Gastroparesis and Functional Dyspepsia
Gastroparesis (GP) and functional dyspepsia (FD) are two of the most common gastric neuromuscular disorders. Disruption of the gastric sensorimotor function is the main factor in the pathogenesis (or development) of upper gastrointestinal symptoms (Tack, 2009). Sensorimotor function encompasses all sensory and motor elements necessary for an individual to interact with their environment (Kalaitzakis, 2007).
These disorders may often be confused, as they have many similarities and differences. Some symptoms include delayed gastric emptying (contents leaving the stomach and moving to the intestine), gastric hypersensitivity, and impaired accommodation of the stomach (leading to feeling full prematurely). The epidemiological and pathophysiological overlap between FD and GP can cause an incorrect diagnosis (Tack, 2009).
Even though considerable progress has been made in the neuromuscular dysfunctions and the gastric sensorimotor dysfunctions of these diseases, more research is required to better understand the etiology and relationship between the dysfunctions and symptoms (Parkman, 2010).
Definitions of the Disorders
Let’s take a look at the definitions of these two ailments.
The definition of gastroparesis is mainly characterized by delayed gastric emptying in the absence of mechanical obstruction (Parkman, 2014).
The Rome IV diagnostic criteria defines functional dyspepsia as the presence of one or more of the following symptoms:
- Postprandial fullness (a prolonged feeling of food remaining in the stomach)
- Early satiation (feeling full quickly after eating only a little)
- Epigastric pain (discomfort below your ribs, in the area of your upper abdomen)
It is also worth noting that there is no evidence of structural disease to explain the symptoms (Stanghellini et al., 2016).
Etiology of gastroparesis and functional dyspepsia
Etiology is used to describe the cause (or causes) of disease. Let’s take a look at the etiology for gastroparesis and functional dyspepsia.
The etiology of gastroparesis is multifactorial, with the key triggers being diabetes mellitus, post-gastric surgery, and disorders of idiopathic origin (meaning the cause is unknown) (Liu, 2017). The most common causes of gastroparesis are neuropathic disorders, including diabetes mellitus, post-vagotomy (a surgery removing part of the vagus nerve), scleroderma (hardening and tightening of the skin and connective tissues), and myopathic diseases (diseases affecting the muscles that control voluntary movement in the body).
Other causes include connective tissue diseases, Parkinson disease, eating disorders, and medications. That being said, an underlying cause cannot be established in approximately 50% of patients classified as having idiopathic GP.
Similar to gastroparesis, the etiology of functional dyspepsia is diverse among patients. While it can be attributed to genetic predisposition in some patients, a prior viral infection, stress, inflammation, surgery, or trauma can be another cause in other patients. Additionally, although no clear cause-effect relationship has been established, hormonal influences can also affect symptoms in some patients with FD.
Pathophysiology is essentially the functional changes that accompany a particular syndrome or disease. Abnormalities of the gastric sensorimotor function identified in both gastroparesis and functional dyspepsia. In addition to delayed gastric emptying, these shared abnormalities can include hypersensitivity to gastric distension (stomach stretching after eating), abnormal intestinal motility, and central nervous system dysfunction (Tack, 2009).
Although the pathophysiology of gastroparesis has yet to be fully explained, known abnormalities include vagal neuropathy (damage to the vagal nerve) and disorders of intrinsic and extrinsic neuropathy, such as diabetes mellitus and viral infection. Interstitial cells of Cajal, which regulate smooth muscle contractions, are also negatively affected. This is a large reason that intestinal motility loses effectiveness.
Most of the pathophysiology of functional dyspepsia overlaps with gastroparesis, but visceral hypersensitivity is fairly unique to FD. Visceral hypersensitivity is the experience of pain within the inner organs at a level that is more intense than normal.
The pathophysiological results we discussed do not necessarily predict the symptoms of gastroparesis and functional dyspepsia, and conversely, investigators have questioned whether symptoms can be used to predict underlying pathophysiology. Some symptoms common to both diseases, like epigastric fullness, nausea, and vomiting, have been associated with delayed gastric emptying (Sarnelli, 2003). Many reports describe the poor relationship between gastric emptying and symptoms; however, the responsiveness of these symptoms to therapeutic interventions (treatment) more convincingly supports the relationship between pathophysiology and symptoms.
Both gastroparesis and functional dyspepsia overlap with each other in regards to sensory dysfunction, but tests for these abnormalities are very limited. Ultimately, there are no validated algorithms for the diagnosis of GP and FD.
While this is problematic, it is critical to clearly distinguish patients with FD from those with GP. Differential diagnosis consists of two steps. First, mechanical obstruction should be excluded by imaging techniques. Second, motility abnormality should be assed using various tests, including a gastric emptying test and manometry, which tests how well the esophagus is working (Lacy, 2012).
Since the symptoms of gastric sensorimotor disorders do not discriminate functional dyspepsia from gastroparesis, patients should be treated based on their predominant symptoms (Stein, 2014). Some treatment options have a positive outcome for patients with either disease, such as dietary modification (frequent, low-fat, small meals) and pharmacological therapy (prokinetic agents, antiemetic agents, acid suppression therapy).
Dietary modification aims to restore hydration and electrolyte balance. Prokinetic agents are drugs that strengthen coordinated gastrointestinal motility and transit of content in the gastrointestinal tract. Antiemetic agents generally act by central or peripheral blockade of neurotransmitters involved in pathways that promote nausea and vomiting. Acid suppression uses an H2 receptor antagonist or proton pump inhibitor to keep acidity levels to a minimum (Camilleri, 2016).
The most important aspect presented in the current understanding of functional dyspepsia and gastroparesis is that these disorders share a similar pathogenesis in many cases, to the point that separating the two may be artificial. Current treatments for the two diseases are limited, but it is expected that the situation will substantially improve as the understanding of the pathophysiology of the two disorders broadens. Additionally, a combination of approaches such as basic research, clinical investigation, and controlled clinical trials are required to improve patient care in these conditions.
Camilleri, M. 2016. Functional Dyspepsia and Gastroparesis. https://pubmed.ncbi.nlm.nih.gov/27332558/
Kalaitzakis, E. 2007. Role of gastric sensorimotor dysfunction in gastrointestinal symptoms and energy intake in liver cirrhosis. https://pubmed.ncbi.nlm.nih.gov/17327944/
Lacy, B. 2012. Functional dyspepsia and gastroparesis: one disease or two? https://pubmed.ncbi.nlm.nih.gov/23160285/
Liu, N. 2017. Gastroparesis Updates on Pathogenesis and Management. https://pubmed.ncbi.nlm.nih.gov/28535580/
Parkman, P. et al. 2010. Gastroparesis and Functional Dyspepsia: Excerpts from the AGA/ANMS Meeting. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2892213/
Parkman, H. 2014. Idiopathic gastroparesis. https://pubmed.ncbi.nlm.nih.gov/25667023/
Sarnelli, G. 2003. Symptoms associated with impaired gastric emptying of solids and liquids in functional dyspepsia. https://pubmed.ncbi.nlm.nih.gov/12738456/
Stanghellini, V. 2016. Gastroduodenal disorders. https://pubmed.ncbi.nlm.nih.gov/27147122/
Stein, B. 2014. Treatment of functional dyspepsia and gastroparesis. https://pubmed.ncbi.nlm.nih.gov/25169218/
Tack, J. 2009. Gastric motor and sensory function. https://pubmed.ncbi.nlm.nih.gov/19726981/