Krylov Petrikov bulbar pseudobulbar syndrome differences. Pseudobulbar syndrome. Causes. Symptoms Symptoms and course

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 of peripheral paralysis are revealed (atrophy of the muscles of the tongue, a 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, and gag reflexes are reduced or absent, and paresis of the orbicularis oris muscle is often noted.

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 cranial nerves 9, 10, 12 are bilaterally interrupted, with a clinical picture of central paresis or paralysis of the muscles innervated by these cranial nerves.

The following diseases are most often accompanied by pseudobulbar palsy: 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 conducting 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 of damage to the frontal lobe of the brain .

Frontal lobe syndrome is the general name for 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 the frontal lobe syndrome are influenced by the law on the functional asymmetry of the cerebral hemispheres; the 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 (in left-handed people - vice versa), the right hemisphere is responsible for non-verbal, gnostic-practical functions (in left-handed people - vice versa).

Posterior frontal lobe syndrome. 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);

Anterior (pole) syndrome. 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 lesion spreads posteriorly, Foster-Kennedy syndrome (primary atrophy of the optic disc, on the side of the lesion, as a result of pressure on the optic nerve) and the presence of congestive optic disc may appear. 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 the proximity of the pathological process to the base of the skull and to the orbit.

Precentral region syndrome. Occurs when the precentral gyrus is damaged (Brodmann's 4th and partially 6th area), which is the motor area of ​​the cerebral cortex. 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 a monoplegic type of paralysis or paresis, a combination of monoparesis of an arm or leg with central paresis of muscles innervated by the facial and hypoglossal nerves - a 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.

Pseudobulbar palsy occurs in vascular diseases of the brain with bilateral supranuclear damage to the motor conductors, i.e. in the presence of multifocal lesions localized in both hemispheres of the brain. Small softenings and cysts are often found. With pseudobulbar palsy, there is a violation of the motor functions of the limbs, tongue, larynx, mastication, pharyngeal and facial as a result of loss of central supranuclear innervation (corticonuclear and corticospinal conductors).

The symptoms of pseudobulbar palsy are varied.

1. Usually there are disorders - impaired articulation (dysarthria, anarthria), phonation (nasal tone of speech, which can be slurred, silent and quiet), sometimes impaired coordination (chanted speech).

2. Swallowing disorders - dysphagia, manifested in choking when particles enter the respiratory tract, leakage of liquid into the nasopharyngeal space, drooling as a result of insufficient swallowing of saliva.

3. Chewing disorder, causing retention in the mouth due to pareticity of the chewing teeth and tongue. Disorder of the function of facial muscles (mask-like appearance due to weakness of the facial muscles); symptoms of oral automatism:

a) proboscis reflex (protrusion of the lips with a “proboscis” when they are percussed);

b) lip reflex (protrusion of the lips forward when tapping on the upper one and bringing the lips closer together when irritating them with strokes);

c) sucking reflex (sucking movements when touching the lips);

d) Astvatsaturov’s nasolabial reflex (proboscis-like protrusion of the lips when tapping on the root of the nose);

e) ankylosing spondylitis (chin contraction when the chin is tapped);

f) palmar-chin reflex Marinesko-Radovici (contraction of the chin upon stroke stimulation of the palm);

g) buccal-labial reflex (raising the mouth or baring the mouth when the cheek is irritated by strokes).

4. Friendly movements on - moving the chin to the side is friendly with turning the eyes, baring the teeth on the side to which the eyeballs are voluntarily retracted; involuntary opening of the mouth when abducted upward; friendly extension of the head when opening, abduction of the protruding tongue to the side is friendly to the rotation of the eyes; friendly turn of the head towards the abduction of the eyeballs.

5. Increased masseter reflex.

6. Changes in gait - gait with small steps, insufficient balancing or lack of friendly balancing of the arms when walking (acheirokinesis), stooping and stiffness.

7. The presence of pyramidal-extrapyramidal tetraparesis (sometimes asymmetrical), more pronounced on one side with increased tone, increased tendon and periosteal reflexes, decreased or absent abdominal reflexes and the presence of pathological reflexes (Babinsky, Rossolimo symptoms, etc.).

8. Sometimes the presence of constant or paroxysmal hyperkinesis in the presence of tetraparesis.

9. Involuntary appearance of emotional-facial discharges, i.e. forced crying, laughter, as a result of disinhibition of thalamostriatal-brain-stem automatisms during a bilateral process in the brain. Violent laughter (also laughter) manifests itself in fits and starts.

