Week Twelve - Developmental Childhood Disorders Flashcards
Neurodevelopmental disorders of childhood involve?
Abnormalities of anatomical development
- hydrocephaly
Genetic and chromosomal disorders
- turner’s syndrome
- williams syndrome
Acquired disorders
- FASD
What is Turners syndrome?
Partial of total deletion of X chromosome affecting females
- do not develop secondary sex characteristics, shorts stature
Often comorbid with learning/behavioural disabilities
Lower IQ, high VIQ tho
Treatment for turner’s syndrome?
Growth and sex hormone therapy
What is Williams syndrome?
Elvin typed facial features (upturned nose etc) - physical features
Strengths & weaknesses of Williams syndrome?
Strengths:
- Social, empathetic and talkative
- remarkable language abilities (but low IQ)
- Near perfect pitch, rhythm, recognise faces
Weaknesses:
- Severe attentional problems
- Poor spatial ability
- Drawing
Brain changes in Williams Syndrome?
General thinning of cortex (parietal and occipital lobes, orbitofrontal cortex)
- spared in temporal gyrus (auditory cortex so explains musical abilities)
What are acquired disorders?
When there is injury to the brain other prenatally or postnatally
What is FASD?
A diagnostic term used to describe impacts on the brain and body of individuals prenatally exposed to alcohol
- worst during first trimester
Characteristics of FASD?
Microcephaly, low birthweight, reduced growth
Poor muscle tone and coordination
Below IQ, inattention, hyperactivity, learning disabilities, poor behaviour
FASD diagnosis?
presence of severe impairment in at least 3 neurodevelopment domains and 3 facial features
Treatment for FASD?
Learning and behavioural therapy
Medication for ADHD like symptoms
What is ASD?
Restricted and repetitive patterns of behaviour, interests or other activities
Early signs of ASD?
Infants: poor eye contact, poor response
Pre-school: limited play
School age: concrete/literal thinking
ASD gender difference?
males 75%
Explain the heterogenous of ASD?
Continuum of impairments for any one symptom
Abilities in ASD?
Have savant abilities (cog and artistic eg memory, drawing)
Causes of ASD?
Genetics: heritability is 50% (many genes have been identified in brain development, NT function, synaptic changes)
GENE-ENVIRONMENT interaction
Environmental:
- prenatal birth complications
- parental age
- infection, pollution, nutritional factors
Post mortem findings of ASD in brain?
Cerebellum (fewer neurons), amygdala, frontal (increased cortical thickness) & temporal cortex (decreased cortical thickness) and white matter connectivity (excess) is implicated
People with ASD spend?
Less time looking at faces (eyes especially)
- lower activity in fusiform face area
Functional findings of ASD in brain?
Increased/decreased glucose metabolism and blood flow in limbic frontal/temporal areas
What social factors are affected in ASD?
Theory of mind and emotion processing
Treatment of ASD?
Learning and behavioural interventions in early childhood
- no recommended pharmacological treatment for core symptoms
Antipsychotics sometimes prescribed
what is ADHD?
Persistent pattern of inattentiveness and hyperactivity/impulsivity
Inattentiveness symptoms? DSM5
6 for at least 6 months difficulty with attention poor listening poor follow through with tasks organisation skills are poor
hyperactivity/impulsivity symptoms? DSM5
6 for at least 6 months fidgeting runs/climbs inappropriately unable to play quietly difficulty with patience
Prevalence of ADHD?
5-7% of children, 2.5% of adults (more males)
Comorbidity of ADHD?
80% have comorbid disorders (eg mood/learning)
Causes of ADHD?
Genetic: heritability (70-80%), multiple genes (dopaminergic system), epigenetic effects
Environment: prenatal and substance exposures, heavy metal/chemical exposure, nutritional factors (vita D, omega 3), lifestyle/psychosocial factors
Structural brain findings of ADHD?
Reduced brain volume (caudate nucleus, amygdala, HC)
Disrupted cortical thinning and white matter connectivity between hemispheres
Functional brain findings of ADHD?
Reduced blood flow in frontal lobes and BG
EEG: greater theta/beta ratio
Cognitive process of ADHD?
Reduced focused, sustain attention
Reduced verbal, working memory
Reduced executive functioning
ADHD is associated with? Dopamine hypothesis
Reduced extracellular dopamine
- treatment with dopamine agonists inhibits the reuptake of dopamine
Maturational delay hypothesis of ADHD?
There is delayed cortical thickness meaning delayed development of higher cognitive functions (inhibitory control, attention) - tends to improve with age
Network dysfunction model of ADHD?
Suggests a hypoactive prefrontal cortex - required for organisation/planning meaning it accounts for the inattention and disorganisation
What are the three separate subsections of the attentional network model?
Alerting model
Orienting model
Executive control network
What is the alerting model?
Governs general level of arousal and vigilance
- maintained by norepinephrine
What is the orienting system?
Directing attention to prioritise external information
- voluntary/involuntary
Dorsal: top-down
Ventral: bottom-up
What is the executive control network?
Higher level regulation
- prioritises information for our current goals
Attention models fronto system, ventral system and dorsal system roles? Cortese et al
FS: goal directed executive control processes
VS: orienting to salient stimuli
DS: select external stimuli based on goals, experience, memory
Reward model of ADHD?
striatum, ACC, OFC central to reward processing
Mind-at-rest model fo ADHD?
Normally out DMN is active when at rest, deactivated when task focused - ADHD children are slow to switch of DMN (can be corrected with methylphenidate)
Treatment of ADHD?
Pharmacological:
- dopamine and norepinephrine agonists (stop reuptake and increase dopamine availability)
Nonpharmacological:
- behaviour interventions (typically less effective than pharm)
What is dyslexia?
A specific reading ability (written texts)
- marked by poor phonological awareness - poor naming, WM, EF
Causes of dyslexia?
Genetic base: 50% heritability (prenatal brain development genes)
Environment: lower SES
Brain changes in Dyslexia?
Various subtle visual, auditory and motor/cerebellar deficits
- likely to stem from a deficit of phonological processing rather than sensorimotor
Dual-route model of word cognition?
Lexical (direct) route: Word recognised as a whole unit and translated directly to meaning - used for reading familiar/irregular words
Phonetic (indirect) route: Letters translated into sounds using grapheme/phoneme conversion - unfamiliar and nonwords
Visual theory of Dyslexia?
Make word reversal errors - failure in establishing hemispheric dominance
Orthographic learning theory of dyslexia?
Establishing ability to mapping between phonemes and graphemes
Phonological theory of dyslexia?
There is a grapheme/phoneme conversion route and this is the issue with reading
Visual attention theory of dyslexia?
Performance on visual tasks is often different in people with dyslexia
Neural mechanisms in dyslexia?
Disrupted activation of the LH language network
- temporoparietal region
- occipito-temporal
- lH inferior frontal gyrus
Treatment of dyslexia?
Intensive instructions to learn how to read phonics
