Symptoms of recurrent laryngeal nerve paresis (paralysis) and its treatment. Method for the treatment of temporary postoperative paresis of the recurrent laryngeal nerve during extensive surgery on the thyroid gland Recurrent laryngeal nerve of the giraffe

An example with tanystropheus was given by Dr. Yuri Viktorovich Tchaikovsky in his monograph “The Science of the Development of Life.”
He gave this as an illustration:
1. Biologically inappropriate trait.
2. Opportunities for successful survival of the species contrary to the presence of biologically inappropriate signs.

We are talking about a fossil lizard (Tanystropheus), the remains of which are dated to the mid-Triassic period.
Tanystropheus is the animal with the longest neck in Earth's history. And what is especially noteworthy here is that this huge neck - badly bent, since the neck contained only 9 (or 10) vertebrae.
As a result, tanystropheus was a kind of "a log with legs":

By comparison, for example, a significant number of aquatic plesiosaurs also had long necks. But they were also “accompanied” by a large number of vertebrae. At least three dozen. And some reached more than 70. This number of vertebrae provided the necks of plesiosaurs with excellent flexibility (probably).
Here, for example, is the skeleton of an Elasmosaurus:


It is he who has a record number of vertebrae (more than 70).

In this regard, the question arises: whose product is tanystropheus best considered:
1. A product of evolution during natural selection?
2. Or a product of evolution during against natural selection?
3. Or a product of design (within the concept of diversity of design in different biological taxa)?

Let us note that today on Earth there is a certain modern semblance of “tanystropheus” - the African giraffe.
In my opinion, this is one of the most beautiful mammals on Earth:

Despite the fact that the giraffe's neck (with seven cervical vertebrae) is significantly shorter than that of the fossil tanystropheus, the giraffe has a serious set of specific biological problems caused by its long neck. And special “engineering solutions” that solve these problems.

For example, the problem of blood circulation (quoting from Wikipedia):
Tall height increases the load on the circulatory system, especially in relation to the supply to the brain. Therefore, giraffes have especially strong hearts. It passes 60 liters of blood per minute, weighs 12 kg and creates a pressure that is three times higher than that of a person. However, it would not be able to withstand the overload of the sudden lowering and raising of the giraffe's head. To ensure that such movements do not cause the death of the animal, the giraffe's blood is thicker and has twice the density of blood cells than that of humans. In addition, the giraffe has special shut-off valves in the great jugular vein that interrupt the flow of blood so that pressure is maintained in the main artery supplying the brain.

And this is how a giraffe is forced to drink :)

P.s. Perhaps those most surprised by the unique design of the giraffe are creationists (since they are supporters of intelligent design in the creation of different biological taxa). They often cite the giraffe as evidence of intelligent design rather than natural (or natural) evolution. unnatural?) selections.
For those interested, here are popular scientific links on this topic.

The internal laryngeal muscles are innervated by branches of the vagus nerve. The anterior cricothyroid muscle is innervated by the superior laryngeal nerve, the remaining muscles of the larynx are recurrent nerves. Various injuries or pathological conditions of the vagus nerve and its branches lead to the development of peripheral neuropathic paresis of the larynx. When the nucleus of the vagus nerve in the brain stem or the higher pathways and cortical centers is damaged, central neuropathic paresis of the larynx occurs.

Neuropathic laryngeal paresis is the most common type of laryngeal paresis. It may be associated with pathology of the larynx, various diseases of the nervous system, and pathological processes in the chest cavity. Therefore, not only otolaryngology, but also neurology and thoracic surgery are involved in the examination and treatment of patients with neuropathic laryngeal paresis.

Causes of neuropathic laryngeal paresis

Peripheral neuropathic laryngeal paresis is most often caused by pathology of the right and left recurrent nerves. The large length of the recurrent nerve, its entry into the larynx from the thoracic cavity and contact with many anatomical structures provide ample opportunities for damage to the nerve in its various parts. The left recurrent nerve bends around the aortic arch and can be compressed by its aneurysm. The right recurrent nerve passes at the apex of the right lung and can be compressed by pleural adhesions in this area. The causes of damage to the recurrent nerves with the development of neuropathic paresis of the larynx can also be: trauma to the larynx, pleurisy, pericarditis, tumors of the pleura and pericardium, lymphadenitis, tumors and cysts of the mediastinum, enlargement of the thyroid gland (with diffuse toxic goiter, autoimmune thyroiditis, iodine deficiency diseases, tumors), thyroid cancer, benign tumors, diverticula and esophageal cancer, tumors and enlarged cervical lymph nodes.

Peripheral neuropathic paresis of the larynx can be of toxic origin and occur as a result of toxic neuritis of the recurrent nerves in case of poisoning with arsenic, alcohol, lead, nicotine, etc. It may develop in diabetes mellitus, as a result of intoxication in certain infections, for example, in diphtheria, typhus or typhoid fever , tuberculosis. The occurrence of neuropathic paresis of the larynx can be observed when the recurrent nerve is damaged during operations on the thyroid gland: thyroidectomy, hemithyroidectomy, subtotal resection.

Central neuropathic paresis of the larynx can be observed with damage to the brain stem (bulbar palsy), which is observed with tumors, neurosyphilis, poliomyelitis, botulism, syringomyelia, severe atherosclerosis of cerebral vessels, hemorrhage in the brain stem with hemorrhagic stroke. Also, neuropathic paresis of the larynx of central origin is observed in pathological processes affecting the corresponding pathways and the cerebral cortex. Cortical neuropathic paresis of the larynx occurs with brain tumors, hemorrhagic and ischemic stroke, and severe traumatic brain injury. It should be noted that cortical neuropathic paresis of the larynx is always bilateral in nature, due to incomplete crossing of the nerve pathways before they enter the brain stem.

Symptoms of neuropathic laryngeal paresis

Reduced mobility of the vocal cords with neuropathic laryngeal paresis leads to disturbances in voice formation (phonation) and respiratory function. Neuropathic paresis of the larynx is characterized by sequential involvement of the internal laryngeal muscles in the pathological process: first, the function of the posterior crico-arytenoid muscle, which is responsible for widening the glottis and abducting the vocal folds, is impaired, then weakness and paralysis of the laryngeal adductors develop, which normally narrow the larynx and bring together the vocal cords . This phenomenon is called the Rosenbach-Semon law. In accordance with it, in neuropathic paresis of the larynx, due to the preserved performance of the adductors at the beginning of the disease, the vocal cord on the affected side occupies a median position, after some time the weakness of the adductors increases and the vocal cord moves to an intermediate position.

Unilateral neuropathic laryngeal paresis at the beginning is characterized by preservation of phonation due to the adjoining of the healthy vocal cord to the ligament occupying the middle position of the affected side. Breathing also remains normal; difficulty can be detected only with significant physical exertion. Further development of neuropathic paresis of the larynx is accompanied by the involvement of the laryngeal adductors and the intermediate position of the vocal cord, due to which the glottis does not completely close during phonation. Hoarseness occurs. After a few months, patients with neuropathic laryngeal paresis develop compensatory hyperadduction of the vocal cord on the healthy side and it begins to fit more tightly to the paretic ligament. As a result, there is a restoration of the normal sound of the voice, but disturbances in vocal function in patients with neuropathic laryngeal paresis persist.

Bilateral neuropathic paresis of the larynx in the initial period is accompanied by severe respiratory disorders, including asphyxia. This is due to the fact that both vocal cords occupy a midline position and can close completely, preventing air from passing into the airways. Clinically, bilateral neuropathic paresis of the larynx is manifested by rare noisy breathing with retraction of the supraclavicular fossa, epigastrium and intercostal spaces during inspiration and protrusion during exhalation. A patient with bilateral neuropathic paresis of the larynx is in a forced position, often sitting, resting his hands on the edge of the sofa. His facial expression reflects extreme fear, his skin is cyanotic in color. Even minor physical effort causes a sharp deterioration in the condition. After 2-3 days from the onset of clinical manifestations of neuropathic paresis of the larynx, the vocal cords take an intermediate position and a gap forms between them. Respiratory function improves, but any physical activity leads to symptoms of hypoxia.

