Disorders of Childhood Flashcards
Myths, realities, and research challenges
Psychological and behavioural problems in children are very common.
Few children receive help.
Traditionally, research on childhood disorders has relied on adult models and intervention approaches.
There is ongoing debate on relative contribution of genetic and environmental factors.
Indigenous youths are at greater risk of emotional and behavioural problems.
Overall, most children are inherently resilient and can deal with some adversity.
Understanding and classifying childhood disorders
Prior to the twentieth century there was almost no recognition of psychological disorders in childhood.
Children were seen as miniature adults.
The early twentieth century saw greater recognition of and interest in childhood disorders.
Separate childhood disorders were not included until DSM-3.
One major criticism of the DSM-5 is that it does not take into account the dimensional nature of many childhood conditions.
Externalising disorders
In children, are behaviours that are under-controlled and directed at others.
Behaviours you can see, usually disruptive.
Internalising disorders
In children, are behaviours that are over-controlled and inner-directed.
Internal eg anxiety, mood disorders.
Diagnosis of attention-deficit/hyperactivity disorder (ADHD)
Neurodevlopmental disorder.
Defined by symptoms of inattention (eg being easily distracted) and/or hyperactivity and impulsivity (eg fidgeting, moving about excessively).
Deficits in executive functioning (ability to plan, think things through).
Prevalence of ADHD
Approx 7.2% across populations
Aetiology of ADHD: genetic contribution
Considerable genetic contribution to the development of ADHD.
May entail some form of neuropsychological impairment, which has been posited as the key factor underlying ADHD.
Autonomic under-arousal seen in preschoolers with ADHD.
Children with ADHD seem to have lower responses to reinforcement, so they need stronger motivated to alter their behaviour.
Aetiology of ADHD: Family and parenting variables
Parental inconsistency and lack of involvement have been associated with ADHD symptomatology.
Aetiology of ADHD: diet
Controversies over the role of diet in the aetiology of ADHD.
Artificial additives contribute to a child becoming hyperactive.
Treatment of ADHD
Pharmacological approaches are common.
Psychostimulant medication (eg Ritalin) have been extensively used and shown to be effective.
Should combine drug treatment with some form of psychosocial treatment.
Specific learning disorder
Disorder of learning characterised by lower than expected performance in a particular area of learning relative to the child’s chronological age and intellectual ability.
Diagnosis of reading disorder
Characterised by difficulties in reading accuracy, fluency, and comprehension which is not the result of a general developmental disability, intellectual disability, sensory impairment (eg vision problems) or lack of access to appropriate education.
Prevalence of reading disorder
One of the most common of childhood disorders.
Between 4 and 7%.
Considerable degree of stability, unlikely to resolve itself.
High rates of comorbidity with behavioural problems and with ADHD.
Aetiology of reading disorder
There is some evidence of a genetic component to reading disorder.
Research suggests deficits in phonological awareness, working memory, and the speed of processing written language may contribute to the development of reading disorder.
Treatment of reading disorder
Only phonological (i.e. sounding out words) approaches led to significantly improved outcomes.
Diagnosis of Autism Spectrum Disorder (ASD)
Impairments in social interaction and social communication such as social-emotional reciprocity.
Abnormalities in eye contact or an absence of interest in peers.
Repetitive and restricted patterns of behaviour eg preoccupation with a specific activity (like collecting footie cards), an insistence on sameness in routines, or motor mannerisms such as body-rocking.
Deficits in ‘theory of mind’ - can’t take other people’s perspective.
Prevalence of ASD
About 1% prevalence rate.
Boys outnumber girls 2:1.
Approx 75% of children with ASD have a poor outcome.
Aetiology of ASD
Evidence of genetic vulnerability.
Prenatal and perinatal insults (eg maternal ill-health during pregnancy) can increase the risk of the disorder.
Extreme social deprivation can lead to ASD.
Treatment of ASD
Early intervention is very important to ensure highest level of adaptation and functioning possible.
Aim of intervention is to help child develop better social and emotional relationships, learn better communication skills, and decrease stereotypic behaviours eg head banging.
