Is bulbar syndrome treatable? Pseudobulbar palsy. Manifestations and causes of pseudobulbar syndrome

Bulbar syndrome is a serious neurological disease. The pathology leads to paralysis of the tongue, muscles of the pharynx, and lips. Progressive bulbar palsy poses a risk to human health and is difficult to treat.

The patient may feel that he is having difficulty eating food on his own. Will need to visit medical institution as soon as the first symptoms appear.

If you ignore the signs, there will be irreversible consequences. Bulbar syndrome dangerous disease and it must be treated promptly.

The bulbar nerves are affected due to neurological development. This leads to changes in the central nervous system. When motor nerve endings are affected, peripheral paralysis occurs.

Observed following reasons bulbar syndrome:

, due to which the medulla oblongata was affected;
infectious head disease;
malignant and benign tumor processes;
bruises and fractures of the base of the skull;
inflammation in the brain;
botulinum toxin intoxication.

It often happens that the cause of bulbar palsy is hypertension. The disease worsens the patient's condition over time. Against this background, atherosclerosis develops, vascular spasm occurs, and this leads to a stroke, which is why bulbar syndrome occurs.

If you feel unwell, you should consult a doctor. If bulbar symptoms are ignored, various complications can occur.

Symptoms

There are several types of bulbar syndrome. The acute form of the pathology passes quickly and develops against the background of a stroke, swelling or contusion of the brain, or encephalitis. If the disease is progressive, then bulbar palsy occurs slowly.

It happens in the background various pathologies, which are connected to the central nervous system. Most often this is Kennedy amyatrophy, tumor formations in the brain. Bulbar syndrome can be bilateral or unilateral. The pathology is often reflected in the movements of the larynx, tongue, and pharynx.

There are three signs that appear with bulbar palsy:

Dysphagia– this is when swallowing is impaired. The patient has difficulty swallowing food due to progressive paralysis of the soft palate. A weak patient may easily choke on food. Over time, progressive bulbar palsy develops, and the patient has difficulty eating even soft foods.
Dysarthria. There is a violation of the pronunciation of words. At first, the patient can make sounds, but bulbar palsy leads to a complete absence of speech.
Dysphonia leads to impaired vocal functions. A person observes how hoarseness and hoarseness develop.

A patient with bulbar palsy may be affected by facial expressions and facial expressions. The mouth may be open and saliva will be released. When eating, food may fall out of the mouth. Bulbar syndrome can lead to serious consequences in the form of disorders of the respiratory and cardiovascular systems.

The patient experiences changes in the oral cavity. The tongue becomes uneven, folded and twitches at times. If the patient has unilateral bulbar syndrome, then the changes will be on one side. With bilateral lesions, the tongue may be completely immobile.

When do sublingual changes occur? nerve ending, then saliva begins to flow heavily. Many patients may suffer from severe salivation, so they use a handkerchief on a regular basis. At the first manifestations of bulbar syndrome, it is necessary to visit a specialist.

Diagnostics

A neurologist prescribes diagnosis and treatment of bulbar palsy. First of all, the specialist conducts a neurological examination and electromyography. Based on the diagnostic results, the doctor identifies the cause of bulbar syndrome and prescribes treatment. The specialist must determine the breathing rate and heartbeat.

The following studies are carried out for bulbar palsy:

Radiography makes it possible to detect fractures and bruises of the head, and tumor processes.

Electromyography helps check the performance of the muscles of the tongue, neck, arms, and legs. This type of diagnosis reveals muscle activity in a calm state and during contraction.
Esophagoscopy. This research method helps to examine the esophagus. The performance of the pharynx muscles and vocal cords is assessed.

Magnetic resonance imaging. A fast and high-quality diagnostic method that identifies various diseases in 90% of cases. MRI makes it possible to evaluate the condition of all organs. Tomography helps identify brain pathologies. The study is most often carried out using a contrast agent.
Electrocardiogram. Makes it possible to find different heart diseases and study heart rhythm.

Laboratory tests are carried out to identify inflammatory processes, infections, hemorrhage. A general analysis of urine, blood and cerebrospinal fluid examination is prescribed.

When conducting computed tomography and MRI, tumor formations, edema, and cysts are detected in the brain. If the first symptoms of bulbar palsy appear, you should immediately visit a doctor. The disease only progresses over time and cannot be avoided without treatment. the disease can be fatal.

Bulbar palsy in children

Bulbar palsy develops in unborn children. There is strong moisture in the oral mucosa; in normal conditions it should be almost dry. If you examine the baby's mouth when he is crying, you will notice that the tongue is slightly turned to the side. This sign appears when the hypoglossal nerve ending is disrupted.

Bulbar syndrome in children occurs in rare cases, as it involves damage to the brain stems. They cease to function, and life without them is impossible. Pseudobulbar palsy often occurs in children and is extremely difficult. The baby suffers not only from loss of speech, but also from changes in muscle tone.

Hyperkinesis and various disorders motor apparatus. This leads to what happens childishly cerebral paralysis. The disease can begin to affect newborns and children under two years of age. Most often, cerebral palsy occurs due to birth injuries.

With bulbar syndrome, the child experiences impaired motor skills. It happens that the upper facial part is damaged, which causes immobility. The child does not have the opportunity to take care of himself. Such children look clumsy, have difficulty chewing and swallowing food, and keep drool in their mouth. Must be assigned correct treatment with bulbar palsy.

