Abstract
The theory of dual motor innervation of striated muscle suggested by the histological studies of Boeck 1 and supported by the physiological observations of DeBoer 2 and Langelaan 3 has led to considerable experimental investigation and controversy. Assuming this theory and the functional hypothesis that the sympathetic nervous system was responsible for the maintenance of plastic tone and that the medullated or sometic fibers served only to initiate contractile tone, Hunter 4 and Royle 5 proceeded experimentally, and later clinically, to give these studies clinical application. They interrupted the sympathetic innervation of one extremity of animals upon which an upper motor neurone (decerebrated spasticity) type of paralysis had been or was subsequently produced, and reported hypotonicity of the muscles of the sympathectomized side. However, no one has been able to duplicate their results experimentally or clinically (Von Lochem excepted).
Recently, Wilkinson 6 has demonstrated quite conclusively that striated muscle tissue receives no sympathetic innervation. Cobb, 7 Tower, 8 Kanavel and Davis, 9 Kuno, 10 and others were unable to show any constant difference in muscle tone as a result of sympathetic deinnervation. If the animals were observed from time to time the normal (control) extremity would show diminished tone as frequently as the operated side.
In an attempt to correlate the definitely recognized interruption of vasomotor control to any alteration in muscle tone (if obtainable) these classical experiments were repeated and frequent skin temperature determinations made. These readings have been tabulated for 2 animals. All the methods commonly used to produce hypertonicity were used. Strychnine was used for 16 observations on 10 animals; parathyroid tetany was induced in 2 animals; ether rigidity 34 times in 20 animals; decerebrated rigidity in 4 animals and spinal cord section in 2 animals.
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