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MINISTRY OF HEALTH OF UKRAINE
BUKOVYNIAN STATE MEDICAL UNIVERSITY
“Approved”
on the methodical meeting
of the Department of neurology, psychiatry
and medical psychology nm. S.M.Savenko
“____” ___________ 2009 (Report № __).
Chief of the Department
_______________________
Professor V.M. Pashkovsky
METHODICAL INSTRUCTION
for 4-th year students of medical faculty №2
(the speciality “medical affair”)
for independent work during preparing to practical class
Theme 29: EARLY CHILD’S AUTISM. ETIOLOGY AND
EPIDEMIOLOGY.
CLINICAL
DISPLAYS.
DIAGNOSTICS.
TREATMENT. PROPHYLAXIS. QUESTION OF EXAMINATION AND
REHABILITATION. CHILDREN AND TEENAGERS HYPERKINETIC
DISORDERS. ETIOLOGY. PATHOGENESIS. CLINICAL DISPLAYS.
DISORDERS OF SOCIAL CONDUCT. CLINIC, RAN ACROSS,
PROPHYLAXIS.
PRINCIPLES
OF
MEDICAL-PEDAGOGIC
CORRECTION AND SOCIAL REHABILITATION.
MODULE 2. SPECIAL (NOSOLOGY) PSYCHIATRY
TOPICAL MODULE 6. DISORDERS OF ADULT PERSONALITY AND
BEHAVIOUR. MENTAL RETARDATION. DISORDERS OF PSYCHOLOGICAL
DEVELOPMENT. BEHAVIOURAL AND EMOTIONAL DISORDERS WITH ONSET
USUALLY OCCURRING IN CHILDHOOD AND ADOLESCENCE.
Сhernivtsi, 2009
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1. ACTUALITY OF THEME:
Autism is a brain development disorder characterized by impaired social interaction and
communication, and by restricted and repetitive behavior. These signs all begin before a child is
three years old. The autism spectrum disorders (ASD) also include related conditions such as
Asperger syndrome that have milder signs and symptoms.
Autism has a strong genetic basis, although the genetics of autism are complex and it is
unclear whether ASD is explained more by multigene interactions or by rare mutations. In rare
cases, autism is strongly associated with agents that cause birth defects. Other proposed causes,
such as childhood vaccines, are controversial, and the vaccine hypotheses lack any convincing
scientific evidence. The prevalence of ASD is about 6 per 1,000 people, with about four times as
many males as females. The number of people known to have autism has increased dramatically
since the 1980s, partly due to changes in diagnostic practice; the question of whether actual
prevalence has increased is unresolved.
Autism affects many parts of the brain; how this occurs is not understood. Parents usually
notice signs in the first two years of their child’s life. Although early behavioral or cognitive
intervention can help children gain self-care, social, and communication skills, there is no known
cure. Not many children with autism live independently after reaching adulthood, though some
become successful, and an autistic culture has developed, with some seeking a cure and others
believing that autism is a condition rather than a disorder.
Attention-deficit/hyperactivity disorder (AD/HD or ADHD) is a neurobehavioral
developmental disorder. It affects about 3 to 5% of children with symptoms starting before seven
years of age. Global prevalence for children is approximately 5%, with wide variability
dependent on research methodologies utilized in studies. It is characterized by a persistent
pattern of impulsiveness and inattention, with or without a component of hyperactivity. ADHD is
twice as common in boys as in girls, though studies suggest this discrepancy may be due to
subjective bias. ADHD is generally a chronic disorder with 30 to 50% of individuals diagnosed
in childhood continuing to have symptoms into adulthood. As they mature, adolescents and
adults with ADHD are likely to develop coping mechanisms to compensate for their impairment.
2. DURATION OF PRACTICAL CLASSES - 2 HOURS.
3. EDUCATIONAL PURPOSE
3.1. To know:
1. Etiology and pathogenesis of child’s autism and hyperkinetic disorders.
2. Clinical picture of child’s autism.
3. Clinical picture of hyperkinetic disorders.
4. Clinical picture of disorders of social conduct.
5. Diagnostic of child’s autism and hyperkinetic disorders.
6. Treatment of patients with child’s autism and hyperkinetic disorders.
7. Prophylactic of child’s autism and hyperkinetic disorders.
8. Principles of medical-pedagogic correction and social rehabilitation.
3.2. Able:
1.To diagnose child’s autism, hyperkinetic disorders and disorders of social conduct.
3.To conduct differential diagnosis.
4.To conduct measures of prophylactic of child’s autism and hyperkinetic disorders.
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3.3. To capture practical skills:
1. To collect anamnesis in patients with child’s autism and hyperkinetic disorders.
2. Clinical psychological examination of children with child’s autism and hyperkinetic
disorders.
3. To conduct psychoprophylactic measures of child’s autism and hyperkinetic
disorders.
4. INTERSUBJECT INTEGRATION (base level of preparation).
Names of previous disciplines
1. Medical genetic.
2. Normal and pathologic physiology.
3. Anatomy
4. Medical psychology
Skills are got
1.To possess of methods reaviling genetic diseases of
human.
2. To know functions of brain, physiology and
pathological physiology HNA.
3. To know structure of brain
4. To know psychology of personality.
5. ADVICES TO STUDENTS.
5.1. CONTENTS OF THEME.
Autism is a highly variable brain development disorder that first appears during infancy
or childhood, and generally follows a steady course without remission. Symptoms tend to
continue through adulthood, although often in more muted form. It is distinguished not by a
single symptom, but by a characteristic triad of symptoms: impairments in social interaction;
impairments in communication; and restricted interests and repetitive behavior. Other aspects,
such as atypical eating, are also common but are not essential for diagnosis. Autism is one of
three related autism spectrum disorders. Its individual symptoms occur in the general population
and appear not to associate highly, without a sharp line separating pathologically severe from
common traits.
Social development
Social deficits distinguish ASD from other developmental disorders. People with autism have
social impairments and often lack the intuition about others that many people take for granted.
Noted autistic Temple Grandin described her inability to understand the social communication of
neurotypicals, or people with normal neural development, as leaving her feeling "like an
anthropologist on Mars".
