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Ovid: Oxford Handbook of Psychiatry

Editors: Semple, David; Smyth, Roger; Burns, Jonathan; Darjee, Rajan; McIntosh, Andrew Title: Oxford Handbook of Psychiatry, 1st Edition Copyright ©2005 Oxford University Press > Table of Contents > Chapter 14 – Child and adolescent psychiatry Chapter 14 Child and adolescent psychiatry P.566
Introduction The ‘normal’ and ‘abnormal’ child The practice of child psychiatry involves the detection, evaluation, and care of children who have mental health needs. This may occur within formal specialist services or at a primary health care level, so it is essential that all individuals involved in the care of children have at least a basic understanding of normal and abnormal childhood experience and behaviour. Differentiating ‘normal’ from ‘abnormal’ can be difficult in young people since they are subject to developmental change and thus ‘normality’ evolves and varies according to differing age. Furthermore, what is normal may vary according to the family, social, religious, and cultural environment. Models of normal childhood experience and behaviour that are based solely on the norms of a particular society may be completely inappropriate in a different context. Having said this, there are a number of core ‘norms’ that transcend societal barriers, and likewise there are a number of core mental syndromes that have been shown to exist worldwide. ‘Adaptive’ and ‘maladaptive’ behaviours Another principle that bears consideration in caring for the mental health needs of young people is the fact that symptoms are not always abnormal. An evolutionary perspective is useful here since it may be helpful to consider whether a specific experience or behaviour that manifests is adaptive or maladaptive. Is the symptom a normal response in a given situation that serves to successfully elicit caring behaviour from the parent or other caregiver? For example, a baby’s persistent crying when hungry is adaptive and therefore ‘normal’ because it is ‘designed’ to elicit prompt feeding. Likewise, anxiety in a 2-year-old who is being separated from his/her parent into the care of a stranger is normal since, at this developmental stage, the child may perceive the attachment figure as the only source of safety. On the other hand, disabling separation anxiety in a 7-year-old is considered abnormal since the child has achieved a level of cognitive development at which he/she should have learned that many non-attachment figures might be considered ‘safe’. P.567
The barb in the arrow of childhood suffering is this: its intense loneliness, its intense ignorance. –Akhenaton (1354 BC), Egyptian king If there is anything we wish to change in the child, we should first examine it and see whether it is not something that could better be changed in ourselves. Carl Gustav Jung (1875–1961) P.568
Assessment (1)—principles The ‘biopsychosocial approach’ Understanding and managing successfully the mental and behavioural problems of children depends upon the thoughtful consideration of all the biological, psychological, and social factors that may play a role in the generation of symptoms. It is important to remember that several factors may interact in a dynamic 2-way fashion, giving rise to symptoms. The ‘biopsychosocial approach’ is useful at all stages of the evaluation and intervention provided to a child. The role of the multidisciplinary team Child and adolescent (C&A) mental health care exemplifies the relevance of and need for a multidisciplinary approach. For medically trained professionals who are used to ‘leading the team’, C&A work may be at first a little bewildering. New trainees may find themselves at a loss as to the nature of their role within a team where social workers and psychologists may be better equipped to manage a specific case. But because young people are embedded within family, social, and educational systems, their problems cannot be medicalised and treated within an exclusively medical model. An holistic management plan for a child or adolescent presenting to health services might include the involvement of some or all of the following professionals:

  • Psychiatrists and psychiatric nurses
  • Psychologists and psychotherapists
  • Occupational therapists, speech therapists, and physiotherapists
  • Social workers, welfare agencies, and other statutory bodies
  • Specialist paediatricians and neurologists
  • Teachers and educational services
  • Police services and the legal/court system

Children and families When a young person comes into contact with mental health services he/she is more likely to have been referred for help than to have brought him or herself. This is important to remember, since ‘the patient’ may have no say in his/her referral and this may have implications for the therapeutic relationship. In addition, one is rarely dealing with the young person alone—young people are usually dependant upon caregivers, whether they are parents or other adults. Thus one is commonly confronted by a room full of people who may have differing experiences, motivations, and interpretations of the young ‘patient’s’ problems and needs. The professional in this situation needs to be aware of the various dynamics and be vigilant in remaining objective and non-partisan. Sometimes a child’s ‘symptoms’ are in fact the presenting symptoms of a family problem. Children may become anxious, depressed, or behaviourally disturbed as a result of marital conflict, parental illness, or dissocial behaviour, or other pathologies within the home. In these cases the challenge is to disentangle and identify the root causes of the child’s symptoms. Likewise, families and other caregivers need to be actively included within the management plan for a child. With adolescents this may not always be the case. P.569
Assessing children and their families Flexibility is important when assessing children and their families. While a general system of assessment works in most cases, not all children have a standard ‘nuclear family’ arrangement. For example, some may live in foster homes or in children’s homes. Older adolescents too, may have variable domestic situations, including being alienated from their families. Thus sensitivity to individual circumstances is mandatory. In general though, an assessment should include the components listed on pages pp. 570, 571.1–2 References 1 Barker P (1988) Basic Child Psychiatry. Blackwell Science Ltd, Oxford. 2 Goodman R and Scott S (1997) Child Psychiatry. Blackwell Science Ltd, Oxford. P.570
Assessment (2)—practice Interviewing the family

  • Where possible it is advisable to see the child or adolescent with all members of the family who live in the house. A good explanation to family members is to stress the importance of individual perspectives and experiences of the problem and the fact that each member can contribute to the solution.
  • Establishing rapport or ‘joining the family’ is a primary objective of the initial interview.
  • Define the problem/s and the desired outcome.
  • Obtain the family history and construct a genogram.
  • Developmental history of the child, parental relationship issues, and parental physical and mental health may best be obtained from parents alone, as it may be inappropriate discussing such information with children present.
  • Observe family functioning and interactions. Note patterns of communication, degree of warmth, power dynamics, alliances, etc.

Interviewing the child alone

  • Establishing rapport and gaining the child’s confidence are primary objectives of the first interview. Young children should be invited to play, draw, etc.
  • Begin with subjects well away from the presenting problem/s (e.g. interests and hobbies, friends and siblings, school, holidays).
  • Progress to enquiring about child’s view of the problem, worries, fears, sleep and appetite, mood, self-image, peer and family relationships, experiences of bullying or teasing, abuse, persistent thoughts, fantasy life, abnormal experiences, suicidality, etc. (It may take several interviews to obtain a full picture.)
  • Observe: levels of activity and attention; physical and mental level of development; mood and emotional state; quality of social interaction.
  • Physical examination—usually have a parent present.

Gathering other information

  • Obtain consent to contact school for meeting or report from teachers, school psychologists, etc. Consider asking teacher to complete a checklist (e.g. Child Behaviour Checklist; Connors’ Teacher Rating Scale).
  • Consult other caregivers, medical professionals who have treated the child, and social agencies that have been involved with the child and/or family.
  • Other rating scales (e.g. K-SADS; BDI).
  • Psychological tests: may include IQ, personality and developmental assessments.
  • Investigations: haematology; chromosome studies; EEG; CT; etc.

Formulation of the problem

  • Consider aetiology in terms of constitutional, temperamental, physical, and environmental factors.
  • Most symptoms fall into one (or several) of the following domains: emotional symptoms; conduct symptoms; developmental symptoms; relationship symptoms.
  • Consider predisposing, precipitating, perpetuating, and protective factors.

Adolescence1 Adolescence is not just a blend of childhood and adulthood; it is a stage with unique biological and social characteristics of its own. Behavioural problems and disorders occurring during adolescence often represent exaggerations or unresolved versions of the normal development tasks of adolescence. Adolescence is a relatively new social phenomenon, since the age of puberty has steadily dropped while education has become prolonged over the last few centuries. This means that, particularly in the developed world, individuals achieve physical and sexual maturity before they assume adult roles. Biological factors defining adolescence include the achievement of sexual maturity as well as the physical and cognitive changes resulting from hormonal shifts. These changes are sexually dimorphic but do not approach the extent of sexual dimorphism apparent in other primates. Some of the psychological and social tasks of adolescence include:

  • Identity formation—during adolescence the individual attempts to develop a strong sense of differentiated self; this includes a social identity, a sexual identity, a work identity, and a moral identity. (DSM-IV provides a coding for ‘Identity Problem’ under the rubric of other conditions that may be a focus of clinical interest.)
  • Self-determination—there is a shift from accepting rules and boundaries imposed by others to setting them oneself; this involves substituting self-imposed control for externally imposed control.
  • Exploration vs. commitment—the dual process of exploring (‘keeping options open’) versus making a commitment to particular options, choices, beliefs, etc. Premature commitment can lead to ‘foreclosure’ while prolonged exploration without commitment is sometimes called ‘the psychosocial moratorium’.
  • Puberty rites—some societies provide structured rituals to assist the adolescent with the transition from childhood to adulthood.

Disorders of adolescence These are normally classified in terms of:

  • Residual childhood problems (e.g. conduct disorder; separation anxiety disorder)
  • Problems of adolescent transition (e.g. anorexia nervosa; parasuicide; substance misuse)
  • Early adult disorders (e.g. bipolar disorder; schizophrenia)

Epidemiology of adolescent disorders The Isle of Wight Study2 remains a classic investigation of adolescent psychopathology. Findings include: 10% had psychiatric disorders; another 10% had feelings of misery and worthlessness (? depression); most had emotional or conduct disorders; half of 14-yr-olds with disorders already had the disorder at 10 yrs of age. P.573
I would there were no age between ten and three-and-twenty, or that youth would sleep out the rest; for there is nothing in the between but getting wenches with child, wronging the ancientry, stealing, fighting. –Shakespeare: The Winter’s Tale (Act III Scene 3) References 1 Goodman R and Scott S (1997) Child Psychiatry. Blackwell Science Ltd, Oxford. 2 Rutter M, Graham P, Chadwick OF, Yule W (1976) Adolescent turmoil: fact or fiction? J Child Psychol Psychiatry 17, 35–56. P.574
An approach to behavioural problems Five categories of behavioural problems:

  • Disruptive—this includes oppositional, aggressive, destructive, disobedient, hyperactive, and substance abuse behaviours.
  • Anxious—may manifest as clinginess, worry, fearfulness, shyness, avoidant behaviour, sleep problems, regressive behaviours (e.g. enuresis, encopresis, separation anxiety), somatisation, hyperactivity, ritualistic behaviours, etc.
  • Moody—may manifest as irritability, sadness, crying, avoidant behaviour, regressive behaviours, ‘acting out’ (oppositional behaviours), poor weight gain, sleep problems, etc.
  • Social deficits—manifests as playing alone, shyness, avoidant behaviours, no friends, unable to read social cues, relationship difficulties, inappropriate behaviours, language problems.
  • Developmental deficits—may be deficits in language, motor function, milestones, etc.

