Model of differential diagnosis of nervous system lesions in young children

Symptoms | Treatment of neonatal depression syndrome

Depression syndrome is the consequences of perinatal damage to the central nervous system in a child during the period from 28 weeks of intrauterine development to 7 days after birth. Perinatal lesions of the central nervous system occur in 85% or more of children.

CNS depression syndrome is the bottom of the manifestations of intrauterine fetal hypoxia, birth injuries, IUI.

CNS depression syndrome in newborns develops somewhat less frequently than hyperexcitability syndrome, but is still one of the most common in childhood.

The main causes of perinatal CNS lesions, including depression syndrome, are:

hypoxia, asphyxia, hemolytic disease of the newborn, injuries at the time of birth due to improper use of obstetric aid, as well as intrauterine infections.

The main infections that affect the brain during the neonatal period are CMV (cytomegalovirus infection), herpes infection, and syphilis.

Oppression syndrome in newborns first appears months and days of life.

The main reasons for the development of CNS HIP:

- anemia in the mother (a decrease in the amount of hemoglobin, which reduces the delivery of oxygen and nutrients to the tissues of the baby’s body) - any chronic diseases and defects: congenital heart defects, lungs of other organs, kidney disease, the presence of diabetes mellitus, which contribute to poor circulation - complications pregnancy and childbirth (gestosis, threat of premature birth, pathology of the placenta and umbilical cord, prematurity and post-term pregnancy, multiple pregnancies, polyhydramnios and oligohydramnios, various anomalies of labor) - fetal diseases (hemolytic disease of the newborn, intrauterine infection, bleeding) Tangible signs of fetal hypoxia mainly are expressed in changes in its motor activity (sudden increase, increased heart rate and movements (movements) of the fetus during acute hypoxia, or a decrease and weakening of them during chronic hypoxia). When a diagnosis of intrauterine fetal hypoxia is made, the expectant mother needs to carry out procedures to identify the causes, followed by comprehensive treatment of their source, with possible hospitalization in a hospital, adherence to bed or home rest and daily routine.

Hypoxic lesions of the central nervous system

Section I

Hypoxic lesions of the central nervous system

I. A) P 91.0 Cerebral ischemia (hypoxic-ischemic encephalopathy, perinatal hypoxic brain damage)

Cerebral ischemia grade I (mild)

a) Intrapartum hypoxia, mild asphyxia at birth;

b) Excitation of the central nervous system is more common in full-term infants, depression - in premature infants, lasting no more than 5-7 days;

c) Moderate hypoxemia, hypercarbia, acidosis;

NSG, CT, MRI - without pathological abnormalities;

DEG - compensatory increase in speed along the main arteries of the brain;

Diagnosis example:

P 91.0 “Cerebral ischemia stage I” or “Hypoxic-ischemic damage to the central nervous system stage I”

Cerebral ischemia degree II (moderate)

a) Factors indicating intrauterine fetal hypoxia; moderate asphyxia at birth; extracerebral causes of cerebral hypoxia that arise postnatally;

b) CNS depression, excitation or change of phases of cerebral activity (lasting more than 7 days);

Convulsions in premature infants are often tonic or atypical (convulsive apnea, stereotypical spontaneous oral automatisms, fluttering of the eyelids, myoclonus of the eyeballs, “rowing” movements of the arms, “pedaling” of the legs); in full-term infants - multifocal clonic; Attacks are usually short-term, single, less often repeated;

Intracranial hypertension (transient, more often in full-term infants);

Autonomic-visceral disorders;

c) Metabolic disorders (hypoxemia, hypercarbia, acidosis are more pronounced and persistent)

NSG - local hyperechoic foci in the brain tissue (in premature infants, more often in the periventricular region; in full-term infants, subcortically.

MRI - focal lesions in the brain parenchyma are determined in the form of changes in the nature of the magnetic resonance signal on T1 and T2-weighted images.

CT scan of the brain shows local foci of low density in the brain tissue (in premature infants, more often in the periventricular region; in full-term infants, subcortically and/or cortically.

DEG are signs of hypoperfusion in the middle cerebral artery in full-term infants and the anterior cerebral artery in premature infants. An increase in the diastolic component of blood flow velocity, a decrease in the resistance index.

Diagnosis example:

P 91.0 “Cerebral ischemia degree II” or “Hypoxic-ischemic damage to the central nervous system II degree.”

In cases of diagnosis of specific structural changes in the brain, an additional code is set (for example, P 91.2 cerebral leukomalacia of a newborn).