Unusual social development becomes apparent early in childhood. Autistic infants show less
attention to social stimuli, smile and look at others less often, and respond less to their own
name. Autistic toddlers have more striking social deviance; for example, they have less eye
contact and anticipatory postures and are more likely to communicate by manipulating another
person's hand. Three- to five-year-old autistic children are less likely to exhibit social
understanding, approach others spontaneously, imitate and respond to emotions, communicate
nonverbally, and take turns with others. However, they do form attachments to their primary
caregivers. They display moderately less attachment security than usual, although this feature
disappears in children with higher mental development or less severe ASD. Older children and
adults with ASD perform worse on tests of face and emotion recognition.
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Contrary to common beliefs, autistic children do not prefer being alone. Making and
maintaining friendships often proves to be difficult for those with autism. For them, the quality
of friendships, not the number of friends, predicts how lonely they feel.
Communication
About a third to a half of individuals with autism do not develop enough natural speech to meet
their daily communication needs. Differences in communication may be present from the first
year of life, and may include delayed onset of babbling, unusual gestures, diminished
responsiveness, and vocal patterns that are not synchronized with the caregiver. In the second
and third years, autistic children have less frequent and less diverse babbling, consonants, words,
and word combinations; their gestures are less often integrated with words. Autistic children are
less likely to make requests or share experiences, and are more likely to simply repeat others'
words (echolalia) or reverse pronouns. Joint attention seems to be necessary for functional
speech, and deficits in joint attention seem to distinguish infants with ASD: for example, they
may look at a pointing hand instead of the pointed-at object, and they consistently fail to point at
objects in order to comment on or share an experience. Autistic children may have difficulty
with imaginative play and with developing symbols into language.
In a pair of studies, high-functioning autistic children aged 8–15 performed equally well, and
adults better than individually matched controls at basic language tasks involving vocabulary and
spelling. Both autistic groups performed worse than controls at complex language tasks such as
figurative language, comprehension and inference. As people are often sized up initially from
their basic language skills, these studies suggest that people speaking to autistic individuals are
more likely to overestimate what their audience comprehends.
Repetitive behavior
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Stereotypy is apparently purposeless movement, such as hand flapping, making sounds,
head rolling, or body rocking.
Compulsive behavior is intended and appears to follow rules, such as arranging objects
in a certain way.
Sameness is resistance to change; for example, insisting that the furniture not be moved
or refusing to be interrupted.
Ritualistic behavior involves the performance of daily activities the same way each
time, such as an unvarying menu or dressing ritual. This is closely associated with
sameness and an independent validation has suggested combining the two factors.
Restricted behavior is limited in focus, interest, or activity, such as preoccupation with a
single television program or toy.
Self-injury includes movements that injure or can injure the person, such as biting
oneself. A 2007 study reported that self-injury at some point affected about 30% of
children with ASD.
Other symptoms
Autistic individuals may have symptoms that are independent of the diagnosis, but that
can affect the individual or the family. An estimated 0.5% to 10% of individuals with ASD show
unusual abilities, ranging from splinter skills such as the memorization of trivia to the
extraordinarily rare talents of prodigious autistic savants.Unusual responses to sensory stimuli
are more common and prominent in autistic children, although there is no good evidence that
sensory symptoms differentiate autism from other developmental disorders. Differences are
greater for under-responsivity (for example, walking into things) than for over-responsivity (for
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example, distress from loud noises) or for sensation seeking (for example, rhythmic
movements). Several studies have reported associated motor problems that include poor muscle
tone, poor motor planning, and toe walking; ASD is not associated with severe motor
disturbances.
Unusual eating behavior occurs in about three-quarters of children with ASD, to the extent that it
was formerly a diagnostic indicator. Selectivity is the most common problem, although eating
rituals and food refusal also occur; this does not appear to result in malnutrition. Although some
children with autism also have gastrointestinal (GI) symptoms, there is a lack of published
rigorous data to support the theory that autistic children have more or different GI symptoms
than usual; studies report conflicting results, and the relationship between GI problems and ASD
is unclear.
Sleep problems are known to be more common in children with developmental disabilities, and
there is some evidence that children with ASD are more likely to have even more sleep problems
than those with other developmental disabilities; autistic children may experience problems
including difficulty in falling asleep, frequent nocturnal awakenings, and early morning
awakenings.
Classification
Autism is one of the five pervasive developmental disorders (PDD), which are characterized by
widespread abnormalities of social interactions and communication, and severely restricted
interests and highly repetitive behavior. These symptoms do not imply sickness, fragility, or
emotional disturbance. Leo Kanner introduced the label early infantile autism in 1943.
Of the five PDD forms, Asperger syndrome is closest to autism in signs and likely
causes; Rett syndrome and childhood disintegrative disorder share several signs with autism, but
may have unrelated causes; PDD not otherwise specified (PDD-NOS; also called atypical
autism) is diagnosed when the criteria are not met for a more specific disorder. Unlike autism,
Asperger's has no substantial delay in language development.The terminology of autism can be
bewildering, with autism, Asperger's and PDD-NOS often called the autism spectrum disorders
(ASD) or sometimes the autistic disorders, whereas autism itself is often called autistic disorder,
childhood autism, or infantile autism. In this article, autism refers to the classic autistic disorder;
in clinical practice, though, autism, ASD, and PDD are often used interchangeably. ASD, in turn,
is a subset of the broader autism phenotype (BAP), which describes individuals who may not
have ASD but do have autistic-like traits, such as avoiding eye contact.
The manifestations of autism cover a wide spectrum, ranging from individuals with
severe impairments—who may be silent, mentally disabled, and locked into hand flapping and
rocking—to high functioning individuals who may have active but distinctly odd social
approaches, narrowly focused interests, and verbose, pedantic communication. Sometimes the
syndrome is divided into low-, medium- and high-functioning autism (LFA, MFA, and HFA),
based on IQ thresholds, or on how much support the individual requires in daily life; these
subdivisions are not standardized and are controversial. Autism can also be divided into
syndromal and non-syndromal autism, where the former is associated with severe or profound
mental retardation or a congenital syndrome with physical symptoms, such as tuberous sclerosis.
Although individuals with Asperger's tend to perform better cognitively than those with autism,
the extent of the overlap between Asperger's, HFA, and non-syndromal autism is unclear.
