Bulbar stroke. Treatment methods for bulbar syndrome

Such a problem as the development of pseudo bulbar syndrome in a child - this is a real test for parents. The point is that the symptoms of this disease manifest themselves quite clearly and, if the reaction is untimely, take a long time to overcome.

What is pseudobulbar syndrome

The essence of this disease comes down to the appearance of multiple large and small foci of hemorrhage, which lead to damage in both hemispheres of the fibers connecting the motor nuclei of the cerebral cortex with the brain stem.

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

With such a problem, as a rule, bulbar functions begin to suffer. It's about about swallowing, chewing, articulation and phonation. Violation of such functions leads to pathologies such as dysphagia, dysphonia, and 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;

Astvatsaturov's nasolabial reflex;

Distant-arial and other similar reflexes.

Pseudobulbar syndrome - causes

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

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

In fact, pseudobulbar syndrome occurs when, against the background of some disease, the central pathways coming from the motor centers of the cortex are interrupted cerebral hemispheres to motor nuclei medulla oblongata.

Pathogenesis

The development of such a syndrome manifests itself through severe atheromatosis of the arteries of the base of the brain, which affects both hemispheres. In childhood, bilateral damage to the corticobulbar conductors is recorded, resulting in cerebral palsy.

If you have to deal with the pyramidal form of pseudobulbar syndrome, the tendon reflex increases. With the extrapyramidal form, slow movements, stiffness, anemia and increased muscle tone. The mixed form implies the total manifestation of the above-described signs indicating pseudobulbar syndrome. Photos of people affected by this syndrome confirm the seriousness of the disease.

Symptoms

One of the main symptoms of this disease includes impaired swallowing and chewing. In this condition, 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 meals. Moreover, changes occur in the voice - it takes on a new shade. The sound becomes hoarse, consonants drop 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 experience attacks of violent convulsive laughter or crying. But such symptoms are not always present.

It is worth mentioning the tendon reflex lower jaw, which can increase sharply during the development of the syndrome.

Often pseudobulbar syndrome is recorded in parallel with a disease such as hemiparesis. Extrapyramidal syndrome may occur, which leads to stiffness, increased muscle tone and slowness of movement. Intellectual impairment, which can be explained by the presence of multiple foci of softening in the brain, is also possible.

Moreover, in contrast to the bulbar form, this syndrome eliminates the occurrence of cardiovascular disorders and respiratory systems. This is explained by the fact that pathological processes do not affect the vital centers, but develop in the medulla oblongata.

The syndrome itself can have either a gradual onset or an acute development. But if we consider the most common indicators, 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 pseudobulbar syndrome in children, it is necessary to differentiate its symptoms from nephritis, parkinsonism, bulbar palsy and nerves. One of distinctive features 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-like paralysis. This disease progresses slowly and late stages apoplectic strokes are recorded. Moreover, signs similar to the syndrome appear: violent crying, speech disorder, etc. Therefore, a qualified doctor must determine the patient’s condition.

Development of the syndrome in children

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

When examining a baby with pseudobulbar syndrome, fibrillation and atrophy are not detected, but the reflex of oral automatism is recorded. Also, such a syndrome can lead to 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 vertebrobasilar artery system, inoperable malignant tumors of the trunk or demyelinating processes.

Treatment of the syndrome

To influence pseudobulbar syndrome in children, you must initially take into account the stage of its occurrence. 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, drugs are usually used that are aimed at normalizing lipid metabolism, coagulation processes and reducing cholesterol in the blood. Drugs that improve microcirculation, bioenergetics of neurons and metabolic processes in the brain would be useful.

Such drugs as Encephabol, Aminalon, Cerebrolysin, etc. have a similar effect. In some cases, doctors may prescribe drugs that have an anticholinesterase effect (Proserin, Oxazil).

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 you may not be able to completely neutralize the disease. This means that the child will suffer from swallowing dysfunction for the rest of his life, and not only that.

But if you react in a timely manner, 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, restoring the functions of cells that have been damaged. Such a restorative effect can return the patient to full functioning.

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 orbicularis oris muscle, feeding through a tube and electrophoresis with proserin on the cervical spine.

Speaking about the first signs of recovery, it is worth noting that they include the appearance of reflexes of the newborn, which were previously absent, stabilization neurological status and positive changes in previously recorded deviations. Also when successful treatment there should be a promotion motor activity against the background of physical inactivity 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, if you do not have to deal with incurable severe lesions, the early recovery period begins within the first 2-3 weeks of the child’s life. When dealing with a problem such as pseudobulbar syndrome, treatment at week 4 and beyond includes recovery therapy.

