Cerebral palsy, spastic tetraplegia, severe course, rehabilitation stage - case history. Cerebral palsy - case history with an open ending

Disease history

The term cerebral palsy has been around for over a century, and the disease itself has probably existed without a name throughout human history. However, despite its long history, there is still no unity of views on this problem.

Along with the generalized term cerebral palsy, the term "Little's disease" is sometimes used in clinical practice. This name was proposed in honor of the British orthopedic surgeon William John Little (William John Little), who in the middle of the 19th century was the first to establish a causal relationship between complications during childbirth and impaired mental and physical development of children after birth.

His views were summarized in the article "On the influence of pathological and difficult childbirth, prematurity and asphyxia of newborns on the mental and physical condition of children, especially with regard to deformities" . This article, addressed to the Obstetrics Society of Great Britain, is most often cited in publications and articles on cerebral palsy.

spastic form

For the implementation of movements, it is necessary that the impulse from the motor area of ​​the cerebral cortex be freely conducted to the muscle. In this form, damage to the motor zone of the cerebral cortex or the main motor (pyramidal) pathway disrupts the conduction of the impulse mainly to the lower limbs, which are paralyzed.

Thus, paralysis, or plegia, is the absence of movement in a muscle or group of muscles as a result of a "breakage" in the motor reflex pathway. Partial loss of motor functions (limitation of strength, volume, range of motion) is called paresis. In the spastic form, the central motor neuron is damaged and central paralysis or paresis develops.

The spastic form is characterized by motor disturbances in the upper and lower extremities, with the legs more affected than the arms. The degree of damage to the hands can be different - from pronounced restrictions in the volume and strength of movements to mild motor awkwardness, which manifests itself only when performing fine differentiated movements (writing, making a mosaic, labor operations, etc.).

There are mild, moderate and severe forms of spastic paralysis.

With a mild degree of spastic paralysis, the intellect of patients is not impaired or impaired, but slightly, patients move independently and serve themselves.

At an average degree, a violation of intelligence, hearing, and vision is often determined, but some of these patients can be adapted to work.

With pronounced forms of the disease, the psyche is often significantly disturbed, there is strobism, salivation, and other symptoms. In severe cases, there is dementia, hyperkinesis, athetosis.

With good and consistent treatment in patients with spastic paralysis, especially mild to moderate, a significant improvement can be achieved. Some of these patients graduate from secondary and even higher educational institutions and work successfully. However, in severe forms, the prognosis may be unfavorable, which is especially true for patients with severe intellectual impairment.

Often hand motility disorders are so insignificant that the spastic form is defined as "spastic paralysis of the limbs, more often lower, less often upper and lower", i.e. with mild dysfunction of the hands, diplegia of the lower extremities comes first.

The defeat of two paired limbs, either upper or lower, is called "diplegia" (or paraplegia). However, in some literary sources, spastic diplegia is characterized as tetraplegia (or tetraparesis), i.e. as a general lesion of four limbs. Indeed, with spastic diplegia, there is a violation of the motor functions of all limbs: the legs are mainly affected, and the upper limbs are affected to a lesser extent. However, the unequal severity of motor disorders in the arms and legs indicates damage to the limbs according to the principle of diplegia. In this regard, both terms complement each other.

With spastic diplegia, the main symptom is an increase in muscle tone (spasticity) in the lower extremities with a limitation in the volume and strength of movements.

Official data

Last name, first name: ...

Age: 5 years old.

Home address:

Date of admission to the clinic:

Curation start date: 05/29/2008.

Complaints

The inability to stand, move independently, limited movements in both legs and arms. On mental retardation: he does not speak well.

Disease history.

According to her grandmother, the girl has been ill since she was 6 months old, when in 2003 her parents noticed a delay in physical development: the child did not sit up on his own, he did not hold his head well. From the age of 7 months, there were signs of movement restriction in the arms first, then in the legs. Have addressed to the doctor. At the age of 9 months, an examination was carried out and a diagnosis was made: cerebral palsy, spastic tetraplegia. From the age of 1, every 6 months, the girl undergoes a course of planned treatment.

She is currently undergoing treatment in the inpatient department of the Children's City Hospital No. 5, the neuropsychiatric department.

Anamnesis of life.

Child from first pregnancy. The pregnancy proceeded normally. The mother did not tolerate infectious diseases during pregnancy. Nutrition is satisfactory, vitamin D2 received in the required quantities.

Childbirth I, at term (40 weeks), independent, rapid, without anesthesia. Child at birth m = 3100 g, l = 51 cm, head circumference = 34 cm, chest circumference = 34 cm; she screamed immediately, she was attached to her chest in the delivery room. Apgar score 7 points. The umbilical cord was removed on the 3rd day. She was discharged home on the 5th day. Weight at discharge 3000 g. Artificial feeding.

Development of motor skills: the girl began to hold her head from 5 months. From 6 months he rolls over on his stomach, from 8 months he sits.

Mental development: smiles from 3 months old, started to walk from 5 months old, pronounce separate syllables from 10 months old, utters the first words from 1.5 years old.

The teeth erupted at 6 months, by the year the child has 8 teeth.

Didn't attend kindergarten.

Family history: tuberculosis, alcoholism, sexually transmitted diseases, relatives denies.

Past illnesses.

Chicken pox - 3 years;

SARS - from 3 years old 1-2 times a year in the autumn-winter period;

There were no operations or blood transfusions.

Vaccinations according to an individual schedule.

Allergological anamnesis is not burdened.

Genealogical tree

Conclusion: heredity is not burdened.

The present state of the patient

General inspection.

The general condition of mild severity, the position of the body is natural. Consciousness is clear. The behavior is active. The constitutional type is asthenic.

The physical development of the child is below average, proportional, harmonious.

Skin and PZhK.

The skin is pink. Severe cyanosis and areas of pathological pigmentation are not observed. Moisture and elasticity of the skin are normal. There are no rashes, scratches, scars, visible tumors. Visible mucous membranes are pink, clean, there is no icteric staining of the frenulum of the tongue and sclera. The conjunctiva of the eyes is pink. Correctly shaped fingers. Fungal infection, increased fragility of the nail plates were not noted.

The layer of subcutaneous fat is moderately developed, evenly distributed. The thickness of the skin fold in the umbilical region was 1 cm. No edema was detected. No crepitus was found.

During external examination, the lymph nodes are not visualized. Occipital, parotid, chin, submandibular, cervical, supraclavicular, subclavian, axillary, ulnar, inguinal, popliteal lymph nodes are not palpable.

Bone-articular system.

The joints are not deformed, painless on palpation, seals are not revealed. Mobility restrictions are not observed. There is no crunch or pain when moving.

The physique is correct, there are no deformations and deformities of the trunk, limbs and skull. The shape of the head is oval. Posture is correct. Body halves are symmetrical. There are no chest deformities. The angles of the shoulder blades are directed downward.

The physiological curves of the spine are sufficiently pronounced, there are no pathological curves.

The bones are not deformed, painless on palpation. The terminal phalanges of the fingers are not thickened. "Bracelets", "strings of pearls" - not defined.

Teething is timely, the condition of the teeth is normal.

Respiratory system.

The skin is pale pink, Frank's symptom is negative. The mucosa of the oropharynx is bright pink, without plaque, the tonsils are not enlarged. Nasal breathing is not disturbed, there is no discharge from the nose. The respiratory rate is 20 times per minute. The chest is not deformed, symmetrical, participates in the act of breathing. The type of breathing is mixed.

Palpation of the chest is painless. The chest is moderately rigid. Voice trembling is carried out in the same way in symmetrical areas. Excursion of the chest - 6 cm. The skin folds on the chest are symmetrical.

Percussion.

Percussion sound clear pulmonary over all symmetrical points.

Topographic percussion without features.

The cardiovascular system.

The skin is flesh-colored, no deformation in the chest area is detected. The apex beat is determined in the 5th intercostal space, 1 cm outward from the midclavicular line. Heart hump, cardiac impulse are not defined. Visible pulsation in the area of ​​large vessels is not determined.

Palpation. The apex beat is palpated in the 5th intercostal space 1 cm outward from the midclavicular line; prevalence 1x1 cm; apical impulse of moderate height, moderate strength.