Sometimes the patient suddenly begins to cry for no apparent reason, but it occurs when trying to start a conversation or during speech, during various emotional experiences. It often occurs in conjunction with various motor manifestations: when actively opening the eyeballs, when moving the eyeballs to the side, when closing the eyes. Hyperkinetic discharges are observed, occurring paroxysmally during emotional discharges during violent crying. Involuntary movements manifest themselves in different ways: in some cases they consist of intermittent waving of the hand, in others - the raised hand jerkily approaches the head. In rare cases, a hyperkinetic discharge consists of a cycle of movements: for example, extending the arm, swinging the hand, then rhythmically patting the chest, and finally rotating the torso to the side.

Based on his own material (over 100 cases of pseudobulbar palsy, varied in clinical picture, localization of vascular foci of the etiology of the vascular process), N. K. Bogolepov developed symptoms and described new symptoms of pseudobulbar palsy.

Pseudobulbar palsy occurs after repeated strokes. In cases, the first stroke passes unnoticed, leaving no trace, and after a second stroke, bilateral motor disorders develop: on the side opposite to the lesion, phenomena of central paralysis occur, on the side of the same name as the lesion, plastic hypertension and hyperkinesis appear in the hand; At the same time, disturbances in speech, phonation, facial expressions and sometimes swallowing develop.

Clinical and anatomical analysis of such cases reveals the presence of foci in both hemispheres of the brain: an old focus of softening, remaining after the first stroke, manifested by no symptoms until the second stroke, and a fresh focus of softening, which caused the development of not only motor disorders in the limbs opposite to the lesion, which contributed to the appearance of extrapyramidal symptoms on the side of the same name. Apparently, the compensation of motor functions that was present after the first stroke is disrupted with a second stroke, and a picture of pseudobulbar palsy appears.

Anatomical control of cases of pseudobulbar palsy reveals multiple small foci of softening; sometimes large white softening, - red softening combined with small foci; in cases of large softening, it is combined with a cyst after softening in the other hemisphere of the brain. The etiological factor of vascular disease of the brain is arteriosclerosis, less often syphilitic endarteritis. There are cases where pseudobulbar palsy develops as a result of repeated embolisms.

M.I. Astvatsaturov points out that pseudobulbar palsy may be based on small cavities in the area of ​​the subcortical nodes and the internal bursa. Symptomatology in such cases may be due to damage not only to the corticobulbar conductors and the striatum. Between the striatal (akinetic) and corticobulbar (paralytic) varieties of pseudobulbar paralysis, according to M.I. Astvatsaturov, there is a difference in that in the first case there is a lack of motor initiative in the corresponding muscles without the phenomena of real paresis or paralysis, the automatic ease of performing swallowing is lost and phonation movements. In the corticobulbar form of pseudobulbar palsy, on the contrary, there is central paralysis caused by damage to the corticospinal tracts, and elementary motor functions are lost. L. M. Shenderovich, in a work devoted to pseudobulbar palsy, identified four forms:

1. paralysis, depending on bilateral damage to the pathways from the nuclei of the pons and medulla oblongata (cortical origin);
2. paralysis caused by symmetrical damage to the striatal bodies (striatal origin);
3. paralysis that occurs when a combination of cortical lesions (including the corticobulbar tract) of one hemisphere and the striatal system of the other hemisphere;
4. special children's uniform.

The first group of pseudobulbar palsies can include cases when multiple foci of softening are localized in both hemispheres of the brain - the cortical form of pseudobulbar palsy. As one example of the form of pseudobulbar palsy, we can point to the case described by V. M. Bekhterev in the city. At the autopsy, atrophy of the brain convolutions was found in the right hemisphere in the region of the middle and upper part of the frontal and upper part of the central gyri, mainly in the upper part of the sulci praecentralis (the first and third frontal gyri, respectively) and in the left hemisphere of the brain - in the upper part of the first frontal gyrus, respectively, the upper part of the sulcus Rolandi and in the posterior segment of the third frontal gyrus. Along with brain atrophy, there was an accumulation of serous fluid in the subarachnoid space. Along with the anomaly of the cerebral vessels was discovered: the left posterior communicating artery was absent, the left posterior cerebral artery departed from the main artery, and the right one from the communicating artery, the left anterior cerebral artery was much thinner than the right one.

This bilateral brain damage caused bilateral motor disorders, speech disorder, convulsive seizures with head abduction and in the direction opposite to the lesion.

In the cortical form of pseudobulbar palsy, the psyche is most clearly disturbed; speech disorder, epileptic seizures, violent crying, and dysfunction of the pelvic organs are pronounced.

