Both before and after treatment, achalasia patients may need to eat slowly, chew very well, drink plenty of water with meals, and avoid eating near bedtime. Raising the head off the bed or sleeping with a wedge pillow promotes emptying of the esophagus by gravity. After surgery or pneumatic dilatation, proton pump inhibitors are required to prevent reflux damage by inhibiting gastric acid secretion, and foods that can aggravate reflux, including ketchup, citrus, chocolate, alcohol, and caffeine, may need to be avoided.

Drugs that reduce LES pressure are useful. These include calcium channel blockers such as nifedipine and nitrates such as isosorbide dinitrate and nitroglycerin. However, many patients experience unpleasant side effects such as headache and swollen feet, and these drugs often stop helping after several months.

Botulinum toxin (Botox) may be injected into the lower esophageal sphincter to paralyze the muscles holding it shut. As in the case of cosmetic Botox, the effect is only temporary and lasts about 6 months. Botox injections cause scarring in the sphincter which may increase the difficulty of later Heller myotomy. This therapy is recommended only for patients who cannot risk surgery, such as elderly people in poor health. Pneumatic dilatation has a better long term effectiveness than botox.

Nutcracker esophagus is a benign, nonprogressive condition, meaning it is not associated with significant complications. Patients are usually reassured by their physicians that the disease is unlikely to worsen. However, the symptoms of chest pain and dysphagia may be severe enough to require treatment with medications, and rarely, surgery.

The initial step of treatment focuses on reducing risk factors. While weight reduction may be useful in reducing symptoms, the role of acid suppression therapy to reduce esophageal reflux is still uncertain. Very cold and very hot beverages may trigger esophageal spasms.

Medical therapy for nutcracker esophagus includes the use of calcium-channel blockers, which relax the lower esophageal sphincter (LES) and palliate the dysphagia symptoms. Diltiazem, a calcium-channel blocker, has been used in randomized control studies with good effect. Nitrate medications, including isosorbide dinitrate, given before meals, may also help relax the LES and improve symptoms. The inexpensive generic combination of belladonna and phenobarbital (Donnatal and other brands) may be taken three times daily as a tablet to prevent attacks or, for patients with only occasional episodes, as an elixir at the onset of symptoms. Phosphodiesterase inhibitors, such as sildenafil, can be given to reduce symptoms, particularly pain, but small trials have not been able to demonstrate clinical improvement. Finally, trazodone, an antidepressant that reduces visceral sensitivity, has also been shown to reduce chest pain symptoms in patients with nutcracker esophagus.

Endoscopic therapy with botulinum toxin, known also as Botox, can also be used to improve dysphagia which stabilizes unintentional weight loss, but the effect has limited effect on other symptoms, including pain, while also being a temporary treatment lasting a few weeks. Finally, pneumatic dilatation of the esophagus, which is an endoscopic technique where a high-pressure balloon is used to stretch the muscles of the LES, can be performed to improve symptoms, but again no clinical improvement is seen in regards to motility.

In patients who have no response to medical or endoscopic therapy, surgery can be performed. A Heller myotomy involves an incision to disrupt the LES and the myenteric plexus that innervates it. The Heller myotomy is used as a final treatment option in patients who do not respond to other therapies.

The patient is generally sent for a GI, pulmonary, or ENT, depending on the suspected underlying cause. Consultations with a speech therapist and registered dietitian nutritionist (RDN) are also needed, as many patients may need dietary modifications such as thickened fluids.

In the great majority of cases, sufferers experience no life-altering discomfort, and no treatment is required. If there is pain or discomfort, 3 or 4 sips of room temperature water will usually relieve the pain. Symptomatic patients should elevate the head of their beds and avoid lying down directly after meals. If the condition has been brought on by stress, stress reduction techniques may be prescribed, or if overweight, weight loss may be indicated. Antisecretory drugs like proton pump inhibitors and H receptor blockers can be used to reduce acid secretion. Medications that reduce the lower esophageal sphincter (LES) pressure should be avoided.