Pulse - correct, firm, full, rhythmic. Heart rate = 90 beats / sec.

Edema is not defined.

Percussion, without features.

Auscultation. Heart tones are crisp, clear, the timbre is soft, normocardia, the rhythm of the tones is correct. The ratio of tones is preserved, no additional tones are heard. Noises are not heard.

Arterial pressure:

Right hand - 110/70 mm Hg. Art.

Digestive organs.

Inspection. Lips pale pink, moist. Cracks, ulcerations, rashes are absent. The tongue is pink, of normal shape and size, the back of the tongue is not lined, the papillae are well defined. The mucous membrane of the tongue is moist, without visible defects. The gums are pink, there is no bleeding or defects. The back wall of the pharynx is not hyperemic, the tonsils are not enlarged. There is no smell from the mouth.

The abdomen is normal, symmetrical. Bloating is not observed. Peristaltic movements are not visible. The umbilicus is retracted. Collaterals on the anterior surface of the abdomen and its lateral surfaces are not expressed. Scars and other changes in the skin are not observed. Hernias are not revealed. The abdominal muscles are involved in breathing.

Palpation.

On superficial palpation: the abdomen is not tense, painless. Hernial ring is not defined. Shchetkin-Blumberg's symptom is negative, Voskresensky's symptom is negative, Dumbadze's symptom is negative. Mendel's sign is negative. The divergence of the abdominal muscles, hernias of the white line was not revealed.

Deep methodical sliding palpation according to Obraztsov-Strazhesko. With deep palpation, pain is noted in the epigastric region and in the navel. A large curvature of the stomach is palpated on both sides of the midline of the body 3 cm above the navel in the form of a roller. The gatekeeper is not determined by palpation. The sigmoid colon is palpable in the left iliac region in the form of a smooth dense cylinder 1.5 cm thick. The caecum is palpated in the form of a moderately tense cylinder 1.5 cm in diameter, painless. The ascending colon and the descending colon are not thickened, 1.5 cm in diameter. The transverse part of the colon is palpated as a cylinder of moderate density 1.5 cm thick one centimeter above the navel, mobile, painless.

On palpation, the liver is soft, smooth, painless, the edge is sharp, located 1 cm below the edge of the costal arch. The spleen is not palpable.

Urinary system.

The skin in the lumbar region is flesh-colored, swelling is not determined. There are no edema.

The kidneys are not palpable.

The bottom of the bladder percussion is not determined. The reduced symptom of Pasternatsky is negative.

Neurological status

The state of the psyche.

Contact with the girl is established with difficulty. Mental development below age. Intelligence is reduced. Speech is difficult, monosyllabic. Vocabulary is poor. Reading, writing, gnosis and praxis cannot be assessed.

Functions of the cranial nerves.

1st pair - olfactory nerves, 2nd pair - optic nerve: the functions could not be investigated.

3rd, 4th, 6th pairs - oculomotor, trochlear, abducens nerves: the width of the palpebral fissures is normal. The size of the pupil is about 4 mm, correct, round; preserved direct reaction to light, friendly reaction from the other eye. The reaction to convergence and accommodation is preserved.

5th pair - trigeminal nerve: paresthesia and pain in the area of ​​innervation of the trigeminal nerve were not detected. The sensitivity of the skin of the face is not changed. Pressure sensitivity of nerve exit points (Valle's points) is normal. The condition of the chewing muscles (movement of the lower jaw, tone, trophism and strength of the chewing muscles) is satisfactory.

7th pair - facial nerve: the symmetry of the face at rest and during movement is preserved. Lagophthalmos, hyperacusis are absent. Lacrimal function is not broken.

8th pair - vestibulocochlear nerve: no tinnitus. Auditory hallucinations were not identified.

9-10th pair - glossopharyngeal and vagus nerves: no pain in the throat, tonsils, ear. Phonation, swallowing, salivary function, pharyngeal and palatine reflexes were within normal limits.

11th pair - accessory nerve: raising the shoulder girdle, turning the head, approaching the shoulder blades, raising the arm above the horizontal are impaired due to the presence of spastic paralysis of the arms.

12th pair - hypoglossal nerve: the tongue is clean, moist, mobile; the mucous membrane is not thinned, normal folding; fibrillar twitchings are absent.

motor functions.

Active and passive movements are limited. Identified hypertonicity in all limbs. Tendon reflexes from the biceps, triceps muscles, carporadial reflexes from both hands are enhanced. Patellar, Achilles, plantar reflexes from both legs are enhanced.

Skin reflexes: abdominal upper, middle, lower - positive.

Pathological reflexes: Babinsky, Oppenheim, Gordon, Schaeffer, Rossolimo, Bekhterev, Zhukovsky are positive on all limbs.

Symptoms of oral automatism: labial, nasolabial, palmar-oral, negative.

Coordination of movements is difficult to assess due to the condition of the child.

Sensitivity.

Pain, tactile sensitivity is approximately not violated. Anesthesia, hypoesthesia are absent. Segmental and conductive type of sensory impairment were not identified.

meningeal symptoms.

Rigidity of the muscles of the neck - muscle tone is not increased, Kernig's symptom, Brudzinsky's (upper, lower, middle) are absent.

Vegetative-trophic sphere: temperature is normal, sweating is intense on the palms and feet. The subcutaneous fat layer is moderately developed.

Preliminary diagnosis and its justification

Based on complaints about the inability to stand and move independently, limited movements in both legs and arms, mental retardation and neurological examination data, it can be assumed that the nervous system is involved in the pathological process.

Syndromes identified:

Syndrome of spastic tetraplegia: based on complaints of the inability to stand independently, move around, limited movements in both legs and arms and on the basis of objective data (active and passive movements are limited. Hypertonicity was detected in all limbs. Tendon reflexes from the biceps, triceps muscles, carporadial from both Strengthened knee, Achilles, plantar reflexes from both legs are strengthened Pathological reflexes: Babinsky, Oppenheim, Gordon, Schaeffer, Rossolimo, Bekhterev, Zhukovsky are positive on all limbs).

Syndrome of mental retardation: based on anamnesis data (the girl began to hold her head from 5 months. From 6 months she rolls over on her stomach, from 8 months she sits, she smiles from 3 months, she began to walk from 5 months, to pronounce separate syllables from 10 months, from 1.5 years she pronounces the first words) and objective data (contact with the girl is difficult to establish, mental development is below age, intelligence is reduced, speech is difficult, monosyllabic, vocabulary is poor).

Based on the identified syndromes, a diagnosis can be assumed: infantile cerebral palsy, spastic tetraplegia, severe course, stage of rehabilitation.

Topical diagnosis and its rationale

Considering the data of neurological examination (hyperreflexia, hypertension, positive pathological reflexes on all limbs - spastic (central) tetraplegia), it can be assumed that the pathological focus is located at the level of the brain.

The presence of central paralysis, together with mental disorders (low mental development, reduced intelligence) suggests the presence of a pathological focus in the frontal lobe of the cerebral cortex, and on both sides, since the disorders were detected symmetrically on both sides.

Plan of additional research methods

Laboratory methods:

General blood analysis;

Blood chemistry;

General urine analysis;

Feces on eggs of worms;

Instrumental methods:

Results of additional research methods.

General blood analysis:

Leukocytes - 5.2 G/l

Segmented - 56%

Eosinophils - 2%

Lymphocytes - 38%

Monocytes - 4%

ESR - 4 mm/h

General urine analysis:

Specific gravity - 1023

Color straw yellow

The reaction is sour

Protein - negative

Sugar - negative

Leukocytes - 3-4 in the field of view

Conclusion: urine parameters without pathological abnormalities.

Feces on the eggs of worms - "negative".

Blood chemistry:

Total protein - 72.0

β-lipoproteins - 44 units

ALT - 16 Ukat/1

ASAT - 36 Ukat/1

Bilirubin - 11.4 µmol/l

Alkaline phosphatase - 532 U/l

GGTP - 28 U/l

Whey sugar - 4.4

Conclusion: the biochemical composition of the blood without pathological abnormalities.

Differential Diagnosis

Volumetric formation of the brain.

Common signs of the formation of the brain and cerebral palsy is the presence of focal neurological symptoms, mental disorders that are present in our case.

