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Bulbar syndrome (or bulbar paralysis) 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 the sonority of speech). A patient suffering from this paralysis cannot swallow solid food, and liquid food will enter the nose due to the paresis of the soft palate. The patient's speech will be incomprehensible with a hint of nasality (nazolium), this violation 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 if the patient has problems swallowing solid and liquid food, whether he chokes on it. During the answer, the patient's speech is carefully listened to, violations characteristic of paralysis, noted above, are noted. Then the doctor examines the oral cavity, performs laryngoscopy (a method for examining the larynx). With unilateral bulbar syndrome, the tip of the tongue will be directed towards the lesion, or completely motionless with bilateral. 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 the deviation of the palatine uvula to the healthy side. Using a special spatula, the doctor checks the palatine and pharyngeal reflexes, irritating the mucous membrane of the soft palate and the posterior pharyngeal wall. The absence of vomiting, coughing movements indicate damage to the vagus and glossopharyngeal nerves. The study ends with laryngoscopy, which will help confirm the paralysis of the true vocal cords.

The danger of bulbar syndrome is vagus nerve injury. Lack of function of this nerve will cause abnormal heart rhythm and respiratory distress, which can immediately lead to death.

Etiology

Depending on the disease caused by bulbar palsy, there are two types of it: acute and progressive. Acute most often occurs due to acute circulatory disorders in the medulla oblongata (heart attack) due to thrombosis, vascular embolism, and also when the brain is wedged into the foramen magnum. Severe damage to the medulla oblongata leads to a violation of the vital functions of the body and the subsequent death of the patient.

Progressive bulbar palsy develops with amyotrophic lateral sclerosis. This rare disease is a degenerative change in the central nervous system that causes damage to motor neurons, causing muscle atrophy and paralysis. ALS is characterized by all the symptoms of bulbar paralysis: dysphagia when taking liquid and solid food, glossoplegia and atrophy of the tongue, sagging of the soft palate. Unfortunately, there is no cure for amyotrophic sclerosis. Paralysis of the respiratory muscles causes the death of the patient due to the development of suffocation.

Bulbar paralysis often accompanies a disease such as myasthenia gravis. No wonder the second name of the disease is asthenic bulbar palsy. The pathogenesis consists in an autoimmune lesion of the body, causing pathological muscle fatigue.

In addition to bulbar lesions, muscle fatigue after exercise, which disappears after rest, joins the symptoms. The treatment of such patients consists in the appointment of anticholinesterase drugs by the doctor, most often Kalimin. The appointment of Prozerin is not advisable because of its short-term effect and a large number of 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 paralysis 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 pathways.

The proboscis reflex is detected when a neurological hammer is gently tapped on the upper and lower lip - the patient pulls them out. The same reaction can be traced when the hammer approaches the lips - a distance-oral reflex. Stroke irritation of the skin of the palm above the elevation of the thumb will be accompanied by a contraction of the mental muscle, causing the skin to pull up on the chin - palmo-chin reflex.

Treatment and prevention

First of all, the treatment of bulbar syndrome is aimed at eliminating the cause that caused it. Symptomatic therapy consists in the elimination of respiratory failure with a ventilator. To restore swallowing, a cholinesterase inhibitor is prescribed -. It blocks cholesterase, 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. All other therapeutic measures will depend on the specific disease.

There is no specific prevention for this syndrome. To prevent the development of bulbar paralysis, it is necessary to treat diseases that can cause it in a timely manner.

Video on how exercise therapy is performed for bulbar syndrome:

BULBAR PARALYSIS(Late Latin bulbaris referring to the medulla oblongata; from Latin bulbus bulb; the old designation of the medulla oblongata is bulbus cerebri) - a clinical syndrome of damage to the IX, X, XII pairs of cranial nerves or their nuclei located in the medulla oblongata, and atrophic paralysis of the muscles of the tongue, lips, soft palate, pharynx, vocal cords and epiglottis. Depending on the localization of the lesion, B. p. can be unilateral (damage to one side of the medulla oblongata) and bilateral (damage to both halves of the medulla oblongata). B. p. observed with syringobulbia, circulatory disorders in the medulla oblongata (ischemic infarction), tumors of the posterior cranial fossa, cranio-spinal tumor, neck injury, polioencephalomyelitis, bulbar form of tick-borne encephalitis, polyneuritis (diphtheria), bulbar form of amyotrophic lateral sclerosis. Depending on the course of B. p. is acute (apoplectic) and gradually progressive.