However, in some unusual instances, as when the hiatal hernia is unusually large, or is of the paraesophageal type, it may cause esophageal stricture or severe discomfort. About 5% of hiatus hernias are paraesophageal. If symptoms from such a hernia are severe for example if chronic acid reflux threatens to severely injure the esophagus or is causing Barrett's esophagus, surgery is sometimes recommended. However surgery has its own risks including death and disability, so that even for large or paraesophageal hernias, watchful waiting may on balance be safer and cause fewer problems than surgery. Complications from surgical procedures to correct a hiatus hernia may include gas bloat syndrome, dysphagia (trouble swallowing), dumping syndrome, excessive scarring, and rarely, achalasia. Surgical procedures sometimes fail over time, requiring a second surgery to make repairs.

One surgical procedure used is called Nissen fundoplication. In fundoplication, the gastric fundus (upper part) of the stomach is wrapped, or plicated, around the inferior part of the esophagus, preventing herniation of the stomach through the hiatus in the diaphragm and the reflux of gastric acid. The procedure is now commonly performed laparoscopically. With proper patient selection, laparoscopic fundoplication recent studies have indicated relatively low complication rates, quick recovery, and relatively good long term results.

It is not clear exactly what causes esophageal spasms. Sometimes esophageal spasms start when someone eats hot or cold foods or drinks. However, they can also occur with eating or drinking. The increased release of acetylcholine may also be a factor, but the triggering event is not known.

If there is dysphagia to both solids and liquids, then it is most likely a motility problem. If there is dysphagia initially to solids but progresses to also involve liquids, then it is most likely a mechanical obstruction. Once a distinction has been made between a motility problem and a mechanical obstruction, it is important to note whether the dysphagia is intermittent or progressive. An intermittent motility dysphagia likely can be diffuse esophageal spasm (DES) or nonspecific esophageal motility disorder (NEMD). Progressive motility dysphagia disorders include scleroderma or achalasia with chronic heartburn, regurgitation, respiratory problems, or weight loss. Intermittent mechanical dysphagia is likely to be an esophageal ring. Progressive mechanical dysphagia is most likely due to peptic stricture or esophageal cancer.

Esophageal spasm or oesophageal spasm is a disorder of esophageal motility. The esophagus is an organ in vertebrates which consists of a fibromuscular tube through which food passes, aided by peristalsis contractions, from the upper esophageal sphincter to the stomach through waves of coordinated muscle contraction, or peristalsis.

There are two types of esophageal spasm:

- Diffuse esophageal spasm (DES), where there is uncoordinated esophageal contractions where several sections of the esophagus can contract at once.

- Nutcracker esophagus (NE) also known as hypertensive peristalsis, where the contractions are coordinated but with an excessive amplitude.

Both conditions can be linked with Gastroesophageal reflux disease (GERD).

When the coordinated muscle contraction are irregular or uncoordinated, this condition may be called diffuse esophageal spasm. These spasms can prevent food from reaching the stomach where food gets stuck in the esophagus. At other times the coordinated muscle contraction is very powerful, which is called nutcracker esophagus. These contractions move food through the esophagus but can cause severe pain.

Esophageal diseases can derive from congenital conditions, or they can be acquired later in life.

Many people experience a burning sensation in their chest occasionally, caused by stomach acids refluxing into the esophagus, normally called heartburn. Extended exposure to heartburn may erode the lining of the esophagus, leading potentially to Barrett's esophagus which is associated with an increased risk of adenocarcinoma most commonly found in the distal one-third of the esophagus.

Some people also experience a sensation known as globus esophagus, where it feels as if a ball is lodged in the lower part of the esophagus.