Treatment

If the patient acute form bulbar palsy, then must be provided in a timely manner health care. Therapy will be aimed at eliminating complications of the pathology. First of all, the patient is connected to a ventilator. This is necessary in order to maintain the patient’s vitality and restore breathing during bulbar syndrome.

Prozerin, Adenosine triphosphate, vitamins are used, they help activate swallowing reflexes and improve gastric motility. By regulating swallowing, the production of gastric juice and saliva is reduced. The patient is given an atropine drip. The drug is available in various forms, but since the patient has a impaired swallowing reflex, the medicine is administered intravenously.

Eating through a tube. This method feeding makes it possible to avoid food getting into respiratory system. If a person is in a comatose state, then he is given a dropper nutritional elements and glucose. Patients suffering from bulbar palsy are sensitive, irritable, and depressed.

It happens that many patients may refuse to eat because they are afraid of choking. Such patients are referred for treatment to a psychotherapist. Drug therapy for bulbar syndrome is also prescribed.

Medicines

The following are used to treat pathology: medications:

Prozerin is prescribed to restore muscle performance. Helps improve swallowing functions and gastric motility. If you have high blood pressure, the drug lowers it.
Atropine is used for severe salivation.
Antibiotics are prescribed if there are infectious diseases.
Torsemide and Furosemide are decongestant diuretics that are needed to relieve swelling in the head.
Parmidine, Alprostan, are used for various diseases vascular system.
Vitamins B, Neuromultivit, Milgamma, Vitagamma, they are prescribed to support and restore the central nervous system.
Products with glutamic acid improve the metabolic process in the nervous system.

All medications must be taken after they are prescribed by a doctor. Some medications have a number of contraindications and side effects. Self-medication is not recommended, as it can only worsen the patient’s condition with bulbar palsy. Must be present special food, since with an advanced disease the patient cannot eat food on his own.

The patient only feeds through a nasogastric or gastric feeding tube, and a special mixture passes through it. The doctor must show how to properly feed a patient at home with bulbar palsy. The specialist selects the necessary diet to provide the patient with all the necessary vitamins for a speedy recovery.

The food is given liquid, without lumps or solid pieces. As a rule, products are used that have a homogeneous mass and easily pass through a special tube. Nutrizon is available in the form of powder and ready-made drink. Part this drug includes all the necessary proteins, fats, carbohydrates, vitamins, microelements.

The patient's feeding tube can be used for about five days. Then it is replaced or washed and treated well. Syringes that are necessary for administering food should be cleaned immediately after feeding.

Traditional methods of treatment

Possible together with drug therapy combine traditional medicine. There are many prescriptions for the treatment of progressive bulbar palsy. The medicinal mixture is prepared on the basis of white mistletoe, valerian root, oregano, and yarrow. To prepare the tincture, take all the listed plants in equal quantities and pour boiling water over them. Use herbal remedy You need one hundred grams three times a day before meals.

The following recipe is prepared from mint, oregano, mistletoe, motherwort, thyme, and lemon balm. You need to mix everything together and pour hot water. Wait until it cools down and strain the contents. A remedy for the treatment of bulbar palsy is taken orally, one hundred grams after meals.
Alcohol tincture based on peony root. To prepare, you need to grate the plant and add alcohol one to ten. Place the tincture in a warm place for seven days; as soon as it is ready, strain it. You need to take 35 drops three times a day before eating.

To make a sage tincture, take the plant and pour boiling water over it. Place in a warm place for eight hours. Strain and consume a tablespoon several times a day after meals. You can take medicinal baths from sage and rose hips for bulbar syndrome. Take about 300 grams of the plant, fill it with water and set it to cook for 15 minutes. Let it sit for about an hour, strain the product and pour it into the bath. The procedure should last at least thirty minutes. In order to achieve an effect in the treatment of bulbar palsy, you need to take a bath a couple of times a week.

You need to take fresh tanning sumac leaves and add hot water. Place in a warm place for an hour and strain the product. You need to take a tablespoon about three times a day. If used correctly traditional methods treatment, this will help reduce bulbar palsy. Before use, you should consult your doctor.

Progressive bulbar palsy is very dangerous if left untreated. At the first symptoms, you must contact a medical facility. A neurologist will conduct an examination and prescribe a comprehensive diagnosis.

With various brain lesions, complexes of characteristic disorders called syndromes develop. One of them is pseudobulbar palsy. This condition occurs when nuclei medulla oblongata cease to receive sufficient regulation from overlying centers. It does not pose an immediate threat to the patient's life, unlike bulbar palsy. Correct differential diagnosis between these two syndromes not only allows the doctor to determine the level of damage, but also helps to assess the prognosis.

How does pseudobulbar syndrome occur?

The brain has “old” sections that can work autonomously, without the regulatory influence of the cortex. This supports vital activity even when the higher parts of the nervous system are damaged. But such basic neuronal activity is accompanied by disruption of complex motor acts. After all, for coordinated work different groups muscles need precise coordination of various nerve impulses, which cannot be provided only by subcortical structures.

Pseudobulbar syndrome (paralysis) occurs when the higher regulation of the motor (motor) nerve nuclei in the medulla oblongata is disrupted. These include the centers of the 9th, 10th and 12th pairs of cranial nerves. Many pathways in the brain are partially or completely crossed. Therefore, complete disappearance of control impulses occurs with bilateral damage to the frontal parts of the cerebral cortex or with extensive damage to the subcortical nerve pathways.

