A further contribution to the subject of vasomotor ataxia / by Solomon Solis Cohen.

  • Solis-Cohen, Solomon, 1857-1948.
Date:
[1902?]
Catalogue details

Licence: In copyright

Credit: A further contribution to the subject of vasomotor ataxia / by Solomon Solis Cohen. Source: Wellcome Collection.

Provider: This material has been provided by The University of Glasgow Library. The original may be consulted at The University of Glasgow Library.

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    inconstant association. Among these, special mention may be made of tingling and numbness—not only in the extremities, but in the face, in the tongue and lips, and sometimes over one-half of the body— and of blood losses—as epistaxis, hemoptysis, hematemesis, hematuria (which may be so slight, however, as to be merely discoverable by the presence of erythrocytes in unusual quantity upon microscopic exami- nation of the urine), hemoglobinuria, retinal hemorrhage, petechise, etc. Slight, transient, but recurrent, albuminuria, is not uncommon. Hives and attacks resembling erythema nodosum are manifested with more or less frequency, while recurrent circumscript edema (angioneurotic edema)—sometimes affecting especially one-half of the tongue—or giant urticaria, local or general, may appear in apparent sequence to trauma, to emotion, to indigestion, to food and drug intoxication, or to sudden chill, etc. In some persons the hands will swell to almost twice their normal size when exposed to cold, even in slight degree. These subjects sometimes have attacks of chromidrosis or hemidrosis. Many persons have at different times what may be termed substitutive crises—as vertigo, migrain, asthma, or nausea and emesis.—But to extend the list of symptoms and syndromes would be to begin the record of cases and to pass beyond the purpose of this paper. That the paroxysms or crises are often precipitated by toxic influences of endogenous or ectogenous origin is probably true, but whatever be the toxico-pathologic mechanism of individual symptoms or of special groups of symptoms, underlying all is the fundamental defect of inhi- bition, which Savill terms vasomotor inco-ordination, and for which I prefer my original term—vasomotor ataxia. Apart from the general relationships discussed, there is a practical clinical value to these observations. It lies in the recognition and assemblage of the cases that as yet do not fall into accepted syndrome groups. Doubtless more or less definite causation and more or less definite toxico-pathologic mechanisms will ere long be established for Oraves's and Raynaud's syndromes, as for Mitchell's erythromelalgia; and other syndrome groups among those described, may—like angio- neurotic edema, hay fever, and migrain—receive limiting descriptions and specific names. I shall, in a future paper, attempt to point out some of the more or less constant associations that may serve as the bases for such diagnostic entities. But beyond all these will remain many vague and inconstant manifestations, recurring irregularly and