CNP Child Neuropsychology Flashcards
Why would hemispherectomy have to be conducted as a treatment? What deficits can be observed in such patients?
- Patient had severe seizures
- Seizures were caused by chronic inflammation (Rasmussen’s encephalitis)
- Right hemispherectomy was the only treatment
- Deficits: if the surgery is done early in the brain development, recovery is good except for slight motor impairment
How does the brain development look like?
When, what first, what happens with neurons, what is overproduced?
- The brain starts to develop by about 21 days after conception
- The neural tube is a cylinder of cells that develops into the nervous system
- The developing brain looks like a human brain by about 100 days after conception
- Sulci and gyri form at about 28 - 30 weeks
- Neurons are formed near the walls of the ventricles and migrate to their destinations
- Brain development involves a massive overproduction of cells and connections, followed by apoptosism (programmed cell death) to remove the excess cell
What do the neural stem cells in the neural tube develop into?
- Give rise to two daugther cells:
1. Progenitor cells: divide to produce neuroblasts or glioblasts, which develop into neurons or glia
2. Stem cells: exist throughout life and produce new neurons in the hippocampus and olfactory bulb
↪ The presence of stem cells suggests that neural injuries could be repaired → doesn’t routinely happen in the brain - The rate of neurogenisis decreases with age, and the function of neurons produced later in life may be different
How do cortical maps develop? Where does it start from?
- Subventricular zone contains a map of the cortex that enables cells from a part of the zone to migrate to a specific part of the cortex
- Neurons migrate along radial glia, which extend from the zone to the related region of the cortex
- Cortex is built from the inside out, so the deepest layer (VI) forms first, then V, and so on until layer I is formed
↪ The new ones go around the old ones
Picture 1
How and why do dendrites develop in neural maturation?
- During maturation, the cells produce dendrites to increase their surface area to form synapses
- Dendritic arborization involves branching
- Dendritic spines are the targets for the synapses
- Dendrites start to form prenatally, and this continues long after birth
- Dendrites grow slowly, only micrometers per day
How do axons develop and how does this influence the development of the dendrites?
Axons grow toward the appropriate targets
- Axons grow at a fairly constant rate of 1 millimeter per day
- The faster axon growth means axons reach their targets before dendrites have developed, so can influence dendritic development
In what order do the corteses’ synapses develop and at what months/years? Why is there synaptic pruning?
Picture 2
There is an overshoot in synaptic density (overproduction) and that decreases over time = synaptic pruning
This is more effective since more connections are created and then if they are not useful they get pruned away
↪ Better than selecting exact dendrites to each axon which would take too long and might not be accurate
Experiments in rats have characterized the effects of injury at different points in development, what are these?
- If cortical injury occurs during neurogenesis (embryonic day 18), recovery tends to be complete, even if the destruction of the cortex is complete
- Damage during neuronal migration and differentiation (postnatal days 1–5) results in permanent damage, regardless of size or location of the lesion
- Damage after migration (postnatal days 7–12) results in nearly complete recovery of cognitive functions and partial recovery of motor functions
Children can grow into deficits because regions that were previously compensating for the lost function can no longer do so
Environment and brain organization
What can be seen from experiments with rats on early life experiences’ influence of brain organization?
- Some cortical regions of domesticated animals are 10% to 20% smaller than animals raised in the wild
- Animals born in the wild and domesticated at a young age have brain sizes similar to animals who live their whole life in the wild
Environment and brain organization
What are the effects of exposure to a complex environment on brain size?
- Brain size increases, especially the cortex
↪ Differences are observed in the density of glial cells, length of dendrites, density of spines, and size of synapses
↪ Young brains and old brains seem to react differently to the same experience
What is the relationship between socioeconomic status and brain development? Examples?
- There is a relationship between socioeconomic status and academic achievement
- Causes likely include parental education, child health, school quality, stress, and language exposure
- At age 3, children from high-SES families are exposed to 11 million words per year, while children from low-SES families are exposed to only 3.2 million words per year
- Lower family income is associated with decreased cortical volume across the frontal, temporal, and parietal cortex, independent of sex or race
What are neurodevelopment disorders?
Characteristics, consequences, incidence
- Characterized by onset between in utero development and the start of formal schooling
- Result in deficits in social, personal, or school functioning
- Impairments may be specific to one function or more global
- Incidence may be as high as 17% of school-age children
- Deficits often emerge gradually, making it difficult to identify the disorder
- Testing and assessment identify variation in the population, so may fail to identify individuals who have difficulties but are still performing close to standard levels
What are the two dimensions in which we can see neurodiversity?
