Atrophic hypoganglionosis in the colon of adults with slow-transit constipation: a morphometric histopathological investigation

BACKGROUND: The diagnostic criteria for hypoganglionosis in colon specimens from adults with chronic slow-transit constipation have not been defined properly. The aim of this study was to evaluate the most important diagnostic parameters for hypoganglionosis in routinely prepared transverse sections. METHODS: Twelve histopathologically diagnosed hypoganglionic hemicolectomy specimens of the left colon, which had been resected due to chronic slow-transit constipation, were compared with 12 control hemicolectomy specimens which had been resected because of pseudodiverticulosis, vaginal prolapse, or rectocele without chronic constipation. All surgical specimens were coiled caudocranially and cut in a cryostat; only native tissue was used. The myenteric plexus was selectively stained by an acetylcholinesterase reaction. Nerve cells were specifically stained by a nitroxide synthase and a lactate dehydrogenase reaction. Morphometric measurements of the myenteric plexus were performed with an optic-electronic image-analysis system. The contrast-rich image of the myenteric plexus and its nerve cells and muscularis propria enabled the various structures to be measured with a semiautomatic grey-level discrimination. RESULTS: In hypoganglionosis of adults, the most striking finding was a significant decrease in nerve-cell number (–43.8%) in the colonic myenteric plexus. The cross-sectional area of the plexus decreased by 30.4%, and the number of ganglia decreased by 19.7%. The distances of myenteric ganglia showed only a moderate increase. The incidence of hypoganglionosis in chronic slow-transit constipation in the distal colon of adults was about 33% in 759 cases. CONCLUSIONS: The study shows that hypoganglionosis of the myenteric plexus can precisely be objectified by morphometric means. The findings also demonstrate that the most characteristic anomaly in atrophic hypoganglionosis is the significantly lowered nerve-cell number in the myenteric plexus. The data support the hypothesis that hypoganglionosis in adults is the result of an atrophic process rather than, as in young children, a primary hypoplastic anomaly.