Bulbar syndrome - what is this diagnosis? Bulbar palsy

1. Small medical encyclopedia. - M.: Medical encyclopedia. 1991-96 2. First aid. - M.: Great Russian Encyclopedia. 1994 3. encyclopedic Dictionary medical terms. - M.: Soviet encyclopedia. - 1982-1984.

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 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 oral cavity, 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 if it is 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 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 gagging 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 defeat vagus nerve . Insufficient function of this nerve will cause impairment heart rate and respiratory distress, 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 disorder blood circulation in the medulla oblongata (infarction) due to thrombosis, vascular embolism, as well as when the brain is wedged into the large foramen magnum. Heavy defeat 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, the symptoms include muscle fatigue after physical activity, which disappears 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 gently tapping the upper and lower lower lip– 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. All other treatment 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:

Bulbar syndrome develops when the caudal parts of the brain stem (medulla oblongata) or its connections with the executive apparatus are damaged. The functions of the medulla oblongata are diverse and have vital significance.

The nuclei of the IX, X and XII nerves are centers for controlling the reflex activity of the pharynx, larynx and tongue and are involved in articulation and swallowing. They receive interoceptive information and are related to many visceral reflexes (coughing, swallowing, sneezing, salivation, sucking) and various secretory reactions. The medulla oblongata contains the medial (posterior) longitudinal fasciculus, which is important in regulating the movements of the head and neck and coordinating the latter with eye movements. It contains the relay nuclei of the auditory and vestibular conductors. Ascending and descending paths, connecting lower and higher levels of the nervous system. The reticular formation plays important role in facilitating or suppressing motor activity, regulating muscle tone, conducting afferentation, in postural and other reflex activity, in the control of consciousness, as well as visceral and autonomic functions. In addition, through the vagal system, the medulla oblongata participates in the regulation of respiratory, cardiovascular, digestive and other metabolic processes in the body.

Here we will look at the advanced forms of bulbar palsy, which develop with bilateral lesions of the nuclei of the IX, X and XII nerves, as well as their roots and nerves inside and outside the skull. Here we also included lesions of the corresponding muscles and synapses, which lead to the same disorders of bulbar motor functions: swallowing, chewing, articulation, phonation and breathing.

The main causes of bulbar syndrome:

1. Motor neuron diseases (ALS, Fazio-Londe spinal amyotrophy, Kennedy bulbospinal amyotrophy).

2. Myopathies (oculopharyngeal, Kearns-Sayre syndrome).

3. Dystrophic myotonia.

4. Paroxysmal myoplegia.

5. Myasthenia gravis.

6. Polyneuropathy (Guillain-Barré, post-vaccination, diphtheria, paraneoplastic, with hyperthyroidism, porphyria).

7. Poliomyelitis.

8. Processes in the brain stem, posterior cranial fossa and craniospinal region (vascular, tumor, syringobulbia, meningitis, encephalitis, granulomatous diseases, bone anomalies).

1. 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.

ALS diagnosis criteria:

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 ALS (just like “primary lateral sclerosis” as another type of ALS that occurs without clinical signs of damage to the anterior horns of the spinal cord).

* For more details, see the section “ALS Syndrome”.

Increasing bulbar palsy may be a manifestation of progressive spinal amyotrophy, in particular ter

the end stage of Werdnig-Hoffmann amyotrophy, and in children - spinal amyotrophy Fazio-Londe. 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 range of 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. 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. Unlike ALS, the process here is always symmetrical, it is not accompanied by symptoms of upper motor neuron involvement and has a more favorable course.

2. Myopathies. Some forms of myopathy (oculopharyngeal, Kearns-Sayre syndrome) may manifest as impaired bulbar function. 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 the later stages of the disease.

One of the forms of mitochondrial encephalomyopathy, namely Kearns-Sayre syndrome (“ophthalmoplegia plus”), manifests itself, in addition to ptosis and ophthalmoplegia, as 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

retinal pigmentary degeneration

cardiac conduction disorders

(bradycardia, atrioventricular block, syncope,

sudden death possible)

increase in protein levels in the cerebrospinal fluid

3. 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. The clinical picture consists of myotonic, myopathic syndromes and extramuscular disorders ( dystrophic changes in the lens, testicles and others 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).

4. Paroxysmal myoplegia (periodic paralysis). Paroxysmal myoplegia is a disease (hypokalemic

skaya, hyperkalemic and normokalemic forms), manifested by generalized or partial seizures 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 in carbohydrates rich food, abuse 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 is carried out with secondary forms of myoplegia, which occur in patients with thyrotoxicosis, with primary hyperaldosteronism, hypokalemia in some gastrointestinal diseases, and kidney diseases. Iat-trogenic variants of periodic paralysis have been described when prescribed drugs that promote the removal of potassium from the body (diuretics, laxatives, licorice).