B. p. from compression of the medulla oblongata, myasthenic B. p., Duchenne bulbar palsy, and laryngeal B. p. are also described as separate forms of B. p.

Clinical picture

With B. p., speech becomes blurry, with a nasal tint (dysarthria), phonation (aphonia) and swallowing (dysphagia), especially liquid food (food enters the nose, the patient choke) are disturbed. The tongue deviates towards the affected side (unilateral B. and.) or is immobile (bilateral B. p.), there is a hanging of the soft palate, the tongue deviates to the healthy side (unilateral B. p.), there is no closure of the vocal cords, the pharyngeal and palatine are not called reflexes. In the atrophied muscles of the tongue of the affected side, fibrillar twitches are observed (with damage to the nucleus of the XII pair), a violation of electrical excitability (rebirth reaction).

Acute bulbar palsy develops as a result of Economo lethargic encephalitis, cerebral hemorrhage or ischemic circulatory disorders in the brain stem (thrombosis or embolism in the vessels of the vertebrobasilar system with softening foci in the medulla oblongata) (Fig. 1), especially with occlusion of the inferior posterior cerebellar or vertebral artery, causing retroolive syndromes of Wallenberg - Zakharchenko, Avellis, Babinsky - Najotte, Jackson (see Alternating syndromes, Stroke). With a mild course (in particular, with thrombosis of the posterior inferior cerebellar artery), the patient recovers, but neurological disorders persist. In severe lesions, the course is unfavorable - patients die due to impaired respiratory and cardiovascular activity.

Progressive bulbar palsy observed in the bulbar form of amyotrophic lateral sclerosis (see), hron, poliomyelitis, in stages III and IV hron, cerebrovascular insufficiency (according to the classification of N. K. Bogolepov) due to multiple cysts and foci of red softening in the brain stem (Fig. 2 and 3).

In this case, the predominantly motor nuclei of the IX, X and XII cranial nerves are affected; wiring systems usually remain intact. The main clinical symptoms are growing disorders of swallowing, chewing and articulation, later - breathing.

Ischemic and inflammatory-degenerative damage to the motor nuclei of the cranial nerves of the medulla oblongata has a progressive course, and patients die as a result of impaired breathing and cardiac activity.

Bulbar palsy from compression of the medulla oblongata(compression B. p.) develops acutely, gradually or paroxysmal, depending on the cause of the disease. Acute development of compression B. p. is observed with hemorrhage with perifocal edema in the brain stem or cerebellum (Fig. 4), progressive - with compression of the medulla oblongata by a tumor of the cerebellum, base of the brain, cerebellopontine angle (see Brain, tumors) or the upper cervical vertebra in case of a fracture or dislocation of it; paroxysmal - with compression by an aneurysm of the vertebral or basilar artery.

Myasthenic bulbar palsy(Erb's disease - Goldflam) occurs as a result of impaired conduction in neuromuscular synapses (see Myasthenia gravis).

Duchenne bulbar palsy, or subacute anterior poliomyelitis. With it, labio-glosso-laryngeal and labio-glosso-pharyngeal B. p. are observed. It is manifested by disorders of swallowing, speech, salivation, breathing due to atrophic paralysis of the lips, tongue, nasopharynx and larynx. B. p. Duchenne has a subacute progressive course without remissions; patients die from respiratory and cardiac disorders. The disease usually lasts up to two years.

laryngeal bulbar palsy can be partial (unilateral lesion of the recurrent nerve) and complete (bilateral lesion of the recurrent nerve). It is mainly manifested by a violation of phonation. Occurs with neck trauma, thyroid disease, aortic aneurysm, mediastinal tumor.

Diagnosis

Diagnosis is based on characteristic clinical symptoms. B. p. is differentiated with pseudobulbar paralysis (see), with Krom there is no atrophy of the muscles of the tongue, pharyngeal and palatine reflexes are increased, there are reflexes of oral automatism, violent crying and laughter.

Forecast

The prognosis is determined by the nature of the pathological process that caused the disease, the severity of clinical symptoms. Most often unfavorable.

Treatment consists in the treatment of the underlying disease. To improve the function of swallowing, prozerin, glutamic acid, vitamins, ATP are prescribed, in case of respiratory failure - artificial respiration, in case of salivation - atropine. Tube feeding. When indicated, dehydration therapy is carried out (see), vasodilators, drugs that normalize blood clotting are prescribed.