N.B. Many ‘symptoms’ cross category boundaries, so it is important to gain as broad a view of the behavioural ‘syndrome’ as possible. It may also be that a dimensional view of childhood behavioural problems is more appropriate than rigid categorisation. Differential diagnosis of various behavioural ‘symptoms’ Since individual ‘symptoms’ can occur in more than one disorder, it is worth considering a differential diagnosis for the presenting behavioural symptom. It is also extremely important to differentiate a clearly maladaptive behaviour from one that is developmentally or situationally appropriate. ‘Normal’ behaviours also include those that form part of the child’s expected testing and experimentation of the world. The child presenting with the following symptoms could have any of the listed conditions (which are discussed individually later in this section):

  • Hyperactive—ADHD, oppositional and conduct disorders, anxiety, depression, mania, PDDs, substance abuse, sexual abuse.
  • Inattention—ADHD, oppositional and conduct disorders, LD/PDDs, mood disorders, anxiety disorders, substance abuse, sexual abuse.
  • Separation problems—attachment disorders, anxiety, depression, developmental problems, sexual abuse.
  • Social problems, avoidance—depression, anxiety, social phobia, PDDs, sexual abuse.
  • Aggression, hostility—oppositional and conduct disorders, ADHD, mania, psychosis, depression, anxiety, developmental disorders, LD/PDDs, substance abuse, sexual abuse.
  • Regressive behaviours—depression, anxiety, developmental problems, LD/PDDs, substance abuse, sexual abuse.
  • Sexually inappropriate behaviours—sexual abuse, conduct disorders, substance abuse, mania, psychosis, LD/PDDs, normal testing.
  • Somatisation—anxiety, depression, LD/PDDs, psychosis, sexual abuse.
  • P.575

  • Tantrums—oppositional and conduct disorders, ADHD, depression, anxiety, LD/PDDs, sexual abuse, physical problems, mania, psychosis.
  • Ritualistic behaviours—normal, anxiety, OCD, LD/PDDs, psychosis.

Assessment of behavioural disorders—general principles

  • Identify the problem behaviour/s—obtain a full description (from parents, child, teachers, etc.) of the problem behaviour/s. This should include the evolution of the behaviour, a chronology of the child’s typical daily activities, the setting in which the behaviour occurs, the effects of it on family, school, relationships, etc, and attitudes of others to the behaviour/s. It is always appropriate to speak to the child alone (if possible) to establish his/her views, desires, and mental state.
  • Determine the parental strategy—it is important to find out how the parents deal with the behaviour/s. This includes information about their expectations, philosophy of parenting, interpretation of the behaviour/s, moral, religious, and cultural views on parenting, etc. Also, how do the parents react or respond to the behaviour/s? How do they discipline or punish? What do they tolerate? Are they permissive or restrictive? Are they overprotective or uninvolved? Do they feel empowered or impotent, helpless, and incompetent as parents? How do they manage their frustrations, anger, etc? What coping mechanisms do they have?
  • Family history and dynamics—as well as gathering a full family history of health, psychiatric problems, social and cultural circumstances, and support structures, it is also important to assess parental and sibling relationships, the presence of any significant stressors or losses, and how the problem behaviour interacts with family dynamics.
  • Social behaviour—the evolution of the child’s social behaviour, including social developmental, attachment behaviour, imaginary play, reading of social cues, relationships, and language use.
  • School behaviour—attendance, changes in school, separation issues, socialisation, performance, peer and teacher interactions and responses, friendships, bullying, etc.
  • Child’s health and development—pregnancy, birth, and developmental milestones. Was the child planned, wanted? How did siblings react? How did parents and siblings cope? Any post-partum problems? Were there supports? Also, child’s temperament, illnesses, treatment, etc.
  • Direct observation of parent-child interaction—during the interview/s it is important to note how the child behaves and how parents respond and interact with the child. If siblings can be present their behaviour and interactions can also be evaluated. A home and/or school visit may add additional information about the behaviour in these settings.
  • Collateral information—teachers, extended family, and social services may be able to provide important input and permission should be sought to contact and involve them where appropriate.

Attention deficit hyperactivity disorder (ADHD) In recent years ADHD has become increasingly diagnosed and is the focus of both a great deal of research and an excess of media publicity. Many C&A mental health services have experienced a major increase in referrals for assessment for ADHD and doctors are under increasing pressure to prescribe stimulant medication for ‘difficult kids’. The accepted definition of ADHD is: ‘a persistent pattern of inattention and/or hyperactivity that is developmentally inappropriate’. DSM-IV specifies that at least some of the symptoms must have their onset before 7 yrs of age. (This is controversial, since studies have demonstrated that up to 90% of the ‘inattentive’ subtype may have a later onset1.) Furthermore, the behaviour should occur in at least 2 settings and should persist for at least 6 months, to fulfil diagnostic criteria. Clinical features (see opposite) Epidemiology In the USA, incidence is estimated at 3–5%, while in the UK the figure of 1% is reported. There is a male predominance of 3:1. Aetiology Genetics: 50% risk in MZ twins; 2x risk in siblings; ↑CD and substance abuse in parents; genes 5, 6, and 11 implicated. Neurological functional imaging shows frontal metabolism. Neurotransmitters DA and NA dysregulation in the prefrontal cortex. Psychosocial stress; family dysfunction; poor attachment, etc. Evolutionary ‘response-ready’ traits may have adaptive benefits. Other food additives, lead and alcohol exposure (little evidence). Comorbidity ADHD is highly comorbid with 50–80% of children having a comorbid disorder: specific learning disorders (60%); CD and ODD (40%); substance abuse; depression; bipolar disorder2 (NB Overlap in symptomatology). Outcome Approximately 20% develop dissocial personality traits; 15–20% develop substance misuse problems; high rates of suicidality, poor self-esteem, unemployment. ADHD symptoms may persist into adulthood (20–30% with full ADHD syndrome and -60% with 1 or more core symptoms). Impulsivity-hyperactivity remits early, while inattention often persists. Studies show a pattern of psychopathology, cognition, and functioning in adults similar to that in children and adolescents.3 Assessment

  • Interview with parents, including full developmental, medical, and family history and assess family functioning.
  • Interview with child: evaluate for physical or comorbid psychiatric disorder and assess attachment style and level of activity.
  • Collateral information from school, agencies, etc. A school visit to observe behaviour in the classroom may be useful.
  • Connor’s Assessment Scale.

Treatment Effort should be made to provide psychological and social interventions before resorting to pharmacological treatment. Principles are:

  • CBT methods, especially behavioural, are often effective
  • Social skills training
  • Parent management training
  • Individual/family/group therapies
  • Educational/remedial interventions
  • Stimulants (e.g. Methylphenidate (Ritalin®); dextroamphetamine; pemoline)

Clinical features of ADHD

  • Hyperactivity-impulsivity symptoms include: fidgeting, moving, getting up and running about, climbing on desks, etc.; talking excessively; unable to play quietly; blurting out answers; jumping the queue; continually interrupting.
  • Inattention symptoms include: cannot sustain attention; easily distracted; poor task completion; dislikes, can’t organize, and makes mistakes with tasks that require attention; doesn’t listen, is forgetful, and loses things for tasks.
  • Very young children are often sensitive, have poor sleep, cry a lot, and are constantly active.
  • Two groups are recognised anecdotally: the ‘organic’ group may have soft neurological signs, subtle motor and visuo-perceptual abnormalities, learning difficulties, and some degree of coordination problems; the ‘dynamic’ group commonly have a history of deprivation, poor attachment, stress and depression, and high levels of frustration.

References 1 Applegate B, Lahey BB, Hart EL, et al. (1997) Validity of the age-of-onset criterion for ADHD: a report from the DSM-IV field trials. J Am Acad Child Adol Psychiatry 36, 1211–21. 2 Giedd JN (2000) Bipolar disorder and attention-deficit/hyperactivity disorder in children and adolescents. J Clin Psychiatry 61 (suppl 9), 31–4. 3 BiedermanJ, Faraone SV, Spencer T, et al. (1993) Patterns of psychiatric comorbidity, cognition, and psychosocial functioning in adults with attention deficit hyperactivity disorder. AJP 150, 1792–8. P.578
Methylphenidate (Ritalin®) Mode of action An indirect sympathomimetic that ↑ release of DA and NA. Indications ADHD and narcolepsy. Clinical effects ↑ concentration and attention and ↓ impulsivity. Side-effects ↓ Appetite and weight; nausea and vomiting; anxiety, insomnia, dysphoria, headaches; rarely tics, cardiac problems, and ↑ BP; high dose can cause psychosis or seizures. Growth suppression may be a long-term outcome of high doses over long periods without ‘drug holidays’. Prescribing practices Vary, with higher doses in the USA (1 mg/kg) than in the UK (0.3 mg/kg). Principles of prescribing (see NICE guidelines opposite)

  • Start with 5–10 mg in morning; can add 5–10 mg at midday; late dose can cause insomnia
  • Start low and titrate weekly
  • Check weight, BP, and liver function regularly
  • Monitor response (Connor’s Rating Scale)
  • May develop ‘tolerance’ over time; can get rebound hyperactivity as effect wears off (NB short t½ 1–2hrs); give ‘drug holidays’ over weekends

N.B. The 1990s saw increasing use and abuse of Ritalin worldwide. Concerns include the possibility of dependence, tardive tic disorders, and growth suppression. Vigilance should be exercised in correct diagnosis and prescription of ritalin. P.579
NICE guidance on the use of methylphenidate (Ritalin®, Equasym®) for attention deficit/hyperactivity disorder (ADHD) in childhood