5. Myasthenia gravis.

Bulbar syndrome is one of the dangerous manifestations 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 dysfunctions of the extraocular muscles (ptosis, diplopia and limited mobility of the eyeballs) and facial muscles, as well as the muscles of the limbs. Approximately one third of patients have masticatory involvement

nary muscles, muscles of the pharynx, larynx and tongue. There are generalized and local (mainly ocular) forms.

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

6. 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.

7. Poliomyelitis.

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. Characteristic period reverse development paralysis soon after their appearance. 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 1X, X (less often XII) nerves, but also the facial nerve are affected. 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 is 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 polio include Guillain-Barré syndrome, acute intermittent porphyria, botulism, toxic polyneuropathies, transverse myelitis, and acute spinal cord compression due to epidural abscess.

8. Processes in the brain stem, posterior cranial fossa and craniospinal region.

Some diseases sometimes easily involve both halves of the medulla oblongata, given small size and a compact form of the caudal part of the brain stem: tumors of an intramedullary (glioma or ependymoma) or extramedullary nature (neurofibromas, meningiomas, hemangiomas, metastatic tumors); tuberculoma, sarcoidosis and other granulomatous processes may resemble the clinical symptoms of a tumor. Volumetric processes are sooner or later accompanied by an increase in intracranial pressure. Parenchymal and subarachnoid hemorrhages, head injury and other processes accompanied by intracranial hypertension and herniation of the medulla oblongata into the foramen magnum can lead to hyperthermia, respiratory disorders, coma and death of the patient from respiratory and cardiac arrest. Other causes: syringobulbia, congenital disorders and anomalies of the craniospinal region (platybasia, Paget's disease), toxic and degenerative processes, meningitis and encephalitis, leading to dysfunction of the caudal parts of the brain stem.

9. Psychogenic dysphonia and dysphagia.

Psychogenic disorders of bulbar functions sometimes require a differential diagnosis with true bulbar palsy. Psychogenic disorders of swallowing and phonation can be observed both in the picture of psychotic disorders and as part of conversion disorders. In the first case, they are usually observed against the background of clinically obvious behavioral disorders, in the second, they are rarely a monosymptomatic manifestation of the disease and in this case their recognition is facilitated by the identification of polysyndromic demonstrative disorders. It is necessary to use both positive criteria for diagnosing psychogenic disorders and excluding organic diseases using modern paraclinical examination methods.

Diagnostic tests for boulevard syndrome

General and biochemical analysis blood; general analysis urine; CT or MRI of the brain; EMG of the muscles of the tongue, neck and limbs; clinical and EMG tests for myasthenia gravis with pharmacological load; examination by an ophthalmologist; ECG; cerebrospinal fluid examination; esophagoscopy; consultation with a therapist.

Bulbar syndrome is a disorder accompanied by simultaneous failure of the function of several nerves - glossopharyngeal, sublingual and vagus. This leads to disruption of the processes of chewing and swallowing, and speech dysfunction. Among dangerous consequences pathologies - changes in the functioning of the heart and respiratory system. Treatment of bulbar syndrome is based on both the use various groups drugs and surgical interventions. The prognosis for the disease is usually cautious. The outcome depends on the etiology of the lesion.

Causes of development of bulbar syndrome

Many unfavorable factors can provoke disruptions in the functioning of the nervous system and reflex arc. These include both infectious agents and non-infectious pathologies. The main causes of bulbar syndrome in children and adults are:

1. Congenital genetic abnormalities. A number of diseases are accompanied by damage to the normal structure and functions of the medulla oblongata, which leads to the appearance specific symptoms defeats. Amyotrophy Kennedy and porphyrin disease can provoke the occurrence of such disorders. Pseudobulbar syndrome in children, often noted against the background of cerebral palsy, is also one of the hereditary pathologies. The peculiarity of the problem is the absence of atrophy of the affected muscles, that is, the paralysis is peripheral.
2. A common cause of bulbar syndrome in newborns is bacterial and viral infections. They lead to inflammation of the membranes of the brain and spinal cord. Meningitis and encephalitis are accompanied by the formation of paralysis, both central and peripheral. Common agents leading to the disorder are Lyme disease and botulism.
3. Neurology describes the occurrence of bulbar and pseudobulbar syndromes against the background of defects in bone structures, for example, due to injuries or osteochondrosis affecting the neck area. Formation mechanism clinical signs associated with compression nerve structures, which interferes with their normal operation.
4. CNS function disorders also occur during the formation oncological processes. Tumors prevent adequate nutrition and blood supply to the affected organs, which leads to the formation of problems.
5. Vascular defects are a common cause of bulbar syndrome. Characteristic violations work of the muscles of the tongue and pharynx occurs as a result of a stroke, since with this problem there is a severe degree of ischemia of the nervous tissue. Congenital anomalies the structure of arteries and veins can also lead to the formation of the disease.
6. To a separate group etiological factors, provoking the occurrence of bulbar syndrome, cause autoimmune problems. A common cause of nervous system disorders is multiple sclerosis, accompanied by damage to the sheaths of the fibers that form the spinal cord and brain.

