Bulbar syndrome treatment prognosis. Bulbar syndrome: causes, symptoms, features of the treatment of pathology in children and adults

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 epiglottal 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 foods, 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 tracts.

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 syndrome It is characterized by peripheral paralysis of the so-called bulbar muscles, innervated by the IX, X, XI and XII cranial nerves, which causes the occurrence of dysphonia, aphonia, dysarthria, choking while eating, ingress of liquid food into the nose through the nasopharynx. There is a descent of the soft palate and the absence of its movements when pronouncing sounds, speech with a nasal tone, sometimes deviation of the tongue to the side, paralysis of the vocal cords, muscles of the tongue with their atrophy and fibrillar twitching. There are no pharyngeal, palatine and sneezing reflexes, there is a cough when eating, vomiting, hiccups, respiratory distress and cardiovascular activity.

Pseudobulbar syndrome It is characterized by disorders of swallowing, phonation, articulation of speech, and often a violation of facial expressions. The reflexes associated with the brain stem are not only preserved, but also pathologically increased. Pseudobulbar syndrome is characterized by the presence of pseudobulbar reflexes (automatic involuntary movements carried out by the circular muscle of the mouth, lips or chewing muscles in response to mechanical or other irritation of skin areas.). Violent laughter and crying, as well as a progressive decrease in mental activity, are noteworthy. Thus, pseudobulbar syndrome is a central paralysis (paresis) of the muscles involved in the processes of swallowing, phonation and articulation of speech, which is caused by a break in the central pathways from the motor centers of the cortex to the nuclei of the nerves. Most often it is caused by vascular lesions with foci of softening in both hemispheres of the brain. The cause of the syndrome may be inflammatory or tumor processes in the brain.

30 Meningeal syndrome.

meningeal syndrome observed with disease or irritation of the meninges. It consists of cerebral symptoms, changes in the cranial nerves, spinal cord roots, inhibition of reflexes and changes in the cerebrospinal fluid. The meningeal syndrome is and true meningeal symptoms(damage to the nervous apparatus located in the meninges of the brain, most of which refers to the nerve fibers of the trigeminal, glossopharyngeal, vagus nerves).

To True meningeal symptoms include headache, cheek symptom ( raising the shoulders and flexing the forearms with pressure on the cheek ), Zygomatic symptom of ankylosing spondylitis(tapping of the zygomatic bone is accompanied by an increase in headache and tonic contraction of the muscles of the face (painful grimace) mainly on the same side) , percussion soreness of the skull, nausea, vomiting and changes in pulse. Headache is the main symptom of meningeal syndrome. It is diffuse in nature and increases with head movement, sharp sounds and bright light, it can be very intense and is often accompanied by vomiting. Usually vomiting of cerebral origin is sudden, profuse, occurs without prior nausea and is not associated with food intake. There is hyperesthesia of the skin, sensory organs (skin, optical, acoustic). Patients painfully endure the touch of clothing or bedding. Among the characteristic signs are symptoms that reveal tonic tension in the muscles of the limbs and trunk (N. I. Grashchenkov): stiff neck muscles, symptoms of Kernig, Brudzinsky, Lessage, Levinson, Guillain, a symptom of rising, bulbo-facial Mondonesi tonic symptom, gunshot syndrome trigger "(a characteristic posture - the head is thrown back, the body is in the position of overextension, the lower limbs are brought to the stomach). Meningeal contractures are often noted.