Differences in brain functioning within the human population are normal
1. Disability vs Impairment:
- Impairment: Physical difference that creates a limitation
- Disability: interaction between personal characteristics and societal barriers
2.Identity vs Disorder:
- Identity: characteristics that define a sense of self (can’t be removed)
- Disorder: characteristics that could be treated or modified (can be removed)
Neurodevelopmental disorders contain all aspects: identity, disorder, disability, impairment
What are the three most common neurodevelopmental disorders in children?
- Attention Deficit Hyperactivity Disorder (ADHD)
- Specific Learing Disorders (SLD)
- Autism Spectrum Disorder (ASD)
What is the history of ADHD?
1775: first mention in a textbook in German
1798: first mention in a textbook in the UK
1902: first scientific article on ADHD
1937: first use of stimulant medications as treatment
1960: FDA approval of Ritalin for treatment
- This is useful info as it shows that ADHD was not made up recently to medicate children or give an accuse for misbehaviour
What are the diagnostic criteria for ADHD according to DSM-5-TR?
- DSM-5-TR (2022) equal weight given to inattention and hyperactivity/impulsivity (child must have 6 or more symptoms of inattention and/or hyperactivity for at least 6 months)
- DSM-5-TR splits ADHD into three sub-categories:
1. predominantly inattentive type
2. predominantly hyperactive-impulsive type
3. combined type - The symptoms must be present in two or more settings
- Several symptoms must have been present before the age of 12
- Lead to impairment in social, academic, or occupational functioning
What are three examples of ADHD behaviours?
Inattentiveness: style of behaviour involving disorganisation and lack of persistence
- Distractible, forgetful
- Can’t follow directions
- Disorganised
Hyperactivity: excess of movement
- Fidgety
- Always on the go
- Talking excessively
Impulsivity: acting without reflecting
- Interrupting people
- Blurting our answers
What is the prevalence of ADHD?
- One of the most common reasons for referral to CAMHS
- 5.9% of youth, 2.5% of adults
- 2 times more common in males
- Inattentive subtype identified more in girls
- The combined type and predominantly hyperactive-impulsive type make 80% of the diagnoses
Is ADHD over-diagnosed? What evidence is there?
- Differences in diagnoses across the world, but no significant difference in prevalence between North America, Europe, Asia, Africa, South America, and Oceania
- Increased number of diagnosis in the past 30-40 years
↪ Could be because of more knowledge but also because of drug companies’ involvement - Higher rates of diagnosis in children ‘young for their year’
What is the heritability of ADHD?
High heritability: 70-80%
* Higher than personality, temperament, or depression
* Similar to schizophrenia, bipolar disorder, ASD
Despite the high heritability, the genetics explanation is very complex, why?
- Not explained by Mendelian inheritance
↪ a child has 50% chance of having a disorder if their parent has the same disorder = not true for ADHD - Not associated with common genetic variants with a large effect size
- Associated with thousands of genetic variants with a small effect size
- High overlap between polygenic risk for ADHD and other disorders, esp. ASD (more general risk for neurodevelopmental disorders)
How many cognitive models are there that try to explain ADHD?
A lot of them, no need to know which or how many, just the ones we will go over now:
1. EF deficit model
2. Delay aversion model
3. Multiple deficits model
↪ Dual Pathway model
Cognitive models of ADHD
What are executive functions?
Higher-order cognitive processes that guide behaviours in pursuit of a goal
- Includes: inhibition, updating, shifting, and planning
Cognitive models of ADHD
What criteria have to be fulfilled for the EF deficit model to explain ADHD?
This model propses that EF deficits are a primary deficit in ADHD
Criteria:
1. Consistency: EF deficits in ADHD must be consistently demonstrated across studies
2. Explanation: EF deficits should account for substantial variance in symptoms
3. Universality: EF weaknesses must be present in most individuals with ADHD
4. Aetiology: EF deficits and ADHD symptoms must have common aetiological influences, e.g. genetic
Cognitive models of ADHD
What evidence is there for the consistency criteria?
EF deficit model
- 83 studies, >6500 participants, 13 EF tasks
- Poorer performance in ADHD found 65% of the time
- Strongest effects for inhibitory control, vigilance, working memory and planning. Perseverative errors (WCST) were only weakly related to ADHD
- Effects not fully explained by IQ, academic achievement, or comorbid disorders
- ✓
Cognitive models of ADHD
What evidence is there for the explanation criteria?
EF deficit model
- Effect sizes for EF deficits were medium, while effect sizes for symptoms are large
- Variance in EF cannot fully explain variance in symptoms
- 𐄂
Cognitive models of ADHD
What evidence is there for the universality criteria?