Main symptoms of pathology

Bulbar syndrome is characterized by specific clinical manifestations. Classic signs include:

1. Changes in facial expressions in patients. The facial muscles atrophy, which leads to the formation characteristic symptoms. Patients appear emotionless.
2. Because of defeat glossopharyngeal nerve the swallowing process is disrupted. Patients have difficulty chewing food and can easily choke.
3. Noted profuse salivation, which arises due to pathological changes in the work of the vagus. The inhibitory effect of the vagus nerve weakens, which leads to active secretion of the secretion of the digestive glands. Due to the paralysis of several structures at once, it is difficult for the patient to completely close the jaws, so saliva may flow out of the corners of the mouth.
4. Damage to the hypoglossal nerve provokes severe speech disorders. Patients find it difficult to speak because the muscles are weakened. Pronounced sounds are slurred and drawn out. Similar problems are diagnosed in both adult patients and children.
5. Most dangerous symptoms bulbar syndrome is associated with a violation of automaticity in the functioning of vital systems. Patients with the disease suffer from changes in heart function and respiratory failure. Respiratory problems get worse high risk aspiration. In severe cases, apnea is observed, requiring emergency medical attention.

Necessary diagnostic tests

Bulbar syndrome is not an independent disease. Therefore, confirming the presence of a problem comes down to discovering the cause of its occurrence, as well as establishing the nature pathological disorders. For this purpose, standard diagnostic studies– blood, urine and stool tests, as well as general examination patient and history taking.

In many cases, the use of visual methods is required, in particular, magnetic resonance imaging, which makes it possible to detect the presence of tumor and ischemic processes in the cranial cavity. Electromyography, used to differentiate central and peripheral paralysis, is also informative.

Therapy methods

Treatment of bulbar syndrome should be aimed at the cause of its occurrence. However, patients often require urgent Care, especially against the background of acute cardiac and respiratory failure. Therapy is also symptomatic in nature and is aimed at improving general condition patient. Both conservative methods, traditional and folk, and radical ones are used.

Drug treatment

1. When an infectious agent that triggers the development of symptoms is identified, antibacterial drugs of various groups are used.
2. To reduce intensity inflammatory processes for injuries, as well as palliative care pseudobulbar syndrome in oncology are used hormonal agents, for example, Prednisolone and Solu-Medrol.
3. In order to restore function autonomic innervation Atropine is prescribed. It helps reduce the active secretion of saliva and also prevents bradycardia.
4. In a number of emergency conditions associated with the development of severe arrhythmia, the use of Lidocaine, which is administered to patients intravenously, is justified.

Physiotherapy

Massage has a pronounced effect in bulbar syndrome. It helps relax muscles and restore normal blood supply to the affected area. Kinesiotherapy improves trophism and functioning of the nervous system, that is, special training that has positive reviews. Exercises are used to help restore the functioning of the facial muscles. Gymnastics is also used to improve the function of the muscles involved in the swallowing process.

Once the patient's condition has stabilized, work with a speech therapist will be required. It is necessary for the correction of formed speech disorders. Expressed therapeutic effect during rehabilitation after brain damage, for example, as a result of a stroke, electrophoresis with Hydrocortisone and Lidocaine is used.

Surgery

In some cases it is necessary to use more radical methods. They are used both to alleviate the condition of patients and to influence the cause of the disease. Some patients have a tracheostomy installed to maintain adequate breathing. Many also require a nasogastric tube. Surgical intervention necessary for patients with operable tumors in the cranial cavity, as well as for those injured as a result of various injuries.