Cerebral ischemia grade III (severe)

a) Factors leading to intrauterine fetal hypoxia and/or severe perinatal asphyxia; extracerebral causes of persistent cerebral hypoxia (CHD, severe forms of SDR, hypovolemic shock, etc.);

b) Progressive loss of cerebral activity - over 10 days

(in the first 12 hours of life there is deep depression or coma, in the period from 12-24 there is a short-term increase in the level of wakefulness, from 24-72 hours there is an increase in depression or coma

• Repeated convulsions, epistatus is possible.
• Dysfunction of the brain stem (disturbances in breathing rhythm, pupillary reactions, oculomotor disorders).
• The position of decortication or decerebration (depending on the extent of the lesion).
• Severe autonomic and visceral disorders.
• Progressive intracranial hypertension.

c) Persistent metabolic disorders.

NSG - a diffuse increase in the echogenicity of the brain parenchyma - is characteristic of full-term infants. Increased echogenicity of periventricular structures is typical for premature infants. Narrowing of the lateral ventricles. Subsequently, cystic periventricular cavities (PVC) are formed in premature infants, and signs of atrophy of the cerebral hemispheres with passive expansion of the cerebrospinal fluid spaces appear.

CT scan - decreased density of brain parenchyma, narrowing of the cerebrospinal fluid spaces, multifocal cortical and subcortical foci of reduced density, changes in the density of the basal ganglia and thalamus - mainly in full-term infants, periventricular cystic cavities - in premature infants (Check with a radiologist)

MRI - lesions in the brain parenchyma are detected as changes in the magnetic resonance signal on T1 and T2-weighted images.

DEG - paralysis of the main arteries of the brain, with transition to persistent cerebral hypoperfusion. Decrease in diastolic blood flow velocity, change in the nature of the curve (its leasing or pendulum-like nature). Increase in resistance index.

Diagnosis example:

P 91.0 “Cerebral ischemia of the third degree” or “Hypoxic-ischemic damage to the central nervous system of the third degree.”

In cases of diagnosis of specific structural changes in the brain, an additional code is set (see Appendix).

I. B) R 52 INTRACRANIAL HEMORRHAGES

(hypoxic, non-traumatic)

P 52.0 Intraventricular hemorrhage of the 1st degree (subependymal)

a) Ante- and - intrapartum hypoxia, mild asphyxia at birth, repeated attacks of apnea, jet administration of hyperosmolar solutions.

b) Develops predominantly in premature or immature newborns Course: asymptomatic, absence of specific neurological disorders

c) Transient metabolic disorders

NSG - hyperechoic areas, unilateral or bilateral localization in the thalamo-caudal notch or in the region of the head of the caudate nucleus. The time frame for transformation of a subependymal hematoma into a cyst is 10-14 days or more.

CT, MRI - do not have diagnostic advantages over NSG.

DEG - without pathological changes.

P 52.1 Intraventricular hemorrhage of the second degree

(subependymal + intraventricular)

Develops predominantly in premature infants (35-65%).

a) Factors indicating intrauterine fetal hypoxia and/or moderate asphyxia at birth. Defects in the provision of primary resuscitation care, arterial hypertension or fluctuation of systemic blood pressure due to SDR, iatrogenic factors (inadequate mechanical ventilation regimens, rapid administration of large volumes or hyperosmolar solutions, functioning fetal communications, pneumothorax, etc.). Coagulopathies.

b) There are 2 main variants of the flow: gradual (wavy) and catastrophic.

• Catastrophic course: short-term motor excitation is suddenly replaced by progressive depression of cerebral activity with transition to coma. Deep apnea, increasing cyanosis and marbling of the skin. Tonic convulsions, oculomotor disorders, bradyarrhythmia, and thermoregulation disorders indicate increasing intraventricular hypertension.
• Gradual course (wavy): periodic changes in phases of cerebral activity, attacks of repeated apnea, muscle hypotension, atypical convulsive attacks.

c) Fluctuation and then a rapid decrease in systemic blood pressure (cf. blood pressure < 30 mm Hg)

Fall in hematocrit and decrease in hemoglobin level

Metabolic disorders: hypoxemia, hypercabia, acidosis, hypocalcemia, fluctuations in serum glucose levels

CSF - with an admixture of blood (the time of occurrence of bleeding and its intensity is judged by the microscopic characteristics and the number of red blood cells), reactive pleocytosis, increased protein levels, decreased glucose. During lumbar puncture, blood pressure is often elevated.

NSG changes depend on the time of the study; at the initial stages, hyperechoic zones are determined in the area of ​​the germinal matrix, then ventriculomegaly develops, and subsequently echo-positive formations (thrombi) are visualized in the lumens of the ventricles. In some cases, blockage of the cerebrospinal fluid pathways with the development of acute hydrocephalus is possible.

CT, MRI, PET - do not have diagnostic advantages in the neonatal period over NSG

DEG - fluctuation of blood flow in the main arteries of the brain before the development of intravetricular bleeding, stabilization - after hemorrhage, with the progression of ventriculomegaly (usually after 10-12 days) - increasing hypoperfusion.