The following are additional diseases and conditions that affect the esophagus:

- Achalasia

- Acute esophageal necrosis

- Barrett's esophagus

- Boerhaave syndrome

- Caustic injury to the esophagus

- Chagas disease

- Diffuse esophageal spasm

- Esophageal atresia and Tracheoesophageal fistula

- Esophageal cancer

- Esophageal dysphagia

- Esophageal varices

- Esophageal web

- Esophagitis

- GERD

- Hiatus hernia

- Jackhammer esophagus (hypercontractile peristalsis)

- Killian–Jamieson diverticulum

- Mallory-Weiss syndrome

- Neurogenic dysphagia

- Nutcracker esophagus

- Schatzki's ring

- Zenker's Diverticulum

Megaesophagus may occur secondary to diseases such as achalasia or Chagas disease. Achalasia is caused by a loss of ganglion cells in the myenteric plexus. There is a marked lack of contraction within the muscles involved in peristalsis with a constant contraction of the lower esophageal sphincter. Dilation of the esophagus results in difficulty swallowing. Retention of food bolus is also noted.

Megaesophagus can also be a symptom of the disease myasthenia gravis. Myasthenia gravis is a neuromuscular disease where the primary symptom is weakness in various body parts of the dog. However, when myasthenia gravis occurs in older dogs it is thought of as an immune-mediated disease. Often when myasthenia gravis is diagnosed in older dogs the first symptom the dog may manifest is megaesophagus.

Myasthenia gravis occurs when acetylcholine receptors (nicotinic acetylcholine receptors) fail to function properly, so that the muslce is not stimulated to contract.

A hiatus hernia is a type of hernia in which abdominal organs (typically the stomach) slip through the diaphragm into the middle compartment of the chest. This may result in gastroesophageal reflux disease (GERD) or laryngopharyngeal reflux (LPR) with symptoms such as a taste of acid in the back of the mouth or heartburn. Other symptoms may include trouble swallowing and chest pains. Complications may include iron deficiency anemia, volvulus, or bowel obstruction.

The most common risk factors are obesity and older age. Other risk factors include major trauma, scoliosis, and certain types of surgery. There are two main types: a sliding hernia, in which the body of the stomach moves up, and a paraesophageal hernia, in which an abdominal organ moves beside the esophagus. The diagnosis may be confirmed with endoscopy or medical imaging. Endoscopy is typically only required when concerning symptoms are present, symptoms are resistant to treatment, or the person is over 50 years of age.

Symptoms from a hiatus hernia may be improved by changes such as raising the head of the bed, weight loss, and adjusting eating habits. Medications that reduce gastric acid such as H2 blockers or proton pump inhibitors may also help with the symptoms although they can also create significant side effects. If the condition does not improve with medications, a surgery to carry out a laparoscopic fundoplication may be an option. Between 10% and 80% of people in the United States are affected.

Diseases of the hepatobiliary system affect the biliary tract (also known as the "biliary tree"), which secretes bile in order to aid digestion of fats. Diseases of the gallbladder and bile ducts are commonly diet-related, and may include the formation of gallstones that impact in the gallbladder (cholecystolithiasis) or in the common bile duct (choledocholithiasis).

Gallstones are a common cause of inflammation of the gallbladder, called cholecystitis. Inflammation of the biliary duct is called cholangitis, which may be associated with autoimmune disease, such as primary sclerosing cholangitis, or a result of bacterial infection, such as ascending cholangitis.

Disease of the biliary tree may cause pain in the upper right abdomen, particularly when pressed. Disease might be investigated using ultrasound or ERCP, and might be treated with drugs such as antibiotics or UDCA, or by the surgical removal of the gallbladder.

Gastric diseases refer to diseases affecting the stomach. Inflammation of the stomach by infection from any cause is called gastritis, and when including other parts of the gastrointestinal tract called gastroenteritis. When gastritis persists in a chronic state, it is associated with several diseases, including atrophic gastritis, pyloric stenosis, and gastric cancer. Another common condition is gastric ulceration, peptic ulcers. Ulceration erodes the gastric mucosa, which protects the tissue of the stomach from the stomach acids. Peptic ulcers are most commonly caused by a bacterial "Helicobacter pylori" infection.