EF deficit model
Within a study, not every individual with ADHD showed an EF deficit = 𐄂
Cognitive models of ADHD
What evidence is there for the aetiology criteria?
EF deficit model
Overlap between genes and brain mechanisms between ADHD and EF ✓
Cognitive models of ADHD
What is delay aversion?
Faster decline in the effectiveness of reward (reinforcement) as the delay between behaviour and reward increases
E.g. Marshmellow experiment
Proposed that children with ADHD prefer the smaller reward over the delayed bigger reward
Cognitive model of ADHD
What evidence of the four criteria is there that does/not support the delay aversion explanation of ADHD?
Consistency: ✓
- Meta-analysis indicated consistent delay aversion in ADHD
Explanation: 𐄂
- The effect size is moderate to small - if you know about one’s delay aversion, you don’t necessarily know ADHD symptoms severity
Universality: 𐄂
- ADHD subgroups without delay aversion can be identified
Aetiology: ✓
- Brain regions implicated in reward processing are also implicated in ADHD
In conclusion, not a good explanation
Cognitive models of ADHD
What do the multiple deficit models propose and What is their criticism? What models are those?
- Recognise that ADHD behaviours can arise from different cognitive deficits
- Different models propose different cognitive routes
- A common criticism is that the multiple deficits models are difficult to test
1. Dual Pathway Model
2. Three Factor Model
Cognitive models of ADHD
What does the Dual Pathway model proposes?
- Independent contributions of executive function (inhibition) deficits and delay aversion
- One or both pathways may contribute in an individual
Cognitive models of ADHD
What is the Three factor model?
- Proposes that there are independent contributions from executive function, delay
discounting, and temporal processing - Temporal processing: tapping a rhythm, estimating durations, anticipating a stimulus
Biological explanation
What could be the biological (brain) explanation for ADHD considering subcortical volumes?
- Mega-analysis
- Some reductions in subcortical volume
- Most effects found in children, not adults
- Effect sizes are very small (found only because it was done on so many people)
Biological explanation
What could be the biological (brain) explanation for ADHD considering cortical morphology?
- Mega-analysis
- Lower total cortical thickness and regional thickness of the fusiform gyrus and temporal pole in children
- Effect are small to very small
Biological explanation
What evidence did a mega-analysis study using task fMRI found to help explain ADHD?
Indicated no consistent differences in task fMRI activation across studies
- no functional brain difference in ADHD
What evidence did a mega-analysis study using resting-state fMRI found to help explain ADHD?
Did not indicate significant hyper- or hypoconnectivity of any specific region in ADHD
Biological explanation
What is the main conclusion from all those mega-analysis?
Even if they are mega-analysis, the effect sizes are small or inconsistent = not good enough evidence to explain ADHD
Pharmacological treatment of ADHD
- Stimulants: Methylphenidate (e.g. Ritalin); Amphetamines (e.g. Adderall) - good efficacy
- Non-stimulants
- SNRIs
Non-pharmacological treatments of ADHD
- Parent training in behaviour management
- School interventions - peer-tutoring, adjustments to curriculum and exam times, more sources of positive reinforcement for work productivity…
What are Specific Learning Disorders? What are the characteristics?
- Specific learning disorders impact the ability to learn and apply reading, writing, or math skills
- Children generally have typical intelligence but are unable to learn or use a particular academic skill, such as reading, writing, mastering calculations, or mathematical reasoning with typical instruction
What does reading involve that people with dyslexia struggle with? What are the 3 types of reading?
- Reading involves identifying letters, converting letters into sounds, combining sounds in sequence, and short-term memory
1. Phonological reading decodes the letters of the words into sounds that can be pronounced
2. Graphemic reading looks at the whole word and produces the sound of that word from memory
3. Fluent reading involves both phonological and graphemic reading
What could be causes for phonological and sensory deficiency?
- Reading deficits do not present in a straightforward way (phonological skills)
- Children may be impaired at decomposing words into the phonemes that make them up
What deficit is there in the brain observed in adult males with developmental dyslexia?
Impairments of phoneme use are associated with the left-hemisphere language regions
- weaker connections between the left medial geniculate body and the left temporal cortex
How could the difference in sound-detection ability explain dyslexia?
- Most people can separate two sounds separated by 10 to 40 ms, but children with learning difficulties required much longer intervals between sounds
- Many consonants contain sounds that change in less than 40 ms
- Timing accuracy and sensory processing of cells might be different in people with dyslexia
What are other theories might explain Dyslexia?