The second group of pseudobulbar palsies is the extrapyramidal form of pseudobulbar palsy. The symptoms of pseudobulbar disorders vary depending on whether pallidal, striatal or thalamic formations are affected in bilateral localization of lesions. Motor disturbances are represented by paresis, which is sometimes deep and more pronounced in the lower extremities. Motor disturbances are of an extrapyramidal nature: the torso and head are bent, half-bent, amicable; there is inactivity, stiffness, akinesis, freezing of the limbs in their assigned position, plastic hypertension, increased postural reflexes, slow gait with small steps. Speech, phonation, swallowing and chewing are impaired primarily due to the inability of the boulevard muscles to perform movements quickly and clearly, and therefore dysarthria, aphonia, and dysphagia develop. Damage to the striatum affects the functions of speech, swallowing and chewing, since in the subcortical nodes and in the thalamus opticus there is a somatotopic distribution according to a functional characteristic (the anterior part of the striatal system is related to the functions of swallowing).

Among pseudobulbar palsies caused by focal lesions in the subcortical nodes, several options can be distinguished: a) Pseudobulbar parkinsonism - a syndrome of pseudobulbar palsy with a predominance of akinetic-rigid disorders, expressed in four limbs, caused by small foci (lacunae or small cysts) localized in pallidal system. The course of pseudobulbar parkinsonism is progressive: akinesis and rigidity gradually lead to the forced position of the patient in bed, to the development of flexion contracture of both. Along with extrapyramidal disorders, pseudobulbar reflexes are expressed, possibly depending on the presence of other small focal lesions in the brain, causing disinhibition of oral automatisms, b) Pseudobulbar striatal syndrome - a syndrome of pseudobulbar palsy with motor extrapyramidal-pyramidal paresis of four limbs (unevenly expressed on both sides), with impaired articulation, phonation and swallowing and with the presence of various hyperkinesis. c) Pseudobulbar thalamo-striatal syndrome - pseudobulbar paralysis as a result of multiple foci involving the area of ​​the thalamus and striatum, accompanied by paroxysmal seizures and hyperkinetic discharges associated with emotional arousals. The importance of the visual thalamus in pseudobulbar palsies was pointed out by V. M. Bekhterev. The occurrence of crying and laughter, which are an expression of emotional experience, must be associated with the function of the visual thalamus, which plays in the implementation of emotional arousals. The appearance of violent crying or laughter in pseudobulbar palsy indicates disinhibition of thalamo-striatal automatisms and occurs with bilateral brain damage. Damage to the thalamus opticum in pseudobulbar palsy can sometimes be indirect (for example, disinhibition of the thalamus opticum due to damage to the frontothalamic connections); in other cases, direct damage to the thalamus occurs by one of the many foci that causes the development of pseudobulbar palsy.

The third group of pseudobulbar palsies consists of the most common cases when there is a combined lesion of one hemisphere and the subcortical nodes of the other hemisphere. Symptoms vary significantly depending on the size and location of the lesion in the brain, the extent of the lesion in the subcortical white matter and the region of the subcortical nodes. What matters is the nature of the vascular process: with the syphilitic process, phenomena of brain irritation often occur along with symptoms of prolapse, and in such cases, paralysis of the limbs is combined with epileptic seizures. A peculiar variant of pseudobulbar paralysis of cortical-subcortical localization is represented by cases when not epileptic seizures are observed, as indicated above, but subcortical seizures that occur during emotional discharges.

The fourth group consists of cases of pseudobulbar palsy that occur when vascular lesions are localized in the pons. This form of pseudobulbar palsy was first described by I. N. Filimonov in the city. Based on a clinical and anatomical study, I. N. Filimonov concluded that with bilateral localization of the lesion at the base of the middle third of the pons, paralysis of four limbs and the trunk occurs (with preservation of tendon reflexes and the appearance of pathological reflexes) and paralysis of the trigeminal, facial, vagus and hypoglossal nerves characteristic of supranuclear lesions develops (with preservation of automatic and reflex functions), pronounced bulbar reflexes and violent crying appear. In the case of S. N. Davidenkov, pseudobulbar palsy developed in connection with syphilitic endarteritis of the paramedian arteries emerging from the trunk of the basilar artery and supplying the ventromedial section of the pons. S. N. Davidenkov established a number of patterns characteristic of the pontine form of pseudobulbar palsy, and emphasized the signs that make it possible to distinguish pseudobulbar palsy when the process is localized in the pons from pseudobulbar palsy of the cortical-subcortical

of different origin. He proposed to call the described pseudobulbar palsy of pontine localization Filimonov's syndrome.

