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K.A. Semyonova, M.D., Prof., Honored Scientist of R.S.F.S.R.


The notion "perinatal encephalopathy" combines etiologically different brain lesions as well as those of uncertain origin that occurred in the perinatal period of life.

The already known causes of perinatal encephalopathy include various viral, bacterial infections that can, as is well known now, affect the fetus brain; toxins and heavy metals. Avitaminoses, stress reactions, therapeutic intoxications, etc. can be classified among triggering mechanisms.

The problem is further complicated by the fact that repeated intrauterine hypoxia may be caused by any adverse influence on the brain and, what is very essential for the disease forecast assessment, by dysontogenetic phenomena. The process that developed intrauterinely as a result of an infectious or some other lesion is also progressing because the impairment of single brain structures which have already significantly matured in this developmental stage delays and disturbs the maturation of those structures that are functionally connected with the former and prevents their further age development.

Thus, a pathologic chain is formed from one brain developmental phase to another; this pathologic chain finds its expression in the clinical picture of the disease, yet it is typically impossible to trace its initial link.

The analysis is also complicated by the fact that the process entailing the deformation and decay of nerve cells, be it inflammation caused by infectious agents, intoxication and so on, may end within the uterus does not preclude the possibility that the process in question and its consequences may occur in the postnatal life period.

Thus, nonspecific autoimmune inflammation may give rise to a specific inflammatory process of this or that etiology that, coupled with hypoxia and cerebral circulation impairment developing on the basis of the inflammation, may affect not only the severe clinical picture in the infant but also that for years to come (Yu.M. Zhabotinsky and V.I. Yoffe, 1975; K.A. Semyonova, N.M. Makhmudova, 1979; S.F. Semyonov, K.A. Semyonova, 1984; A.S. Semyonov, 1983; V.M. Yevtushenko, 1992, et al.).

Complex immune system disorders identified in children with perinatal encephalopathy examined below, such as first ICP manifestations in patients born from mothers who suffered from diverse infectious diseases prior or during pregnancy - cytomegalia, herpes, influenza and other diseases - as well as from mothers who had various hazards in pregnancy - give reasons not to consider ICP only as a residual disease. It seems likely that current processes, first of all, autoimmune nonspecific inflammations, may occur along with residual phenomena caused by mechanical birth injures.

This circumstance causes us to carefully analyze the mother's and father's medical history and monitor the child's disease dynamics not only over the early developmental period but over a number of years as well. Hence, a program of therapeutic restoration should be based on the mentioned dynamic observation.

An evaluation of the infant's condition in the first weeks of life can provide important data on the state of its organism and the severity of perinatal encephalopathy.

Currently, perinatal encephalopathy is subdivided, as recommended by Yu. Yakunin et al. (1976), into hypoxic, traumatic (mechanical injury at birth), infectious and metabolic related to intoxications, endocrine and hormonal stress effects, autoimmune conflicts. At the same time, the authors single out both unaccounted for and unclassifiable factors. Nevertheless, therapeutic procedures prescribed in infants who are diagnosed this way or another are practically uniform: drug therapy, including vitamins, nootropic drugs, mydocalm, occasionally, ATP, massage and some light physiotherapeutic procedures.

Dehydration and anticonvulsive therapy are conducted in the presence of a hypertensive or spasmodic syndrome, even irrespective of assumed etiologic factor or factors.

According to diverse statistic data, a clear-cut picture of infantile cerebral palsy is formed by the 6th-10th month in 6-10% of children who sustained perinatal encephalopathy. The incidence of this disease can be judged by the fact that while in 1964 the average share of ICP patients was 0.64 per 1,000 of the child population, so in 1989 this share accounted for 5.6-8.9 per 1,000 of the child population.

Perinatal encephalopathy can be manifested by oligophrenia, hydrocephaly, many genetic diseases, etc.

The child's clinical examination should be preceded by an in-depth analysis of the medical history of pregnancy and birth as well as the child's assessment at birth.

The main clinical syndromes of perinatal encephalopathy are the following: general suppression syndrome, or the so-called neoreflex excitability syndrome; hypertensive, convulsive syndrome and motor-reflex disturbance syndrome, including pathology of congenital motor reflexes and muscle tonicity disturbances. Later, towards the 2nd-6th-8th month are analyzed, pre-speech development, sequentially its 1st-2nd-3rd and 4th periods, orienting, visual and auditory reactions, presence of the cognitive component in the above reactions, development of mimic adequate reactions, gradual formation of normal stage-by-stage mental development.

A complex of the listed pathologic syndromes that are manifested with varying intensity in the first months of life and ensuing pathology of mental and speech development can be observed in children with perinatal encephalopathy. Retardation of mental and speech development can be considered as the most prognostically relevant factors in the formation of subsequent infantile cerebral palsy.

The latter syndrome is manifested by this or that degree of muscle tone disturbance and congenital motor reflexes. Healthy infants of the first months of life when they are in the dorsal position have a moderately increased tone of the flexors of upper and lower limbs. From the 2nd-3rd months of life on, the child tries to raise and keep raised the head from the dorsal and prone position. This is due to the fact that he is forming a labyrinthine righting reflex.

