Irritable Bowel Syndrome (IBS)

Populations and Risk Factors

• Women affected approximately 2:1 over men; hormonal fluctuations (menstruation, perimenopause) exacerbate symptoms — estrogen and progesterone influence gut motility and visceral sensitivity
• Most common onset between ages 20 and 40; can occur at any age but rarely presents initially after age 50 (new onset after 50 is a red flag for organic pathology)
• Strong association with anxiety, depression, and somatization disorders — psychological comorbidity is present in 50–90% of patients seeking treatment
• Co-occurs with fibromyalgia (up to 60% overlap), chronic fatigue syndrome (51% overlap), and temporomandibular disorders — shared central sensitization mechanism
• Prior gastrointestinal infection increases risk 6-fold (post-infectious IBS develops in 10–15% of patients following bacterial gastroenteritis)
• Dietary triggers: FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols), gluten sensitivity, caffeine, alcohol, fatty foods
• Psychosocial stressors — childhood adversity and chronic life stress are independent risk factors

Causes and Pathophysiology

Brain-Gut Axis Dysregulation

IBS is fundamentally a disorder of the brain-gut axis — the bidirectional communication network between the central nervous system and the enteric nervous system (ENS). The ENS contains approximately 100 million neurons embedded in the gut wall and operates semi-autonomously, but is modulated by the CNS via vagal afferents and sympathetic pathways.

• Serotonin (5-HT) is the key neurotransmitter: approximately 95% of the body's serotonin is produced by enterochromaffin cells in the gut mucosa. Serotonin regulates peristalsis, visceral sensation, and intestinal secretion. In IBS, serotonin signaling is dysregulated — elevated 5-HT levels correlate with IBS-D (increased motility and secretion), while reduced 5-HT availability correlates with IBS-C (slowed transit). This is why SSRIs and tricyclic antidepressants are sometimes used to manage IBS — they modulate serotonin at both the gut and central level.
• Vagal afferents carry visceral pain signals from the gut to the nucleus tractus solitarius in the brainstem, which relays to the hypothalamus, amygdala, and anterior cingulate cortex — the same brain regions that process emotional distress. This neuroanatomy explains why emotional states directly influence gut symptoms and why gut symptoms intensify emotional distress (bidirectional amplification loop).

Visceral Hypersensitivity

The defining pathophysiological feature of IBS is visceral hyperalgesia — normal physiological distension of the intestinal lumen (from gas, stool, or peristaltic contractions) is perceived as painful.

• At the peripheral level, enterochromaffin cells in the gut mucosa have a lower activation threshold, releasing excess serotonin in response to normal luminal stimuli
• At the spinal level, dorsal horn neurons receiving visceral afferents from the gut become sensitized (wind-up), amplifying pain signals — this is the visceral equivalent of central sensitization seen in conditions like fibromyalgia
• At the cortical level, functional imaging shows hyperactivation of the anterior cingulate cortex and prefrontal cortex during rectal distension in IBS patients compared to controls — the brain amplifies what the gut reports

This three-level sensitization explains why light abdominal palpation may be painful in IBS patients — the examiner is compressing viscera that are already at a lowered pain threshold.

Stress-Gut Mechanism

Stress worsens IBS through a well-characterized neuroimmune cascade:

• Psychological or physical stress activates the hypothalamic-pituitary-adrenal (HPA) axis, releasing corticotropin-releasing factor (CRF) from the hypothalamus
• CRF acts directly on CRF receptors on intestinal mast cells, triggering mast cell degranulation
• Degranulating mast cells release histamine, proteases, and pro-inflammatory cytokines that increase intestinal permeability ("leaky gut"), stimulate visceral afferent nerve endings, and disorganize peristalsis
• The resulting symptoms (cramping, urgency, diarrhea, or constipation) further amplify the stress response — creating a self-reinforcing cycle

This mechanism is the neurobiological rationale for stress reduction as a primary therapeutic strategy in IBS, and for why MT's parasympathetic activation effect is clinically relevant.

Post-Infectious IBS

In 10–15% of patients who experience acute bacterial gastroenteritis (e.g., Salmonella, Campylobacter, Shigella), IBS symptoms persist for months to years after the infection has cleared. The mechanism involves:

• Residual low-grade mucosal inflammation and increased mucosal mast cell density in the gut wall even after the pathogen is eliminated
• Persistent alterations in the gut microbiome (dysbiosis) that fail to return to baseline
• Sensitization of enteric sensory neurons during the acute infection that does not resolve — a form of peripheral nerve "memory"

Microbiome Dysbiosis

IBS patients consistently show altered gut microbiome composition compared to healthy controls — reduced microbial diversity and shifts in the relative abundance of Firmicutes and Bacteroidetes. While the causal direction remains debated, dysbiosis contributes to IBS through:

• Altered fermentation patterns producing excess gas (contributing to bloating and distension)
• Disrupted bile acid metabolism (contributing to IBS-D)
• Impaired intestinal barrier function

Disorganized Motility

Intestinal motility in IBS is not simply increased or decreased — it is disorganized. Normal coordinated peristalsis is replaced by irregular, high-amplitude propagating contractions (HAPCs) in IBS-D, or reduced propagating contractions in IBS-C. In IBS-M, the pattern alternates unpredictably. This disorganized motility, combined with visceral hypersensitivity, produces the characteristic cramping, urgency, incomplete evacuation, and unpredictable bowel patterns.