Diagnosis of intellectual disability
Deficits in intellectual functioning eg reasoning, problem solving, planning, abstract thinking.
Deficits in adaptive functioning that result in a failure to meet developmental and sociocultural standards for person independence and social responsibility.
Prevalence of intellectual disability
Approx 1%.
Approx 85% of those with the condition have an IQ within the mild range of intellectual impairment.
Co-occurs with many disorders including epilepsy, cerebral palsy, sensory deficits, and pervasive developmental disorders.
Increased risk of anxiety and depression.
Aetiology of intellectual disability
Wide range of causes, many with genetic components (eg Down syndrome).
Exposure to toxic agents such as cigarette smoke and alcohol during pregnancy can also cause intellectual disability.
Perinatal conditions such as maternal infection and low birth weight, and postnatal causes like exposure to contaminants like lead contribute to the disability.
Traumatic injury to the head.
Treatment of intellectual disability
Early intervention to treat underlying condition.
Physical therapy, occupational therapy, speech therapy, family support.
Any associated physical conditions (eg epilepsy) and mental health problems also need to be identified and treated properly.
Diagnosis of oppositional defiant disorder (ODD)
Characterised by a persistent pattern of angry/irritable mood, argumentative/defiant behaviour, and vindictiveness.
Difficulty regulating emotion and negative affect style.
Prevalence of ODD
One of the most common childhood disorders, affecting approx 3% of children.
Aetiology of ODD: biological and psychological factors
Alterations in androgen (hormone related to aggressiveness).
Differences in patterns of frontal brain activation may be biological basis for negative affect.
Autonomic under-arousal results in increasing arousal through problem behaviours.
Traumatic brain injury.
Difficult temperament and problems understanding social cues are psychologist factors.
Aetiology of ODD: parenting practices
Highly punitive and critical parents.
Use of restrictive control - entails behaviours intended to stop or punish the child such as giving negative instructions, removing objects from the child, scolding and smacking.
Aetiology of ODD: interaction between parent and child
Coercive processes model: parents and children engage in progressively more coercive interactions with each other through learning processes. Parent gives instruction, child throw tantrum, parent retracts instruction (reinforces tantrum behaviour). Next time child will throw tantrum for longer/louder.
Diagnosis of conduct disorder
Persistent pattern of violation of rules and the rights of others.
Thought to develop from ODD and be a precursor to adult criminality and antisocial personality disorder.
Behaviours include stealing, fighting, being cruel to people or animals, destroying property and skipping school.
Prevalence of conduct disorder
More common in boys.
Approx prevalence rate is 3% in childhood and 6% in adolescence.
Aetiology of conduct disorder: biological and psychological factors
Appears to be a common genetic element to conduct disorder.
Low cortisol levels (underlie aggression).
Higher levels of androgen levels (hormone related to aggression).
Temperament characteristics: negativity, volatility, and low persistence.
Manipulative behaviour and lack of guilt, remorse and empathy.
Aetiology of conduct disorder: social factors
Poor social skills
Associating with antisocial peers and peer rejection.
Parenting practices: monitor and supervise child less, less warm, harsher discipline.
Difficulties in family relationships.
Behavioural intervention for ODD
Reward pro-social behaviour.
Punish anti-social behaviour.
Contingency management.
Reduce stressors eg don’t do things you know will end poorly (grocery shopping).
Treatment for conduct disorder
Good parent role modelling. Learning about how to get needs met (in a pro-social way). Acceptance by peers. Teaching about rules. Reward pro-social behaviour. Consequences for antisocial behaviour.
The treatment and prevention of externalising disorders (ODD, conduct disorder)
Parenting interventions
Attachment-based approaches emphasise the quality of the parents relationship with the child.
Family therapy focuses on the family as a system.
Child-focused approaches include cognitive-behavioural interventions and problem-solving skills training.
School-based approaches are guided by behaviour change principles.
Combined approaches for longstanding externalising problems, and complicating family members.
Separation anxiety disorder
Internalising disorder.
Distress in anticipation of, or on separation from an attachment figure, the need to know where they are, extreme homesickness, and worried about harm coming to them.