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Causes
It has long been presumed that there is a common cause at the genetic, cognitive, and neural
levels for autism's characteristic triad of symptoms. However, there is increasing suspicion that
autism is instead a complex disorder whose core aspects have distinct causes that often co-occur.
Autism has a strong genetic basis, although the genetics of autism are complex and it is unclear
whether ASD is explained more by multigene interactions or by rare mutations with major
effects.Complexity arises due to interactions among multiple genes, the environment, and
epigenetic factors which do not change DNA but are heritable and influence gene expression.
Early studies of twins estimated heritability explains more than 90% of the risk of autism,
assuming a shared environment and no other genetic or medical syndromes. However, most of
the mutations that increase autism risk have not been identified. Typically, autism cannot be
traced to a Mendelian (single-gene) mutation or to a single chromosome abnormality like
Angelman syndrome or fragile X syndrome, and none of the genetic syndromes associated with
ASDs has been shown to selectively cause ASD. Numerous candidate genes have been located,
with only small effects attributable to any particular gene. The large number of autistic
individuals with unaffected family members may result from copy number variations—
spontaneous deletions or duplications in genetic material during meiosis. Hence, a substantial
fraction of autism cases may be traceable to genetic causes that are highly heritable but not
inherited: that is, the mutation that causes the autism is not present in the parental genome. Gene
replacement studies in mice suggest that autistic symptoms are closely related to later
developmental steps that depend on activity in synapses and on activity-dependent changes, and
that the symptoms may be reversed or reduced by replacing or modulating gene function after
birth. All known teratogens related to the risk of autism appear to act during the first eight
weeks from conception, and though this does not exclude the possibility that autism can be
initiated or affected later, it is strong evidence that autism arises very early in development.
Although evidence for other environmental causes is anecdotal and has not been confirmed by
reliable studies, extensive searches are underway. Environmental factors that have been claimed
to contribute to or exacerbate autism, or may be important in future research, include certain
foods, infectious disease, heavy metals, solvents, diesel exhaust, PCBs, phthalates and phenols
used in plastic products, pesticides, brominated flame retardants, alcohol, smoking, illicit drugs,
vaccines, and prenatal stress. Although parents may first become aware of autistic symptoms in
their child around the time of a routine vaccination (and parental concern about vaccines has led
to a decreasing uptake of childhood immunizations and an increasing likelihood of measles
outbreaks), the overwhelming majority of scientific studies show no causal association between
the measles–mumps–rubella vaccine and autism, and there is no convincing scientific evidence
showing that the vaccine preservative thiomersal helps cause autism.
Mechanism
Autism's symptoms result from maturation-related changes in various systems of the brain.
Despite extensive investigation, how autism occurs is not well understood. Its mechanism can be
divided into two areas: the pathophysiology of brain structures and processes associated with
autism, and the neuropsychological linkages between brain structures and behaviors. The
behaviors appear to have multiple pathophysiologies.
Pathophysiology
Autism affects many parts of the brain. Unlike many other brain disorders such as
Parkinson's, autism does not have a clear unifying mechanism at either the molecular, cellular, or
systems level; it is not known whether autism is a few disorders caused by mutations converging
on a few common molecular pathways, or is (like intellectual disability) a large set of disorders
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with diverse mechanisms. Autism appears to result from developmental factors that affect many
or all functional brain systems, and to disturb the timing of brain development more than the
final product. Neuroanatomical studies and the associations with teratogens strongly suggest that
autism's mechanism includes alteration of brain development soon after conception.[5] This
anomaly appears to start a cascade of pathological events in the brain that are significantly
influenced by environmental factors. Although many major structures of the human brain have
been implicated, almost all postmortem studies have been of individuals who also had mental
retardation, making it difficult to draw conclusions. Brain weight and volume and head
circumference tend to be greater in autistic children. The cellular and molecular bases of
pathological early overgrowth are not known, nor is it known whether the overgrown neural
systems cause autism's characteristic signs. Current hypotheses include:
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An excess of neurons that causes local overconnectivity in key brain regions.
Disturbed neuronal migration during early gestation.
Unbalanced excitatory–inhibitory networks.
Abnormal formation of synapses and dendritic spines, for example, by modulation of the
neurexin–neuroligin cell-adhesion system, or by poorly regulated synthesis of synaptic
protein. Disrupted synaptic development may also contribute to epilepsy, which may
explain why the two conditions are associated.
Neuropsychology
Two major categories of cognitive theories have been proposed about the links between autistic
brains and behavior.
The first category focuses on deficits in social cognition. The empathizing–systemizing
theory postulates that autistic individuals can systemize—that is, they can develop internal rules
of operation to handle events inside the brain—but are less effective at empathizing by handling
events generated by other agents. An extension, the extreme male brain theory, hypothesizes that
autism is an extreme case of the male brain, defined psychometrically as individuals in whom
systemizing is better than empathizing; this extension is controversial, as many studies contradict
the idea that baby boys and girls respond differently to people and objects. These theories are
related to the earlier theory of mind approach, which hypothesizes that autistic behavior arises
from an inability to ascribe mental states to oneself and others.
The second category focuses on nonsocial or general processing. Executive dysfunction
hypothesizes that autistic behavior results in part from deficits in working memory, planning,
inhibition, and other forms of executive function. Tests of core executive processes such as eye
movement tasks indicate improvement from late childhood to adolescence, but performance
never reaches typical adult levels. A strength of the theory is predicting stereotyped behavior and
narrow interests; two weaknesses are that executive function is hard to measure and that
executive function deficits have not been found in young autistic children. Weak central
coherence theory hypothesizes that a limited ability to see the big picture underlies the central
disturbance in autism. One strength of this theory is predicting special talents and peaks in
performance in autistic people. A related theory—enhanced perceptual functioning—focuses
more on the superiority of locally oriented and perceptual operations in autistic individuals.
These theories map well from the underconnectivity theory of autism.
Neither category is satisfactory on its own; social cognition theories poorly address autism's rigid
and repetitive behaviors, while the nonsocial theories have difficulty explaining social
impairment and communication difficulties. A combined theory based on multiple deficits may
prove to be more useful.