  • Methylphenidate is recommended for use as part of a comprehensive treatment programme for children with a diagnosis of severe attention deficit/hyperactivity disorder (ADHD). ‘Severe ADHD’ is broadly similar to a diagnosis of hyperkinetic disorder (HKD), although in some cases treatment may be appropriate for children and adolescents who do not fit the diagnostic criteria for HKD but are experiencing severe problems due to inattention or hyperactivity/impulsiveness.
  • Methylphenidate is not currently licensed for children under the age of six or for children with marked anxiety, agitation, or tension; symptoms or family history of tics or Tourette’s syndrome; hyperthyroidism; severe angina or cardiac arrhythmia; glaucoma; or thyrotoxicosis. Caution is required in the prescribing of methylphenidate for children and young people with epilepsy, psychotic disorders, or a history of drug or alcohol dependence.
  • Diagnosis should be based on a timely, comprehensive assessment conducted by a child/adolescent psychiatrist or a paediatrician with expertise in ADHD. It should also involve children, parents and carers, and the child’s school, and take into account cultural factors in the child’s environment. Multidisciplinary assessment, which may include educational or clinical psychologists and social workers, is advisable for children who present with indications of significant comorbidity.
  • Treatment with methylphenidate should only be initiated by C&A psychiatrists or paediatricians with expertise in ADHD, but continued prescribing and monitoring may be performed by GPs, under shared care arrangements with specialists.
  • Careful titration is required to determine the optimal dose level and timing. The drug should be discontinued if improvement of symptoms is not observed after appropriate dose adjustment.
  • A comprehensive treatment programme should involve advice and support to parents and teachers, and could, but does not need to, include specific psychological treatment (such as behavioural therapy). While this wider service is desirable, any shortfall in its provision should not be used as a reason for delaying the appropriate use of medication.
  • Children on methylphenidate therapy should receive regular monitoring. When improvement has occurred and the child’s condition is stable, treatment can be discontinued at intervals, under careful specialist supervision, in order to assess both the child’s progress and the need for continuation of therapy.

Conduct disorder (CD)1,2 Essence A repetitive and persistent pattern of behaviour in which the basic rights of others or major age-appropriate societal norms or rules are violated. These violations include aggression or cruelty to people and animals, destruction of property, deceitfulness or theft and serious violation of rules (e.g. truanting or running away). The term ‘delinquent’ is unfashionable and refers to the individual whose behaviour leads them into the criminal justice system—‘young offender’ is the modern term. CD is important because it is common; it is the cause of great suffering in both the individual and in society; it is a risk factor for adult antisocial behaviour; and it is a major burden on public resources. In many countries it constitutes one of the major public mental health problems, making prevention strategies important (see opposite). Epidemiology In North America CD is the most common reason for psychiatric evaluation in children and adolescents. It has an earlier onset and is more common in boys than in girls. Aetiology A family history of antisocial behaviour or substance abuse, low CSF serotonin, low IQ, and brain injury are biological factors associated with risk for CD. Psychosocial risk factors include: parental criminality and substance abuse; harsh and inconsistent parenting; domestic chaos and violence; large family size; low socio-economic status and poverty; early loss and deprivation; lack of a warm parental relationship; school failure; social isolation; and exposure to abuse and societal violence. Comorbidity ADHD; substance abuse; suicidality. Clinical features (As above) Other common features: early sexual behaviour, gang involvement, low self-esteem, lack of empathy. Course and outcome CD is often chronic and unamenable to treatment. Adult outcomes include: dissocial personality disorder; criminality; substance abuse; and mental disorders. However, less than 50% of CD cases have severe and persistent antisocial problems as adults. Predictors of poor outcome are: early onset (before 10 yrs); low IQ; poor school achievement; attentional problems and hyperactivity; family criminality; low socio-economic status; and poor parenting. Protective factors are: female gender; high intelligence; resilient temperament; competence at a skill; warm relationship with a key adult; commitment to social values; strong and stable community institutions; increased economic equality. Assessment

  • Clarify the purpose of the assessment (clinical, community, forensic).
  • Obtain a full history with collateral from school, community, and legal system.
  • Identify causal risk and protective factors.
  • Assess for comorbidity and make a diagnosis (±psychometric testing).
  • Formulate the problem and establish management plan (see opposite.)

Management of CD3 Multiple strategies are indicated:

  • Ensure the safety of the child
  • CBT problem-solving skills-in individual/group setting
  • Parent management training-to improve social exchanges/stability
  • Functional family therapy-combined CBT/systems approach
  • Multi-systemic therapy-family-based, including school and community
  • Medication-only for comorbid disorders (e.g. ADHD—p. 576)
  • Academic and social support-referral to relevant agencies/groups

Prevention strategies and policy implications

  • Preschool child development programmes—identifying parents and families at risk and instituting home visits and support
  • School programmes—identify children at risk and institute classroom enrichment, home visits, and parent and teacher training
  • Community programmes—identify children and adolescents through their involvement with social agencies and institute interventions such as enhanced recreation programmes, parent training and adult mentoring of youth
  • Social and economic restructuring to reduce poverty and to improve family and community stability.

Oppositional defiant disorder (ODD) Essence An enduring pattern of negative, hostile, and defiant behaviour, without serious violations of societal norms or the rights of others. Behaviour may occur in one situation only (e.g. home) and may lead to social isolation, depression, or substance abuse. Epidemiology Onset is between 3 and 8 years old. More common in boys during childhood but equal rates in adolescence. A common condition affecting 15–20 % of C & As. Aetiology Temperamental factors; sick or traumatised child; power struggle between parents and child (NB differentiate from normal autonomous ‘struggle’ of the young child and adolescent). Outcome ¼ show no symptoms later in life but many progress to CD and/or substance abuse. Management Same management principles as for CD (see above). References 1 Bassarath L (2001) Conduct disorder: a biopsychosocial review. Can J Psychiatry 46, 609–16. 2 Waddell C, Lipman E, Offord D (1999) Conduct disorder: practice parameters for assessment, treatment, and prevention. Can J Psychiatry 44 (supp 2), 35s–39s. 3 Kazdin AE (2000) Treatments for aggressive and antisocial children. Child Adolesc Psych Clinics N America 9, 841–58. P.582
Pervasive developmental disorders (PDDs)1 Pervasive developmental disorders (PDDs) define a spectrum of behavioural problems commonly associated with autism. They frequently involve a triad of deficits in social skills, communication/language, and behaviour. The feature that all have in common is a difficulty with social behaviour. DSM-IV categorises PDDs as follows:

  • Autism (pp. 584, 585)
  • Asperger’s syndrome
  • Rett’s syndrome
  • Childhood disintegrative disorder

PDDs are characterised by either a lack of normal development of skills or the loss of already acquired skills. There is a gender bias with male > female predominance in all syndromes except Rett’s syndrome (female predominance). Prevalence of PDD ranges from 10–20 cases per 10 000 individuals. Asperger’s syndrome (AS)2 Essence A syndrome first described by Hans Asperger in 1944 characterised by severe persistent impairment in social interactions, repetitive behaviour patterns, and restricted interests. IQ and language are normal or, in some cases, superior. Mild motor clumsiness (ICD-10) and a family history of autism may be present. Newton and Einstein may have had AS. Epidemiology Male predominance. Prevalence may be as high as 1 in 300 as AS is almost certainly under-recognised. ‘Autistic spectrum’ There is some evidence that AS forms a spectrum with autism and high-functioning autism in terms of aetiology, pathology, and clinical presentation. Children with AS may have more striking autistic features before age 5, but later develop ‘normally’ in most spheres excepting social behaviour. Social deficits commonly manifest in adolescence or early adulthood when the individual experiences difficulty with intimate relationships. Psychiatric comorbidity is high with depression most common. BPAD and schizophrenia are more common than in the general population. Rett’s syndrome (RS)3 A genetic disorder (X-linked) of arrested neuro-development that affects almost exclusively females. Prevalence is 1 per 10–20 000. The first 6 months of life are normal, but between 6 and 18 months there is progressive head growth, loss of motor skills, loss of hand skills, stereotypies, abnormal hand movements, loss of social skills and language development. Seizures occur in 75% while spasticity, scoliosis, and respiratory difficulties are common outcomes. Developmental arrest plateaus and many may reach adulthood, although disability is great and prognosis poor. P.583
Childhood disintegrative disorder (CDD)4 Rare, occurring in fewer than 5 in 10 000 children. Male predominance. There is normal development for 2–3 years, followed by a loss of acquired motor, language, and social skills between ages 3 and 4 years. Stereotypies and compulsions are common. Cause is unknown and prognosis is poor. PDD-NOS Also termed ‘atypical autism’, PDD-NOS is relatively common and encompasses sub-threshold cases where there are impairments of social interaction, communication, and/or stereotyped behaviour patterns or interest, but where full criteria for other PDDs are not met. Did Newton and Einstein have AS? Isaac Newton may well have had AS. He hardly spoke, was so engrossed in his work that he often forgot to eat, and was lukewarm or bad-tempered with the few friends he had. If no one turned up to his lectures, he gave them anyway, talking to an empty room. He had a nervous breakdown at 50, brought on by depression and paranoia. As a child, Albert Einstein was a loner, and repeated sentences obsessively until he was seven years old. He became a notoriously confusing lecturer. In spite of this, he made intimate friends, had numerous affairs, and was outspoken on political issues. References 1 Shaw JA (1999) Practice parameters for the assessment and treatment of children and adolescents who are sexually abusive of others. American Academy of Child and Adolescent Psychiatry Working Group on Quality Issues. J Am Acad Child Adolesc Psychiatry 38 (12 supp), 32s–54s. 2 Gillberg C (1998) Asperger syndrome and high-functioning autism. BJP 172, 200–9. 3 Schneider JH and Glaze DG (2002) http://www.emedicine.com 4 Bernstein BE (2002) http://www.emedicine.com P.584
Autism1 Essence Autism was first described by Maudsley in 1867 and named ‘infantile autism’ by Leo Kanner in 1943. It is a syndrome that has engendered controversy in terms of its definition, relationship to other syndromes (e.g. schizophrenia), and aetiology. It is characterised by a triad of symptoms:

  • Abnormal social relatedness
  • A qualitative abnormality in communication or play
  • Restricted, repetitive, and/or stereotyped behaviour, interests, and activities

