Neurogastroenterology: Brain-Gut Axis, Stress, and Psychological Factors

Irritable bowel syndrome (IBS) is now conceptualized with disorders of gut-brain interaction (DGBI). It should be noted that interactions between the brain and the gut are reciprocal. Microbiota and mucosal inflammation relate to pathophysiology of IBS. Visceral afferent neurons are mainly ascend via the sympathetic nervous system and parasympathetic nervous system (vagus nerve). Increase in intraluminal pressure of the colon causes a reflex action and gastrointestinal perception. This activity comprises (1) the peristaltic reflex, (2) the colo-colonic inhibitory reflex, and (3) colonic perception. The nociceptive signal ascends the primary afferent neurons whose cell bodies are in the dorsal root ganglia. They form synapse with the lamina I neurons of the dorsal horn of the spinal cord. Then the parabrachial nucleus, the thalamus, the hypothalamus, and the amygdala are activated. A meta-analysis showed that colorectal distension in IBS patients activates the anterior cingulate cortex, amygdala, and midbrain but deactivates the medial and lateral prefrontal cortex, thereby revealing an association between IBS symptoms and functional changes in the neuronal network centering on the amygdala. Psychosocial stress activates paraventricular nucleus of the hypothalamus. Moreover, hormones, especially the main stress-related peptide corticotropin-releasing hormone (CRH), contribute to the pathological state of IBS patients. In IBS patiments, bowel movement, visceral perception, mucosal permeability, and low-grade inflammation are exaggerated when CRH is released. Possibly relating to the common neurotransmission and/or neuroendocrine changes, IBS patients have high comorbidity with anxiety disorder or depressive disorder. Further research of IBS based on the neurogastroenterology especially brain-gut axis, stress, and psychological factors is warranted in the future.