The cores left without a “commander” begin to work autonomously. In this case, the following processes occur:

the function of the respiratory muscles and heart is preserved, that is, vital acts remain unchanged;
articulation (pronunciation of sounds) changes;
due to paralysis of the soft palate, swallowing is impaired;
involuntary stereotypical grimaces appear with imitation of emotional reactions;
vocal cords become inactive, phonation is impaired;
deep unconditioned reflexes of oral automatism are activated, which normally can only be found in infants.

The nuclei of the medulla oblongata, the cerebellum, the brainstem, the limbic system and many pathways between individual subcortical structures of the brain take part in the formation of such changes. Their disinhibition and discoordination of work occurs.

Difference between bulbar syndrome and pseudobulbar syndrome

Bulbar syndrome is a complex of disorders that occur when the nuclei themselves in the medulla oblongata are damaged. These centers are located in a thickening of the brain called the bulba, which gives the syndrome its name. And with pseudobulbar palsy, the nuclei continue to function, although coordination between them and other nerve formations is disrupted.

In both cases, articulation, phonation and swallowing are affected. But the mechanism of development of these disorders is different. With bulbar syndrome, severe peripheral paralysis of the muscles of the pharynx and soft palate occurs with degeneration of the muscles themselves, often accompanied by a violation of vital functions. important functions. And with pseudobulbar syndrome, the paralysis is central in nature, the muscles remain unchanged.

Causes of pseudobulbar syndrome

Atherosclerosis can lead to damage to neurons in the cerebral cortex and, as a result, to pseudobulbar syndrome.

Pseudobulbar syndrome results from damage to neurons in the frontal cortex or the nerve pathways leading from these cells to nuclei in the medulla oblongata. The following conditions can lead to this:

hypertonic disease with the formation of multiple small or repeated strokes;
atherosclerosis of small vessels of the brain;
unilateral damage to the brain arteries of medium and small caliber, which leads to steal syndrome (blood supply deficiency) in symmetrical areas;
vasculitis with systemic lupus erythematosus, tuberculosis, syphilis, rheumatism;
degenerative diseases (Pick's disease, supranuclear palsy, and others);
consequences ;
consequences of brain damage in utero or as a result of birth trauma;
consequences of severe ischemia after clinical death and comatose states;
severe metabolic disorders due to long-term use of valproic acid drugs;
tumors frontal lobes or subcortical structures;

Most often, pseudobulbar syndrome occurs in chronic progressive conditions, but it can also appear in acute oxygen starvation many parts of the brain.

Clinical picture

Such patients may laugh or cry against their own will.

Pseudobulbar syndrome is characterized by a combination of impaired swallowing, speech, the appearance of violent grimaces (laughter and crying) and symptoms of oral automatism.

The appearance of choking and pauses before swallowing is explained by paresis (weakness) of the muscles of the pharynx and soft palate. In this case, the disturbances are symmetrical and not as severe as with bulbar palsy. There is no atrophy or twitching of the affected muscles. And the pharyngeal reflex can even be increased.

Speech impairments with pseudobulbar syndrome affect only pronunciation - speech becomes unclear and blurred. This is called dysarthria and can be caused by paralysis or spastic muscle tone. In addition, the voice becomes dull. This symptom is called dysphonia.

The syndrome necessarily includes symptoms of oral automatism. Moreover, the patient himself does not notice them; these signs are detected during special tests during a neurological examination. Mild irritation of some areas leads to contraction of the mental or perioral muscles. These movements resemble sucking or kissing. For example, such a reaction appears after touching the palm or corner of the mouth, or tapping the back of the nose. And with a light blow to the chin, the chewing muscles contract, closing the slightly open mouth.

Violent laughter and crying often occur. This is the name given to characteristic short-term contractions facial muscles, similar to emotional reactions. These involuntary grimaces are not associated with any impressions and cannot be stopped by an effort of will. Voluntary movements of the facial muscles are also impaired, which is why a person may open his mouth when asked to close his eyes.

Pseudobulbar syndrome is not isolated; it appears against the background of other neurological disorders. The big picture depends on the root cause. For example, damage to the frontal lobes is usually accompanied by emotional and volitional disorders. In this case, a person may become inactive, lacking initiative, or, conversely, disinhibited in his desires. Dysarthria is often combined with memory loss and speech disorders (aphasia). When subcortical zones are damaged, various motor disorders often occur.

How to treat

When pseudobulbar syndrome is detected, the underlying disease must first be treated. If it is hypertension, antihypertensive and vascular therapy is prescribed. For specific vasculitis (syphilitic, tuberculosis), antimicrobial agents and antibiotics must be used. In this case, treatment can be carried out jointly with specialized specialists - a dermatovenerologist or a phthisiatrician.

In addition to specialized therapy, drugs are prescribed to improve microcirculation in the brain, normalize the functioning of nerve cells and improve the transmission of nerve impulses. For this purpose, various vascular, metabolic and nootropic agents, anticholinesterase drugs are used.

No universal remedy for the treatment of pseudobulbar syndrome. The doctor selects a scheme complex therapy taking into account all existing violations. In addition to taking medications, special exercises for the affected muscles, breathing exercises according to Strelnikova, and physiotherapy can be used. If children have speech disorders, classes with a speech therapist are required; this will significantly improve the child’s adaptation in society.