At the same time, for children who have had to endure seizures, drugs are selected more carefully. Cortexin is often used, the course of treatment is 10 injections. In addition to these measures, Pantogam and Nootropil are administered orally 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 carried out 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. Wherein this method treatment is combined with taking 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 resulting from pseudobulbar syndrome. Its essence comes down to disruption of the pathways connecting the nuclei of the bulbar group with the cerebral cortex.

This disease can have three degrees:

- Lightweight. The violations are minor and manifest themselves in the fact that children have difficulty pronouncing growling and hissing sounds. When writing a text, the child sometimes confuses letters.

- Average. It occurs more often than others. In this case, there is virtually a complete absence of facial movements. Children have difficulty chewing and swallowing food. The tongue also moves poorly. In this state, the child cannot speak clearly.

- Severe (anarthria). Facial movements are completely absent, as well as muscle mobility speech apparatus. In such children, the lower jaw droops, but the tongue remains motionless.

For this disease, drug treatment methods, massage and reflexology are used.

It is not difficult to conclude that this syndrome is quite serious threat the health of the child, therefore the disease requires parents to quickly respond to symptoms and be patient during the treatment process.

Pseudobulbar syndrome or pseudobulbar palsy- This pathological condition, in which damage to the cranial nerves develops, which leads to paralysis of the facial muscles, muscles involved in speaking, chewing and swallowing. The disease is similar in symptoms to bulbar palsy, but is milder. leads to atrophy of muscle fibers, but this is not observed with pseudobulbar syndrome.

The development of the syndrome is associated with damage to the brain (in particular, its frontal lobes) with vascular disorders or as a result of injury, inflammatory or degenerative process. Characteristic signs of pathology: disturbances in swallowing processes, changes in voice and articulation, spontaneous crying and laughter, disruption of the facial muscles. Most often, this syndrome develops in combination with other neurological disorders.

Since the cause of the disease is brain damage and vascular disorders, then for treatment it is recommended to use drugs that improve cerebral circulation and metabolic processes V nerve tissue. Effectively apply folk remedies nootropic action based on medicinal plants.

How does the disease develop?

The brain is divided into the cortex and subcortical structures. The cortex appeared evolutionarily at a later stage, and it is responsible for the highest nervous activity. Subcortical structures, in particular the medulla oblongata, exist for a longer time. They can work autonomously, without the participation of the cerebral cortex. This structure provides the basic processes of life: breathing, heartbeat, the centers of which are located in the medulla oblongata. Normally, all parts of the brain are interconnected, and there is a clear regulation of human life. However, if these connections are disrupted, the subcortical structures continue to function autonomously.

The development of pseudobulbar syndrome is precisely caused by a disruption in the connection of the cortex with the nuclei motor neurons pyramidal centers of the medulla oblongata, from which the cranial nerves arise. Disruption of this connection is not life-threatening, since the medulla oblongata itself was not damaged in this case, but causes symptoms associated with disruption of the normal functioning of the cranial nerves: facial paralysis, speech impairment and others.

Pathology develops when the frontal lobes are affected. For pseudobulbar syndrome to occur, bilateral damage to the frontal lobes is necessary, since bilateral connections are formed in the brain: between the nuclei of motor neurons and the right and left hemispheres of the brain.

Causes of paralysis

Bulbar and pseudobulbar palsy have similar manifestations: in both cases, there is a disruption of the innervation of the facial, chewing, swallowing muscles, structures responsible for speech and breathing. With bulbar palsy, damage occurs to the cranial nerves themselves or to the structures of the medulla oblongata, and such damage leads to muscle atrophy and can be life-threatening for the patient. With pseudobulbar palsy, a violation of intracerebral regulation occurs. In this case, the nuclei of the medulla oblongata do not receive signals from other parts of the brain. In this case, however, there is no damage to the nervous tissue itself and there is no danger to human life.

Various reasons can lead to the development of pseudobulbar palsy:

Pathologies of cerebral vessels. This reason is the most common. Pseudobulbar palsy is caused by ischemic or hemorrhagic stroke, vasculitis, atherosclerosis and other vascular pathologies. The development of this disorder is more common in older people.
Violations embryonic development and congenital brain injuries.Hypoxia or birth injury can lead to the development of cerebral palsy in an infant, one of the manifestations of which can be pseudobulbar syndrome. Also, such paralysis can develop with congenital plumbing syndrome. Manifestations of pseudobulbar syndrome in this case are observed already in childhood. The child suffers not only from bulbur disorders, but also from a number of other neurological pathologies.
Traumatic brain injury.
Epilepsy with damage to the corresponding structures.
Degenerative and demyelinating processes in nervous tissue.
Inflammation of the brain or meninges.
Benign or malignant tumor, in particular, glioma. Manifestations of the disorder depend on the location of the tumor. If the growth of the neoplasm affects the regulation of the pyramidal structures of the medulla oblongata, the patient will develop pseudobulbar syndrome.
Brain damage due to hypoxia. Lack of oxygen has a complex negative effect. Brain tissue is extremely sensitive to oxygen starvation and is the first to suffer from hypoxia. The damage in this case is often complex and includes, among other things, pseudobulbar syndrome.