Pseudobulbar palsy of pontine localization, described by I. N. Filimonov N. Davidenkov, is characterized by the following signs: 1. With the development of pseudobulbar palsy of pontine localization, absolute immobility of the patient occurs, caused by deep paralysis of the limbs; consciousness remains intact. The picture of pseudobulbar paralysis reveals (in the case of I.N. Filimonov) a peculiar dissociation of motor disorders. Paralysis of four limbs with anarthria, dysphagia, paralysis of the tongue, lips and lower jaw is combined with the preservation of the oculomotor system and partial preservation of the function of the muscles that rotate the head and the muscles innervated by the superior branch of the facial nerve; severe impairment of the motor functions of the lips and tongue). 3. Cervical tonic reflexes (in the case of S.N. Davidenkov) can be expressed in the first days of the development of pseudobulbar palsy and, with passive rotation of the head, manifest themselves in automatic extension and after a few seconds in the protective flexion reflex of the same name (without the participation of the opposite limbs). 4. Pseudobulbar palsy in the case of I. N. Filimonov was flaccid; in the case of S.N. Davidenkov, the phenomena of early contracture with tonic tensions were noted, leading to tonic changes in the position of the limbs in spontaneous movements with protective reflexes in both arms and legs (clearly expressed in the first time of development of pseudobulbar paralysis). the period of recovery of motor functions in pseudobulbar palsy of pontine localization revealed a significant similarity in the form of active movements with involuntary reflex movements, the absence of friendly global movements characteristic of capsular hemiplegia and the appearance of imitative kinesia, i.e. symmetrical flexion or extension synergies of the forearm with active movements of the opposite ( active movements of the lower extremities were not accompanied by friendly movements).

Cerebellar abnormalities were noted in cases of pseudobulb palsy of pontine origin. With pronounced pseudobulbar palsy, a combination of various pseudobulbar symptoms is observed.

Based on a clinical and anatomical study of a case of pseudobulbar palsy, I. N. Filimonov proved the separate course of the conduction pathways for the extremities (at the base of the pons) and for the cervical and ocular (in the tegmentum of the pons), causing the dissociation of paralysis during obliteration of the paramedian arteries.

Pseudobulbar pontine syndrome should always be differentiated from apoplectic bulbar palsy, when there is paralysis of the limbs with partial damage to the cranial nerves.

The presence of amyotrophies in pseudobulbar palsies is not a reason to single out a special group. We have repeatedly observed trophic disorders in pseudobulbar paralysis, which in some cases manifested themselves in excessively pronounced progressive general emaciation (lack of subcutaneous fat layer, diffuse muscle atrophy, thinning and atrophy of the skin) or partial atrophy developing in the paralyzed limbs in the proximal part. In the origin of general exhaustion, damage to the subcortical formations (especially the putamen) and the hypothalamic region undoubtedly plays a role; development

partial atrophy of paralyzed limbs in pseudobulbar palsies may be associated with cortical damage.

Sometimes pseudobulbar syndrome due to arteriosclerosis manifests itself as short-term crises and micro-strokes. Patients experience memory loss, choking on food, difficulty writing, speaking, insomnia, decreased intelligence, mental disorders and mild pseudobulbar symptoms.

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 a 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, suppression of reflexes and changes in the 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 the nerve fibers of the trigeminal, glossopharyngeal, and 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 of 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. Characteristic signs include symptoms that reveal tonic tension of 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, standing up symptom, bulbo-facial tonic Mondonesi symptom, “gunshot” syndrome trigger" (characteristic posture - the head is thrown back, the torso is in a hyperextension position, the lower limbs are 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. Additional examination reveals stagnant optic discs and characteristic changes on craniograms (“finger impressions,” thinning of the dorsum sella, suture dehiscence). Focal symptoms depend on the immediate location 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 the most informative diagnostic method currently is 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 route - the occurrence of meningitis occurs in the conditions of an already existing purulent infection. The development of sinusogenic meningitis is promoted by purulent infection of the 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 the entrance gates (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 (tachycardia at the beginning of the disease, bradycardia as the disease progresses). Meningeal syndrome includes general cerebral symptoms, manifested by tonic tension of 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 impaired control of the pelvic organs (in the case of the 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). With serous meningitis, the cerebrospinal fluid is clear; with purulent meningitis, it is cloudy and yellow-green in color. Laboratory tests of cerebrospinal fluid determine pleocytosis, changes in the cell number ratio, and increased protein content. 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. In case of 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 administration of sulfonamides (etazol, norsulfazole) in an average daily dose of 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, and less commonly, a repeat spinal puncture. In case of 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 the formation of the chronic phase, a major role is played by 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 develops focal symptoms characteristic of epidemic encephalitis. Diagnostics It is important to correctly assess the state of consciousness, promptly identify the first symptoms of focal brain damage, in particular sleep disorders, oculomotor, vestibular, autonomic-endocrine disorders; it is necessary to collect accurate anamnestic data on previously suffered acute infectious diseases with general cerebral symptoms, disturbances of consciousness, sleep, and diplopia. Treatment. There are currently no specific treatment methods for epidemic encephalitis. It is advisable to carry out vitamin therapy recommended for viral infections (ascorbic acid, B vitamins), prescribing 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 dehydration therapy is indicated: diuretics, hypertonic solutions of fructose, sodium chloride, calcium chloride. For convulsions, enemas are prescribed.