P 52.2 Intraventricular hemorrhage of the third degree

(subependymal + intraventricular + periventricular)

Among all variants of IVH, their share accounts for 12 to 17%.

b) Most often observed in premature infants with extremely low body weight.

• Typically catastrophic. Rapid depression of cerebral activity with the development of coma, progressive disorder of vital functions (bradycardia, arrhythmia, apnea, respiratory rhythm pathology).
• Tonic convulsions and oculomotor disorders occur due to dislocation of the brain stem. High incidence of deaths in the first days of life.

c) Severe, difficult to correct, metabolic disorders (hypoxemia, hypercarbia, acidosis, electrolyte disturbances), disseminated intravascular coagulation syndrome.

A progressive fall in systemic blood pressure and cardiac arrhythmias. Critical drop in hematocrit and hemoglobin levels

CSF - with a significant admixture of blood (the time of occurrence of bleeding and its intensity is judged by the microscopic characteristics and the number of red blood cells), reactive pleocytosis, increased protein levels are often observed, and cerebrospinal fluid pressure is often increased.

Diagnostic lumbar puncture is performed according to strict indications and with extreme caution, due to the high risk of herniation of the brain stem into the foramen magnum.

NSG is an extensive hyperechoic area of ​​periventricular localization (hemorrhagic infarction - often unilateral in the fronto-parietal region), the lateral ventricle on the side of the hemorrhage is practically not visualized, later ventriculomegaly and deformation of the lateral ventricle are revealed due to the formation of a porencephalic post-hemorrhagic cystic cavity. Thrombi are often visualized in the lumen of the ventricles, in combination with pronounced dilatation of the ventricular system. Subsequently, an increase in the echogenicity of the ventricular walls is caused by the development of aseptic ventriculitis and hemosiderosis of the periventricular parenchyma. In a significant percentage of cases, occlusive hydrocephalus is formed.

CT, MRI, PET - do not have diagnostic advantages in the neonatal period over NSG

DEG - in the initial stages, a decrease in systolic and diastolic blood flow rates, an increase in the resistance index

Reduced diastolic blood flow velocity, decreased resistance index.

P 52.5 Primary subarachnoid hemorrhage (non-traumatic)

The frequency is about 20%, of which 75% are in premature and immature

a) Intranatal hypoxia, asphyxia at birth. Short gestation period, immaturity. Coagulopathies.

b) Clinical course options:

• Asymptomatic,
• Excitement syndrome with hyperesthesia and acute intracranial hypertension (tension and bulging of the large fontanel, divergence of the sagittal and coronal sutures, profuse regurgitation, intermittent Graefe's symptom);
• Convulsions that suddenly occur on the 2-3rd day of life (focal clonic - more often in full-term infants), atypical convulsions (in premature infants).

c) Metabolic disorders are not typical

NSG is not very informative for diagnosing PSC. In some cases, the expansion of the Sylvian fissure and/or interhemispheric fissure is visualized.

CT and MRI - accumulation of blood is detected in various parts of the subarachnoid space, but more often in the temporal regions.

DEG is not very informative (primary and secondary vasospasm).

CSF - increased pressure, increased erythrocyte content (including changed ones), increased protein concentration, neutrophilic pleocytosis.

R 52.4 Hemorrhage into the substance of the brain (non-traumatic)

parenchymal

P 52.6 hemorrhage in the cerebellum and posterior cranial fossa

(rare)

a) Intrauterine fetal hypoxia, severe or moderate asphyxia at birth. Coagulopathies. Prematurity. Vascular malformations.

b) The clinical picture depends on the location and volume of the hemorrhagic infarction.

• With scattered petechial hemorrhages of subcortical localization, an asymptomatic course is possible.
• With extensive parenchymal hematomas of hemispheric localization, the clinical course is similar to stage III IVH. Progressive loss of cerebral activity with transition to stupor or coma, focal neurological symptoms contralateral to the lesion (distinct asymmetry of muscle tone, focal or tonic convulsions, oculomotor disturbances, etc.); increasing intracranial hypertension.
• Hemorrhages in the posterior cranial fossa and cerebellum are characterized by increasing signs of intracranial hypertension (tension of the fontanelles, dehiscence of the nuchal suture, agitation, frequent tonic convulsions) and brainstem disorders (respiratory, cardiovascular disorders, oculomotor disorders, bulbar syndrome).

c) Severe metabolic disorders that are difficult to correct (hypoxemia, hypercarbia, acidosis, disseminated intravascular coagulation) are usually accompanied by massive hematomas. A progressive increase in systemic blood pressure is subsequently replaced by a fall. Heart rhythm disturbances. Decreases in hematocrit and hemoglobin levels correlate with the amount of bleeding.