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Screening
About half of parents of children with ASD notice their child's unusual behaviors by age 18
months, and about four-fifths notice by age 24 months. As postponing treatment may affect longterm outcome, any of the following signs is reason to have a child evaluated by a specialist
without delay:
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No babbling by 12 months.
No gesturing (pointing, waving goodbye, etc.) by 12 months.
No single words by 16 months.
No two-word spontaneous phrases (other than instances of echolalia) by 24 months.
Any loss of any language or social skills, at any age.
Diagnosis
Diagnosis is based on behavior, not cause or mechanism. Autism is defined in the DSMIV-TR as exhibiting at least six symptoms total, including at least two symptoms of qualitative
impairment in social interaction, at least one symptom of qualitative impairment in
communication, and at least one symptom of restricted and repetitive behavior. Sample
symptoms include lack of social or emotional reciprocity, stereotyped and repetitive use of
language or idiosyncratic language, and persistent preoccupation with parts of objects. Onset
must be prior to age three years, with delays or abnormal functioning in either social interaction,
language as used in social communication, or symbolic or imaginative play. The disturbance
must not be better accounted for by Rett syndrome or childhood disintegrative disorder. ICD-10
uses essentially the same definition. A pediatrician commonly performs a preliminary
investigation by taking developmental history and physically examining the child. If warranted,
diagnosis and evaluations are conducted with help from ASD specialists, observing and
assessing cognitive, communication, family, and other factors using standardized tools, and
taking into account any associated medical conditions. A pediatric neuropsychologist is often
asked to assess behavior and cognitive skills, both to aid diagnosis and to help recommend
educational interventions.
Disorders of psychological development
(F80-F89)
The disorders included in this block have in common: (a) onset invariably during infancy or
childhood; (b) impairment or delay in development of functions that are strongly related to
biological maturation of the central nervous system; and (c) a steady course without remissions
and relapses. In most cases, the functions affected include language, visuo-spatial skills, and
motor coordination. Usually, the delay or impairment has been present from as early as it could
be detected reliably and will diminish progressively as the child grows older, although milder
deficits often remain in adult life.
F80
F80.0
Specific developmental disorders of speech and language
Disorders in which normal patterns of language acquisition are disturbed from the
early stages of development. The conditions are not directly attributable to
neurological or speech mechanism abnormalities, sensory impairments, mental
retardation, or environmental factors. Specific developmental disorders of speech and
language are often followed by associated problems, such as difficulties in reading and
spelling, abnormalities in interpersonal relationships, and emotional and behavioural
disorders.
Specific speech articulation disorder
A specific developmental disorder in which the child's use of speech sounds is below
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F80.1
F80.2
F80.3
F81
F81.0
F81.1
F81.2
the appropriate level for its mental age, but in which there is a normal level of
language skills.
Expressive language disorder
A specific developmental disorder in which the child's ability to use expressive spoken
language is markedly below the appropriate level for its mental age, but in which
language comprehension is within normal limits. There may or may not be
abnormalities in articulation.
Receptive language disorder
A specific developmental disorder in which the child's understanding of language is
below the appropriate level for its mental age. In virtually all cases expressive
language will also be markedly affected and abnormalities in word-sound production
are common.
Acquired aphasia with epilepsy [Landau-Kleffner]
A disorder in which the child, having previously made normal progress in language
development, loses both receptive and expressive language skills but retains general
intelligence; the onset of the disorder is accompanied by paroxysmal abnormalities on
the EEG, and in the majority of cases also by epileptic seizures. Usually the onset is
between the ages of three and seven years, with skills being lost over days or weeks.
The temporal association between the onset of seizures and loss of language is
variable, with one preceding the other (either way round) by a few months to two
years. An inflammatory encephalitic process has been suggested as a possible cause of
this disorder. About two-thirds of patients are left with a more or less severe receptive
language deficit.
Specific developmental disorders of scholastic skills
Disorders in which the normal patterns of skill acquisition are disturbed from the
early stages of development. This is not simply a consequence of a lack of
opportunity to learn, it is not solely a result of mental retardation, and it is not due
to any form of acquired brain trauma or disease.
Specific reading disorder
The main feature is a specific and significant impairment in the development of
reading skills that is not solely accounted for by mental age, visual acuity
problems, or inadequate schooling. Reading comprehension skill, reading word
recognition, oral reading skill, and performance of tasks requiring reading may all
be affected. Spelling difficulties are frequently associated with specific reading
disorder and often remain into adolescence even after some progress in reading has
been made. Specific developmental disorders of reading are commonly preceded by
a history of disorders in speech or language development. Associated emotional
and behavioural disturbances are common during the school age period.
Specific spelling disorder
The main feature is a specific and significant impairment in the development of
spelling skills in the absence of a history of specific reading disorder, which is not
solely accounted for by low mental age, visual acuity problems, or inadequate
schooling. The ability to spell orally and to write out words correctly are both
affected.
Specific disorder of arithmetical skills
Involves a specific impairment in arithmetical skills that is not solely explicable on
the basis of general mental retardation or of inadequate schooling. The deficit
concerns mastery of basic computational skills of addition, subtraction,
multiplication, and division rather than of the more abstract mathematical skills
involved in algebra, trigonometry, geometry, or calculus.
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F82
F83
F84
F84.0
F84.1
F84.2
Specific developmental disorder of motor function
A disorder in which the main feature is a serious impairment in the development of
motor coordination that is not solely explicable in terms of general intellectual
retardation or of any specific congenital or acquired neurological disorder.
Nevertheless, in most cases a careful clinical examination shows marked
neurodevelopmental immaturities such as choreiform movements of unsupported
limbs or mirror movements and other associated motor features, as well as signs of
impaired fine and gross motor coordination.
Mixed specific developmental disorders
A residual category for disorders in which there is some admixture of specific
developmental disorders of speech and language, of scholastic skills, and of motor
function, but in which none predominates sufficiently to constitute the prime
diagnosis. This mixed category should be used only when there is a major overlap
between each of these specific developmental disorders. The disorders are usually,
but not always, associated with some degree of general impairment of cognitive
functions. Thus, the category should be used when there are dysfunctions meeting
the criteria for two or more of F80.-, F81.- and F82.