In addition, 70% have mild to moderate LD. The remaining 30% with normal IQ are classified as either high-functioning autism (with language difficulties) or Asperger’s syndrome (with normal language). NB This last point is controversial and many would consider AS not to be classified as a form of autism. In general terms, 1–2% of those with autism have a ‘normal’ life; 5–20% have a ‘borderline’ prognosis (i.e. varying degrees of independence); but 70% are totally dependent upon support. Epidemiology The onset of symptoms is typically before age 3. Male: female ratio is 3–4:1. Prevalence is 5–10 per 1000 individuals. Aetiology The cause is unknown but a number of hypotheses exist: genetic (↑ in Down’s syndrome and fragile X); obstetric complications; toxic agents; pre/postnatal infections (↑ with maternal rubella); autoimmune (anecdotal MMR-not proven);↑ association with neurological disorders (e.g. tuberous sclerosis) Pathophysiology MRI: some have ↑brain size; ↑lateral and 4th ventricles; frontal lobe and cerebellar abnormalities. Pathology: abnormal purkinje cells in cerebellar vermis; abnormal limbic architecture. Biochemistry: 1/3 have ↑ serum 5HT; some have ↑ β-endorphin immunoreactivity. Clinical features

  • Abnormal social relatedness: impaired non-verbal behaviour; poor eye contact; impaired mentation; failure to develop peer relationships; reduced interest in shared enjoyment; lack of social or emotional reciprocity and empathy; attachment to unusual objects.
  • Abnormal communication or play: delay or lack of spoken language; difficulty in initiating or sustaining conversation; stereotyped and repetitive (or idiosyncratic) language; mixing of pronouns; lack of developmentally appropriate fantasy, symbolic, or social play.
  • Restricted interests or activities: encompassing preoccupations and interests; adherence to non-functional routines or rituals; resistance to change; stereotypies and motor mannerisms (e.g. hand or finger flapping or body rocking); preoccupation with parts of objects.
  • Neurological features: seizures; motor tics; ↑ head circumference; abnormal gaze monitoring; ↑ ambidexterity.
  • Physiological features: unusually intense sensory responsiveness (e.g. to bright lights, loud noise, rough textures); absence of typical P.585
    response to pain or injury; abnormal temperature regulation; ↑ paediatric illnesses.
  • Behavioural problems: irritability; temper tantrums; self-injury; hyperactivity; aggression.
  • ‘Savants’: a minority may have ‘islands of precocity’ against a background of LD (i.e. isolated abilities).

Differential diagnosis Other PDDs; childhood schizophrenia; LD; language disorders; neurological disorders; sensory impairment (deafness or blindness); OCD; psychosocial deprivation. Assessment of autism

  • A multidisciplinary approach is required, involving psychiatrists, psychologists, paediatricians, neurologists, speech therapists, OT, and primary care teams.
  • Full clinical evaluation: including physical and mental state as well as specific developmental, psychometric, and educational assessments.
  • Rating scales: Autism Behaviour Checklist (ABC); Childhood Autism Rating Scales (CARS); Autism Diagnostic Interview-Revised (ADI-R); Autism Diagnostic Observation Schedule (ADOS).

Treatment strategies for autism

  • Educational and vocational interventions: special versus mainstream
  • Behavioural interventions: includes behaviour modification, social skills training, and CBT methods
  • Family interventions: education; support; advocacy
  • Speech and language therapy; OT; physiotherapy; dietary advice; etc.,
  • Pharmacotherapy: symptom management (e.g. antipsychotics, for stereotypies); SSRIs for compulsive and self-harming behaviours and depression/anxiety
  • Treat medical conditions (e.g. epilepsy, GIT problems)

References 1 Brasic JR (2002) http://www.emedicine.com P.586
Language and learning disorders (LLDs)1 DSM-IV groups together a number of LLDs that share the following:

  • Performance significantly below that expected for IQ or age
  • A discrete developmental disability in the absence of LD
  • Commonly present as emotional or behavioural problems
  • 50% have a comorbid psychiatric disorder and many have other LLDs
  • Most show strong evidence of heritability

Reading disorder (‘dyslexia’) Difficulty with reading, in most cases involving a deficit in phonological-processing skills. 4% of school-age children. Male predominance. There is often a family history of dyslexia. 20% have comorbid ADHD or CD. Management includes 1:1 remedial teaching and parent involvement improves long-term outcome. Disorder of written expression Often coexists with dyslexia and manifests as difficulties with spelling, syntax, grammar, and composition. Occurs in 2–8% of school-age children with a 3:1 male predominance. Difficulties may first emerge with the shift from narrative to expository writing assignments. Mathematics disorder Female predominance and occurs in 1–6% of school-age children. Often associated with visuo-spatial deficits and attributed to right parietal dysfunction. Language disorders Includes expressive and receptive language disorders, phonological disorder and stuttering. There are delays or difficulties in language use that are not attributable to sensory or motor deficit or environmental deprivation, in excess of that based on scores of non-verbal intelligence. These disorders are highly heritable and may relate to impaired rapid temporal processing of auditory information. Male predominance and occurs in 5–10% of school-age children. Treatment includes speech therapy. Stuttering2 A disturbance in the normal fluency and time patterning of speech. Usually struggle with initial syllables. Male predominance of 3:1. Most children grow out of it but stuttering affects 1–2% of adults. Majority of cases are developmental but occasionally there are acquired cases (e.g. head injury). Aetiology: genetic; incomplete cerebral dominance; hyperdopaminergic state. Management: speech therapy; antipsychotics (risperidone); (SSRIs may have some effect). References 1 AACAP (1998) Practice parameters for the assessment and treatment of children and adolescents with language and learning disorders. J Am Acad Child Adolesc Psychiatry 37 (10 supp), 46s–62s. 2 Costa D and Kroll R (2000) Stuttering: an update for physicians. CMAJ 162, 1849–55. P.587
Enuresis Essence Voluntary or involuntary voiding of urine, usually at night, in a child of 5 years or older. More common in males than females. Approximately 3–7% of 7-year-olds. Enuresis commonly results in low self-esteem and often becomes a focus for family conflict. Aetiology Genetic—75% have a family history of enuresis; generalised developmental delay; poor potty training; psychosocial stressors (e.g. birth of a sibling, hospitalisation, starting school, domestic conflict); comorbid psychopathology (e.g. depression); organic causes. N.B. Very important to exclude organic cause: UTI; obstructive uropathy; neurological problems; diabetes mellitus; seizures; drug side-effects. Course Distinguish between 1°(never dry) and 2° (previously dry) enuresis. Management Behavioural modification is the mainstay and includes:

  • Restrict fluids at night
  • ‘Night lifting’
  • Record-keeping (e.g. starcharts)
  • Mattress alarm
  • Rewards
  • Imipramine—anticholinergic effect of increasing sphincter tone. 80% have some improvements but tolerance may develop after 6 weeks. NB Potential hazards of TCAs in children.

Encopresis Essence Voluntary or involuntary soiling of stool in inappropriate places or in a child of 4 years or older. More common in males than females. Approximately 5% of children over 4 years of age. Aetiology Regression under stress; power struggle with parents; child is preoccupied or distracted; organic causes. (Mechanism often involves retention/constipation with overflow.) N.B. Very important to exclude organic cause: Hirschprung’s disease; anal pathology; drug side-effects; neurological problems; nutritional disorders. Course Usually stops by adolescence. Encopresis commonly results in low self-esteem, ostracism, and family over-involvement. Management It is important to manage family stress and discord, educate parents about minimising shame (change pants often), and support the child psychologically. A paediatric referral is always indicated. Behavioural methods (see above) are the mainstay of treatment, but imipramine may offer some improvement. P.589
Other behavioural disorders Motor skills disorder There are a number of conditions affecting children where the primary problem involves an impairment of motor function. This may manifest as a delay in developmental milestones and includes impairments of coordination, fine motor skills, and gross movement. Gross motor impairments suggest genetic aetiology while fine motor impairments suggest environmental causation. Treatment involves physiotherapy, OT, and educational assistance. Sleep disorders Classified as for adult sleep disorders (see pp. 388, 389, 390, 391, 392, 393, 394, 395, 396, 397, 398, 399, 400, 401, 402, 403, 404, 405, 406, 407, 408, 409, 410, 411, 412, 413, 414, 415, 416, 417, 418, 419, 420, 421, 422, 423, 424, 425). The main syndromes that manifest in children and adolescents are: nightmare disorder (p. 418); sleep terror disorder (p. 415); and sleepwalking disorder (pp. 414, 415). Management is the same as for adults. Feeding and eating disorders of infancy and early childhood1 Pica This is a common condition where there is persistent (>1month) eating of non-nutritive substances at a developmentally inappropriate age (>1½ yrs). Common substances are: dirt, stones, hair, faeces, plastic, paper, wood, string, etc. It is particularly common in individuals with developmental disabilities and may be dangerous or life-threatening depending on the substance ingested. Consequences may include toxicity, infection, or GIT ulceration/obstruction. Typically occurs during 2nd and 3rd yrs of life, although young pregnant women may exhibit pica during pregnancy. Hypothesised causes include: nutritional deficiencies; cultural factors (e.g. clay); psychosocial stress; malnutrition and hunger; brain disorders (e.g. hypothalamic problem). Rumination This is the voluntary or involuntary regurgitation and rechewing of partially digested food. Occurs within a few minutes post-prandial and may last 1–2 hrs. Regurgitation appears effortless and is preceded by belching. Typical onset 3–6 months of age, may persist for several months and then spontaneously remit. Also occurs in older individuals with LD. May result in weight loss, halitosis, dental decay, aspiration, recurrent RTI, and sometimes asphyxiation and death (5–10% of cases). Causes include: LD; GIT pathology; psychiatric disorders; psychosocial stress. Treatment includes physical examination and investigations; behavioural methods; nutritional advice. References 1 Ellis CR and Schnoes CJ (2002) http://www.emedicine.com P.590
Attachment disorders Normal attachment Attachment refers to the strong emotional bond that exists between a child and the primary caregiver. John Bowlby described the formation of healthy secure attachment from early infancy, as well as a normal pattern of separation anxiety commencing between 6 and 9 months, peaking between 12 and 18 months and decreasing during the 3rd year. Disorders of attachment Insecure attachment manifests as anxious, avoidant, or reactive attachment and predisposes the child to other neurotic disorders later on. Separation anxiety disorder This represents increased and inappropriate anxiety around separation from attachment figures or home, which is developmentally abnormal and results in impaired normal functioning. It occurs in about 3.5% of children and 0.8% of adolescents. Causes genetic vulnerability; anxious, inconsistent, or over-involved parenting; and regression during periods of stress, illness, or abandonment. Symptoms anxiety about actual or anticipated separation from or danger to attachment figure; sleep disturbances and nightmares; somatisation; and school refusal (especially in adolescents). Comorbidity depression; anxiety disorders (panic with agoraphobia in older children); ADHD; oppositional disorders; learning disorders; and developmental disorders. Assessment full physical examination; attempt interview on own; parental interview including full developmental and family history; collateral from school if consented. Treatment family/group therapies; CBT and play therapies; bridging back to school; SSRIs (e.g. fluoxetine, paroxetine).1 Reactive attachment disorder This disorder reflects a disturbed pattern of social relatedness, is diagnosed before age 5 yrs, and may manifest as either inhibited or disinhibited subtypes. Causes: deprivation and neglect, and this usually reflects a disturbance in the dyadic relationship between caretaker and child. Contributing factors include: caretaker may be young, isolated, inexperienced, and/or depressed; child may have difficult temperament and/or have a sensory impairment. It is more common in poverty-stricken and socially disrupted environments. Symptoms failure to thrive; malnutrition; listlessness; vigilance; withdrawal; diffuse attachments in disinhibited subtype. Differential LD; PDD; neurological disorders; psychosocial dwarfism. Management hospitalise and secure protection if indicated; therapy focuses on caretaker-child dyad; involve social services. P.591
Ethology and attachment The history of attachment theory is closely allied to the development of ethology, the study of animal behaviour in its natural environment. Konrad Lorenz (an Austrian doctor) and Nico Tinbergen (a Dutch biologist) are recognised as the fathers of ethology, and shared the Nobel Prize in 1973 for their contributions to the field. Some of their most important discoveries were the identification of imprinting, fixed action patterns (FAPs), and innate releasing mechanisms (IRMs)—all of which have informed the understanding of infant attachment behaviour. Lorenz classically described imprinting in ducklings and Greylag goslings, the phenomenon where young animals form an immediate and irreversible social bond with the first moving object they encounter. The phenomena of FAPs and IRMs were first observed in the herring gull and the stickleback, and formed a basis for understanding the complex innate mechanisms that facilitate mother-infant bonding during the first weeks. During the 1950s and 1960s, John Bowlby and Margaret Ainsworth used ethological principles to study the formation of healthy and abnormal attachment in children. Ainsworth developed the Strange Situation Procedure, an experiment that she used in several cultural settings to establish universal patterns of attachment. Healthy attachment was classically described as ‘secure’, while ‘insecure’ attachment encompassed ‘anxious’, ‘resistant’, and ‘avoidant’ types. These latter concepts are recognised in contemporary nomenclature under the diagnoses ‘separation anxiety disorder’ and ‘reactive attachment disorder’. Bowlby also coined the term ‘critical period’ to describe the stage during which the infant is most responsive to developing secure attachment. References 1 Bernstein BE (2002) http://www.emedicine.com P.592
Anxiety disorders—overview1,2 Anxiety and fear are an inherent part of the human condition and in times of danger are often adaptive. As a result of changing developmental and cognitive abilities during childhood, the content of normal fears and anxieties shifts from concerns about concrete external things to abstract internalised anxieties. Anxiety disorders are characterised by irrational fear or worry causing significant distress and/or impairment in functioning and their relative prevalence reflects this shift in content. Thus specific disorders appear more common during specific stages of development. Epidemiology Anxiety disorders are among the most common psychiatric disorders in youth. Prevalence rates range from 5–15% with 8% requiring clinical treatment. Age of onset varies for each disorder but range from 7 to 12 yrs. Separation anxiety disorder and specific phobia usually have onset in early childhood, Generalised anxiety disorder occurs across all age groups, while obsessive-compulsive disorder, social phobia, and panic disorder tend to occur in later childhood and adolescence. Aetiological factors Genetic vulnerability; temperament that exhibits ‘behavioural inhibition’ (timidity, shyness, and emotional restraint with unfamiliar people or situations); anxious attachment; negative life events; dysregulation of 5HT and NA systems. Organic causes of anxiety Medical conditions: hyperthyroidism; cardiomyopathy; arrythmias; respiratory and neurological diseases. Substances: alcohol; caffeine; cocaine; amphetamines; cannabis; SSRIs; LSD; ecstasy; etc. Assessment