Diagnosis of neuropathic laryngeal paresis

The goal of diagnosing neuropathic laryngeal paresis is not only to establish a diagnosis, but also to identify the cause of the paresis. To do this, the patient is referred to a consultation with an otolaryngologist, neurologist, neurosurgeon, thoracic surgeon and endocrinologist. Examination of a patient with neuropathic laryngeal paresis is a fairly large list of studies. These are CT and radiography of the larynx, laryngoscopy, study of vocal function (stroboscopy, electroglottography, phonetography, determination of the time of maximum phonation), electromyography of the laryngeal muscles. To exclude the occurrence of neuropathic paresis of the larynx due to damage to the recurrent nerve in pathological processes of the chest cavity, radiography of the chest organs, CT scan of the mediastinum, ultrasound of the heart, and radiography of the esophagus are performed. The condition of the thyroid gland is examined using ultrasound of the thyroid gland. If a central nature of neuropathic paresis of the larynx is suspected, MRI and CT of the brain are indicated.

Neuropathic paresis of the larynx should be differentiated from myopathic and functional paresis of the larynx, as well as from arthritis or subluxation of the arytenoid joint, false croup, diphtheria, an attack of bronchial asthma, and congenital stridor.

Classification

Classification of paresis is carried out depending on the factors contributing to the disease.

1. Myopathic.

• Deviations in the functioning of the muscles that open the glottis. Infrequent cases of the disease, sometimes develop as a result of multiple sclerosis, acute poisoning with chemicals.
• Malfunction of the muscles that close the opening between the vocal cords. As a result of unilateral or bilateral lesions, the vocal folds do not close enough. This is sometimes caused by tumors, injuries, diphtheria, and thyroid diseases.
• Changes in the activity of the muscles responsible for the tension of the vocal cords. A very rare pathology, the result is a hoarse voice.

2. Neuropathic.

The degree of disturbance of the nervous system can be different, based on this, paresis is distinguished:

• peripheral - provoked by injuries, tumors of the cervical, thoracic, in the esophagus - usually one-sided;
• bulbar – caused by tumors, cerebral hemorrhages, sclerosis; can be one or two-sided;
• cortical – processes occur in the superficial layer covering the cerebral hemispheres; usually bilateral.

When affected by neuropathic paresis, one side is mainly affected (phonation is impaired). A healthy vocal fold balances the work of the affected one, and after some period the voice resumes. Bilateral damage is fraught with a sharp lack of oxygen (a particular risk at the onset of the disease).

3. Functional.

Develops as a result of disruption of activation-slowdown processes in the cerebral cortex. Temporary loss of voice occurs as a result of nervous strain and autonomic dysfunction. Such laryngeal paresis are always bilateral.

Reasons

Laryngeal paralysis is a serious common disease, ranking second among ENT diseases.

The causes of paresis are different. The most common provoking factors are:

• impaired blood circulation in the vessels (stroke, atherosclerosis);
• diseases of the brain and spinal cord;
• neck and spine injuries;
• contusions (blast injuries);
• trauma during operations: cervical region, chest, skull;
• tumors or metastases, hematomas;
• laryngitis, tracheitis;
• harmful effects on the nerve of harmful microorganisms and chemotherapy drugs;
• prolonged overstrain of the vocal cords in actors, singers, and speakers;
• metabolic disorders in the body due to hyperthyroidism of the thyroid gland;
• pronounced neuroses (hysteria) as a result - motor disorders, malfunction of internal organs.

Clinical picture

To make an accurate diagnosis, make a prognosis of the patient’s condition and prescribe effective treatment for laryngeal paralysis, it is necessary to draw up a clinical picture. To do this, you should analyze the patient’s complaints, data from external examination and laboratory tests.

Paresis of the larynx is characterized by pronounced disorders of the main activities of the throat: breathing and voice formation. The expression of clinical symptoms of laryngeal paresis is directly related to the degree of damage (unilateral or bilateral) and the duration of the disease.

Unilateral paralysis characterizes:

• severe hoarseness of the voice (in children it is more pronounced after crying), its loss is possible;
• violation of the depth and frequency of breathing, intensifies during a conversation;
• soreness, presence of coma.

Bilateral laryngeal paresis is accompanied by difficulty in inhaling due to a narrowed space between the vocal folds:

• shortness of breath, especially during movement (in severe cases - during inactivity);
• wheezing;
• lifelessness (sometimes bluishness) of the skin;
• increased sweating;
• fatigue during vocal stress;
• increase/decrease in blood pressure.

Sometimes laryngeal paresis is asymptomatic, and the problem is discovered during a medical examination.

Difficulty breathing during paresis as a result of failure of free access of air into the respiratory tract due to a narrowed glottis can sometimes cause suffocation.

Often patients with paresis feel lethargy, indifference to life, or vice versa - they are restless. Shortness of breath appears both at rest and with light exertion, breathing is loud and frequent, blood pressure increases noticeably.

Carrying out diagnostics

Since laryngeal paresis is caused by many factors, the disease is diagnosed and treated by different specialists: endocrinologists, otolaryngologists, neurologists, neurosurgeons, cardiologists, psychologists and psychiatrists.

1. Analysis of complaints: the emotional state of the patient, breathing, recent infectious diseases, injuries, problems with the thyroid gland (especially operations on the thyroid gland and chest).
2. Inspection (feeling the neck).
3. The microlaryngoscopy method is an opportunity to analyze the condition of the vocal cords, mucous membrane, the presence or absence of inflammatory processes.
4. Computed tomography or x-ray of the larynx, chest to be able to fully see the condition of the upper respiratory passages, soft tissues, and blood vessels.
5. Electroglottography, phonetography - methods for testing vocal activity in case of laryngeal paresis.
6. Fibrolaryngoscopy - diagnosing the larynx using a flexible endoscope - determines the condition of the vocal apparatus and the level of closure of the glottis.
7. Video surveillance examines how mobile the vocal cords are.
8. Ultrasound examination of the thyroid gland and heart (thyroid disease is one of the main causes leading to paresis).
9. To exclude neuropathic laryngeal paresis, brain tomography or MRI is prescribed.
10. Electromyography is the study of disturbances in nerve impulses.

Psychiatrists necessarily examine the patient and prescribe psychological tests. During the examination, it is important to distinguish between other ailments - arthritis, croup - with paresis.

Treatment of paresis

Whatever the severity of the disease, its treatment is aimed at restoring the motor functions of the larynx. The choice of the main method of therapy is influenced by the severity and duration of the disease.

For paresis, causal healing is recommended - determining the cause and getting rid of it, that is, the disease that caused the paralysis. If the underlying disease is inflammation, then anti-inflammatory therapy is recommended; if it is the consequences of an injury, thermal procedures are prescribed. When the cause is toxicosis due to an infectious disease, this disease is cured.

Symptomatic therapy with:

• electrical stimulation of nerves and laryngeal muscles;
• acupuncture;
• phonopedia;
• surgical methods (laryngoplasty, implantation surgery, tracheostomy).

Laryngeal paralysis involves drug treatment, the following are prescribed:

• antibacterial and antiviral drugs;
• vitamin complex – neuropathic paralysis;
• activators of muscle activity – myopathic paralysis;
• psychotropic substances, antidepressants, antipsychotics, sedatives;
• vascular and effects on brain function drugs (presence of injuries, strokes).

It is important to treat paralysis resulting from injury or surgery in the neck area immediately; delay can lead to atrophy - loss of motor ability.

Indications for surgery

• it is necessary to remove the tumor in the esophagus;
• perform operations on the thyroid gland;
• tension of the vocal muscle is required;
• respiratory failure in case of bilateral paresis (removal of the vocal fold or its fixation);
• the onset of suffocation (asphyxia) - a tracheostomy or tracheotomy is performed.

Non-drug treatment

In addition to medication or surgery, physiotherapy methods are also prescribed:

• medicinal electrophoresis;
• magnetic therapy;
• breathing exercises, voice exercises;
• acupuncture;
• for functional paresis, hydrotherapy, electrosleep, massage and reflexology are effective;
• psychotherapy;
• phonopedia – exercises that restore the function of the vocal apparatus, applicable at any stage of the disease caused by various factors, at all stages of treatment.

Prevention

To prevent laryngeal paresis, you should:

• promptly identify and treat ailments that can contribute to paralysis (tumors, acute inflammatory processes in the ENT organs);
• treat promptly injuries to the larynx;
• exclude (if possible) laryngeal injuries during thyroid surgery;
• adjust voice mode;
• beware of hypothermia, refrain from long stays in dusty rooms, beware of getting acids and alkalis into the respiratory system;
• Treat in a timely manner, with the help of doctors, inflammatory processes, infections, neuroses, and thyroid diseases.