Unfortunately, it is usually not possible to completely get rid of pseudobulbar syndrome, because such disorders occur with severe bilateral brain lesions, which are often accompanied by the death of many neurons and destruction of nerve pathways. But treatment will compensate for the disorders, and rehabilitation activities will help the person adapt to the problems that have arisen. Therefore, you should not neglect your doctor’s recommendations, because it is important to slow down the progression of the underlying disease and preserve nerve cells.

Motor neuron diseases (amyotrophic lateral sclerosis, Fazio-Londe spinal amyotrophy, Kennedy bulbospinal amyotrophy).
Myopathies (oculopharyngeal, Kearns-Sayre syndrome).
Dystrophic myotonia.
Paroxysmal myoplegia.
Myasthenia.
Polyneuropathy (Guillain-Barré, post-vaccination, diphtheria, paraneoplastic, with hyperthyroidism, porphyria).
Polio.
Processes in the brain stem, posterior cranial fossa and craniospinal region (vascular, tumor, syringobulbia, meningitis, encephalitis, granulomatous diseases, bone anomalies).
Psychogenic dysphonia and dysphagia.

Motor neuron diseases

The end stage of all forms of amyotrophic lateral syndrome (ALS) or the onset of its bulbar form are typical examples of bulbar dysfunction. Usually the disease begins with bilateral damage to the nucleus of the XII nerve and its first manifestations are atrophy, fasciculations and paralysis of the tongue. In the first stages, dysarthria without dysphagia or dysphagia without dysarthria may occur, but quite quickly there is a progressive deterioration of all bulbar functions. At the onset of the disease, difficulty swallowing liquid food is observed more often than solid food, but as the disease progresses, dysphagia develops when eating solid food. In this case, the weakness of the tongue is accompanied by weakness of the masticatory and then facial muscles, the soft palate hangs down, the tongue in the oral cavity is motionless and atrophic. Fasciculations are visible in it. Anarthria. Constant drooling. Weakness of the respiratory muscles. In the same area or in other regions of the body, symptoms of upper motor neuron involvement are detected.

Criteria for the diagnosis of amyotrophic lateral sclerosis

the presence of signs of damage to the lower motor neuron (including EMG - confirmation of the anterior horn process in clinically intact muscles); clinical symptoms upper motor neuron lesions (pyramidal syndrome); progressive course.

“Progressive bulbar palsy” is today considered as one of the variants of the bulbar form of amyotrophic lateral sclerosis (just like “primary lateral sclerosis” as another type of amyotrophic lateral sclerosis, occurring without clinical signs of damage to the anterior horns spinal cord).

Increasing bulbar palsy can be a manifestation of progressive spinal amyotrophy, in particular, the terminal stage of Werdnig-Hoffmann amyotrophy, and in children, Fazio-Londe spinal amyotrophy. The latter refers to autosomal recessive spinal amyotrophies with onset in early childhood. In adults, X-linked bulbar spinal amyotrophy is known, beginning at the age of 40 years and older (Kennedy disease). Characterized by weakness and atrophy of the proximal muscles upper limbs, spontaneous fasciculations, limited volumes active movements in the arms, decreased tendon reflexes in the biceps and triceps brachii muscles. As the disease progresses, bulbar (usually mild) disorders develop: choking, tongue atrophy, dysarthria. The leg muscles are involved later. Characteristics: gynecomastia and pseudohypertrophy of the calf muscles.

With progressive spinal amyotrophies the process is limited to damage to the cells of the anterior horns of the spinal cord. Unlike amyotrophic lateral sclerosis, the process here is always symmetrical, it is not accompanied by symptoms of upper motor neuron involvement and has a more favorable course.

Myopathies

Some forms of myopathies (oculopharyngeal, Kearns-Sayre syndrome) may manifest as impaired bulbar functions. Oculopharyngeal myopathy (dystrophy) is a hereditary (autosomal dominant) disease, characterized by a late onset (usually after 45 years) and muscle weakness, which is limited to the facial muscles (bilateral ptosis) and bulbar muscles (dysphagia). Ptosis, swallowing disorders and dysphonia progress slowly. The main maladaptive syndrome is dysphagia. The process extends to the limbs only in some patients and in late stages diseases.

One of the forms of mitochondrial encephalomyopathy, namely Kearns-Sayre syndrome (“ophthalmoplegia plus”), manifests itself, in addition to ptosis and ophthalmoplegia, with a myopathic symptom complex that develops later eye symptoms. Involvement of the bulbar muscles (larynx and pharynx) is usually not severe enough, but can lead to changes in phonation and articulation, and choking.

Obligate signs of Kearns-Sayre syndrome:

external ophthalmoplegia
pigmentary degeneration retina
cardiac conduction disturbances (bradycardia, atrioventricular block, syncope, possible sudden death)
increased protein levels in the cerebrospinal fluid

Dystrophic myotonia

Dystrophic myotonia (or Rossolimo-Kurshman-Steinert-Batten myotonic dystorophy) is inherited in an autosomal dominant manner and affects men 3 times more often than women. Her debut occurs at the age of 16-20 years. Clinical picture consists of myotonic, myopathic syndromes and extramuscular disorders ( dystrophic changes in the lens, testes and other endocrine glands, skin, esophagus, heart and sometimes in the brain). Myopathic syndrome is most pronounced in the muscles of the face (masticatory and temporal muscles, which leads to a characteristic facial expression), neck and, in some patients, in the limbs. Damage to the bulbar muscles leads to a nasal tone of voice, dysphagia and choking, and sometimes to respiratory disorders (including sleep apnea).

