Pseudobulbar syndrome in children and adults. Reasons for the development of the 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 lesions hemorrhages that lead to damage on both hemispheres of the fibers connecting the motor nuclei 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. Yours Negative influence is capable of providing 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 of the 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 the distinguishing features of the pseudoform will be the absence of atrophy.

It is worth noting that in some cases it can be quite difficult to distinguish PS from Parkinson-like paralysis. This disease progresses slowly, and in the later stages apoplectic strokes are recorded. Moreover, signs similar to the syndrome appear: violent crying, speech disorder, etc. Therefore, a qualified doctor 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 proserine on cervical region 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 of the neurological status and positive changes in the deviations recorded earlier. 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, it is actually observed complete absence 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 is 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, however, it proceeds more easily. 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, it is recommended for treatment to use drugs that improve cerebral circulation and metabolic processes in the brain. 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 higher 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.

The development of pseudobulbar palsy can lead to various reasons:

1. 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.
2. Disorders of embryonic development and congenital brain injuries. Hypoxia or birth trauma 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.
3. Traumatic brain injury.
4. Epilepsy with damage to the corresponding structures.
5. Degenerative and demyelinating processes in nervous tissue.
6. Inflammation of the brain or meninges.
7. 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.
8. 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 pseudobulbar syndrome is oral automatism. 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 involuntary movements Such people are characterized by disturbances in the voluntary regulation of 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. Most often, the 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.

Paralysis)

dysfunction of the muscles (paralysis) innervated by the IX, X and XII pairs of cranial nerves as a result of bilateral damage to the central motor neurons and corticonuclear pathways, going to the nuclei of these nerves.

Pseudobulbar palsy often develops with severe cerebral atherosclerosis. Bilateral neurological disorders occur after repeated ischemic or hemorrhagic strokes, which result in the formation of multiple small lesions in the cerebral hemispheres. Corticonuclear conductors (see Pyramidal system) at this may cause damage to various levels, often in the internal capsule, the pons of the brain. The development of P. p. is also possible with unilateral switching off of blood flow in a large cerebral artery, as a result of which the opposite hemisphere also decreases (the so-called steal), and chronic brain damage develops. The cause of P. p. can also be diffuse cerebral vessels in vasculitis, for example, syphilitic, tuberculous, rheumatic, periarteritis nodosa, systemic lupus erythematosus, Degos disease, etc. In addition, P. p. is observed in perinatal brain damage, damage to the cortical nuclear tracts in hereditary degenerative diseases, Pick's disease, Creutzfeldt-Jakob disease, post-resuscitation complications in persons who have suffered cerebral hypoxia. IN acute period cerebral hypoxia P. p. may develop as a result diffuse damage cerebral cortex.

Clinically characterized by a swallowing disorder - dysphagia (Dysphagia), articulation disorder - dysarthria (Dysarthria) or anarthria, changes in phonation - dysphonia (hoarseness). tongue muscles, soft palate and pharynx is not accompanied by atrophy and is significantly less pronounced than with bulbar palsy (Bulbar palsy). Caused by oral automatism (see Reflexes), which are associated with concomitant dysfunction of central motor neurons and corticonuclear pathways to the nuclei of the facial and trigeminal nerves. Patients are forced to eat food slowly, choking when swallowing due to liquid food entering the (soft palate); salivation is noted. Often P. p. is accompanied by attacks of violent laughter or crying, which are not associated with emotions and arise as a result of spastic contraction of the facial muscles. At the same time, weakness, impaired attention and memory, with a subsequent decrease in intelligence, can be observed.

Based on the nature of the accompanying symptoms, pyramidal, extrapyramidal, pontine, as well as hereditary and childhood forms of P. p. are distinguished. In the pyramidal form, in addition to the manifestations of P. p., diparesis of the limbs is observed, deep reflexes almost always increase and pathological carpal and foot reflexes are caused. In the extrapyramidal form, the signs of P. p. are combined with akineticorid syndrome (Akinetic-rigid syndrome). The pontine form is characterized by a combination of signs of P. p. with central paralysis of the muscles innervated by the V, VII and VI pairs of cranial nerves. The hereditary form of P. p. is one of the components of a complex of neurological manifestations caused by genetic disorder brain metabolism with degeneration of pyramidal neurons. The childhood form of P. p. develops as a result of the birth brain or intrauterine encephalitis and is characterized by a combination of P. p. with spastic diparesis, choreic, athetoid or torsion hyperkinesis (Hyperkinesis).

