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The Effect of Therapeutic Mobilization on Hypercalciuria Following Acute Poliomyelitis
FRED PLUM, M.D.;
MARCELLE F. DUNNING, M.D.
AMA Arch Intern Med. 1958;101(3):528-536.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
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Hypercalciuria and extensive osseous demineralization predictably follow illnesses in which there is either flaccid or spastic muscle paralysis. In poliomyelitis, in particular, previous work in this laboratory1 has demonstrated that there are two aspects in the mineral loss. During approximately the first three to eight weeks after the onset of illness, urinary calcium values rise to about twice the normal maximum of excretion. This rise is as marked in mildly paralyzed subjects as it is in patients suffering extensive muscle denervation; thus there is no direct quantitative relationship between the extent of paralysis and the degree of daily hypercalciuria in this early phase. During the period of from 2 to 12 months after the onset of poliomyelitis, however, the duration of hypercalciuria is directly related to the extent of paralysis. Excessive calcium loss may last as long as 40 weeks in patients with motor paraplegia, while quadriplegic subjects continue
. . . [Full Text PDF of this Article]
Author Affiliations
Seattle
From The Division of Neurology, Department of Medicine, University of Washington School of Medicine.
Footnotes
Submitted for publication June 24, 1957.
Aided by an annual grant from the National Foundation for Infantile Paralysis to the Northwest Respirator and Rehabilitation Center and by a research grant (B-1034 [C]) from the National Institute of Neurological Diseases and Blindness, National Institutes of Health, United States Public Health Service.
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