Bibliography: Bogolepov N. K. Disorders of motor functions in vascular lesions of the brain, M., 1953, bibliogr.; he, Neuropathology, Emergency states, M., 1967; Zakharchenko M. A. Vascular diseases of the brain stem, blockage art. cerebelli inferior posterior, M., 1911; M and N about in-with and y B. N. Progressive bulbar paralysis, Mnogotomn, the guide to neurol., under the editorship of. N. I. Grashchenkova, vol. 7, p. 109, D., 1960; D u c h e n e G. B. A. Paralysie musculaire progressive de la langue, du voile, du palais et des livres, affection non encore decrite comme espfece morbide distincte, Arch. gin. M6d., t. 16, p. 283, 1860; Erb W. H. Zur Gasuistik der bulbaren Lahmungen, Arch. Psychiatry. Nervenkr., Bd 9, S. 325, 1878-1879; G o 1 d f 1 a m S. t)ber einen scheinbar heilbaren bulbarparalytischen Symptomen Komplex mit Beteiligung der Extremitaten, Dtsch. Z. Nervenheilk., Bd 4, S. 312, 1893; Wallenberg A. Verschluss der Arteria cerebelli inferior posterior dextra (mit Sektionsbefund), ibid., Bd 73, S. 189, 1922.

H. K. Bogolepov.

1. Motor neuron diseases (amyotrophic lateral sclerosis, Fazio-Londe spinal amyotrophy, Kennedy bulbospinal amyotrophy).
2. Myopathies (oculopharyngeal, Kearns-Sayre syndrome).
3. Dystrophic myotonia.
4. Paroxysmal myoplegia.
5. Myasthenia.
6. Polyneuropathy (Guillain-Barré, post-vaccination, diphtheria, paraneoplastic, with hyperthyroidism, porphyria).
7. Polio.
8. Processes in the brain stem, posterior cranial fossa and cranio-spinal region (vascular, tumor, syringobulbia, meningitis, encephalitis, granulomatous diseases, bone anomalies).
9. 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 a bilateral lesion of the nucleus XII of the nerve and its first manifestations are atrophy, fasciculations and paralysis of the tongue. In the early stages, dysarthria without dysarthria or dysarthria without dysarthria may occur, but a progressive deterioration of all bulbar functions is observed rather quickly. At the beginning of the disease, difficulty in swallowing liquid food is observed more often than solid food, but as the disease progresses, dysphagia develops when taking solid food. At the same time, weakness of the masticatory and then facial muscles joins the weakness of the tongue, the soft palate hangs down, the tongue in the oral cavity is motionless and atrophic. It shows fasciculations. Anartria. Constant salivation. 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 of damage to the upper motor neuron (pyramidal syndrome); progressive course.

"Progressive bulbar palsy" is now 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 of the spinal cord).

Increasing bulbar paralysis may be a manifestation of progressive spinal amyotrophy, in particular, the terminal stage of Werdnig-Hoffmann amyotrophy (Werdnig-Hoffmann), and in children, Fazio-Londe spinal amyotrophy. The latter refers to autosomal recessive spinal amyotrophies with a debut in early childhood. X-linked bulbar spinal amyotrophy is known in adults, beginning at the age of 40 years and older (Kennedy's disease). Characterized by weakness and atrophy of the muscles of the proximal upper limbs, spontaneous fasciculations, limited range of active movements in the arms, decreased tendon reflexes with the biceps and triceps muscles of the shoulder. As the disease progresses, bulbar (usually mild) disorders develop: choking, tongue atrophy, dysarthria. Leg muscles are involved later. Characteristic features: 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. In contrast to amyotrophic lateral sclerosis, here the process is always symmetrical, it is not accompanied by symptoms of involvement of the upper motor neuron and has a more favorable course.