Symptoms of pathology

Manifestations of pseudobulbar syndrome are complex. The patient experiences disturbances in the processes of chewing, swallowing, and speech. The patient may also experience spontaneous laughter or crying. The disturbances are less pronounced than with bulbar palsy. Also in this case there is no muscle atrophy.

Pseudobulbar palsy leads to speech impairment. It becomes unclear, articulation is impaired. The patient's voice also becomes duller. These symptoms are associated with paralysis or, on the contrary, spasm of the muscles responsible for articulation.

One of the most key symptoms of pseudobulbar syndrome is oral automaticity. These are reflexes that are characteristic only of infants, but never occur in healthy adults.

A common sign of this disease is spontaneous laughter or crying. This condition occurs due to uncontrolled contraction of facial muscles. A person is not able to control these reactions. You also need to understand that they cannot be provoked by anything. In addition to the occurrence of involuntary movements, such people are characterized by disturbances in the voluntary regulation of the facial muscles. For example, when intending to close their eyes, a person may open their mouth instead.

The development of pseudobulbar palsy is associated with damage to the tissue of the cerebral cortex. In most cases, such damage is complex in nature and is manifested not only by dysregulation of the motor neuron nuclei of the medulla oblongata, but also by other neurological disorders.

Treatment of the disease

Treatment of the disease should primarily be aimed at eliminating the cause of the pathology. The most common cause of paralysis is vascular diseases, so therapy is aimed at improving cerebral circulation. Nootropic drugs that improve metabolic processes in the brain are also used in therapy.

It is also useful to practice physical therapy and execute breathing exercises. It is important to stretch your neck muscles 2-3 times a day: tilt your head forward, backward and to the sides, in circular movements. After warming up, you need to rub your neck muscles with your hands and massage your scalp with your fingertips. This will help relieve the symptom oxygen starvation and improve brain nutrition. If speech is impaired, you need to perform articulation gymnastics. If symptoms of pseudobulbar palsy appear in childhood, it is necessary to conduct classes with a speech therapist, as well as independently develop the child’s speech.

Folk remedies that have a nootropic effect will also help in treatment. Many commercial nootropic drugs are based specifically on plant components. Folk medicines have a similar but milder effect and do not cause negative side effects. Medicinal drugs must be taken in courses. The duration of the course is 2–4 weeks, after which you need to take a break. It is also recommended to alternate medicines so that addiction does not occur and the healing effect does not disappear.

Bulbar syndrome, or bulbar palsy- combined lesion of the bulbar group cranial nerves : glossopharyngeal, vagus, accessory and sublingual. Occurs when the function of their nuclei, roots, and trunks is impaired. Manifests:

bulbar dysarthria or anarthria
nasal tone of speech (nasolalia) or loss of sonority of the voice (aphonia)
swallowing disorder (dysphagia)
atrophy, fibrillary and fascicular twitching in the tongue
manifestations of flaccid paresis of the sternocleidomastoid and trapezius muscles

The palatal, pharyngeal and cough reflexes also fade away. Particularly dangerous are those associated with this respiratory disorders and cardiovascular disorders.

Dysarthria with bulbar syndrome is a speech disorder caused by flaccid paresis or paralysis of the muscles that support it (muscles of the tongue, lips, soft palate, pharynx, larynx, muscles that lift the mandible, respiratory muscles). Speech is slow, the patient quickly tires, speech defects are recognized by him, but overcoming them is impossible. The voice is weak, dull, depleted. Vowels and voiced consonants are deafened. The timbre of speech is changed into an open nasal type, and the articulation of consonant sounds is blurred. The articulation of fricative consonants (d, b, t, p) has been simplified. Possible selective disorders in the pronunciation of the mentioned sounds due to varying degrees involvement of muscles in the pathological process.

Brissot's syndrome(Described by the French neurologist E. Brissaud) is characterized by periodic occurrence trembling, pale skin, cold sweat, respiratory and circulatory disorders, accompanied by a state of anxiety, vital fear in patients with bulbar syndrome. (A consequence of dysfunction of the reticular formation in the brain stem).

