Anomalies of the innervation of the gastrointestinal tract. Irritable bowel syndrome

Cells of the intramural ganglia of the gastrointestinal tract migrate from the ganglion plate along the branches of the vagus and pelvic nerves and are found at the 5-7th week of intrauterine life in the esophagus and stomach, and at the 7-8th week in the small and rectum and at 10-12 week in the remaining parts of the intestine. According to another point of view, fibers are not the route of movement of neuroblasts. The latter differentiate in place from precursor cells located in the mesenchyme and, apparently, previously migrated from the nerve rudiment. Congenital intestinal aganglionosis (Hirschsprung's disease, true congenital megacolon) is agenesis of the ganglia of the intermuscular (Auerbach) and submucosal (Meissierian) nerve plexuses in certain areas of the intestine. Isolated as an independent nosological unit by the Danish pediatrician N. Hirschsprung Frequency 0.2 cases in 1000 newborns The zone of aganglionosis extends to various distances upward from anal canal. In this regard, a division into long- and short-segmental (rectosigmoid) types is accepted. A.I. Leyushkin distinguishes the rectal form (21.9% of all cases of aganglionosis of the colon), rectosigmoidal (69.2%), subtotal - with damage to the transverse colon or more proximal parts of the colon (3.2%), total - aganglionosis the entire colon (0.6%) and segmental (5.1%). In the latter case, an aganglionic zone is found between two sections of the intestine with preserved nerve plexuses, or a section of healthy intestine is located between two aganglionic ones. In 1% of cases, aganglionosis involves small intestine, in addition to aplasia of ganglion cells, nerve fibers may also be absent. In 82.2% of cases of Hirschsprung's disease, the cellular component of ganglia is completely absent, in 17.8% of cases there is a deficiency of neurons with their morphological changes. At the site of the nerve plexuses, bundles of highly convoluted, intensely impregnated non-myelinated nerve fibers are revealed. Using histochemical methods, their cholinergic nature was shown and the pathogenesis of the diseases was deciphered. The triggering point in the development of Hirschsprung's disease is aplasia of cholipergic neurons of the intermuscular plexus, which coordinate intestinal motility. This is accompanied by the absence of sympathetic terminals, which have an inhibitory effect on the ganglia. As a result, the relaxation reflex of the internal anal sphincter in response to rectal stretching is disrupted. The condition is aggravated by an excess of cholinergic nerve fibers in the muscular layer, causing persistent spasm of the intestinal muscles. An important factor disturbances of peristalsis are also insufficiency of peptidergic innervation.

Presence of aganglionic. spasmodic, non-peristaltic segment leads to the development of persistent constipation or dynamic intestinal obstruction. The overlying sections of the intestine expand, their walls hypertrophy, and megacolon occurs. Under the influence of constant fecal intoxication, fatty liver degeneration develops. The condition may be complicated by perforation of the dilated colon and the development of enterocolitis. An X-ray examination reveals a characteristic cone-shaped transition zone between the narrowed and expanded suprasteiotic segments. At. In a morphological study, the most appropriate is to determine acetylcholinesterase in a biopsy specimen, the content of which in the nerve fibers of the lamina propria and muscular plates of the mucous membrane of the aganglionic zone is sharply increased. The technique is safe and gives 3-4% false positive and false negative results. Silver impregnation requires a long time for fixing and processing the material; To diagnose using this method, fragments of the entire thickness of the intestinal wall should be excised in order to detect the nerve ganglia of the intermuscular plexus.

Treatment surgical - removal of the aganglionic zone and pathologically changed expanded overlying sections.

Development of Hirschsprung's disease is associated with a disruption of the process of migration of cervical elements into the intestinal tube or with a disruption of the differentiation of migrated proeuryoblasts. The combination with megaureter (2.5-4%) and other anomalies of the urinary organs indicates damage to the pelvic parasympathetic system, but this concept cannot explain cases of total intestinal aganglionosis. TTP - before the 10th week of intrauterine development, however, the longer the zone of aganglionosis, the shorter the TTP.

The transmission of congenital aganglionosis obeys the laws of polygenic inheritance and is different for the short- and long-segmental type of the disease. In the presence of a short aganglionic segment, the risk for male siblings is 5%, female siblings - 1%; in the second type, the risk for male and female siblings is 10%; the short-segmental type occurs in boys almost 5 times more often than in girls, the long-segmental type occurs with equal frequency in boys and girls. In 15.2% of cases, congenital aganglionosis is combined with other defects, in 2-3.2% of cases trisomy 21 is observed. Hirschsprung's disease is also described in Waardenburg, Aarskog, Smith-Lemli-Opitz syndromes.

Esophageal achalasia(achalasia cardia, megaloesophagus, cardiospasm) - a violation of the reflex relaxation of the cardiac sphincter in response to stretching of the esophagus, leading to expansion and hypertrophy of the latter. The congenital nature of esophageal achalasia has not yet been reliably proven.

The morphological substrate of esophageal achalasia is a decrease or complete absence ganglion cells in the cardiac part of the esophagus, which normally coordinate peristaltic waves (in Hirschsprung's disease a similar mechanism occurs).

Trypanosomes, which are known to cause ganglionosis of the colon (Chagas disease), vitamin deficiency, bacterial or viral infection, emotional stress. At the same time, there are a number of cases of esophageal achalasia in 2, 3 and even 4 siblings, suggesting a hereditary nature of the disease with late manifestation. The combination of achalasia and microcephaly was described in 3 sisters and, possibly, their brother and, according to the authors, is inherited in an autosomal recessive manner.