Pseudobulbar syndrome or pseudobulbar palsy is a pathological condition in which damage to the cranial nerves develops, leading 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) due to vascular disorders or as a result of injury, inflammatory or degenerative processes. 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 nervous tissue. Effectively use folk nootropic remedies based on medicinal plants.

How does pseudobulbar syndrome 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 of motor neurons of the 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 it 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:

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 that can help identify pseudobulbar syndrome

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, muscle atrophy does not occur.

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.

How to treat pseudobulbar syndrome?

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 engage in physical therapy and 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 eliminate the symptom of 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 herbal components. Traditional 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 medications so that addiction does not occur and the healing effect is not lost.

Traditional recipes:

1. 1. Medicinal collection No. 1. Mix thyme, mint, motherwort and borage herb in equal proportions. 3 tbsp. l. This collection needs to be poured with half a liter of boiling water, left to infuse for several hours and filtered. Standard dosage: ½ glass 2 times a day after meals.
   2. Medicinal collection No. 2. Mix equal amounts of celandine grass and birch leaves or buds. Prepare an infusion of these herbs: take 2 tbsp per 2 ml. l. mixture, leave for 3 hours, then filter. You need to take 50 ml of infusion after each meal.
   3. Medicinal collection No. 3. The collection consists of lemon balm, lily of the valley, oregano, wild carrot seeds and hawthorn flowers. Plants need to be taken in equal quantities, chopped and mixed. To prepare the infusion, pour 2 tablespoons of the mixture with a glass of boiling water, leave to infuse for 3 hours, then strain. The entire infusion is drunk in one day in small portions.
   4. Sweet clover officinalis. You need to prepare an infusion of crushed dried plant in a standard dosage (1 tbsp per 200 ml of boiling water). You need to take 0.5 cups 2 times a day after meals.

1. Celandine. The dried ground part of celandine is used in therapy. An infusion is prepared from plant materials: for 200 ml of boiling water you need to take 1 tbsp. l. medicine, leave for 15 minutes and strain. Celandine is taken 3-4 times a day, 2 tbsp. l. The full course of treatment should last three weeks, after which a break must be taken.
2. Periwinkle and hawthorn. For treatment, a healing potion is prepared. First, boil the periwinkle leaves over low heat for 5 minutes (1 tsp per 500 ml of boiling water), then remove from the heat and add a mixture of hawthorn leaves and flowers (1 tbsp). This decoction must be left to steep for several hours and then filtered. Standard dosage: 0.5 cups before meals.
3. Cranberry. Cranberries are very useful for improving cerebral circulation. 0.5 kg of berries are ground with 350 g of honey, 150 g of grated horseradish are added and mixed thoroughly. This medicine is stored in a glass container in the refrigerator. The patient is given 1 tbsp. l. drugs 3 times a day after meals.
4. Alfalfa. Alfalfa seeds are poured with warm boiled water (3 tsp per 300 ml of water), left overnight and drunk the next day in three doses 30 minutes before meals, and the seeds are eaten. Therapy lasts at least 9 months.

Such a problem as the development of pseudobulbar syndrome in a child is a real test for parents. The fact is that the symptoms of this disease manifest themselves quite clearly and, 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. We are talking 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. The vascular form of syphilis of the brain, as well as neuroinfections, degenerative processes, infections and tumors affecting both hemispheres, can also have a negative impact.

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

Pathogenesis

The development of such a syndrome 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 are first recorded. 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, unlike the bulbar form, this syndrome excludes the occurrence of disorders of the cardiovascular 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 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 of the neurological status and positive changes in the deviations recorded earlier. Also, with successful treatment, there should be an increase in motor activity against the background of physical inactivity or an increase in muscle tone in the 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. Moreover, this method of 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 the mobility of the muscles of the 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 a fairly serious threat to the child’s health, so the disease requires parents to quickly respond to symptoms and be patient during the treatment process.