Paroxysmal myoplegia (periodic paralysis)

Paroxysmal myoplegia is a disease (hypokalemic, hyperkalemic and normokalemic forms), manifested by generalized or partial attacks of muscle weakness (without loss of consciousness) in the form of paresis or plegia (up to tetraplegia) with decreased tendon reflexes and muscle hypotonia. The duration of attacks varies from 30 minutes to several days. Provoking factors: rich food rich in carbohydrates, abuse of table salt, negative emotions, physical activity, night sleep. Only in some attacks there is involvement of the cervical and cranial muscles. Rarely the respiratory muscles are involved in the process to one degree or another.

Differential diagnosis carried out with secondary forms of myoplegia, which occur in patients with thyrotoxicosis, with primary hyperaldosteronism, hypokalemia in some gastrointestinal diseases, and kidney diseases. Iattrogenic variants of periodic paralysis have been described when prescribed drugs that promote the removal of potassium from the body (diuretics, laxatives, licorice).

Myasthenia gravis

Bulbar syndrome is one of the dangerous manifestations of myasthenia gravis. Myasthenia gravis is a disease whose leading clinical manifestation is pathological muscle fatigue, which decreases until complete recovery after taking anticholinesterase drugs. The first symptoms are often dysfunction of the extraocular muscles (ptosis, diplopia and limited mobility eyeballs) and facial muscles, as well as muscles of the limbs. In approximately one third of patients, involvement of the masticatory muscles, muscles of the pharynx, larynx and tongue is observed. There are generalized and local (mainly ocular) forms.

Differential diagnosis myasthenia gravis is carried out with myasthenic syndromes (Lambert-Eaton syndrome, myasthenic syndrome with polyneuropathies, myasthenia-polymyositis complex, myasthenic syndrome with botulinum intoxication).

Polyneuropathy

Bulbar palsy in polyneuropathies is observed in the picture of a generalized polyneuropathic syndrome against the background of tetraparesis or tetraplegia with characteristic sensory disorders, which facilitates the diagnosis of the nature of bulbar disorders. The latter are characteristic of such forms as acute demyelinating polyneuropathy Guillain-Barré, post-infectious and post-vaccination polyneuropathy, diphtheria and paraneoplastic polyneuropathy, as well as polyneuropathy in hyperthyroidism and porphyria.

Polio

Acute poliomyelitis, as a cause of bulbar palsy, is recognized by the presence of general infectious (preparalytic) symptoms, the rapid development of paralysis (usually in the first 5 days of illness) with greater damage to the proximal parts than the distal ones. A period of reverse development of paralysis soon after its appearance is characteristic. There are spinal, bulbar and bulbospinal forms. More often affected lower limbs(in 80% of cases), but the development of hemitype or cross-type syndromes is possible. Paralysis is sluggish in nature with loss of tendon reflexes and rapid development of atrophy. Bulbar palsy can be observed in the bulbar form (10-15% of the entire paralytic form of the disease), in which the nuclei of not only the IX, X (less often XII) nerves, but also facial nerve. Damage to the anterior horns of segments IV-V can cause respiratory paralysis. In adults, the bulbospinal form more often develops. Involvement of the reticular formation of the brain stem can lead to cardiovascular (hypotension, hypertension, cardiac arrhythmias), respiratory (“atactic breathing”) disorders, swallowing disorders, and disturbances in the level of wakefulness.

Differential diagnosis carried out with others viral infections, capable of affecting the lower motor neuron: rabies and herpes zoster. Other diseases that often require a differential diagnosis from acute polio include Guillain-Barré syndrome, acute intermittent porphyria, botulism, toxic polyneuropathies, transverse myelitis, and acute spinal cord compression due to epidural abscess.

Bulbar syndrome is a neurological pathology caused by dysfunction of three pairs of cranial nerves simultaneously: IX, X and XII. A disorder of the motor innervation of the muscles of the head and neck is manifested by a violation of the swallowing process, throwing food into the respiratory organs, speech abnormalities, hoarseness of the voice, pathological change taste sensations and vegetative symptoms.

Bulbar syndrome is characterized by blocking of nerve impulses at the level of cranial nuclei or motor fibers. Light form pathology develops with unilateral damage to the IX, X and XII nerves. Bilateral damage to the same nerves leads to the development of severe disease.

Bulbar syndrome, in contrast, has a more severe course and is manifested by life-threatening dysfunctions: arrhythmia, atrophy of paralyzed muscles and respiratory arrest. A triad of symptoms is characteristic: dysphonia, dysphagia, dysarthria. Some patients are not even able to eat on their own. Diagnosis of the syndrome is based on patient examination data and results additional examinations. Typically, treatment begins with emergency measures, and then moves on to etiotropic, pathogenetic and symptomatic therapy.

Bulbar syndrome is a severe progressive process leading to loss of ability to work and deterioration in quality of life. A quickly emerging syndrome with a rapid increase in clinical symptoms is deadly and requires emergency medical care and hospitalization of patients in the intensive care unit.

Classification

Bulbar syndrome can be acute, progressive, alternating with one- or two-sided lesions.

Acute paralysis is characterized by a sudden onset and rapid development. Its main causes are strokes, encephalitis and neuroinfections.
Progressive paralysis is a less critical condition, characterized by a gradual increase in clinical symptoms. It develops in chronic degenerative diseases of the nervous system.
Alternating syndrome - damage to the nuclei of the bulbar zone with unilateral damage to the muscles of the trunk.