But brain tumors are characterized by shell symptoms: impaired consciousness, headaches; symptoms of increased intracranial pressure, which was not detected in our case. Also, the formations of the central nervous system are characterized by a progressive course of the disease, with a gradual increase in the clinic, the absence of signs of regression. In our case, the girl's condition is stable, without progression of neurological symptoms.

In addition, for the development of such a clinic (spastic tetraplegia), there must be a bilateral lesion of the cerebral cortex, which is extremely rare.

Treatment

Medical treatment of cerebral palsy

Medicines are used in the treatment of an acute period of brain damage in a newborn child, mainly in the first half of life.

In the formation of cerebral palsy, drug treatment is mainly prescribed for those patients in whom cerebral palsy is accompanied by convulsions, and is also sometimes used to reduce muscle spasticity and spontaneous movements.

To combat seizures, two groups of medicines are used:

Anticonvulsants, which quickly stop seizure activity and prevent its recurrence. There are a large number of drugs in this group, which differ in the mechanism of action and require long-term treatment.

Drugs of the benzodiazepine group are used in emergency cases to stop frequent convulsions or status epilepticus. They act on the chemical processes in the brain. The most common of these is diazepam.

In the treatment of cerebral palsy, medications are also sometimes used to reduce muscle spasticity, especially after orthopedic interventions.

For this purpose, the following medicines are most often used: diazepam, which acts as a general relaxant of the brain and body; baclofen (lioresal), which blocks signals (commands to contract) from the spinal cord to the muscles; and dantrolene, which affects the process of muscle contraction. When taken in pill form, these medications can reduce muscle tone for only a short period of time. Their benefits for a long-term decrease in muscle tone have not yet been proven by anyone. These drugs can cause significant side effects, such as drowsiness or allergic reactions, and their effect on children's nervous system is not yet fully understood.

The introduction of botulinum toxin A can also be attributed to drug treatment.

Physical rehabilitation.

One of the most important methods of treating cerebral palsy is physical rehabilitation, which begins in the first months of a child's life, immediately after the diagnosis is made. At the same time, sets of exercises are used aimed at two important goals - to prevent weakening and atrophy of muscles due to their insufficient use, and also to avoid the development of contractures, in which spastically tense muscles become inactive and fix the patient's limbs in a pathological position.

Surgery.

One of the additional methods of treatment of cerebral palsy are surgical operations. The most common of these are orthopedic interventions aimed at eliminating muscle shortening and bone deformities. The purpose of these operations in a child with the potential to walk is to improve his ability to move. For children who do not have the prospect of independent walking, the goal of surgery may be to improve the ability to sit, facilitate the performance of hygienic functions, and, in some cases, eliminate pain syndromes.

RCHD (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Archive - Clinical Protocols of the Ministry of Health of the Republic of Kazakhstan - 2010 (Order No. 239)

Other type of cerebral palsy (G80.8)

general information

Short description

Infantile cerebral palsy (CP)- a group of syndromes that are the result of brain damage that occurred in the perinatal period.

A characteristic feature of cerebral palsy is a variety of motor disorders that are manifested by paralysis, discoordination of movements, often combined with various disorders of speech, mentality, and sometimes epileptic seizures.

Cerebral palsy is a polyetiological disease of the brain that can occur during its intrauterine formation, during childbirth and the newborn, as well as in the postnatal period. Cerebral palsy is the most common cause of childhood disability (30-70%), among which diseases of the nervous system are in the first place. In most cases, the physical condition of patients improves, but activity restrictions remain: reduced mobility, speech disorders, and others.

According to the literature, the incidence of cerebral palsy in the population is 2 per 1000 newborns; according to L. O. Badalyan (1987) - from 3 to 6 cases per 1000 births. The main causes of cerebral palsy are associated with the development of pregnancy and childbirth (perinatal period): chronic diseases of the mother, infectious diseases, medication during pregnancy, premature birth, protracted labor, hemolytic disease of the newborn, entanglement of the umbilical cord and others.

Protocol"Cerebral palsy"

ICD-10 code:

G 80.0 Spastic cerebral palsy

Congenital spastic (cerebral)

G 80.1 Spasmodic diplegia

G 80.2 Childhood hemiplegia

Classification

Classification

G 80 Infantile cerebral palsy.

Includes: Little's disease

Excludes: hereditary spastic paraplegia

G 80.0 Spastic cerebral palsy.

Congenital spastic palsy (cerebral)

G 80.1 Spasmodic diplegia.

G 80.2 Children's hemiplegia.

G 80.3 Dyskinetic cerebral palsy.

G 80.8 Another type of cerebral palsy.

Mixed syndromes of cerebral palsy.

G 80.9 Cerebral palsy, unspecified.

Classification of cerebral palsy(K. A. Semenova et al. 1974)

1. Double spastic hemiplegia.

2. Spastic diplegia.

3. Hemiparesis.

4. Hyperkinetic form with subforms: double athetosis, athetous ballism, choreatetous form, choreic hyperkinesis.

5. Atonic-astatic form.

By the severity of the injury: mild, moderate, severe form.

Period:

Early recovery;

late recovery;

residual period.

Diagnostics

Diagnostic criteria

Complaints to a delay in psychoverbal and motor development, movement disorders, involuntary movements in the limbs, seizures.

History- perinatal pathology (prematurity, birth asphyxia, birth trauma, prolonged conjugative jaundice, intrauterine infections, etc.), previous neuroinfections, stroke, TBI in early childhood.

Physical examinations: movement disorders - paresis, paralysis, contractures and stiffness in the joints, hyperkinesis, delayed psycho-speech development, intellectual disability, epileptic seizures, pseudobulbar disorders (impaired swallowing, chewing), pathology of the organs of vision (strabismus, atrophy of the optic nerves, nystagmus ).

The spastic form of cerebral palsy is characterized by:

Increased muscle tone in the central type;

High tendon reflexes with extended reflexogenic zones, clonuses of the feet and patella;

Pathological reflexes: Babinsky, Rossolimo, Mendel-Bekhterev, Oppenheim, Gordon, Schaeffer. Among them, the Babinsky reflex is most constantly detected.

The hyperkinetic form of cerebral palsy is characterized by: hyperkinesis - choreic, athetoid, choreoathetoid, double athetosis, torsion dystonia.

At the age of 2-3 months, "dystonic attacks" appear, characterized by a sudden increase in muscle tone during movements, with positive and negative emotions, loud sounds, bright light; accompanied by a sharp cry, pronounced vegetative reactions - sweating, redness of the skin and tachycardia.

Tendon reflexes in most patients of normal living creatures or somewhat brisk, pathological reflexes are not detected.

Hyperkinesis in the muscles of the tongue appears at the age of 2-3 months of life, earlier than hyperkinesis in the muscles of the body - they appear at 4-6 months and become more pronounced with age. Hyperkinesis is minimal at rest, disappears during sleep, increases with voluntary movements, is provoked by emotions, and is more pronounced in the supine and standing position. Speech disorders are hyperkinetic in nature - dysarthria. Mental development is disturbed less than in other forms of cerebral palsy.

The atonic-astatic form of cerebral palsy is characterized by:

1. Muscle tone is sharply reduced. Against the background of general muscular hypotension, the tone in the upper limbs is higher than in the lower limbs, and movements in the upper part of the body are more active than in the lower.

2. Tendon reflexes are high, pathological reflexes are absent.

3. Recurvation in the knee joints, flat-valgus feet.

4. In the mental sphere, 87-90% of patients have a pronounced decrease in intelligence, speech disorders are of a cerebellar nature.

Laboratory research:

1. Complete blood count.

2. General analysis of urine.

3. Feces on the eggs of the worm.

4. ELISA for toxoplasmosis, cytomegalovirus - according to indications.

5. Definition of TTG - according to indications.

Instrumental research:

1. Computed tomography (CT) of the brain: there is a different atrophic process - expansion of the lateral ventricles, subarachnoid spaces, cortical atrophy, porencephalic cysts and other organic pathology.

2. Electroencephalography (EEG) - general disorganization of the rhythm, low-voltage EEG, peaks, hypsarrhythmia, generalized paroxysmal activity are detected.

3. EMG - according to indications.

4. MRI of the brain - according to indications.

5. Neurosonography - to exclude internal hydrocephalus.

6. Optometrist - examination of the fundus reveals the expansion of veins, narrowing of the arteries. In some cases, congenital atrophy of the optic nerve, strabismus are found.

