The exact mechanism is not known. The probable explanation is imbalance in the regulation of colonic motor activity by the
autonomic nervous system. Acute megacolon develops because of abnormal
intestinal motility. Normal colonic motility requires integration of myogenic, neural, and hormonal influences. The enteric nervous system is independent but is connected to the
central nervous system by
sympathetic and
parasympathetic nerves. The targets of the
enteric neurons are
muscle cells, secretory cells,
endocrine cells,
microvasculature, and inflammatory cells. The neurons in the enteric plexuses are stimulated by a food
bolus, which both distends the gut and stimulates the mucosal surface, leading to the release of factors that stimulate
interneurons. The stimulated interneurons transmit excitatory signals proximally, which cause contraction and inhibitory signals distally, and these in turn cause relaxation. These signals are transmitted by the
neurotransmitters
acetylcholine and
serotonin, among others. Acute megacolon can also lead to
ischemic necrosis in massively dilated intestinal segments. This is explained by
Pascal's law and
Laplaces's law. Pascal's principle states that a change in pressure at any point in an enclosed fluid at rest is transmitted undiminished to all points in the fluid; the pressure across all parts of the lumen is equal. Laplace's law states that: T=\frac{P r}{2t} where
T is wall tension,
P is pressure,
r is the radius, and
t is wall thickness. Since the wall tension is proportionate to the radius, a dilated intestinal segment has a greater wall tension than a nondilated segment; if the dilatation and tension are sufficiently great, blood flow may be obstructed and ischemia of the bowel will occur. Ogilivie syndrome may precipitate
volvulus. ==Diagnosis==