This is what esophageal achalasia is all about

Esophageal achalasia is an esophageal motility disorder, mainly caused by lack of esophageal peristalsis. The cause is still unclear, but its impact on human health is huge. Therefore, people should not take esophageal achalasia lightly.

The cause of esophageal achalasia is unknown. Some people believe that viral infection, toxins, nutritional deficiencies and local inflammation may be the causes of this disease, but no viral particles were found in electron microscopic examination of the vagus nerve and intramural plexus, which does not support the viral infection theory. Some children have a family history of the disease, suggesting that the disease is related to genes. Clinical studies have found that mental concerns can aggravate the symptoms of children, and it is considered whether mental stimulation may cause cortical nerve dysfunction, leading to central and autonomic nervous system dysfunction and the onset of the disease. Recent studies have found that the HLADQw antigen is closely related to the disease and that an autoantibody that antagonizes gastrointestinal nerves has been found in the patient's serum, suggesting that the disease has autoimmune factors.

It is generally believed that this disease is a neurogenic disease. The lesions show a decrease or even complete absence of ganglion cells in the vagus nerve and its dorsal nucleus in the esophageal wall and in the myenteric plexus of the esophageal wall, but the decrease in the LES is milder than that in the esophageal body. Animal experiments have shown that freezing stimulation or cutting of the vagus nerve (bilaterally) above the thoracic level can cause lack of peristalsis in the lower esophagus and poor relaxation of the LES. However, cutting the vagus nerve unilaterally or below the lower thoracic level does not affect the function of the LES. It can be seen from this that the vagus nerve's innervation is limited to the upper part of the esophagus, while the function of the lower end of the esophagus is controlled by the myenteric nerve plexus of the esophageal wall, whose neurotransmitters are purine nucleotides and vasoactive intestinal peptide (VIP). It has been measured that the VIP in the LES of patients with this disease is 8.5±3.6 mol/g, which is significantly lower than that of normal people (95.6±28.6 mol/g). VIP has the effect of inhibiting LES tension in the resting state. The obvious reduction of VIP in LES causes achalasia due to the loss of LES inhibitory function and increased tension.

Several chronic animal models of esophageal achalasia are produced by bilateral cervical vagotomy or by toxins that destroy ganglion cells in the dorsal nucleus of the vagus nerve or in the myenteric plexus of the esophageal wall. In addition, Chagas' invasion of the muscular layer of the esophagus releases exotoxins that damage the nerve plexus, causing tension in the LES and enlargement of the esophagus (Chageas disease). Gastric cancer invading the muscular layer of the LES can also cause symptoms similar to this disease. Some patients with esophageal achalasia often experience dysphagia suddenly, and have degenerative changes in the vagus nerve and the muscular plexus of the esophageal wall. Therefore, some people believe that the disease may be caused by a neurotoxic virus, but this has not been confirmed so far. Although there have been literature reports that multiple people in the same family suffer from this disease, and occasionally twins suffer from this disease, it is still not certain whether the occurrence of this disease has a genetic background.

When normal swallowing begins, the LES relaxes reflexively and its pressure drops, making it easier for food to enter the stomach cavity. When the vagus nerve is dysfunctional or the intramuscular plexus of the esophageal wall is damaged, LES pressure may rise to around 6.67 kPa (50 mmHg). After swallowing, the pressure does not drop and the LES cannot relax, so that food cannot enter the stomach smoothly; in addition, the propulsive peristalsis of the esophagus cannot push the food forward. As a result, a large amount of food and water accumulate in the esophagus until their weight exceeds the LES pressure and then they can enter the stomach. Due to food retention, the esophagus initially expands in a fusiform shape, and then gradually elongates and bends. The degree of esophageal dilation is far greater than that caused by esophageal cancer or other esophageal diseases, and its maximum capacity can reach more than 1L. In addition, the esophageal wall may have intermittent hypertrophy, inflammation, diverticula, ulcers or cancer, resulting in corresponding clinical symptoms.