  • Physical examination and interview with child
  • Interview with parents including developmental and family history
  • Rating scales: K-SADS; Hamilton Anxiety Rating Scale; DISC; CBCL

Treatment principles

  • CBT is supported by a number of controlled studies as the psychological treatment of choice for paediatric anxiety disorders. Focuses on relaxation training, exposure and response prevention, and cognitive restructuring.
  • Psycho-education and parent training.
  • Psychodynamic therapies include group, family, and individual/play techniques.
  • Pharmacological: SSRIs are first-line agents, but there are some data supporting specialist use of buspirone, alprazolam, and clonazepam in older children and adolescents with resistant symptoms.

References 1 Labellarte MJ, Ginsburg GS, Walkup JT, Riddle MA (1999) The treatment of anxiety disorders in children and adolescents. Biological Psychiatry 46, 1567–78. 2 Dadds MR and Barrett PM (2001) Practitioner review: psychological management of anxiety disorders in childhood. J Child Psychol Psychiat 42, 999–1011. P.593
Generalised anxiety disorder Essence Characterised by developmentally inappropriate and excessive worry and anxiety on most days about things not under one’s own control. Severe enough to cause distress and/or dysfunction. Children are often perfectionist and self-critical. Most common anxiety disorder of adolescence with approximately 4% prevalence in this group. More common in females during adolescence. Only 11/3 seek treatment. Symptoms Excessive worry; restlessness, irritability and fatigue; poor concentration; sleep disturbances; muscle tension. In children: somatic symptoms (headache; stomach pains or ‘irritable bowel’; rapid heart beat; shortness of breath); nail biting and hair pulling; and school refusal. Comorbidity Very high rates—up to 90%. Other anxiety disorders, depression, conduct disorders, and substance abuse are most common. Management CBT; SSRIs; benzodiazepines (see p. 356 for overview). P.595
Panic disorder/agoraphobia1 Essence Recurrent, unexpected panic attacks are the hallmark of this disorder, together with a period during which the child is concerned about having another attack and the possible consequences of an attack and exhibits significant behavioural changes related to the attacks. These latter features are referred to as anticipatory anxiety. The first attack must be uncued. A panic attack is described as a discrete period of increased fear peaking at about 10 minutes and lasting about 1½ to 1 hr. Symptoms Sweating, flushing, trembling, palpitations and tachycardia, chest pain, shortness of breath and choking, nausea and vomiting, dizziness, paraesthesia, depersonalisation and derealisation, and a fear of dying. N.B. In young children somatic symptoms predominate rather than classic symptoms. Agoraphobia may or may not coexist with the disorder, but is usually present. The essential feature is anxiety about being in a situation in which escape would be difficult or help unavailable should a panic attack occur. This leads to avoidance of places or situations and may result in school refusal and separation anxiety. Epidemiology Panic disorder has an estimated prevalence of 3–6% and is more common in females post-puberty. Peak onset is 15–19 yrs. Comorbidity Depression, substance abuse, and other anxiety disorders (especially social phobia) are most common. Management Exclude organic causes (pp. 344, 345); CBT; SSRIs; benzodiazepines (see pp. 348, 349 for details). References 1 Larsen LH (2002) http://www.eMedicine.com P.596
Social phobia and selective mutism Essence Social phobia (SP) is extremely common and often undiagnosed and is the 3rd most common mental health disorder in America. It is characterised by marked fear of one or more social or performance-related situations where the person is exposed to scrutiny and in which embarrassment may occur. Exposure to social situations usually causes an anxiety reaction (may be a panic attack) that is distressing and recognised as inappropriate. Thus situations are either avoided or endured with discomfort. This may lead to agoraphobia and in severe cases school refusal. Selective mutism (SM) primarily affects children and often manifests at school when the child cannot speak when called upon by teachers. The child may designate a friend or family member to serve as an interpreter and whispers in that person’s ear in order to communicate. Epidemiology SP is most common in adolescents with an estimated prevalence of 5–15% as opposed to only 1% in children. SM is seen in less than 1% of children in community settings and may represent SP with early onset. SP is more common in girls and the average age of onset for both genders is 12 yrs. Family studies demonstrate a 2x increased risk for SP in the relatives of SP probands, while twin studies show a 3x increased risk in monozygotic twins. Comorbidity High rates of other anxiety disorders (especially GAD, simple phobia, and panic disorder) in approximately 30–60% cases, with mood disorders (20%) and substance abuse also frequent comorbidly. Prognosis Although the prognosis for treated SP is fair to good, comorbid conditions may persist and hinder educational and social progress. Those who experience symptoms in 2 or more situations have a poorer outcome than those experiencing symptoms in a single situation only. Management High levels of clinician awareness in diagnosing SP; individual and family assessments; K-SADS rating scale; CBT; SSRIs; moclobemide (specialist use only). P.597
Simple phobias1,2 Essence Excessive fear of an object or situation with distress and phobic avoidance. There may be anticipatory anxiety and exposure can precipitate a panic attack. Causes Familial pattern in some cases; paired conditioning and sensitisation. Epidemiology Very common (10% in some studies); ♀:♂ = 2:1. Comorbidity Depression; substance abuse. Subtypes Animal phobias; natural environment phobias (especially 5–10 yr-olds); blood/infection/injury phobias; situational phobias (e.g. lifts, closed spaces); other. Management CBT is the mainstay, including relaxation training and graded exposure. References 1 Velting ON and Albano AM (2001) Current trends in the understanding and treatment of social phobia in youth. J Child Psychol Psychiat 42, 127–40. 2 Bernstein BE (2002) http://www.eMedicine.com. P.598
Post-traumatic stress disorder1,2 Essence A syndrome characterised by a triad of symptoms: intrusive re-experiencing of a traumatic event; avoidance; and hyperarousal. Recognised in children since the 1980s. Symptoms variable in young children, but similar to adult pattern in older children. Traumatic event Require exposure to a trauma with response involving fear, helplessness, or disorganized, agitated play (in young children). Epidemiology Prevalence varies according to age, but develops in approximately 3–6% of children exposed to a trauma. Most exposed do not develop the disorder and those that are affected usually have a pre-existing vulnerability (i.e. ‘an unnatural response to an unnatural event’). Clinical presentation in young children (Scheeringa criteria3):

  • Compulsive repetitive play representing part of the trauma and failing to relieve anxiety
  • Recurrent recollections of the event
  • Nightmares, night terrors, and difficulty going to sleep
  • Constriction of play
  • Social withdrawal
  • Restricted affect
  • Loss of acquired developmental skills especially language regression and toilet training
  • Decreased concentration and attention
  • New aggression
  • New separation anxiety

Depression is common in older children and adolescents. Comorbidity Common in PTSD with depression, anxiety disorders, and substance abuse frequent in adolescents. Behavioural disorders common in young children. Clinical assessment

  • Interview with child (drawing and play methods useful in young child).
  • Interview with parents including developmental and family history and account of the trauma.
  • Instruments include K-SADS-PL and the Children’s Post-Traumatic Stress Reaction Index.