Forecast

For patients with unilateral paralysis, the prognosis is favorable: in almost all cases, the voice can be restored and breathing can be improved (however, physical activity should be reduced).

Bilateral paralysis most often requires the involvement of surgeons. After a full course of rehabilitation, the voice is partially restored, breathing returns to normal.

If the causative factor of paralysis is eliminated and a course of treatment is carried out in time, then although the singing data will be lost, the voice will return.

Delayed treatment can lead to irreparable changes in the laryngeal muscles and voice disorders.

Causes of laryngeal paresis

Laryngeal paresis is a polyetiological pathology that often develops against the background of another disease. For example, laryngeal paresis can occur during an inflammatory disease, which can be laryngitis. Also, laryngeal paresis can occur in parallel with infections such as influenza, ARVI, tuberculosis, typhoid (or typhus), secondary (tertiary) syphilis or botulism. Traumatic brain injury, myasthenia gravis, polymyositis, syringomyelia, as well as tumors and vascular disorders (ischemic stroke, atherosclerosis, etc.) - all this can also accompany laryngeal paresis.

The development of laryngeal paresis may also be associated with damage to the branch of the vagus nerve, that is, the recurrent nerve, which leaves the chest cavity and passes to the larynx, contacting the aortic arch, heart, mediastinum, thyroid gland and other organs.

Among the pathological changes in organs that can damage or compress the recurrent nerve are pericarditis, aortic aneurysm, tumor (or enlargement) of the mediastinal lymph nodes, as well as a tumor of the esophagus, possible cervical lymphadenitis, and thyroid cancer, which occurs with the formation of a goiter.

Paresis of the larynx can also be provoked by increased vocal strain, as well as inhalation of cold or dusty air. The functional type of laryngeal paresis can occur as a result of stress or strong psycho-emotional experience. It happens that laryngeal paresis develops against the background of hysteria, neurasthenia, psychopathy and VSD.

Symptoms of laryngeal paresis

The first and main symptom of developing laryngeal paresis is voice disturbance (or dysphonia), as well as disturbance of the breathing process. Manifestations of voice impairment are a decrease in its sonority (sometimes there is complete aphonia, that is, absence of voice), a transition to speaking in a whisper, loss of the usual timbre of the voice, hoarseness, hoarseness of the voice or its rattling, and rapid fatigue during vocal stress.

Impaired breathing in the case of paresis of the larynx is associated with a very difficult flow of air into the respiratory tract due to a narrowing of the glottis. The latter can be expressed to varying degrees, including even asphyxia. Also, breathing problems can be caused by forced exhalation in order to perform phonation. Clinical manifestations of laryngeal paresis depend on its type.

So, for example, myopathic laryngeal paresis is usually characterized by bilateral lesions. It is characterized by disturbances in phonation or breathing, which is expressed in the form of asphyxia (in the case of paresis of the dilator larynx muscles).

If we talk about neuropathic paresis of the larynx, it is often unilateral, characterized by the slow development of weakness in the muscle itself, as well as an enlarged glottis. A few months after the disease, restoration of phonation begins by compensatory adduction of the vocal cords on the side that is healthy. Asphyxia threatens bilateral neuropathic paresis of the larynx only in the first days of the disease.

If we are talking about functional paresis of the larynx, then this type is observed in those people who have a labile nervous system. The latter, as a rule, happens after severe emotional stress or during a respiratory disease. This type of paresis is characterized by the incoming nature of impaired phonation. The voice with this type of paresis is quite loud, especially when crying or laughing, and pronounced sensations such as tickling, tickling or grinding are observed. The latter is characteristic of the larynx and pharynx. Irritability, sleep disturbance, headache, anxiety and imbalance can also be characteristic symptoms of this type of laryngeal paresis.

Diagnosis of laryngeal paresis

Several specialists will be needed to diagnose laryngeal paresis. So, for example, a patient cannot do without an otolaryngologist, neurologist, neuropsychiatrist, thoracic surgeon, endocrinologist, phoniologist and psychiatrist. Taking an anamnesis is of great importance. It is the anamnesis that can determine the type of underlying disease, due to which laryngeal paresis subsequently occurred, as well as the patient’s tendency to have a psychogenic reaction. Great importance is also given to previously undergone operations performed in the chest area, on the thyroid gland, due to which the recurrent nerve could be damaged.

Any examination of a patient with laryngeal paresis begins with microlaryngoscopy, which allows us to assess the position of the vocal cords, as well as the distance between them and their condition. The study helps determine the condition of the laryngeal mucosa, the presence of various inflammatory processes, including hemorrhages.

An effective diagnostic method can be a CT scan of the larynx or radiography. The contractility of the laryngeal muscles can be assessed using electromyography or electroneurography. Any study of vocal function in the case of laryngeal paresis also involves stroboscopy, electroglottography, phonetography, and more.

If peripheral laryngeal paresis is suspected, additional CT scanning, chest x-ray, ultrasound of the heart and thyroid gland, x-ray of the esophagus and CT of the mediastinum may be used. In order to exclude central laryngeal paralysis, doctors prescribe a CT scan of the brain and an MRI. If the examination does not reveal morphological changes, then laryngeal paresis is most likely of a functional type. In order to confirm the latter, psychological testing and examination of the patient by a psychiatrist are carried out. During the examination, the doctor’s task is also to differentiate laryngeal paresis from croup, arthritis, congenital stridor or subluxation.

Treatment of laryngeal paresis

Of course, therapy for laryngeal paresis depends on its etiology. This therapy consists of eliminating the main disease, which subsequently caused laryngeal paresis. The treatment of laryngeal paresis itself is carried out both medically and surgically.

Medicinal methods include antibiotic therapy, antiviral therapy (in the case of infectious-inflammatory etiology of laryngeal paresis), the use of neuroprotectors, as well as B vitamins (in the case of recurrent neuritis). Biogenic stimulants, as well as muscle activity stimulants, can be part of drug therapy. The use of psychotropic drugs such as antidepressants, various tranquilizers, and antipsychotics will also serve as good treatment if the patient has functional paresis of the larynx. An integral component in the treatment of laryngeal paresis can be one of the vascular drugs or a nootropic.

If we talk about surgical methods for treating laryngeal paresis, then first of all, it involves surgery to tension the vocal cord, as well as removal of diverticula, possible tumors in the esophagus, removal of tumors in the mediastinum, resection of the thyroid gland, and more. Sometimes a tracheostomy or tracheotomy procedure is an emergency.

Regardless of the type of laryngeal paresis and the primary type of treatment prescribed (medical or surgical), in addition, doctors also prescribe physiotherapeutic methods. In the case of neuropathic or myopathic paresis of the larynx, electrical stimulation, magnetic therapy, drug electrophoresis, DDT, and microwave therapy are used. If we talk about functional paresis of the larynx, then physiotherapy includes massage, reflexology, hydrotherapy and electrosleep. The doctor also prescribes a course of psychotherapy.

Sources

• http://www.krasotaimedicina.ru/diseases/zabolevanija_lor/neuropathic-laryngeal-paresis
• http://InfoGorlo.ru/gortan/parez-gortani.html
• https://www.mosmedportal.ru/illness/parez-gortani/