Indications for specialist consultations:

1. Speech therapist - detection of speech disorders and their correction.

2. Psychologist - to clarify mental disorders and their correction.

3. Orthopedist - identifying contractures, resolving the issue of surgical treatment.

4. Prosthetist - to provide orthopedic care.

5. Optometrist - examination of the fundus, detection and correction of eye pathology.

6. Neurosurgeon - in order to exclude neurosurgical pathology.

7. Physical therapy doctor - appointment of individual lessons, styling.

8. Physiotherapist - for the appointment of physiotherapy procedures.

Minimum examination when referring to a hospital:

1. Complete blood count.

2. General analysis of urine.

3. Feces on the eggs of the worm.

The main diagnostic measures:

1. Complete blood count.

2. General analysis of urine.

3. Speech therapist.

4. Psychologist.

5. Optometrist.

6. Orthopedist.

7. Prosthetist.

9. Physical therapy doctor.

10. Physiotherapist.

11. Computed tomography of the brain.

List of additional diagnostic measures:

1. Neurosonography.

2. Neurosurgeon.

3. MRI of the brain.

4. ELISA for toxoplasmosis.

5. ELISA for cytomegalovirus.

6. Infectionist.

8. Cardiologist.

9. Ultrasound of the abdominal organs.

10. Geneticist.

11. Endocrinologist.

Differential Diagnosis

Medical tourism

Get treatment in Korea, Israel, Germany, USA

Medical tourism

Get advice on medical tourism

Treatment

Treatment tactics

It is extremely important to suspect or make a diagnosis in the first year of life, since the child's brain has a huge potential to compensate for the damage received. The child's brain is extremely plastic, so it is necessary to try to stimulate its recovery capabilities. The complex treatment of cerebral palsy includes medications, exercise therapy, orthopedic care, various types of massage, reflexology, physiotherapy, sessions with a speech therapist and psychologist. Rehabilitation therapy is most effective in patients in the early recovery period, the sooner you start preventing or reducing the development of pathological phenomena, the greater the effect of therapeutic measures.

Basic principles of treatment of cerebral palsy in the recovery period:

1. With the help of medications, a decrease in the zone of excitation and a decrease in muscle tone. Fight against delayed tonic reflexes and pathological muscle tone.

2. To achieve the formation of the vertical position of the child, his movements and manual manipulations, the cultivation of the skill of standing, moving initially with outside help, and then independently or with the help of crutches, sticks, orthopedic shoes, splints, devices.

3. Improvement of general mobility and coordination of movements.

4. Promoting the normalization of mobility in the joints and muscle performance, elimination of joint contractures.

5. Education and training of support and balance.

6. Stimulation of cognitive and psycho-speech development, mental development and education of correct speech.

7. Teaching vital, applied, labor skills, self-service skills education.

Purpose of treatment:

Improving motor and psycho-speech activity;

Prevention of pathological postures and contractures;

Acquisition of self-service skills;

Social adaptation, the emergence of motivations;

Relief of seizures.

Non-drug treatment:

1. General massage.

2. Exercise therapy - individual and group classes.

3. Physiotherapy - ozocerite applications, SMT, magnetotherapy.

4. Conductive pedagogy.

5. Classes with a speech therapist, psychologist.

6. Acupuncture.

7. Adele suit.

8. Hippotherapy.

Medical treatment

Recently, drugs of the nootropic series - neuroprotectors, have been widely used in order to improve metabolic processes in the brain. Most nootropic drugs, due to their psychostimulating effect, are prescribed in the first half of the day. The duration of nootropic treatment courses is from one to two to three months.

Cerebrolysin, ampoules 1 ml / m, piracetam, 5 ml ampoules 20%, tablets 0.2 and 0.4, ginkgo biloba (tanakan), tablets 40 mg, pyritinol hydrochloride (encephabol), dragee 100 mg, suspension - 5 ml contain 80.5 mg pyritinol (corresponding to 100 mg pyritinol hydrochloride).
Encephabol - a minimum of contraindications, approved for use from the first year of life. Dosage of the suspension (with a content of 20 mg of encephabol in 1 ml) for children 3-5 years old, a daily dose of 200-300 mg (12-15 mg of body weight) is prescribed in 2 doses - in the morning (after breakfast) and in the afternoon (after daytime sleep and afternoon tea) . The duration of the course is 6-12 weeks, long-term use is advisable, which increases working capacity and learning ability, improves higher mental functions.

Actovegin, ampoules 2 ml 80 mg, dragee-forte 200 mg of the active substance. Neurometabolic drug containing exclusively physiological components. Children are prescribed in dragee-forte, taking before meals ½ -1 dragee 2-3 times a day (depending on age and severity of symptoms of the disease), up to 17 hours. The duration of therapy is 1-2 months. Instenon tablets (1 tablet contains etamivan 50 mg, hexobendine 20 mg, etophylline 60 mg). Multicomponent neurometabolic drug. The daily dose is 1.5-2 tablets, administered in 2 divided doses (morning and afternoon) after meals. To avoid side effects, a gradual dose increase over 5-8 days is recommended. The duration of treatment is 4-6 weeks.

With spastic forms of cerebral palsy Myospasmolytics are widely used in practice: tolperisone, tizanidine, baclofen.
Tolperisone (mydocalm) is a centrally acting muscle relaxant, has membrane stabilizing activity, due to which it suppresses the formation and conduction of action potentials in hyperstimulated motor neurons of the brain stem and in peripheral nerves.
The mechanism of action is associated with a depressing effect on the caudal part of the reticular formation, suppression of pathologically increased spinal reflex activity and effects on peripheral nerve endings, as well as central n-anticholinergic properties. It also has a vasodilatory effect. This leads to a decrease in abnormally high muscle tone, reduces pathologically increased muscle tone, muscle rigidity, and improves voluntary active movements.
Mydocalm suppresses the functions of activating and inhibitory reticulospinal tracts and inhibits the conduction of mono- and polysynaptic reflexes in the spinal cord.
Dosage regimen: children from 3 months. up to 6 years, mydocalm is prescribed orally at a daily dose of 5-10 mg / kg (in 3 doses during the day); at the age of 7-14 years - at a daily dose of 2-4 mg / kg; adults 50 mg - 150 mg (1-3 tablets) 3 times a day.

Tizanidin (sirdalud) is a centrally acting myospasmolytic. The main point of application of its action is in the spinal cord. It selectively suppresses the polysynaptic mechanisms responsible for increasing muscle tone, mainly by reducing the release of excitatory amino acids from interneurons. The drug does not affect neuromuscular transmission.
Sirdalud is well tolerated and effective for cerebral and spinal spasticity. It reduces resistance to passive movements, reduces spasms and clonic convulsions, and increases the strength of voluntary contractions.

Baclofen is a centrally acting muscle relaxant; GABA receptor agonist. It inhibits mono- and polysynaptic reflexes, apparently due to a decrease in the release of excitatory amino acids (glutamate and aspartate) and terminals, which occurs as a result of stimulation of presynaptic GABA receptors. Against the background of the use of the drug, the motor and functional activity of patients increases.

Angioprotectors: vinpocetine, cinnarizine.

B vitamins: thiamine bromide, pyridoxine hydrochloride, cyanocobalamid; neuromultivit - a special complex of B vitamins with directed neurotropic action; neurobex.

Vitamins: folic acid, tocopherol, retinol, ergocalciferrol.

Anticonvulsants in epileptic syndrome: valproic acid, carbamzazepine, diazepam, clonazepam, topamax, lamotrigine.

With a combination of cerebral palsy with hydrocephalus, hypertensive-hydrocephalic syndrome, the appointment of dehydration agents is indicated: acetozolamide, furosemide, at the same time potassium preparations: panangin, asparkam, potassium orotate.

With severe anxiety, a syndrome of neuro-reflex excitability, sedatives are prescribed: novo-passit, noofen, a mixture with citral.

