Causes of Gastroparesis

The term ‘idiopathic’ means that the cause for a condition cannot be identified. This is very common in gastroparesis, with over 30% of cases being idiopathic. In these cases, the patient exhibits the signs and symptoms of gastroparesis, but the cause is not understood. Some patients with normal stomach emptying suffer from identical symptoms and are treated using the same techniques.

Post-infectious gastroparesis is also considered to be idiopathic. Post-infectious gastroparesis refers to the onset of gastroparesis symptoms after an infection (e.g. gastroenteritis, Epstein-Barr, Hawaii and Norwalk viruses, rotavirus). The patient can experience gastroparesis symptoms long after the virus has passed.

Diabetes is common among people with gastroparesis, with nearly 1 in 3 gastroparesis sufferers also having diabetes.

In diabetes, high blood glucose levels can cause nerve damage that affects stomach function. This nerve damage can slow down gastric emptying and lead to gastroparesis symptoms.

Gastroparesis symptoms can also make blood glucose levels more difficult to control.

Improving control of blood glucose is an important focus of treatment for people with diabetic gastroparesis.

Around 13% of gastroparesis cases are post-surgical. Post-surgical gastroparesis occurs when the vagus nerve is damaged or intentionally cut during surgery. The vagus nerve is a pathway of communication between the gut and the brain. The nerve may be damaged during a number of operations, including those targeting: Gastroesophageal Reflux Disease (GERD), bariatric surgery, peptic ulcers, heart or lung transplants.

The digestive tract is packed with 100+ million nerve cells that form the enteric nervous system. The enteric nervous system communicates extensively with the brain and shares similar nerve endings and chemicals that are used to relay signals and messages.

The communication between the brain and the gut is referred to as the brain-gut axis or the gut-brain axis.

The function of the brain-gut axis is to control digestion without conscious awareness. Normal digestive function requires a high degree of coordination between the gut and the brain. This involves bi-directional communication relating to

• Chemical and immune processes (e.g. inflammation)
• Microbiology (e.g. intestinal bacterial flora)
• Amount and movement of intestinal contents (e.g. distension, motility)

The relationship between the brain and the gut is complex and occurs through several pathways (e.g. vagus nerve, endocrine signals, autonomic nervous system). When communication between the brain and gut is disrupted in some way, this can lead to abnormal digestive function (e.g. hypersensitivity, abnormal gut motility).

The brain-gut axis can have a profound impact on our thoughts, feelings and behaviours. For example, feelings of gut pain or discomfort can lead to anxiety or worry. Also, as mentioned in the section on Stress, thoughts and feelings that cause stress within the body can make gastrointestinal symptoms worse. In some cases, this relationship can become a vicious cycle of deteriorating gastrointestinal and psychological health.

Comorbidity refers to the co-occurrence of two or more conditions in a person. If a condition is described as a common comorbidity of gastroparesis, it means that the condition is often experienced alongside gastroparesis.

Some of the most common comorbidities of gastroparesis are described separately in this section, however listed below are some other conditions associated with gastroparesis

• Anorexia nervosa and bulimia
• Anxiety and depression
• Gastroesophageal Reflux Disease (GERD)
• Metabolic and endocrine disorder (e.g. hypothyroidism)

In connective tissue disorders (e.g. scleroderma) the stomach muscles can degenerate and slow down gastric emptying.

Women generally have a slower rate of gastric emptying than men. Gastric emptying is also affected by the menstrual cycle and is slower during the luteal phase of the cycle, which suggests that hormones might play a role in gastroparesis.

Some hormones that are being researched in relation to gastroparesis include

• Estrogen and progesterone (important for sexual and reproductive development in women)
• Ghrelin (stimulates appetite and gastric motility)
• Motilin (stimulates contractions of the gastrointestinal tract)

A number of medications can slow down gastric emptying and lead to gastroparesis symptoms.

For example

• Pain medications (e.g. morphine, oxycodone)
• Diabetes medications (e.g. exenatide)
• Organ transplantation anti-rejection drugs (e.g. cyclosporine)

If you are experiencing medication side-effects, consult your doctor. Do not stop or reduce medication without medical advice—this may lead to deterioration in the condition that the medication was prescribed for.

Neurological conditions that may lead to gastroparesis include Parkinson’s disease, multiple sclerosis, amyloidosis, and paraneoplastic disease.

In these disorders, neurological control of the stomach can be affected, leading to delayed gastric emptying.

Psychological stress can have an impact on all systems in the body, including the gastrointestinal system.

Stress can cause the following symptoms

• Indigestion
• Abdominal pain
• Diarrhea
• Constipation
• Nausea and vomiting
• Delayed gastric emptying

Stress can also exacerbate any current symptoms—making gastroparesis symptoms more severe. Stress influences symptoms through an interaction with the brain-gut axis.