Theodor Weber,[17] rejecting the above theories on the ground that neither bronchial spasm nor tonic contraction of the diaphragm is capable of explaining why catarrhal secretion should come on at the close of an attack in which at the commencement there was no catarrh, attributes the phenomena of asthma to sudden swelling of the bronchial mucous membrane, the result of dilatation of its blood-vessels produced through the agency of the vaso-motor nerves; thus reviving the fluxionary theory of Traube. In support of this theory he cites the result of Von Loven's[18] experiments, which prove that irritation of the sensory nerves is followed by reflex engorgement of the territory to which they are distributed. Weber considers that this engorgement of the bronchial mucous membrane is somewhat similar to the acute swelling and stoppage of the nostrils to which many persons are subject--a closure which often does not last longer than a few moments, and which is attended with increased redness and swelling of the Schneiderian membrane. The mucous membrane of the nostril and that of the bronchi being both parts of the respiratory tract, and somewhat similar in structure, he concludes that the process in the nostrils is analogous to that which occurs in the bronchi during the asthmatic paroxysm. As additional proof of the correctness of his hypothesis he cites the fact that such occlusion of the nostrils is often the precursor of the asthmatic attack, and in some cases continues throughout the paroxysm. See investigations of Daly, Roe, Allen, and Hack, further on. [Footnote 17: "Ueber Asthma Nervosum," _Tageblatt der 45 Versammlung deutscher Naturforscher u. Aertze in Leipzig, etc._, 1872, p. 159.] [Footnote 18: _Naturforscher u. Aertze in Leipzig, etc._, 1872, p. 159.] The idea that asthma is due to swelling and engorgement of the bronchial mucous membrane appears to have been confirmed by the tracheoscopic observations of Stoerk.[19] On examining the air-passages with the laryngoscope, he could see the mucous membrane of the trachea as far as visible (that is, to the bifurcation) grow red with the onset of the paroxysm, and resume its normal appearance after the termination of the attack. He opposes the spasm theory, denies the correctness of Biermer's conclusions, and adopts Weber's explanation of the asthmatic phenomena. He agrees with Wintrich that spasm of the diaphragm occurs, but claims that it results from the tension to which it is subjected by the inflated alveolæ: the diaphragm being forced downward by the distended lung, its fibres are stretched, and the result is a tonic spasm of that muscle. His objections, although well stated, are not sufficiently conclusive to cause us to accept his opinion in preference to that of Biermer and other supporters of the spasm theory. [Footnote 19: _Mittheilungen über Asthma bronchiale, etc._, Stuttgart, 1875.]