In recent years, in spastic forms of cerebral palsy, botulinum toxin has been used to reduce the spasticity of individual muscle groups. The mechanism of action of botulinum toxin (Dysport) is to inhibit the release of acetylcholine at neuromuscular synapses. Injection of the drug leads to relaxation of the spastic muscle.
The main indication for prescribing dysport in children with various forms of cerebral palsy is equinovarus deformity of the foot. The introduction of Dysport is technically simple and is not accompanied by significant adverse reactions.
The standard dose of Dysport per procedure is 20-30 mg per 1 kg of body weight. The maximum allowable dose in children is 1000 units. the average dose for each head of the gastrocnemius muscle is 100-150 units, for the soleus and posterior tibial muscles - 200 units.
Injection technique: 500 units Dysport is diluted in 2.5 ml of physiological saline (i.e. 1 ml of solution contains 200 units of the drug). The solution is injected into the muscle at one or two points. The effect of the drug (relaxation of spastic muscles) begins to appear on the 5-7th day after the administration of the drug, with the maximum effect achieved by 10-14 days.
The duration of the muscle relaxant is individual and varies from 3 to 6 months. after the introduction. Dysport should be introduced into the complex scheme as early as possible, before the formation of joint contractures.

Preventive actions:

Prevention of contractures, pathological postures;

Prevention of viral and bacterial infections.

Further management: dispensary registration with a neurologist at the place of residence, regular physical therapy classes, training parents in massage skills, exercise therapy, orthopedic styling, caring for children with cerebral palsy.

List of essential medicines:

1. Actovegin ampoules 80 mg, 2 ml

2. Vinpocetine, (Cavinton), tablets, 5 mg

3. Piracetam in 5 ml ampoules 20%

4. Pyridoxine hydrochloride ampoules 1 ml 5%

5. Folic acid tablets 0.001

6. Cerebrolysin, ampoules 1 ml

7. Cyanocobalamin, ampoules 200 mcg and 500 mcg

Additional medicines:

1. Aevit, capsules

2. Asparkam, tablets

3. Acetozolamide, tablets 250 mg

4. Baclofen 10 mg and 25 mg tablets

5. Valproic acid, syrup

6. Valproic acid tablets 300 mg and 500 mg

7. Gingo-Biloba 40 mg tablets

8. Glycine, tablets 0.1

9. Hopantenic acid, (Pantocalcin), tablets 0.25

10. Diazepam, ampoules 2 ml 0.5%

11. Dysport, ampoules 500 IU

12. Carbamazepine tablets 200 mg

13. Clonazepam, tablets 2 mg

14. Konvuleks, capsules 150 mg, 300 mg, 500 mg, solution in drops

15. Lamotrigine 25 mg and 50 mg tablets

16. Magne B6 tablets

17. Neuromidin tablets 20 mg

18. Novo-Passit, tablets, solution 100 ml

19. Noofen, tablets 0.25

20. Panangin, tablets

21. Piracetam tablets 0.2

22. Pyritinol, suspension or tablets 0.1

23. Thiamine bromide ampoules, 1 ml 5%

24. Tizanidine (Sirdalud), tablets 2.4 and 6 mg

25. Tolpirisone, (mydocalm) ampoules 1 ml, 100 mg

26. Tolpirisone, dragee 50 mg and 150 mg

27. Topamax, capsules 15 mg and 25 mg, tablets 25 mg

28. Cinnarizine tablets 25 mg

Treatment effectiveness indicators:

1. Improving motor and speech activity.

2. Decreased muscle tone in spastic forms of cerebral palsy.

3. An increase in the volume of active and passive movements in the paretic limbs.

4. Relief of seizures with concomitant epilepsy.

5. Reduction of hyperkinesis.

6. Acquisition of self-service skills.

7. Replenishment of active and passive vocabulary.

8. Improving the emotional and mental tone of the child.

Hospitalization

Indications for hospitalization: movement disorders, paresis, paralysis, delayed psychomotor and speech development from their peers, seizures, hyperkinesis, contractures, joint stiffness

Information

Sources and literature

1. Protocols for the diagnosis and treatment of diseases of the Ministry of Health of the Republic of Kazakhstan (Order No. 239 of 04/07/2010)
   1. L.O. Badalyan. Children's neurology. 1975 Moscow Handbook of a child psychiatrist and neuropathologist, edited by L.A. Bulakhova. Kyiv 1997 L.Z. Kazantsev. Rett syndrome in children. Moscow 1998 Clinic and diagnosis of cerebral palsy. Teaching aid. Zhukabaeva S.S. 2005

Information

List of developers:

The history of each disease has its heroes, who directed a huge amount of effort to treat or eradicate a particular disease. The history of cerebral palsy is no exception. Dedicated medical professionals and other professionals have worked hard to create a better world for people with special needs. .

William John Little (1810-1894)

First to study and try to define cerebral palsy

Dr. William John Little, the first person to determine that the development of cerebral palsy is caused by a lack of oxygen caused by a traumatic brain injury at birth. He used his experience of illness in childhood to apply it in medical practice..

Path to start

As a child, Little suffered mumps, measles, and whooping cough, three diseases that still exist today. The consequence of polio was a small clubfoot - a violation in which the leg is turned inward. When William was 15 years old, his illnesses and handicap sparked his interest in medicine. At the age of 27, he received his medical degree.

During his studies, Little met Dr. Georg Friedrich Louis Stromeyer, a German orthopedic surgeon who performed innovative reconstructive surgeries. Using his new techniques, Strohmeyer was able to correct Little's clubfoot. The operation was so successful that Little began to introduce it in England, which marked the beginning of the development of orthopedic surgery in the UK. Many of his techniques are still used in modern medicine today.

"Beginning" cerebral palsy

Little's work in Cerebral Palsy, which was not yet called by that name at the time, actually began in the late 1830s when he lectured on birth injuries. In 1853, he published his research in a paper entitled "On the Nature and Treatment of the Deformities of the Human Body", noting "congenital defects" and "their ability to recover to an amazing degree of perfection."

His work on cerebral palsy culminated in 1861 when Little attempted to give the first definition of cerebral palsy in a paper presented at the Obstetrical Society in London. In it, he stated that the "abnormal course of childbirth", during which "the child practically suffocated," traumatizes the nervous system and leads to spasticity, and sometimes to paralytic contractures.

It was here that he first identified what is now known as cerebral palsy. His work was so innovative that spastic cerebral palsy was at first called Little's disease.

In his 1861 paper, Little noted the role of treatment and early rehabilitation. "Many of the most helpless were restored to considerable activity and began to enjoy life," he wrote.

Dynasty

Little continued his medical practice until 1884, but his legacy does not end there. Two of his sons followed in their father's footsteps in orthopedic surgery. Muirhead Little became the first President of the British Orthopedic Association in 1918.

Sir William Osler (1849 - 1928)

Wrote the first book about cerebral palsy and came up with a name for cerebral palsy

Sir William Osler is regarded as one of the most significant figures in the history of medicine. He was also one of the earliest investigators of cerebral palsy and is often credited with pioneering the use of the term "CP".

While Dr. William John Little began the study of cerebral palsy, he described "Little's disease", which, as we know today, is only one form of this disease. Osler's book, Cerebral Palsy, describes many other forms of cerebral palsy. The book brings together Osler's lectures, which are numerous case studies and highlight the possible causes of impairment. Just as Little Osler points out that the right treatment can significantly improve the quality of life.

father of medicine

Sir William Osler is considered by many to be the father of modern medicine. In 1889, when Cerebral Palsy was written, Sir Osler became Chief of the newly established Johns Hopkins School of Medicine. His textbook, The Principles and Practice of Medicine: For Use in the Practical Work of Medical Students, was published in 1892 and translated into four languages. It became one of the most important medical textbooks in use for the next forty years.

Sir Osler also revolutionized North American medical education when, at Johns Hopkins, he began teaching students medicine at the bedside rather than in the classroom. He went even further by developing post-education programs that continue medical training. This principle of teaching is still used today.

In 1905 Osler was awarded the highest title in the English-speaking world of medicine: Royal Professor of Medicine at the University of Oxford. It was an honor that seemed irresistible until 1911, when he was knighted for his contributions to the medical field.

Sigmund Freud (1865-1939)

First to combine a wide range of movement disorders

Dr. Sigmund Freud, the neurologist who first argued that cerebral palsy could be caused by abnormal development before birth. Prior to this, orthopedic surgeon Dr. William Little postulated that cerebral palsy develops due to a complicated birth. Freud did not disagree with this statement, stating that difficult childbirth is "only a symptom of deeper effects that affect the development of the fetus." At the time, this conclusion was largely ignored. Only decades later did researchers begin to support Freud's theories.