Fear is specifically related to the separation experience and is greatly reduced in the presence of the attachment figure.
Separation anxiety disorder prevalence
Occurs in approx 4% of children.
More common in girls.
Occurs most commonly in middle childhood.
Most cases improve over time.
Aetiology of separation anxiety disorder: genetic component
Evidence that children inherit a non-specific, genetic vulnerability to separation anxiety disorder, characterised as a predisposition to anxiety in general.
Aetiology of separation anxiety disorder: parenting and parental anxiety
Many parents also show symptoms of anxiety suggesting inheritance.
Parents model anxious behaviours and poor coping skills.
Parents provide less opportunities for their child to confront and master fearful situations.
Grant their child less autonomy and are overprotective - less practicing separation.
Treatment of separation anxiety disorder
CBT is treatment of choice Psychoeducation Exposure Coping-skills training Reinforcement Relaxation skills
Diagnosis of enuresis
The involuntary emptying of the bladder in the absence of any organise causes, either at night (nocturnal enuresis) or daytime (diurnal enuresis).
Child must be at least 5 years old.
Occurs at least twice a week for 3 months.
Two categories: primary enuresis (never dry) and secondary enuresis (period of dry for at least 6 months).
Prevalence of enuresis
Relatively common
Boys 15-22%
Girls 7-15%
Most grow out of the disorder.
Aetiology of enuresis
Inherited factors thought to play a significant role.
No specific factor that is inherited has been pinpointed but may be related to general developmental immaturity as well as hormonal and physical factors.
Children with enuresis tend to have lower than average height and later development of milestones.
Other possible factors include: hyperactivity of the parasympathetic system, dysregulation of vasopressin (chemical linked to sensation of full bladder) and abnormal sleep patterns.
Treatment of enuresis
Conditioning approaches are most successful.
Bell and pad method is most effective intervention. (Urine-sensitive lad placed in bed, sets off alarm when wet, wakes child up, teaches child to avoid negative situation of being woken up).
Diagnosis of encopresis
Repetitive soiling in inappropriate places at least once a month for 3 months.
Child must be at least 4 years old.
Medical or physical problems needs to be ruled out first.
Can be retentive (child tends to hold on as long as possible) or non-retentive (soiling is intermittent).
Prevalence of encopresis
Approx 1.5-7.5% of children.
Tends to decline with age.
Tend to have more anxiety/desperation symptoms, attention difficulties, greater social problems, more disruptive behaviour, poorer school performance.
Aetiology of encopresis
Model by Cox et al suggests that the child experienced constipation (resulting from physical or psychological factors) which leads to faecal impaction and hard stools.
Passing stools may be painful, and so child anticipates future difficulties. Tries to avoid going to toilet, results in chronic constipation and overflow incontinence.
Can lead to parent-child conflict (child refuses to go to the toilet), and shame and rejection can lead child to hide or lie about dirty underwear.
Treatment of encopresis
Medical management combined with behavioural treatment is more effective than medical treatment alone.
Behavioural interventions include psychoeducation for parents and children, combined with an appropriate reinforcement schedule to encourage children to use the toilet.
Diagnosis of selective mutism
Persistent failure to speak in selected settings for at least 1 month after the beginning of the school year, even though the child understands spoken language and has the ability to speak.
Prevalence of selective mutism
Occurs in less than 1% of children.
More common in girls.
Onset is usually gradual.
Some experience it for short periods of time, some for many years.
98% of children with selective mutism meet criteria for another disorder; anxiety disorders, elimination disorders.
Aetiology of selective mutism
Manifestation of shy, inhibited temperament.
Strong link with social phobia.
Anxiety symptoms related.
Treatment of selective mutism
Little research on treatment.
Seems to be quite resistant to treatment.
Pharmacotherapy may have some benefit.
Behavioural interventions are most used. Eliminating all reinforcement for mutism and bolstering self-confidence and decreasing anxiety (graded exposure).
Treatment aims to reduce child’s high anxiety in social situations, improve limited experience child has in speaking to people outside of family, and reduce high level of reinforcement of non-verbal communication.