Etiology and pathogenesis. The causes of PG can be stroke, traumatic brain injury, neck and spine injuries, surgery on the neck, chest organs, skull, diverticulum of the trachea and esophagus, enlargement of the heart and aortic arch (tetralogy of Fallot, mitral valve disease, aortic aneurysm, ventricular hypertrophy , dilatation of the pulmonary artery). Disruption of the innervation of the larynx can develop due to compression of the recurrent nerve or its involvement in the pathological process by hematoma, inflammatory infiltrate, tumor or metastatic process. Recurrent neuritis of inflammatory, toxic and metabolic origin (viral etiology, poisoning with barbiturates, organophosphates and alkaloids, hypocalcemia, hypokalemia, diabetes and thyrotoxicosis) can also be causes of PG.
Most often, damage to the recurrent nerve develops during operations for thyroid diseases. It was noted that with primary intervention the rate of complications is 3%, with repeated intervention - 9%. A number of authors refer to complications in the form of paresis or paralysis of the recurrent nerve after surgery on the thyroid gland and vascular bundle of the neck with the general term “crash injuries” without specifying the nature of the injury. It has been noted that a violation of the innervation of the larynx develops as a result of the impact on the recurrent nerve with instruments during surgery, with hemostasis (pressure with a napkin), trauma with suture material, hematoma, wound exudate, toxic effects of anesthetics, disinfectant solutions.
Diagnostics. Diagnosis of PG is based on data from the laryngoscopic picture and anamnesis. For PG, a voiced breath is characteristic - inspiratory stridor. During laryngoscopy, the vocal folds are in the median or paramedian position. In addition, paralysis of central origin is characterized by impaired mobility of the tongue, soft palate and changes in speech articulation.
Examination of a patient with suspected paresis or PG involves the following algorithm: microlaryngoscopy, computed tomography (CT) or X-ray tomography of the larynx and trachea in direct and lateral projections, chest radiography. Clinical and biochemical blood tests are required. In case of respiratory decompensation, emergency measures are first taken to normalize breathing to the required extent, and then an examination.
Differential diagnosis of PG is carried out with other diseases that cause respiratory failure: laryngospasm, myocardial infarction, pulmonary embolism, brainstem stroke. In cases where the patient's condition does not require urgent surgery, patients with PG undergo a general clinical examination, CT scan of the neck and chest, endoscopic examination of the larynx, trachea, esophagus, lungs, ultrasound of the neck and thyroid gland, and tomographic examination of the brain. To establish the etiology of PG when its genesis is unclear, consultations with an endocrinologist, neurologist, pulmonologist, and thoracic surgeon are indicated.
Clinic. For an adequate assessment of the severity of the condition, the correct choice of treatment method and accurate prediction of the course of the disease, an assessment of the patient’s complaints and medical history is of great importance. The degree of stenosis of the lumen of the larynx and, accordingly, the severity of the patient’s condition is determined during a general examination and a general clinical examination.
With PG, all 3 functions of the larynx are affected: respiratory, protective and vocal. The voice with bilateral PH can be sonorous, sometimes there is an aspirated hoarseness. A sonorous voice in combination with inspiratory stridor, the absence of a clinical picture of acute inflammation (normal temperature, absence of pain), as well as anamnestic data (surgery performed on the neck, thyroid gland, chest, cranial cavity, etc.) should lead the doctor to think about the possibility of airway stenosis, which is caused by PG.
Impaired respiratory function develops with unilateral and bilateral PG in cases where the size of the glottis does not correspond to the anthropometric characteristics of a person, with increased body weight, small size of the larynx, significant physical activity, concomitant pathology (with acute and chronic laryngitis), acute respiratory diseases, lung disease, other factors causing respiratory failure of mixed origin.
The severity of the clinical manifestations of airway stenosis depends on the size of the glottis. The patient’s condition is also influenced by concomitant somatic pathology: cardiovascular and pulmonary, metabolic disorders (hypothyroidism, hypoparathyroidism, etc.), deformation of the cervical and thoracic spine. With laryngeal stenosis and breathing compensation, a shortening of the pause between inhalation and exhalation, prolongation of inspiration (inspiratory dyspnea), and a decrease in the number of respiratory movements per minute are noted. and distortion of the normal ratio of the number of respiratory movements and pulse beats, when instead of the normal ratio of 1:4, a ratio of 1:6, 1:7 and 1:8 appears. In this case, breathing becomes noisy, and a change in frequency, tension and pulse rhythm occurs.
With respiratory decompensation, the patient's general condition is severe, characterized by weakness, apathy or extreme anxiety. Cyanosis of the fingers and face, shortness of breath at rest and with little physical exertion, noisy breathing, loud inhalation (inspiratory dyspnea), increased breathing, involvement of auxiliary muscles in breathing, tachycardia, and increased blood pressure are noted.
In acute laryngeal stenosis, the clinical picture of the disease is more pronounced than in chronic stenosis, even with a relatively wide glottis. The clinical picture of chronic stenosis can be “blurred” due to the body’s adaptation to hypoxia due to compensatory and adaptive reactions.
Treatment. Bilateral laryngeal paresis that developed in the early postoperative period as a result of damage to the recurrent nerve, in the absence of symptoms of acute respiratory failure, is treated conservatively for 10-14 days.
Therapy includes the prescription of broad-spectrum antibacterial drugs and hormone therapy. If a hematoma is present, drugs that affect blood clotting, vitamin therapy, hyperbaric oxygenation sessions, stimulating therapy, drugs that improve the rheological properties of blood, and vascular therapy are prescribed. If the dynamics are positive, a course of phonopedic exercises is carried out. Until the symptoms of respiratory failure are compensated, the patient should be under the supervision of an otolaryngologist.
Treatment regimen for patients with bilateral PG after strumectomy in the acute phase (1-4 weeks):
- broad-spectrum antibiotics intramuscularly or intravenously - 7-9 days;
- hormones intravenously (dexamethasone, prednisolone);
- etamsylate 2.0 intramuscularly - 1-3 days. after surgery;
- HBO - 8-10 sessions from the 1st day;
- cocarboxylase 100 mg intravenously 2 times/day;
- angioprotectors (pentoxifylline) intravenously;
- pentoxifylline 5.0 intravenous drip from 6-8 days. after surgery;
- multivitamins 2.0 after 2 days. No. 5 intravenously;
- drugs with a combined metabolic effect - actovegin, intravenous vinpocetine No. 10;
- physiotherapy (phonophoresis of medicinal substances, magnetic laser);
- neuroprotectors - neostigmine methyl sulfate subcutaneously.
After 1 month. after surgery and in the presence of bilateral laryngeal paresis, we can talk about PG. Treatment tactics are determined individually depending on the following factors: the severity of symptoms of respiratory failure, the size of the glottis, the underlying disease, and concomitant pathology. Under favorable circumstances, it is possible to simultaneously perform tracheostomy and laryngoplasty to the required extent. To restore breathing, emergency tracheostomy is performed under local anesthesia or general anesthesia. Surgery under anesthesia is possible with fiberoptic tracheal intubation without the use of muscle relaxants. Most patients with bilateral PG require surgical treatment. Indications for reconstructive surgery are impaired mobility of the vocal folds and the inability to adequately breathe through natural channels, and the ineffectiveness of conservative treatment. Contraindications for plastic surgery are old age, severe concomitant pathology, and malignant diseases of the thyroid gland.
The question of the nature of palliative treatment is decided individually on the basis of objective data and laryngoscopic data (Fig. 1).

Functional surgery of bilateral PG has a number of features:
1. A thorough preoperative examination is necessary to clarify the extent of damage and factors complicating the operation.
2. The surgical approach must be carefully planned. It is necessary to choose a single method of intervention from all the alternatives. The primary operation should be 99.9% successful, because... the supply of healthy tissue is exhausted.
3. Plastic surgery of the vocal tract on the side of the operation with auto- or allo-tissues significantly improves the functional result of the operation (Fig. 2).
Rehabilitation of patients with bilateral paresis or PG allows for complete restoration of respiratory function and partial restoration of vocal function. The rehabilitation period for patients with simultaneous tracheostomy and laryngoplasty is 3-4 months.

Literature
1. Palchun V.T. Otorhinolaryngology. National leadership. M., 2008. pp. 760-766.
2. Encyclopedic Dictionary of Medical Terms. T.I.M., 1983.
3. Banar I.M. Microsurgery in the elimination of paralytic stenoses of the larynx: Abstracts of reports at the IX Congress of Otorhinolaryngologists of the USSR. November 15-17, 1988, Chisinau. pp. 314-315.
4. Kirasirova E.A. Rehabilitation of patients with traumatic injuries of the larynx and trachea of ​​various etiologies: Dis. ...doc. honey. Sci. M., 2004.
5. Continuous laryngeal nerve integrity monitoring during thyroidectomy: does it reduce the risk of injury? /M.L. Robertson et al. // Otolaryngol Head Neck Surg. 2004. Nov. Vol. 131. No. 5. P. 596-600.
6. F. Procacciante et al. Palpatory method used to identify the recurrent laryngeal nerve during thyroidectomy // World J Surg. 2001 Feb. Vol. 25. No. 2. P. 252-253.
7. Valdina E.A. Thyroid diseases. St. Petersburg, 2006. P. 368.

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X pair - vagus nerves

(n. vagus), mixed, develops in connection with the fourth and fifth gill arches, and is widely distributed due to which it got its name. Innervates the respiratory organs, organs of the digestive system (up to the sigmoid colon), thyroid and parathyroid glands, adrenal glands, kidneys, and participates in the innervation of the heart and blood vessels (Fig. 1).

