ANGIONEUROTIC EDEMA 285 
scratching and rubbing, and with this fatigue the per- 
meability of the wall increases with resultant limited 
serum oozing, i. e., wheal formation. 
In simple urticarias this wheal formation is of short 
duration. With no marked vasoconstricting impulse 
ensuing, tonus gradually returns to the fatigued vaso- 
dilators, increased vessel wall permeability disappears, 
exuded serum is taken up by the normal processes of 
tissue drainage, and the wheal fades. It is unlikely that 
local deposits of toxins and osmosis thereto enter into 
the creation of such lesions, since disappearance of the 
wheal follows so promptly upon the cessation of exter- 
nal irritation. 
Here then it would seem that hyperthyroid action 
plus local vasodilator fatigue are the direct cause of 
simple urticarial lesions. 
Between the short-lived manifestations of simple 
urticaria and the long-lived lesions of angioneurotic 
edema there appear to be differences only as to the ex- 
citing cause and the duration of the individual swell- 
ings. In the angioneurotic type nervous stress or 
fatigue seem to be the predominating features in the 
etiology. We know these factors, absent in simple 
urticatria, cause profound adrenal irritation, rather 
than thyroid stimulation. Adrenal excitation, however, 
always entails thyroid stimulation, so that in angioneu- 
rotic types thyroid stimulation is present. Further- 
more, in profound nervous excitation or fatigue, diges- 
tion often is curtailed or temporarily stopped, and pro- 
teins, whose digestion is interfered with, may be assimi- 
lated later in forms particularly irritating to the 
organism, and capable of producing as components 
of the blood any or all the phenomena ascribed to 
foreign proteins in the blood, including both thy- 
roid and adrenal irritation. Except in cases of se- 
vere nervous reaction a temporary hyperthyroid secre- 
tion either occurs first or quickly supervenes after 