31. Tumors of the nervous system. Tumors of the nervous system are neoplasms that grow from the substance, membranes and vessels of the brain,peripheral nerves, as well as metastatic ones. In terms of frequency of occurrence, they are in 5th place among other tumors. They mainly affect: (45-50 years old), their ethnology is unclear, but there are hormonal, infectious, traumatic and radiation theories. There are tumors primary and secondary (metastatic), benignmalignant and intracerebral and extracerebral. Clinical manifestations of brain tumors are divided into 3 groups: cerebral, focal symptoms and displacement symptoms. The dynamics of the disease is characterized first by an increase in hypertensive and focal symptoms, and already at later stages, symptoms of displacement appear. Cerebral symptoms are caused by an increase in intracranial pressure, impaired liquorodynamics and intoxication of the body. These include the following symptoms: headache, vomiting, dizziness, seizures, impaired consciousness, mental disorders, changes in pulse and breathing rhythm, shell symptoms. An additional study determines congestive optic discs, characteristic changes on craniograms (“finger impressions”, thinning of the back of the Turkish saddle, divergence of sutures). Focal symptoms depend on the immediate localization of the tumor. Tumor the frontal lobe is manifested by the “frontal psyche” (weakness, foolishness, slovenliness), paresis, impaired speech, smell, grasping reflexes, epileptiform seizures. Tumors of the parietal lobe are characterized by violations of sensitivity, especially complex types of it, a violation of reading, counting, writing. Tumors of the temporal lobe accompanied by gustatory, olfactory, auditory hallucinations, memory disorders and psychomotor paroxysms. Tumors of the occipital lobe manifested by visual impairment, hemianopsia, visual agnosia, photopsia, visual hallucinations. pituitary tumors characterized by endocrine dysfunctions - obesity, menstrual irregularities, acromegaly. Tumors cerebellum accompanied by impaired gait, coordination, muscle tone. Tumors of the cerebellopontine angle begin with tinnitus, hearing loss, then paresis of the facial muscles, nystagmus, dizziness, disorders of sensitivity and vision join. At brain stem tumors cranial nerves are affected. Tumor IV brain ventricle characterized by paroxysmal headache in the back of the head, dizziness, vomiting, tonic convulsions, respiratory and cardiac disorders. If a brain tumor is suspected, the patient should be urgently referred to a neurologist. To clarify the diagnosis, a number of additional studies are carried out. On the EEG, slow pathological waves are determined; on EchoEG - displacement of M-Echo up to 10 mm; The most important angiographic sign of a tumor is the displacement of vessels or the appearance of newly formed vessels. But the most informative diagnostic method at present is computed and magnetic nuclear tomography.

32. Meningitis. Etiology, clinic, diagnostics, treatment, prevention. Meningitis is an inflammation of the membranes of the brain and spinal cord, and the soft and arachnoid membranes are more often affected. Etiology. Meningitis can occur through several routes of infection. Contact way - the occurrence of meningitis occurs in the conditions of an already existing purulent infection. The development of sinusogenic meningitis is promoted by a purulent infection of the paranasal sinuses (sinusitis), otogenic-mastoid process or middle ear (otitis), odontogenic - pathology of the teeth. The introduction of infectious agents into the meninges is possible by lymphogenous, hematogenous, transplacental, perineural routes, as well as in conditions of liquorrhea with an open craniocerebral injury or spinal cord injury, a crack or fracture of the base of the skull. The causative agents of infection, entering the body through the entrance gate (bronchi, gastrointestinal tract, nasopharynx), cause inflammation (serous or purulent type) of the meninges and adjacent brain tissues. Their subsequent edema leads to disruption of microcirculation in the vessels of the brain and its membranes, slowing down the resorption of cerebrospinal fluid and its hypersecretion. At the same time, intracranial pressure rises, dropsy of the brain develops. It is possible to further spread the inflammatory process to the substance of the brain, the roots of the cranial and spinal nerves. Clinic. The symptom complex of any form of meningitis includes general infectious symptoms (fever, chills, fever), increased respiration and disturbance of its rhythm, changes in heart rate (tachycardia at the onset of the disease, bradycardia as the disease progresses). The meningeal syndrome includes cerebral symptoms, manifested by tonic tension of the muscles of the trunk and limbs. Often there are prodormal symptoms (runny nose, abdominal pain, etc.). Vomiting in meningitis is not associated with food intake. Headaches can be localized in the occipital region and radiate to the cervical spine. Patients react painfully to the slightest noise, touch, light. Seizures may occur in childhood. Meningitis is characterized by hyperesthesia of the skin and soreness of the skull during percussion. At the onset of the disease, there is an increase in tendon reflexes, but with the development of the disease they decrease and often disappear. In the case of involvement in the inflammatory process of the substance of the brain, paralysis, pathological reflexes and paresis develop. Severe meningitis is usually accompanied by dilated pupils, diplopia, strabismus, impaired control of the pelvic organs (in the case of mental disorders). Symptoms of meningitis in old age: a weak manifestation of headaches or their complete absence, tremor of the head and limbs, drowsiness, mental disorders (apathy or, conversely, psychomotor agitation). Diagnostics. The main method for diagnosing meningitis is a lumbar puncture followed by examination of the cerebrospinal fluid. All forms of meningitis are characterized by fluid leakage under high pressure (sometimes a jet). With serous meningitis, the cerebrospinal fluid is transparent, with purulent meningitis, it is cloudy, yellow-green in color. With the help of laboratory studies of cerebrospinal fluid, pleocytosis, a change in the ratio of the number of cells and an increased protein content are determined. In order to determine the etiological factors of the disease, it is recommended to determine the level of glucose in the cerebrospinal fluid. In the case of tuberculous meningitis, as well as meningitis caused by fungi, the glucose level decreases. For purulent meningitis, a significant (to zero) decrease in glucose levels. The main landmarks of a neurologist in the differentiation of meningitis are the study of cerebrospinal fluid, namely the determination of the ratio of cells, the level of sugar and protein. Treatment. In case of suspected meningitis, hospitalization of the patient is mandatory. In severe prehospital stage (depression of consciousness, fever), the patient is administered 50 mg of prednisolone and 3 million units of benzylpenicillin. Lumbar puncture at the prehospital stage is contraindicated! The basis for the treatment of purulent meningitis is the early appointment of sulfonamides (etazol, norsulfazol) at an average daily dose of 5-6 g or antibiotics (penicillin) at an average daily dose of 12-24 million units. If such treatment of meningitis during the first 3 days is ineffective, therapy with semi-synthetic antibiotics (ampiox, carbenicillin) in combination with monomycin, gentamicin, nitrofurans should be continued. The basis of the complex treatment of tuberculous meningitis is the continuous administration of bacteriostatic doses of 2-3 antibiotics. Treatment of viral meningitis may be limited to the use of drugs (glucose, analgin, vitamins, methyluracil). In severe cases (pronounced cerebral symptoms), corticosteroids and diuretics are prescribed, less often - repeated spinal puncture. In the case of a layering bacterial infection, antibiotics may be prescribed. Prevention. Regular hardening (water procedures, sports), timely treatment of chronic and acute infectious diseases.