Myopathies

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

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

Obligate signs of Kearns-Sayre syndrome:

• external ophthalmoplegia
• retinitis pigmentosa
• cardiac conduction disorders (bradycardia, atrioventricular block, syncope, sudden death is possible)
• increased levels of protein in the cerebrospinal fluid

Dystrophic myotonia

Dystrophic myotonia (or Rossolimo-Kurshman-Steinert-Batten myotonic dystorophia) is inherited in an autosomal dominant manner and affects men 3 times more often than women. Her debut falls on the age of 16-20 years. The clinical picture consists of myotonic, myopathic syndromes and extramuscular disorders (dystrophic changes in the lens, testicles and other endocrine glands, skin, esophagus, heart and sometimes in the brain). Myopathic syndrome is most pronounced in the muscles of the face (chewing 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 a decrease in tendon reflexes and muscle hypotension. The duration of the attacks varies from 30 minutes to several days. Provoking factors: rich in carbohydrates rich food, salt abuse, negative emotions, physical activity, night sleep. Only in some attacks the involvement of the cervical and cranial muscles is noted. 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 certain gastrointestinal diseases, kidney diseases. Iattrogenic variants of periodic paralysis are described when prescribing drugs that promote the excretion of potassium from the body (diuretics, laxatives, licorice).

myasthenia gravis

Bulbar syndrome is one of the dangerous manifestations of myasthenia gravis. Myasthenia (myasthenia gravis) is a disease, the leading clinical manifestation of which is pathological muscle fatigue, decreasing until complete recovery after taking anticholinesterase drugs. The first symptoms are more often violations of the functions of the oculomotor muscles (ptosis, diplopia and limitation of the mobility of the eyeballs) and facial muscles, as well as the muscles of the limbs. Approximately one third of patients have involvement of the muscles of mastication, muscles of the pharynx, larynx, and tongue. There are generalized and local (mainly eye) forms.

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

Polyneuropathies

Bulbar paralysis 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 typical for such forms as acute demyelinating polyneuropathy of Guillain-Barré, post-infectious and post-vaccination polyneuropathy, diphtheria and paraneoplastic polyneuropathy, as well as polyneuropathy in hyperthyroidism and porphyria.

Polio

Acute poliomyelitis, as the cause of bulbar palsy, is recognized by the presence of general infectious (pre-paralytic) symptoms, the rapid development of paralysis (usually in the first 5 days of illness) with a greater lesion of the proximal than distal. The period of reverse development of paralysis shortly after their appearance is characteristic. There are spinal, bulbar and bulbospinal forms. The lower extremities are more often affected (in 80% of cases), but the development of syndromes by hemitype or cross is possible. Paralysis is sluggish in nature with the loss of tendon reflexes and the rapid development of atrophy. Bulbar paralysis 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 the facial nerve suffer. Damage to the anterior horns of the IV-V segments can cause respiratory paralysis. Adults are more likely to develop the bulbospinal form. Involvement of the reticular formation of the brainstem can lead to cardiovascular (hypotension, hypertension, cardiac arrhythmias), respiratory ("atactic breathing") disorders, swallowing disorders, disturbances in the level of wakefulness.

Differential Diagnosis carried out with other viral infections that can affect the lower motor neuron: rabies and herpes zoster. Other diseases that often require a differential diagnosis from acute poliomyelitis are Guillain-Barré syndrome, acute intermittent porphyria, botulism, toxic polyneuropathies, transverse myelitis, and acute spinal cord compression due to epidural abscess.

Bulbar syndrome or, as it is also called bulbar paralysis, is a disease caused by a change in the activity or damage to some parts of the brain that provoke a malfunction of the organs of the mouth or pharynx.

This is a paralysis of the organs of direct eating or speech, in which the lips, palate, pharynx (upper esophagus, tongue, small tongue, lower jaw) are paralyzed. This disease can be bilateral or unilateral, affecting half of the pharynx in a longitudinal section.

With the disease, the following symptoms are observed:

• Lack of facial expressions of the mouth: the patient simply cannot use it.
• Constantly open mouth.
• Entry of liquid food into the nasopharynx or trachea.
• There are no palatine and pharyngeal reflexes, the person ceases to involuntarily swallow, including saliva).
• Because of the previous symptom, salivation develops.
• If unilateral paralysis occurs, the soft palate hangs down, and the tongue is pulled to the healthy side.
• Slurred speech.
• Inability to swallow
• Paralysis of the tongue, which may be constantly twitching or hanging outward from the mouth.
• Breathing is disturbed.
• There is deterioration in the activity of the heart.
• The voice disappears or becomes deaf, barely audible, changes its tone and becomes completely different from the previous one.

Patients are often unable to swallow, so they are forced to eat liquid food through a tube.

In medicine, bulbar and pseudobulbar syndromes are distinguished, which have very similar symptoms, but still differ slightly, have different causes, although they are related by origin.