CSF - increased pressure, increased erythrocyte content (including changed ones), increased protein concentration, neutrophilic pleocytosis in the cerebrospinal fluid. With the exception of cases of small focal parenchymal hemorrhages.

NSG is not very informative for small-point hemorrhages; massive hemorrhagic infarctions are visualized as asymmetric hyperechoic foci in the brain parenchyma. After 2-3 weeks, echo-negative cavities (pseudocysts, leukomalacia) form in their place. Possible contralateral displacement of the interhemispheric fissure and homolateral compression of the lateral ventricle.

CT scan shows areas of increased density in the brain parenchyma, varying in size and location, with concomitant deformation of the cerebrospinal fluid spaces.

MRI - change in the MR signal from foci of hemorrhage not in the acute stage.

DEG is asymmetric hypoperfusion in the cerebral arteries on the affected side.

I. B) Combined ischemic and hemorrhagic

CNS lesions (non-traumatic)

Occurs much more often

than all isolated forms of CNS damage discussed above

(occurs predominantly in premature infants)

a) Intrauterine hypoxia and asphyxia at birth. Premature infants with low body weight (1000-1500 g). Defects in the provision of primary resuscitation care, arterial hypotension, hypertension or fluctuations in systemic blood pressure. Coagulopathies, DIC syndrome.

B) The clinical picture depends on the leading type of damage to the central nervous system (ischemia or hemorrhage), its severity and location. There is significant variability in neurological symptoms and their dynamics. These types of damage are the most severe.

c) Metabolic disorders that are difficult to correct.

CSF - pressure is usually increased; morphological characteristics depend on the degree of hemorrhage into the cerebrospinal fluid spaces.

NSG, CT, MRI - various variants of deformation of the liquor-conducting system, foci of altered density, differing in intensity, predominantly periventricular localization.

DEG—fluctuation of cerebral blood flow; paralysis of the main arteries of the brain, decreased blood flow.

Diagnosis example:

“Combined (non-traumatic) ischemic-hemorrhagic damage to the central nervous system.”

In cases of diagnosing specific structural changes in the brain, combinations of codes corresponding to ischemic and hemorrhagic intracranial injuries are set (see Appendix).

Section II

Traumatic damage to the nervous system.

II. A) P 10 Intracranial birth injury

(Rupture of intracranial tissues and hemorrhage due to birth trauma)

R 10.8 Epidural hemorrhage

(occurs mainly in full-term,

with a frequency of about 2% among all intracranial hemorrhages).

a) Anomalies of childbirth: discrepancy between the birth canal and the size of the fetal head, anomalies of presentation, instrumental delivery.

b) Rapidly increasing intracranial hypertension in the first hours of life;

• Hyperexcitability;
• Convulsions;
• On the side of the hematoma, the pupil is sometimes dilated. Often combined with cephalhematoma.

c) Metabolic disorders in isolated epidural hematoma are not typical.

CSF is not informative.

NSG is not very informative (depends on the location and volume of the hematoma).

CT scan shows a ribbon-shaped, high-density formation between the dura mater and the covering bones of the skull. In some cases, the hematoma area has the shape of a “biconvex lens” adjacent to the integumentary bones of the skull.

DEG is not informative.

P 10.0 Subdural supratentorial hemorrhage

(True prevalence unknown, more common in full-term

over 4000 and post-term, in 40% of cases bilateral,)

a) See section “Epidural hemorrhage”

b) The following variants of clinical manifestations are found:

• Asymptomatic;
• Focal neurological disorders developing in the first 72 hours of life: hemiparesis (on the side opposite to the hematoma); deviation of the eyes in the direction opposite to hemiparesis (“eyes look” at the hematoma); dilation of the pupil on the side of the injury;
• Focal (focal) seizures
• Hypertension syndrome of varying severity or hyperexcitability.

c) Metabolic disorders in isolated subdural hematoma of convexital localization are not typical.

Transillumination of the skull is an accessible and informative diagnostic method. A limited focus of low luminescence above the hematoma is determined.

NSG - for small and flat subdural hematomas of convexital localization, is not very informative; for hemorrhages of significant size, there are signs of compression of the homolateral hemisphere and displacement of the median structures towards the side opposite to the focus.

CT and MRI are the most informative methods for diagnosing SDC of suprahemispheric localization. Hemorrhage is visualized as a “sickle-shaped” area of ​​​​increased density adjacent to the calvarium.

DEG is a decrease in blood flow velocity in the middle cerebral artery on the side of the hematoma.

CSF changes are not very specific; lumbar puncture should be performed with great caution due to the high risk of herniation of the cerebellar tonsils into the foramen magnum, or the temporal lobe into the notch of the tentorium of the cerebellum.