Pervasive developmental disorders
A group of disorders characterized by qualitative abnormalities in reciprocal social
interactions and in patterns of communication, and by a restricted, stereotyped,
repetitive repertoire of interests and activities. These qualitative abnormalities are a
pervasive feature of the individual's functioning in all situations.
Use additional code, if desired, to identify any associated medical condition and mental
retardation.
Childhood autism
A type of pervasive developmental disorder that is defined by: (a) the presence of
abnormal or impaired development that is manifest before the age of three years, and
(b) the characteristic type of abnormal functioning in all the three areas of
psychopathology: reciprocal social interaction, communication, and restricted,
stereotyped, repetitive behaviour. In addition to these specific diagnostic features, a
range of other nonspecific problems are common, such as phobias, sleeping and eating
disturbances, temper tantrums, and (self-directed) aggression.
Autistic disorder
Infantile: autism , psychosis
Kanner's syndrome
Atypical autism
A type of pervasive developmental disorder that differs from childhood autism either in
age of onset or in failing to fulfil all three sets of diagnostic criteria. This subcategory
should be used when there is abnormal and impaired development that is present only
after age three years, and a lack of sufficient demonstrable abnormalities in one or two
of the three areas of psychopathology required for the diagnosis of autism (namely,
reciprocal social interactions, communication, and restricted, stereotyped, repetitive
behaviour) in spite of characteristic abnormalities in the other area(s). Atypical autism
arises most often in profoundly retarded individuals and in individuals with a severe
specific developmental disorder of receptive language.
Rett's syndrome
A condition, so far found only in girls, in which apparently normal early development
is followed by partial or complete loss of speech and of skills in locomotion and use of
hands, together with deceleration in head growth, usually with an onset between seven
and 24 months of age. Loss of purposive hand movements, hand-wringing stereotypies,
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F84.3
F84.4
F84.5
and hyperventilation are characteristic. Social and play development are arrested but
social interest tends to be maintained. Trunk ataxia and apraxia start to develop by age
four years and choreoathetoid movements frequently follow. Severe mental retardation
almost invariably results.
Other childhood disintegrative disorder
A type of pervasive developmental disorder that is defined by a period of entirely
normal development before the onset of the disorder, followed by a definite loss of
previously acquired skills in several areas of development over the course of a few
months. Typically, this is accompanied by a general loss of interest in the environment,
by stereotyped, repetitive motor mannerisms, and by autistic-like abnormalities in
social interaction and communication. In some cases the disorder can be shown to be
due to some associated encephalopathy but the diagnosis should be made on the
behavioural features.
Overactive disorder associated with mental retardation and stereotyped
movements
An ill-defined disorder of uncertain nosological validity. The category is designed to
include a group of children with severe mental retardation (IQ below 35) who show
major problems in hyperactivity and in attention, as well as stereotyped behaviours.
They tend not to benefit from stimulant drugs (unlike those with an IQ in the normal
range) and may exhibit a severe dysphoric reaction (sometimes with psychomotor
retardation) when given stimulants. In adolescence, the overactivity tends to be
replaced by underactivity (a pattern that is not usual in hyperkinetic children with
normal intelligence). This syndrome is also often associated with a variety of
developmental delays, either specific or global. The extent to which the behavioural
pattern is a function of low IQ or of organic brain damage is not known.
Asperger's syndrome
A disorder of uncertain nosological validity, characterized by the same type of
qualitative abnormalities of reciprocal social interaction that typify autism, together
with a restricted, stereotyped, repetitive repertoire of interests and activities. It differs
from autism primarily in the fact that there is no general delay or retardation in
language or in cognitive development. This disorder is often associated with marked
clumsiness. There is a strong tendency for the abnormalities to persist into adolescence
and adult life. Psychotic episodes occasionally occur in early adult life.
Management
A three-year-old with autism points to fish in an aquarium, as part of an experiment on
the effect of intensive shared-attention training on language development.The main goals of
treatment are to lessen associated deficits and family distress, and to increase quality of life and
functional independence. No single treatment is best and treatment is typically tailored to the
child's needs. Studies of interventions have methodological problems that prevent definitive
conclusions about efficacy. Although many psychosocial interventions have some positive
evidence, suggesting that some form of treatment is preferable to no treatment, the
methodological quality of systematic reviews of these studies has generally been poor, their
clinical results are mostly tentative, and there is little evidence for the relative effectiveness of
treatment options. Intensive, sustained special education programs and behavior therapy early in
life can help children acquire self-care, social, and job skills, and often improve functioning and
decrease symptom severity and maladaptive behaviors; claims that intervention by around age
three years is crucial are not substantiated. Available approaches include applied behavior
analysis (ABA), developmental models, structured teaching, speech and language therapy, social
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skills therapy, and occupational therapy. Educational interventions have some effectiveness in
children: intensive ABA treatment has demonstrated effectiveness in enhancing global
functioning in preschool children and is well-established for improving intellectual performance
of young children. Neuropsychological reports are often poorly communicated to educators,
resulting in a gap between what a report recommends and what education is provided. It is not
known whether treatment programs for children lead to significant improvements after the
children grow up, and the limited research on the effectiveness of adult residential programs
shows mixed results.
Many medications are used to treat ASD symptoms that interfere with integrating a child
into home or school when behavioral treatment fails. More than half of U.S. children diagnosed
with ASD are prescribed psychoactive drugs or anticonvulsants, with the most common drug
classes being antidepressants, stimulants, and antipsychotics. Aside from antipsychotics, there is
scant reliable research about the effectiveness or safety of drug treatments for adolescents and
adults with ASD. A person with ASD may respond atypically to medications, the medications
can have adverse effects, and no known medication relieves autism's core symptoms of social
and communication impairments.
Prognosis
There is no known cure. Children recover occasionally, so that they lose their diagnosis of ASD;
this occurs sometimes after intensive treatment and sometimes not. It is not known how often
recovery happens; reported rates in unselected samples of children with ASD have ranged from
3% to 25%. Most children with autism lack social support, meaningful relationships, future
employment opportunities or self-determination. Although core difficulties tend to persist,
symptoms often become less severe with age. Few high-quality studies address long-term
prognosis. Some adults show modest improvement in communication skills, but a few decline;
no study has focused on autism after midlife. Acquiring language before age six, having an IQ
above 50, and having a marketable skill all predict better outcomes; independent living is
unlikely with severe autism.
