Normal and abnormal development
Development and plasticity
Timing is of essence
Protracted developmental changes: changes from childhood into adulthood continue across cortical areas
Heterochronous developmental changes
Rise and fall of synaptic density differs in timing for visual, auditory and prefrontal cortex
Clinical relevance of developmental timing
Language effects children who suffered brain injury prenatally or within 1st 6 months of life
Right hemisphere injuries- great risk for delays in word comprehension – however in adults damage occurs in the left hemisphere
Left posterior injuries: greater risk for production difficulties whereas in adults injury is in the left inferior prefrontal cortex (more anterior-broca’s)
Children with early unilateral brain injury- their brain difficulties seem to resolve, regardless of the side of lesions. Results of study
Child had smaller mean length of utterance with LHD compared to RHD
In Adults people with LHD had much greater decrease in length of utterance compared to child. But with RHD the mean length of utterance was greater
Spatial processing
Children with early LHD have difficulties with processing and producing both local and global aspects of their visual environment when tested with navon figures (Big M made from lots of little z). In contrast adults with LHD can process the global image but not the local image- can see the M but not the z
Children with early RHD have difficulties with the global aspects of these tasks only, they can spot the local letters. This is the same with adults
Executive function
Prenatal insults to the frontal lobe performed more poorly across the board on executive tasks such as Tower of London; Fluency tests
Children with lesions between 7-9 years did best
Children with lesions in early childhood and after 10 years of age was task dependent and generally poorer than controls
Summary
Differences in the effect of lesions in children and adults shows that multiple heterchronous processes are involved in pre and post natal changes in brain structure and function
Some processes seem too be less vulnerable to early brain damage than to later lesions and recover more effectively overall (E.g expressive language). Spatail processing seems to be severely and permanently affected and outcome is variable for executive functions
Understanding aediatric brain injury cases require moving away from the adult model as risk and recovery differ in terms of localisation of the risk
Childhood onset developmental disorders
Functionally defined disorders
Unlike cases of acquired brain damage, these are identified by behavioural characteristics and may be heterogenous in aetiology
Age of diagnosis and progression may differ
Examples
Attention deficit Hyperactivity disorder (ADHD)
Autistic spectrum disorder (ASD)
ADHD
Diagnosis: American Psychiatric Association (DSM-IV)
Criterion A
Symptoms in 2 categories – inattention + hyperactivity
Child must exhibit 6 or more in either category
Symptoms must have persisted for at least 6 months to an extent that is inconsistent for developmental level
Criterion B
Some inattentive/ hyperactive impulsive symptoms present before age 7 years
Criterion C
Symptoms are exhibiting in two or more settings
Criterion D
Must be clear evidence of clinically significant impairment in social or scholastic functioning
Criterion E
Symptoms don’t occur exclusively during the course of or can’t be accounted for by another disorder
| Inattention | Hyperactivity |
|---|---|
| Has difficulty sustaining attention in tasks or play | Fidgets with hands/feet/squirms in seat |
| Fails to give close attention to details | Leaves seat when sitting is expected |
| Doesn’t listen when spoken to | Runs about when inappropriate |
| Doesn’t follow through on instructions | Has difficulties in playing or engaging in leisure activities quietly |
| Has difficulty organising tasks/ activities | Is always on the go |
| Avoids tasks that require mental effort | Talks excessively/ blurts out answers |
| Loses things necessary for task | Has difficulty awaiting turns |
| Is easily distracted by external stimuli | Interrupts or intrudes on others- butts into conversations or games |
| Is forgetful on daily activities |
Prevalence
3-5% school children suffer from ADHD
Different types of ADHD determined by the balance of inattention and hyperactivity/impulsivity symptoms (however this subdivision was dropped in DSM-V)
AD/HD inattentive type
AD/HD combined
AD/HD hyperactive type
Neurocognitive theories
Inhibition deficit- inability to override natural/habitual behavioural responses (prepotent response) in order to implement more adaptive goal-orientated behaviour. In people with ADHD there is inhibition of the following:
Working memory: acting on events held in memory
Self regulation: emotional self control
Speech internalisation: description and reflection
Reconstitution: analysis of synthesis and behaviour
No go trials- children with ADHD had greater number of errors compared to controls
Found there was lower levels of activity for control related circuits (caudate nucleus/ globus pallidus, parietal lobe/prefrontal cortex0
Pathophysiology
Brain structure
Children with ADHD there is a proportionally greater decrease in volume in Left sided prefrontal cortex. The posterior parietal cortex also shows thinning compared to controls
Prefrontal-strial-cerebellar and prefrontal striatal-thalamic circuits have been found to differ in ADHD
Neurotransmitter pathways
Dopamine deficiency is thought to be involved as ADHD pts respond to drugs that increase dopamine levels
Noradrenaline also likely to play a role
Alternative theories
Inhibition deficits characterise many children wil AD/HD but not all
Working memory difficulties
Sustained attention
Motivational difficulties
Autism spectrum disorder
Diagnosis DSM IV
Social impairment (2+ of)
Marked impairment in the use of non-verbal behaviours (eye-contact)
Failure to develop age appropriate peer relations
Lack of spontaneous sharing of enjoyment, interests, achievements with other people
Lack of...