Diagnosis in typical cases is not difficult. P. p. should be differentiated from bulbar palsy. With the latter, there are no reflexes of oral automatism, the pharyngeal reflex from the soft palate is not evoked, there are also fascicular twitching of the muscles of the tongue, nasality is more pronounced. Treatment depends on the form of P. and its stage of the underlying disease. As P. progresses, agents are used that normalize blood clotting processes and reduce cholesterol levels in the blood. Drugs that improve microcirculation in the brain, metabolic processes and bioenergetics of neurons (aminalon, encephabol, cerebrolysin, etc.), and anticholinesterase agents (prozerin, oxazil, etc.) are indicated. At acute development P. p. are necessary in the hospital, probe. In case of severe swallowing disorders, food masses with obstruction are possible respiratory tract, which requires resuscitation measures (see Asphyxia).

Bibliography.: Gusev E.I., Grechko V.E. and Burd G.S. Nervous diseases, M., 1988; Collins R.Ts. Diagnosis of nervous diseases. from English, M., 1986.

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

See what “Pseudobulbar palsy” is in other dictionaries:

PSEUDOBULBAR PARALYSIS- (false bulbar palsy), loss of function of the lingual, chewing, facial, pharyngeal and laryngeal muscles, and sometimes corresponding eye movements due to damage to the central, cortical nuclear conductors motor nuclei… … Great Medical Encyclopedia

PSEUDOBULBAR PARALYSIS- [from Greek. pseudos lie lat. bulbus is a bulb whose shape resembles the medulla oblongata and the Greek. paralysis relaxation] central paralysis facial expression of articulatory muscles, muscles of the tongue, pharynx, soft palate and larynx, caused by... ...

ICD 10 G12.212.2 ICD 9 335.23335.23 DiseasesDB ... Wikipedia

Loss or impairment of movement in one or more parts of the body. Paralysis is a symptom of many organic diseases nervous system. A condition in which voluntary movements are not completely lost is called paresis. Causes. Paralysis is not... Collier's Encyclopedia

PSEUDOBULBAR PARALYSIS- [from Greek. pseudos lie and lat. bulbus bulb, the shape of which resembles the medulla oblongata] paralysis of facial articulatory muscles innervated by cranial motor muscles brain nerves, caused by bilateral damage to the cortical stem... ... Psychomotorics: dictionary-reference book

- (paralysis pseudobulbaris; synonym: false bulbar palsy, supranuclear bulbar palsy) paresis of muscles innervated by motor cranial nerves, caused by bilateral damage to the cortical nuclear fibers in the hemispheres or in the trunk... ... Large medical dictionary

Pseudobulbar palsy- Syn.: Pseudobulbar syndrome. Combined dysfunction of the caudal group of cranial nerves, caused by bilateral damage to the corticonuclear pathways leading to their nuclei. In this case, the clinical picture resembles manifestations of bulbar... ... Encyclopedic Dictionary of Psychology and Pedagogy Great Psychological Encyclopedia

Bulbar and pseudobulbar palsies.

Bulbar palsy.

This is a symptom complex that occurs as a result of damage to the motor nuclei, roots, or the 9, 10, 12 pairs of cranial nerves themselves, with a clinical picture of flaccid atrophic (peripheral) paresis, paralysis of the muscles innervated by these nerves. Particularly pronounced with bilateral lesions.

Bulbar palsy is characteristic of amyotrophic lateral sclerosis, progressive Duchenne bulbar palsy, poliomyelitis, polio-like diseases, tick-borne encephalitis, tumors of the tegmentum of the medulla oblongata and cerebellum, syringobulbia.

