACE FLIGHT , 1985, The Lancet.

[7]  F. Plum,et al.  The effect of therapeutic mobilization on hypercalciuria following acute poliomyelitis. , 1958, A.M.A. archives of internal medicine.

[8]  R. Wright,et al.  DIAGNOSIS OF ALPHA1-ANTITRYPSIN DEFICIENCY , 1975, The Lancet.

[9]  P. Meunier,et al.  Effects of disodium dichloromethylene diphosphonate on bone loss in paraplegic patients. , 1981, The Journal of clinical investigation.

[10]  A. Chantraine Actual concept of osteoporosis in paraplegia , 1978, Paraplegia.

[11]  W. A. Spencer,et al.  Hypercalcemia in early traumatic quadriplegia. , 1975, Journal of chronic diseases.

[12]  A. Chantraine Clinical investigation of bone metabolism in spinal cord lesions , 1971, Paraplegia.

[13]  A. F. Stewart,et al.  Calcium homeostasis in immobilization: an example of resorptive hypercalciuria. , 1982, The New England journal of medicine.

[14]  G. D. Whedon,et al.  Effects of immobilization upon various metabolic and physiologic functions of normal men. , 1948, The American journal of medicine.

[15]  R. Heaney,et al.  Radiocalcium metabolism in disuse osteoporosis in man. , 1962, The American journal of medicine.

[16]  K. Klose,et al.  Bone mineral density after bicycle ergometry training. , 1990, Archives of physical medicine and rehabilitation.

[17]  C. J. Pattee,et al.  Effect of the oscillating bed and tilt table on calcium, phosphorus and nitrogen metabolism in paraplegia. , 1954, The American journal of medicine.

[18]  A. Ohry,et al.  Zinc and osteoporosis in patients with spinal cord injury , 1980, Paraplegia.

[19]  L. Halstead,et al.  Metabolic and endocrine changes in spinal cord injury: II (section 1). Consequences of partial decentralization of the autonomic nervous system. , 1982, Archives of physical medicine and rehabilitation.

[20]  J. Ditunno,et al.  Immobilization hypercalcemia in acute spinal cord injury treated with etidronate. , 1984, Archives of internal medicine.

[21]  B. J. Winer Statistical Principles in Experimental Design , 1992 .

[22]  F. Biering-Sørensen,et al.  Bone mineral content of the lumbar spine and lower extremities years after spinal cord lesion , 1988, Paraplegia.

[23]  P. Saville,et al.  Etidronate disodium in postmenopausal osteoporosis , 1976, Clinical pharmacology and therapeutics.

[24]  A. Schoutens,et al.  Longitudinal study of calcium and bone metabolism in paraplegic patients , 1977, Paraplegia.

[25]  P. Kaplan,et al.  Calcium balance in paraplegic patients: influence of injury duration and ambulation. , 1978, Archives of physical medicine and rehabilitation.

[26]  E. Lowman,et al.  Mineral metabolism in spinal cord injury. , 1980, Archives of physical medicine and rehabilitation.

[27]  R. Keagy,et al.  Congenital absence of lumbar articular facets. A report of three cases. , 1967, The Journal of bone and joint surgery. American volume.

[28]  J. Claus-Walker,et al.  Collagen metabolite excretion as a predictor of bone- and skin-related complications in spinal cord injury. , 1989, Archives of physical medicine and rehabilitation.

[29]  A. Abramson Bone disturbances in injuries to the spinal cord and cauda equina (paraplegia) their prevention by ambulation. , 1948, The Journal of bone and joint surgery. American volume.

[30]  E R Morey,et al.  Inhibition of bone formation during space flight. , 1978, Science.

[31]  O. Cope,et al.  Acute Atrophy of Bone (Osteoporosis) Simulating Hyperparathyroidism12 , 1941 .

[32]  Sell Gh,et al.  Lower extremity fractures after spinal cord injury: a retrospective study. , 1981 .