Mechanism of Gastroparesis
Gastroparesis results from a complex interplay of neuromuscular dysfunction affecting gastric motility, accommodation, and sensory function, leading to delayed gastric emptying in the absence of mechanical obstruction. 1
Key Pathophysiological Mechanisms
Gastric Motility Disorders
- Antral hypomotility: Reduced contractility of the gastric antrum impairs grinding and propulsion of food particles 1
- Pyloric dysfunction: Characterized by prolonged intermittent contractions and increased baseline tone at the pylorus, impeding gastric emptying 2, 1
- Antroduodenal and pyloric dyscoordination: Disrupted coordination between antral contractions and pyloric relaxation prevents proper food passage 2, 1
Nervous System Damage
- Vagal nerve injury: Disruption of vagal afferent and efferent pathways significantly contributes to gastroparesis 2, 1
- Enteric nervous system damage: Loss of interstitial cells of Cajal (ICC), the pacemaker cells that regulate gastric motility 1
- Autonomic neuropathy: Particularly relevant in diabetic gastroparesis, impairing both gastric motility and sensation 1
Gastric Accommodation and Sensory Function
- Impaired gastric accommodation: Reduced ability of the proximal stomach (fundus) to relax and accommodate food, associated with early satiety and postprandial fullness 1
- Increased visceral perception: Exaggerated sensitivity to gastric stimuli contributes to symptom generation and intensity 2, 1
Etiology-Specific Mechanisms
Diabetic Gastroparesis (25% of cases)
- Diabetic neuropathy linked to antral hypomotility and pylorospasm 2
- Hyperglycemia directly impairs gastric motility and increases perception of gastrointestinal sensations 1
Post-Surgical Gastroparesis
- Typically results from partial or complete vagotomy (intended or unintended) 2, 1
- Common after procedures like esophagectomy, gastrectomy, and fundoplication 1
Idiopathic Gastroparesis
- Most common form, often following viral infections 1
- May involve immune-mediated damage to the enteric nervous system 1
Additional Contributing Factors
- Altered intestinal permeability: Changes in gut barrier function may contribute to symptom generation 2, 1
- Abnormal gut microbiome: Changes in gastric and small bowel microbiota may play a role in pathophysiology 2, 1
- Central nervous system processing abnormalities: Affect symptom perception and intensity 1
- Learned behaviors: Food aversion and disordered eating patterns can develop and perpetuate symptoms 2
Clinical Manifestations Related to Pathophysiology
- Nausea and vomiting: Related to gastric dysrhythmias, antral hypomotility, and increased visceral sensitivity 1
- Early satiety and postprandial fullness: Associated with impaired gastric accommodation and delayed emptying 1
- Abdominal pain: Linked to visceral hypersensitivity and altered central processing of sensory signals 1
- Bloating: Results from impaired gastric emptying and intestinal dysmotility 1
Important Clinical Considerations
- Gastroparesis and functional dyspepsia may represent a spectrum of the same pathophysiological disorder rather than distinct entities 1
- Symptoms often overlap significantly with functional dyspepsia, making diagnosis challenging 2
- The severity of symptoms does not always correlate with the degree of delayed gastric emptying 2
- Multiple pathophysiological mechanisms often coexist in individual patients, requiring targeted therapeutic approaches 2, 1