(Stroke. 1999;30:1974-1981.)
© 1999 American Heart Association, Inc.
Letters to the Editor |
Hemiosteoporosis Following Stroke: Importance of Pathophysiologic Understanding and Histologic Evidence
Department of Neurology, Kurume University Medical Center, Kurume, Japan
First Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan
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To the Editor:
We read with interest the article by Ramnemark et al1 reporting that patients developed hemiosteoporosis during the first year after severe stroke. These authors concluded that hemiosteoporosis occurred independently of any weight change after stroke. Other reports have indicated that bone mass or bone mineral density (BMD) is reduced in stroke patients on the hemiplegic side, reflecting both degree of paralysis and vitamin D deficiency.2 3 4 In these investigations, bone changes were determined by bone mass or BMD with x-ray radiodensitometry2 3 or dual-energy x-ray absorptiometry,4 without histologic assessment. However, the diagnosis of osteoporosis requires histological demonstration that both bone matrix and bone mineral area are lost. Ramnemark's report1 does not mention quantitative assessment of bone biopsy specimens. To our knowledge, histologically proved osteoporosis in patients after stroke has not been reported, although a well-established relationship exists between prolonged immobilization and osteoporosis in spinal cord injury.5
Our previous findings3 have shown lower serum 25-hydroxyvitamin (25-OHD) concentrations in patients following stroke (9.1±4.9 ng/mL for 42 outpatients, 5.9±4.1 ng/mL for 45 inpatients) than in control subjects (21.6±3.1 ng/mL), which correlates well with decreased bone mass as measured by radiodensity. Among the patients, 7 of the outpatients (17%) and 21 of the inpatients (47%) had 25-OHD concentrations below 5 ng/mL, which are considered osteomalacic levels. These deficiencies were caused by malnutrition and sunlight deprivation. In vitamin D deficiency, bone mineralization is impaired, which leads to accumulation of unmineralized matrix or osteoid in the skeleton. Reduction in bone formation occurs with prolonged immobilization from spinal cord injury, as evidenced by diminished osteoid thickness and mineralization rates observed in biopsy specimens.6 Accordingly, a combination of disuse and hypovitaminosis D may act on bone on the paretic sides of immobilized stroke patients.
As stated by Ramnemark et al,1 hip fractures are a serious complication after stroke; between 4% and 15% of hip fractures occur as a late complication of cerebrovascular disease.7 8 The article postulated that hip fractures after stroke reflect both a high incidence of accidental falls and progressive hemiosteoporosis on the paretic side. However, osteoporosis on the paretic side must be distinguished from bone loss on that side caused by a combination of disuse and hypovitaminosis D, because clear identification of the process has important therapeutic implications for the prevention of hip fractures. If only disuse osteoporosis is acting on the paretic side, agents that inhibit bone resorption, such as bisphosphonate9 or calcitonin,10 are needed to prevent further bone loss.11 On the other hand, if the bone changes on the paretic side are caused by disuse and by hypovitaminosis D, vitamin D supplementation is needed to prevent hip fractures. A recent study has found that daily supplementation with vitamin D (800 IU) and calcium (1200 mg) can reduce hip fracture by 43% in postmenopausal women.12 The incidence of hip fracture in hemiplegic stroke patients may be similarly reduced by routine use of active vitamin D supplements.13
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1. Ramnemark A, Nyberg L, Lorentzon R, Olsson T, Gustafson Y. Hemiosteoporosis after severe stroke, independent of changes in body composition and weight. Stroke. 1999;30:755–760.
2. Sato Y, Maruoka H, Honda Y, Asoh T, Fujimatsu Y, Oizumi K. Development osteopenia in the hemiplegic finger in patients with stroke. Eur Neurol. 1996;36:278–283.[Medline] [Order article via Infotrieve]
3.
Sato Y, Maruoka H, Oizumi K, Kikuyama M. Vitamin D
deficiency and osteopenia in the hemiplegic limbs of stroke patients.
Stroke. 1996;27:2183–2187.
4. Hamdy RC, Moore SW, Cancellaro VA, Harvill LM. Long-term effects of strokes on bone mass. Am J Phys Med Rehabil. 1995;74:351–356.[Medline] [Order article via Infotrieve]
5. Minaire P. Immobilization osteoporosis: a review. Clin Rheumatol. 1989;8(suppl):95–103.
6. Minaire P, Meunier P, Edouard C, Bernard J, Courpron P, Bourret J. Quantitative histological data on disuse osteoporosis: comparison with biological data. Calcif Tissue Res. 1974;17:57–73.[Medline] [Order article via Infotrieve]
7. Chiu KY, Pun WK, Luk KDK, Chow SP. A prospective study on hip fractures in patients with previous cerebrovascular accidents. Injury. 1992;23:297–299.[Medline] [Order article via Infotrieve]
8.