Epidemiology
Reports of autism cases grew dramatically in the U.S. from 1996 to 2007. It is unknown how
much, if any, growth came from changes in autism's prevalence. Most recent reviews tend to
estimate a prevalence of 1–2 per 1,000 for autism and close to 6 per 1,000 for ASD; because of
inadequate data, these numbers may underestimate ASD's true prevalence. PDD-NOS's
prevalence has been estimated at 3.7 per 1,000, Asperger's at roughly 0.6 per 1,000, and
childhood disintegrative disorder at 0.02 per 1,000. The number of reported cases of autism
increased dramatically in the 1990s and early 2000s. This increase is largely attributable to
changes in diagnostic practices, referral patterns, availability of services, age at diagnosis, and
public awareness, though unidentified contributing environmental risk factors cannot be ruled
out. The available evidence does not rule out the possibility that autism's true prevalence has
increased; a real increase would suggest directing more attention and funding toward changing
environmental factors instead of continuing to focus on genetics.
Autism is associated with several other conditions:


Genetic disorders. About 10–15% of autism cases have an identifiable Mendelian
(single-gene) condition, chromosome abnormality, or other genetic syndrome, and ASD
is associated with several genetic disorders.
Mental retardation. The fraction of autistic individuals who also meet criteria for
mental retardation has been reported as anywhere from 25% to 70%, a wide variation
13



illustrating the difficulty of assessing autistic intelligence. For ASD other than autism,
the association with mental retardation is much weaker.
Anxiety disorders are common among children with ASD; there are no firm data, but
studies have reported prevalences ranging from 11% to 84%. Many anxiety disorders
have symptoms that are better explained by ASD itself, or are hard to distinguish from
ASD's symptoms.
Epilepsy, with variations in risk of epilepsy due to age, cognitive level, and type of
language disorder.
Several metabolic defects, such as phenylketonuria, are associated with autistic
symptoms.
Behavioural and emotional disorders with onset usually occurring in
childhood and adolescence
(F90-F98)
F90
F91
F91.0
F91.1
Hyperkinetic disorders
A group of disorders characterized by an early onset (usually in the first five years of
life), lack of persistence in activities that require cognitive involvement, and a
tendency to move from one activity to another without completing any one, together
with disorganized, ill-regulated, and excessive activity. Several other abnormalities
may be associated. Hyperkinetic children are often reckless and impulsive, prone to
accidents, and find themselves in disciplinary trouble because of unthinking breaches
of rules rather than deliberate defiance. Their relationships with adults are often
socially disinhibited, with a lack of normal caution and reserve. They are unpopular
with other children and may become isolated. Impairment of cognitive functions is
common, and specific delays in motor and language development are
disproportionately frequent. Secondary complications include dissocial behaviour and
low self-esteem.
Conduct disorders
Disorders characterized by a repetitive and persistent pattern of dissocial,
aggressive, or defiant conduct. Such behaviour should amount to major violations
of age-appropriate social expectations; it should therefore be more severe than
ordinary childish mischief or adolescent rebelliousness and should imply an
enduring pattern of behaviour (six months or longer). Features of conduct disorder
can also be symptomatic of other psychiatric conditions, in which case the
underlying diagnosis should be preferred.
Examples of the behaviours on which the diagnosis is based include excessive
levels of fighting or bullying, cruelty to other people or animals, severe
destructiveness to property, fire-setting, stealing, repeated lying, truancy from
school and running away from home, unusually frequent and severe temper
tantrums, and disobedience. Any one of these behaviours, if marked, is sufficient
for the diagnosis, but isolated dissocial acts are not.
Conduct disorder confined to the family context
Conduct disorder involving dissocial or aggressive behaviour (and not merely
oppositional, defiant, disruptive behaviour), in which the abnormal behaviour is
entirely, or almost entirely, confined to the home and to interactions with
members of the nuclear family or immediate household. The disorder requires that
the overall criteria for F91.- be met; even severely disturbed parent-child
relationships are not of themselves sufficient for diagnosis.
Unsocialized conduct disorder
Disorder characterized by the combination of persistent dissocial or aggressive
F91.2
F91.3
F92
14
behaviour (meeting the overall criteria for F91.- and not merely comprising
oppositional, defiant, disruptive behaviour) with significant pervasive
abnormalities in the individual's relationships with other children.
Socialized conduct disorder
Disorder involving persistent dissocial or aggressive behaviour (meeting the
overall criteria for F91.- and not merely comprising oppositional, defiant,
disruptive behaviour) occurring in individuals who are generally well integrated
into their peer group.
Oppositional defiant disorder
Conduct disorder, usually occurring in younger children, primarily characterized
by markedly defiant, disobedient, disruptive behaviour that does not include
delinquent acts or the more extreme forms of aggressive or dissocial behaviour.
The disorder requires that the overall criteria for F91.- be met; even severely
mischievous or naughty behaviour is not in itself sufficient for diagnosis. Caution
should be employed before using this category, especially with older children,
because clinically significant conduct disorder will usually be accompanied by
dissocial or aggressive behaviour that goes beyond mere defiance, disobedience,
or disruptiveness.
Mixed disorders of conduct and emotions
A group of disorders characterized by the combination of persistently aggressive,
dissocial or defiant behaviour with overt and marked symptoms of depression,
anxiety or other emotional upsets. The criteria for both conduct disorders of
childhood and emotional disorders of childhood or an adult-type neurotic
diagnosis or a mood disorder must be met.
Symptoms
The most common symptoms of ADHD are:



Impulsiveness: acting before thinking of consequences, jumping from one activity to
another, disorganization, tendency to interrupt other peoples' conversations.
Hyperactivity: restlessness, often characterized by an inability to sit still, fidgeting,
squirminess, climbing on things, restless sleep.
Inattention: easily distracted, day-dreaming, not finishing work, difficulty listening.
Some of the associated conditions are:





Oppositional defiant disorder (35%) and conduct disorder (26%) which both are
characterized by anti-social behaviors such as stubbornness, aggression, frequent temper
tantrums, deceitfulness, lying, or stealing.
