Child psychiatry

Introduction:

Child psychiatry is the branch of psychiatry concerned with the assessment and treatment of children’s emotional behavioural and relationship problems.

Children are immature individual passing through stages of growth and development till they reach adulthood.

The development is the product of the continuous interaction heredity and the maturation of different systems and the environmental influences.

The childhood period start from birth till eighteen years old (0-18) passing from infancy(0-2), childhood from three years till puberty(3-13) and adolescence from(14-18)

The abnormality in child psychiatry is elicited by comparing the child behaviour to the corresponding normal range of the age group.

It is truly that we obtain the majority of our information from the observation made by the parents, caregivers, and teachers, but also we have to observe the child.

We always should take in consideration the developmental stage of the child, for example temper tantrums in a two years old child is not considered pathological, however, in a nine years old it is considered pathological.

The children are developing physically, emotionally, intellectually, and socially.

The assessment of the child follows the usual steps of the adult assessment, taking in consideration the following steps:

-Flexibility

-Preferably the two parents should attend the assessment interview.

- Ideally the child is left with his parents in the room which should be large, with different set of toys put in each corner of the room, or put it separately on a table, the room should be safe and secure and the child is watched by the therapist through a camera,given enough time for play. The therapist should observe the choice of toys, the degree of attachment to parents, any abnormal

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movements, the nutritional status, evidence of neglect or abuse. The therapist introduce himself to the patient, and the history and assessment are done as usual. To observe the ease of separation the therapist could ask the parents to go away after explaining to the child that they will be outside.

A detailed personal history should be obtained, the family history should be taken with special emphasis on the following points:

-Quality of parenting

-Parent –child relationship.

-Pattern of family relationship

-Separation from the care giver for more than a week

-General health (eating, elimination, sleeping, and physical complaints.

-School (achievement, sociability with schoolmates, relationship with teacher, and if he likes or dislikes the school .

-Attention span, concentration, and activity.

The treatment of children depends mainly on non pharmacological treatment mainly play therapy ,behaviour therapy and training, changing the attitude of the parents towards their children, working with the family and teachers and coordinating the efforts to help him.

The ICD-10 or the DSM IV is nearly describing the same disorders with different names. All categories used in DSM-IV are found in ICD-10, but not all ICD-10 categories are in DSM-IV.

-Mental Retardation is the same on both classification

-Learning disorders(DSMIV) is Specific developmental disorders of scholastic skills(iICD-10)

-Motor Skills Disorder (DSMIV) is Specific developmental disorder of motor

Function (ICD-10)

-Communication Disorders (DSMIV) is Specific development disorders of speech and language (ICD-10)

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-Pervasive Developmental Disorders is the same in both classifications.

-Attention deficit and disruptive behaviour (DSMIV) is the Behavioural and emotional disorders with onset Usually occurring in childhood and adolescence(ICD-10) including conduct and hyperkinetic disorder

Feeding and Eating Disorders of Infancy or Early Childhood in(DSMIV)is Other behavioral and emotional disorders with onset usually occurring in childhood and adolescence (ICD-10)

TIC Disorders is the same in both classifications.

Elimination Disorders(DSMIV) is included in Other behavioral and emotional disorders with onset usually occurring in childhood and adolescence (ICD-10)

The DSM-IV contains 5 axis

Axis I consists of mental disorders .

Axis II consists of mental retardation and personality disorders.

Axis III lists any physical disorder or general medical condition that is present in addition to the mental disorder.

Axis IV is used to code psychosocial and environmental problems

Axis V Global Assessment of Functioning (GAF)

ICD-10 is composed of three axes:

I. Clinical DiagnosesII. Disablement III. Contextual Factors.

We will discuss the most important diagnostic entities which are (autism, attention deficit hyperactivity disorder, mental retardation, tic disorders, separation anxiety disorder,childhood phobias , elimination disorders)

AUTISM

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This is a condition in which there is delay or deviance in the development of social skills,

language and communication and behavioural repertoire. It affect s multiple areas of development,

manifested early in life and causes persistent dysfunction

Epidemiology:

Life time prevalence is 5/10.000 children (0.05%)

The onset is before three years.