Pseudobulbar palsy- combined dysfunction of the bulbar group of cranial nerves caused by bilateral damage going to their cores corticonuclear pathways . The clinical picture in this case resembles the manifestations of bulbar syndrome, but the paresis is central in nature (the tone of paretic or paralyzed muscles is increased, there is no hypotrophy, fibrillary and fascicular twitching), and the pharyngeal, palatal, cough, and mandibular reflexes are increased.

With pseudobulbar palsy, violent laughter and crying are noted, as well as reflexes of oral automatism

Oral automatism reflexes are a group of phylogenetically ancient proprioceptive reflexes, in the formation of reflex arcs of which the V and VII cranial nerves and their nuclei, as well as cells of the XII cranial nerve nucleus, the axons of which innervate the orbicularis oris muscle, take part. They are physiological in children under 2-3 years of age. Later, the subcortical nodes and the cerebral cortex exert an inhibitory influence on them. When these brain structures are damaged, as well as their connections with the marked nuclei of the cranial nerves, reflexes of oral automatism appear. They are caused by irritation of the oral part of the face and are manifested by stretching the lips forward - a sucking or kissing movement. These reflexes are characteristic, in particular, of clinical picture pseudobulbar syndrome.

Dysarthria with pseudobulbar syndrome- speech disorder caused by central paresis or paralysis of the muscles supporting it (pseudobulbar syndrome). The voice is weak, hoarse, hoarse; the pace of speech is slow, its timbre is nasal, especially when pronouncing consonants with a complex articulatory structure (r, l, sh, zh, ch, c) and vowels “e”, “i”. In this case, stop consonants and “r” are usually replaced by fricative consonants, the pronunciation of which is simplified. The articulation of hard consonants is impaired to a greater extent than soft ones. The ends of words are often not agreed upon. The patient is aware of articulation defects and actively tries to overcome them, but this only increases the tone of the muscles that provide speech and increases the manifestations of dysarthria.

Violent crying and laughter- spontaneous (often inappropriate), not amenable to volitional suppression and without adequate reasons, a facial emotional reaction inherent in crying or laughter, which does not contribute to the resolution of internal emotional tension.

Oral automaticity reflexes:

Proboscis reflex (oral ankylosing spondylitis reflex)- involuntary protrusion of the lips in response to light tapping with a hammer on the upper lip or on the subject’s finger placed on the lips. Described by Russian neurologist V.M. Bekhterev.
Oral Oppenheim reflex- chewing and sometimes swallowing movements (except for the sucking reflex) in response to line irritation of the lips. Refers to the reflexes of oral automatism. Described by the German neuropathologist N. Oppenheim.
Oppenheim's sucking reflex- the appearance of sucking movements in response to line irritation of the lips. Described by the German neuropathologist N. Orrengeim.
Nasolabial reflex (nasolabial reflex Astvatsaturov)- contraction of the orbicularis oris muscle and protrusion of the lips in response to tapping with a hammer on the back or tip of the nose. Described by domestic neuropathologist M.I. Astvatsaturov.
Palmomental reflex (Marinescu-Radovici reflex)- contraction of the mental muscle in response to line irritation of the skin of the palm in the area of elevation thumb on the side of the same name. Later extra-receptive skin reflex (compared to oral reflexes). Reflex arc closes in the striatum. Inhibition of the reflex is provided by the cerebral cortex. Normally caused in children under 4 years of age. In adults, it can be caused by cortical pathology and damage to cortical-subcortical, cortical-nuclear connections, in particular with pseudobulbar syndrome. Described by the Romanian neurologist G. Marinesku and the French doctor I.G. Radovici.
Wurp-Toulouse reflex (labial Wurp reflex)- involuntary stretching of the lips, reminiscent of a sucking movement, occurring in response to line irritation of the upper lip or its percussion. French doctors S. Vurpas and E. Toulouse described it.
Escherich reflex- sharp stretching of the lips and freezing them in this position with the formation of a “goat muzzle” in response to irritation of the mucous membrane of the lips or oral cavity. Refers to the reflexes of oral automatism. Described by the German doctor E. Escherich.
Remote-oral reflex Karchikyan-Rasvorov- protrusion of the lips when approaching the lips with a hammer or any other object. Refers to symptoms of oral automatism. Described by domestic neuropathologists I.S. Karchikyan and I.I. Solutions
Bogolepov's distant-oral reflex. After inducing the proboscis reflex, the approach of the malleus to the mouth leads to the fact that it opens and freezes in the “ready to eat” position. Described by Russian neuropathologist N.K. Bogolepov.
Babkin's distant chin reflex- contraction of the chin muscles when the hammer approaches the face. Described by domestic neuropathologist P.S. Babkin.
Oral Henneberg reflex- contraction of the orbicularis oris muscle in response to irritation with a spatula hard palate. Described by the German psychoneurologist R. Genneberg.
Labiomental reflex- contraction of the chin muscles when the lips are irritated.
Rybalkin mandibular reflex- intense closing of the slightly open mouth when a hammer hits a spatula placed across the lower jaw on her teeth. May be positive in cases of bilateral lesions of the corticonuclear tracts. Described by domestic doctor Ya.V. Rybalkin.
Bulldog reflex (Janiszewski reflex)- tonic closing of the jaws in response to irritation with a spatula of the lips, hard palate, and gums. It usually occurs when the frontal lobes of the brain are affected. Described by domestic neuropathologist A.E. Yanishevsky.
Guillain's nasopharyngeal reflex- closing the eyes while tapping the back of the nose with a hammer. May be caused by pseudobulbar syndrome. Described by the French neurologist G. Guillein
Mandibular clonus (Dana's sign)- clonus of the lower jaw when tapping with a hammer on the chin or on a spatula placed on the teeth of the lower jaw of a patient whose mouth is slightly open. It can be detected with bilateral damage to the corticonuclear pathways. Described by the American doctor Ch.L. Dana