Clinically manifested by dysphagia, vomiting, followed by exhaustion and the development of pneumonia. Fluoroscopy reveals a sharply dilated esophagus, narrowing like a cigar in the cardiac region; a small amount of barium penetrates the stomach after a long time.

Treatment surgical - longitudinal dissection (myotomy) of the cardioesophageal sphincter. The prognosis after surgical treatment is favorable.

- this is a lack of tone smooth muscle organ due to organic or functional reasons. May develop with various diseases internal organs, poor diet with little dietary fiber in the diet as a result of taking certain medications. Diagnosis is based on a detailed interview with the patient, identification of dietary and lifestyle habits, results of laboratory tests, irrigoscopy and colonoscopy, prescribed to exclude organic lesions and assess intestinal motility. Treatment involves normalizing lifestyle, diet therapy, prescribing prokinetic drugs, and, if necessary, laxatives.

ICD-10

K59.8 Other specified functional intestinal disorders

General information

Intestinal atony - functional state characterized by a sharp decrease in smooth muscle tone intestinal wall, disruption of the process of emptying it. Normally, contractions of the intestinal muscles (peristalsis) ensure the movement of food mass to its final sections. Within a minute, each section of the colon makes about fifteen peristaltic movements. If the tone is impaired, peristalsis is weakened, in severe cases it is absent.

The pathology is accompanied by prolongation of the intervals between acts of defecation and the appearance of difficulties during bowel movements. Constipation is an extremely common complaint, but in most cases, patients do not consult a gastroenterologist for a long time and take laxatives and medications on their own. traditional medicine. However, symptoms persist because the cause of the condition is not identified and eliminated, and incorrect treatment only aggravates the violation of tone. Intestinal atony can be a symptom of other diseases, so the appearance of constipation requires a visit to a doctor for adequate diagnosis and treatment.

Causes

The causes of intestinal atony can be diseases of internal organs, the use of certain medications, or lifestyle features. A common etiology of decreased intestinal muscle tone and the development of constipation is a sedentary lifestyle. Physical inactivity leads to deterioration of the innervation of the intestinal wall, resulting in a decrease in the number and strength of peristaltic movements. It does not lead to such consequences proper nutrition– use large quantity carbohydrate high-calorie foods with insufficient fiber intake. The cause of disruption of the intestinal innervation by the central nervous system can be constant stress.

The development of intestinal atony can be caused by taking medications such as antispasmodics, morphine-like analgesics, antidepressants, antiulcers, antiepileptics, antacids, some sorbents, as well as certain intestinal infections, disruption of intestinal microbiocenosis (dysbacteriosis), and the presence of helminths that produce substances that inhibit peristalsis. Nicotine also negatively affects the tone of the intestinal wall. The tone may be reduced due to hereditary factors, at endocrine pathology(obesity, hypothyroidism), during pregnancy, menopause, if present oncological pathology, due to surgical interventions into the abdominal cavity and the development of adhesive disease.

Very often intestinal atony varying degrees severity is observed during pregnancy. This is due to both mechanical compression of the intestines and high content progesterone, one of the effects of which is to relax the smooth muscle tissue of internal organs, including the intestinal muscles. Intestinal tone is reduced in older people, which is explained both by the processes of physiological aging and by the high frequency of atherosclerotic damage to the blood vessels supplying it.

Symptoms of intestinal atony

The symptoms of this pathology are characterized by polymorphism and are determined by the degree of motor impairment, features nervous system patient, age. Signs of intestinal atony are associated with stool retention, as well as impaired digestive processes. The main symptom is constipation (slow or systematically insufficient bowel movements). The norm is when bowel movements occur at least three times a week and no more than three times a day. Accordingly, constipation is the frequency of bowel movements less than three times a week, which is characterized by increased dryness and hardness of stool. Also an important diagnostic criterion is a decrease in the person’s usual frequency of stool.

Intestinal atony is accompanied by symptoms such as cramping abdominal pain, imperative ineffectual urge to defecate, frequent belching, abdominal discomfort, nausea. Often there is a feeling of heaviness and bloating. Characteristic and general symptoms: neurovegetative disorders, increased fatigue.

Complications

Since when the processes of cavity digestion are disrupted, the absorption of nutrients and vitamins deteriorates, signs of hypovitaminosis are characteristic, anemia is possible due to impaired absorption of iron, and the development of iron deficiency anemia. Complete intestinal atony leads to intestinal obstruction.

Diagnostics

Diagnosis of intestinal atony is based on identifying the cause of the pathology, since disturbances in intestinal tone are usually a consequence of some disease. A consultation with a gastroenterologist is indicated, including a detailed questioning of the patient, clarification of lifestyle features, eating habits, level of physical activity, and previous diseases. For effective correction Secondary atony requires treatment of the causative pathology.

An objective examination reveals bloating and decreased peristaltic sounds. General clinical laboratory research in order to assess the condition of the hepatobiliary system. Mandatory method research is a coprogram, as well as stool analysis for dysbacteriosis. The presence of protozoa and helminths is assessed. A study of the level of thyroid hormones (hormones) is carried out thyroid gland), since hypothyroidism can cause a significant decrease in intestinal tone.

Assess motor function small intestine allows radiography of the barium passage. To exclude organic causes of damage to the large intestine, irrigoscopy may be performed. This method consists of an x-ray examination of the large intestine after retrograde injection into it contrast agent. It makes it possible to assess the extensibility of the intestinal wall, the relief of the mucosa, as well as the functional state.

An informative research method is colonoscopy - endoscopic method, which allows you to visually assess the condition of the intestines, to exclude the presence of Crohn's disease, oncological pathology and other conditions that may cause atony. In order to exclude Hirschsprung's disease (a pathology characterized by congenital absence nerve ganglia in the muscular and submucosal layer of the intestine) a biopsy is performed and histological examination biopsy with a specific test for cholinesterase.

If the measures taken do not reveal the cause of intestinal atony, it is advisable to consult a neurologist, psychologist or psychotherapist with a full psychoneurological and psychological examination, since reduced tone may be psychogenic in nature.

Treatment of intestinal atony

Treatment of this condition in modern gastroenterology begins with diet. In some cases, only proper nutrition is enough to correct the frequency of bowel movements. For constipation, diet table No. 3 is prescribed. It is recommended to consume vegetables and fruits in fresh. Should be in daily diet include products that contain anthraglycosides - dried apricots, figs, prunes. It is mandatory to include fermented milk dishes, juices with pulp (plum, apricot) in the menu. vegetable fats. It is necessary to limit products containing tannin (tea, blueberries, cocoa). Food should be chemically and mechanically irritating; food should not be prepared in the form of puree or jelly.

A very important role in regulating the frequency of bowel movements belongs to drinking regime. It is recommended to drink at least two liters of fluid per day (taking into account the absence of kidney pathology, of cardio-vascular system), optimally in the form of mineral waters. Also important correct mode nutrition: the maximum volume of food intake should be in morning time when the propulsive ability of the intestines is maximum. It is advisable to eat about 5-6 times a day.

The introduction of bran into the diet significantly improves the transit of intestinal contents. Wheat bran should be poured with boiling water and after twenty minutes added to kefir, soups and other dishes. The mechanism of action is based on the fact that bran fibers are not digested and have the ability to absorb water abundantly, increasing the volume of feces. Volume stimulates intestinal motility.

A sufficient level of physical activity is of great importance. This is especially important for patients who have been hospitalized for a long time due to illness. bed rest(for example, after myocardial infarction, stroke, severe head injury, spinal injury, polytrauma), as well as for people who are obese due to physical inactivity.

Regulating lifestyle and nutrition in many cases allows you to achieve positive effect without the use of laxatives. However, unfortunately, the prevalence, over-the-counter availability and low cost of many laxatives, as well as the neglect medical recommendations leads to their mass uncontrollable independent use patients. Introduction drug therapy should be carried out only after the measures described above and only by a doctor.

Drug therapy for intestinal atony begins with the use of prokinetics - drugs that increase tone and improve intestinal motility. Cholinesterase inhibitors have this effect. Treatment usually also includes medicines choleretic action, having a pronounced irritant effect to the intestinal wall.

Laxatives are not a means of permanent treatment for intestinal atony, as patients often use them. They are used only on initial stages treatment to normalize the impaired defecation reflex. There are several groups of laxatives that differ in their mechanism of action.

The most commonly used secretory drugs plant origin or synthetic. Their action is based on reducing the absorption of water in the intestines, diluting stool, and irritating the chemoreceptors of the mucous membrane. This group includes such common remedies as preparations of hay leaves, rhubarb root, castor oil, bisacodyl, sodium picosulfate and others. These drugs accelerate the transit of intestinal contents and also directly stimulate the process of defecation. The main disadvantage of this group is the loss of electrolytes and water during systematic use, the development of addiction, requiring dosage adjustment, as well as pain.

The second group of laxative drugs - osmotic agents. This group includes lactulose, a non-absorbable disaccharide, as well as high-molecular-weight polymers that retain water. Being in the intestinal lumen, such substances increase the osmotic pressure of feces and thereby stimulate the secretion of water into the intestinal lumen. Fecal masses become more liquid, which contributes to their better movement and stimulates motility.

The third group is products whose action is based on increasing the volume of feces (bran, plantain seeds, seaweed, calcium polycarbophil and others). These are the only natural laxatives suitable for systematic use. They have no side effects and stimulate peristalsis naturally– due to the mechanical effect of the volume of feces. Products that facilitate the passage of feces due to a lubricating effect are also used: olive, almond oil, liquid paraffin. According to indications, intestinal cleansing is carried out: colon hydrotherapy or subaqueous baths.

Prognosis and prevention

Intestinal atony has a favorable prognosis: when comprehensive examination, detection and elimination of the cause, correction of nutrition and lifestyle (if necessary, prescribing reasonable, adequate drug treatment), the pathology responds well to therapy. The exception is cases of organic damage, lack of innervation (as in Hirschsprung's disease) and others serious illnesses. Prevention of intestinal atony is rational nutrition, beginning with childhood, mandatory sufficient physical activity, as well as timely detection and treatment of diseases that may cause decreased intestinal tone.

ICD-10 code

Constipation is a disease caused by intestinal atony. Many patients do not pay due attention to constipation, citing the fact that it can go away on its own, and are embarrassed to consult a doctor on such an “intimate” issue. In fact, fecal retention in the intestines can have a very negative impact on general condition patient, lead to intoxication, the appearance of inflammatory processes, and even the need for surgery.

Intestinal atony - what is it?

Intestinal atony is a violation of the tone of the intestinal walls, as a result of which they cannot contract and relax normally to push feces to the rectum and subsequent exit. With atony, intestinal motility is impaired ( contractility muscles of the walls of the gastrointestinal tract), which leads to constipation in humans, difficulty or impossibility of excreting feces. In summary, atony is not constipation, but a dysfunction of intestinal motility, which leads to stagnation of feces.

Causes of intestinal atony in adults

Atony occurs as a consequence of one or more factors that adversely affect gastrointestinal motility. Maybe like independent disease(for example, genetically determined), a side effect of another disease or taking pills (for example, intestinal infections, helminthiasis, taking antispasmodics), or poor lifestyle ( overuse alcohol, sedentary lifestyle). In Group increased risk development of atony are people who:

They experience constant stress that overloads the human central nervous system, which can lead to organ failures;
Poor diet (eating high-calorie foods with low fiber content);
Lead a sedentary lifestyle (as a result - a decrease in the innervation/impulse conductivity of the intestinal muscles, which forms peristalsis);
Antispasmodics and painkillers/anesthesia containing morphine are taken for a long time, in large doses;
Suffer from intestinal dysbiosis (toxins produced during indigestion reduce peristalsis);
Suffer from intestinal infections;
Have a genetic predisposition to atony;
Have malignant tumors intestines (they release toxins that disrupt the functioning of the nervous system);
Smoking, abusing alcohol (affect the functioning of the nervous system);
Use opiate drugs (reduce tone hollow organs);
They suffer from helminthiasis (worms produce toxins that affect peristalsis);
Survived an unsuccessful caesarean section.

In children

Atony in a child may occur for the following reasons:

Hereditary during pregnancy and lactation;
Stress various kinds;
Change in the nature of nutrition (for example, as a result of weaning from food);
Insufficient water consumption.

The appearance of childhood atony can be prevented by proper abdominal massage. Prescribed for treatment glycerin suppositories which promote reflexive rejection of feces (placed 20 minutes after the first meal), improve gastrointestinal motility.

In older people

Senile atony occurs:

due to a sedentary lifestyle;
as a side effect of operations.

Steps to treat and reduce the risk of intestinal atony in older people:

frequent walks, chamomile enemas;
introducing an abundance of vegetable and dairy foods into the diet,
eating grated, liquid and soft foods, as well as foods that have a laxative effect, improves gastrointestinal motility.

Symptoms of the disease

There are a number of symptoms by which a patient may suspect atony. If such signs are detected, you should consult a doctor, because... they indicate a disruption in intestinal motility, and this, without appropriate treatment, can lead to dangerous complications. Symptoms of atony are as follows:

Constipation (you should pay attention even when bowel movements occur less than once a day);
Bloating and gas;
Hard stool;
Weakness and bad dream;
Pale color faces;
Anemia (anemia);
The skin takes on a marbled color.

Signs	Spastic type	Atonic type
Intestinal colic	Pulling, aching	Rumbling, flatulence (increased gas production)
Rectal condition	Mostly empty	More often filled
Type of stool	Most often fragmented (“sheep”)	More often voluminous
Feeling in the intestines with constipation	Tension, compression	Expansion, fullness
Acidity gastric juice	Promoted	Reduced or zero

Diagnostics

If you suspect a disturbance in intestinal motility, including the presence of atony, you must consult a proctologist or gastroenterologist to determine accurate diagnosis, determining the severity of the disease and the cause of its occurrence. Since self-medication can lead to worsening of the condition and atony!

Doctors easily diagnose atony by asking the patient about the symptoms of the disease that are bothering him. It is much more difficult to establish the cause of the disease. For this purpose they use following methods treatment of atony:

A survey to find out the patient’s lifestyle, the characteristics of his diet and hereditary predispositions to atony;
Stool analysis and stool culture;
Colonoscopy;
X-ray (in some cases, X-ray images reveal areas of accumulation of stool, which helps identify places of possible adhesions or fecal blood clots in the intestine).

How to cure intestinal atony?

Treatment of intestinal atony should be comprehensive, aimed at eliminating the cause of the disease and eliminating factors that negatively affect intestinal motility.

For atony, the following are used simultaneously:

drug treatment (homeopathic remedies that restore normal innervation of the muscular walls of the intestine, remove the effects of fecal stagnation, regulate fecal excretion, eliminate the underlying diseases);
treatment with a diet that helps normalize stool (liquid, laxative, plenty of fiber);
physical exercise ( special gymnastics, contributing to the normalization of fecal excretion);
general normalization of lifestyle (fighting a sedentary lifestyle, bad habits and stress).

By combining all of the above treatment methods, you can quickly achieve a good result and prevent the recurrence of atony by improving gastrointestinal motility.

Treatment with drugs

When treating intestinal atony, medicine uses the following medications:

Laxatives (for example, Regulax);
Enzyme preparations aimed at improving food digestion (for example, pancreatin);
Anti-bloating medications (for example, espumisan);
Antiemetics and peristalsis enhancers (for example, cerucal, metoclopramide);
Drugs that improve impulse transmission to muscles (for example, amiridine). Use only under medical supervision;
Proserin (used on an outpatient basis if other medications have not led to an improvement in intestinal motility).

Special diet and nutrition regimen

When diagnosing “intestinal atony”, the patient needs to include in his menu products that facilitate the passage of feces through the colon:

Vegetable juices, fruit compotes, jelly;
Curdled milk, yoghurts, sour cream, kefir;
Stale bread, dry biscuits;
Vegetable soups, borscht, cabbage soup;
Lean meat, poultry, veal;
Sausages;
Cauliflower, zucchini, tomatoes, carrots;
Barley, millet and buckwheat;
Pasta;
Sea kale, greenery;
Baked apples;
Prunes, dried apricots;
Lingonberries, oranges, peaches;
Pumpkin;
Rhubarb.

It is advisable to eat small portions - 5 times a day, at the same time, combine proper nutrition with walks and exercises. It is advisable to eat food not dry, cook or bake food, and not smoke or fry. By adhering to this treatment, you can improve gastrointestinal motility.

The absence of the following products in the diet also helps to normalize intestinal function and motility:

Canned food;
Salty fish;
Rich broths;
Peas, beans;
Mushrooms;
Garlic;
Chocolate, coffee;
Pomegranates, quince;
Smoked meats;
Blueberries, pears.

Folk remedies

Promote the treatment of atony and folk remedies, including in the diet frequent consumption of mixtures made from products that have a beneficial effect on intestinal motility.

Aloe mixtures: wash several aloe leaves, remove thorns, and chop. Heat one and a half cups of honey in a saucepan (the temperature should not be higher than 40 degrees, otherwise the honey may lose its beneficial features), add aloe there and leave for 24 hours. Reheat again, take 1 tbsp every day 1 hour before breakfast. within 7-10 days. After completing the treatment, take a week break and repeat the course again.
Leaf tea powder: Grind loose leaf tea in a coffee grinder and take half a dessert spoon in powder form four times a day before meals.
Roast pumpkin and beans: cut a quarter of the pumpkin into cubes, chop the onion, mix with the pumpkin and simmer in a frying pan for vegetable oil. When the pumpkin becomes soft, add the boiled beans and simmer for another 5 minutes.
Semolina porridge: cook semolina porridge without salt and sugar. Add a little honey (optional). Consume regularly.

Video: exercises for intestinal atony

The work of intestinal motility at home can be improved by doing physical exercise, as well as properly massaging the abdominal area. This will help the intestines move feces to the exit, normalize the process of emptying and recover from atony.

Remember that all this is done only when the person does not experience critical complications due to fecal retention (bleeding, inflammatory processes, tears and perforations). In this case physical activity may aggravate the patient's condition with atony. Watch a video that will teach you how to properly perform exercises and abdominal massage to improve the functions of intestinal motility:

Innervation of the gastrointestinal tract (up to the sigmoid colon), pancreas and liver

Afferent pathways from these organs they go as part of the vagus nerve.

Efferent parasympathetic innervation. Preganglionic fibers originate from the dorsal vegetative nucleus the vagus nerve (nucleus dorsalis n. vagi) and pass in its composition (n. vagus) to the terminal nodes located in the thickness of the organs.
Function: enhancing peristalsis of the stomach, intestines, gall bladder and relaxation of the sphincter of the pylorus of the duodenum, vasodilation. With regard to the secretion of the intestinal glands, we can say that the vagus nerve contains fibers that excite and inhibit it.

Efferent sympathetic innervation. Preganglionic fibers originate in the lateral horns of the spinal cord Th V – Th XII (thoracic segments) and go along the corresponding branches to sympathetic trunk and further without interruption to intermediate nodes...
Function: slowing down the peristalsis of the stomach, intestines, gall bladder, vasoconstriction and inhibition of gland secretion.

If vertebral displacements occur in the lower thoracic spine and the influence of sympathetic innervation decreases, we will receive increased peristalsis. The situation can result in diarrhea (diarrhea), and is often interpreted as “intestinal neurosis”. In some cases, there may be sharp pain in the abdomen due to cramping individual areas intestines. Moreover, the pain can be so severe that it leads to an erroneous diagnosis - " acute stomach", and, accordingly, to solving the problem through surgical intervention!
Personally, while still a student medical institute, assisted the surgeon (operator) during appendectomy (removal vermiform appendix), and, unfortunately, only on operating table, already after access to the abdominal cavity was opened, the fact that the appendix was not inflamed became obvious! Although the Shchetkin-Blumberg symptom was positive, the number of leukocytes in the blood increased to 12 10 9 per liter and the ESR (erythrocyte sedimentation rate) increased. And, alas, I think a great many such examples can be given.
In addition, I dare to suggest that a prolonged spasm automatically leads directly to the emergence of a specific acute pathology V abdominal cavity- the same appendicitis, cholecystitis, pancreatitis, adnexitis, etc., etc.!
The sharply contracted intestinal muscles can compress the mesetherial vessels, thereby bleeding parts of the intestines, to which the nerve endings instantly react with pain and the occurrence of a local inflammatory reaction.
By the way, you can get rid of sharp abdominal pain by adopting a stretching cat pose (leaning on your arms bent at the elbows and legs bent at the knees), when the pelvic end of the body is located above the head.
This static exercise, aimed at stretching (pulling) the spinal column, helps to increase the distance between articulated vertebrae, thereby stopping compression spinal nerves, and, as a consequence, restoration of the conduction of bioelectric impulses through the sympathetic nervous system to the intestines. As a result, intestinal peristalsis slows down (i.e., the tone of their smooth muscles decreases), blood circulation improves (there is no compression of mesetherial vessels) and, as a result, pain decreases and inflammation subsides.
At one time, albeit for a very short time, doctors made attempts to treat gastric ulcers by denervation of the suffering organ, i.e. using the so-called trunk or selective vagotomy, when the trunk of the vagus nerve or one of its branches innervating the stomach was cut. Thanks to this operation, it was possible to avoid a complex and difficult gastric resection operation. But this gentle operation (vagotomy) had to be subsequently abandoned, because Some patients experienced an exacerbation of the disease (relapse). However, it was this method of treatment that gave impetus to thinking about the paramount importance nervous regulation, and about the reasons for the recurrence of the disease, and a little later about the primacy of its vegetative part, the functioning of which is affected by adjustments, problems (displacements or blocks) in the spinal column!
In this regard, I decided to try to treat patients with this pathology using spinal manipulation, i.e. using manual therapy. I had four such patients - gastric and duodenal ulcers - and all four had excellent results!

In 2000, in my territorial area, there was a case when a patient who occasionally abused alcohol, after another alcoholic excess, created a problem in his stomach: upon examination he had signs of " erosive gastritis", the clinical picture somewhat resembles an acute abdomen. That is, there was spontaneous bleeding, which, by the way, also stopped spontaneously! The diagnosis during urgent (urgent) hospitalization was subsequently confirmed by gastroscopic examination.
And the same bleeding in the stomach occurred in a patient suffering from duodenal ulcer, which arose after lifting weights. And also stopped spontaneously! (1996, August).
The year before (1995), it was at this young man duodenal ulcer during periods of exacerbation was manifested by severe pain and pronounced dyspeptic disorders. At my suggestion, I worked with his spine just during periods of exacerbations (spring and autumn) - and he and I got an excellent result - the next year he had no seasonal exacerbations of the disease!
But after lifting weights, he had, in his words, black feces (melena), and the next day he was brought from work to the clinic and led onto the porch of the building by his arms (the young man was very pale!). The patient was immediately hospitalized surgery department City Emergency Hospital, where upon admission he immediately underwent an endoscopic examination of the stomach and duodenum. But the old healed ulcerative defect did not bleed - there was no exacerbation of the chronic disease! However, melena confirmed bleeding from the overlying parts of the intestine, i.e. from the stomach. (Blood exposed to hydrochloric acid in the stomach acquires a black color). Apparently, there was a short-term bleeding of the entire inner surface stomach, due to temporary denervation of precapillary vessels - arterioles, which ruptured and poured blood into the lumen of the hollow organ.
The lifting of significant weight "flattened" intervertebral discs and instead of being biconvex, they became flat - which is why the intervertebral foramina became smaller, which resulted in compression of the spinal nerves. As we remember, when a nerve fiber is compressed, the conduction of a bioelectric impulse is disrupted. As a result, the tone of the smooth muscles inside the walls of the arterioles sharply decreased, and the vessels could not withstand the blood pressure and simply began to tear! I describe this mechanism in more detail below – in the second part of the “Concept”. Therefore, I will not dwell on this here.
After two days of observation of the admitted patient and conservative treatment measures, the young man was discharged from the clinic.

Exposure to sound vibrations
One of the most striking examples of disorders in the spinal column, in the area responsible for the functioning of the gastrointestinal tract, can be a case that took place in the lives of people close to me, and mine too!
Our entire family (my wife and I, son and youngest daughter, my mother) after several hours spent sitting with their backs to powerful sound-reproducing speakers - this was at a wedding, i.e., also due to drinking alcohol, got intestinal dysfunction, lasted three days! The reason, presumably, was the impact of sound vibrations in the air, and, in particular, low-frequency ones. Not only did mechanical displacements of the vertebrae occur, but switches (short circuits) also occurred in the spinal cord itself. Blocking the conduction of bioelectric impulses through the sympathetic autonomic nervous system (it, as we remember, slows down intestinal motility, constricts blood vessels and inhibits the secretion of glands) leads to predominance parasympathetic innervation, enhancing intestinal motility, dilating intestinal vessels (and this is an additional flow of blood, i.e. fluid). The consequence of such an imbalance in the autonomic innervation of the intestines was diarrhea (diarrhea) in several people. The funny thing is that many regarded this situation as related to eating fried food. river fish, fatty at that. But our youngest daughter, Dasha, did not eat that fish! However, she also had a so-called intestinal disorder.
I will give another example of the pathogenic effects of sound vibrations on a living organism.
During preparations for the Victory Parade, in November 1945 in Moscow, the combined orchestra of the Moscow garrison held rehearsals in the arena in Khamovniki. An experienced cavalry rider, Nikolai Sitko, decided to take the opportunity and try to tame a horse named Polyus, who was supposed to participate in the parade on Red Square, to the music of a brass band.
The officer entered the arena at the Pole at a time when the orchestra was not yet playing. But further... Loud, unexpected music in a confined space, unfortunately, became disastrous for the horse. Pole was very frightened, he trembled and sweated, and then he began to rush around and... fell! The orchestra immediately stopped playing. With difficulty they lifted the horse to his feet and calmed him down. Subsequently, the efforts of veterinarians, unfortunately, turned out to be ineffective - they could not help the injured animal. He had a strong nervous breakdown. And Polyus was sent to his native stud farm.

And more about the impact of sound frequency fluctuations
In Regensburg, Germany, in 1996, seventeen-year-old Christiane Kittel suffered a thromboembolism (blockage from a blood clot) pulmonary artery, but the doctors managed to save the girl - she was operated on. However, it was not possible to bring Christiane Kittel out of her coma either in the immediate hours after the operation or in the next seven years!
In 2003, the popular performer Bryan Adams arrived in the city on tour, whose fan, unfortunately, was Christiane Kittel. The patient’s mother, Adelheid Kittel, decided to bring the comatose girl to the concert of her daughter’s favorite performer right into the hall where the show was to take place. With the last hope for healing. And - a miracle happened! At the very first sounds of music and the singer’s voice, the girl moved and opened her eyes!
“For joy, I wanted to hug the whole world. When we returned to the clinic, she called me three times, saying “Mom,” said the happy Frau Kittel.
It must be assumed that the cerebral cortex of the unfortunate girl, as if by a short circuit, was turned off seven years ago. And electromagnetic vibrations of the sound range, from 20 Hz to 20 KHz, and even of high power, led to the severing of pathological connections in the brain, and returned a person to an active, full life. And besides, sound vibrations high power, like a shock wave, could displace the vertebrae of a girl lying in a coma. And thus, create new combinations of displacements in the spine, and, accordingly, connections in the central nervous system. (Since there was maximum relaxation of all muscles, including the spine).

During an air show in the city of Sknyliv near Lvov, even before the tragedy associated with the SU-29 crash, during the flight of a combat vehicle over people (the plane flew at a very low altitude), a six-year-old boy suffered a myocardial infarction and died in the arms of his grandfathers.

In Anton Pavlovich Chekhov's story “The Death of an Official,” the general barked at the official Chervyakov: “Get out!” And immediately “something came off” in his stomach. And further in the text. “Seeing nothing, hearing nothing, he backed away to the door, went out into the street and trudged... Arriving mechanically home, without taking off his uniform, he lay down on the sofa and... died” (52).

Viral hepatitis A (jaundice), or Botkin's disease
This happened to me in 1958, when I was four years old and attending kindergarten.
It was early spring, and it was still cool - we were in coats. It was getting late in the evening; our parents were going to pick us up soon. And we, the children, together with the teacher, were on the street, in the courtyard kindergarten, when I wanted to go to the toilet, and just to recover. I was a shy boy and therefore, without saying anything to the teacher, I ran to the building to our group’s room, where there was a toilet. The door to the building was locked, and I also ran and returned under the canopy of the gazebo. Jogging slightly relieved the tension, but not for long, because after 10–15 seconds the urge to defecate arose again, and it was imperative, requiring an immediate solution to the problem.
And I found it - this is the solution - I crossed my legs and squeezed them tightly, straining both the thigh muscles and the muscles of the pelvic floor with all my might. And in the blink of an eye everything changed.
I still clearly remember that evening, the gazebo and that bench... and my feelings: the urge to defecate disappeared instantly, my legs gave way - my body seemed to go limp, and I felt the need to lie down immediately. I lay down on the bench and felt very cold. I really wanted to sleep. I closed my eyes and remember that I fell asleep almost instantly... (By the way, about memory: in general, my very first memory was leaving a city in Ukraine for a village in Russia, when I was exactly 1 year old).
But I didn’t fall asleep, I lost consciousness. It was a coma. Later, while already in the hospital, I turned yellow. And subsequently, in all questionnaires, he indicated that he suffered from viral hepatitis A, i.e. Botkin's disease, or jaundice.
I was unconscious for four days - the treatment had no effect. Until my paternal aunt, Lidia Sergeevna, found the whispering grandmother. And that grandmother read prayers, whispering them in my ear - and I came to my senses.
The first memory after I came out of the coma was an unsuccessful injection in the left buttock - it was very painful, as if I had been burned, and I cried a lot. And now, right in the center of the left buttock, there is a scar measuring 3?4 cm, which confirms the complete imbalance of the entire nervous system. Although the injection was indeed carried out incorrectly (there are a lot of nerve endings in this area of the buttock, and the least of them are in the outer upper quadrant).
And I remember the first time I went out to Fresh air and the recovering children and I danced in a circle. The sun was shining. And the first grass has already begun to emerge. Moreover, I remember it very well - everything around was as if permeated with white light - it was painful for me to look even at the crowns of the trees with their still sparse foliage. We walked in a circle, holding each other's hands, and rejoiced at the recovery. And I, smiling weakly, staggered, barely able to stand on my feet.
What happened to me then?
The brain (cortex) interfered with the natural course of processes with powerful tension, which was tantamount to an explosion or short circuit.
Apparently, the hypothalamus was also partially blocked (with the destruction of the dorsolateral nuclei of the posterior hypothalamus, a complete loss of thermoregulation occurs - normal temperature cannot be maintained, and the body cools down to 35? C!); and cerebellum (vasomotor reflexes, skin trophism, wound healing rate); and reticular formation (vasomotor, temperature and respiratory centers).
There was no anatomical destruction, but there was a kind of short circuit in the central nervous system, at the level of subcortical formations (reticular formation, hypothalamus, cerebellum). And of course, all these processes were not without displacements in the spinal column.
This was confirmed by severe weakness, and the fact that I felt cold (a sharp cooling of the body was setting in!), and an almost instantaneous loss of consciousness. Yes, and the same injection, which resulted in a rather large and rough skin defect, really reminiscent of a post-burn scar.
And, of course, verbal vibrations (the prayers of a whispering grandmother), which probably broke pathological connections in the brain, as in the case of a girl from Germany who lay in a coma for seven whole years.
And I would lie in a coma for who knows how long... And, most likely, I would die - and not for long.
And I turned yellow because of a spasm of both the bile ducts of the liver and the sphincter of Oddi. That is, the bile produced by the liver could not enter any gallbladder, neither in duodenum, but got directly into the blood, which led to coloration of the skin.

Non-specific ulcerative colitis(NYAK)
Among the great variety of human diseases, there is one complex and very delicate one, in which bleeding ulcers form on the walls of the large intestine and are accompanied by diarrhea (stool up to 10-15 times a day) - ulcerative colitis (UC). The pathology can spread both to the ascending and descending parts of the colon, and to transverse colon, and, in addition, total UC also occurs, when all mentioned parts of the large intestine are affected.
So, on X-ray photographs, the affected part of the intestine is, as a rule, two times wider than the unaffected part! And this is simply partial (or complete) sympathetic denervation of any part of the colon. The comprehensive influence of parasympathetic innervation (due to the absence of sympathetic) leads to increased peristalsis, vasodilation and increased secretion of glands - and hence bleeding ulcers and, therefore, excess fluid into the intestinal lumen. And it is enough to restore innervation, as the pathology will practically disappear within a week. That's all. But now this disease leads to disability of sick people and large material costs for medications.
By the way, in 2005 I encountered a patient who had suffered from this disease for a number of years and had retired due to disability. However, something else is interesting. After some time, this sufferer (it’s a joke - loose stool, i.e. diarrhea up to 15 times a day), UC spontaneously gave way to another disease - obliterating endarteritis occurred. (Arteries lower limbs, in this case, are gradually clogged by circular deposits on internal walls atherosclerotic layers).

Dystonia or intestinal dyskinesia is a dysfunction of the small and, to a greater extent, large intestine, which is accompanied by changes in tone and motor activity intestinal wall, consisting of several layers of smooth muscle. This disease does not pose a threat to the patient's life, but causes noticeable discomfort.

Types of dyskinesia

Modern classification dyskinesia divides the primary (congenital) and secondary forms (acquired) of this functional disorder. By clinical course acquired dyskinesia is distinguished:

with the predominant development of intestinal disorders (constipation or diarrhea);
with manifestation of abdominal pain;
with a predominance of general neurotic symptoms.

Depending on the motor disorders intestines, there are two types of dystonia:

hypertensive (spastic);
hypotonic.

Depending on the type of dyskinesia, one or another type of treatment is prescribed, of course, in the absence of evidence organic diseases intestines (peptic ulcer, ulcerative colitis, Crohn's disease).

Causes of colon dystonia

The disease is localized within the ascending, transverse colon and descending colon, which suffer from functional disorders innervation with the subsequent formation of characteristic symptoms.

Causes of impaired motor function of the gastrointestinal tract:

Nervous overstrain and chronic stress - lead to the formation of pathological impulses in the brain, which leads to disorders of the functioning of internal organs.
Errors in nutrition. Lack of fiber, vitamins and minerals often provokes a violation of the motor activity of the colon with the development of characteristic clinical picture.
Sedentary image life. Lack of physical activity leads to stagnation of the food bolus and the development of intestinal dystonia.
Endocrine disorders, hypertension, pathology of the autonomic nervous system.
Abuse medications.
Inflammatory or infectious processes in the body.
Genetic predisposition to functional failure of the colon.

Since intestinal dyskinesia is caused by a number of factors, the cause is first determined (an accurate diagnosis is made), and then methods of treatment and correction of the patient’s condition are chosen.

Symptoms

Signs characteristic of dyskinesia occur in different time sequences and differ in severity. Distributed following symptoms:

Pain in the abdominal area. They are spastic, stabbing, aching in nature, occur against the background of food intake, and are accompanied by disruption of the defecation process. Feature- no pain at night and immediately after waking up.
Dyspeptic symptoms: loss of appetite, nausea, belching, vomiting, flatulence (bloating).
Violation of the process of defecation. Depending on the type of damage to the colon (hypertensive or hypotonic), diarrhea or constipation progresses.
Symptoms of neuroses. Against the background of dyskinesia, a person notes emotional instability, anxiety, and sleep disorders.

There is the following difference between the spastic and hypotonic forms of dystonia:

If we're talking about about hyperkinesis of the muscular wall of the organ, then its excessive contraction occurs. Areas of spasmodic intestine appear, which cause constipation due to difficulty in further movement of feces or diarrhea due to increased peristalsis. In this case, the person is bothered by severe, often sudden, pain in the abdomen. Numerous scanty bowel movements or the simultaneous release of large amounts of feces are observed.
The hypotonic type of colon dyskinesia is accompanied by a decrease in intestinal motor activity. The patient complains of aching, nagging pain in the abdomen, flatulence, and constipation. Notes fatigue, weakness. Pathology can cause the development of dynamic intestinal obstruction, which may even require urgent surgical intervention.

Diagnosis of intestinal dystonia

It is easy to identify the symptoms of intestinal dyskinesia (dystonia) in typical cases. The doctor will suspect the presence of pathology based on the patient’s complaints and collecting a history of the disease. The process takes much longer differential diagnosis, that is, excluding a likely “candidate” for the diagnosis of conditions with similar symptoms. This requires various instrumental studies and taking tests.

During the survey, special attention is paid to describing the nature of the pain syndrome and its relationship with food intake. Disruption of the defecation process will tell you a lot.

Dystonia of the large intestine sometimes becomes a “mask” for other diseases. Differential diagnosis is carried out with the following diseases:

Acute food intoxication or toxic infection.
Infectious diseases. Gastroenterocolitis, which is caused by pathogenic microorganisms(Shigella, amoeba, salmonella), often develop as a type of gastrointestinal motility disorder. Chronic amoebiasis, or amoebic dysentery, is also possible.
Nonspecific ulcerative colitis and Crohn's disease - serious illnesses gastrointestinal tract, which are accompanied by dyskinesia.
Malignant neoplasms.

For differential diagnosis, auxiliary examination methods are used:

sigmoidoscopy;
colonoscopy;
ultrasonography abdominal organs;
computed tomography, magnetic resonance imaging (rare);
stool analysis (coprogram).

Establishing an accurate diagnosis is the key to selecting optimal therapy and eliminating pathology.

In the treatment of intestinal dystonia, the doctor proceeds from the type of lesion when selecting therapy.

For hypotension, increased fiber content in the diet, abdominal massage, and increased physical activity are prescribed. Intensifying your lifestyle leads to improved peristalsis and a reduction in complaints. Rotting and fermentation in the intestines stop due to the long presence of food in its lumen, passage through the large intestine is normalized, signs of autointoxication are reduced, and mood and performance are improved.
In case of intestinal hypertonicity, a massage is also prescribed, but a relaxing one. The use of laxatives is indicated, copious amounts water, which softens stool, taking antispasmodic drugs.