Etiology

The etiopathogenetic factors of paralysis are very diverse: impaired blood supply to the brain, head injury, acute infections, neoplasms, swelling of brain tissue, inflammation, exposure to neurotoxins.

Bulbar syndrome is a manifestation of various mental and somatic diseases, which by origin can be divided into the following groups:

genetic - acute intermittent porphyria, Kennedy's disease, Chiari malformation, paroxysmal myoplegia;
vascular - ischemic and hemorrhagic stroke of the brain, hypertensive crisis, thrombosis of the venous sinuses, discirculatory encephalopathy;
degenerative - syringobulbia, Guillain-Barré syndrome, myasthenia gravis, dystrophic myotonia, Alzheimer's disease;
infectious – encephalitis, tick-borne borreliosis, polio, neurosyphilis, Lyme disease, diphtheria polyneuropathy, botulism, meningitis, encephalitis;
oncological – cerebellar tumors, gliomas, ependymomas, tuberculomas, cysts;
demyelinating – multiple sclerosis;
endocrine - hyperthyroidism;
traumatic – fractures of the base of the skull.

Factors provoking the development of the syndrome:

abuse of salty foods,
frequent inclusion of high-carbohydrate and fatty foods and dishes in the diet,
chronic stress, frequent conflict situations,
excessive physical stress.

Pathogenesis

Electrical impulses from the brain enter the cortex and then to the motor nuclei of the bulbar zone. Nerve fibers begin from them, through which signals are sent to the skeletal muscles of the upper body. Centers of the medulla oblongata healthy people are responsible for hearing, facial expressions, swallowing processes and sound pronunciation. All cranial nerves are structural components CNS.

The vagus nerve has many branches that span the entire body. The tenth pair of nerves starts from the bulbar nuclei and reaches the organs abdominal cavity. Thanks to its proper functioning, the respiratory organs, stomach, and heart function at an optimal level. The vagus nerve provides swallowing, coughing, vomiting, and speech.
The glossopharyngeal nerve innervates the muscles of the pharynx and the parotid salivary gland, providing its secretory function.
The hypoglossal nerve innervates the muscles of the tongue and facilitates swallowing, chewing, sucking and licking.

Under influence etiological factor The synaptic transmission of nerve impulses is disrupted and simultaneous destruction of the nuclei of the IX, X and XII pairs of cranial nerves occurs.

An etiopathogenetic factor can exert its negative impact at one of three levels:

in the nuclei of the medulla oblongata,
in the roots and trunks inside the cranial cavity,
in fully formed nerve fibers outside the cranial cavity.

As a result of damage to the nuclei and fibers of these nerves, the trophism of muscle tissue is disrupted. The muscles decrease in volume, become thinner, and their number decreases until they disappear completely. Bulbar palsy is accompanied by hypo- or areflexia, hypo- or atony, hypo- or atrophy of the paralyzed muscles. When the nerves innervating the respiratory muscles are involved in the process, patients die from suffocation.

Symptoms

The clinical picture of the syndrome is caused by impaired innervation of the muscles of the throat and tongue, as well as dysfunction of these organs. Patients develop a specific symptom complex – dysphagia, dysarthria, dysphonia.

Swallowing disorders are manifested by frequent choking, salivation from the corners of the mouth, and the inability to swallow even liquid food.
Bulbar dysarthria and dysphonia are characterized by a weak and muffled voice, nasal sound and “blurred” sounds. Consonant sounds become uniform, vowels become difficult to distinguish from each other, speech becomes slow, tedious, slurred, and impossible. Nasality and slurred speech are associated with the immobility of the soft palate.
The patient's voice becomes weak, dull, and depleted to the point of complete aphonia - a disturbance in the sound of speech. The reason for the altered timbre of the voice is incomplete closure of the glottis, caused by paresis of the laryngeal muscles.
Disturbances in facial activity or its complete absence. Facial functions lose their specificity, their general weakening occurs, and normal coordination is disrupted. The patient's facial features become expressionless - the mouth is half open, profuse salivation and loss of chewed food.
Decrease and gradual extinction of the palatal and pharyngeal reflexes.
Weakness of the masticatory muscles due to paralysis of the corresponding nerves. Impaired chewing of food.
Atrophy of the muscles of the tongue and its immobility.
Entry of liquid and solid food into the nasopharynx.
Twitching of the tongue and drooping of the velum.
In severe cases - disruption of the heart, vascular tone, and breathing rhythm.

When examining patients, specialists detect deviation of the tongue towards the lesion, its hypotonia and immobility, and isolated fasciculations. In severe cases, glossoplegia is noted, which sooner or later ends in pathological thinning or folding of the tongue. Stiffness and weakness of the palatine arches, uvula and pharyngeal muscles lead to dysphagia. Constant reflux of food into the respiratory tract can result in aspiration and the development of inflammation. Violation autonomic innervation salivary glands manifests itself as hypersalivation and requires constant use of a scarf.

In newborns, bulbar syndrome is a manifestation of cerebral palsy caused by birth trauma. Babies develop motor and sensory disorders, the sucking process is disrupted, and they often spit up. In children over 2 years of age, the symptoms of the pathology are similar to those in adults.

Diagnostics

Diagnosis and treatment of bulbar palsy is carried out by specialists in the field of neurology. Diagnostic measures are aimed at identifying the immediate cause of the pathology and consist of examining the patient, identifying all the symptoms of the disease and conducting electromyography. The obtained clinical data and research results make it possible to determine the severity of paralysis and prescribe treatment. These are mandatory diagnostic techniques that are complemented general analysis blood and urine, brain tomography, esophagoscopy, cerebrospinal fluid examination, electrocardiography, consultation with an ophthalmologist.

