TY - JOUR
T1 - Upright activity and higher motor function may preserve bone mineral density within 6 months of stroke: a longitudinal study
AU - Borschmann, Karen
AU - Iuliano, Sandra
AU - Ghasem-Zadeh, Ali
AU - Churilov, Leonid
AU - Pang, Marco Yiu Chung
AU - Bernhardt, Julie
PY - 2018/12/1
Y1 - 2018/12/1
N2 - Purpose: Bone fragility contributes to increased fracture risk, but little is known about the emergence of post-stroke bone loss. We investigated skeletal changes and relationships with physical activity, stroke severity, motor control and lean mass within 6 months of stroke. Methods: This is a prospective observational study. Participants were non-diabetic but unable to walk within 2 weeks of first stroke. Distal tibial volumetric bone mineral density (vBMD, primary outcome), bone geometry and microstructure (high-resolution peripheral quantitative computed tomography) were assessed at baseline and 6 months, as were secondary outcomes total body bone mineral content and lean mass (dual energy X-ray absorptiometry), bone metabolism (serum osteocalcin, N-terminal propeptide of type 1 procollagen (P1NP), C-terminal telopeptide of type 1 collagen (CTX)), physical activity (PAL2 accelerometer) and motor control (Chedoke McMaster) which were also measured at 1 and 3 months. Results: Thirty-seven participants (69.7 years (SD 11.6), 37.8% females, NIHSS 12.6 (SD 4.7)) were included. The magnitude of difference in vBMD between paretic and non-paretic legs increased within 6 months, with a greater reduction observed in paretic legs (mean difference = 1.5% (95% CI 0.5, 2.6), p = 0.007). At 6 months, better motor control was associated with less bone loss since stroke (r = 0.46, p = 0.02). A trend towards less bone loss was observed in people who regained independent walking compared to those who did not (p = 0.053). Higher baseline daily count of standing up was associated with less change in bone turnover over 6 months: osteocalcin (r = −0.51, p = 0.01), P1NP (r = −0.47, p = 0.01), CTX (r = −0.53, p = 0.01). Conclusion: Better motor control and walking recovery were associated with reduced bone loss. Interventions targeting these impairments from early post-stroke are warranted. Clinical trial registration: URL: http://www.anzctr.org.au. Unique identifier: ACTRN12612000123842.
AB - Purpose: Bone fragility contributes to increased fracture risk, but little is known about the emergence of post-stroke bone loss. We investigated skeletal changes and relationships with physical activity, stroke severity, motor control and lean mass within 6 months of stroke. Methods: This is a prospective observational study. Participants were non-diabetic but unable to walk within 2 weeks of first stroke. Distal tibial volumetric bone mineral density (vBMD, primary outcome), bone geometry and microstructure (high-resolution peripheral quantitative computed tomography) were assessed at baseline and 6 months, as were secondary outcomes total body bone mineral content and lean mass (dual energy X-ray absorptiometry), bone metabolism (serum osteocalcin, N-terminal propeptide of type 1 procollagen (P1NP), C-terminal telopeptide of type 1 collagen (CTX)), physical activity (PAL2 accelerometer) and motor control (Chedoke McMaster) which were also measured at 1 and 3 months. Results: Thirty-seven participants (69.7 years (SD 11.6), 37.8% females, NIHSS 12.6 (SD 4.7)) were included. The magnitude of difference in vBMD between paretic and non-paretic legs increased within 6 months, with a greater reduction observed in paretic legs (mean difference = 1.5% (95% CI 0.5, 2.6), p = 0.007). At 6 months, better motor control was associated with less bone loss since stroke (r = 0.46, p = 0.02). A trend towards less bone loss was observed in people who regained independent walking compared to those who did not (p = 0.053). Higher baseline daily count of standing up was associated with less change in bone turnover over 6 months: osteocalcin (r = −0.51, p = 0.01), P1NP (r = −0.47, p = 0.01), CTX (r = −0.53, p = 0.01). Conclusion: Better motor control and walking recovery were associated with reduced bone loss. Interventions targeting these impairments from early post-stroke are warranted. Clinical trial registration: URL: http://www.anzctr.org.au. Unique identifier: ACTRN12612000123842.
KW - Bone loss
KW - Bone mineral density
KW - HR-pQCT
KW - Microstructure
KW - Physical activity
KW - Stroke
UR - http://www.scopus.com/inward/record.url?scp=85040222471&partnerID=8YFLogxK
U2 - 10.1007/s11657-017-0414-4
DO - 10.1007/s11657-017-0414-4
M3 - Journal article
SN - 1862-3522
VL - 13
JO - Archives of Osteoporosis
JF - Archives of Osteoporosis
IS - 1
M1 - 5
ER -