33. Encephalitis. epidemic encephalitis. Clinic, diagnosis, treatment. Encephalitis is inflammation of the brain. The primary lesion of gray matter is called polioencephalitis, white - leukoencephalitis. Encephalitis can be limited (stem, subcortical) or diffuse; primary and secondary. The causative agents of the disease are viruses and bacteria. Often the causative agent is unknown. Economo epidemic encephalitis (lethargicencephalitis). Most often people aged 20-30 years get sick. Etiology. The causative agent of the disease is a filterable virus, but so far it has not been possible to isolate it. The routes of penetration of the virus into the nervous system have not been studied enough. It is assumed that viremia initially occurs, and then the virus penetrates the brain through the perineural spaces. In the clinical course of epidemic encephalitis, acute and chronic phases are distinguished. In the formation of the chronic phase, an important role belongs to autoimmune processes that cause the degeneration of the cells of the substantia nigra and the globus pallidus, the hypothalamus. Clinic The incubation period usually lasts from 1 to 14 "days, however, it can reach several months and even years. The disease begins acutely, the body temperature rises to 39-40 ° C, headache occurs, often vomiting, general malaise. Catarrhal phenomena may be observed. in the pharynx.It is important that during epidemic encephalitis, already in the first hours of the disease, the child becomes lethargic, drowsy; psychomotor agitation is less common.Unlike adults, epidemic encephalitis in children occurs with a predominance of cerebral symptoms.After a few hours after the onset of the disease, loss of consciousness may occur ,generalized convulsions are often observed.The defeat of the nuclei of the hypothalamic region contributes to the violation of cerebral hemodynamics.The phenomena of edema develop - swelling of the brain, often leading to death on the 1-2nd day, even before the child develops focal symptoms characteristic of epidemic encephalitis. Diagnostics It is important to correctly assess the state of consciousness, timely identify the first symptoms of focal brain damage, in particular sleep disorder, oculomotor, vestibular, vegetative-endocrine disorders, it is required to collect accurate anamnestic data on previous acute infectious diseases with cerebral symptoms, impaired consciousness, sleep, diplopia. Treatment. There are currently no specific treatments for epidemic encephalitis. It is advisable to carry out the vitamin therapy recommended for viral infections (ascorbic acid, B vitamins), the appointment of desensitizing drugs (antihistamines - diphenhydramine, suprastin, diazolin, tavegil; 5-10% solutions of calcium chloride, calcium gluconate orally or intravenously; prednisolone, etc.) , To combat the phenomena of cerebral edema, intensive dehydrating therapy is shown diuretics, hypertonic solutions of fructose, sodium chloride, calcium chloride. For convulsions, enemas are prescribed.