Rice. 1.

1 - dorsal nucleus of the vagus nerve; 2 - nucleus of the solitary tract; 3 - nucleus of the spinal tract of the trigeminal nerve; 4 - double core; 5 - cranial root of the accessory nerve; 6 - vagus nerve; 7 - jugular foramen; 8 - superior node of the vagus nerve; 9 - lower node of the vagus nerve; 10 - pharyngeal branches of the vagus nerve; 11 - connecting branch of the vagus nerve to the sinus branch of the glossopharyngeal nerve; 12 - pharyngeal plexus; 13 - superior laryngeal nerve; 14 - internal branch of the superior laryngeal nerve; 15 - external branch of the superior laryngeal nerve; 16 - superior cardiac branch of the vagus nerve; 17 - lower cardiac branch of the vagus nerve; 18 - left recurrent laryngeal nerve; 19 - trachea; 20 - cricothyroid muscle; 21 - lower constrictor of the pharynx; 22 - middle pharyngeal constrictor; 23 - stylopharyngeal muscle; 24 - superior pharyngeal constrictor; 25 - velopharyngeal muscle; 26 - muscle that lifts the velum palatine, 27 - auditory tube; 28 - auricular branch of the vagus nerve; 29 - meningeal branch of the vagus nerve; 30 - glossopharyngeal nerve

The vagus nerve contains sensory, motor and autonomic parasympathetic and sympathetic fibers, as well as small intra-stem nerve ganglia.

Sensitive nerve fibers of the vagus nerve originate from afferent pseudounipolar nerve cells, clusters of which form 2 sensory nodes: upper (ganglion superior), located in the jugular foramen, and lower (ganglion inferior), lying at the exit from the hole. The central processes of the cells go into the medulla oblongata to the sensitive nucleus - nucleus of the solitary tract (nucleus tractus solitarii), and peripheral ones - as part of the nerve to the vessels, heart and viscera, where they end with receptor apparatus.

Motor fibers for the muscles of the soft palate, pharynx and larynx originate from the upper cells of the motor dual core.

Parasympathetic fibers originate from the autonomic dorsal nucleus(nucleus dorsalis nervi vagi) and spread as part of the nerve to the heart muscle, muscle tissue of the membranes of blood vessels and viscera. Impulses traveling along parasympathetic fibers reduce the heart rate, dilate blood vessels, narrow the bronchi, and increase peristalsis of the tubular organs of the gastrointestinal tract.

Autonomous postganglionic sympathetic fibers enter the vagus nerve along its connecting branches with the sympathetic trunk from the cells of the sympathetic ganglia and spread along the branches of the vagus nerve to the heart, blood vessels and viscera.

As noted, the glossopharyngeal and accessory nerves are separated from the vagus nerve during development, so the vagus nerve maintains connections with these nerves, as well as with the hypoglossal nerve and the sympathetic trunk through connecting branches.

The vagus nerve leaves the medulla oblongata behind the olive through numerous roots, merging into a common trunk, which leaves the skull through the jugular foramen. Next, the vagus nerve goes downward as part of the cervical neurovascular bundle, between the internal jugular vein and the internal carotid artery, and below the level of the upper edge of the thyroid cartilage - between the same vein and the common carotid artery. Through the superior thoracic aperture, the vagus nerve penetrates the posterior mediastinum between the subclavian vein and artery on the right and in front of the aortic arch on the left. Here, by branching and connections between the branches, it forms in front of the esophagus (left nerve) and behind it (right nerve) esophageal nerve plexus(plexus oesophagealis), which forms 2 near the esophageal opening of the diaphragm wandering trunk: anterior (tractus vagalis anterior) And posterior (tractus vagalis posterior), corresponding to the left and right vagus nerves. Both trunks exit the chest cavity through the esophageal opening, give branches to the stomach and end with a number of terminal branches in celiac plexus. From this plexus, fibers of the vagus nerve spread along its branches. Throughout the entire length of the vagus nerve, branches extend from it.

Branches of the cerebral vagus nerve.

1. Meningeal branch (r. meningeus) starts from the superior node and through the jugular foramen reaches the dura mater of the posterior cranial fossa.

2. Auricular branch (r. auricularis) goes from the superior node along the anterolateral surface of the jugular vein bulb to the entrance to the mastoid canal and further along it to the posterior wall of the external auditory canal and part of the skin of the auricle. On its way it forms connecting branches with the glossopharyngeal and facial nerves.

Branches of the cervical vagus nerve.

1. Pharyngeal branches (rr. pharyngeales) originate from the bottom node or immediately below it. They receive thin branches from the upper cervical ganglion of the sympathetic trunk and, between the external and internal carotid arteries, penetrate to the lateral wall of the pharynx, on which, together with the pharyngeal branches of the glossopharyngeal nerve and the sympathetic trunk, they form the pharyngeal plexus.

2. Superior laryngeal nerve (rr. laryngeus superior) branches off from the lower node and descends down and forward along the lateral wall of the pharynx medially from the internal carotid artery (Fig. 2). At the greater horn, the hyoid bone is divided into two branches: external (r. externus) And internal (r. internus). The external branch connects with branches from the superior cervical ganglion of the sympathetic trunk and runs along the posterior edge of the thyroid cartilage to the cricothyroid muscle and the inferior constrictor of the pharynx, and also intermittently gives branches to the arytenoid and lateral cricoarytenoid muscles. In addition, branches extend from it to the mucous membrane of the pharynx and the thyroid gland. The internal branch is thicker, more sensitive, pierces the thyrohyoid membrane and branches in the mucous membrane of the larynx above the glottis, as well as in the mucous membrane of the epiglottis and the anterior wall of the nasal pharynx. Forms a connecting branch with the inferior laryngeal nerve.

Rice. 2.

a — right view: 1 — superior laryngeal nerve; 2 - internal branch; 3 - outer branch; 4 - lower pharyngeal constrictor; 5 - cricopharyngeal part of the lower pharyngeal constrictor; 6 - recurrent laryngeal nerve;

b — the plate of the thyroid cartilage is removed: 1 — the internal branch of the superior laryngeal nerve; 2 - sensitive branches to the mucous membrane of the larynx; 3 - anterior and posterior branches of the inferior laryngeal nerve; 4 - recurrent laryngeal nerve

3. Superior cervical cardiac branches (rr. cardiaci cervicales superiors) - branches varying in thickness and level, usually thin, originate between the superior and recurrent laryngeal nerves and go down to the thoracic nerve plexus.

4. Inferior cervical cardiac branches (rr. cardiaci cervicales inferiors) depart from the laryngeal recurrent nerve and from the trunk of the vagus nerve; participate in the formation of the cervicothoracic nerve plexus.

Branches of the thoracic vagus nerve.

1. Recurrent laryngeal nerve (n. laryngeus recurrens) arises from the vagus nerve as it enters the chest cavity. The right recurrent laryngeal nerve bends around the subclavian artery from below and behind, and the left one around the aortic arch. Both nerves rise in the groove between the esophagus and trachea, giving branches to these organs. Final branch - inferior laryngeal nerve(n. laryngeus inferior) approaches the larynx and innervates all the muscles of the larynx, with the exception of the cricothyroid, and the mucous membrane of the larynx below the vocal cords.

Branches from the recurrent laryngeal nerve extend to the trachea, esophagus, thyroid and parathyroid glands.

2. Thoracic cardiac branches (rr. cardiaci thoracici) begin from the vagus and left laryngeal recurrent nerves; participate in the formation of the cervicothoracic plexus.

3. Tracheal branches go to the thoracic trachea.

4. Bronchial branches are directed to the bronchi.

5. Esophageal branches approach the thoracic esophagus.

6. Pericardial branches innervate the pericardium.

Within the cavities of the neck and chest, the branches of the vagus, recurrent and sympathetic trunks form the cervicothoracic nerve plexus, which includes the following organ plexuses: thyroid, tracheal, esophageal, pulmonary, cardiac:

Branches of the vagus trunks (ventral part).

1) anterior gastric branches start from the anterior trunk and form the anterior gastric plexus on the anterior surface of the stomach;

2) posterior gastric branches originate from the posterior trunk and form the posterior gastric plexus;

3)celiac branches originate mainly from the posterior trunk and take part in the formation of the celiac plexus;

4) hepatic branches are part of the hepatic plexus;

5) renal branches form renal plexuses.