In children with manifest perinatal encephalopathy (PE) this reflex is not formed or else it is much weaker. In the prone position of such children the defense reflex is weak or absent: the infant does not turn his head to free the mouth or nose for breathing.

The intensity of the grasp reflex is increased and, the main thing, it is not extinguished after 2-3 months of life.

The neck asymmetric tonic reflex and the neck symmetric tonic reflex are either poorly marked or absent in healthy children.

In children with progressing PE symptomatology, the labyrinthine tonic and neck asymmetric and symmetric tonic reflexes increase forming pathologic muscular synergies that result in motor disability of children towards 2-3 years and even earlier if the course of disease is severe. The tonicity of the flexors of both upper and lower limbs increases under the influence of the labyrinthine tonic reflex in children in the dorsal position. The same muscular tone pathology occurs in the vertical body position by stimulating a triple flexion in lower limbs, that is, flexing righting as well as contractures in hip, knee and ankle joints; under the effect of the labyrinthine tonic reflex the tonicity of the extensors of lower and upper limbs of the child in the dorsal position is increased; the tongue is adducted to the root, speech development is essentially impaired.

The influence of the neck symmetric tonic reflex is different: the tone of the extensors and adductors of lower limbs of the child in a vertical position with his head dropped to the chest increases forming a "ballerina's pose" described by Little and characteristic of spastic diplegia, the commonest ICP form. On the contrary, if the head is dropped backwards, then the tone of the flexors of lower limbs and extensors of upper limbs increases.

Under the influence of the neck asymmetric tonic reflex and if the child's head is turned sideways, the hand towards which the face is turned is extended in all joints; inversely, the hand facing the neck is bent in all joints forming a "fencer's pose".

All the three reflexes that are absent in the child already in 2-3 months of life grow in children with PE which is one of the main ICP prognostic symptoms, especially, if retardation and pathology of pre-speech and later of mental development are observed.

The whole complex of the above-mentioned syndromes in children with PE is particularly clearly identified if pathology was recorded in the ECHO-EG which points to the presence of a hypertensive syndrome and, more importantly, if there was an EEG shift by more than 2 mm which are indicative of atrophic processes in brain tissues, most frequently, of hemiatrophy; furthermore, the whole complex of the above syndromes is manifestable in case of pathology in neurosonography - encephalomalacia in sub-ependymal spaces; in pathology of vascular plexuses (most frequently, hemorrhages in the ventricular region of ventricle); in atrophies that can be most frequently detected in the region of the frontal and temporal lobes, cysts in the substance of the large hemispheres, displasias, more frequently, of the cerebellum, etc. It should be stressed, however, that in the majority of cases, even in clearly marked ECHO-EG and neurosonography changes, a stabilization of the process can be brought about p

Encephalography recordings in children of the first 2-4 months of life are made rarely and in children under 2 months still more rarely. Nevertheless, despite the difficulties associated with its performance, the EEG provides information that is essentially relevant for the assessment of the true condition of the child's CNS and of the prognosis. EEG recordings make it possible to judge on the following: degree of age-linked brain development retardation; presence of interhemispheric asymmetries; disturbance of zonal distribution of bioelectric activity that indicate particularities of the state of different regions of the large hemispheres which is also substantiated by the pathology of own bioelectric activity in these regions and, finally, the presence of epiactivity on the EEG, including its foci in different areas of the brain.

Convulsive attacks differing in their manifestations form part of the complex of syndromes characteristic of PE. They may occur already in the first hours and days of the child's life. In this age period they are typically clonic and spread to mimic facial musculature, muscles of upper limbs and, more rarely, those of lower limbs.

Spasms in the infant may be a result of marginal encephalitis produced by intrauterine neuroinfection; a result of hypoglycemia originated by the destruction of the endothelium of the ventricles producing glycogen in the first months of intrauterine life; a result of other metabolic disorders, sicatricial processes in the brain membranes and medullary substance, etc.

In all these instances anticonvulsive therapies, including luminal that is generally administered do not produce the desired effect. Meanwhile, every convulsive seizure is known to sharply inhibit further motor and, especially, mental development of the child. This is the reason why the most detailed possible clinical, neurophysiologic and biochemical examination of children with PE complicated by a convulsive syndrome may help conduct adequate anticonvulsive therapy, that is, antiinflammatory treatment, handle disturbances of metabolic and autoimmune processes which noticeably contribute to spasmodic activity.

The hypertensive syndrome recorded, according to diverse statistical data, in 50-75% of children with PE severely impairs motor, mental and pre-speech development. Clinically, it is displayed by the well-known Graefe's syndrome, a disjunction of cranial bone sutures and dilatation of the large and, in severe cases, small fontanels which dilatation does not reach big sizes in those children who subsequently develop ICP as opposed to children developing hydrocephaly, whose scull circumference can exceed 50-60 cm already in the first 2-5 months.