As well as peptic ulcers, vomiting blood may result from abnormal arteries or veins that have ruptured, including Dieulafoy's lesion and Gastric antral vascular ectasia. Congenital disorders of the stomach include pernicious anaemia, in which a targeted immune response against parietal cells results in an inability to absorb vitamin B12. Other common symptoms that stomach disease might cause include indigestion or dyspepsia, vomiting, and in chronic disease, digestive problems leading to forms of malnutrition. In addition to routine tests, an endoscopy might be used to examine or take a biopsy from the stomach.

Antiparasitic treatment is most effective early in the course of infection, but is not limited to cases in the acute phase. Drugs of choice include azole or nitro derivatives, such as benznidazole or nifurtimox. Both agents are limited in their capacity to completely eliminate "T. cruzi" from the body (parasitologic cure), especially in chronically infected patients, and resistance to these drugs has been reported.

Studies suggest antiparasitic treatment leads to parasitological cure in more than 90% of infants but only about 60–85% of adults treated in the first year of acute phase Chagas disease. Children aged six to 12 years with chronic disease have a cure rate of about 60% with benznidazole. While the rate of cure declines the longer an adult has been infected with Chagas, treatment with benznidazole has been shown to slow the onset of heart disease in adults with chronic Chagas infections.

Treatment of chronic infection in women prior to or during pregnancy does not appear to reduce the probability the disease will be passed on to the infant. Likewise, it is unclear whether prophylactic treatment of chronic infection is beneficial in persons who will undergo immunosuppression (for example, organ transplant recipients) or in persons who are already immunosuppressed (for example, those with HIV infection).

There are two approaches to treating Chagas disease: antiparasitic treatment, to kill the parasite; and symptomatic treatment, to manage the symptoms and signs of the infection. Management uniquely involves addressing selective incremental failure of the parasympathetic nervous system. Autonomic disease imparted by Chagas may eventually result in megaesophagus, megacolon and accelerated dilated cardiomyopathy. The mechanisms that explain why Chagas targets the parasympathetic autonomic nervous system and spares the sympathetic autonomic nervous system remain poorly understood.

A stenosis is an abnormal narrowing in a blood vessel or other tubular organ or structure. It is also sometimes called a stricture (as in urethral stricture).

Stricture as a term is usually used when narrowing is caused by contraction of smooth muscle (e.g., achalasia, prinzmetal angina); stenosis is usually used when narrowing is caused by lesion that reduces the space of lumen (e.g., atherosclerosis). The term coarctation is another synonym, but is commonly used only in the context of aortic coarctation.

Restenosis is the recurrence of stenosis after a procedure. The term is from Ancient Greek στενός, "narrow".

The resulting syndrome depends on the structure affected.

Examples of vascular stenotic lesions include:

- Intermittent claudication (peripheral artery stenosis)

- Angina (coronary artery stenosis)

- Carotid artery stenosis which predispose to (strokes and transient ischaemic episodes)

- Renal artery stenosis

The types of stenoses in heart valves are:

- Pulmonary valve stenosis, which is the thickening of the pulmonary valve, therefore causing narrowing

- Mitral valve stenosis, which is the thickening of the mitral valve (of the left heart), therefore causing narrowing

- Tricuspid valve stenosis, which is the thickening of the tricuspid valve (of the right heart), therefore causing narrowing

- Aortic valve stenosis, which is the thickening of the aortic valve, therefore causing narrowing

Stenoses/strictures of other bodily structures/organs include:

- Pyloric stenosis (gastric outflow obstruction)

- Lumbar, cervical or thoracic spinal stenosis

- Subglottic stenosis (SGS)

- Tracheal stenosis

- Obstructive jaundice (biliary tract stenosis)