Etiology: for tumors and arachnoiditis in the posterior cranial fossa, carcinomatosis, sarcomatosis, granulomatous processes, meningitis with predominant localization in the posterior cranial fossa, diphtheria polyneuritis, infectious-allergic polyradiculoneuritis.

Clinic: There is a violation of articulation (dysarthria, anarthria), swallowing (dysphagia, aphagia), phonation (dysphonia, aphonia), a nasal tone of speech is noted (nasolalia). There is a prolapse of the soft palate, its immobility when pronouncing sounds, and sometimes deviation of the uvula. Damage to the 10th nerve results in respiratory and cardiovascular disorders. Signs are revealed peripheral paralysis(atrophy of the muscles of the tongue, decrease in its volume, folding of the mucous membrane of the tongue). Damage to the nuclei is characterized by fasciculation of the tongue. Palatal, pharyngeal, cough, gag reflexes reduced or absent, paresis of the orbicularis oris muscle is often observed.

Diagnosis is based on the clinic. Differential diagnosis is carried out with pseudobulbar palsy. Treatment consists of treating the underlying disease. With bilateral damage to the 10th pair, the outcome is fatal.

Pseudobulbar palsy.

This is a symptom complex that occurs when the corticonuclear tracts of the 9th, 10th, 12th cranial nerves are interrupted bilaterally, with clinical picture central paresis or paralysis of the muscles innervated by these cranial nerves.

Most often accompanied by pseudobulbar palsy the following diseases: multiple sclerosis, basal gliomas and other tumors of the base of the pons, circulatory disorders in the vertebrobasilar region, central pontine myelinolysis. Lesions of corticonuclear fibers in the region of the cerebral peduncles are often associated with cerebrovascular accidents and tumors. More orally located bilateral lesions of the corticonuclear tracts are usually observed in diffuse or multifocal processes in both hemispheres - vascular diseases of the brain, demyelinating diseases, encephalitis, intoxication, brain injuries and their consequences.

Damage to the corticonuclear tracts of the 9th, 10th, 12th pairs of cranial nerves leads to the appearance of a picture of central paralysis.

Clinic: Manifested by disorders of swallowing (dysphagia), phonation (dysphonia), and speech articulation (dysarthria). There is a tendency to violent laughter and crying, which is due to bilateral interruption of the descending cortical fibers that conduct inhibitory impulses.

Unlike bulbar palsy, with pseudobulbar syndrome, the paralyzed muscles do not atrophy and there is no degeneration reaction. At the same time, reflexes associated with the brain stem are not only preserved, but also pathologically increased - palatal, pharyngeal, cough, gag. The presence of symptoms of oral automatism is characteristic.

Diagnosis is based on the clinic. Differential diagnosis with bulbar palsy. Treatment and prognosis depend on the nature and severity of the disease that caused this pathological condition.

16. Clinical manifestations lesions of the frontal lobe of the brain .

Frontal lobe syndrome – common name a set of syndromes of various, functionally significant structures of the frontal lobe of the cerebral hemispheres. Each of these syndromes can be presented in 2 variants - irritative and prolapsed. In addition, the characteristics of frontal lobe syndrome are influenced by the law on functional asymmetry cerebral hemispheres, syndromes of the left and right hemispheres have significant differences. In accordance with this law, the left hemisphere in right-handed people is responsible for verbal functions(for left-handers - on the contrary), the right - for non-verbal, gnostic-practical functions (for left-handers - on the contrary).

Syndrome posterior sections frontal lobe. Occurs when the following Brodmann fields are affected: 6 (agraphia), 8 (comfortable rotation of the eyes and head in the opposite direction and “cortical” gaze paralysis to the side, aspantine, astasia-abasia), 44 (motor aphasia).

Middle compartment syndrome. Occurs when the 9, 45, 46, 47 Brodmann areas are damaged. The main symptoms of this syndrome are mental disorders, which can be represented by 2 main syndromes:

· Apathetic-abulic syndrome – lack of initiative for any movement.