Mulley G, Espley AJ. Hip fracture after hemiplegia.
Postgrad Med J. 1979;55:264–265.
9. Strom T, Steiniche T, Thamsborg G, Melsen F. Changes in bone histomorphometry after long-term treatment with intermittent, cyclic etidronate for postmenopausal osteoporosis. J Bone Miner Res. 1993;8:199–208.[Medline] [Order article via Infotrieve]
10. Wimalawansa SJ. Long- and short-term side effects and safety of calcitonin in man: a prospective study. Calcif Tissue Int. 1993;52:90–93.[Medline] [Order article via Infotrieve]
11.
Sato Y, Kuno H, Kaji M, Ohshima Y, Asoh T, Oizumi K.
Increased bone resorption during the first year following a stroke.
Stroke. 1998;29:1373–1377.
12. Chapuy MC, Arlot ME, Duboeuf F, Brun J, Crouzet B, Arnaud S, Delmas PD, Meunier PJ. Vitamin D3 and calcium to prevent hip fractures in elderly women. N Engl J Med. 1992;327:1637–1642.[Abstract]
13.
Sato Y, Maruoka H, Oizumi K. Amelioration of
hemiplegia-associated osteopenia over 4 years following stroke by
1
-hydroxyvitamin D3 and calcium supplementation.
Stroke. 1997;28:736–739.
Response
Geriatric Medicine, Department of Community Medicine and Rehabilitation
Sports Medicine Unit, Department of Surgical and Perioperative Science
Department of Public Health and Clinical Medicine, Medicine, Umeå University, Umeå, Sweden
Key Words: bone density • hemiplegia • osteoporosis
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We thank Dr Sato and his colleagues for their valuable comments on our article.
Bone loss after stroke occurs exclusively on the paretic side, is most pronounced the first year after stroke, and continues significantly the first year after the acute onset of stroke.1 2 Preliminary data indicate that stroke patients continue to lose bone mass between 1 and 3 years after stroke onset (Ramnemark et al, unpublished data, 1999). A main reason for development of hemiosteoporosis is likely to be the paresis itself (ie, disuse). Vitamin D deficiency cannot be excluded as an additional cause, because stroke patients may be malnourished3 and stay indoors most of the time. However, in our study we saw only the normal rate of bone loss over the total body during the first year after stroke. This argues against hypovitaminosis D and general immobilization being the main cause of hemiosteoporosis.
We agree with Sato and his colleagues that bone histopathology studies
in hemiplegic patients would be of value, although this is rarely
performed in clinical praxis. One previous study4 analysed
histopathological changes in bone biopsies in stroke patients who had
suffered femoral neck fracture. However, biopsies were not strictly
from the paretic side, and the sample size was too small to draw any
conclusions. The diagnosis of osteoporosis in our study was set,
according to WHO, as a BMD value (in grams per square centimeter) 
2.5
SDs below the young adult mean value of BMD (T score),5
and 84% of patients in our study fulfilled the criteria for
osteoporosis in paretic hip at the 12-month follow-up.
Further intervention studies with the aim of reducing fracture risk in stroke patients are of major interest. Sato et al have been instrumental in this area by demonstrating the effects of very interesting treatments on osteoporosis by vitamin D and calcium in this patient group.6
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References |
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TopIntroductionReferencesIntroduction References |
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1. Ramnemark A, Nyberg L, Lorentzon R, Olsson T, Gustafson Y. Hemiosteoporosis after severe stroke, independent of changes in body composition and weight. Stroke.. 1999;30:755–760.
2. Ramnemark A, Nyberg L, Lorentzon R, Englund U, Gustafson Y. Progressive hemiosteoporosis on paretic side and increased bone mineral density in non-paretic arm first year after severe stroke. Osteoporos Int. 1999;9;269–275.
3. Finestone HM, Greene Finestone LS, Wilson ES, Teasell RW. Malnutrition in stroke patients on the rehabilitation service and at follow-up: prevalence and predictors. Arch Phys Med Rehabil.. 1995;76:310–316.[Medline] [Order article via Infotrieve]
4.
McClure J, Goldsborough S. Fractured neck of femur and
contralateral intracerebral lesions. J Clin
Pathol.. 1986;39:920–922.
5. Kanis JA, Melton LJ III, Christiansen C, Johnston CC, Khaltaev N. The diagnosis of osteoporosis. J Bone Miner Res.. 1994;9:1137–1141.[Medline] [Order article via Infotrieve]
6. Sato Y, Maruoka H, Oizumi K. Amelioration of hemiplegia-associated osteopenia more than 4 years after stroke by 1 alpha-hydroxyvitamin D3 and calcium supplementation. Stroke.. 1997;28:736–739.
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