Sex Distribution :male to female ratio is 4-5 :1 .

socio- economic status : No association between autistic disorder and any socioeconomic status

Etiology and pathogenesis.

Autistic disorder is a developmental behavioural disorder biological in origin and the emotionally

unresponsive refrigerator mother of Kanner is obsolete.

Psychosocial and Family factors:

All recent studies show no significant changes in rearing practice of autistic parents.

However autistic children are responding with exacerbated symptoms to psychosocial stressors

including family discord, the birth of a new sibling or a family move, and they are extremely sensitive

to even small changes in their families and immediate environment.

Biological factors:

The high rate of mental retardation and seizure disorders suggest a biological basis for autistic

disorder. 75% of autistic are mentally retarded, one third are mild to moderate and close to half are

severely mentally retarded they show marked deficits in abstract reasoning social understanding and

verbal tasks than in performance tasks such as block design and digit recall in which details can be

remembered without reference to the "Gestalt " meaning.

1- 32% have grand mal epilepsy.

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20-25% ventricular enlargement.

E.E.G abnormalities from 10-83%, there is some indication of failed cerebral

lateralization.

Hypoplasia of cerebellar vermal lobules VI& VII.

Cortical abnormalities (polymicrogyria) these abnormalities reflect abnormal cell

migration in the first six months of gestation.

Fewer Purkinje's cells.

Increase diffuse cortical metabolism by P.E.T.

It is associated with neurological conditions, congenital rubella phenyl ketonuria,

tuberous sclerosis.

More perinatal complications.

More minor congenital physical anomalies suggests abnormal development within the

first trimester of pregnancy.

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Genetic factors:

2-4% of siblings of autistic children are autistic, 50 times more than in general population.

Concordance rate in two studies 36in monozygotic to zero in dizygotic, 96in monozygotic to

27 in dizygotic.

Fragile x syndrome 1% have fragile X

Tuberous sclerosis 2% have this disorder

Chromosomes 2&7 there is two region

16,17 have autism related genes.

Immunological factors:

Maternal antibodies directed to fetus (lymphocytes of fetus react with maternal antibodies

raising the possibility that embryonic neural or extraembryonic tissues may be damaged

during gestation.

Perinatal factors: Maternal bleeding, meconium in the amniotic fluid, respiratory distress

syndrome and neonatal anaemia.

Neuroanatomical factors: total brain volume is larger than normal but mentally retarded

autistic have smaller brain.

Increase in size in the occipital lobe, parietal and temporal lobe, no differences were found in

the frontal lobes. Specific origins of these enlargement are unknown. It could be explained by

increase neurogenesis, decreased neuronal death and increased production of nonneuronal

brain tissue, such as glial cells or blood vessels. Brain enlargement has been suggested as a

possible biological marker for autistic disorder.

The temporal lobe is believed to be a critical area of brain abnormality in autistic disorder.

Biochemical factors:

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Increase serotonin in autism and in mental retardation , increase in HVA in C.S.F with increase

withdrawal and stereotypes

Physical characteristics:

Attractive look, minor physical anomalies such ear malformations indicating the particular

fetal developmental period in which the abnormality arises, ambidexterity, abnormal

dermatoglyphics suggesting a disturbance in neuroectodermal development.

DSM-IV - TR Diagnostic Criteria for Autistic Disorder

A-A total of Six (or more) items from (1), (2) and (3), with at least two from (1), and one each from

(2) and (3(.

(1) Qualitative impairment in social interaction, as manifested by at least two of the following:

a) Marked impairment in the use of multiple nonverbal behaviours such as eye-to-eye gaze, facial

expression, body postures, and gestures to regulate social interaction.

b) Failure to develop peer relationships appropriate to the developmental level.

c) a lack of spontaneous seeking to share enjoyment, interests, or achievements with other people

(e.g., by a lack of showing, bringing, or pointing out objects of interest(.

d) lack of social or emotional reciprocity.