During the first neurological examination, the patient’s neurological status is determined: speech intelligibility, voice timbre, salivation, swallowing reflex. Be sure to study appearance tongue, identify atrophies and fasciculations, and evaluate its mobility. Assessment of respiratory rate and heart rate is of important diagnostic importance.

Then the patient is sent for additional diagnostic examination.

Using a laryngoscope, the larynx is examined and sagging of the vocal cord on the affected side is detected.
X-ray of the skull - determination of bone structure, the presence of fractures, injuries, neoplasms, areas of hemorrhage.
Electromyography is a research method that evaluates the bioelectrical activity of muscles and allows one to determine the peripheral nature of paralysis.
Computed tomography - the most accurate images of any part of the body and internal organs made using X-rays.
Esophagoscopy - determining the functioning of the muscles of the pharynx and vocal cords by examining their inner surface using an esophagoscope.
Electrocardiography is the simplest, most accessible and informative method diagnosis of heart diseases.
MRI - layer-by-layer images of any area of the body, allowing you to study the structure of a particular organ as accurately as possible.
IN laboratory tests there are characteristic changes: in the cerebrospinal fluid - signs of infection or hemorrhage, in the hemogram - inflammation, in the immunogram - specific antibodies.

Treatment

Emergency medical care should be provided in full to patients with acute bulbar syndrome, accompanied by signs of respiratory and cardiovascular dysfunction. Resuscitation measures are aimed at maintaining the vital functions of the body.

Patients are connected to a ventilator or have their trachea intubated;
Proserin is administered, which restores muscle activity, improves the swallowing reflex and gastric motility, and reduces the pulse;
"Atropine" eliminates hypersalivation;
Antibiotics are administered when there are clear signs of an infectious process in the brain;
Diuretics help cope with cerebral edema;
Drugs that improve cerebral circulation are indicated in the presence of vascular disorders;
Patients with respiratory and cardiac problems are hospitalized in the intensive care unit.

The main goal of treatment is to eliminate the threat to the patient’s life. All patients with severe neurological disorder are transported to a medical facility, where adequate treatment is selected for them.

Stages of therapy:

Etiotropic therapy is the elimination of diseases that have become the root cause of bulbar syndrome. In most cases, these diseases are not treated and progress throughout life. If the cause of the pathology is infection, take antibacterial agents wide range- “Ceftriaxone”, “Azithromycin”, “Clarithromycin”.
Pathogenetic treatment: anti-inflammatory - glucocorticoids "Prednisolone", decongestant - diuretics "Furosemide", metabolic - "Cortexin", "Actovegin", nootropic - "Mexidol", "Piracetam", antitumor - cytostatics "Methotrexate".
Symptomatic therapy aimed at improving general condition patients and reducing the severity clinical manifestations. B vitamins and preparations with glutamic acid stimulate metabolic processes in nerve tissue. For severe dysphagia - administration of vasodilators and antispasmodics, infusion therapy, correction of vascular disorders. "Neostigmine" and "ATP" reduce the severity of diaphagia.
Currently, the use of stem cells that actively function instead of the damaged ones has a good therapeutic effect.
Patients with bulbar syndrome in severe cases are fed through an enteral tube with special mixtures. Relatives need to monitor the condition of the oral cavity and observe the patient while eating to prevent aspiration.

Bulbar syndrome is difficult to respond to even adequate therapy. Recovery occurs in isolated cases. During the treatment process, the condition of the patients improves, paralysis weakens, and muscle function is restored.

Physiotherapeutic methods used to treat bulbar syndrome:

electrophoresis, laser therapy, magnetic therapy and mud therapy,
therapeutic massage to develop muscles and accelerate their recovery process,
kinesitherapy - performing certain exercises that help restore the functioning of the human musculoskeletal system,
breathing exercises - a system of exercises aimed at improving health and developing the lungs,
physical therapy – certain exercises that speed up recovery,
V recovery period classes with a speech therapist are shown.

TO surgical intervention resorted to in cases where conservative treatment does not give positive results. Operations are performed in the presence of tumors and fractures:

Shunt operations prevent the development of dislocation syndrome.
Craniotomy is performed in patients with epidural and subdural hematomas of the brain.
Clipping of pathologically dilated cerebral vessels is surgical method, allowing to effectively eliminate abnormal changes in the circulatory system.
Cholesterol plaques are removed by performing endarterectomy and prosthetic replacement of the damaged area.
In case of skull fractures, the skull is opened, the source of bleeding and bone fragments are eliminated, and the defect is closed. bone tissue removed bone or a special plate, and then proceed to long-term rehabilitation.

Facilities traditional medicine used to treat paralysis: infusions and decoctions medicinal herbs, alcohol tincture of peony, strong solution of sage - medicines that strengthen the nervous system and relieve tension. Patients are recommended to take healing baths with a decoction of sage or rose hips.

Prevention and prognosis

Preventive measures to prevent the development of bulbar syndrome:

immunization by vaccination against major infectious diseases,
fight against atherosclerosis,
control blood pressure and blood sugar levels,
timely detection of neoplasms,
balanced diet with limited carbohydrates and fats,
playing sports and maintaining an active lifestyle,
compliance with the work and rest schedule,
undergoing medical examinations with doctors,
fight against smoking and alcohol consumption,
full sleep.