- Bowel obstruction

- Phimosis

- Non-communicating hydrocephalus

- Stenosing tenosynovitis

- Atherosclerosis

- Esophageal stricture

- Achalasia

- Prinzmetal angina

- Vaginal stenosis

There is no cure for this disease. Drugs such as antiplatelet agents (including aspirin) are usually given to prevent clots, but surgery is usually recommended. Since moyamoya tends to affect only the internal carotid artery and nearby sections of the adjacent anterior and middle cerebral arteries, surgeons can direct other arteries, such as the external carotid artery or the superficial temporal artery to replace its circulation. The arteries are either sewn directly into the brain circulation, or placed on the surface of the brain to reestablish new circulation after a few weeks.

There are many operations that have been developed for the condition, but currently the most favored are the in-direct procedures EDAS, EMS, and multiple burr holes and the direct procedure STA-MCA. Direct superficial temporal artery (STA) to middle cerebral artery (MCA) bypass is considered the treatment of choice, although its efficacy, particularly for hemorrhagic disease, remains uncertain. Multiple burr holes have been used in frontal and parietal lobes with good neovascularisation achieved.

The EDAS (encephaloduroarteriosynangiosis) procedure is a synangiosis procedure that requires dissection of a scalp artery over a course of several centimeters and then making a small temporary opening in the skull directly beneath the artery. The artery is then sutured to a branch of the middle cerebral artery on the surface of the brain and the bone is replaced.

In the EMS (encephalomyosynangiosis) procedure, the temporalis muscle, which is in the temple region of the forehead, is dissected and through an opening in the skull placed onto the surface of the brain.

In the multiple burr holes procedure, multiple small holes (burr holes) are placed in the skull to allow for growth of new vessels into the brain from the scalp.

In the STA-MCA procedure, the scalp artery (superficial temporal artery or STA) is directly sutured to an artery on the surface of the brain (middle cerebral artery or MCA). This procedure is also commonly referred to as an EC-IC (External Carotid-Internal Carotid) bypass.

All of these operations have in common the concept of a blood and oxygen "starved" brain reaching out to grasp and develop new and more efficient means of bringing blood to the brain and bypassing the areas of blockage. The modified direct anastomosis and encephalo-myo-arterio-synangiosis play a role in this improvement by increasing cerebral blood flow (CBF) after the operation. A significant correlation is found between the postoperative effect and the stages of preoperative angiograms. It is crucial for surgery that the anesthesiologist have experience in managing children being treated for moyamoya, as the type of anesthesia they require is very different from the standard anesthetic children get for almost any other type of neurosurgical procedure.

Some of the most up to date treatments for Moyamoya are explained by top rated surgeons at Boston Children's Hospital in Massachusetts in these

The natural history of this disorder is not well known. The long term outlook for patients with treated moyamoya seems to be good. While symptoms may seem to improve almost immediately after the in-direct EDAS, EMS, and multiple burr holes surgeries, it will take probably 6–12 months before new vessels can develop to give a sufficient blood supply. With the direct STA-MCA surgery, increased blood supply is immediate.

Once major stroke or bleeding take place, even with treatment, the patient may be left with permanent loss of function so it is very important to treat this condition promptly.

Dr. Michael Scott, MD discusses the success rate for Moyamoya surgery in

Some of the differential or comorbid medical diagnoses may include:

- achalasia – There have been cases where achalasia, a disorder of the esophagus which affects peristalsis, has been misdiagnosed as AN. It has been reported in cases where there is sub-clinical manifestation of anorexia nervosa and also in cases where the full diagnostic criteria AN have been met.

- acute pandysautonomia is one form of an autonomic neuropathy, which is a collection of various syndromes and diseases which affect the autonomic neurons of the autonomic nervous system (ANS). Autonomic neuropathies may be the result of an inherited condition or they may be acquired due to various premorbid conditions such as diabetes and alcoholism, bacterial infection such as Lyme disease or a viral illness. Some of the symptoms of ANS which may be associated with an ED include nausea, dysphagia, constipation, pain in the salivary glands, early saiety. It also affects peristalsis in the stomach. Acute pandysautonomia may cause emotional instability and has been misdiagnosed as various psychiatric disorders including hysterical neurosis and anorexia nervosa.