P 10.4 Subdural subtentorial (infratentorial) hemorrhage

(They are rare, more often in full-term babies weighing

over 4000 and post-term)

a) Anomalies of childbirth: (discrepancy between the birth canal and the size of the fetal head, rigid birth canal, etc.), pathological variants of fetal presentation (usually breech), instrumental delivery.

b) Flow options:

• Catastrophic - from the first minutes and hours of life, signs of compression of the brain stem develop: progressive loss of cerebral activity - coma, opisthotonus posture, divergent strabismus, impaired pupillary reactions, floating movements of the eyeballs, fixed gaze. Progression of respiratory and cardiovascular disorders.
• Delayed or subacute-progressive - after a period of relative well-being (lasting from several hours or days, less often weeks), signs of intracranial hypertension (tension of the fontanelles, dehiscence of the nuchal suture, agitation, frequent tonic convulsions) and compression of the brain stem (respiratory and cardiovascular) increase. disorders, oculomotor, bulbar syndrome).

The most common outcome is death.

c) Metabolic disorders that are difficult to correct. Progressive decrease in blood pressure, bradyarrhythmia, anemia.

NSG is a deformation of the fourth ventricle; in some cases, zones of increased echogenicity are identified in the area of ​​the structures of the posterior cranial fossa. Blood clots are detected in the cistern magna of the brain.

CT - allows you to detect extensive hematomas of the posterior cranial fossa, which are visualized as areas of increased density

MRI is the most informative for detecting hematomas of small volume in subacute cases.

CSF - lumbar puncture is not indicated due to the high risk of herniation of the cerebellar tonsils into the foramen magnum.

DEG is not informative.

R 10.2 Intraventricular hemorrhage, traumatic

(rarely encountered, mainly in full-term infants)

a) Prolonged labor, especially in combination with perinatal hypoxia, rapid rotation of the head, forced extraction of the fetus. Coagulopathies.

b) Manifestation - 1-2 days of life (in newborns with trauma and/or asphyxia) in newborns with unclear etiology (in 25%) - sometimes at 2-4 weeks of life.

• Hyperexcitability alternating with depression, convulsions (focal or multifocal), respiratory rhythm disturbances (secondary apnea).
• Progressive intracranial hypertension (vomiting, bulging fontanelle, dehiscence of cranial sutures).
• Hydrocephalus

c) There are no specific metabolic disorders.

NSG - ventriculomegaly, an uneven increase in the echogenicity of the choroid plexuses, deformation of their contours and an increase in size. Determination of echo-positive thrombi in the lumens of the ventricles.

CT, MRI - do not have obvious diagnostic advantages.

DEG is not informative

CSF - pressure is increased, blood admixture is determined in cases of blood penetration into the subarachnoid spaces, protein levels are increased, mixed pleocytosis (see above).

P 10.1 Parenchymal hemorrhage (hemorrhagic infarction)

(They are rare, more often in full-term babies weighing

over 4000 and post-term)

a) Anomalies of childbirth: (discrepancy between the birth canal and the size of the fetal head, rigid birth canal, etc.), pathological variants of fetal presentation, instrumental delivery. (Predisposing factors - hypoxia, foci of ischemia, coagulopathy, vascular malformations, tumors)

b) The clinical picture depends on the location and volume of hemorrhage.

Hemorrhages in the cerebral hemispheres - course:

• Asymptomatic;
• Increasing depression with a gradual loss of cerebral activity, transition to coma, often with focal symptoms (hemisyndromes, focal clonic convulsions),
• Intracranial hypertension (due to perifocal cerebral edema).

Intracerebellar hemorrhages - course

• Asymptomatic (with hemorrhage in the marginal parts of the cerebellar hemisphere);
• Increasing intracranial hypertension (tension of the fontanelles, dehiscence of the nuchal suture, agitation, frequent tonic convulsions).
• Compression of the brainstem (respiratory and cardiovascular disorders, oculomotor, bulbar syndrome) - with massive hemorrhages in the cerebellar hemispheres.

c) Metabolic disorders are not specific.

NSG - asymmetric hyperechoic areas of different size and location in the cerebral hemispheres; with a massive hematoma - signs of compression of the homolateral ventricle and displacement of the interhemispheric fissure. In the cerebellar hemispheres, hyperechoic foci are visualized (with significant intracerebellar hemorrhages).

CT and MRI are more informative for identifying parenchymal hematomas of various locations and sizes (especially subcortical and small ones).

DEG is not very informative in the acute period; later there are signs of cerebral hypoperfusion.