Bulbar palsy (BP) - which 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 lesions of brain regions.

Symptoms of the disease

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

The main symptoms of bulbar paralysis:

1. Swallowing problems. With bulbar syndrome, there are disturbances in the work of the muscles that carry out the process of swallowing. This leads to the development of dysphagia. With dysphagia, the muscles of the tongue, soft palate, epiglottis, pharynx and larynx lose their working capacity. In addition to dysphagia, aphagia develops - the absence of a swallowing reflex. Water and other liquids enter the nasal cavity, solid food - into the larynx. There is profuse salivation 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 made 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 deaf, nasality occurs - speech “in the nose”. Vowel sounds become almost indistinguishable from each other, and consonants are slurred. Speech is perceived as incomprehensible and barely distinguishable; when trying to pronounce words, a person gets tired very quickly.

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

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

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

Emergence factors

The occurrence of bulbar paralysis 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 and infectious nature (Lyme disease, Guyon-Barré syndrome).
6. This violation is a manifestation of other complex pathologies occurring in the body.

Therapeutic measures

Treatment of bulbar paralysis directly depends on the primary (main) disease. The more efforts are made to eliminate it, the more likely it is to improve the clinical picture of the pathology.

Treatment of paralysis consists in resuscitation of lost functions, maintaining the viability of the organism as a whole. For this, vitamins are prescribed to restore the function of swallowing, in addition, ATP, Prozerin are recommended.

To restore normal breathing, artificial lung ventilation is prescribed. Atropine is used to reduce saliva volume. The appointment of Atropine is caused by the need to reduce the amount of secretion secreted - in a sick person, its amount can reach 1 liter. But even the ongoing activities 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-fledged work of the bulbar nerve fibers. Unlike bulbar palsy, which is characterized by both unilateral and bilateral lesions, pseudobulbar syndrome occurs only with the 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 work of the muscles of the pharynx, vocal cords, and articulation of speech are disrupted. As with the development of PD, pseudobulbar syndrome may be accompanied by dysphagia, dysphonia or aphonia, dysarthria. But the main difference is that in PBP there is no atrophy of the tongue muscles and defibrillary reflexes.

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

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

In PBP, there are no changes in the functioning of the respiratory and cardiovascular systems. This is due to the fact that destructive processes take place higher than the medulla oblongata. From which it follows that PBS does not have the consequences characteristic of bulbar palsy, with the development of the disease, vital functions are not violated.

Observed reflexes in violation

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 you run something over them, such as 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 established by lightly tapping on the chin or on a spatula or ruler, which lie on the lower row of teeth. A positive result is the case if there is a sharp contraction of the masticatory muscles or clenching of the jaws.
2. Proboscis reflex. In specialized literature, you can find other names, for example, kissing. To call it, they make light taps on the upper lip or near the mouth, but at the same time it is necessary to touch the circular muscle.
3. Distance-oral Korchikian reflex. When checking this reflex, the patient's lips do not touch, a positive result occurs only if the lips are automatically pulled out by the tube without touching them, only when an object is presented.
4. Naso-labial reflex of Astvatsaturov. The presence of contractions of the facial muscles occurs with a slight tapping on the back of the nose.
5. Marinescu-Radovic's palmo-chin reflex. It is called in case of irritation of the skin in the area under the thumb. If the facial muscles on the side of the irritated hand contract involuntarily, then the reflex test is positive.
6. Yanyshevsky's syndrome is characterized by convulsive compression of the jaws. To test for the presence of this reflex, the stimulus is applied to the lips, gums, or hard palate.

Although without the presence of reflexes, the symptoms of PBP are quite extensive. First of all, this is due to the defeat of many parts of the brain. In addition to positive reactions to 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, a decrease or complete loss of intelligence. This leads to the presence of many softened foci of the brain.

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

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 conjunction with such disorders as:

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

In order to alleviate the symptoms of the disease as much as possible, the drug Prozerin is most often prescribed. The treatment process in PBS is aimed at treating the underlying disease. Be sure to prescribe drugs that improve blood clotting and accelerate metabolic processes. For enhanced nutrition of the brain with oxygen, the drug Cerebrolysin and others are prescribed.