XI pair - accessory nerve

(p. accessories) is mainly motor, separated during development from the vagus nerve. It begins in two parts - the vagus and the spinal cord - from the corresponding motor nuclei in the medulla oblongata and spinal cord. Afferent fibers enter the trunk through the spinal part from the cells of the sensory nodes (Fig. 3).

Rice. 3.

1 - double core; 2 - vagus nerve; 3 - cranial root of the accessory nerve; 4 - spinal root of the accessory nerve; 5 - large hole; 6 - jugular foramen; 7 - superior node of the vagus nerve; 8 - accessory nerve; 9 - lower node of the vagus nerve; 10 - first spinal nerve; 11 - sternocleidomastoid muscle; 12 - second spinal nerve; 13 - branches of the accessory nerve to the trapezius and sternocleidomastoid muscles; 14 - trapezius muscle

The wandering part comes out cranial root(radix cranialis) from the medulla oblongata below the exit of the vagus nerve, the spinal part is formed spinal root(radix spinalis), emerging from the spinal cord between the dorsal and anterior roots.

The spinal part of the nerve rises to the large foramen, enters through it into the cranial cavity, where it connects with the vagus part and forms the common trunk of the nerve.

In the cranial cavity, the accessory nerve divides into two branches: internal And external.

1. Internal branch (r. internus) approaches the vagus nerve. Through this branch, motor nerve fibers are included in the vagus nerve, which leave it through the laryngeal nerves. It can be assumed that sensory fibers also pass into the vagus and further into the laryngeal nerve.

2. Outer branch (r. externus) exits the cranial cavity through the jugular foramen to the neck and goes first behind the posterior belly of the digastric muscle, and then from inside the sternocleidomastoid muscle. Perforating the latter, the external branch goes down and ends in the trapezius muscle. Connections are formed between the accessory and cervical nerves. Innervates the sternocleidomastoid and trapezius muscles.

XII pair - hypoglossal nerve

(n. hypoglossus) is predominantly motor, formed as a result of the fusion of several primary spinal segmental nerves innervating the hypoglossal muscles.

The nerve fibers that make up the hypoglossal nerve extend from its cells motor nucleus located in the medulla oblongata. The nerve emerges from it between the pyramid and the olive with several roots. The formed nerve trunk passes through the canal of the hypoglossal nerve to the neck, where it is located first between the external (outside) and internal carotid arteries, and then descends under the posterior belly of the digastric muscle in the form of an open upward arc along the lateral surface of the hyoglossus muscle, constituting the upper side of Pirogov's triangle (lingual triangle) (Fig. 4); branches into terminal lingual branches(rr. linguales), innervating the muscles of the tongue.

Rice. 4.

1 - hypoglossal nerve in the canal of the same name; 2 - nucleus of the hypoglossal nerve; 3 - lower node of the vagus nerve; 4 - anterior branches of the 1st-3rd cervical spinal nerves (form the cervical loop); 5 - superior cervical ganglion of the sympathetic trunk; 6 - upper root of the neck loop; 7 - internal carotid artery; 8 - lower root of the neck loop; 9 - neck loop; 10 - internal jugular vein; 11—common carotid artery; 12—lower belly of the omohyoid muscle; 13 - sternothyroid muscle; 14 - sternohyoid muscle; 15 - upper belly of the omohyoid muscle; 16 - thyrohyoid muscle; 17 - hypoglossus muscle; 18 - geniohyoid muscle; 19—genioglossus muscle; 20—own muscles of the tongue; 21 - styloglossus muscle

From the middle of the nerve arch goes down along the common carotid artery superior root of the cervical loop (radix superior ansae cervicalis), which connects with her lower root (radix inferior) from the cervical plexus, resulting in the formation neck loop (ansa cervicalis). Several branches extend from the cervical loop to the neck muscles located below the hyoid bone.

The position of the hypoglossal nerve in the neck can vary. In people with long necks, the arc formed by the nerve lies relatively low, while in people with short necks it lies high. This is important to consider when performing nerve operations.

The hypoglossal nerve also contains other types of fibers. Sensory nerve fibers come from the cells of the inferior ganglion of the vagus nerve and, possibly, from the cells of the spinal ganglia along the connecting branches between the hypoglossal, vagus and cervical nerves. Sympathetic fibers enter the hypoglossal nerve along its connecting branch with the superior ganglion of the sympathetic trunk.

The areas of innervation, fiber composition and names of the cranial nerve nuclei are presented in Table. 1.

Table 1. Areas of innervation, fiber composition and names of cranial nerve nuclei

Pair	Nerve	Fiber composition (predominant)	Names of nuclei located in the brain stem	Innervated organs
	Nervus terminalis	Sympathetic(?)		Blood vessels and glands of the nasal mucosa
	Nervi olfactorii	Sensitive		Regio olfactoria of the nasal mucosa
		Sensitive		Retina of the eyeball
		Motor	Nucleus n. oculomotorii	M. Levator palpebrae superioris, m. rectus medialis, m. rectus superior, m. rectus inferior, m. obliquus inferior
		Parasympathetic	Nucleus n. oculomotorius accessorius	M. ciliaris, m. sphincterpupillae
	Nervus trochlearis	Motor	Nucleus n. trochlearis	M. obliquus superior
	Nervus trigeminus	Motor	Nucleus motorius n. trigemini	Mm. masticatorii, m. tensoris veli palatini, m. tensor tympani, venter anterior m. digastrici
		Sensitive	Nucleus mesence-phalicus n. trigemini	Skin of the frontal and temporal parts of the head, facial skin. Mucous membranes of the nasal and oral cavities, anterior 2/3 of the tongue, teeth, salivary glands, organs of the orbit, dura mater of the brain in the region of the anterior and middle cranial fossae
		Sensitive	Nucleus pontinus n. trigemini
		Sensitive	Nucleus spinalis n. trigemini
		Motor	Nucleus n. abducentis	M. rectus lateralis
		Motor	Nucleus n. facialis	Mm.faciales, t. platysma, venter posterior t. digastrici, m. styloideus, m. stapedius
	Nervus intermedius	Sensitive	Nucleus solitarius	Taste sensitivity of the anterior 2/3 of the tongue
		Parasympathetic	Nucleus salivatorius superior	Glandula lacrimalis, tunica mucosa oris, tunica mucosa nasi (glands), gl. sublingualis, gl. submandibularis, glandulae salivatoria minores
	Nervus vestibulo-cochlearis	Sensitive	Nervus cochlearis: nucl. cochlearis anterior, nucl. cochlearis posterior	Organon spirale, spiral organ
			Nervus vestibularis: nucl. vestibularis medialis, nucl. vestibularis superior, nucl. inferior	Crista ampullares. Macula urticuli, macula sacculi, membranous labyrinth of the inner ear
	Nervus glossopharyngeus	Motor	Nucleus ambiguus	M. stylopharingeus, muscles of the pharynx
		Sensitive	Nucleus solitarius	Cavum tympani, tuba auditiva, tunica mucosa radicis linguae, pharingis, tonsilla palatina, glomus caroticus, auditory tube
		Parasympathetic	Nucleus salivatorius inferior	Glandula parotidea
		Motor	Nucleus ambiquus	Tunica muscutarispharingis, m. levator velipalatini, m. uvulae, m. palatoglossus, m. palatopharyngeus, mm. laryngis
		Sensitive	Nucleus solitarius	Dura mater encephali in the area of ​​the posterior cranial fossa, skin of the external auditory canal. Organs of the neck, chest and abdomen (excluding the left side of the colon)
		Parasympathetic	Nucleus dorsalis n. vagi	Smooth muscles and glands of the thoracic and abdominal organs (except for the left side of the colon)
	Nervus accessorius	Motor	Nuclei nervi accessorii (nucl. accessorius)	M. sternocleidomastoideus, T. trapezius
	Nervus hypoglossus	Motor	Nucleus n. hypoglossi	Muscles of the tongue, musculi infrahyoids

Human anatomy S.S. Mikhailov, A.V. Chukbar, A.G. Tsybulkin

PARESIS AND PARALYSIS OF THE LARYNX

National Medical Association of Otolaryngologists

Ministry of Health of the Russian Federation

Doctor - otorhinolaryngologist Maxim Aleksandrovich Dementyev

I CONFIRM:

Chief freelancer

specialist

otorhinolaryngologist

Ministry of Health of Russia

Doctor of Medical Sciences, Professor N. A. Dykhes

President of the National Medical Association of Otorhinolaryngologists, Honored Doctor of Russia,

corresponding member RAS

INTRODUCTION

Vocal fold paralysis is more of a symptom complex of disorders caused by pathology in the vocal larynx. It is usually observed as a result of a pathological process affecting the vagus nerve or its superior and/or recurrent laryngeal branches.

