Causes

Gastroparesis may be chronic or transient; transient gastroparesis may arise in acute illness of any kind, with the use of certain cancer treatments or other drugs which affect digestive action, or due to anorexia nervosa, bulimia and other abnormal eating patterns.

Chronic gastroparesis is frequently due to autonomic neuropathy. This may occur in people with type 1 diabetes or type 2 diabetes. The vagus nerve becomes damaged by years of high blood glucose, resulting in gastroparesis. Gastroparesis has also been associated with various autoimmune diseases and syndromes, such as fibromyalgia and Parkinson's disease, and may occur as part of a mitochondrial disorder.

Chronic gastroparesis can also be caused by other types of damage to the vagus nerve, such as abdominal surgery.

Idiopathic gastroparesis (gastroparesis with no known cause) accounts for a third of all chronic cases; it is thought that many of these cases are due to an autoimmune response triggered by an acute viral infection. "Stomach flu", mononucleosis, and others have been anecdotally linked to the onset of the condition, but no systematic study has proven a link.

Gastroparesis sufferers are disproportionately female. One possible explanation for this finding is that women have an inherently slower stomach emptying time than men. A hormonal link has also been suggested, as gastroparesis symptoms tend to worsen the week before menstruation, when progesterone levels are highest. Neither theory has been proven definitively.

Signs and Symptoms

The most common symptoms of gastroparesis are:

• Chronic nausea
• Vomiting (especially of undigested food)
• Early satiety

Other symptoms include:

• Heartburn
• Weight loss
• Abdominal bloating
• Erratic blood glucose levels
• Lack of appetite
• Gastroesophageal reflux
• Spasms of the stomach wall
• Morning nausea may also indicate gastroparesis. It is important to note that vomiting may not occur in all cases, as sufferers may learn to adjust their diets to include only small amounts of food.

Diagnosis and Treatment

Gastroparesis can be diagnosed with tests such as x rays, manometry, and gastric emptying scans. The clinical definition for gastroparesis is based solely on the emptying time of the stomach and not on other symptoms, and severity of symptoms does not necessarily correlate with the severity of gastroparesis. Therefore, some patients may have marked gastroparesis with few, if any, serious complications.

Treatment includes dietary changes (low-fiber and low-residue diets, and in some cases, restrictions on fat and/or solids), oral medications such as Metoclopramide (Reglan, Maxolon, Clopra), Cisapride (Propulsid), Erythromycin (E-Mycin, Erythrocin, Ery-Tab, EES) and Domperidone (Motilium); adjustments in insulin dosage for those with diabetes, a jejunostomy tube, parenteral nutrition, implanted gastric neurostimulators ("stomach pacemakers"), or botulinum toxin.

Viagra, which increases blood flow to the genital area, is also being used by some practitioners to stimulate the GI tract in diabetic gastroparesis.

The antidepressant Mirtazapine has also proven effective in the treatment of gastroparesis unresponsive to conventional treatment. This is due to its anti-emetic and appetite stimulant properties. Mirtazapine acts on the same serotonin receptor (5-HT3) as the popular anti-emetic Ondansetron.

Complications

Primary complications of gastroparesis include:

• Fluctuations in blood glucose due to unpredictable digestion times (in diabetic patients)
• General malnutrition due to the symptoms of the disease (which frequently include vomiting and reduced appetite) as well as the dietary changes necessary to manage it
• Severe fatigue and weight loss due to calorie deficit
• Intestinal obstruction due to the formation of bezoars (solid masses of undigested food)
• Bacterial infection due to overgrowth in undigested food

Bulimia nervosa was named and first described by the British psychiatrist Gerald Russell in 1979.

Diagnosis

According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV TR) published by the American Psychiatric Association, the criteria for diagnosing a patient with bulimia are:

• Recurrent episodes of binge eating. An episode of binge eating is characterized by both of the following:
• Eating, in a fixed period of time, an amount of food that is definitely larger than most people would eat under similar circumstances. Mainly eating binge foods.
• A lack of control over eating during the episode: a feeling that one cannot stop eating or control what or how much one is eating.
• Recurrent inappropriate compensatory behavior to prevent weight gain, such as: self-induced vomiting; misuse of laxatives, diuretics, or other medications; fasting; excessive exercise.
• Triggers include periods of stress, traumatic events, and self-evaluation of body shape and weight.
• These symptoms may occur after every meal, on a daily basis, or once every few months.
• The disturbance does not occur exclusively during episodes of anorexia nervosa.