(2) Qualitative impairments in communication as manifested by at least

one of the following:

a) delay in, or total lack of , the development of spoken language not accompanied by an attempt to

compensate through alternative modes of communication such as gesture or mime.

b) in individuals with adequate speech, marked impairment in the ability to initiate or sustain a

conversation with others.

c) Stereotyped and repetitive use of language or idiosyncratic language.

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d) lack of varied, spontaneous make-believe play or social imitative play appropriate

to developmental level.

(3) Restricted repetitive and stereotyped patterns of behaviour, interests,

and activities, as manifested by at least one of the following:

a) encompassing preoccupation with one or more stereotyped and restricted patterns of interest

that is abnormal either in intensity or focus.

b) Apparently inflexible adherence to specific, non-functional rational routines or rituals.

c) Stereotyped and repetitive motor mannerisms (e.g., hand or finger flapping or twisting, or

complex whole-body movements).

B. Delays or abnormal functioning in at least one of the following areas, with onset prior to age 3

years: (1) social interaction, (2) language as used in social communication, or (3) symbolic or

imaginative play.

C. The disturbance is not better accounted for by Rett's disorder or childhood disintegrative disorder

.Differential Diagnosis:

The major differential diagnosis are

1- Schizophrenia with childhood onset.

2- Mental retardation with behavioural symptoms.

3- Mixed receptive – expressive language disorder.

4- Congenital deafness or severe hearing disorder.

5- Psychosocial deprivation.

6- Disintegrative psychoses.

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Children with pervasive developmental disorder usually have many concurrent problems, therefore

a step –wise approach to the differential diagnosis is suggested.

1- Determine I.Q.

2- Determine level of Language development.

3- Child's behaviour is appropriate for

a) chronological age.

b) Mental age.

c) Language age.

4- if not appropriate consider differential diagnosis of psychiatric disorder according to.

i- Pattern of social interaction.

ii- Pattern of Language.

iii- Pattern of play.

iv- Other behaviour.

5- Identify any relevant condition.

6- Consider whether there are any relevant psychosocial factors.

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Course and prognosis:

1- Life long disorder with guarded prognosis, those who have I.Q > 70 and use communicative

language by age 5-7 tend to have the best prognosis . High I.Q. autistic at age of 13 no longer

met criteria for autism but have some features. They show positive changes in

communication and social domains overtime. The symptoms that did not improve overtime

those related to ritualistic and repetitive behaviours. 2/3 of autistic live in complete or semi

dependence either with relative or institutions. Only 1- 2% acquire abnormal independent

status with gainful employment and 5-20% achieve a borderline line normal status the

prognosis improve if the environment is supportive and capable of meeting their needs. In

some cases self mutilation or aggressiveness and regression. 4-32% have G.M.E in late

childhood and adolescence it affects the prognosis.

Treatment: the goals of treatment are to increase socially acceptable and prosocial behaviour

to decrease odd behavioural symptoms and to improve verbal and non verbal communication.

Language remediation – Academic remediation.

Appropriate behavioural interventions to reinforce socially acceptable behaviours and

encourage self – care skills for M.R. autistic.

Insight – oriented individual psychotherapy proved ineffective.

Educational and behavioural interventions are considered the treatment of choice.

Structured classroom training in combination with behavioural method, is the most effective

treatment.

Parental support and counselling and training of parents in the concepts and skills of

behaviour modification.

Resolution of the parent's concern lead to considerable gain in children, language cognitive

and social areas of behaviour.

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"Facilitated communication" is a technique by which autistic with some language is aided in

communication by a teacher who helps the child pick out letters on a computer or letter

board.

There are no specific medications to treat the core symptoms of autistic disorder.

Pyschopharmacotherapy is a valuable adjunctive treatment to ameliorate associated

behavioural symptoms.