· Disinhibited-euphoric syndrome is the opposite of the first syndrome. Those. infantilism, foolishness, euphoria.

Other symptoms of damage to the middle part of the frontal lobe may include:

· Symptom of “facial facialis” (Vincent’s symptom) – the presence of insufficiency of lower facial innervation when crying, laughing, smiling.

· Grasping phenomena – Janiszewski reflex (at the slightest touch to the palmar surface, the hand reflexively clenches into a fist), Robinson reflex (the phenomenon of automatic obsessive grasping and pursuit);

· Typical changes in posture (reminiscent of parkinsonian posture);

Syndrome anterior section(poles). Occurs when the 10th and 11th fields according to Brodmann are affected. The leading symptoms of this syndrome are disturbances in statics and coordination, referred to as frontal ataxia (deflection of the body to the side at rest, overshooting), adiadochokinesis and impaired coordination on the side opposite to the lesion, less often on the side of the lesion. Sometimes these symptoms are referred to as pseudocerebellar. They differ from true cerebellar ones in the lower intensity of disturbances, the absence of hypotonia of the muscles of the limbs and their combination with changes in muscle tone of the extrapyramidal type (rigor, the phenomena of “cogwheel” and “countercontinence”). The described symptoms are caused by damage to the frontopontine and pontocerebellar pathways, which begin primarily at the poles of the frontal lobes.

Inferior surface syndrome. It is similar to the syndromes of the middle part of the frontal lobe and the frontal pole, differing in the presence of obligatory damage to the olfactory nerve. The leading symptom, in addition to mental disorders (apathetic-abulic or disinhibited-euphoric syndromes), is hypo- or anosmia (decreased or absent sense of smell) on the side of the lesion. When the pathological focus spreads posteriorly, Foster-Kennedy syndrome (primary disc atrophy) may appear optic nerve, on the side of the lesion, as a result of pressure on the optic nerve) and the presence of congestive optic disc. Pain on percussion along the zygomatic process or the frontal region of the head and the presence of exophthalmos homolateral to the focus may also occur, indicating proximity pathological process to the base of the skull and to the orbit.

Precentral region syndrome. Occurs when the precentral gyrus is damaged (4 and partially 6 areas according to Brodmann), which is the motor area of ​​the cortex big brain. Here are the centers of elementary motor functions - flexion, extension, adduction, abduction, pronation, supination, etc. The syndrome is known in 2 variants:

· Variant of irritation (irritation). Gives the syndrome of partial (focal) epilepsy. These seizures (Jackson's, Kozhevnikov's) are expressed by clonic or tonic-clonic convulsions, stereotypically starting from a certain part of the body according to the somatotopic projection: irritation of the lower parts of the precentral gyrus gives partial seizures starting in the muscles of the pharynx, tongue and lower facial group (opercular syndrome - attacks of chewing or swallowing movements, licking lips, smacking). Unilateral irritation of the cerebral cortex in the region of the middle part of the precentral gyrus produces clonic-tonic paroxysms - irritative syndrome of the anterior central gyrus - clonic or clonic-tonic convulsions in the arm contralateral to the lesion, starting from the distal parts (hand, fingers) of the latter. Irritation of the cerebral cortex in the region of the paracentral lobule causes the appearance of clonic or clonic-tonic convulsions, starting from the muscles of the foot of the opposite part of the body.

· Variant of cerebral prolapse. It manifests itself as a violation of voluntary motor function - central paresis (paralysis). A characteristic sign of cortical disorders of motor function is the monoplegic type of paralysis or paresis, a combination of monoparesis of the arm or leg with central paresis of the muscles innervated by the facial and hypoglossal nerves– syndrome of loss of functions of the anterior central gyrus, caused by unilateral damage to a certain area of ​​the cerebral cortex in the region of the anterior central gyrus.