Modern techniques offer the treatment of paralysis with stem cell injections.

And in order to alleviate the suffering of the patient, careful oral care is necessary. When eating, be as careful as possible to prevent food particles from entering the trachea. It is desirable that nutrition is carried out through a tube passed through the nose into the esophagus.

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

With the defeat of the caudal parts of the brain stem, bulbar syndrome develops. Pathology can arise from the action of several factors on which the treatment of the disease depends.

Causes of the disease

Bulbar disorders are manifested by paralysis of the muscles of the pharynx, epiglottis, tongue, lips, soft palate, and vocal cords. Such changes occur as a result of a violation of brain activity, namely, the medulla oblongata.

For accurate diagnosis and subsequent treatment of bulbar syndrome, which could give high positive results, it is important to establish the causes of the pathology.

Among the factors experts call the following:

• hereditary;
• vascular;
• degenerative;
• infectious.

Infectious causes of bulbar syndrome lie in acute intermittent porphyria and Kennedy's bulbospinal amyotrophy. The degenerative factor occurs when a person develops syringobulbia, polio, and Guillain-Barré syndrome.

Those who have had an ischemic stroke also fall into the risk group. Among the common causes of the disease are amyotrophic sclerosis, and paroxysmal myoplegia, and Fazio-Londe's spinal amyotrophy.

Do not forget about the danger for a person of post-vaccination and paraneoplastic polyneuropathy, hyperthyroidism, because these pathologies can also lead to the appearance of symptoms of bulbar syndrome.

Among other causes of the syndrome, experts also name such diseases and processes:

• botulism;
• spinal cord tumor;
• bone anomalies;
• meningitis;
• encephalitis.

Thus, many factors can provoke the occurrence in a person’s life of such a dangerous pathology. Only a group of highly qualified specialists can establish these causes with maximum accuracy using modern diagnostic methods and tools.

Bulbar Syndrome Symptoms

It is possible to recognize the development of a disease caused by brain damage by its characteristic signs. It is important to distinguish between bulbar and pseudobulbar syndromes, the symptoms of which are slightly different.

Bulbar palsy is characterized by the following symptoms:

Each person may experience symptoms in varying degrees of complexity. Pseudobulbar, or false paralysis, occurs with bilateral brain damage.

Clinically, these two disorders are manifested by the same symptoms, only with pseudobulbar paralysis, atrophy, the reaction of degeneration and distortion of the tongue do not develop. In addition, the pseudobulbar syndrome, unlike the bulbar syndrome, does not lead to respiratory and cardiac arrest.

How the disease progresses in children

With the development of bulbar syndrome in newborns, there is an increased humidity of the oral mucosa, which should normally be relatively dry. If you look into the baby's mouth while screaming or crying, you can find that the tip of the tongue is slightly retracted to the side. This symptom occurs when the hypoglossal nerve is damaged.

In children, bulbar palsy can rarely be observed, since it affects the brain stems, without the functioning of which life becomes impossible. More often, children develop pseudobulbar palsy, which is clinically very severe. In a child, in addition to paralysis of the muscles of the speech apparatus, there is also a change in muscle tone, hyperkinesis and other movement disorders.

This form of damage to the brain stems in newborns is often a manifestation of cerebral palsy. Pathology can manifest itself immediately after birth or in children under two years of age. Quite often, cerebral palsy becomes a consequence of birth injuries.

With bulbar and pseudobulbar syndromes, parents notice a violation of motor skills in a child. Often the upper part of the face is affected, due to which it becomes motionless.

Such children are unable to serve themselves on their own, they look awkward and awkward, they cannot chew and swallow food normally, and retain saliva in their mouths.

How is the treatment carried out

The health of people with this pathology must be given special attention. Often, urgent medical attention is required to save the patient's life. Our main actions are to neutralize the threat to the life of the patient until the moment when he is hospitalized and he is prescribed treatment. It usually requires support for body functions that have been impaired due to damage to the brain stems.

To do this, experts carry out the following actions:

• artificial ventilation of the lungs in order to restore breathing;
• the use of Prozerin, adenosine triphosphate and vitamins to activate the swallowing reflex;
• the appointment of Atropine to reduce salivation.

Be sure to carry out symptomatic treatment aimed at alleviating the patient's condition. It is also important to cure the disease that caused the development of bulbar syndrome.

