In a preceding study it was established that changes of the left colon, usuaUy limited to the sigmoid, formerly believed to represent a pre-diverticular stage or the sequelae of extensive diverticular inflammation, are not inflammatory in nature. These changes, such as crowded haustration and saw-tooth pattern, are caused by contraction and rearrangement of the musculature of the sigmoid and most likely represent a late, irreversible stage of the spastic colon syndrome. Superficial inflammation in dlverticula probably occurs often but is usuaUy self-limited and without clinical significance. The substratum of the clinical syndrome of acute diverticulitis is a perforation of a diverticulum. This is a self-limited process in many cases. It consists of extravasation of colonic contents, associated with an intramural inflammation, foreign-body granuloma, or abscess formation. These processes can be recognized radioiogically by the extravasation of barium, often in minute amounts, and by the sweUing of the colonic waU or paracolic abscess formation causing unilateral marginal filling defects or circular narrowing and obstruction. Frank perforation into the general peritoneal cavity may occur. A severe fecal peritonitis is rare. The better understanding of the pathology of so-called diverticulitis[long dash]diverticular deep sigmoiditis or pericolitis would be better terms[long dash]and stricter and more detailed roentgen criteria make a re-orientation in therapeutic indications and a reevaluation of therapeutic results desirable.