Neurologists will highlight the following main causes of pseudobulbar palsy:

1. Vascular diseases affecting both hemispheres (lacunar state with hypertension, atherosclerosis; vasculitis).
2. Perinatal pathology and birth trauma, including.
3. Congenital bilateral periaqueductal syndrome.
4. Traumatic brain injury.
5. Episodic pseudobulbar palsy in epileptiform opercular syndrome in children.
6. Degenerative diseases affecting the pyramidal and extrapyramidal systems: ALS, primary lateral sclerosis, familial spastic paraplegia (rare), OPCA, Pick's disease, Creutzfeldt-Jakob disease, progressive supranuclear palsy, Parkinson's disease, multiple system atrophy, other extrapyramidal diseases.
7. Demyelinating diseases.
8. Consequences of encephalitis or meningitis.
9. Multiple or diffuse (glioma) neoplasm.
10. Hypoxic (anoxic) encephalopathy (“disease of the revitalized brain”).
11. Other reasons.

Vascular diseases

Vascular diseases affecting both hemispheres are the most common reason pseudobulbar palsy. Repeated ischemic disorders of cerebral circulation, usually in people over 50 years of age, with hypertension, atherosclerosis, vasculitis, systemic diseases, heart and blood diseases, multiple lacunar cerebral infarctions, etc., as a rule, lead to a picture of pseudobulbar palsy. The latter can sometimes develop with a single stroke, apparently due to decompensation of the latent vascular brain failure in the other hemisphere. With vascular pseudobulbar palsy, the latter may be accompanied by hemiparesis, tetraparesis, or bilateral pyramidal insufficiency without paresis. Revealed vascular disease brain, usually confirmed by MRI.

Perinatal pathology and birth trauma

Due to perinatal hypoxia or asphyxia, as well as birth trauma, various forms of childhood cerebral palsy(cerebral palsy) with the development of spastic-paretic (diplegic, hemiplegic, tetraplegic), dyskinetic (mainly dystonic), atactic and mixed syndromes, including with a picture of pseudobulbar palsy. In addition to periventricular leukomalacia, these children often have unilateral hemorrhagic infarction. More than half of these children show symptoms of mental retardation; approximately one third develop epileptic seizures. The history usually contains indications of perinatal pathology, delayed psychomotor development and in neurological status residual symptoms of perinatal encephalopathy are revealed.

Differential diagnosis Cerebral palsy includes some degenerative and hereditary metabolic disorders (glutaric aciduria type I; arginase deficiency; dopa-responsive dystonia; hyperekplexia (with rigidity); Lesch-Nyhan disease), as well as progressive hydrocephalus, subdural hematoma. MRI detects certain abnormalities in the brain in almost 93% of patients with cerebral palsy.

Congenital bilateral aqueduct syndrome

This defect occurs in children's neurological practice. It leads (like congenital bilateral sclerosis of the hippocampus) to a pronounced disorder speech development, which sometimes even mimics childhood autism and the picture of pseudobulbar palsy (mainly with speech disorders and dysphagia). Mental retardation and epileptic seizures are observed in approximately 85% of cases. MRI reveals malformation of the perisylvian gyri.

Severe traumatic brain injury (TBI)

Severe traumatic brain injury in adults and children often leads to various types of pyramidal syndrome (spastic mono-, hemi-, tri- and tetraparesis or plegia) and pseudobulbar disorders with severe speech and swallowing disorders. The association with a history of trauma leaves no room for diagnostic doubt.

Epilepsy

Episodic pseudobulbar palsy has been described in children with epileptiform opercular syndrome (paroxysmal oral apraxia, dysarthria and drooling), observed in slow phase night sleep. The diagnosis is confirmed by epileptic discharges in the EEG during a nocturnal attack.

Degenerative diseases

Many degenerative diseases, occurring with the involvement of the pyramidal and extrapyramidal systems, may be accompanied by pseudobulbar syndrome. Such diseases include lateral amyotrophic sclerosis, progressive supranuclear palsy (these forms as the cause of pseudobulbar syndrome are more common than others), primary lateral sclerosis, familial spastic paraplegia (rarely leads to severe pseudobulbar syndrome), Pick's disease, Creutzfeldt-Jakob disease, Parkinson's disease, secondary parkinsonism, multiple system atrophy, less commonly - other extrapyramidal diseases.