Dehydration therapy falls far short of being successful because the formation of both the hypertensive and convulsive syndromes is a function of many causes, whereas dehydration therapy is symptomatic.

Present-day biochemical studies give reasons to look forward to a successful search for a pathogenetically meaningful anticonvulsive and dehydration therapy, but so far it has been symptomatic.

Cerebral hypotrophy observed in 60-70% of children with PE, especially, of premature ones is a syndrome that resists all forms of therapeutic recovery. Insufficiency of the body mass and growth of the child at birth remains not only in the first weeks and months of life, but also, non infrequently, in the following years of his life. Growth and body mass deficiency may be concomitant with cardiovascular insufficiency and very often with respiratory and digestive insufficiency. This entire complex of functional and morphofunctional deficiency may seriously inhibit the formation of the nervous system due mainly to chronic hypoxia, hemopoiesis, nutrition disturbances, etc.

Now, we would like to discuss those children with PE who subsequently will develop the hyperkinetic form of ICP since the latter may be diagnosed in a late stage, whereas initially it was considered to be a "flabby child" manifestation; only when hyperkineses are clearly manifested towards 1.5-2 days, an accurate diagnosis is made and it is proceeded to adequate treatment. Meanwhile, hyperkineses can be detected much more earlier, beginning with 4-6 months of life, in the lingual muscles, Typically, these are "back and forth" kineses that imitate the sucking act. In similar cases the tongue may often and later permanently, protrude beyond the lower tip. Only later on, it expands to mimic musculature and muscles of upper extremities. Most frequently, choreoathetosis-type hyperkinesis is noted. Temple-Fay remedial gymnastics, cycladol, ridinol when used in similar cases, are in a position to inhibit and extinguish the intensity of the developing hyperkinetic form of ICP.

Perinatal encephalopathy may also be the first syndrome of oligophrenia. Infants of several weeks of life may lack orienting visual and auditory reactions while retaining visual unconditioned reflexes and simplest sound reactions. They lack adequate mimic reactions, the complex of livening up when communicating with adults, reactions to moving objects or adults' faces; they also lack differentiated voice reactions. The sounds they utter are monotonous, modulations are absent. The child does not try to catch bright or sounding toys. In these children motor development also turns out to be retarded, but in another way compared with children in whom ICP will be diagnosed in the future. They do not develop any pronounced increase in tonic reflexes, nor do they form pathologic muscular synergies; yet, all the motor development phases prove to be delayed by this or that period or time - from 6-8 months to 1-1.5 years. In this case all of the child's movements are awkward and indicative of "m

Later on, the latter may turn into heightened motor activity and the ability to perform a lot of movements: climbing, running, etc., which even healthy people are unable of. At the age of 1-2 years and more pre-speech and speech retardation will come to the fore and will determine the basic diagnosis, oligophrenia.

In children with ICP (following mental and speech retardation due to limited sensory-visual and auditory-afferentation - 15-20% of children suffer from phonemic hearing impairment - afferentation being proprioceptive in children with pathologic motility and socially neglected children) oligophrenia much more frequently is not truly primary, it is secondary and may occur in children with primarily intact intelligence.

Accordingly, a careful analysis of the medical history of the mother's pregnancy period, a detailed clinical examination and, where possible, a number of laboratory tests enabling an approach to pathogenic therapy are required to carry out adequate recovery therapy in children with PE.

But at present, this remaines a very difficult problem, which is demonstrated by the fact that mentally and neurologically impaired patients account for 85% of those who are handicapped since childhood.

REFERENCES (in Russian):

Zhabotinsky, Yu.M.; Yoffe, V.I. Experimental and allergic demyelinating diseases of the nervous system. L., 1975.

Semyonova, K.A.; Makhmudova, N.M. Medicinal rehabilitation and social adaptation of infantile cerebral palsy patients. Tashkent, 1979.

Semyonov, A.S. Impairment of the immunocompetent system in congenital cerebral lesions. Ph.D. (Med.) thesis. M., 1983.

Semyonov, S.F.; Semyonova, K.A. Immunobiologic principles of the pathogenesis of nervous and mental diseases. Tashkent, 1984.

Yakunin, Yu.A.; Yampolskaya; Kipnis, S.L.; Sysoyeva, I.M. Nervous system diseases in neonates and infants of early age. M., 1979.

Yevtushenko, S.K. Neurogenic immunodeficiency due to cerebral pathology and neurohormonal supply insufficiency. Collection of theses "New technologies in the rehabilitation of infantile cerebral palsy". Donetsk, 1994, p 183.

Yevtushenko, S.K.; Yevtushenko, O.S. On new views on the pathogenesis of infantile cerebral palsy. Journ. "Clinical and Experimental Medicine Archives", vol. 11, # 2, 1993.

Lisyanyi, V.I.; Tsimbalyuk, S.A.; Yavorskaya, O.V. et al. Peculiarities of the immune status in patients with different forms of infantile cerebral palsy. Collection "Managerial and clinical problems of child neurology and psychiatry", Samara, 1993, p. 162.