A brief summary table of syndromes for ease of remembering:

	Bulbar syndrome	Pseudobulbar syndrome
Similarities		Dysphagia, dysphonia and dysarthria; drooping temples soft palate, decrease in their mobility; paralysis vocal cords(with laryngoscopy)
Differences	Loss of palatal and pharyngeal reflexes	Revitalization of the palatal and pharyngeal reflexes; symptoms of oral automatism, violent patterns, or crying
Localization of the lesion	Medulla oblongata (nucleus ambiguus) or glossopharyngeal, vagus and hypoglossal nerves	Bilateral damage to the corticonuclear tracts at the level of the cerebral hemispheres or brain stem

When some areas of the brain are damaged, serious pathological processes can appear that reduce a person’s standard of living, and in some cases, threaten death.

Bulbar and pseudobulbar syndrome are disorders of the central nervous system, the symptoms of which are similar to each other, but their etiology is different.

Bulbar occurs as a result of damage to the medulla oblongata - the glossopharyngeal, vagus and hypoglossal nerves that are in it.

Pseudobulbar syndrome (paralysis) manifests itself due to disruption of the conductivity of the corticonuclear pathways.

Clinical picture of bulbar syndrome

The main diseases during or after which bulbar palsy occurs:

stroke affecting the medulla oblongata;
infections ( tick-borne borreliosis, acute polyradiculoneuritis);
trunk glioma;
botulism;
displacement of brain structures with damage to the medulla oblongata;
genetic disorders (porphyrin disease, bulbospinal amyotrophy Kennedy);
Syringomyelia.

Porphyria – genetic disorder, in which bulbar palsy often appears. The unofficial name - vampire disease - is given because of man's fear of the sun and the effects of light on skin, which begin to burst, become covered with ulcers and scars. Due to involvement in inflammatory process cartilage and deformation of the nose, ears, as well as exposure of teeth, the patient becomes like a vampire. There is no specific treatment for this pathology.

Isolated bulbar palsies are uncommon due to the involvement of the nuclei of nearby structures of the medulla oblongata during damage.

The main symptoms that occur in the patient:

speech disorders (dysarthria);
swallowing disorders (dysphagia);
voice changes (dysphonia).

Patients have difficulty speaking indistinctly, their voice becomes weak, to the point that it becomes impossible to make a sound. The patient begins to pronounce sounds through the nose, his speech is blurred and slow. Vowel sounds become indistinguishable from each other. Not only paresis of the tongue muscles, but their complete paralysis may occur.

Patients choke on food and often cannot swallow it. Liquid food enters the nose, and aphagia may occur (complete inability to swallow).

The neurologist diagnoses the disappearance of the soft palate and pharyngeal reflexes and notes the appearance of twitching of individual muscle fibers and muscle degeneration.

In case of severe damage, when cardiovascular and respiratory centers, disturbances in the rhythm of breathing and heart activity occur, which can lead to death.

Manifestations and causes of pseudobulbar syndrome

Diseases after or during which pseudobulbar palsy develops:

vascular disorders affecting both hemispheres (vasculitis, atherosclerosis, hypertensive lacunar cerebral infarctions);
traumatic brain injuries;
brain damage due to severe hypoxia;
epileptoform syndrome in children (a single episode of paralysis may occur);
demyelinating disorders;
Pick's disease;
bilateral perisylvian syndrome;
multiple system atrophy;
intrauterine pathology or birth trauma in newborns;
genetic disorders (lateral amyotrophic sclerosis, olivopontocerebellar degenerations, Creutzfeldt-Jakob disease, familial spastic paraplegia, etc.);
Parkinson's disease;
glioma;
neurological conditions after inflammation of the brain and its membranes.