Primary disorder of vigilance, which is characterized by poor attention and concentration,
as well as difficulties staying awake. These children tend to fidget, yawn and stretch, and
appear to be hyperactive in order to remain alert and active.
Mood disorders. Boys diagnosed with the combined subtype have been shown more
likely to suffer from a mood disorder.
Bipolar disorder. As many as 25% of children with ADHD have bipolar disorder.
Children with this combination may demonstrate more aggression and behavioral
problems than those with ADHD alone.
Anxiety disorder, which has been found to be more common in girls diagnosed with the
inattentive subtype of ADHD.
15

Obsessive-compulsive disorder. OCD is believed to share a genetic component with
ADHD, and shares many of its characteristics.
Causes
A specific cause of ADHD is not known. There are, however, a number of factors that may
contribute to ADHD including genetics, diet and social and physical environments.
Genetic factors. Twin studies indicate that the disorder is highly heritable and that genetics are
a factor in about 75% of ADHD cases. Hyperactivity also seems to be primarily a genetic
condition; however, other causes do have an effect.
Environmental factors.Twin studies to date have also suggested that approximately 9% to 20%
of the variance in hyperactive-impulsive-inattentive behavior or ADHD symptoms can be
attributed to nonshared environmental (nongenetic) factors.
Diet. A meta-analysis has found that dietary elimination of artificial food coloring and
preservatives provides a statistically significant benefit in children with ADHD. Other more
recent studies agree with these conclusions. The European Food Safety Authority (EFSA)
reviewed the literature on the association between food additives and hyperactivity and
concluded that there is only limited evidence of an association between the intake of additives
and activity and attention, and then only in some children studied. They further indicated that the
effects reported in the study were not consistent for the two age groups and for the two food
additive mixtures used in the study. Others have suggested a trial of removing additives from the
diet for children with ADHD as it is harmless and might be helpful. A number of studies have
found that sucrose (sugar) has no effect on behavior and in particular it does not exacerbate the
symptoms of children diagnosed with ADHD.Corn syrup and high fructose corn syrup, the
sugars found in most sweets, were not part of any of these studies.
Social factors. There is no compelling evidence that social factors alone can cause ADHD.
Many researchers believe that relationships with caregivers have a profound effect on attentional
and self-regulatory abilities. A study of foster children found that a high number of them had
symptoms closely resembling ADHD, while other researchers have found behavior typical of
ADHD in children who have suffered violence and emotional abuse. Furthermore, Complex
Post Traumatic Stress Disorder can result in attention problems that can look like ADHD.
ADHD is considered a contributing factor to Sensory Integration Disorders.
Neurodiversit. Proponents of this theory assert that atypical (neurodivergent) neurological
development is a normal human difference that is to be tolerated and respected just like any other
human difference. Social critics argue that while biological factors may play a large role in
difficulties with sitting still in class and/or concentrating on schoolwork in some children, these
children could have failed to integrate others' social expectations of their behavior for a variety
of other reasons.
Diagnosis
No objective test exists to make a diagnosis of ADHD. It thus remains a clinical diagnosis.
Based on the DSM-IV criteria listed below, three types of ADHD are classified:
1. ADHD, Combined Type: if both criteria 1A and 1B are met for the past 6 months
2. ADHD Predominantly Inattentive Type: if criterion 1A is met but criterion 1B is not met
for the past six months
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3. ADHD, Predominantly Hyperactive-Impulsive Type: if Criterion 1B is met but
Criterion 1A is not met for the past six months.
I. Either A or B:
A. Six or more of the following symptoms of inattention have been present for at least 6
months to a point that is disruptive and inappropriate for developmental level:
1. Often does not give close attention to details or makes careless mistakes in
schoolwork, work, or other activities.
2. Often has trouble keeping attention on tasks or play activities.
3. Often does not seem to listen when spoken to directly.
4. Often does not follow instructions and fails to finish schoolwork, chores, or duties
in the workplace (not due to oppositional behavior or failure to understand
instructions).
5. Often has trouble organizing activities.
6. Often avoids, dislikes, or doesn't want to do things that take a lot of mental effort
for a long period of time (such as schoolwork or homework).
7. Often loses things needed for tasks and activities (e.g. toys, school assignments,
pencils, books, or tools).
8. Is often easily distracted.
9. Often forgetful in daily activities.
B. Six or more of the following symptoms of hyperactivity-impulsivity have been present
for at least 6 months to an extent that is disruptive and inappropriate for developmental
level:
Hyperactivity:
1. Often fidgets with hands or feet or squirms in seat.
2. Often gets up from seat when remaining in seat is expected.
3. Often runs about or climbs when and where it is not appropriate (adolescents or
adults may feel very restless).
4. Often has trouble playing or enjoying leisure activities quietly.
5. Is often "on the go" or often acts as if "driven by a motor".
6. Often talks excessively.
Impulsiveness:
1. Often blurts out answers before questions have been finished.
2. Often has trouble waiting one's turn.
3. Often interrupts or intrudes on others (e.g., butts into conversations or games).
II. Some symptoms that cause impairment were present before age 7 years.
III. Some impairment from the symptoms is present in two or more settings (e.g. at school/work
and at home).
IV. There must be clear evidence of significant impairment in social, school, or work
functioning.
Differential diagnoses: 1. Medical conditions that must be excluded include: hypothyroidism,
anemia, lead poisoning, chronic illness, hearing or vision impairment, substance abuse,
medication side effects, sleep impairment, and child abuse, among others.2.Sleep
17
conditions.Among other psychological and neurological issues, the relationship between
ADHD and sleep is complex. In addition to clinical observations, there is substantial empirical
evidence from a neuroanatomic standpoint to suggest that there is considerable overlap in the
central nervous system centers that regulate sleep and those that regulate attention/arousal.
Primary sleep disorders play a role in the clinical presentation of symptoms of inattention and
behavioral dysregulation. There are multilevel and bidirectional relationships among sleep,
neurobehavioral functioning, and the clinical syndrome of ADHD.
Management
Behavioral interventions. Psychological therapies use to treat ADHD include
psychoeducational input, behavior therapy, cognitive behavioral therapy (CBT), interpersonal
psychotherapy (IPT), family therapy, school-based interventions, social skills training, and
parent management training.