During pseudobulbar paralysis, palatine and pharyngeal reflexes are preserved, and paralysis of the tongue does not occur, but swallowing disorders still develop, most patients show symptoms of violent laughter or crying when touching the palate.

Both paralysis occur as a result of damage to the same parts of the brain for the same reasons, but the bulbar syndrome develops due to damage to the brain nuclei responsible for the functions of swallowing, heartbeat, speech or breathing, and the pseudobulbar syndrome develops from damage to the subcortical pathways from these nuclei to the nerves bulbar group responsible for these functions.

At the same time, pseudobulbar syndrome is a less dangerous pathology that does not entail the risk of sudden cardiac or respiratory arrest.

What causes symptoms

Symptoms of pathology are caused by damage to a whole group of brain organs, and specifically, the nuclei of several nerves embedded in the medulla oblongata, their intracranial or external roots. With bulbar syndrome, almost never a single nucleus is affected with the loss of only one function, since these organs are located very close to each other, and also have a very small size, which is why they are affected simultaneously.

Due to the defeat, the nervous system loses contact with the organs of the pharynx and can no longer control them either consciously or unconsciously at the level of reflexes (when a person automatically swallows saliva).

A person has 12 pairs of cranial nerves that appear as early as the second month of the prenatal period of life, which consist of the medulla and are located in the very center of the brain between its hemispheres. They are responsible for the human senses and the functioning of the face as a whole. At the same time, they have a motor function, a sensitive function, or both at once.

The nuclei of the nerves are a kind of command posts: ternary, facial, glossopharyngeal, hypoglossal, etc. Each nerve is paired, so the pairs are also their nuclei, which are located symmetrically with respect to the medulla oblongata. With bulbar syndrome, the nuclei responsible for the glossopharyngeal, hypoglossal or vagus nerve are affected, which has mixed functions for the innervation of the pharynx, soft palate, larynx, esophagus, has a parasympathetic effect (excitatory and contracting) on ​​the stomach, lungs, heart, intestines, pancreas, responsible for the sensitivity of the mucous membrane of the lower jaw, pharynx, larynx, part of the auditory canal, eardrum and other less important parts of the body. Since the nuclei are paired, either completely or only half of them, located on one side of the medulla oblongata, can suffer.

Disruption or damage to the vagus nerve in bulbar palsy can cause a sudden stop of contractions of the heart, respiratory organs, or disruption of the gastrointestinal tract.

Causes of the disease

Brain disorders that cause bulbar syndrome can have a huge number of causes that can be grouped into several general groups:

• Hereditary deviations, mutations and changes in organs.
• Brain diseases, both traumatic and infectious.
• Other infectious diseases.
• Toxic poisoning.
• Vascular changes and tumors.
• Degenerative changes in the brain and nervous tissues.
• Bone anomalies.
• Violations of intrauterine development.
• Autoimmune failures.

Each group contains a large number of individual diseases, each of which is capable of giving complications to the bulbar group of the nuclei of the brain and to other parts of it.

Bulbar palsy in children

In newborns, bulbar palsy is very difficult to determine, it is diagnosed by two signs:

• Too high humidity of the mucous membrane of the baby's mouth, which in infants is almost dry.
• Retraction of the tip of the tongue to the side if the hypoglossal nerve is affected.

Bulbar syndrome in children is extremely rare, since all brain stems are affected in them, which is fatal. Such babies simply die immediately. But pseudobulbar syndrome in children is common and is a type of cerebral palsy.

Treatment Methods

Bulbar paralysis and pseudobulbar syndromes are diagnosed using the following methods:

• General urine and blood tests.
• An electromyogram is a study of the conduction of nerves in the muscles of the face and neck.
• Tomography of the brain.
• Ophthalmologist's examination.
• Esophagoscopy - examination of the esophagus with a probe with a video camera.
• Analysis of cerebrospinal fluid - cerebral fluid.
• Tests for myasthenia gravis is an autoimmune disease characterized by extreme fatigue of the striated muscles. Autoimmune diseases are disorders in which one's own enraged immunity begins to kill.

Methods of treatment and the possibility of complete healing from bulbar or pseudobulbar palsy depends on the exact cause of their occurrence, since it is a consequence of other diseases. Sometimes it is possible to completely restore all functions, for example, if the disease was not caused by a complete lesion, but only by irritation of the brain due to an infection, but more often during treatment, the main goal is to restore vital functions: breathing, heartbeat and the ability to digest food, and it is also possible relieve some of the symptoms.