Demyelinating diseases

Demyelinating diseases often involve the corticobulbar tracts bilaterally, leading to pseudobulbar syndrome (multiple sclerosis, post-infectious and post-vaccination encephalomyelitis, progressive multifocal leukoencephalopathy, subacute sclerosing panencephalitis, AIDS-dementia complex, adrenoleukodystrophy).

This same group (“myelin diseases”) includes metabolic diseases myelin (Pelizius-Merzbacher disease, Alexander disease, metachromatic leukodystrophy, globoid leukodystrophy).

Consequences of encephalitis and meningitis

Encephalitis, meningitis and meningoencephalitis, along with other neurological syndromes, may also include pseudobulbar syndrome in their manifestations. Symptoms of an underlying infectious brain lesion are always identified.

Multiple or diffuse glioma

Some variants of brainstem glioma exhibit variable clinical symptoms depending on its location within the caudal, middle (pons) or oral parts of the brain stem. Most often, this tumor begins in childhood (in 80% of cases before the age of 21) with symptoms of involvement of one or more cranial nerves (usually VI and VII on one side), progressive hemiparesis or paraparesis, and ataxia. Sometimes conduction symptoms precede damage to the cranial nerves. Headaches, vomiting, and swelling in the fundus occur. Pseudobulbar syndrome develops.

Differential diagnosis with pontine shape multiple sclerosis, vascular malformation (usually cavernous hemangioma) and brainstem encephalitis. IN differential diagnosis MRI provides significant assistance. It is important to distinguish between focal and diffuse forms of glioma (astrocytoma).

Hypoxic (anoxic) encephalopathy

Hypoxic encephalopathy with serious neurological complications typical for patients who have experienced resuscitation measures after asphyxia, clinical death, long comatose state and so on. The consequences of severe hypoxia, in addition to prolonged coma in the acute period, include several clinical options, including dementia with (or without) extrapyramidal syndromes, cerebellar ataxia, myoclonic syndromes, Korsakoff's amnestic syndrome. Separately considered delayed postanoxic encephalopathy with a bad outcome.

Sometimes there are patients with hypoxic encephalopathy who have persistent residual effects consist in predominant hypokinesia of bulbar functions (hypokinetic dysarthria and dysphagia) against the background of minimally expressed or completely regressing general hypokinesia and hypomimia (this variant of pseudobulbar disorders is called “extrapyramidal pseudobulbar syndrome” or “pseudopseudobulbar syndrome”). These patients do not have any abnormalities in the limbs and trunk, but are disabled due to the above-mentioned manifestations of a peculiar pseudobulbar syndrome.

Other causes of pseudobulbar syndrome

Sometimes pseudobulbar syndrome manifests itself as component more extensive neurological syndromes. For example, pseudobulbar syndrome in the picture of central pontine myelinolysis ( malignant neoplasm, liver failure, sepsis, alcoholism, chronic renal failure, lymphoma, cachexia, severe dehydration and electrolyte disturbances, hemorrhagic pancreatitis, pellagra) and the overlapping “locked-in man” syndrome (occlusion of the basilar artery, traumatic brain injury, viral encephalitis, post-vaccination encephalitis, tumor, hemorrhage, central pontine myelinolysis).

Central pontine myelinolysis is a rare and potentially fatal syndrome that manifests itself with the rapid development of tetraplegia (due to medical illness or Wernicke encephalopathy), and pseudobulbar palsy due to demyelination central departments bridge, which is visible on MRI and in turn can lead to “locked-in” syndrome. "Locked-in man" syndrome ("isolation" syndrome, de-efferentation syndrome) is a condition in which selective supranuclear motor de-efferentation leads to paralysis of all four limbs and caudal parts of the cranial innervation without impairment of consciousness. The syndrome is manifested by tetraplegia, mutism (aphonia and anarthria of pseudobulbar origin) and the inability to swallow while conscious; in this case, the possibility of communication is limited only by vertical movements of the eyes and eyelids. CT or MRI reveals destruction of the medioventral part of the pons.