The prognosis of the pathology is determined by the course of the underlying disease that became the root cause of the syndrome. Damage to the nuclei of infectious etiology is completely cured, and the processes of swallowing and speech are gradually restored. Acute disorder cerebral circulation, manifested by the clinical syndrome, has an unfavorable prognosis in 50% of cases. With degenerative pathologies and chronic diseases of the nervous system, paralysis progresses. Patients usually die from cardiopulmonary failure.

Video: bulbar syndrome - clinical options and physiotherapeutic treatment

Bulbar syndrome (or bulbar palsy) is a complex lesion of the IX, X and XII cranial nerves (vagus, glossopharyngeal and hypoglossal nerves), whose nuclei are located in the medulla oblongata. They innervate the muscles of the lips, soft palate, tongue, pharynx, larynx, as well as the vocal cords and epiglottic cartilage.

Symptoms

Bulbar palsy is a triad of three leading symptoms: dysphagia(swallowing disorder), dysarthria(violation of the correct pronunciation of articulate speech sounds) and aphonia(violation of speech sonority). A patient suffering from this paralysis cannot swallow solid food, and liquid food will enter the nose due to paresis of the soft palate. The patient’s speech will be incomprehensible with a hint of nasalism (nasalism), this disturbance is especially noticeable when the patient pronounces words containing such complex sounds as “l” and “r”.

To make a diagnosis, the doctor must conduct a study of the functions of the IX, X and XII pairs of cranial nerves. Diagnosis begins with finding out whether the patient has problems swallowing solid and liquid food, or whether he chokes on it. During the answer, the patient’s speech is carefully listened to, and the disturbances characteristic of paralysis noted above are noted. Then the doctor examines the oral cavity and performs laryngoscopy (a method of examining the larynx). With unilateral bulbar syndrome, the tip of the tongue will be directed towards the lesion, or completely motionless with bilateral one. The mucous membrane of the tongue will be thinned and folded - atrophic.

Examination of the soft palate will reveal its lag in pronunciation, as well as deviation of the uvula in the healthy direction. Using a special spatula, the doctor checks the palatal and pharyngeal reflexes, irritating the mucous membrane of the soft palate and back wall throats. The absence of vomiting and coughing movements indicates damage to the vagus and glossopharyngeal nerves. The study ends with laryngoscopy, which will help confirm paralysis of the true vocal cords.

The danger of bulbar syndrome lies in damage to the vagus nerve. Insufficient function of this nerve will cause abnormal heart rhythm and breathing problems, which can immediately lead to death.

Etiology

Depending on what disease causes bulbar palsy, there are two types: acute and progressive. Acute most often occurs due to acute circulatory disturbance in the medulla oblongata (infarction) due to thrombosis, vascular embolism, and also when the brain is wedged into the foramen magnum. Severe damage to the medulla oblongata leads to disruption of the vital functions of the body and subsequent death of the patient.

Progressive bulbar palsy develops in amyotrophic lateral sclerosis. This rare disease represents degenerative change central nervous system, in which damage to motor neurons occurs, which serves as a source of muscle atrophy and paralysis. ALS is characterized by all the symptoms of bulbar palsy: dysphagia when taking liquid and solid food, glossoplegia and tongue atrophy, sagging of the soft palate. Unfortunately, treatment for amyotrophic sclerosis has not been developed. Paralysis of the respiratory muscles causes the death of the patient due to the development of suffocation.

Bulbar palsy often accompanies a disease such as myasthenia gravis. It is not for nothing that the second name of the disease is asthenic bulbar palsy. The pathogenesis consists of an autoimmune lesion of the body, causing pathological muscle fatigue.

In addition to bulbar lesions, muscle fatigue is added to the symptoms after physical activity, disappearing after rest. Treatment of such patients consists of the doctor prescribing anticholinesterase drugs, most often Kalimin. Prescribing Proserin is not advisable due to its short-term effect and large quantity side effects.

Differential diagnosis

It is necessary to correctly differentiate bulbar syndrome from pseudobulbar palsy. Their manifestations are very similar, however, there is a significant difference. Pseudobulbar palsy is characterized by reflexes of oral automatism (proboscis reflex, distance-oral and palmar-plantar reflex), the occurrence of which is associated with damage to the pyramidal tracts.

The proboscis reflex is detected by carefully tapping the upper and lower lips with a neurological hammer - the patient pulls them out. The same reaction can be observed when the hammer approaches the lips - the distance-oral reflex. Line irritation of the skin of the palm above the eminence thumb will be accompanied by contraction of the mentalis muscle, causing the skin to pull up on the chin - the palmomental reflex.

Treatment and prevention

First of all, treatment of bulbar syndrome is aimed at eliminating the cause that caused it. Symptomatic therapy consists of eliminating respiratory failure using a ventilator. To restore swallowing, a cholinesterase inhibitor is prescribed. It blocks cholyesterase, as a result of which the action of acetylcholine is enhanced, leading to the restoration of conduction along the neuromuscular fiber.

M-anticholinergic Atropine blocks M-cholinergic receptors, thereby eliminating increased salivation. Patients are fed through a tube. Other therapeutic measures will depend on the specific disease.

Specific prevention of this syndrome does not exist. To prevent the development of bulbar palsy, it is necessary to promptly treat diseases that can cause it.

Video about how exercise therapy is performed for bulbar syndrome: