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I
ntroduction. At an international seminar devoted to CCP
(Maryland, USA, 2004), researchers concluded that CCP
is a clinical descriptive term, not an etiologic diagnosis, and
includes a group of developmental disorders and div postures
that limit activity that are caused by non-progressive defeat of the
developing brain of the fetus or child. Attention was drawn to the
fact that motor disorders in cerebral palsy are often accompanied
by sensory defects, changes in cognitive and communicative
functions, perceptual disorders, behavior, and convulsive attacks
[1,9].
The risk factors for the development of epilepsy in children
with cerebral palsy are very diverse and can be both etiologic
and conditionally pathogenetic. First of all, pathogenetic
factors include: short term gestation, infectious diseases during
pregnancy, miscarriage in the mother's history, the threat of
miscarriage during this pregnancy, a violation of the fetoplacental
blood flow, a long duration of the anhydrous period during labor,
low birth weight, prematurity, low scores on the Apgar scale,
history of neonatal revitalization, neonatal respiratory disorders
(respiratory distress), neonatal seizures, neonatal infections,
seizures in the first year of life, defects of the brain development
[11,18,24].
The maximum risk of epilepsy in cerebral palsy provides the
developmental defects of the cerebral cortex (cortical dysplasia).
With their presence, the incidence of epilepsy increases 3.5
times. A somewhat smaller role in the pathogenesis of epilepsy
development plays role neonatal seizures. The severity of motor
disorders and mental underdevelopment increases the risk of
epilepsy in cerebral palsy [3].
An analysis of the literature available to us showed a lack
of classification of epileptic seizures in cerebral palsy. There is
a legitimate question about the nosological evaluation of the
epileptic process in patients with cerebral palsy: symptomatic
epilepsy or epileptic syndrome? According to some authors [5,6],
epileptic syndrome should be attributed to various attacks (specific
and nonspecific) in organic cerebral pathology with pronounced
neurological disorders to emphasize their fundamental difference
from symptomatic epilepsy.
According to Belousova E.D. [3], the classification of seizures
in children with CCP should be carried out in accordance with the
International Classification of Epilepsy and Epileptic Syndromes
(1989), which all seizures are divided into neonatal seizures -
seizures that occur from the first to fourth week of a child's life
and have a different genesis, can both accompany neurological,
somatic and endocrine disorders, and be nosologically
independent epileptic syndrome; febrile convulsions - seizures
in children aged from 3 months to 6 years due to fever, but not a
symptom of neuroinfections (meningitis, encephalitis); epilepsy
and epileptic syndromes - diseases that manifest themselves
spontaneously arising convulsive attacks.
CCP and epilepsy are among the most disabling diseases in
childhood neurology. Despite the frequent occurrence (epilepsy
- 2-3%, children’s cerebral palsy - 1-2% of the children's
population), they still remain hard-to-learn in practical health
care [7]. The combination of these two diseases increases make
worser course and prognosis, which makes this problem urgent
in pediatric neurology.
The existing types of epileptic seizures in cerebral palsy
УДК: 616.853-053.2:616.988.23-025.4-009.12
EPILEPSIA IN CHILDREN WITH CHILDREN'S CEREBRAL
PALSY TO THE QUESTION OF CLASSIFICATION OF
SEIZURES
Madjidova yo.n., abdusattarova g.Sh.
Tashkent Pediatric Medical Institute (Republic of Uzbekistan) Department: Neurology, Pediatric Neurology and Medical
Genetics
Keywords: Children’s cerebral palsy (children’s cerebral palsy), symptomatic epilepsy, classification.
should be reflected in the classification of epileptic seizures
and syndromes (myoclonic seizures, atypical frontal absences,
undifferentiated seizures). Cerebral palsy is a pathology
associated with disrupting the sequence of the ontogenetic
development phases [22]. The starting point of the disturbance
of the phylogenetically conditioned sequence of ontogenetic
development and the common denominator of the action of
various risk factors for the development of cerebral palsy is the
inability to manifest antigravitational locomotor activity in the early
postnatal period [2]. Little's disease, as a nosological unit, exists
more than 100 years. William John Little, a British orthopedic
surgeon, in 1862, first established a causal relationship between
complications during childbirth and a violation of the mental and
physical development of children after birth. His conclusions
were set out in the article «On the impact of pathological and
difficult births, prematurity and asphyxia of newborns on the
mental and physical state of children, especially with respect to
deformities» [23]. William Osler in 1889 for the clinical evaluation
of this pathological condition first used the term «infantile
cerebral palsy» [28]. In 1957, Ronald MacCaith and Paul Polani
defined cerebral palsy as a non-progressive lesion of the brain,
appearing in early years and characterized by a violation of the
movement and position of the div. According to Semenova K.A.
(1980), cerebral palsy is an association of groups of different
clinical manifestations of syndromes that arise as a result of
brain underdevelopment and its damage at various stages of
ontogenesis, leading to the inability to maintain normal posture
and perform arbitrary movements.
The risk of developing seizures and epilepsy is especially high
in children with cerebral palsy [3]. The tendency of epilepsy is 15-
90% of children with this pathology [18]. It has been established
that epilepsy develops more often with spastic forms of cerebral
palsy [826]. Almost half of patients with spastic tetraplegia
suffers from epilepsy (45-65.5%) and spastic hemiplegia (52%);
it is more rare in children with spastic diplegia (32%) [6.29].
According to Belousova E.D. (2004), the form of infantile cerebral
palsy determines one form or another of epilepsy [3]. Half of
patients with spastic hemiplegia have focal seizures, simple and
complex, seizures with secondary generalization; in the other
half, generalized clonic seizures are recorded. It is significant
that the latter prevail in all other forms of cerebral palsy. A high
predisposition to the development of Vest syndrome and Lennox-
Gasto syndrome is observed in patients with spastic tetraplegia
[32]. In most patients with the last debut of seizures observed
in the first year of life. On the contrary, in children with spastic
hemiplegia, the development of epileptic seizures is noted several
years later [15].According to Singhi P., Jagir S., Khandelwal N.,
Malhi P. [31], the mean age of the first epileptic seizure in children
with cerebral palsy is 18.9 months. In turn, as the authors note,
about 60% of children with this disease have developed a seizure
attack in the first year of life. The methods of neuroimaging
(MRI, CT, PET) acquire decisive importance for diagnosis and
prognosis of the severity of the course of both cerebral palsy
and epilepsy in cerebral palsy. The most significant in terms of
informativeness and scope from recent international projects
can be considered the European study of infantile cerebral
palsy, devoted to the analysis of the relationship between clinical
symptoms and MRI data [20]. Children with spastic hemiplegia
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(26.2%), spastic diplegia (34.4%), spastic tetraplegia (18.6%),
dyskinesia (14.4%) and ataxia (3.9%) were examined. In addition
to motor disorders, 28% of children had epilepsy, which was most
common in patients with spastic tetraplegia.
Communicative disorders were registered in 58% of patients,
with maximum frequency they were noted in the group of children
with dyskinesia. The average age of children undergoing MRI
was 38 months. (1-87 months).
Most often (42.5%) revealed White Brain Damage (WBD) as
periventricular leukomalacia and periventricular hemorrhages,
less often - basal ganglia lesions (12.8%), cortical and subcortical
lesions (9.4%), malformations ( 9.1%), focal infarctions (7.4%)
and mixed lesions (7.1%). In 11.7% of cases, an MRI study of
pathological changes in the brain did not reveal.
WBD was most often observed in patients with diplegia
(71.3%), as well as hemiplegia (34.1%) and tetraplegia (25.1%).
It was recorded in more than 80% of children born before 34
weeks pregnancy, but in 25% of cases it was full-term children.
With spastic diplegia, this morphological defect was localized
only in the posterior or in the posterior and middle zones. These
children were often able to walk and had some communication
skills [10,16]. With spastic tetraplegia, WBD captured all the
zones, these patients could not move and had very limited
communication possibilities. The defeat of basal ganglia and
thalamus was mainly associated with dystonic cerebral palsy
(75.6%), single cases were with spastic tetraplegia, diplegia,
and there was not a single patient with hemiplegia. Focal cortical
infarction often led to hemiplegia, in one case tetraplegia was
noted. Cortical and subcortical lesions (multicystic leukemalacia,
etc.) were detected in 33% of children who had all types of
cerebral palsy, except ataxia. The developmental defects of the
brain were detected, mainly in children with hemiplegia [17].
Other types of malformations were represented by lissencephaly,
polymicrogyria, schizencephaly and dysplasia of the cortex. In all
subgroups of cerebral palsy there were mixed variants of brain
lesions (7%); such patients had, as a rule, concomitant pathology
- epilepsy, malformation of internal organs, pathology of vision,
etc. At the same time, 11.7% of the subjects of all MRI scans did
not reveal any cerebral changes, but nevertheless 61% of these
children had moderate and 17% - severe functional disorders,
probably determined by genetic disorders [4].
This study proved the necessity of MRI for all children
with cerebral palsy to determine the time and extent of brain
damage. The frequent defeat of white matter in premature
newborns testifies to the influence of pathological factors on the
development of the brain in the early stages of pregnancy. In
addition, an important conclusion of the study is that obstetric
errors among all causes leading to the development of cerebral
palsy are less than 20% [13,25].
According to Belousova E.D. [3], of all types of brain
damage the most epileptogenic are cortical dysplasias. A similar
study of children suffering from spastic forms of cerebral palsy
was conducted in Poland [19]. It showed the presence of brain
damage in 95.3% of patients. Periventricular leukomalacia was
detected more often in children with spastic diplegia than in
children with tetraplegia and hemiplegia. Cerebral atrophy was
found more often in the group of patients with spastic tetraplegia,
compared with patients with diplegia. Ecephalic cysts were
more often recorded in children with spastic hemiplegia. Also,
congenital brain anomalies (10.7%) were found, represented
by schizencephalus, agenesis of the corpus callosum,
polymicrogyria, haloproencephaly and lissencephaly. As a result
of the obtained data, the etiology and prognosis of epilepsy was
clearly defined [12].
Japanese experts Okumura A., Hayakawa F., Kato T., Kuno
K., [27], after an analysis of 5-year clinical-MRI monitoring,
concluded that patients with congenital malformations of the
brain are characterized by a higher predisposition to epilepsy by
treatment of patients with perinatal cerebral involvement.
EEG studies in cerebral palsy are devoted to an article by
the Spanish authors Zelnik N, Konopnicki M., Bennett-Back O.
etal [30] who studied the random sample of patients with cerebral
palsy. It was concluded that more than 50% of children with
cerebral palsy develop epilepsy and it is always accompanied by
pathological changes in the EEG. The epileptic activity recorded
by the EEG, in their opinion, is usually formed no later than 4
years after the onset of the disease and leads to a deterioration of
intellectual disorders, which, as a rule, existed before. According
to Gururaj A.K. et al. (2003), EEG-study in patients with cerebral
palsy reveals focal epileptiform discharges with secondary
generalization in 39.3% [15].
Some researchers believe that the prognosis of epilepsy
is determined by the form of infantile cerebral palsy [3]. Others
believe that cerebral palsy leads to an increase in the course
of epilepsy and its pharmacological resistance, and the epileptic
process, in turn, aggravates motor and intellectual disorders in
this group of patients [14].
Difficulty of epilepsy in cerebral palsy reaches 51.2%, control
of seizures can be achieved with spastic tetraplegia in more than
60% of cases, spastic hemiplegia - 72.7%, spastic diplegia - in
83.3% of cases.
Polytherapy is more often used in cases of spastic tetraplegia
- 59.5% [18]. Remission of the course of the epileptic process,
according to Zafeiriou D.J. etal. [29] can be achieved in 75.3%
of cases with cerebral palsy, when the period free from seizures
is three years or more. Complete control of seizures is possible
in 65.2% of cases, and approximately 25% of patients are forced
to receive antiepileptic drugs for a considerable time. Long-term
therapy, they say, is necessary for patients prone to pharmaco-
resistant attacks and status epilepticus. Control over convulsive
attacks in cerebral palsy can be achieved in 75% of patients
at normal and borderline intellectual level and in 50% - with a
reduced level of intelligence. In addition, there is a positive
correlation between the age of onset of convulsive seizures and
the effectiveness of control over them.
Kwong K.L., Wong S.N. [21].Kwong K.L. etal. give the
following list of factors that determine a period free from seizures
from one or more years in children with epilepsy in cerebral palsy:
normal and subnormal intellectual development; rare (isolated)
convulsive attacks with late onset; monotherapy; spasticdiaplegia
[21].Factors for the adverse prognosis of epilepsy in children
with cerebral palsy include spasmodic tetraplegia, neonatal
convulsions in the anamnesis, the onset of epileptic seizures
before the age of 1 year, infantile spasms and complex partial
seizures with secondary generalization.
Thus, the types of epileptic seizures in cerebral palsy have
not been fully reflected in the current classification of epileptic
seizures and syndromes. In particular, the undifferentiated
paroxysms, myoclonic seizures, atypical frontal absences, which
require discussion of the need to correct the currently used
classification of the types of epileptic seizures in cerebral palsy,
are not taken into account.
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