Such a problem as the development of pseudobulbar syndrome in a child is a real test for parents. The fact is that the symptoms of this disease manifest themselves quite clearly and, with an untimely reaction, are overcome for a long time.

What is pseudobulbar syndrome

The essence of this disease is reduced to the appearance of multiple large and small foci of hemorrhage, which lead to damage on both hemispheres of the fibers that connect the motor nuclei of the cerebral cortex with the brain stem.

This type of lesion may develop due to recurrent strokes. But there are cases when pseudobulbar syndrome (PS) makes itself felt without previous cases of hemorrhage.

With such a problem, as a rule, bulbar functions begin to suffer. These are swallowing, chewing, articulation and phonation. Violation of such functions leads to such pathologies as dysphagia, dysphonia, dysarthria. The main difference between this syndrome and the bulbar syndrome is that there is no development of muscle atrophy and reflexes of oral automatism are observed:

Increased proboscis reflex;

Oppenheim reflex;

Nasolabial reflex of Astvatsaturov;

Distant-arial and other similar reflexes.

Pseudobulbar syndrome - causes

The development of this syndrome is a consequence of atherosclerosis of the cerebral vessels and the resulting softening foci, which can be localized in both hemispheres.

But this is not the only factor leading to such a syndrome. The vascular form of syphilis of the brain, as well as neuroinfections, degenerative processes, infections and tumors that affect both hemispheres, can also have a negative impact.

In fact, pseudobulbar syndrome occurs when, against the background of any disease, the central paths leading from the motor centers of the cerebral cortex to the motor nuclei of the medulla oblongata are interrupted.

Pathogenesis

The development of such a syndrome is manifested by severe atheromatosis of the arteries of the base of the brain, which affects both hemispheres. In childhood, a bilateral lesion of the corticobulbar conductors is fixed, resulting in cerebral palsy.

If you have to deal with the pyramidal form of pseudobulbar syndrome, then the tendon reflex increases. In the extrapyramidal form, slow movements, stiffness, anemia and increased muscle tone are first recorded. The mixed form implies the total manifestation of the above symptoms, indicating a pseudobulbar syndrome. Photos of people affected by this syndrome confirm the seriousness of the disease.

Symptoms

One of the main symptoms of this disease is a violation of swallowing and chewing. In this state, food begins to get stuck on the gums and behind the teeth, liquid food can flow out through the nose, and the patient often chokes during the meal. Moreover, there are changes in the voice - it acquires a new shade. The sound becomes hoarse, consonants fall out, and some intonations are completely lost. Sometimes patients lose the ability to speak in a whisper.

With a problem such as pseudobulbar syndrome, symptoms can also be expressed through bilateral paresis of the facial muscles. This means that the face takes on a mask-like anemic appearance. It is also possible to manifest attacks of violent convulsive laughter or crying. But these symptoms are not always present.

It is worth mentioning the tendon reflex of the lower jaw, which in the process of developing the syndrome can increase dramatically.

Often pseudobulbar syndrome is fixed in parallel with a disease such as hemiparesis. Possible manifestation of extrapyramidal syndrome, which leads to stiffness, increased muscle tone and slowness of movement. Intellectual impairments are not excluded, which can be explained by the presence of multiple foci of softening in the brain.

At the same time, unlike the bulbar form, this syndrome excludes the occurrence of disorders of the cardiovascular and respiratory systems. This is due to the fact that pathological processes do not affect the vital centers, but develop in the medulla oblongata.

The syndrome itself can have both a gradual onset and an acute development. But if we consider the most common indicators, then it can be argued that in the vast majority of cases, the appearance of pseudobulbar syndrome is preceded by two or more attacks of cerebrovascular accident.

Diagnostics

To determine the pseudobulbar syndrome in children, it is necessary to differentiate its symptoms from nephritis, parkinsonism, bulbar palsy and nerves. One of the distinguishing features of the pseudoform will be the absence of atrophy.

It is worth noting that in some cases it can be quite difficult to distinguish PS from Parkinson's palsy. Such a disease proceeds slowly, and in the later stages apoplectic strokes are recorded. Moreover, signs similar to the syndrome appear: violent crying, speech disorder, etc. Therefore, a qualified doctor should determine the patient's condition.

