1943
DOI: 10.1001/archsurg.1943.01220100013003
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Post-Traumatic Dystrophy of the Extremities

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Cited by 45 publications
(8 citation statements)
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“…Duff et al (1951) reported that an intravenous injection of 7,500 units of heparin resulted in lengthening of the clotting-time to twice normal for only three to four hours. The response of different subjects to a single dose of dextran sulphate was variable, as with heparin (de Takats, 1943).…”
Section: Discussionmentioning
confidence: 99%
“…Duff et al (1951) reported that an intravenous injection of 7,500 units of heparin resulted in lengthening of the clotting-time to twice normal for only three to four hours. The response of different subjects to a single dose of dextran sulphate was variable, as with heparin (de Takats, 1943).…”
Section: Discussionmentioning
confidence: 99%
“…Decalcification -excessive antidromic impulses (AN.AX) are transmitted to blood vessels in the bony attachment and stimulate a release of excess neurohumoral substance 16,32 which induces a neurovascular vasodilation edema that interferes with osteogenesis while osteoclysis continues. It is an interference with bone metabolism (dystrophy) in which decalcification (DD) further weakens the fibroosseous attachment and increases the disability 20,21,23,25 in intensity and area such as occurs within the attachments of tendon fibers to the occipital bone. [7][8][9][10][11] Inflamation Neuritis -other antidromic impulses are transmitted to blood vessels in nerves and surrounding tissues stimulating a release of excess neurohumoral mediator substance which causes a neurovascular vasodilation-edema-sterile inflammation-neuritis, 16,44 as in spinal nerves emerging through weak attachments of ligament/tendon to vertebra.…”
Section: Ligament and Tendon Relaxationmentioning
confidence: 99%
“…and decalcification (dystrophy), 7,9,[20][21][22][23][24][25] and, in association with sympathetic impulse overstimulation from the same source, there is an accompanying dysfunction of the neural, vascular and visceral systems and lowering of the pain threshold. 4,7,16,[26][27][28] Investigation of antidromic impulses in afferent nerves from over-stimulation has been under investigation since 1874 by Goltz, Stickler, Bayliss, Gaskell, Langlcy, Foerster, Hinsey, Gasser, de Takats.…”
mentioning
confidence: 99%
“…Many descriptive terms have since been used, each emphasizing one particular clinical facet or etiology (Steinbrocker and Argyros, 1958). The terms reflex dystrophy and RSD were used by Leriche (1939), de Takats and Miller (1943), Evans (1946), and Holden (1948). Although still used in its original sense by some investigators (International Association, 1979), the term causalgia has become almost synonymous with the term RSD.…”
mentioning
confidence: 99%