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 process of swallowing, throwing food into the respiratory organs, speech deviations, hoarseness of the voice, a pathological change in taste sensations and vegetative symptoms.

Bulbar syndrome is characterized by blocking of nerve impulses at the level of cranial nuclei or motor fibers. A mild form of pathology develops with unilateral damage to the IX, X and XII nerves. Bilateral damage to the same nerves leads to the development of a severe degree of the 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. The 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 the patient's examination data and the results of additional examinations. Usually, treatment begins with urgent measures, and then proceeds to etiotropic, pathogenetic and symptomatic therapy.

Bulbar syndrome is a severe progressive process that leads to disability and deterioration in the quality of life. The syndrome that quickly appeared 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 is acute, progressive, alternating with one- or two-sided nature of the lesion.

• 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 body.

Etiology

The etiopathogenetic factors of paralysis are very diverse: impaired blood supply to the brain, TBI, acute infections, neoplasms, swelling of the 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:

1. genetic - acute intermittent porphyria, Kennedy's disease, Chiari anomaly, paroxysmal myoplegia;
2. vascular - ischemic and hemorrhagic stroke of the brain, hypertensive crisis, thrombosis of the venous sinuses, dyscirculatory encephalopathy;
3. degenerative - syringobulbia, Guillain-Barré syndrome, myasthenia gravis, dystrophic myotonia, Alzheimer's disease;
4. infectious - encephalitis, tick-borne borreliosis, poliomyelitis, neurosyphilis, Lyme disease, diphtheria polyneuropathy, botulism, meningitis, encephalitis;
5. oncological - tumors of the cerebellum, gliomas, ependymomas, tuberculomas, cysts;
6. demyelinating - multiple sclerosis;
7. endocrine - hyperthyroidism;
8. traumatic - fractures of the base of the skull.

Factors provoking the development of the syndrome:

• salty food abuse
• frequent inclusion in the diet of high-carbohydrate and fatty foods and dishes,
• 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, along which signals are sent to the skeletal muscles of the upper body. The centers of the medulla oblongata in healthy people are responsible for hearing, facial expressions, swallowing and sound pronunciation. All cranial nerves are structural components of the CNS.

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

Under the influence of the etiological factor, the synaptic transmission of nerve impulses is disrupted and the nuclei of the IX, X and XII pairs of cranial nerves are simultaneously destroyed.

The etiopathogenetic factor can exert its negative impact on 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. Muscles decrease in volume, become thinner, their number is reduced to complete disappearance. Bulbar paralysis is accompanied by hypo- or areflexia, hypo- or atony, hypo- or atrophy of paralyzed muscles. When the nerves innervating the respiratory muscles are involved in the process, patients die from suffocation.

Symptoms

The clinic of the syndrome is due to a violation of the 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.

1. Swallowing disorder is manifested by frequent choking, salivation from the corners of the mouth, inability to swallow even liquid food.
2. Bulbar dysarthria and dysphonia are characterized by a weak and muffled voice, nasality and "blurring" of sounds. Consonant sounds become the same type, vowels become difficult to distinguish from each other, speech becomes slow, tedious, slurred, impossible. Nasal and slurred speech is associated with the immobility of the soft palate.
3. The voice of patients becomes weak, deaf, dwindling up to complete aphonia - a violation of the sound of speech. The reason for the changed voice timbre is the incomplete closure of the glottis, due to paresis of the laryngeal muscles.
4. Violations of mimic activity or its complete absence. Mimic functions lose their specificity, there is a general weakening of them, a violation of normal coordination. The facial features of the patient become inexpressive - the mouth is half open, profuse salivation and loss of chewed food.
5. Decrease and gradual extinction of the palatine and pharyngeal reflexes.
6. Weakness of the masticatory muscles due to paralysis of the corresponding nerves. Violation of the full chewing of food.
7. Atrophy of the muscles of the tongue and its immobility.
8. Entry of liquid and solid food into the nasopharynx.
9. Twitching of the tongue and drooping of the veil of the palate.
10. In severe cases - a violation of the heart, vascular tone, respiratory rhythm.