Treatment (see p. 370)

  • CBT focusing on psychoeducation and managing anxiety symptoms.
  • Group treatments in case of mass trauma (N.B. debriefing controversial).
  • SSRIs may be indicated for severe anxiety or depressive symptoms.

Terr classification of childhood trauma* Type 1 Classic single, acute, traumatic event; the most common form in children. Symptoms:

  • full, detailed memories
  • ‘omens’ or ‘cognitive reappraisal’
  • misperceptions

Type 2 Follows longstanding or repeated exposure to extreme external events, (e.g. chronic abuse). Symptoms:

  • denial and psychic numbing
  • self-hypnosis, depersonalization, and dissociation
  • rage, self-harm, and/or extreme passivity

Common outcomes include: borderline, antisocial, and narcissistic personality disorder or dissociative identity disorder. Footnote * Terr L (1991) Childhood traumas: an outline and overview. AJP 148, 10–20. References 1 Perrin S, Smith P, Yule W (2000) The assessment and treatment of post-traumatic stress Disorder in children and adolescents. J Child Psychol Psychiat 41, 277–89. 2 Yule W (2001) Posttraumatic stress disorder in the general population and in children. J Clin Psychiatry 62 (suppl 17), 23–8. 3 Scheeringa MS and Gaensbauer TJ (2000) Post-traumatic stress disorder. In Handbook of Infant Mental Health. Zeanah CH (ed.). The Guildford Press. P.600
Obsessive–compulsive disorder (OCD)1,2 Essence (see p. 358) OCD is characterised by recurrent obsessions and/or compulsions that cause impairment in terms of time (>1hr/day), distress, or interference in functioning. Epidemiology Prevalence in adolescents 1–3.6%. May occur as early as 5 yrs of age and mean age of onset is 10 yrs. Male predominance (3:2) in childhood, with equal gender distribution in adolescence. Mild subclinical obsessions and compulsions are common in the general population (4–19%). Although 50% of all cases have their onset by age 15, paediatric OCD is usually recognised only when severe, often years after onset. Often a chronic course with 50–70% still symptomatic after 5 years. Aetiology Increased incidence in 1st degree relatives and in monozygotic twins; possible autoimmune process; reduced volume of caudate nucleus; hyperactive orbitofrontal circuits (SPET); 5HT receptor dysfunction. Symptoms Contamination fears with ritualised washing and avoidance; repetitive doubting and checking (e.g. locks); repetitive counting, arranging, or touching. Differential diagnosis Normal developmental rituals; Tourette’s/tic disorder; Sydenham’s chorea; PANDAS (see opposite); OCD ‘spectrum’ disorders (see p. 358); trichotillomania; OC personality disorder; psychotic disorders; side-effects of stimulants; rarely, basal ganglia disease. Comorbidity 70% have at least one comorbid disorder. Includes other anxiety disorders, OCD spectrum disorders, ADHD, conduct disorders, developmental disabilities, substance abuse, eating disorders, and mood disorders. Clinical assessment

  • Full physical including neurological examination
  • Psychiatric interview with the child
  • Symptom rating and monitoring of severity over time: Children’s Yale-Brown Obsessive Compulsive Scale (CY-BOCS)
  • Interview with parents including full developmental and family history

Treatment approaches

  • CBT, especially graded exposure and response prevention. Shown to reduce relapse.
  • Pharmacological: 1st line agents include SSRIs (fluoxetine and sertraline) and clomipramine. Augmentation with clonazepam, haloperidol, and risperidone. Maintenance therapy for at least 1–2 years. Relapses common and long-term treatment advised after 2 relapses. (See p. 621 for dosages.)
  • Psycho-education: important for both parents and child.

PANDAS3 (paediatric autoimmune neurological disorder associated with streptococcus) An autoimmune syndrome associated with OCD and/or tic disorder, with pre-pubertal onset, characterised by episodic exacerbations of symptoms in association with evidence of Group A β haemolytic streptococcal infection. References 1 Rapoport JL, Inoff-Germain G (2000) Treatment of obsessive-compulsive disorder in children and adolescents. J Child Psychol Psychiat 41, 419–31. 2 AACAP (1998) Practice parameters for the assessment and treatment of children and adolescents with obsessive-compulsive disorder. AACAP. J Am Acad Child Adolesc Psychiatry 37 (10 supp), 27s–45s. 3 Swedo SE, Leonard HL, Garvey M, et al (1998) Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections: clinical description of the first 50 cases. AJP 55, 264–71. P.602
(Gilles de la) Tourette’s syndrome Essence Characterised by multiple motor and one or more vocal tics, present for at least a year, causing distress and impaired function.

  • Facial tics are often the initial symptoms, but tics involving the neck, shoulders, and upper extremities are also common.
  • Vocal tics range from meaningless sounds to clear words and coprolalia (expletives).
  • Typically, tics vary over time with more complex tics emerging after some years.
  • Frequency of tics wax and wane, with exacerbations often related to physical and emotional stress.

Epidemiology Mean age of onset is 7 years and ♂:♀ = 3:1. Prevalence is approximately 5/10 000. Aetiology enetic factors—autosomal dominant and polygenic common (with increase in monozygotic twins and 1° degree relatives); dopamine system (antipsychotics reduce symptoms), basal ganglia implicated; Post-infectious (see PANDAS above). Comorbidity OCD and ADHD common; also other tic disorders, LD, depression, anxiety, impulse and conduct disorders. Management Psychoeducation; CBT; medication if tics are disabling and non-responsive to other therapies—haloperidol (pimozide, sulpiride, and clonidine for specialist use). Other tic disorders Chronic motor or vocal tic disorder More common that Tourette’s syndrome, with a better long-term outcome. Transient tic disorder Motor and/or vocal tics are present transiently for less than one year. P.603
Depression in children and adolescents Both major depressive and dysthymic disorders are common, familial, and recurrent in young people, and usually persist into adulthood. These disorders seem to be manifesting at earlier ages with successive cohorts, and comorbidity is high (approx. 50–70%). They are commonly associated with poor psychosocial, family, and academic function. Risk of suicide is high and so early detection and treatment are a priority. Major depressive disorder Epidemiology Prepubescent: prevalence up to 3% with 1:1 gender ratio. Adolescent: prevalence approx. 8% for males and 14% for females. Notably, during the last 50 years, there has been a steady increase in the risk for depression in children and adolescents. Risk factors Family history/parent with mood disorder; loss of a parent or parental divorce; abuse; negative life events; family conflict; etc. Clinical features

  • Young children Apathy, poor feeding, failure to thrive, separation anxiety, irritability, aggression, tantrums, hyperactivity, somatisation, regressed behaviour (enuresis, soiling, etc).
  • Older children Somatisation, school refusal, poor school performance, and sleep disturbance are common. Also ‘acting out’ vs. ‘regression’.
  • Adolescents Melancholia, low self-esteem, substance abuse, suicidal acts, school refusal, behavioural problems, biological symptoms, psychotic symptoms.

Note: 20% with an MDE will later manifest bipolar disorder. Risk factors include: psychosis; psychomotor retardation; family history of BPD; pharmacologically induced hypomania. Comorbidity Dysthymia and anxiety disorders (50–80%); substance abuse (20–30%); disruptive disorders; somatisation; suicide (see p. 606). Differential Medical conditions; substances; adjustment disorders; other psychiatric disorders. Dysthymic disorder Epidemiology 0.5–1.5% in children and 1.5–8% in adolescents. Clinical features and course

  • Depressed mood or irritability for at least 1 year.
  • Other features are:poor energy and concentration; low self-esteem; feel unloved; anger; anxiety.
  • High comorbidity (esp. MDD) and protracted course (3–4 years).

Management of depression1 Assessment

  • Initial conjoint interview with parents/family and child.
  • Physical examination and interview with child (play techniques may be useful with young child). NB. Check for comorbid problems. May require several interviews to develop rapport and ensure a full assessment. Evaluate suicide risk at every stage.
  • Interview with parents to assess developmental and family history.
  • Collateral from teachers, GP, social services, etc.
  • Rating scales include Beck Depression Inventory and Child Depression Inventory, but are more useful for symptom screening, assessing severity, or monitoring improvement than for diagnosing depression.
  • Laboratory investigations as indicated.


  • Establish therapeutic alliance and provide education to child and family.
  • Psychotherapy is a reasonable initial treatment in mild to moderate depression. This may be individual, group, or family therapy and the mode should be decided individually in each case. Factors such as patient preference, availability of resources and expertise, and family context may influence choice. CBT is one of the most researched techniques, but IPT, behaviour therapy, psychodynamic therapy, and supportive therapy are used.
  • Pharmacotherapy
    • SSRIs are regarded as 1st line therapy. Best evidence for use of fluoxetine. Starting dose: 5 mg/day for 4 weeks; then review.
    • TCAs are not supported by trials and have been associated with cardiac toxicity. However, individual cases may respond better to TCAs than to SSRIs. NB Check ECG, BP, Resting pulse, and weight prior to commencing a TCA. Starting dose: 1.5 mg/kg/day in children; 25–50 mg/day in adolescents. (Repeat ECG prior to increasing dose.)
    • Combination treatment should be considered in all cases (i.e. psychotherapy + medication). Also multidisciplinary involvement (e.g. social worker, OT).

Maintenance treatment

  • Psychotherapies are particularly useful in maintenance phase and have been shown to reduce relapse.
  • Pharmacotherapy: there are no studies of maintenance therapy in depressed C&A so similar principles should be used as for adults. Multiple episodes, complicated episodes (e.g. psychosis), and chronic symptoms are indications for maintenance. 2 or 3 episodes—maintenance for 1–3 years; >3 episodes, psychosis, or treatment resistance—consider longer treatment. Therapy should be continued at the dose required for remission.