Freud on the causes of cerebral palsy

Freud did not agree with Little's conclusions, so he raised questions that are still debated in the medical community today. Freud observed that many children who experienced asphyxia at birth developed normally without cerebral palsy. Little believed that asphyxia was the cause of cerebral palsy.

Little's research was in the field of orthopedic surgery, and Freud believed that this limited the type of patients Little could observe and examine. In addition, Freud studied the brain and its pathology, which allowed him to identify links between cerebral palsy and other conditions such as intellectual disabilities and epilepsy. All of this led Freud to conclude that these conditions were probably caused by problems occurring very early in the development of the brain and central nervous system, certainly before birth.

Despite this observation, researchers and physicians continued to follow Little's findings. Freud's theory was not proven until almost a century later, studies showed that only a small percentage of cerebral palsy - approximately 10 percent - is caused by birth asphyxia.

Freud was the first to combine movement disorders under one definition of "cerebral palsy"

Although the term "infantile cerebral palsy" was not used in the mid-1800s, Freud was the first to group the wide range of movement disorders caused by abnormal brain development under one term: cerebral palsy. This association is still valid today, although Freud proposed it as a temporary classification. Today, doctors and researchers continue to work on better methods for classifying cerebral palsy.

The Peculiar Birth of Sigmund Freud

Ironically, Freud was protected from asphyxia at birth. He was born with a shirt on, which means he was born with an intact amniotic sac. This happens most often during preterm labor and can allow the baby to develop as if it were still in the womb: not needing to breathe on its own, protected from infection, and fed from amniotic fluid. According to folklore, Freud was born on the day of the Caul holiday, which was an omen of future success. He was destined to become a great man.

History and origin of cerebral palsy

Send your good work in the knowledge base is simple. Use the form below

Students, graduate students, young scientists who use the knowledge base in their studies and work will be very grateful to you.

Hosted at http://www.allbest.ru/

GOU VPO "Voronezh State Medical Academy named after N.N. Burdenko

Ministry of Health and Social Development of the Russian Federation"

Department of Neurology

Head department: Lutsky M.A

Teacher: Uvarova M.V.

Disease history

Clinical diagnosis:

Cerebral palsy. Spastic tetraparesis. Hydrocephalus. Convergent strabismus. Right-sided hearing loss

student of group P-409

Voronezh 2012

I. Passport part

1. Full name: N

2. Age: 3 years 1 month

3. Gender: male

4. Home address: Voronezh region, Vorobyevsky district,

5. Place of work of parents:

6. Nationality - Russian

7. Date of admission to the hospital: 27.02.2012

8. Date of supervision: 02/27/2012 - 03/03/2012

II. Complaints

Complaints at the time of admission and curation made by the mother: instability, staggering, uncertainty when walking, limited movements in the limbs, delayed psychoverbal development: does not pronounce meaningful words, does not understand addressed speech.

III. History of present illness

(Anamnesis morbi)

The child is sick from birth. The perinatal anamnesis is aggravated (during pregnancy, toxicosis of the first half, exacerbation of chronic pyelonephritis, premature birth, prolonged, long anhydrous period, conjugative jaundice, cerebral edema, cardiac arrest, prolonged mechanical ventilation).

From an early age, there is a decrease in motor activity, an increase in tone in the limbs, a delay in motor and psychoverbal development. He holds his head from 8 months, sits from 1.5 years, walks independently from 2 years 9 months. There are no recognized words.

The diagnosis was established at 1 year. Periodically enters for planned treatment in the psycho-neurological department of young children of the Children's Clinical Hospital No. 2. Last hospitalization XI/11. The present hospitalization is the ninth.

IV. Anamnesis of life

(Anamnesis vitae)

Pregnancy I, toxicosis of the first half, exacerbation of chronic pyelonephritis. Childbirth I at 36 weeks, protracted, long anhydrous period. Birth weight 3140g, height 53 cm. At birth: Apgar score 7-8, conjugative jaundice, cerebral edema, cardiac arrest, prolonged mechanical ventilation. Artificial feeding with adapted infant formulas. He holds his head from 8 months, sits from 1.5 years, walks independently from 2 years 9 months. Produces individual sounds.

Past illnesses: He suffers from viral and catarrhal diseases 1-2 times a year. The mother denies syphilis, tuberculosis, toxoplasmosis.

Allergic history: food allergy.

Hereditary history: My grandmother has pyelonephritis, my great-grandmother on my mother's side has bronchial asthma.

Epidemiological history: The mother denies contact with infectious during the last 3 weeks.

Living conditions, food - satisfactory.

V. Objective research

General status.

General condition of the patient: satisfactory. Consciousness: clear. The position of the patient is active. Behavior and facial expressions are calm.

Body type - normosthenic. Height 94 cm. Weight 13 kg. Physical development is average, harmonious.

Skin and visible mucous membranes: moderately moist, clean, pale pink. Healthy nails and hair. Tissue turgor and skin elasticity are normal. Subcutaneous veins are visible on the forehead.

Subcutaneous fat: moderately developed, evenly distributed. The thickness of the skin fold in the navel is 1 cm. There are no edema.

Lymph nodes: not visible on examination. On palpation, the occipital, behind the ear, parotid, chin, submandibular, superficial anterior and posterior cervical, supraclavicular, subclavian, axillary, ulnar, inguinal, popliteal are undetectable.

Muscular system: developed moderately, evenly, symmetrically. The tone in the proximal sections is reduced, in the distal - increased. Muscle strength is reduced. Pain on palpation and movement is absent.

Osteo-articular system: The head is enlarged in size. Circumference 52.5 cm. Bones and joints are not deformed, painless. The springs are closed.

Cardiovascular system: Pulse rate 88 per minute. Blood pressure 90/60 mmm. rt. Art. Heart sounds are clear, rhythmic. Heart murmurs are not heard. There is no cardiac impulse. The apex beat is palpated in the fifth intercostal space 1 cm outward from the left midclavicular line. The symptom of "cat's purr" was not detected. Percussion of the heart:

Limits of relative stupidity:

Right - 0.5 cm medially from the right parasternal line in the fourth intercostal space;

Upper - at the level of the II intercostal space of the rib along the parasternal line

Left - 1 cm outward from the left midclavicular line in the fifth intercostal space;

Limits of absolute dullness of the heart:

right - left edge of the sternum;

upper - at the level of the III rib;

left - on the left midclavicular line;

Respiratory system: respiratory rate 22 per minute. Rhythmic breathing, no shortness of breath. When conducting comparative percussion, the sound is clear (pulmonary), the same on both sides. On auscultation: vesicular breathing is heard over the entire surface of the lungs. Topographic percussion data:

Inferior borders of the lungs:

Digestive system: Tongue pink, moist, clean, taste buds visible. The mucous throat is not hyperemic. The tonsils protrude slightly from behind the palatine arches, dense, pink in color, the lacunae are clean. The abdomen is rounded, symmetrical, not swollen. Palpation - soft, painless. The liver is palpated 1 cm below the edge of the costal arch. The size of the liver according to Kurlov: along the right midclavicular line - 9 cm, along the anterior midline - 7 cm, along the left costal arch - 6 cm. The gallbladder and spleen are not palpable. Percussion of the spleen: length - 5 cm, diameter - 3 cm. The chair is regular, independent, formed, without pathological impurities.

urinary system. Visually, no pathological changes were detected in the lumbar region. The kidneys are not palpable, painless. The effleurage symptom is negative on both sides. Pressure on the ureteral points and pain does not cause. Urination painless, free, 4-5 times a day.

Endocrine system: Examination and palpation of the thyroid gland showed no increase in size. The gland is of soft consistency, painless, mobile.

neurological status.

1. Cranial nerves.

I pair - olfactory nerve, II pair - optic nerve - the functions could not be investigated. Based on previous studies, partial atrophy of the optic nerve was revealed.

III, IV, VI pairs - oculomotor, trochlear, abducens nerves: round pupils, the same size. Convergence is reduced. The reaction of the pupils to light could not be determined. The width of the palpebral fissures is normal. Full eyeball movements. Convergent strabismus.