The development of the syndrome in children

A problem such as pseudobulbar syndrome in newborns can manifest itself quite clearly. Already in the first month of life, signs of such a disease become noticeable.

When examining a baby with pseudobulbar syndrome, fibrillation and atrophy are not detected, but a reflex of oral automatism is recorded. Also, a similar syndrome can lead to the appearance of pathological crying and laughter.

Sometimes doctors diagnose combined forms of pseudobulbar and bulbar syndrome. This form of the disease is a consequence of amyotrophic lateral sclerosis, thrombosis in the system of vertebrobasilar arteries, inoperable malignant tumors of the trunk, or demyelinating processes.

Treatment of the syndrome

In order to influence the pseudobulbar syndrome in children, one must initially take into account the stage of its course. In any case, the treatment will be more effective the sooner the parents take the child to the doctor.

In the event that this syndrome progresses, agents are usually used that are focused on normalizing lipid metabolism, coagulation processes and lowering cholesterol in the blood. Useful will be drugs that improve microcirculation, bioenergetics of neurons and metabolic processes in the brain.

A similar effect is exerted by drugs such as Encephabol, Aminalon, Cerebrolysin, etc. In some cases, doctors may prescribe drugs that have anticholinesterase effects (Proserin, Oksazil).

Considering what disorders pseudobulbar syndrome causes in children, it is extremely important to know the signs indicating its development. After all, if you ignore the obvious symptoms and do not start the treatment process on time, then it may not be possible to completely neutralize the disease. This means that the child will suffer from swallowing disorders for the rest of his life, and not only.

But if you respond in a timely manner, then the chances of recovery will be quite high. Especially if stem cells are used in the treatment process. Their administration in a disease such as pseudobulbar syndrome can have the effect of physically replacing the myelin sheath and, moreover, restore the functions of cells that have been damaged. Such a restorative effect is able to return the patient to a full life.

How to influence the condition in newly born children

If pseudobulbar syndrome has been diagnosed in newborns, treatment will involve an integrated approach. First of all, this is a massage of the circular muscle of the mouth, feeding through a probe and electrophoresis with prozerin on the cervical spine.

Speaking about the first signs of recovery, it is worth noting that they include the appearance of newborn reflexes, which were absent before, stabilization of the neurological status and positive changes in the deviations recorded earlier. Also, with successful treatment, there should be an increase in motor activity against the background of hypodynamia or an increase in muscle tone in case of severe hypotension. In children with long gestational ages, a meaningful reaction to contact and emotional tone improves.

Recovery period in the treatment of newborns

In most cases, unless you have to deal with untreated severe lesions, the early recovery period begins within the first 2-3 weeks of a child's life. When dealing with a problem such as pseudobulbar syndrome, treatment at week 4 and beyond includes a recovery period therapy.

At the same time, for children who had to undergo convulsions, drugs are selected more carefully. Cortexin is often used, the course of which is 10 injections. In addition to these measures, Pantogam and Nootropil are orally administered to children during treatment.

Massage and physiotherapy

Regarding the use of massage, it is worth noting that it has a predominantly tonic and, in rare cases, relaxing effect. It is also held for all children. For those newborns who have spasticity of the limbs, massage is indicated earlier - on the 10th day of life. But it is important not to exceed the current norm - 15 sessions. In this case, this method of treatment is combined with the adoption of "Mydocalm" (twice a day).

Physiotherapy, in turn, is focused on electrophoresis of magnesium sulfate with aloe or lidase on the cervical spine.

Pseudobulbar dysarthia

This is one of the diseases that are the result of pseudobulbar syndrome. Its essence is reduced to a violation of the pathways connecting the nuclei of the bulbar group with the cerebral cortex.

This disease can have three degrees:

- Light. Violations are minor and manifest themselves in the fact that children do not pronounce growling and hissing sounds well. While writing the text, the child sometimes confuses the letters.

- Medium. Occurs more often than others. In this case, there is actually a complete absence of mimic movements. Children have difficulty chewing and swallowing food. At the same time, the tongue also moves poorly. In this state, the child cannot speak clearly.

- Severe degree (anarthria). Mimic movements are completely absent, as well as the mobility of the muscles of the speech apparatus. In such children, the lower jaw sags, while the tongue remains motionless.

With this disease, medical treatment methods, massage and reflexology are used.

It is easy to conclude that this syndrome is a fairly serious threat to the health of the child, so the disease requires parents to quickly respond to symptoms and patience in the treatment process.