- Lupus: various neuropsychiatric symptoms are associated with systemic lupus erythematosus (SLE), including depression. Anorexia and weight loss also may occur with SLE and while rare it may be misdiagnosed as AN.

- Lyme disease is known as the "great imitator", as it may present as a variety of psychiatric or neurologic disorders including anorexia nervosa. "A 12 year old boy with confirmed Lyme arthritis treated with oral antibiotics subsequently became depressed and anorectic. After being admitted to a psychiatric hospital with the diagnosis of anorexia nervosa, he was noted to have positive serologic tests for Borrelia burgdorferi. Treatment with a 14 day course of intravenous antibiotics led to a resolution of his depression and anorexia; this improvement was sustained on 3 year follow-up." Serologic testing can be helpful but should not be the sole basis for diagnosis. The Centers for Disease Control (CDC) issued a cautionary statement (MMWR 54;125) regarding the use of several commercial tests. Clinical diagnostic criteria have been issued by the CDC (CDC, MMWR 1997; 46: 531-535).

- Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) is a rare genetic disorder characterized by gastrointestinal dysmotility, severe cachexia progressive external ophthalmoplegia, post-prandial emesis (vomiting after eating), peripheral neuropathy, and diffuse leukoencephalopathy. Onset is prior to age 20 in 60% of cases. ""Miss A" was a 21-year-old Indian woman diagnosed as having treatment-resistant anorexia nervosa." It was subsequently proven to be MNGIE

- superior mesenteric artery syndrome (SMA syndrome) "is a gastrointestinal disorder characterized by the compression of the third or transverse portion of the duodenum against the aorta by the superior mesenteric artery resulting in chronic partial, incomplete, acute or intermittent duodenal obstruction". It may occur as a complication of AN or as a differential diagnosis. There have been reported cases of a tentative diagnosis of AN, where upon treatment for SMA syndrome the patient is asymptomatic.

- Addison's disease is a disorder of the adrenal cortex which results in decreased hormonal production. Addison's disease, even in subclinical form, may mimic many of the symptoms of anorexia nervosa.

- Brain tumors: There are multiple cases were the neuropsychiatric symptoms of a brain tumor were attributed to AN, resulting in misdiagnosis. The tumors in these cases were noted in various regions of the brain including the medulla oblongata, hypothalamus, pituitary gland, pineal gland and the obex.

- Simmond's disease (organic hypopituitarism) – "A 20-year-old Japanese man with a hypothalamic tumor which caused hypopituitarism and diabetes insipidus was mistakenly diagnosed as anorexia nervosa because of anorexia, weight loss, denial of being ill, changes in personality, and abnormal behavior resembling the clinical characteristics of anorexia nervosa"

- Brain calcification either dystrophic calcification or metastatic calcification can present with neuropsychiatric symptoms including those associated with AN and comorbid disorders such as obsessive compulsive disorder.

- cysts that occur in the central nervous system such as dermoid cysts and arachnoid cysts can cause neuropsychiatric symptoms including psychosis.

- Celiac disease is an inflammatory disorder triggered by peptides from wheat and similar grains which cause an immune reaction in the small intestine. "information on the role of the gastrointestinal system in causing or mimicking eating disorders is scarce."(Leffler DA "et al.")

- Gall bladder disease which may be caused by inflammation, infection, gallstones, obstruction of the gallbladder or torsion of the gall bladder – Many of the symptoms of gall bladder disease may mimic anorexia nervosa (AN). Laura Daly, a woman from Missouri, suffered from an inherited disorder in which the gall bladder was not properly attached; the resultant complications led to multiple erroneous diagnoses of AN. Upon performance of a CCK test, standard imaging techniques are done with the patient lying prone, in this instance it was done with the patient in an upright position. The gall bladder was shown to be in an abnormal position having flipped over the liver. The gallbladder was removed and the patient has since recovered. The treatment was performed by William P. Smedley in Pennsylvania.

