The Effect of Therapeutic Mobilization on Hypercalciuria Following Acute Poliomyelitis

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Abstract
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

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