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Mental retardation

Definition:

Intellectual impairment starting early in life associated with educational and social disabilities

Level of mental retardation:

Classified according to the I.Q determined by standard psychometric tests

Mild mental retardation: IQ level 50–55 to approximately 70 about 75%

Moderate retardation: IQ level 35–40 to 50–55 about 15%

Severe mental retardation: IQ level 20–25 to 35–40 about 8%

Profound mental retardation: IQ level below 20 or 25 about 2%

N.B -Borderline mental retardation <90

Co- morbidity with other psychiatric disorders is high because of the possible genetic etiology, presence of organic brain disease, reaction to the stigma of subnormality, parental attitude either rejection or overprotection, as a consequences of the abnormality e.g. deficient social skills

N.B making the diagnosis of the co- morbid disorder is sometimes difficult due to the low level of intelligence and the poor verbal fluency.

1-Depression is common but not expressed verbally

2-adjustment disorders prominent in the mild mental retardation

3-personality disorder may lead to problem specially legal

4-75% of autistic are mentally retarded

5-Schizophrenia (gifted schizophrenia)more deterioration of mental functions, delusion and hallucination are less likely to be expressed clearly

Causes:

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-congenital,chromosomes or gene defects

Clinical Findings and Laboratory Abnormalities That Increase Suspicion for Underlying Metabolic Disorder

Growth abnormality

Recurrent, unexplained illness

Seizures

Ataxia

Loss of psychomotor skills

Hypotonia

"Coarse" appearance

Eye abnormalities (cataracts, ophthalmoplegia, corneal clouding, retinal abnormality)

Recurrent somnolence/coma

Abnormal sexual differentiation

Arachnodactyly

Hepatosplenomegaly

Metabolic/lactic acidosis

Hyperuricemia

Hyperammonemia

Low cholesterol

Structural hair abnormalities

Unexplained deafness

Bone abnormalities (dysostosis, occipital horns, punctate calcifications)

Skin abnormalities (angiokeratoma, "orange-peel" skin, icthyosis)

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-intrauterine infections

-perinatal complication: anoxia, intraventricular hemorrhage, kernicterus ,etc..

-postnatal complication: encephalitis meningitis,trauma , etc...

-Psychosocial factors : sensory deprivation or poor stimulating environment.

Assessment

-detailed history including:family history of inherited diseases, prenatal perinatal and neonatal history,milestones.

-physical examination

-behavioural assessment

-psychometric assessment of I.Q

N.B clinically we can have a rough idea about the intelligence of a child

One to two year old can imitate drawing a line

Three year old can imitate drawing a circle

four year old can imitate drawing a square

five year old can imitate drawing a triangle

seven year old can imitate drawing a lozenge.

Management:

-Special education and training

-Family support and education

-Regular reassessment and follow up

Physical and psychological treatment .

Tic disorders

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Definition: A tic is a sudden, rapid, recurrent, non rhythmic, stereotyped motor movement or vocalization.

There is three types of tics :

-chronic motor or vocal tics

-transient tic disorder

-Tourette’s disorder

Tourette’s disorder (Gilles de la Tourette’s syndrome)

Tourette's disorder is a neuropsychiatric disorder with onset in childhood that is characterized by chronic intermittent motor and vocal tics.

Epidemiology:

-Prevalence is about 4-5 /10.000

-Mean age of onset seven years of age

-Boys to girls ratio is 3:1

DSM-IV Diagnostic Criteria for Tourette's Disorder

A. Both multiple motor and one or more vocal tics have been present at some time during the illness, although not necessarily concurrently.

B. The tics occur many times a day (usually in bouts), nearly every day or intermittently throughout a period of more than 1 year, and during this period there was never a tic-free period of more than 3 consecutive months.

C. The onset is before age 18 years.

D. The disturbance is not due to the direct physiological effects of a substance (e.g., stimulants) or a general medical condition (e.g., Huntington's disease or postviral encephalitis).

Motor and vocal tics can be simple or complex. Simple tics are the first to appear.

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Examples:

Simple motor tics: eye blinking, head jerking, facial grimacing.

Simple vocal tics: coughing , grunting , sniffing.

Complex motor tics: hitting self, jumping.

Complex vocal tics: coprolalia (use of vulgar words ),Palilalia(repetition of own words, echolalia (repeating other’s word).

Aetiology:

-Definite aetiology is unknown.

-Evidence of genetic transmission:

i- it runs in families

ii- higher incidence in monozygotic twins than dizygotic

-Evidence of neurobiologic causes : E.E.G abnormalities in about 50% of patients.