- colonic tuberculosis misdiagnosed as anorexia nervosa in a physician at the hospital where she worked – "This patient, who had severe wasting, was misdiagnosed as having anorexia nervosa despite the presence of other symptoms suggestive of an organic disease, namely, fever and diarrhea"(Madani, A 2002).

- Crohn's disease: "We report three cases of young 18 to 25 year-old girls, initially treated for anorexia nervosa in a psychiatric department. Diagnosis of Crohn's disease was made within 5 to 13 years."(Blanchet C, Luton JP. 2002)"This disease should be diagnostically excluded before accepting anorexia nervosa as final diagnosis". (Wellmann W "et al.")

- hypothyroidism, hyperthyroidism, hypoparathyroidism and hyperparathyroidism may mimic some of the symptoms of, can occur concurrently with, be masked by or exacerbate an eating disorder and/or various comorbid disorders such as anxiety and depression.

- Insulinomas are (pancreatic tumors) that cause an overproduction of insulin, causing hypoglycemia. Various neurological deficits have been ascribed to this condition including misdiagnosis as an eating disorder.

- Multiple sclerosis (encephalomyelitis disseminata) is a progressive autoimmune disorder in which the protective covering (myelin sheath) of nerve cells is damaged as a result of inflammation and resultant attack by the bodies own immune system. In its initial presentation, MS has been misdiagnosed as an eating disorder.

Triple-A syndrome or AAA syndrome, also known as achalasia-addisonianism-alacrima syndrome or Allgrove syndrome, is a rare autosomal recessive congenital disorder. In most cases, there is no family history of it. The syndrome was first identified by Jeremy Allgrove and colleagues in 1978. The syndrome involves achalasia, addisonianism (adrenal insufficiency of primary type), and alacrima (insufficiency of tears). Alacrima is usually the earliest manifestation. It is a progressive disorder that can take years to develop the full blown clinical picture.

The differential diagnoses of anorexia nervosa (AN) includes various types of medical and psychological conditions, which may be misdiagnosed as AN. In some cases, these conditions may be comorbid with AN because the misdiagnosis of AN is not uncommon. For example, a case of achalasia was misdiagnosed as AN and the patient spent two months confined to a psychiatric hospital. A reason for the differential diagnoses that surround AN arise mainly because, like other disorders, it is primarily, albeit defensively and adaptive for, the individual concerned.

Anorexia Nervosa is a psychological disorder characterized by extremely reduced intake of food. People suffering from Aneroxia Nervosa have a low self-image and consider themselves overweight.

Common behaviors and signs of someone suffering from AN:

- Forcing oneself to vigorously exercise even in adverse conditions or when their health does not permit it.

- Forcing own self to urinate and excrete waste product from the body.

- Using substituted amphetamines (stimulants that can reduce appetite) to reduce appetite.

- Skin turning yellow

Individuals affected by AAA have adrenal insufficiency/Addison's disease due to ACTH resistance, alacrima (absence of tear secretion), and achalasia (a failure of a ring of muscle fibers, such as a sphincter, to relax) of the lower esophageal sphincter at the cardia which delays food going to the stomach and causes dilation of the thoracic esophagus. There may also be signs of autonomic dysfunction with AAA, such as pupillary abnormalities, an abnormal reaction to intradermal histamine, abnormal sweating, orthostatic hypotension, and disturbances of the heart rate. Hypoglycemia (low blood sugar) is often mentioned as an early sign. The disorder has also been associated with mild mental retardation.

The syndrome is highly variable. Managed effectively, affected individuals can have a normal lifespan and bear children.