V pair - trigeminal nerve: The sensitivity of the skin of the face is not changed, the trigeminal points are painless on palpation. The position of the lower jaw when opening the mouth in the midline. The tone and function of masticatory muscles are not changed. The movements of the lower jaw are made in full. Corneal, conjunctival, superciliary and mandibular reflexes are preserved.

VII pair - facial nerve: The face is symmetrical. The nasolabial folds are the same on both sides. The taste of the anterior 2/3 of the tongue could not be investigated.

VIII pair - vestibule - cochlear nerve. Hearing in the right ear is reduced. Nystagmus is not noted.

IX, X pair - glossopharyngeal and vagus nerves: There are no cardiac arrhythmias and respiratory disorders. The position of the soft palate and uvula at rest and during phonation is median, movements without deviation to the side. Phonation, swallowing, salivary function, pharyngeal and palatine reflexes are preserved. Taste sensitivity of the posterior 1/3 of the tongue could not be investigated.

XI pair - accessory nerve. The strength, tension and trophism of the cervical muscles are preserved. There is no wryneck. The head is in the midline. Raising the shoulders and turning the head is not difficult.

XII pair - hypoglossal nerve. The tongue is located in the mouth in the midline. Atrophy and fibrillar twitching of the muscles of the tongue are absent.

2. Motor area:

Atrophy, hypertrophy, fibrillar and fascicular twitches were not revealed. There are no contracts. Chvostek's symptom is negative. Hyperkinesis, convulsive seizures are not observed. Active and passive movements are limited. Muscle strength is reduced. Muscle tone in the proximal limbs is reduced, in the distal it is increased. Pathological synkinesis is absent. The expression is expressed.

3. Coordination of movements:

Motor coordination is difficult to assess due to the child's age and difficult to reach contact. Unsteady, unsteady gait, staggering when walking.

4. Reflexes:

Proprioceptive reflexes in the face: (superciliary and mandibular) are not changed. Tendon reflexes of the arms (flexion-elbow, extensor-elbow, carpo-radial, Mayer, Leri) and legs (knee, akhilova) revived.

Exterocepural reflexes: corneal, pharyngeal, abdominal (upper, middle, lower) cremaster, plantar are not changed.

Pathological and conditionally pathological reflexes: in the face (proboscis, nasolabial, labial, nasolabial, searching, palmar-chin), hands (Tromner-Rusetsky, grasping), legs (Oppenheim, Gordon, Rossolimo, Zhukovsky, Bekhterev) - negative. Babinski's reflex is positive.

Pathological protective reflexes are positive. Tonic reflexes are absent.

5. Sensitive sphere.

Superficial sensitivity is not broken. Deep and complex types of sensitivity due to the age of the child and hard-to-reach contact are difficult to assess.

There is no pain on palpation in the paravertebral points and along the nerve trunks on the extremities. Radicular and stem tension symptoms (Lasega, Bekhterev, Dejerine, Neri, Vaserman) are negative.

Tonic reflex phenomena of Kernig, Brudzinsky (upper, middle, lower), stiff neck, zygomatic symptom of Bechterew were not detected.

Vomiting, hyperesthesia to light and sounds are not noted.

6. Functions of the pelvic organs:

There are no urination and defecation disorders.

7. Autonomic nervous system.

Vasomotor, secretory, trophic disorders were not detected. Dermographism pink, early, unstable. The pilomotor reflex was preserved. The Dagnini-Ashner reflex causes a decrease in heart rate by 7 beats. Horner's sign is negative. Body temperature is normal.

8. Speech, psyche:

The development of motor and sensory speech is delayed. The child pronounces separate sounds, does not understand the addressed speech - motor and sensory aphasia.

The child lags behind in mental development. When interacting with him, he does not look into his eyes.

VI. Data of additional research methods:

1. Complete blood count:

Hemoglobin - 127 g/l

Erythrocytes - 4 *1012/l

ESR - 4 mm/h

Platelets - 220*109/l

Leukocytes - 6*109/l

Stab - 5%

Segmented - 60%

Eosinophils - 2%

Basophils - 0%

Lymphocytes - 31%

Monocytes 2%

Conclusion is the norm.

2. General analysis of urine:

Specific gravity - 1023

Color straw yellow

The reaction is sour

Protein - negative

Sugar - negative

Leukocytes - 3-4 in the field of view

Conclusion: urine parameters without pathological abnormalities.

3. EEG: Against the background of a pronounced dysfunction of the median structures, mainly stem and limbic-reticular, clearly expressed epileptic activity was not detected.

4. MRI: picture of perinatal changes in the periventricular white matter. Hypoplasia of the cerebellar vermis. A variant of the Dandy-Walker anomaly, open internal hydrocephalus. Atrophic changes in the frontal, temporal lobes of a mixed type.

VII. Topical diagnosis

Tendon reflexes are brisk, hypertonicity in the distal parts of the upper and lower extremities, a positive pathological Babinski reflex, muscle strength in the extremities is reduced - it can be assumed that the pyramidal system is affected.

Instability, uncertainty, staggering when walking, decreased tone in the proximal limbs may indicate damage to the cerebellum.

Violation of cortical functions (delayed psychoverbal development, motor aphasia) indicates a possible lesion of the frontal lobe.

Sensory aphasia may result from damage to the temporal lobe.

VIII. Clinical diagnosis:

Based:

Complaints (for instability, staggering, uncertainty when walking, for limited movements in the limbs, for a delay in psychoverbal development: he does not pronounce meaningful words, he does not understand addressed speech);

History of the disease (aggravated obstetric and perinatal history, lag in psychomotor development);

Objective examination data (restriction of active movements in the limbs, increased tendon reflexes, increased tone in the distal limbs and a decrease in the proximal ones, the presence of a pathological Babinski reflex, delayed psychomotor and speech development, converging strabismus);

Data from instrumental studies (MRI: picture of perinatal changes in the periventricular white matter. Hypoplasia of the cerebellar vermis. A variant of the Dandy-Walker anomaly, open internal hydrocephalus. Atrophic changes in the frontal, temporal lobes of a mixed type)

Previous studies (hearing loss, partial atrophy of the optic nerves).

can be diagnosed:

IX. Differential Diagnosis

With other forms of cerebral palsy:

1) With spastic hemiplegia: Violation of muscle strength, tone, tendon reflexes is detected only on one side - a violation of gait and manipulation is formed. The Wernicke-Mann pose is formed. With this form, motor and psychoverbal development usually occurs in accordance with age.

2) Double hemiplegia. Movement disorders are also manifested by damage to the arms and legs, while the hands are more affected. Characterized by delayed motor and psychoverbal development and treatment-resistant symptomatic epilepsy.

3) Atactic form - muscle tone is reduced, tendon reflexes are increased. When walking dynamic and static ataxia. Delay in motor and psychoverbal development. Elements of intentional tremor.

X. Etiology and pathogenesis

Cerebral palsy is a term that unites a group of non-progressive brain diseases that have arisen as a result of underdevelopment or damage to brain structures in the antenatal, intranatal and early postnatal periods, characterized by movement disorders, postural, speech, and mental disorders.

Factors that determine structural and functional changes in the brain, in 80% of cases, act in the process of intrauterine development of the fetus, in 20% - postnatally. Among the pathogenic factors that damage the brain in utero, the leading role belongs to infections (flu, rubella, toxoplasmosis), somatic and endogenous diseases of the mother (congenital heart disease, chronic lung disease, diabetes mellitus, hypo- and hyperthyroidism, etc.), immunological incompatibility of the mother's blood and fetus (by Rh factor, ABO system and other antigens), occupational hazards, alcoholism. Of the factors causing brain damage during childbirth, birth trauma, birth asphyxia, and encephalitis in the early postpartum period are of primary importance.

Changes in the nervous system are associated with hypoxia and metabolic disorders, which have a direct and indirect (through products of impaired metabolism) effect on the development and function of the brain.

XI. Pathomorphology

brain limited movement change

Morphological changes in the brain depend on the etiology and time of damage to the structures.

In 30% of children with cerebral palsy, brain anomalies are found - micropolygyria, pachygyria, porencephaly, agenesis of the corpus callosum, which are the result of brain damage at an early stage of ontogenesis. Microscopic examination reveals glial proliferation and neuronal degeneration.