When examining patients, specialists detect a deviation of the tongue towards the lesion, its hypotension and immobility, and single fasciculations. In severe cases, glossoplegia is noted, which sooner or later ends with pathological thinning or folding of the tongue. Immobility and weakness of the palatine arches, uvula, and pharyngeal muscles lead to dysphagia. The constant reflux of food into the respiratory tract can result in aspiration and the development of inflammation. Violation of the autonomic innervation of the salivary glands is manifested by hypersalivation and requires constant use of a handkerchief.

In newborns, bulbar syndrome is a manifestation of cerebral palsy due to birth trauma. Babies have motor and sensory disorders, the sucking process is disturbed, they often burp. In children older than 2 years, the symptoms of the pathology are similar to those in adults.

Diagnostics

Diagnosis and treatment of bulbar palsy are carried out by specialists in the field of neurology. Diagnostic measures are aimed at identifying the immediate cause of the pathology and consist in examining the patient, identifying all the symptoms of the disease and conducting electromyography. The obtained clinical data and research results allow to determine the severity of paralysis and prescribe treatment. These are mandatory diagnostic methods, which are supplemented by a general blood and urine test, brain tomography, esophagoscopy, cerebrospinal fluid examination, electrocardiography, and an ophthalmologist's consultation.

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

Then the patient is sent for additional diagnostic examination.

• Using a laryngoscope, the larynx is examined and sagging of the vocal cord is found on the side of the lesion.
• X-ray of the skull - determination of the structure of bones, the presence of fractures, injuries, neoplasms, foci of hemorrhage.
• Electromyography is a research method that evaluates the bioelectric activity of muscles and allows you 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 - determination of the work 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 for diagnosing heart diseases.
• MRI - layered images of any area of ​​the body, allowing the most accurate study of the structure of a particular organ.
• 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.

1. Patients are connected to a ventilator or their trachea is intubated;
2. "Prozerin" is introduced, which restores muscle activity, improves the swallowing reflex and gastric motility, and slows down the pulse;
3. "Atropine" eliminates hypersalivation;
4. Antibiotics are administered with obvious signs of an infectious process in the brain;
5. Diuretics allow you to cope with cerebral edema;
6. Drugs that improve cerebral circulation are indicated in the presence of vascular disorders;
7. Patients with impaired breathing and heart activity are hospitalized in the intensive care unit.

The main goal of therapeutic measures is to eliminate the threat to the life of the patient. All patients with severe neurological disorders are transported to a medical facility, where they are given adequate treatment.

Stages of therapy:

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

The bulbar syndrome hardly gives in even to adequate therapy. Recovery occurs in isolated cases. In the process of treatment, the condition of patients improves, paralysis weakens, muscle work is restored.

Physiotherapeutic methods used to treat bulbar syndrome:

1. electrophoresis, laser therapy, magnetotherapy and mud therapy,
2. therapeutic massage to develop muscles and speed up the process of their recovery,
3. kinesitherapy - performing certain exercises that help restore the work of the human musculoskeletal system,
4. breathing exercises - a system of exercises aimed at strengthening health and developing the lungs,
5. physiotherapy exercises - certain exercises that accelerate recovery,
6. in the recovery period, classes with a speech therapist are shown.

Surgical intervention is 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 a surgical method that effectively eliminates abnormal changes in the circulatory system.
• Cholesterol plaques are removed by endarterectomy and prosthesis of the damaged area.
• In case of skull fractures, the skull is opened, the source of bleeding and bone fragments are eliminated, the bone tissue defect is closed with a removed bone or a special plate, and then they proceed to long-term rehabilitation.

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

Prevention and prognosis

Preventive measures to prevent the development of bulbar syndrome:

1. immunization by vaccination against major infectious diseases,
2. fight against atherosclerosis
3. control of blood pressure and blood sugar levels,
4. timely detection of neoplasms,
5. balanced diet with restriction of carbohydrates and fats,
6. playing sports and leading a mobile lifestyle,
7. observance of the regime of work and rest,
8. passing medical examinations with doctors,
9. the fight against smoking and alcohol consumption,
10. complete sleep.

The prognosis of the pathology is determined by the course of the underlying disease, which has become the root cause of the syndrome. The defeat of the nuclei of infectious etiology is completely cured, and the processes of swallowing and speech are gradually restored. Acute cerebrovascular accident, manifested by the clinic of the syndrome, in 50% of cases has an unfavorable prognosis. With degenerative pathologies and chronic ailments of the nervous system, paralysis progresses. Patients usually die of cardiopulmonary failure.

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