Creutzfeldt-Jakob disease, in which not only pseudobulbar syndrome is observed, but also symptoms of rapidly progressing dementia, is a serious disease, the predisposition to which is genetically determined. It develops due to the entry into the body of abnormal tertiary proteins, similar in their action to viruses. In most cases, death occurs within a year or two from the onset of the disease. There is no treatment to eliminate the cause.

The symptoms that accompany pseudobulbar palsy, like bulbar palsy, are expressed in dysphonia, dysphagia and dysarthria (in a milder version). But these two lesions of the nervous system have differences.

If with bulbar palsy atrophy and degeneration of muscles occurs, then these phenomena are absent with pseudobulbar palsy. Defibrillar reflexes also do not occur.

Pseudobulbar syndrome is characterized by uniform paresis of the facial muscles, which are spastic in nature: disorders of differentiated and voluntary movements are observed.

Since disturbances in pseudobulbar palsy occur above the medulla oblongata, there is no threat to life due to arrest of the respiratory or cardiovascular systems.

The main symptoms that indicate that pseudobulbar palsy has developed, and not bulbar, are expressed in violent crying or laughter, as well as reflexes of oral automatism, which are normally characteristic of children, and in adults indicate the development of pathology. This could be, for example, a proboscis reflex, when the patient stretches out his lips with a tube if light tapping is done near the mouth. The same action is performed by the patient if he brings any object to his lips. Contractions of the facial muscles can be caused by tapping the bridge of the nose or pressing the palm under thumb hands.

Pseudobulbar palsy leads to multiple softened foci of the brain substance, so the patient experiences a decrease in motor activity, disorders and weakening of memory and attention, a decrease in intelligence and the development of dementia.

Patients may develop hemiparesis, a condition in which the muscles on one side of the body become paralyzed. Paresis of all limbs may occur.

With severe brain damage, pseudobulbar palsy can appear together with bulbar palsy.

Therapeutic effects

Since pseudobulbar syndrome and bulbar syndrome are secondary diseases, treatment should be aimed at the causes of the underlying disease, if possible. When symptoms subside primary disease, signs of paralysis may be smoothed out.

The main goal of treatment for severe forms of bulbar palsy is to maintain vital important functions body. For this purpose they prescribe:

artificial ventilation;
tube feeding;
prozerin (it is used to restore the swallowing reflex);
atropine for excessive salivation.

After resuscitation measures complex treatment should be prescribed, which can affect the primary and secondary diseases. Thanks to this, life is preserved and its quality is improved, and the patient’s condition is alleviated.

The issue of treating bulbar and pseudobulbar syndromes through the introduction of stem cells remains controversial: supporters believe that these cells can produce the effect of physical replacement of myelin and restore the functions of neurons, opponents point out that the effectiveness of using stem cells has not been proven and, on the contrary, increases the risk of developing cancerous tumors.

Restoration of reflexes in a newborn begins in the first 2 to 3 weeks of life. Besides drug treatment he undergoes massage and physiotherapy, which should have a tonic effect. Doctors give an uncertain prognosis because full recovery even with adequately selected treatment does not occur, and the underlying disease may progress.

Bulbar and pseudobulbar syndrome are severe secondary lesions of the nervous system. Their treatment must be comprehensive and must be aimed at the underlying disease. In severe cases of bulbar palsy, respiratory and cardiac arrest may occur. The prognosis is unclear and depends on the course of the underlying disease.

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 dysphonia, aphonia, dysarthria, choking while eating, and liquid food entering the nose through the nasopharynx. There is a drooping of the soft palate and the absence of its movements when pronouncing sounds, speech with a nasal tint, sometimes deviation of the tongue to the side, paralysis of the vocal cords, tongue muscles with their atrophy and fibrillary twitching. There are no pharyngeal, palatal and sneezing reflexes, coughing when eating, vomiting, hiccups, respiratory and cardiovascular problems.

Pseudobulbar syndrome characterized by disorders of swallowing, phonation, speech articulation and often impaired facial expressions. 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 orbicularis oris muscle, lips or masticatory 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 central paralysis(paresis) of the muscles involved in the processes of swallowing, phonation and speech articulation, which is caused by a break in the central pathways running from the motor centers of the cortex to the nerve nuclei. Most often it is caused by vascular lesions with softening foci 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. Consists of general cerebral symptoms, changes in the cranial nerves, spinal cord roots, depression of reflexes and changes cerebrospinal fluid. Meningeal syndrome includes and true meningeal symptoms(damage to the nervous apparatus located in the meninges of the brain, most of which belong to nerve fibers trigeminal, glossopharyngeal, vagus nerves).