In many cases, treatment is only symptomatic. No exact protocols have been developed to combat bulbar syndrome, since therapy is aimed at the cause of the disease. However, there are recommendations that are used in most European countries to alleviate the condition of patients with lateral amyotrophic sclerosis. The same principles can be used to treat bulbar syndrome:

1. Widely used medications, helping to relieve spasms, as well as anticonvulsants that provide relaxation of the affected muscles.
2. The use of heat and water helps to improve the well-being of patients.
3. Important and moderate exercise stress. In this case, it is recommended to use both general exercises and special ones aimed at training the affected muscle groups.
4. To maintain adequate body weight, as well as meet the body's needs for nutrients You will need to consult a doctor to create the right diet.
5. Classes with a speech therapist, both group and individual, are used not only for the purpose of correcting speech dysfunctions. They also contribute to the social rehabilitation of patients, which greatly facilitates the further treatment process.

Nutritional Features

In many cases, patients with bulbar syndrome cannot eat normally. For this purpose, a special tube is installed through which food is supplied. Such features require the use of liquid products. The diet should be balanced and provide good nutrition body.

Prognosis and possible complications

The outcome of the lesion largely depends on the cause of the disease. Timely provision of medical care is also important, although even with adequate therapy it is not always possible to cure the disease. Moreover, the prognosis for pseudobulbar syndrome is much better, since the pathology is not accompanied by dysfunction of vital organs.

The greatest danger in the disorder is cardiac and respiratory failure. Patients often die due to severe arrhythmia, aspiration pneumonia, as well as asphyxia when food enters the respiratory tract.

Prevention

Preventing the development of the problem is based on preventing the occurrence of infections and non-communicable diseases that can lead to the formation of pathology. For this it is important to conduct healthy image life, and also undergo regular preventive examinations with doctors.

Bulbar palsy (BP) is characterized by damage to groups of nerve fibers and their nuclei. The main symptom of the disease is a decrease in the motor activity of muscle groups. Bulbar syndrome leads to unilateral and bilateral damage to areas of the brain.

Symptoms of the disease

This pathology causes partial or complete paralysis of the muscles of the face, tongue, palate, and larynx, for which the glossopharyngeal, vagus, and sublingual nerve fibers are responsible.

The main symptoms of bulbar palsy:

1. Swallowing problems. With bulbar syndrome, disturbances occur in the functioning of the muscles that carry out the swallowing process. This leads to the development of dysphagia. With dysphagia, the muscles of the tongue, soft palate, epiglottis, pharynx and larynx lose their functionality. In addition to dysphagia, aphagia develops - the absence of a swallowing reflex. Water and other liquids enter the nasal cavity, solid food enters the larynx. Observed profuse drooling from the corners of the mouth. It is not uncommon for food to enter the trachea or lung cavity. This leads to the development of aspiration pneumonia, which, in turn, can be fatal.
2. Speech impairment and complete or partial loss of the ability to speak. The sounds produced by the patient become muffled, often incomprehensible to perception - this indicates the development of dysphonia. Complete loss of voice—progressive aphonia.
3. During the development of bulbar palsy, the voice becomes weak and muffled, and nasal sound occurs—speech “in the nose.” Vowel sounds become almost indistinguishable from each other, and consonants become indistinct. Speech is perceived as incomprehensible and barely audible; when trying to pronounce words, a person gets very and quickly tired.

Paralysis of the tongue leads to problematic articulation or its complete disruption, and dysarthria appears. Complete paralysis of the tongue muscles may develop - anarthria.

With these symptoms, the patient is able to hear and understand the speech of the interlocutor, but he cannot answer.

Bulbar palsy can lead to the development of problems in the functioning of other organs. First of all, the respiratory system and cardiovascular system suffer. The reason for this is the close proximity of the affected areas of nerve fibers to these organs.

Factors of occurrence

The occurrence of bulbar palsy is associated with many diseases of various origins and is their consequence. These include:

1. Oncological diseases. With the development of neoplasms in the posterior cranial fossa. For example, brainstem glioma.
2. Ischemic stroke of cerebral vessels, infarction of the medulla oblongata.
3. Amyotrophic sclerosis.
4. Genetic diseases, such as Kennedy's disease.
5. Diseases of an inflammatory-infectious nature (Lyme disease, Guyon-Barré syndrome).
6. This disorder is a manifestation of other complex pathologies occurring in the body.

Therapeutic measures

Treatment of bulbar palsy directly depends on the primary (main) disease. The more effort is put into eliminating it, the greater the chance of improving the clinical picture of the pathology.

Treatment of paralysis consists of resuscitating lost functions and maintaining the vitality of the body as a whole. For this, vitamins are prescribed to restore swallowing function; in addition, ATP and Prozerin are recommended.

