seven cases at autopsy and one clinical case. All but two of the patients were under 1 year of age and the oldest was 3% years. Robinson3 in 1927 reported an autopsy specimen from a man aged 19. Dodson and Lorraine4 observed during life a youth aged 19 in whom hypertrophy of the verumontanum was a cause of urinary obstruction and retention, and a good result followed fulguration of the verumontanum. Baldridge5 reported another case in which cure followed fulguration of the verumontanum in an 11 year old patient. Somerforde in 1936 again observed this lesion at autopsy in a child aged 11 years. The latest report is that of Grant7 in 1938 in which he mentions a boy aged 13 years in whom hypertrophy of the verumontanum was noted during life and relief of obstruction followed fulguration of the verumontanum. COMMENT There is no satisfactory explanation for congenital hypertrophy of the verumontanum. The greatly enlarged verumontanum probably acts as a ball valve just in front of the external sphincter in the same way that median lobe prostatic hypertrophy acts in the region of the internal sphincter. Mechanical obstruction to the flow of urine is produced.The pathologic changes in the urinary tract and the symptoms are similar to those resulting from enlargement of the prostate gland or any other type of infravesical obstruction. There is dilatation of the posterior urethra behind the verumontanum. During the earlier stages of obstruction there are hypertrophy of the bladder with trabeculation, hypertrophy of the trigon, perhaps diverticulum formation and inflammation, dependent on the degree of associated infection. Later, when decompensation of the bladder occurs, there follows dilatation of the bladder, which together with inflammatory changes in the bladder wall result in incompetence of the ureterovesical valve mechanism. Ureteral and pelvic dilatation occur, and in the most advanced cases the renal parenchyma becomes a thin shell. This compression atrophy, accompanied in many cases by infection, eventually reduces renal function to a point at which it will no longer support life.The early symptoms are those of urinary obstruction. Later there are renal insufficiency and uremia. Frequency of urination is the most common symptom. With associated infection, frequency often becomes very marked with almost constant dribbling. Enuresis may be the most prominent symptom. One may observe in older children considerable straining, hesitancy and difficulty in voiding. When bladder distention occurs it may be observed as a mass in the lower part of the abdomen. Recurrent episodes of fever, often diagnosed as pyelitis, are common. As renal damage advances, the symptoms of renal insufficiency appear. There may be failure to gain, or even loss of weight. Loss of appetite and gastrointestinal upsets are common, as well as headaches and lassitude. With a lowered renal reserve these patients are more susceptible to intercurrent infections and often die of them. They may lapse into uremic coma. The true cause of the trouble ma...