Gastroparesis is a chronic syndrome characterized by delayed gastric emptying in the absence of mechanical obstruction. The condition primarily arises from neuromuscular dysfunction of the stomach, involving the interstitial cells of Cajal (the "pacemakers" of the gut), the enteric nervous system, and the vagus nerve. The most common etiologies include diabetes mellitus (diabetic gastroparesis), post-surgical complications (iatrogenic), and idiopathic cases where the underlying cause remains unknown.

The clinical presentation is dominated by symptoms of upper gastrointestinal distress, including nausea, vomiting, early satiety, and postprandial fullness. In diabetic patients, the mechanism is often linked to chronic hyperglycemia, which induces oxidative stress and autonomic neuropathy, leading to antral hypomotility and pylorospasm. For a detailed analysis of the clinical burden and therapeutic landscape, the Gastroparesis Treatment Market overview provides a technical breakdown of current drug classes. The resulting malnutrition and glycemic instability create a cyclical health decline that requires aggressive clinical intervention.

Beyond the stomach, gastroparesis affects systemic health through fluid and electrolyte imbalances. Severe cases can lead to the formation of "bezoars"—solid masses of undigested food that can cause secondary obstructions. Understanding the cellular-level changes, such as the loss of neuronal nitric oxide synthase, is critical for the development of targeted therapies that aim to restore the natural motility of the gastric antrum and coordinate pyloric relaxation.