To restore normal breathing, it is prescribed artificial ventilation lungs. Atropine is used to reduce saliva volume. The prescription of Atropine is caused by the need to reduce the volume of secreted secretions - in a sick person its amount can reach 1 liter. But even the measures taken do not guarantee recovery - only an improvement in overall well-being.

Characteristics of pseudobulbar palsy

Pseudobulbar palsy (PBP) is a centralized paresis of muscles, the activity of which directly depends on the full functioning of the bulbar nerve fibers. Unlike bulbar palsy, which is characterized by both unilateral and bilateral lesions, pseudobulbar syndrome occurs only with complete destruction of the nuclear pathways, which include the entire length from the cortical centers to the nuclei of the nerve fibers of the bulbar group.

With PBP, the functioning of the muscles of the pharynx, vocal cords, and speech articulation are disrupted. As with the development of PD, pseudobulbar syndrome may be accompanied by dysphagia, dysphonia or aphonia, and dysarthria. But the main difference is that with PBP there is no atrophy of the lingual muscles and defibrillary reflexes.

A sign of PBS is considered to be uniform paresis of the facial muscles; it is rather centralized in nature - spastic, when muscle tone is increased. This is most expressed in a disorder of differentiated and voluntary movements. At the same time, reflexes increase sharply lower jaw and chin.

Unlike PD, atrophy of the muscles of the lips, pharynx and soft palate is not diagnosed during the development of PBP.

With PBP, there are no changes in the functioning of the respiratory and cardiovascular systems. This is due to the fact that destructive processes occur higher than the medulla oblongata. From which it follows that PPS does not have the consequences characteristic of bulbar palsy; vital functions are not impaired during the development of the disease.

Observable reflexes when disrupted

The main sign of the development of this disease is considered to be involuntary crying or laughter when a person exposes his teeth, and if something is passed over them, for example, a feather or a small sheet of paper.

PBS is characterized by reflexes of oral automatism:

1. Bekhterev's reflex. The presence of this reflex is determined by lightly tapping the chin or using a spatula or ruler that lies on the lower row of teeth. A positive result is considered to be the case if there is a sharp contraction of the chewing muscles or clenching of the jaws.
2. Proboscis reflex. In specialized literature you can find other names, for example, kissing. To call it up, lightly tap on the upper lip or near the mouth, but it is necessary to touch the orbicularis muscle.
3. Korchikyan's distance-oral reflex. When checking this reflex, the patient’s lips do not touch, positive result happens only if the lips are automatically extended with a tube without touching them, only when any object is presented.
4. Naso-labial reflex Astvatsaturov. The presence of contractions of the facial muscles occurs when lightly tapping the back of the nose.
5. Marinescu-Radovic palmomental reflex. Called in case of irritation skin on the site under thumb hands. If the facial muscles on the side of the irritated hand contract involuntarily, then the reflex test is positive.
6. Janyshevsky's syndrome is characterized by convulsive clenching of the jaws. To test for the presence of this reflex, a stimulus is applied to the lips, gums, or hard palate.

Although even without the presence of reflexes, the symptoms of PBP are quite extensive. This is primarily due to damage to many areas of the brain. Except positive reactions for the presence of reflexes, a sign of PBS is a noticeable decrease in motor activity. The development of PBS is also indicated by memory deterioration, lack of concentration, decreased or total loss intelligence. This is caused by the presence of many softened brain foci.

A manifestation of PBS is an almost motionless face that resembles a mask. This is due to paresis of the facial muscles.

When diagnosing pseudobulbar palsy, in some cases a clinical picture similar to the symptoms of central tetraparesis may be observed.

Concomitant diseases and treatment

PBS appears in combination with such disorders as:

1. Acute disorders cerebral circulation in both hemispheres.
2. Encephalopathy.
3. Amyotrophic lateral sclerosis.
4. Atherosclerosis of cerebral vessels.
5. Multiple sclerosis.
6. Motor neuron disease.
7. Tumors of some parts of the brain.
8. Traumatic brain injuries.

In order to alleviate the symptoms of the disease as much as possible, the drug Proserin is most often prescribed. The treatment process for PBS is aimed at treating the underlying disease. Drugs that improve blood clotting and accelerate metabolic processes. To enhance oxygen supply to the brain, the drug Cerebrolysin and others are prescribed.

Modern techniques offer treatment for paralysis with stem cell injections.

And to alleviate the suffering of the patient, careful oral care is necessary. When eating, be as careful as possible to prevent pieces of food from entering the trachea. It is advisable that nutrition be provided through a tube passed through the nose into the esophagus.

Bulbar and pseudobulbar palsy- secondary diseases, the cure of which depends on the improvement of the overall clinical picture.