There are two sub-types of bulimia nervosa:

• Purging type bulimics self-induce vomiting (usually by triggering the gag reflex or ingesting emetics such as syrup of ipecac) to rapidly remove food from the body before it can be digested, or use laxatives, diuretics, or enemas.
• Non-purging type bulimics (approximately 6%-8% of cases) exercise or fast excessively after a binge to offset the caloric intake after eating. Purging-type bulimics may also exercise or fast, but as a secondary form of weight control.

The onset of bulimia nervosa is often during adolescence (between 13 and 20 years of age) and many cases have previously suffered obesity, with many sufferers relapsing in adulthood into episodic binging and purging even after initially successful treatment and remission.

Bulimia nervosa can be difficult to detect, compared to anorexia nervosa, because bulimics tend to be of average or slightly above or below average weight. Many bulimics may also engage in significantly disordered eating and exercising patterns without meeting the full diagnostic criteria for bulimia nervosa.

Effects

These cycles often involve rapid and out-of-control eating, which may stop when the bulimic is interrupted by another person or the stomach hurts from overextension, followed by self-induced vomiting or other forms of purging. This cycle may be repeated several times a week or, in more serious cases, several times a day, and may directly cause:

• Chronic gastric reflux after eating
• Dehydration and hypokalemia caused by frequent vomiting
• Electrolyte imbalance, which can lead to cardiac arrhythmia, cardiac arrest, and even death
• Esophagitis, or inflammation of the esophagus
• Oral trauma, in which repetitive insertion of fingers or other objects causes lacerations to the lining of the mouth or throat
• Gastroparesis or delayed emptying
• Constipation
• Enlarged glands in the neck, under the jaw line
• Peptic ulcers
• Calluses or scars on back of hands due to repeated trauma from incisors
• Constant weight fluctuations

The frequent contact between teeth and gastric acid, in particular, may cause:

• Severe caries
• Perimolysis, or the erosion of tooth enamel
• Swollen salivary glands

Related disorders

Bulimics are much more likely than non-bulimics to have an affective disorder, such as depression or general anxiety disorder: A 1985 Columbia University study on female bulimics at New York State Psychiatric Institute found 70% had suffered depression some time in their lives (as opposed to 25.8% for adult females in a control sample from the general population), rising to 88% for all affective disorders combined. Another study by the Royal Children's Hospital in Melbourne on a cohort of 2000 adolescents similarly found that those meeting at least two of the DSM-IV criteria for bulimia nervosa or anorexia nervosa had a sixfold increase in risk of anxiety and a doubling of risk for substance dependency. Bulimia also has negative effects on the sufferer's dental health due to the acid passed through the mouth from frequent vomiting causing acid erosion, mainly on the posterior dental surface.

Treatment

Pharmacological

Some researchers have hypothesized a relationship to mood disorders and clinical trials have been conducted with tricyclic antidepressants, MAO inhibitors, mianserin, fluoxetine, lithium carbonate, nomifensine, trazodone, and bupropion.

Research groups who have seen a relationship to seizure disorders have attempted treatment with phenytoin, carbamazepine, and valproic acid. Opiate antagonists naloxone and naltrexone, which block cravings for gambling, have also been used.

There has also been some research characterizing bulimia nervosa as an addiction disorder, and limited clinical use of topiramate, which blocks cravings for opiates, cocaine, alcohol and food. Researchers have also report positive outcomes when bulimics are treated in an addiction-disorders inpatient unit.

Brain-derived neurotrophic factor (BDNF) is also under investigation as a possible cause.

Psychotherapy

There are several empirically-supported psychosocial treatments for bulimia nervosa. Cognitive behavioral therapy (CBT), which involves teaching clients to challenge automatic thoughts and engage in behavioral experiments (e.g., in session eating of "forbidden foods") has demonstrated efficacy both with and without concurrent antidepressant medication. Researchers have also reported some positive outcomes for interpersonal psychotherapy and dialectical behavior therapy.

Some researchers have also claimed positive outcomes in hypnotherapy treatment.