What is Visceral Hypersensitivity
Visceral hypersensitivity is enhanced pain sensitivity to experimental gut stimulation, occurring in approximately two-thirds of IBS patients, where normal or mildly noxious stimuli in the gastrointestinal tract are perceived as painful or intensely uncomfortable. 1
Core Definition and Clinical Significance
Visceral hypersensitivity represents a phenomenon where the gut becomes abnormally sensitive to stimuli that would not typically cause pain or discomfort in healthy individuals. 1 This heightened sensitivity plays a crucial role in the development of chronic abdominal pain and discomfort, particularly in patients with irritable bowel syndrome. 1
The condition manifests as both hyperalgesia (increased sensitivity to painful stimuli) and allodynia (non-painful stimuli perceived as painful). 1
Underlying Mechanisms
Visceral hypersensitivity results from a combination of factors involving heightened sensitivity of both peripheral and central nervous systems. 1
Peripheral Sensitization
During tissue injury and inflammation, peripheral nociceptor terminals are exposed to immune and inflammatory mediators including prostaglandins, leukotrienes, serotonin, histamine, cytokines, neurotrophic factors, and reactive metabolites. 1 These mediators activate intracellular signaling pathways that upregulate the sensitivity and excitability of nociceptor terminals, causing primary hyperalgesia at the site of injury or inflammation. 1
Between 6% and 17% of IBS patients report symptom onset following gastroenteritis, with increased mucosal T lymphocytes documented in postinfectious IBS, suggesting an altered environment around nociceptor terminals. 1
Central Sensitization
Central sensitization develops as a secondary consequence of peripheral sensitization, creating hypersensitivity in surrounding uninjured tissue (secondary hyperalgesia/allodynia). 1 This occurs through increased excitability and expanded receptive fields of spinal neurons, resulting in recruitment and amplification of both non-nociceptive and nociceptive inputs from adjacent healthy tissue. 1
Evidence for central sensitization in IBS includes three key observations: 1
- Greater radiation of pain to somatic structures during colonic stimulation compared to healthy subjects
- Coexistence with fibromyalgia (characterized by somatic hyperalgesia) in some IBS patients
- Hypersensitivity extending to more proximal gut regions
These findings are explained by the overlap and convergence of innervation from different gut organs with somatic structures at the spinal cord level. 1
Central Pain Processing
Beyond peripheral and central sensitization, visceral hypersensitivity involves complex processing of sensory inputs in cortical and subcortical brain structures. 1 Functional brain imaging studies demonstrate that visceral sensation is represented in: 1
- Primary (S1) and secondary somatosensory cortex (S2) - mediating sensory discriminative aspects
- Paralimbic and limbic structures (anterior insula, anterior cingulate, prefrontal cortices) - mediating affective and cognitive components
- Subcortical regions (thalamus, periaqueductal grey matter)
Clinical Characteristics
Visceral hypersensitivity, while frequent in IBS, is not a constant finding and cannot be considered a diagnostic marker. 2 The prevalence ranges from 20% to 90% of IBS patients depending on the study methodology. 3
Hypersensitive IBS patients demonstrate lower sensory thresholds for pain, first perception, urge to defecate, and discomfort, rating both painful and non-painful sensations as more intense than normosensitive patients. 4
Important Clinical Pitfall
IBS patients demonstrate decreased pain thresholds to rectal distension, meaning they may perceive symptoms more acutely than non-IBS patients. 5 This heightened perception can complicate clinical assessment, as symptoms may be disproportionate to objective findings.
Modulating Factors
Psychological factors (anxiety, depression, somatization) selectively increase pain perception during distension in hypersensitive IBS patients, but not in normosensitive patients. 4 Anxiety specifically increases intensity ratings of non-painful sensations regardless of sensitivity status. 4
Visceral hypersensitivity may increase during psychosocial stress and symptom exacerbation periods, though this requires further confirmation. 6