Signs and Symptoms

By Subtype

Common Features Across All Subtypes

• Abdominal pain at least 1 day per week (Rome IV criterion) associated with defecation, change in stool frequency, or change in stool form
• Bloating and visible abdominal distension — often worse in the evening and after meals
• Sensation of incomplete evacuation
• Pain relieved (partially or fully) by defecation — a Manning criterion
• Mucus passage — present in IBS but absent in simple functional diarrhea
• Symptoms exacerbated by stress, specific foods, and hormonal changes (menstruation)
• No nocturnal symptoms (being woken from sleep by GI symptoms is a red flag for organic disease)
• No fever, rectal bleeding, unexplained weight loss, or anemia — these are red flags indicating possible IBD, celiac disease, or colorectal cancer

Assessment Profile

Subjective Presentation

• Chief complaint: Recurrent abdominal pain with bloating and irregular bowel habits; patient may describe "my stomach is always upset" or "I never know what my bowels are going to do"; significant impact on daily activities and quality of life; many patients report a strong correlation between stress and symptom flares
• Pain quality: Cramping or dull aching; diffuse or localized to the lower abdomen (particularly left lower quadrant along the descending and sigmoid colon); pain intensity fluctuates with bowel activity; ask patient to identify their predominant pattern — diarrhea-predominant (IBS-D), constipation-predominant (IBS-C), or mixed/alternating (IBS-M) — as this guides treatment approach
• Onset: Gradual onset typically in early adulthood; may follow a significant life stressor or gastrointestinal infection; symptoms are chronic and relapsing — patients describe good periods and bad periods; ask about dietary triggers (FODMAPs, dairy, gluten, caffeine), stress correlation, and menstrual cycle relationship
• Aggravating factors: Emotional stress (primary trigger), specific foods (varies by patient — common culprits include dairy, wheat, caffeine, alcohol, fatty foods, artificial sweeteners), large meals, menstruation, disrupted sleep, travel, antibiotics
• Easing factors: Defecation (partial or complete relief — a diagnostic criterion); heat application to abdomen (IBS-C); stress management; dietary modification; prone or side-lying with knees drawn up; regular routine and sleep schedule
• Red flags: Onset after age 50 → organic pathology; rectal bleeding → IBD or colorectal cancer; unexplained weight loss → malignancy or malabsorption; nocturnal symptoms waking patient from sleep → organic disease; fever → infection or IBD; family history of colorectal cancer, IBD, or celiac disease → refer for investigation before treating as IBS

Observation

• Local inspection: Visible abdominal distension (bloating), particularly in the lower abdomen; may be absent during quiescent periods; no skin changes, bruising, or masses expected; note any surgical scars (previous abdominal surgery can mimic or coexist with IBS)
• Posture: Protective flexed posture during flares — patient may lean forward or draw knees up; habitual guarding posture with shoulders elevated and thoracolumbar flexion if chronic; shallow upper-chest breathing pattern (loss of diaphragmatic excursion from chronic abdominal guarding)
• Gait: Not typically affected; omit from assessment unless patient reports hip or low back pain secondary to chronic guarding

Palpation

• Tone: Abdominal wall musculature — voluntary and involuntary guarding, particularly over the lower abdomen; rectus abdominis and obliques may show chronic hypertonicity from sustained protective guarding; paraspinal tension (thoracolumbar junction T10–L2) secondary to visceral-somatic reflex — visceral afferents from the gut converge on the same dorsal horn segments as somatic afferents from the thoracolumbar paraspinals, producing referred muscle tension; diaphragm restriction palpable at costal margin — chronic shallow breathing pattern
• Tenderness: Diffuse abdominal tenderness, often more pronounced in the left lower quadrant (sigmoid colon); periumbilical tenderness to light palpation — visceral hypersensitivity means the threshold is lowered and normal palpation pressure may be painful; palpable colonic loading (firm, tubular structures along the colon path — particularly descending and sigmoid colon in IBS-C); differentiate from rebound tenderness (pain on release of palpation pressure) — rebound tenderness indicates peritoneal irritation and is a red flag requiring immediate referral (appendicitis, peritonitis, ruptured viscus); thoracolumbar paraspinal tenderness at T10–L2 from visceral-somatic reflex
• Temperature: Normal; no inflammatory heat expected (heat in the abdominal wall would suggest infection or acute inflammation — refer)
• Tissue quality: Abdominal wall — may feel rigid or board-like during flares (involuntary guarding); between flares, tissue may be soft but demonstrate increased sensitivity to palpation; thoracolumbar paraspinals — fibrotic, ropy quality from chronic guarding; reduced fascial mobility through the abdominal wall and thoracolumbar fascia

Motion Assessment

• AROM: Trunk flexion, extension, and rotation may be limited by abdominal guarding, particularly during active flares; patients may avoid full trunk extension (which stretches the abdominal wall and increases intra-abdominal pressure); lateral flexion toward the symptomatic side may reproduce abdominal discomfort
• PROM / end-feel: Not directly applicable to abdominal assessment; trunk PROM limited by guarding shows a protective/muscle spasm end-feel; no joint pathology expected
• Resisted testing: Normal strength; abdominal muscle testing may be deferred during flares due to pain provocation; core weakness may develop over time from chronic guarding and avoidance of abdominal engagement

Special Test Cluster

IBS is a clinical diagnosis based on symptom criteria and exclusion of organic disease. The SOT cluster is oriented toward confirming the symptom pattern and ruling out red flags, not toward direct confirmation via orthopedic tests.

Rome IV Criteria (diagnostic standard): Recurrent abdominal pain on average at least 1 day per week in the last 3 months, associated with 2 or more of: (1) related to defecation, (2) associated with a change in stool frequency, (3) associated with a change in stool form. Symptom onset must be at least 6 months prior to diagnosis. The MT does not diagnose IBS but should recognize these criteria to confirm working within an established diagnosis.

Differential Diagnoses