TO true meningeal symptoms include headache, buccal symptom( raising the shoulders and flexing the forearms while pressing on the cheek ), Zygomatic ankylosing spondylitis sign(tapping the cheekbone is accompanied by increased headache and tonic contraction of the facial muscles (painful grimace) mainly on the same side) , percussion soreness of the skull, nausea, vomiting and changes in pulse. Headache is the main symptom meningeal syndrome. It is diffuse in nature and intensifies with head movement, sharp sounds and bright light, it can be very intense and is often accompanied by vomiting. Typically, vomiting of cerebral origin is sudden, profuse, occurs without preliminary nausea and is not associated with food intake. Hyperesthesia of the skin and sensory organs (cutaneous, optical, acoustic) is noted. Patients are painfully sensitive to the touch of clothing or bedding. To the number characteristic features include symptoms that reveal tonic tension in the muscles of the limbs and trunk (N.I. Grashchenkov): rigidity of the muscles of the back of the head, symptoms of Kernig, Brudzinsky, Lessage, Levinson, Guillain, rising symptom, bulbo-facial tonic Mondonesi symptom, “gun trigger” syndrome ( characteristic pose- the head is thrown back, the torso is in a hyperextension position, lower limbs brought to the stomach). Meningeal contractures are often observed.

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 primarily affect: (45-50 years old). Their ethnology is unclear, but there are hormonal, infectious, traumatic and radiation theories. There are primary and secondary (metastatic) tumors, benignnatural and malignant, intracerebral and extracerebral. Clinical manifestations of brain tumors are divided into 3 groups: general cerebral, focal symptoms and displacement symptoms. The dynamics of the disease are characterized first by an increase in hypertensive and focal symptoms, and in later stages symptoms of displacement appear. General cerebral symptoms are caused by increased intracranial pressure, impaired cerebrospinal fluid circulation and intoxication of the body. These include the following signs: headache, vomiting, dizziness, convulsive seizures, disturbances of consciousness, mental disorders, changes in pulse and breathing rhythm, membrane symptoms. At additional research congestive optic discs, characteristic changes on craniograms (“finger impressions”, thinning of the back of the sella turcica, suture dehiscence) are determined. Focal symptoms depend on the immediate localization of the tumor. Tumor frontal lobe is manifested by “frontal psyche” (weakness, foolishness, sloppiness), paresis, impaired speech, smell, grasping reflexes, epileptiform seizures. Tumors of the parietal lobe are characterized by disturbances of sensitivity, especially complex types of it, disturbances in reading, counting, and writing. Temporal lobe tumors 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 disturbances of endocrine functions - obesity, menstrual irregularities, acromegaly. Tumors cerebellum accompanied by disturbances in gait, coordination, and muscle tone. Tumors of the cerebellopontine angle begin with tinnitus, hearing loss, then paresis of the facial muscles, nystagmus, dizziness, sensitivity and vision disorders are added. At brain stem tumors cranial nerves are affected. Tumor IV cerebral ventricle characterized by paroxysmal headaches in the back of the head, dizziness, vomiting, tonic convulsions, respiratory and cardiac dysfunction. 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. The EEG reveals slow pathological waves; on EchoEG - M-Echo displacement up to 10 mm; The most important angiographic sign of a tumor is the displacement of blood vessels or the appearance of newly formed vessels. But most informative method diagnostics currently include computed tomography and nuclear magnetic tomography.