R 10.3 Traumatic subarachnoid hemorrhage

(rarely found, predominantly in full-term infants)

a) Anomalies of childbirth: (discrepancy between the birth canal and the size of the fetal head, rapid labor, rigid birth canal, etc.), pathological variants of fetal presentation, instrumental delivery, combined in 25% of cases with linear and depressed skull fractures. (Predisposing factors - hypoxia, coagulopathies, vascular malformations, tumors)

b) During the first 12 hours of life, depression of cerebral activity increases, up to coma. In some cases, a “waking” coma is observed: the eyes are wide open, a piercing cerebral scream, a decortication posture (flexion of the arms, extension of the legs).

• Hyperesthesia;
• Hyperexcitability;
• Rapidly growing external hydrocephalus (dehiscence of cranial sutures, bulging fontanelles);
• Generalized convulsions (occurring in the first hours of life).

c) Metabolic disorders are not specific. Posthemorrhagic anemia, blood pressure is reduced (vascular shock) in the first hours, subsequently uncontrolled systemic arterial hypertension.

NSG - possible increase in the echo density of the subcortical white matter on the side of the hemorrhage, expansion of the interhemispheric fissure and/or Sylvian fissure of the basal subarachnoid spaces. Subsequently, a progressive expansion of the convexital subarachnoid spaces is noted.

CT scan shows an increase in the density of the subarachnoid spaces, with their subsequent expansion.

MRI is not very informative in the acute period.

DEG is not very informative in the acute period; later there are signs of cerebral hypoperfusion.

CSF - high pressure, hemorrhagic cerebrospinal fluid, often reactive pleocytosis, elevated protein levels, by 3-6 days the macrophage reaction is pronounced.

II. B) Birth injury of the spinal cord

R 11.5 Hemorrhage into the spinal cord

(sprain, rupture, tear with or without spinal injury)

(rare, about 1% and mainly in full-term babies)

a) Anomalies of fetal presentation (gluteal and leg), incorrect implementation of obstetric aids (for example, excessive lateral traction or rotation of the body with a fixed head). Predisposing factors are hypoxia, coagulopathies, vascular malformations.

b) Three options for the clinical course:

• Catastrophic - stillbirth or death in the first hours after birth due to progressive respiratory and cardiovascular disorders. Observed at the craniospinal level of damage.
• Severe - accompanied by a picture of spinal shock lasting from several days to several weeks (adynamia, areflexia, atony), the abdomen is swollen, intestinal paresis, “paradoxical” diaphragmatic breathing, atony of the anal sphincter and bladder muscles, lack of pain sensitivity below the level of the lesion. Sometimes - Claude Bernard-Horner syndrome. Reflex reactions and sensitivity in the face and head are preserved.

The progression of respiratory failure often leads to death in the neonatal period. It is observed with damage to the middle and lower cervical, upper thoracic parts of the spinal cord.

• Moderately severe - the clinical picture of spinal shock is more short-lived, motor and reflex disorders are less pronounced.

c) Metabolic disorders characteristic of severe respiratory failure. Decreased systemic blood pressure, bradycardia, hypothermia.

NSG is not very informative.

CT, MRI - allow you to visualize the area and nature of the damage (MRI is more preferable).

ENMG - signs of denervation of skeletal muscles at the level of the lesion.

CSF - with hemorrhage, tears, ruptures - the cerebrospinal fluid is hemorrhagic, with ischemia - there may be an increase in protein levels.

II. B) P 14 Birth injury of the peripheral nervous system

Frequency of occurrence 0.1%, mainly in full-term infants

a) Incorrect implementation of obstetric care provided when it is difficult to remove the shoulders and head, or when the fetus’s arms are thrown back.

Traumatic injuries of the brachial plexus

b) P 14.0 Proximal (upper) Erb-Duchenne type

Flaccid paresis of the proximal arm: the arm is brought to the body, extended in all joints, the forearm is pronated, the hand is in palmar flexion, the head is tilted towards the sore shoulder, movements in the shoulder and elbow joints are limited, there is no reflex from the biceps brachii muscle, pain and tactile sensitivity reduced.

In approximately 5% of cases it is combined with paresis of the phrenic nerve.

P 14.1 Distal (lower) Dejerine-Klumpke type

Flaccid paresis of the distal arm: the arm is extended in all joints, lies along the body, pronated, the hand hangs passively. There are no spontaneous movements in the elbow and wrist joints, and movements in the fingers are limited. The grasping and palmo-oral reflexes on the affected side are not evoked. Often trophic disorders (edema, cyanosis, etc.). Sometimes this damage is accompanied by Claude Bernard-Horner syndrome on the affected side.

R 14.3 Total type (paresis of the brachial plexus).

Spontaneous movements in all parts of the arm are completely absent, diffuse muscle hypotonia, areflexia, impaired all types of sensitivity, trophic disorders. Often combined with Claude Bernard-Horner syndrome on the affected side.

c) There are no characteristic metabolic disorders.

NSG, CT, MRI, DEG are not informative.