In recent years, there has been a tendency to increase the number of patients with this pathology. This is due to an increase in surgical interventions on organs in contact with the lower laryngeal nerve of the larynx, the thyroid gland, trachea and esophagus, an increase in injuries in everyday life and the number of surgical interventions for tumors of the bronchi, upper and middle lobes of the lungs, the mediastinum, and an increase in the number of operations for cardiovascular anomalies.

Breathing and voice disorders worsen a person’s quality of life, lead to decreased ability to work and deterioration of interpersonal relationships. The study of diagnosis, treatment and early rehabilitation for this pathology is within the competence of otorhinolaryngologists, therapists, surgeons, and general practitioners.

Definition. Classification.

In clinical practice, the terms “paralysis” and “paresis” of the larynx are used to indicate immobility of the vocal folds.

Paresis implies a temporary impairment of the mobility of the laryngeal muscles and this diagnosis is established for patients with a disease duration of up to 6 months. It is possible to restore mobility within a period of several months to 2 years.

Paralysis is a disorder of motor function in the form of a complete absence of voluntary movements due to impaired innervation of the corresponding muscles.

Laryngeal paralysis is a condition that is one of the causes of stenosis of the upper respiratory tract, characterized by a persistent unilateral or bilateral disorder of the motor function of the larynx in the form of impairment or complete absence of voluntary movements of the vocal folds due to impaired innervation of the corresponding muscles, ankylosis of the cricoarytenoid joints, and inflammatory process.

Depending on the level of damage, laryngeal paralysis is divided into central and peripheral, unilateral and bilateral, and can be congenital or acquired. Central, in turn, are divided into organic and functional.

In the International Classification of Diseases, 10th revision, paralysis (paresis) of the larynx is classified as a respiratory disease:

Class X. Diseases of the respiratory system (J00–J99)

J30–J39 Other upper respiratory tract diseases

Clinical anatomy

Fig.1 Fig.2

a – middle position;

b – paramedian position;

c – intermediate position;

d – lateral (respiratory) position.

It is impossible to predict the final position of the vocal folds after damage to the superior and recurrent laryngeal nerves, since the nerves may regenerate and the loss of function may be partial. The pathological position of the vocal folds may be associated with fibrosis of the vocal muscle, or ankylosis of the cricoarytenoid joints.

The vagus nerve and its branches

The innervation of the larynx is bilateral and is carried out by the superior laryngeal and recurrent laryngeal nerves, which are branches of the vagus nerve.

The superior laryngeal nerve innervates the cricothyroid muscle, which provides tension on the vocal folds when singers sing high notes. Paresis or paralysis of this nerve leads to a change in the timbre of the voice and the inability to move to higher notes when singing. Sometimes with superior laryngeal nerve palsy, patients may have a normal speaking voice, but the quality of their voice when singing is impaired.

The inferior laryngeal nerve innervates the muscles of the larynx responsible for opening the glottis (during breathing, coughing), closing the glottis for phonation and during swallowing.

When identifying a picture of paralysis of the recurrent laryngeal nerve, the cause of its damage should be sought all along the base of the skull in the area of ​​the jugular foramen, further along its course in the neck, as well as in the chest, in the mediastinum.

Epidemiology, etiology and pathogenesis.

The most common cause of unilateral paralysis larynx are:

Injury to the inferior laryngeal nerve or, less commonly, the superior laryngeal nerve during thyroid surgery is one of the most common complications, accounting for 5%–9%.

Bilateral laryngeal paresis may occur as a result of the following reasons:

Organic central laryngeal paralysis occur with cortical and bulbar lesions, with the involvement of the intracranial part of the vagus nerve. Cortical paralysis is always bilateral, in accordance with the innervation from the motor nucleus. Possible causes are contusion, cerebral palsy, encephalitis, diffuse cerebral atherosclerosis, neoplastic meningitis, brain tumors.

Corticobulbar palsy occurs as a result of damage to the corticobulbar tract, for example, due to circulatory failure in the vertebral artery. Bulbar palsy can be the result of circulatory disorders in the cerebellar arteries, multiple sclerosis, syringobulbia, syphilis, rabies, poliomyelitis, encephalitis, intracerebellar tumors. At the same time, isolated paralysis of the larynx was not detected; they are usually combined with damage to the IX, XI and XII pairs of cranial nerves, which is confirmed by neurological examination. Wallenberg syndrome occurs when the vertebral or posterior inferior cerebellar artery is occluded as a result of ischemia of the lateral medulla oblongata. Symptoms include difficulty breathing, hoarseness, dizziness, nausea, vomiting, nystagmus, and disturbances in balance and gait.

Functional central palsies larynx occur in neuropsychiatric disorders due to disruption of the interaction between the processes of excitation and inhibition in the cerebral cortex.

The superior laryngeal nerve may be damaged during thyroidectomy in hypersthenic patients with a low larynx position. Damage to the external branch of the superior laryngeal nerve accompanied by a violation of the innervation of the thyroid cricoid muscle:

Causes of pathology of the recurrent nerve

Damage to the laryngeal nerves is possible with influenza, herpetic infections (unilateral paresis of the larynx is described in combination with unilateral hearing loss in Ramsay Hunt syndrome, as a result of an infection that affects the geniculate ganglion of the facial nerve, as well as other cranial nerves, including the vagus), rheumatism , syphilis, intoxication with lead, arsenic, organic solvents, streptomycin, vincristine.

If the main etiological causes of recurrent nerve paresis are excluded, its disorder is considered idiopathic.

Clinic

For an adequate assessment of the severity of the condition, the correct choice of treatment method and accurate prediction of the course of the disease, an assessment of the patient’s complaints and medical history is of great importance. The degree of stenosis of the lumen of the larynx and, accordingly, the severity of the patient’s condition is determined during a general examination and a general clinical examination. With laryngeal paresis, all 3 functions of the larynx are affected: respiratory, protective and vocal.

With unilateral paralysis of the larynx, as a result of the immobility of the paralyzed vocal fold located in the lateral or paramedian position, persistent disturbances in phonatory function are observed - hoarseness, bitonality or complete loss of voice occurs. Failure to completely close the glottis leads to aspiration. Cough and irritation of the laryngeal mucosa contribute to the development of laryngitis, tracheitis, and aspiration pneumonia. I am concerned about shortness of breath, which intensifies with vocal strain.

With bilateral laryngeal paresis, patients are more concerned about breathing problems. During physical activity, during sleep or conversation, inspiratory stridor appears. The voice may be sonorous, sometimes there is an aspirated hoarseness, and long inspiratory phases are characteristic when speaking. There may be no symptoms of aspiration or dysphagia.

The severity of the clinical manifestations of airway stenosis depends on the size of the glottis. The patient’s condition is also influenced by concomitant somatic pathology: cardiovascular and pulmonary, metabolic disorders (hypothyroidism, hypoparathyroidism, etc.), deformation of the cervical and thoracic spine. With laryngeal stenosis and breathing compensation, a shortening of the pause between inhalation and exhalation and prolongation of inspiration (inspiratory dyspnea) are noted. In this case, breathing becomes noisy, and a change in frequency, tension and pulse rhythm occurs.

With respiratory decompensation, the patient’s general condition is severe, characterized by weakness,

apathy or extreme anxiety. Cyanosis of the fingers and face, shortness of breath at rest and with little physical exertion, noisy breathing, loud inhalation (inspiratory dyspnea), increased breathing, involvement of auxiliary muscles in breathing, tachycardia, and increased blood pressure are noted.

Diagnostics

Diagnosis of laryngeal paresis is based on the following data:

In addition, paralysis of central origin is characterized by impaired mobility of the tongue, soft palate and changes in speech articulation.

Algorithm for examining a patient to determine the cause of laryngeal paresis:

If the origin of laryngeal paresis is unclear, consultations with an endocrinologist, neurologist, pulmonologist, or thoracic surgeon are indicated.

In case of respiratory decompensation, emergency measures are first taken to normalize breathing to the required extent, and then an examination.

Long-term absence of vocal function leads to loss of the image fixed in memory, muscle atrophy, fibrosis of the capsule of the cricoarytenoid joint and dysfunction of the posterior cricoarytenoid muscle. These factors hinder voice improvement.

