Progressive Hemiosteoporosis on the Paretic Side and Increased Bone Mineral Density in the Nonparetic Arm the First Year after Severe Stroke

Fractures are a common and serious complication after stroke and the risk of hip fractures among stroke patients is 2 to 4 times greater than among other elderly people. The aim of this study was to investigate prospectively the change in bone mineral density (BMD) after severe stroke and to study the association between motor impairment, disability and the development of hemiosteoporosis. The study comprised 24 stroke patients, with no persistent paresis from previous strokes or previous osteoporotic fractures, included 1 month after stroke onset. BMD, motor function, ambulation and activities of daily living (ADL) were assessed at 1, 4, 7 and 12 months after stroke onset. At inclusion, the patients’ BMD was normal for their age. During the study, there was a significant loss of BMD in the total body (−2.0%; p<0.05), but not in the head or spine. BMD differed significantly between the paretic and the non-paretic arm at inclusion (−4.8%; p<0.001). Decrease in BMD was most pronounced in the affected humerus (−17.4%; p<0.001) and proximal femur (−12.2%; p<0.01). BMD decreased significantly in both lower extremities during follow-up, but the losses were more pronounced on the paretic side (p<0.01). In the nonaffected ultradistal radius there was a significant increase in BMD from inclusion to the end of the study (+5.8%; p<0.01). There was no pattern in the bone losses correlating with presumptive risk factors for hemiosteoporosis such as motor function, ability to perform ADL or ambulation. Two patients had fractures at follow-up, both on the paretic side. Loss of bone mineral density in the paretic extremities is thus pronounced and progressive during the first year after stroke, indicating that loss of BMD is probably an important risk factor for post-stroke fractures. Surprisingly, BMD in the nonaffected arm increased significantly during the first year after stroke, most likely due to increased physical activity, and perhaps a redistribution of bone minerals from the paretic extremities. Received: 13 January 1998 / Accepted: 24 July 1998