References 1 AACAP (1998) Practice parameters for the assessment and treatment of children and adolescents with depressive disorders. J Am Acad Child Adolesc Psychiatry 37 Supp 10, 63S–83S. P.606
Suicide and suicidal risk in young people1 Epidemiology verall increase during the 20th Century, suicide now represents the 3rd cause of death in adolescents (12% of mortality in this group); represents 2% of child deaths. More prevalent in males than females. 2 important points:

  • Completed suicide is only the tip of the iceberg of suicidal behaviour/ideation.
  • There is a very strong association between depression and suicidality.

5 factors common to children and adolescents who attempt suicide:

  • Life stressors
  • Impulsivity
  • Can’t tolerate negative affect
  • Cognitive distortions
  • Hopelessness

Risk factors for suicide Mood disorder; other comorbid psychiatric disorder (e.g. substance use, anxiety, disruptive and personality problems); previous suicidal behaviour; family history of mood disorder or suicidal behaviour; exposure to family violence, to trauma, or abuse; availability of lethal agents (e.g. guns); poor parent-child communication; school problems; negative life events. Management

  • Consider the need to hospitalise—either to remove a child from a bad environment, or to observe closely for risk, or to intervene if risk is high. Factors indicating hospitalisation include:
    • Young child
    • Toxic environment
    • Runaway
    • Previous attempt
    • Serious attempt
    • Serious lethal method
    • Comorbid psychiatric disorder
  • Outpatient—involve the family; commence treatment for psychiatric disorder (N.B. consider risk of overdose); follow-up regularly.

Prevention General measures include:

  • Screening and treating psychiatric disorders
  • Crisis lines/access to help
  • Education of parents, the public, and the media
  • Intervene in cluster situations (e.g. several suicides in a school)
  • Gun control

A pathway to suicidal behaviour

Predisposing factors e.g. previous attempt; psychiatric disorder
Precipitating factors e.g. ‘domino effect’ (suicide in community or in the media)
Opportunity e.g. access (e.g. to a gun); privacy

Gun control and adolescent suicide (a U.S. perspective) Accessibility to firearms, particularly handguns, influences the rate of teen suicides. Firearms are the most common method of suicide by youth. The increase in the rate of youth suicide (and the number of deaths by suicide) over the past four decades is largely related to the use of firearms as a method. Handguns were used in nearly 70% of teen suicides in 1990, up 20% since 1970. The most common location for the occurrence of firearm suicides by youth is the home. A home with a handgun is almost ten times more likely to have a teen suicide than a home without. There is a positive association between the accessibility and availability of firearms in the home and the risk for youth suicide. The risk conferred by guns in the home is proportional to the accessibility (e.g. loaded and unsecured firearms) and the number of guns in the home. If a gun is used to attempt suicide, a fatal outcome will result 78% to 90% of the time. Public policy initiatives that restrict access to guns (especially handguns) are associated with a reduction of firearm suicide and suicide overall, especially among youth. –Youth Suicide by Firearms Task Force References 1 Flisher AJ (1999) Annotation: mood disorder in suicidal children and adolescents: recent developments. J Child Psychol Psychiat 42, 439–49. P.608
Bipolar disorder in children and adolescents1,2 Epidemiology BPD is rare in prepubescent children but rates of diagnosis are increasing. Adults with BPD report onset in childhood in only 0.5% of cases. Males predominate in childhood cases, while gender rates are equal in adolescents. Prevalence in adolescents is approximately 1%. (NB. Rates may be underestimated as 70% of initial presentations are a depressive episode). Familial factors are important with a 4 times greater risk of mood disorder in offspring of parents with BPD. Clinical presentation Standard ICD-10 and DSM-IV criteria apply but several differences in C&A presentation should be noted:

  • Manic children typically present with atypical or mixed features (e.g. irritability, labile mood, rapid cycling course and behavioural problems).
  • Behavioural problems include: school problems, fighting, substance abuse, and sexual behaviour.
  • The course is often non-episodic and chronic.
  • There is wide developmental variability in presentation.
  • Normal childhood imaginative play, boastfulness, overactivity, exuberance, and grandiosity may be mistaken for symptoms of BPD.
  • Adolescent presentation may be bizarre, mood-incongruent, and/or paranoid. Schneiderian 1st rank symptoms occur in 20% cases.
  • N.B. Early onset BPD is misdiagnosed as schizophrenia in -50%.
  • There is a high degree of symptom overlap between ADHD, ODD, and BPD in C&A.

Comorbidity ADHD (70%), substance abuse (40%), ODD (40%), anxiety disorders (30%), borderline PD, Tourette’s syndrome (8%), bulimia nervosa (3%). Outcome Early onset BPD has a poor outcome with 50% showing long-term decline in function. There is commonly a family history, suggesting that this is a highly genetic form of BPD. The course is often chronic and less responsive to treatment, with atypical and rapid-cycling features especially difficult to treat. Suicide risk is high with rates of completed suicide approximately 10%. Management

  • A full evaluation is required with collateral from family and school. Important factors include: +ve family history of mood disorder; the pattern of mood change; comorbid conditions; suicide risk.
  • Clinical examination to exclude medical cause (e.g. hyperthyroidism).
  • Admission to child or adolescent unit is preferable, for the purposes of observation, treatment, and safety.
  • Psychological therapies include patient and family education, behavioural methods, and supportive therapy.
Treatment guidelines for early-onset BPD (see p. 312).

References 1 James A and Javaloyes A (2001) The treatment of bipolar disorder in children and adolescents. J Child Psychol Psychiat 42, 439–49. 2 Giedd JN (2000) Bipolar disorder and attention-deficit/hyperactivity disorder in children and adolescents. J Clin Psychiatry 61 (suppl 9), 31–4. P.609
Schizophrenia in children and adolescents1,2 Background and definitions Historically, rare cases of schizophrenia in children were noted as early as Kraepelin and were distinguished from autism and other PDDs. However, by the 1970s, ‘childhood schizophrenia’ included a broad spectrum of early-onset psychoses including infantile autism. Then, beginning with DSM-III, the distinction was again recognised with the same diagnostic criteria used in both adult and childhood-onset schizophrenia. Current research supports the notion of continuity between childhood and adult-onset disorder, with appropriate developmental adjustments in the former. Current classification (DSM-IV) recognises both ‘early-onset schizophrenia’ (EOS) with onset before age 18 and ‘very early-onset schizophrenia’ (VEOS) with onset before 13 yrs. Epidemiology VEOS is extremely rare and the rate of onset then increases sharply during adolescence, peaking during late adolescence and early adulthood. There is a 2:1 male predominance during childhood, but this evens out with increasing age. Clinical presentation Clinically, early-onset disorder resembles poor-outcome adult schizophrenia in that it is a chronic severe illness with a poor prognosis. The majority of cases have premorbid abnormalities, including social withdrawal, disruptive behaviour, learning difficulties, speech and language problems, and developmental delays. Symptoms hallucinations, thought disorder, and restricted affect are evident, but delusions and catatonia are rare. Cognition about 10–20% of early-onset cases have IQs in the borderline LD range, while cognitive deficits involving speech and language, memory, and attention occur more commonly than in later-onset cases. Differential diagnosis (see opposite) Biological features

  • Genetic Schizophrenia-spectrum disorders are more common in relatives of EOS probands, suggesting greater vulnerability in EO cases; cytogenetic abnormalities are more common in EOS (than in AOS).
  • Premorbid course EOS cases have increased language, motor, and social delays than AOS cases.
  • Brain imaging ↑ lateral ventricles and total grey matter volume compared with AOS; similar functional deficits to AOS.
  • Obstetric complications similarly implicated as in AOS.

Course and outcome

  • EOS has a more insidious onset and poorer long-term outcome than AOS.
  • Onset before 15 yrs is associated with lower IQ, ↑ cognitive deficits, and ↑ negative symptoms.
  • Onset before 21 yrs results in ↑ social deficits in adulthood and only 20% have a favourable long-term outcome.
  • EOS also seems to be associated with a poorer treatment response.
  • P.611

  • Approx. 30% receive a later diagnosis of schizo-affective disorder or BPAD.

Management The principles of management are similar to that in AOS. However, several points are important:

  • The emphasis should be upon early detection and intervention. This may include screening of high-risk individuals.
  • Avoid depot and sedating antipsychotics—atypicals are commonly used as first-line agents in EOS.
  • Psychosocial treatments should include family work and focus on psychoeducation, social skills, and problem-solving strategies and CBT methods. Therapies should address age-appropriate developmental tasks.

Psychosis in children and adolescents Psychotic illnesses are rare in young children and present a particular challenge in both diagnosis and management. Very young children under 6 yrs have preoperational cognitions and thus ‘reality testing’ is blurred by a range of normal fantasy material. Imagined friends, transient hallucinations under stress, and loose associations may all occur as part of the normal spectrum of childhood experience. Differential diagnosis There are many causes of psychotic symptoms in children and adolescents. This means that the assessment of a child with symptoms requires extreme care and thoroughness. Possible causes include:

  • Normal experience
  • Organic conditions (e.g. TLE, thyroid disease, brain tumour, SLE, and substance misuse disorders)
  • Mood disorders
  • PDD/Autism
  • OCD
  • Schizophrenia
  • Language disorders
  • Dissociative disorders
  • Culture-bound syndromes

References 1 AACAP (2000) AACAP official action. Summary of the practice parameters for the assessment and treatment of children and adolescents with schizophrenia. J Am Acad Child Adolesc Psychiatry 39, 1580–2. 2 Nicolson R, Lenane M, Hamburger SD, et al. (2000) Lessons from childhood-onset schizophrenia. Brain Research Reviews 31, 147–56. P.612
Substance abuse in children and adolescents1 Substance abuse is increasingly common in young people. It may occur in a number of different contexts. These include:

  • Experimentation
  • Educational pressures
  • Entanglements (e.g. relationship break-ups)
  • Employment (unemployment)
  • Extrication (from bad domestic situations)

Risk factors

  • Biological vulnerability
  • Personality traits (high novelty-seeking and low harmavoidance)
  • Comorbid psychiatric disorders
  • Parental problems (poor communication and rolemodelling, antisocial behaviour, substance abuse)
  • Socio-economic deprivation
  • Peer involvement (e.g. increasing association with the ‘rave’ culture)

Comorbidity Conduct disorders; ADHD; depression; poor cognitive, social, and emotional development. Management

  • Early identification of high-risk children (e.g. parents are substance abusers)
  • Treat comorbid psychiatric disorders (N.B. antidepressant is contra-indicated if comorbid stimulant abuse)
  • CBT methods
  • Involve the family early on
  • Legal and social interventions

