Hypercalciuria following poliomyelitis; its relationship to site and degree of paralysis.

Hypercalciuria and demineralization are frequent sequels to severe paralytic illnesses. Freeman1and many others* emphasized that osteoporosis and calcium-containing genitourinary calculi commonly complicate traumatic paraplegia. Excess calcium loss also may be inferred to occur in many patients with multiple sclerosis and polyneuritis, since calcium-containing stones often develop during these illnesses. Whedon and Shorr2recently demonstrated that every one of seven extensively paralyzed patients developed profound losses of calcium and phosphorus after poliomyelitis. The studies cited above were all performed on patients suffering marked paralysis and immobilization. Except for Whedon and Shorr's investigation, they give relatively little quantitative data on serial patterns of mineral excretion. There are few data available to indicate whether, with paralysis, the intensity or duration of hypercalciuria bears any relationship to the site, degree, or extent of denervation. Few investigations have been directed toward determining whether nervous system illnesses produce decalcification in the absence of