CSF is not informative

ENMG - spontaneous bioelectrical activity in rest mode is absent; with active muscle effort, an interference type of curve is recorded with a reduced amplitude of oscillations in paretic muscles.

R 14.2 Traumatic injuries of the phrenic nerves

In 80-90% of cases it is combined with traumatic injuries of the brachial plexus

(total and proximal type), isolated paresis is extremely rare.

b) Unilateral paresis is clinically practically asymptomatic or with minimal manifestations of respiratory failure.

Bilateral paresis of the diaphragm leads to severe respiratory disorders from the first hours of life, which requires respiratory support in some cases.

c) Metabolic disorders characteristic of respiratory failure.

Ultrasound, chest X-ray - high standing and low mobility (relaxation) of the dome of the diaphragm on the affected side/sides.

R 11.3 Traumatic injury to the facial nerve

a) Abnormal presentation of the fetus, operative delivery - incorrect application of abdominal and exit obstetric forceps.

b) On the losing side:

• Lagophthalmos;
• Smoothness of the nasolabial fold;
• When screaming, the mouth is pulled to the healthy side, the search reflex is weakened.

c) NSG, CT, MRI are not informative.

ENMG - reveals a decrease in conductivity along the facial nerve.

R 14.8 Traumatic injuries to other peripheral nerves

(rare)

a) Anomalies of fetal presentation (breech and leg presentation), improper implementation of obstetric care. In the postnatal period - as a rule, of iatrogenic origin or of a secondary nature (inflammatory and traumatic changes in the bones and joints of the extremities).

b) Damage to the nerves of the extremities is clinically manifested by impaired movements and muscle tone in the corresponding areas of innervation: ulnar, radial, sciatic, obturator and tibial nerves.

c) If symptoms characteristic of damage to a particular peripheral nerve are identified, it is necessary to conduct a comprehensive examination to exclude traumatic and purulent-inflammatory processes in the bones, joints and soft tissues.

Continued >>

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Diagnostics:

It is necessary to conduct an ultrasound examination of the fetus, use cardiotocography (recording of the fetal cardiac activity) and Dopplerometry (study of the blood flow of the vessels of the uterus and umbilical cord of the fetus) with the frequency prescribed by the attending physician. Auscultation (listening) of the fetal heartbeat with a stethoscope is also used. It should be noted that not every pregnancy occurs against the background of the above diseases, complicating intrauterine fetal hypoxia. To prevent the possible occurrence of hypoxia, special attention is paid to its prevention: long walks in the fresh air, mandatory dosed physical activity (gymnastics, exercises, exercises for pregnant women and breathing exercises, swimming, yoga). It is possible to use hyperbaric oxygen therapy (HBO) as prescribed by the attending physician. It must be remembered that treatment must be prescribed by a gynecologist, be comprehensive and take into account an individual approach to each expectant mother.

Our help

Specialists from the Department of Developmental Neurobiology of the Research Institute of Pediatrics and Health Protection of the Central Clinical Hospital of the Russian Academy of Sciences work on the basis of the CDC:

• Diagnosis, observation and treatment are carried out by experienced neurologists, candidates of medical sciences with 20 years of experience working with this problem. Our specialists are the authors of the book “Modern neurobiological aspects of perinatal lesions of the central nervous system”, published by the publishing house of the Russian Academy of Sciences.
• Defectologists and clinical psychologists are involved in the diagnosis, who help clarify the presence of developmental disorders. Development assessment is carried out using unified development tables.
• If necessary, children can receive specialized therapeutic, correctional, developmental classes with early development specialists, aimed at stimulating sensory, visual, auditory, tactile, and coordination functions.
• There is the possibility of comprehensive monitoring of children with perinatal damage to the central nervous system with the involvement of qualified specialists, candidates of medical sciences.
• Accompaniment by an experienced pediatrician who will answer all questions about care, nutrition, prevention of rickets and ARVI, and hardening.
• Vaccine prevention department: consultation with a vaccinologist-immunologist in order to draw up an individual vaccination calendar and direct vaccination under his supervision.
• Involvement of any other pediatric specialists, including orthopedists and ophthalmologists.

Early symptoms that should be addressed to a pediatric neurologist

- sluggish breastfeeding, choking during feeding, leakage of milk through the baby's nose - weak cry of the child, nasal or hoarse voice - frequent regurgitation and insufficient weight gain - decreased motor activity of the child, drowsiness, lethargy or severe anxiety - trembling of the chin, upper and/or or lower extremities, frequent startlings - difficulty falling asleep, frequent awakenings during sleep - throwing back the head - slowing or rapid increase in head circumference - low (flabby muscles) or high tone of the muscles of the limbs and torso - decreased activity of movements of the arm or leg on any side , limited hip separation or the presence of a “frog” position with pronounced hip separation, unusual position of the child - strabismus, torticollis - birth of a child by caesarean section, in breech presentation, with an anomaly of labor or with the use of obstetric forceps, extrusion, with the umbilical cord entwined around the neck - prematurity of the child - presence of convulsions during childbirth or in the postpartum period

Signs of hypoxia. Apgar score

The baby's condition is assessed immediately after birth, in the first minute and 5 minutes later. For this purpose, a scale developed by Virginia Apgar is used, taking into account and summing up the following indicators, each of which is scored from 0 to 2 points:

• skin coloring;
• breathing rate;
• reflex activity;
• heart rate;
• muscle tone.