References 1 Gilvarry E (2000) Substance abuse in young people. J Child Psychol Psychiatry 41, 55–80. P.613
Child abuse (1)—general issues1 In recent decades there has been growing awareness that the abuse of children can take many forms. All forms of child abuse involve the elements of power imbalance, exploitation, and the absence of true consent. They may concern acts of commission or acts of omission. Lord Clyde2 suggested, ‘Abuse is the wrongful application of power by someone in a dominant position’. The management of child abuse involves many professionals including police, social workers, educationalists, and health workers. Thus a multidisciplinary approach is required in order to fully assess the extent or risk of abuse and to provide the appropriate interventions. Working with child abuse is stressful and may invoke strong feelings and opinions (e.g. regarding the relative cost to the child of investigation versus non-investigation). Categories of abuse Physical abuse Where there is physical injury to the child and it is known, admitted, or reasonably suspected that the injury was inflicted by a carer or member of the same household; or where a carer knowingly fails to prevent injury or acted without due regard for the safety of the child; or where the nature of the injury is inconsistent with the account of how it occurred. (Includes Munchausen syndrome by proxy—see opposite). Physical neglect Persistent or severe exposure of a child to danger or the persistent failure to fulfill the child’s basic needs (food, sleep, nappy changing, clothing, warmth, shelter, or medical needs) which is likely to result in serious impairment of the child’s health and development. This may also occur when an adult carer persistently pursues or allows a child to follow a lifestyle inappropriate to the child’s developmental needs or which jeopardises his/her health. Leaving a child unattended or inadequately supervised may also qualify as physical neglect. Non-organic failure to thrive Failure to meet expected weight and growth norms or developmental milestones, which does not have a basis in an hereditary or medical condition. Emotional abuse Failure to provide for the child’s basic emotional needs such as to have a severe effect on the behaviour and development of the child. This may include persistent coldness, hostility, or rejection by the caregiver and can be seen as the ‘willful destruction or significant impairment of a child’s confidence’. Other types of abuse are likely to result in emotional abuse. Sexual abuse Any child below the age of consent will be deemed to have been sexually abused when any person, by design or by neglect, causes that child to be involved in any activity that might reasonably be expected to lead to the sexual arousal or gratification of that or any other person, including organised networks. This definition holds whether or not there has been genital contact and whether or not the child is said to have initiated the behaviour. P.615
Abuse by young people or children This involves activities between children/young people of a sexual or physical nature where one or more of the following characteristics is present: lack of true consent; inequalities in power (such as age, developmental stage, or size); actual or threatened coercion. A distinction must be made between behaviour normally expected between young people/ children and that which is clearly of an abusive nature. Munchausen’s syndrome by proxy (Factitious or induced illness syndrome—FIIS)

  • Part of a factitious syndrome that is manifest by a person feigning or inducing illness in a child (or others) in order to obtain medical attention.
  • A form of child abuse in that it subjects the child to emotional abuse, unnecessary medical procedures, hospitalisation or other treatments that are harmful to the child.
  • Can be very difficult to detect as the perpetrating (and colluding) adult/s often deny and disguise their behaviour.
  • It is essential for professionals to be alert to it, especially where a child repetitively presents for medical attention.

Undetected, this form of abuse can result in very serious consequences (including fatality) for the child. References 1 Adapted from the NHS Child Protection Guidelines of the Social Work Department, Lothian Health, Edinburgh, Scotland. 2 Report of enquiry into the removal of children from Orkney in February 1991. P.616
Child abuse (2)—alerting signs The following are signs that may alert one to abuse, but it is important to remember that other causes may exist, and also that these behaviours should be viewed within the context of other information at one’s disposal. Signs of possible physical abuse

  • unexplained injuries or burns, especially if recurrent
  • improbable excuses given for injuries
  • refusal to discuss injuries
  • untreated injuries or delay in reporting them
  • excessive physical punishment
  • limbs kept covered in hot weather; avoidance of swimming, PE, etc.
  • fear of returning home
  • aggression towards others
  • running away

(N.B. ‘Injuries’ may occur for other reasons such as: genuine accidents; haematological disorders; Mongolian blue spots (normal in some darker skinned people); skin conditions such as impetigo or naevi; rare bone diseases; swelling of eye due to tumour; undiagnosed birth injury such as fractured clavicle.) Signs of possible physical neglect

  • constant hunger
  • poor personal hygiene
  • constant tiredness
  • poor state of clothing
  • frequent lateness or non-attendance at school
  • untreated medical problems
  • low self-esteem
  • poor peer relationships
  • stealing

Signs of possible non-organic failure to thrive

  • significant lack of growth
  • weight loss
  • hair loss
  • poor skin or muscle tone
  • circulatory disorders

Signs of possible emotional abuse

  • low self-esteem, continual self-deprecation
  • sudden speech disorder
  • significant decline in concentration
  • socio-emotional immaturity
  • rocking, head-banging, or other neurotic behaviour
  • self-mutilation
  • compulsive stealing
  • extremes of passivity or aggression
  • running away
  • indiscriminate friendliness

Signs of possible sexual abuse Behavioural

  • lack of trust in adults or over-familiarity with adults
  • fear of a particular individual
  • social isolation, withdrawal, and introversion
  • sleep disturbances (nightmares, irrational fears, bed wetting, fear of sleeping alone, needing a nightlight)
  • running away from home
  • girls taking over the mothering role
  • reluctance or refusal to participate in physical activities or to change clothes for activities
  • low self-esteem
  • drug, alcohol, or solvent abuse
  • display of sexual knowledge beyond child’s years
  • unusual interest in genitals of adults, children, or animals
  • expressing affection in inappropriate ways
  • fears of bathrooms, showers, or closed doors
  • abnormal sexualised drawing
  • fear of medical examinations
  • developmental regression
  • poor peer relations
  • over-sexualised behaviour
  • eating disorders
  • compulsive masturbation
  • stealing
  • psychosomatic complaints
  • sexual promiscuity


  • bruises, scratches, or other marks to the thighs or genital area
  • itch, soreness, discharge, unexplained bleeding from the rectum, vagina, or penis
  • pain on passing urine or recurrent urinary tract infection
  • recurrent vaginal infection
  • venereal disease
  • stained underwear
  • unusual genital odour
  • soiling or wetting in children who have been trained
  • discomfort/difficulty walking or sitting
  • pregnancy, particularly when reluctance to name father

Child abuse (3)—assessment, management, and psychiatric outcome Principles of assessment and management of child abuse

  • Early detection in children at high-risk or presenting with alerting signs
  • A multi-disciplinary approach is essential with early consultation across disciplines
  • Maintain confidentiality where necessary and possible
  • Assessment should be measured, sympathetic, and above all child-centred
  • Attempt to engage and involve parents/carers at all stages and keep them informed in all but the most exceptional circumstances
  • Evaluate the child’s physical, emotional, cognitive, and sexual development, as well as the child’s position in the family
  • Evaluate the family in terms of: degree of social isolation and support; levels of stress; emotional maturity of the parents; parental relationship; role of non-abusing parent; and family dynamics
  • Consider extra-familial factors such as: deficiencies in support services; failure of inter-professional communication; socio-political environment
  • Important to clarify the family’s perception of the problem and to gain their cooperation with changes/interventions required
  • Remove/hospitalise child if there is an immediate risk of, or ongoing, abuse
  • Consider whether siblings are at risk
  • Involve social services early
  • Consider whether police involvement is required immediately or whether there is time for a measured multidisciplinary response
  • Balance the benefits/costs of non-intervention versus that of intervention
  • Above all, put the needs of the child first

Psychiatric outcome of chronic abuse Children who are abused have an extremely high rate of psychiatric disorders, both during the abuse and later on. Some of the most common disorders associated with previous abuse:

  • PTSD
  • dissociative disorders
  • conversion disorders
  • borderline personality disorder
  • depression
  • paraphilias
  • substance abuse

Prescribing in children and adolescents1,2 Principles

  • They are not small adults! This is particularly important in regard to the dynamics and kinetics of drugs. Some drugs are metabolised faster while others more readily cross the BBB. Susceptibility to side-effects also varies with age (e.g. children are more likely to develop dystonias and less likely to develop akathisia with neuroleptic treatment).
  • Due to variability in drug response according to weight, dosage is calculated in mg/kg rather than at fixed doses.
  • Medication should be considered as just one component of treatment—it should be accompanied by psychological, social and educational interventions.
  • Drugs are often prescribed for symptoms rather than syndromes (e.g. stimulants for hyperactivity in PDDs).
  • Drug trials in children are problematic both ethically and practically, so there is inadequate data regarding safety and efficacy for many psychotropics. Thus clinicians are often faced with ethical decisions regarding the use of drugs not licensed for use in these age groups.

Guidance for specific psychotropics

Indication Suggested dosage range for children and adolescents
Psychotic disorder 1st line: atypical antipsychotics

  • Risperidone 2–4 mg/day
  • Olanzapine 2.5–15 mg/day
  • Amisulpiride 100–400 mg/day
  • Quetiapine 100–400 mg/day
2nd line: typical antipsychotics

  • Haloperidol 0.5–5 mg/day
  • Chlorpromazine 10–100 mg/day

Clozapine—start with 12.5 mg/day; increase to maximum of 500 mg/day

Aggression/acute behaviour disturbance
  • Risperidone 0.25–2 mg/day
  • Amisulpiride 50–300 mg/day
  • Haloperidol 0.02–0.08 mg/kg/day
  • Fluoxetine 10–20 mg/day
  • Sertraline 25–100 mg/day
  • Citalopram 10–20 mg/day

N.B. Paroxetine in C&As is now specifically contraindicated, due to increased risk of suicide.

Nocturnal enuresis
  • Desmopressin 20–40 µg nocte intranasally
  • Imipramine 0.5–1 mg/kg nocte (N.B. ECG prior to therapy)
Mania/bipolar disorder
  • Lithium 30 mg/kg/day (N.B. short half-life in children)
  • Sodium valproate 500–2000 mg/day
  • Carbamazepine 100–600 mg/day

References 1 Taylor D, Paton C, Kerwin R (2003) The Maudsley Prescribing Guidelines, 7th Ed. Martin Dunitz: London. 2 Riddle MA, Kastelic EA, Frosch E (2001) Pediatric psychopharmacology. J Child Psychol Psychiat 42, 73–90.

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