Pharmacological treatment. Stimulant medications are the most clinically and cost effective
method of treating ADHD. A 2008 review found that the use of stimulants improved teachers'
and parents' ratings of disruptive behavior; however, it did not improve academic achievement
Stimulants neither increased nor decreased rates of delinquency or substance abuse at 3 years.
Intensive treatment for 14 months has no effect on long term outcomes 8 years later. No
significant differences between the various drugs in terms of efficacy or side effects have been
found. About 70% of children improve after being treated with stimulants. Medications,
however, are not recommended for pre-school children with ADHD. Stimulants, in the short
term, have been found to be safe in the appropriately selected patient and appear well tolerated
over 5 years of treatment.
Dietary supplements and specialized diets are sometimes used by people with ADHD with the
intent to mitigate some or all of the symptoms. For example, Omega-3 supplementation may
reduce ADHD symptoms for a subgroup of children and adolescents with ADHD "characterized
by inattention and associated neurodevelopmental disorders." The effectiveness of these dietary
supplements and specialized diets is debated because in many cases preliminary studies
investigating their efficacy are small in scope or followup investigations have conflicting results.
In the United States, no dietary supplement has been approved for the treatment for ADHD by
the FDA.
Psychological & Emotional Support. Several ADHD specific support groups exist as
informational sources and to help families cope with challenges associated with dealing with
ADHD.
Lifestyle. Aerobic fitness may improve cognitive functioning and neural organization related to
executive control during pre-adolescent development, though more studies are needed in this
area. One study suggests that athletic performance in boys with ADHD may increase peer
acceptance when accompanied by fewer negative behaviors.
Prognosis. The proportion of children meeting the diagnostic criteria for ADHD dropped by
about 50% over three years after the diagnosis. This occurred regardless of the treatments used.
It persists into adulthood in about 30-50% of cases. Those affected are likely to develop coping
mechanisms as they mature thus compensating for their previous ADHD.
Epidemiology. ADHD's global prevalence is estimated at 3-5% in people under the age of 19.
There is, however, both geographical and local variability among studies. Geographically,
children in North America appear to have a higher rate of ADHD than children in Africa and the
Middle East,[ well published studies have found rates of ADHD as low as 2% and as high as
18
14% among school aged children. The rates of diagnosis and treatment of ADHD are also
much higher on the east coast of the USA than on the west coast.
5.2. THEORETIC QUESTIONS:
1.Etiology and pathogenesis of child’s autism and hyperkinetic disorders.
2.Clinical picture of child’s autism.
3.Clinical picture of hyperkinetic disorders.
4.Clinical picture of disorders of social conduct.
5.Diagnostic of child’s autism and hyperkinetic disorders.
6.Treatment of patients with child’s autism and hyperkinetic disorders.
7.Prophylactic of child’s autism and hyperkinetic disorders.
8.Principles of medical-pedagogic correction and social rehabilitation.
5.3. PRACTICAL TASKS ON THE CLASS:
1. To collect anamnesis, clinical psychopathological examination of patients with child’s
autism, hyperkinetic disorders and disorders of social conduct.
2. Make up plan of examination and treatment of patients with child’s autism,
hyperkinetic disorders and disorders of social conduct.
3. To solve the tasks and tests.
5.4. MATERIAL FOR SELF-CONTRROL.
A. Questions of self-controls:
1.Etiology and pathogenesis of child’s autism and hyperkinetic disorders.
2.Clinical picture of child’s autism.
3.Clinical picture of hyperkinetic disorders.
4.Clinical picture of disorders of social conduct.
5.Diagnostic of child’s autism and hyperkinetic disorders.
6.Treatment of patients with child’s autism and hyperkinetic disorders.
7.Prophylactic of child’s autism and hyperkinetic disorders.
8.Principles of medical-pedagogic correction and social rehabilitation.
B. TESTS:
1. The hyperkinetic disorders display in:
A. 2-4 y.o.
B. 6-8 y.o.
C. 10-14 y.o.
D. 14-15 y.o.
E. 15-18 y.o.
2. The hyperkinetic syndrome are present in next disease:
A. Epilepsy
B. Schisophrenia
C. Mental retardation
D. Personality disorders
E. All mentioned
3. Who did describe autism syndrome for the first time:
A. Kanner
B. Asperger
C. Jaspers
D. Blejcher
E. Korsakov
19
4. When does autism syndrome display:
A. 1-3 y.o.
B. 2-4 y.o.
C. 5-6 y.o.
D. 8-10 y.o.
E. 10-12 y.o.
5. What signs does autism syndrome have:
A. Emotional idifference
B.Fear
C. Speek disoders
D.All above mentioned
E. Hallucination
6. Normal or high level IQ is about next syndrome:
A. Kanner’s syndrome
B. Asperger’s syndrome
C. Heboid syndrome
D. Korsakov’s syndrome
E. All above mentioned
7. The children don’t want to associate about next syndrome:
A.Hyperdynamic syndrome
B.Autism syndrome
C. Fear syndrome
D. Pathologic fantasy syndrome
E. Paranoid syndrome
8. What syndrome is present in patient with motional anxiety, restlessness, impulsive
actions:
A.Hyperdynamic syndrome
B.Autism syndrome
C. Fear syndrome
D. Pathologic fantasy syndrome
E. Heboid syndrome
1.
2.
3.
4.
6. RECOMMENDED LITERATURE IS:
6.1. Basic:
Clinical Psychiatry from Synopsis of Psychiatry by H.I.Kaplan, B.J.Sadock. – New York:
Williams @ Wilkins. – 1997.
Psychiatry. Course of lectures. – Odessa: The Odessa State Medical University. – 2005. –
336 p.
Lectures.
Internet resource.
6.2. Additional:
1. Морозов Т.В., Шумский Н.Г. Введение в клиническую психиатрию. – Н.Новгород:
Изд-во НГМА, 1998.
2. Попов Ю.В., Вид В.Д. Современная клиническая психиатрия. – М., 1997.
3. Сонник Г.Т. Психіатрія: Підручник / Г.Т.Сонник, О.К.Напрєєнко, А.М.Скрипніков.
– К.: Здоров’я, 2006.
Prepared by assistant
S.D.Savka