Based on the score obtained, the absence or presence of hypoxia and its degree are determined:

• norm – number of points 8-10;
• mild hypoxia – 6-7 points;
• moderate hypoxia – 4-5 points;
• severe hypoxia – 0-3 points.

Mild hypoxia is detected in almost all newborns in the first minute of life and disappears within 5 minutes on its own.

Moderate hypoxia in a newborn requires certain treatment; the child’s condition returns to normal after a few days. In case of severe hypoxia or asphyxia, immediate resuscitation measures are carried out, complex treatment and further monitoring of the child are prescribed.

The clinical picture of neonatal hypoxia is usually pronounced and the diagnosis is established immediately after the birth of the child. Signs of this condition include tachycardia, with gradual replacement by bradycardia (less than 100 beats per minute), irregular heartbeat, auscultation of heart murmurs, pallor of the skin and cyanosis of the nasolabial triangle and extremities.

Irregular breathing or its absence is noted, motor activity is reduced or absent (the child is lethargic or does not move), and the presence of meconium (green water) in the amniotic fluid. Blood clotting rates increase, which leads to thrombosis in the vessels and hemorrhage in the tissue.

Subsequently, if hypoxia was missed in the first minutes of the child’s life, the following signs are added:

• constant drowsiness;
• restless sleep, trembling;
• marbled skin tone of the extremities;
• the child freezes quickly (when bathing, changing clothes);
• restless, capricious behavior, causeless crying;
• trembling of the facial muscles while crying or at rest.

Hypoxic encephalopathy

Hypoxia in a newborn leads to the development of hypoxic encephalopathy (brain damage), which is divided into degrees of severity:

mild – drowsiness or agitation of the newborn, disappearing after 5-7 days;

moderate - in addition to drowsiness and/or agitation, there is crying for no reason, convulsions, aversion to being carried, rapid freezing;

severe - severe drowsiness and lethargy, development of psychomotor agitation or coma with ongoing convulsions.

Late symptoms of birth trauma

There are cases when at birth a baby has minimal impairments, but years later, under the influence of certain stresses - physical, mental, emotional - neurological impairments manifest themselves with varying degrees of severity. These are the so-called late manifestations of birth trauma. Among them: - decreased muscle tone (flexibility), which is so often an additional advantage when playing sports. Often such children are gladly accepted into sports and rhythmic gymnastics sections and choreographic clubs. But most of them cannot stand the physical activity that takes place in these sections. - decreased visual acuity, the presence of asymmetry of the shoulder girdle, angles of the shoulder blades, curvature of the spine, stoop - signs of a possible birth injury of the cervical spine - headaches, dizziness

If you have the above complaints, do not delay your visit to a pediatric neurologist! The specialist will prescribe certain examinations, a course of treatment and will definitely help you!

Symptoms

The depression syndrome is manifested by the main symptoms: lethargy, physical inactivity, sluggish sucking, hyporeflexia, suppressed reflexes of newborns, decreased swallowing reflex.

The syndrome of depression in newborns can be combined with excitement up to the development of convulsions, strabismus, nystagmus and drooping of the lower jaw, asymmetry of the facial muscles, sometimes bulbar (impaired pronunciation of sounds, swallowing due to paresis of the muscles of the pharynx, soft palate and tongue), pseudobulbar (appearance of violent crying, laughing) syndrome.

Often, CNS depression syndrome in newborns is accompanied by lethargy, decreased emotional tone and decreased response to pain; in extreme cases, a coma state can form. CNS depression syndrome is a common reason why parents turn to a neurologist for specialized help.

The depression syndrome can be corrected by physiotherapy and massage.

Symptoms depend on the severity of the disease, mild depression syndrome can be hidden and parents very often do not notice the slight lethargy of the baby in

his daily behavior. In moderate cases, the syndrome of central nervous system depression is usually manifested by symptoms of muscle hypotonia, hyporeflexia, which can be replaced by muscle hypertonicity, and sometimes convulsions, anxiety and hyperesthesia may appear.

CNS depression syndrome in newborns may also accompany vegetative-visceral disorders. Severe central nervous system depression syndrome is manifested by convulsions, intestinal paresis, respiratory disorders, and adrenal hypofunction.