32.Meningitis. Etiology, clinical picture, diagnosis, treatment, prevention . Meningitis is an inflammation of the membranes of the brain and spinal cord, with the soft and arachnoid membranes most often affected. Etiology. Meningitis can occur through several routes of infection. Contact path- the occurrence of meningitis occurs in conditions of an already existing purulent infection. The development of sinusogenic meningitis contributes to purulent infection paranasal sinuses (sinusitis), otogenic mastoid process or middle ear (otitis), odontogenic - dental pathology. 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, crack or fracture of the base of the skull. Infectious agents entering the body through entrance gate(bronchi, gastrointestinal tract, nasopharynx), cause inflammation (serous or purulent type) of the meninges and adjacent brain tissue. Their subsequent swelling 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 increases, and cerebral hydrocele develops. Further spread of the inflammatory process to the substance of the brain, the roots of the cranial and spinal nerves is possible. Clinic. The symptom complex of any form of meningitis includes general infectious symptoms (fever, chills, increased body temperature), increased breathing and disturbance of its rhythm, changes in heart rate (at the beginning diseases tachycardia, as the disease progresses, bradycardia). Meningeal syndrome includes cerebral symptoms, manifested by tonic tension in the muscles of the trunk and limbs. Prodormal symptoms (runny nose, abdominal pain, etc.) often appear. Vomiting with 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, or light. In childhood, seizures may occur. Meningitis is characterized by hyperesthesia of the skin and pain of the skull upon percussion. At the beginning of the disease, there is an increase in tendon reflexes, but as the disease progresses, they decrease and often disappear. If brain matter is involved in the inflammatory process, paralysis, pathological reflexes and paresis develop. Severe meningitis is usually accompanied by dilated pupils, diplopia, strabismus, and loss of control over pelvic organs(in case of development of mental disorders). Symptoms of meningitis in old age: mild or complete absence of headaches, tremors of the head and limbs, drowsiness, mental disorders (apathy or, conversely, psychomotor agitation). Diagnostics. The main method for diagnosing meningitis is lumbar puncture followed by examination of cerebrospinal fluid. All forms of meningitis are characterized by leakage of fluid under high pressure(sometimes in a stream). In serous meningitis, cerebrospinal transparent liquid, with purulent meningitis - cloudy, yellow-green in color. By using laboratory research cerebrospinal fluid is determined by pleocytosis, a change in the ratio of the number of cells and increased content squirrel. In order to clarify 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, glucose levels decrease. For purulent meningitis there is a significant (to zero) decrease in glucose levels. The main guidelines for a neurologist in differentiating meningitis are the study of cerebrospinal fluid, namely the determination of the cell ratio, sugar and protein levels. Treatment. If meningitis is suspected, hospitalization of the patient is mandatory. At severe course 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! Basis of treatment purulent meningitis- early administration of sulfonamides (etazol, norsulfazole) in the middle daily dose 5-6 g or antibiotics (penicillin) in an average daily dose of 12-24 million units. If such treatment of meningitis is ineffective during the first 3 days, therapy with semisynthetic antibiotics (ampiox, carbenicillin) in combination with monomycin, gentamicin, and nitrofurans should be continued. The basis of 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 medications (glucose, analgin, vitamins, methyluracil). In severe cases (severe cerebral symptoms), corticosteroids and diuretics are prescribed, less often - repeated spinal tap. In case of layering bacterial infection antibiotics may be prescribed. Prevention. Regular hardening (water treatments, sports), timely treatment of chronic and acute infectious diseases.

33. Encephalitis. Epidemic encephalitis. Clinic, diagnosis, treatment . Encephalitis is inflammation of the brain. Predominant damage to the gray matter is called polioencephalitis, white matter - leukoencephalitis. Encephalitis can be limited (trunk, subcortical) or diffuse; primary and secondary. The causative agents of the disease are viruses and bacteria. Often the causative agent is unknown. Epidemic encephalitis Economo (lethargicencephalitis). People aged 20-30 years are more likely to 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 sufficiently studied. It is believed that viremia initially occurs, and then the virus enters the brain through the perineural spaces. In the clinical course of epidemic encephalitis, acute and chronic phases are distinguished. In formation chronic phase A major role belongs to autoimmune processes that cause degeneration of cells of the substantia nigra, globus pallidus, and 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, body temperature rises to 39-40 ° C, headache occurs, often vomiting, and general malaise. Catarrhal symptoms may occur. in the throat. It is important that with 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. Already a few hours after the onset of the disease, loss of consciousness may occur , generalized convulsions are often observed. Damage to the nuclei of the hypothalamic region contributes to disruption of cerebral hemodynamics. Phenomena of edema develop - swelling of the brain, often leading to death on the 1st-2nd day, even before the child appears focal symptoms, characteristic of epidemic encephalitis. Diagnostics It is important to correctly assess the state of consciousness and promptly identify the first symptoms focal lesion brain, in particular sleep disorders, oculomotor, vestibular, autonomic-endocrine disorders, requires the collection of accurate anamnestic data on previously suffered acute infectious diseases with general cerebral symptoms, disturbances of consciousness, sleep, diplopia. Treatment. There are currently no specific treatment methods for epidemic encephalitis. It is advisable to carry out the recommended viral infections vitamin therapy (ascorbic acid, B vitamins), prescription of desensitizing drugs (antihistamines - diphenhydramine, suprastin, diazolin, tavegil; 5-10% solutions of calcium chloride, calcium gluconate orally or intravenously; prednisolone, etc.), To combat the symptoms of edema brain, intensive dehydration therapy is indicated: diuretics, hypertonic solutions of fructose, sodium chloride, calcium chloride. For convulsions, enemas are prescribed.