Differential diagnosis of laryngeal paralysis is carried out with other diseases that cause respiratory failure: laryngospasm, myocardial infarction, pulmonary embolism, brainstem stroke.

The vocal folds may be immobile due to dislocations, subluxations, ankylosis or arthritis of the cricoarytenoid joints. In this case, there is asymmetry of the joints with signs of inflammation on the affected side.

According to "Clinical Practice Guideline: Improving Voice Outcomes after Thyroid Surgery" It is recommended to examine the vocal folds in patients with both normal voice and voice disorders before surgery on the thyroid gland. It is necessary to warn the patient about possible postoperative voice and breathing disorders, discuss intervention tactics with the anesthesiologist, conduct intraoperative monitoring of the recurrent nerves, including laryngeal electromyography (LEMG), try to prevent damage to the upper laryngeal nerves (if possible, leave the upper pole of the thyroid gland), in the postoperative period, monitor changes in the patient’s voice (with documentation 2 weeks and 2 months after surgery), consultation with an otolaryngologist is required with examination of the larynx and assessment of the vocal folds; if the patient’s voice changes, rehabilitation is necessary.

Features in children

A special group consists of congenital laryngeal paralysis. Congenital laryngeal paralysis is associated with such hereditary syndromes and diseases as Charcot-Marie-Tooth disease, Arnold-Chiari malformation, Leigh syndrome, Williams syndrome, neuromuscular diseases, Down syndrome, Mobius-Poland syndrome.

The cause of unilateral laryngeal paresis in children can be: neoplasms (29%), postoperative complications (24%), inflammatory processes (21%), postintubation and external injuries of the larynx (8%), central (5%) and idiopathic paralysis (13%). ).

In patients with congenital bilateral laryngeal paralysis, a selective approach is required when considering tracheostomy, since in some cases spontaneous restoration of mobility of the paralyzed vocal folds occurs.

Damage to the recurrent nerve occurs during cardiac surgery in children. The incidence of damage is up to 4% according to various sources, especially often during surgical interventions for coarctation of the aorta - 2.5%.

Surgical closure of the ductus Botalov, especially in neonates with extremely low body weight (< 1000г),часто приводит к парезу (параличу) левого возвратного нерва и проявляется стридором в послеоперационном периоде, осиплостью голоса, проблемами при кормлении и аспирацией. По истечении 9 месяцев жизни у части пациентов наблюдается компенсаторная гипертрофия правой голосовой складки, не возникает проблем при кормлении, но длительно сохраняется слабый плач. Некоторым детям требуется наложение гастростомы для предотвращения аспирации пищи в нижние дыхательные пути.

Laryngeal paresis in rare diseases

Tapia syndrome, accompanied by unilateral paresis of the larynx and tongue, involving the sternocleidomastoid and trapezius muscles, can develop as a complication during mask ventilation due to displacement of the head, during tracheal intubation during surgery or bronchoscopy.

Neuralgic amyotrophy (Personage-Turner syndrome) is an idiopathic brachial plexopathy with an acute onset in the form of pain in the shoulder and shoulder girdle, after which paresis and atrophy of the muscles of the shoulder girdle develop. After a few weeks/months, the symptoms completely regress. With this disease, unilateral, or less often bilateral, paresis of the larynx is possible, with complete restoration of the function of the affected fold with regression of the symptoms of the underlying disease.

Multiple system atrophy is a progressive neurodegenerative disease that causes pyramidal, cerebellar and autonomic dysfunction. Manifested by arterial hypotension, urinary retention, constipation, ataxia, rigidity and postural disturbances. One of the symptoms can be either unilateral (usually with damage to the left vocal fold) or bilateral laryngeal paresis.

Treatment tactics

The disease that caused laryngeal paresis is treated.

Conservative treatment

In the early stages of rehabilitation of vocal function with unilateral laryngeal paresis Stimulating therapy is used:(proserine, galantamine, nimodipine, glucocorticosteroids), neuromuscular electrophonopedic stimulation in combination with phonopedia, which contribute to the early restoration of voice sonority in 60% of cases and can significantly reduce the rehabilitation time of patients (level of evidence III). Stimulating therapy is contraindicated after surgery for a malignant neoplasm of the thyroid gland, organs of the neck, mediastinum and chest, and in the case of an unoperated thyroid gland - hyperthyroidism, the presence of nodes in the thyroid gland, benign skin formations at the locations of the electrodes, and somatic pathology.

It is mandatory to perform stroboscopy of the larynx when observing patients during treatment. A favorable prognostic sign of restoration of the function of the affected nerve is vibrations of the mucous membrane along the edge of the paralyzed vocal fold, the so-called displacement of the mucous “wave”.

With bilateral paresis, restoration of normal airway patency is of paramount importance. In case of respiratory decompensation, tracheotomy is indicated.

Bilateral laryngeal paresis in the early postoperative period as a result of damage to the recurrent nerve, in the absence of symptoms of acute respiratory failure, is treated conservatively for 10–14 days. Therapy includes the prescription of broad-spectrum antibacterial drugs and hormone therapy (level of evidence III). In the presence of a hematoma, medications that affect blood clotting, vitamin therapy, hyperbaric oxygenation sessions, drugs that improve the rheological properties of blood, and vascular therapy are prescribed (level of evidence III). If the dynamics are positive, a course of phonopedic exercises is carried out.

Surgical treatment

Various methods of surgical treatment of peripheral paralysis of the larynx are aimed not only at widening the glottis and restoring adequate breathing, but also, if possible, at preserving phonatory function. The difficulty of treatment lies in the fact that restoration of both functions of the larynx requires the creation of opposite functional conditions: for the respiratory one, a sufficiently wide glottis, for the phonatory one, its narrowing.

Treatment tactics are determined individually depending on the following factors: the severity of symptoms of respiratory failure, the size of the glottis, the underlying disease, and concomitant pathology. Under favorable circumstances, it is possible to simultaneously perform tracheostomy and laryngoplasty to the required extent. To restore breathing, an urgent tracheotomy is performed under local anesthesia or general anesthesia. Surgery under anesthesia is possible with fiberoptic tracheal intubation without the use of muscle relaxants.

Surgical interventions for bilateral laryngeal paralysis

Most patients with bilateral laryngeal paralysis require surgical treatment. Indications for reconstructive surgery are impaired mobility of the vocal folds and the inability to adequately breathe through natural channels, and the ineffectiveness of conservative treatment. Contraindications for plastic surgery are old age, severe concomitant pathology, and malignant diseases of the thyroid gland.

The question of the nature of surgical treatment is decided individually on the basis of objective data and laryngoscopic data.

Functional surgery for bilateral paralysis has a number of features:

1. A thorough preoperative examination is necessary to clarify the extent of damage and factors complicating the operation.

2. The surgical approach must be carefully planned. It is necessary to choose a single method of intervention from all the alternatives. The primary operation should be 99.9% successful, because... the supply of healthy tissue is exhausted.

Surgical interventions for unilateral laryngeal paralysis

Surgical interventions for unilateral laryngeal paralysis include three main groups:

1. Neuroplasty - a method of reinnervation of the larynx includes neuroraphy ansacervicalis with the stump of the recurrent laryngeal nerve, which leads to medialization of the vocal fold, helps restore its tone, while improving the parameters of voice formation.

2. Implantation of various substances into the vocal fold often leads to complications such as the formation of a foreign body granuloma, migration or absorption of the implanted substance, infection with the development of an abscess, medialization of the false fold and ventricle, leading to even greater dysphonia.

3. Surgery of the laryngeal skeleton is represented by three types of interventions: thyroplasty, adduction of the arytenoid cartilage, traction of the lateral cricoarytenoid muscle.

If there is no effect from conservative treatment, surgical methods are used, but not earlier than 12 months after the onset of laryngeal paresis.

Injection laryngoplasty is a procedure performed to change the shape of the vocal cords or their mobility, and can be performed under general anesthesia or local anesthesia. Some doctors prefer to perform this procedure under local anesthesia, since this allows you to immediately verify the effectiveness of the treatment. If more injections are needed, they can be given right away. In case of unilateral paralysis of the larynx, in order to improve vocal function, the technique of medialization of the affected vocal fold is used with the help of various agents: derivatives of hyaluronic acid of own adipose tissue, carboxymethylcellulose, polydimethylsiloxane.

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