-Dopamine abnormality:

i- abnormal levels of homovanilic acid in CSF

ii-Stimulants (methyl phenidate) which are dopamine agonists worsen tics or precipitate their occurrence.

iii-Dopamine antagonists(haloperidol) improve tics

Differential diagnosis:

- Dyskinesia- Syndenham’s chorea- Huntington’s disease

Prognosis:

-Social ostracism is frequent

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If the condition is untreated, the course is usually chronic with periods of lessening alternating with period of exacerbation of tics.

Treatment:

- Psychopharmacological:a-Dopaminergic antagonist: carries the risk od inducind tardive dyskinesia.

i-Haloperidol gives good results in 85 % of casesii-Pimozideb-Alpha-2 adrenergic agonist:Clonidine gives fair results in treating tics but it has the benefit of not producing tardive dyskinesia.

- Psychological counselling is necessary to the family and the child- Psycho education to the family and child(nature of the disorder, how to

cope with it)- Group psychotherapy to deal with the social ostracism and reduce the

social isolation.Chronic motor or vocal tic disorder

Similar to tourette’s, but it comes either with vocal tics or motor tics whether single or multiple.Higher prevalence than Tourette’sSeverity and social impairment are less than in Tourette’sGenetically chronic motor or vocal tic disorders occur in the same families.The neurobiology and the treatment of both disorders are the same

Transient tic disorderEpidemiology:-5-24 % of school children have some sort of tics.-Boys to girls ratio is 3:1- Same diagnostic features as Tourette’s disorder but the duration is less than twelve months.- In the majority of cases it is precipitated by stress and tends to remit spontaneously, in few cases it turns to be Tourette’s disorder or chronic vocal or motor disorder.

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- Psycho education to the family and behaviour modification to the child and rarely interference with psychopharmacological treatment in severe cases.

Separation Anxiety DisordersDefinition: Excessive anxiety concerning separation from home or from major attachment figure for at least four weeks DSM-IV Diagnostic Criteria for Separation Anxiety DisorderA. Developmentally inappropriate and excessive anxiety concerning separation from home or from those to whom the individual is attached, as evidenced by three (or more) of the following: (1) recurrent excessive distress when separation from home or major attachment figures occurs or is anticipated (2) persistent and excessive worry about losing, or about possible harm befalling, major attachment figures (3) persistent and excessive worry that an untoward event will lead to separation from a major attachment figure (e.g., getting lost or being kidnapped) (4) persistent reluctance or refusal to go to school or elsewhere because of fear of separation (5) persistently and excessively fearful or reluctant to be alone or without major attachment figures at home or without significant adults in other settings (6) persistent reluctance or refusal to go to sleep without being near a major attachment figure or to sleep away from home (7) repeated nightmares involving the theme of separation (8) repeated complaints of physical symptoms (such as headaches, stomach aches, nausea, or vomiting) when separation from major attachment figures occurs or is anticipatedB. The duration of the disturbance is at least 4 weeks.C. The onset is before age 18 years.D. The disturbance causes clinically significant distress or impairment in social, academic (occupational), or other important areas of functioning.E. The disturbance does not occur exclusively during the course of a pervasive developmental disorder, schizophrenia, or other psychotic

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disorder and, in adolescents and adults, is not better accounted for by panic disorder with agoraphobia.Specify if:Early onset: if onset occurs before age 6 years

N.B the disorder may be precipitated by a frightening experience or insecurity in the family, and is often maintained by the overprotective attitude of the family.

Treatment:

Psychotherapy(individual, family therapy)

Behaviour therapy

Pharmacotherapy:

-Tricyclic antidepressants.

-Selective serotonin re-uptake inhibitors.

Phobias in children

Phobias are common, and usually normal in children. Common feared objects and situations include: animals, strangers, darkness, and loud noisy voices. Most childhood phobias improve without specific treatment measures. Parents should adopt a reasonable reassuring approach. Behaviour treatment is required if phobia persists.