In some cases, gross focal defects are found - atrophic lobar sclerosis, atrophy of the cells of the basal ganglia and thalamus, pituitary gland, cerebellum. Atrophic lobar sclerosis is manifested by massive localized atrophy of the frontal lobe, underdevelopment of the cerebral cortex, midbrain. The defeat of the basal ganglia and the thalamus is characterized by the growth of myelin fibers with an annular arrangement around the vessels. Usually these changes occur with kernicterus. In the cerebellum, insufficient myelination of pathways and changes in neurons are found.

Often marginal encephalitis in the form of focal fusion of the meninges with a small cell layer of the cortex of the cerebral hemispheres, granulomas, thrombo- and perivasculitis, neoplasm of capillaries.

XII. Treatment

1) stationary mode.

2) drugs that improve metabolism and microcirculation in the brain piracetam, aminalon, glutamic acid, cavinton, cerebrolysin, cortexin, actovegin, glycine.

3) means for removing the pathological tone - mydocalm, baclofen.

4) drugs that improve the metabolism of muscle tissue - nerabol, methandrostenolone

5) vitamins - B1, B6, B12, C, nicotinic acid

6) electrophoresis

7) therapeutic limb massage

8) classes with a speech therapist and a psychologist.

XIII. observation diary

February 28, 2012

AD 90/60. t = 36.5 C.

Heart rate 88 per minute

NPV 22 min.

4) Multivitamins

6) Electrophoresis

7) Classes with a speech therapist

8) Consultation with an ophthalmologist

February 29, 2012

AD 90/60. t = 36.5 C.

Heart rate 85 per minute

NPV 23 per min.

The patient's condition is satisfactory, stable. Limitation of active movements in the limbs, increased tendon reflexes, increased tone in the distal limbs and a decrease in the proximal. Pathological Babinski's reflexes. No changes were found in other organs.

1) Sol. Cavintoni 1.0 with physical solution

2) Cortexin 0.005 IM with 1 ml 0.5% novocaine

3) Tab. Mydocalm 0.2 3 times a day

4) Multivitamins

6) Electrophoresis

7) Classes with a speech therapist

8) Consultation of a psychologist

AD 95/60. t = 36.5 C.

Heart rate 86 per minute

NPV 21 min.

The patient's condition is satisfactory, no negative dynamics are observed. Limitation of active movements in the limbs, increased tendon reflexes, increased tone in the distal limbs and a decrease in the proximal. Pathological Babinski's reflexes. No changes were found in other organs.

1) Sol. Cavintoni 1.0 with physical solution

2) Cortexin 0.005 IM with 1 ml 0.5% novocaine

3) Tab. Mydocalm 0.2 3 times a day

4) Multivitamins

6) Electrophoresis

7) Classes with a speech therapist

March 02, 2012

AD 95/60. t = 36.5 C.

Heart rate 86 per minute

NPV 21 min.

The patient's condition is satisfactory. The child is more mobile, actively trying to pronounce sounds. Limitation of active movements in the limbs, increased tendon reflexes, increased tone in the distal limbs and a decrease in the proximal. Pathological Babinski's reflexes. No changes were found in other organs.

1) Sol. Cavintoni 1.0 with physical solution

2) Cortexin 0.005 IM with 1 ml 0.5% novocaine

3) Tab. Mydocalm 0.2 3 times a day

4) Multivitamins

6) Electrophoresis

7) Classes with a speech therapist

03.02.2012

AD 95/60. t = 36.5 C.

Heart rate 86 per minute

NPV 21 min.

The patient's condition is satisfactory. Limitation of active movements in the limbs, increased tendon reflexes, increased tone in the distal limbs and a decrease in the proximal. Pathological Babinski's reflexes. No changes were found in other organs.

1) Sol. Cavintoni 1.0 with physical solution

2) Cortexin 0.005 IM with 1 ml 0.5% novocaine

3) Tab. Mydocalm 0.2 3 times a day

4) Multivitamins

6) Electrophoresis

7) Classes with a speech therapist

8) Consultation of a psychologist

XIV. Epicrisis

N. was hospitalized on 02.27.12 for planned treatment in the psycho-neurological department of young children of the Children's Clinical Hospital No. 2 with complaints of instability, staggering, uncertainty when walking, limited movements in the limbs, and delayed psychoverbal development.

Ill from birth. In 2010, I was diagnosed with cerebral palsy. Spastic tetraparesis.

Objectively: limitation of active movements in the extremities, increased tendon reflexes, increased tone in the distal extremities and decrease in the proximal ones, the presence of a pathological Babinski reflex, delayed psychomotor and speech development, converging strabismus.

Based on complaints, anamnesis of the disease, objective examination data, laboratory and instrumental analyzes, and a differential diagnosis, the following diagnosis was made:

Cerebral palsy, spastic tetraparesis. Partial atrophy of the optic nerve, convergent strabismus. Communicating hydrocephalus. Dandy-Walker anomaly. Gross delay in psychoverbal development.

Treatment is carried out: drugs that improve cerebral circulation, nootropics, vitamins, massage, electrophoresis. Against the background of ongoing therapy, the dynamics is not observed. She is currently undergoing inpatient treatment.

XVI. References

1) Petrukhin A. S. "Children's neurology": textbook: in two volumes - M.: GOETAR-Media, 2009. - T.2.-560s.:il

2) "Neurology: A National Guide". Under the editorship of E. I. Guseva - M: GOETAR-Media, 2009

3) E. I. Gusev, A. N. Konovalov, G. S. Burd "Neurology and Neurosurgery" M: Medicine, 2000

4) Badalyan L.O. Zhurba L. T., Vsevolozhskaya N. M. "Guide to the neurology of early childhood - Kyiv, 1980

5) L. O. Badalyan "Children's neurology" - M .: Medicine, 1984

Hosted on Allbest.ru

Similar Documents

Study on the basis of clinical, psychological and social health of the characteristics of a child diagnosed with cerebral palsy. Factors that determine the specifics of the emotional development of children with disorders of the musculoskeletal system.

term paper, added 11/15/2014


Cerebral palsy is a severe disease of the nervous system, which often leads to disability of the child. Cerebral palsy is a polyetiological brain disease that occurs under the influence of various harmful effects on the child's body.

report, added 12/12/2008


Infantile cerebral palsy (ICP). A group of disorders of the motor functions of the brain that arose as a result of its damage in infancy. Violation of intellectual development and speech. degree of brain damage. Therapeutic exercise and massage.

abstract, added 02/27/2009


Topographic anatomy of the brain: meninges, ventricles of the brain, boundaries of the lobes, blood supply system. Histological classification of intracranial tumors. Characteristics of the main methods of surgical intervention on the brain in tumors.

term paper, added 11/13/2011


General information and provoking factors, the history of the study of cerebral palsy, its causes and forms. Clinical signs and the course of this disease, the principles of diagnosis and the development of a treatment regimen. Prognosis for recovery and life.

abstract, added 05/20/2015


Case history of a five year old child. Complaints about the inability to stand independently, move around, limited movements in both legs and arms. Isolation of symptoms and preliminary diagnosis: volumetric formation of the brain. Methods of treatment.

case history, added 03/12/2009


Cerebral palsy as a developmental disorder. A disorder in the development of the brain or damage to one or more parts of it. Scientific activity of clinician K.A. Semenova. Formation of reflex mechanisms. Pathological motor reactions.

abstract, added 06/09/2015


Cerebral palsy: concept, risk factors for development. Spastic diplegia. Hemiplegic, hyperkinetic, atonic-astatic form. The main manifestations of the disease. Characterization of the features of the process of education and upbringing of children.

presentation, added 01/24/2018


The consumption of oxygen and glucose by the brain. Aerobic oxidation of glucose in the brain and mechanisms of its regulation. The tricarboxylic acid cycle and mechanisms controlling its rate in the brain. Energy supply of specific functions of the nervous tissue.

term paper, added 08/26/2009


Polyetiological disease of the brain, manifested by motor, mental and speech disorders. Forms of cerebral palsy (ICP). Comprehensive rehabilitation measures in children with cerebral palsy. General massage techniques to relax muscles.