School Phobia

-Irrational fear of going to school associated with unexplained physical complaints such as headache, abdominal pain, or feeling sick. Boys and girls are equally affected.

-Complaints occur on school days and not in holidays

-It occurs at the beginning of school, changing school, in transition between elementary and secondary school.

-Astonishing usually the academic achievement is good or superior.

Precipitating Factors:

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-Separation anxiety (mainly in younger children) child wants to stay with a major attachment figure. Mothers are usually overprotective.

-Minor physical illness

-Emotionally disturbing event at home (parental discord) or at school (criticism, quarrel with a close friend)

- Co morbid psychiatric conditions such as depression in adolescent, or low self –esteem.

Treatment:

-Identify ant treat the precipitating factors.

-gradual desensitisation to the school phobia by early graded return to school

-Both parents should participate in the treatment

-School and teachers should be involved

-In some cases drug can decrease the anxiety or the depressive features.

Elimination disorders

They are :

-Functional enuresis

- Functional encopresis

Functional enuresis: It is repeated involuntaty voiding of urine after the age of five years (usual age of continence) in the absence of any physical disorders.

There are two types of functional enuresis

i-Primary enuresis: the individual has never been urinary continent.

ii-Secondary enuresis : the individual becomes incontinent after being continent , and it usually starts after a sibling birth or parental discord.

- Epidemiology:The point prevalence as cited by D.S.M.IV is

- 7% of boys and 3% of girls at the age of 5 years

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- 3% of boys and 2% of girls at the age of10 years- 1% of boys at age of 18years and still fewer of girls.- Usually secondary enuresis starts at age of 5-8 years.- Spontaneous remission rate between5% to 10% per year after the age of

five.Eatiology:-No specific aetiology but could be explained by delay in the maturation of brain.- There is definite psychosocial sequelae:i-Conflicts with parentsii-Low self esteemiii- social ostracismTreatment:First approach is education for the parents and the childBehavioural treatment is given the priority , if failed we try the biological treatment, and we can combine it with psychotherapy especially if there is low self esteem or social ostracism.We should start by :-search and treat any possible physical disease e.g repeated urinary infections, infestation with entrobius vermicularis.-Treat any emotional problems-advising the parents to stop criticism, or put special regulation on him because he is enuretic.-Fluid restriction before bed time.-going to toilet before bed time-training of the bladder through”retention-control” technique. The aim is to increase the capacity of the bladder and strengthen the power of the sphincter.This is done by whenever he goes to pass urine he passes only a small amount and stop urination, then he counts for 10 and he voids the rest of the amount.Behavior therapy:-Star chart technique: record dry nights with a star and seven consecutive dry nights with a gift.

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-A bell and pad apparatus is helpful . A pad is placed on the bed with a wire running to a bell. When the child wets, the moisture completes a circuit in the pad, ringing the bell and waking the child. With repeated use the child learns to awaken before wetting occurs. -Training of the bladder through”retention-control” techniqueBiological treatment:-Start treatment at a daily dosage of 25 mg, titrating up by 25 mg every 4 to 7 days,till reaching a dose of 75- to 125-mg (5 mg/kg body weight). electrocardiographic (ECG) monitoring is recommended at dosages above 3.5 mg/kg. A pretreatment baseline ECG is also recommended. - Desmopressin oral tablets in a dosage of 200-400 mg for primary nocturnal enuresis . Be cautious about the risk of fluid overload.

Functional encopresis

-It is repeated passing of faeces into iappropriate places after the age at which bowel control is usual (4 years old)

-Physical causes should be ruled out e.g. chronic constipation with overflow incontinence.

-Stressful events at home may precipitate the condition (marital discord, arrival of a new born sibling, separation from the caregiver to whom he is attached)

-Assessment should include parental attitude, emotional disturbances in the child, his I.Q(level of intelligence) and the child’s concern about the problem.

Behaviour therapy in form of rewarding success and ignoring failure often is helpful.

Use of laxatives which increase the bulk of stools is helpful to regulate the time of voiding.

Parental guidance , family therapy is required in certain cases especially when the incontinence is seen by the child as a way to annoy the parents.

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