1.Attentional deficiency - reading problems result from difficulty shifting attention to relevant cues
- This would be associated with the parietal-lobe association areas
2.Motor deficiency - cerebellum is involved in timing, coordination, and attention
- Damage to cerebellum might result in problems with reading
3.Multicausal approaches
- It is possible the reading disorders are not one single condition, but multiple conditions with different causes
What is dyscalculia? Characteristics? Incidence?
- Difficulty representing and processing numbers in a typical way
- Characterized by difficulty with number sense, calculation, or mathematical reasoning
- Incidence is about 5 per 100 students
- Often comorbid with other learning difficulties
How can SLD be detected using neuropsychological evaluation?
- Neuropsychological testing can identify individuals with specific cognitive profiles
- IQ tests are commonly used to assess overall cognitive function and the pattern of performance on subtests
- The ACID profile (arithmetic, coding, information, digit span) on the Wechsler Intelligence Scale for Children suggests a specific learning difficulty
↪ Reading disabled scored lower on all of the subtests than controls
What are the adult outcomes? What can be done to ensure well-being of individuals with SLD?
- Early studies of adult outcomes of neurodevelopmental disorders were optimistic, but later assessments were more pessimistic
- Parents perceive greater impacts of learning disabilities on well-being, happiness, and social interactions than do the individuals with the disability
- Assessment of the strengths and weaknesses of the individual, followed by instruction to address those weaknesses, is important
- Counselling to focus on strategies to work around the individual’s challenges can play a large role
What are the characteritics of autism? Who described it first?
- First described by Leo Kanner and Hans Asperger
- Intellectual disability is common
- Difficulties vary considerably
- Sleep problems, anxiety, depression, epilepsy are more common than in people without ASD
What is prevalence of ASD?
- Around 16.8 in 1,000 children
- Among children aged 8, increase in prevalence from 1.1% in 2008 to 2.3% (likely due to changes to diagnostic criteria (includes broader spectrum), increased awarness of ASD, greater access to services…)
- More common in males (though, likely diagnostic bias)
What are ASD DSM-5-TR criteria?
- Deficits in social communication and social interaction
- Restricted and repetitive behaviours, interests, or activities
- Symptoms must be present in the early developmental period
- Symptoms must cause clinically significant impairment in social, occupational, or other important areas of functioning
- Symptoms are not better explained by intellectual disability or global developmental delay
What are the social communication and interaction difficulties in ASD?
- Social reciprocity (turn-taking)
- Non-verbal communication
- Understanding, maintaining, and developing social relationships
What are the restricted and repititive behaviours and interests?
- Stereotyped or repetitive motor movements, use of objects, or speech
- Insistence on sameness, inflexible adherence to routines
- Highly restricted, fixated interests
- Hyper- or hypo-reactivity to sensory input (not part of the diagnostic criteria but very common)
What is the development of ASD like?
Diagnosis typically around 3 years
At specialist clinics from about 12 months
Early signs (<12 months):
- Lack of eye contact
- No orienting to name
- Little social engagement
Signs (12-24 months):
- Delay in language and/or motor development
- No or limited use of gestures in communication
- Repetitive and stereotyped movements become apparent
- Lack of imaginative play
Persistent differences across the lifespan
What causes autism?
No one knows
How do genetics explain ASD? What is the problem with this?
- Highly heritable (90% in twin studies)
- Some single-gene disorders have a similar presentation, e.g. Fragile-X, Rett syndrome
However:
- Most cases are idiopathic (no genetic explanation why someone has autism)
- Unaffected family members may share traits
How does neuroanatomy differ in people with ASD? What are the problems with this?
Difference in head size trajectory
- Larger head size in infancy
- Typical head size later
- May be tied to differences in neurogenesis and synaptogenesis
Some differences in subcortical structures, mainly amygdala and striatum
Problems:
- Findings are not consistent across studies
- Interactions with age and gender have been reported
- Considerably heterogeneity in study samples
What are the results from a resting-state mega-analysis studying brain function of people with ASD?
- Autism related to hypoconnectivity of sensory and attentional areas, and hyperconnectivity of the default mode network and subcortical structures
- Sensory and attention hypoconnectivity was associated with social impairment, RRBIs, and sensory processing
- DMN hyperconnectivity related to social impairment and sensory processing
Cognitive theories of ASD
Theory of Mind deficit?
- Impairment in the ability to know the thoughts, beliefs, and desires of others
- Explains social difficulties in some autistic people
Cognitive theories of ASD
Weak Central Coherence theory?
- Bias towards local instead of global processing
↪ focus on detail rather than the big picture - Explains some perceptual differences
Cognitive theories of ASD
Systematising vs Empathising theory
- Bias towards systems and objects (systematising)
- Very sexist theory: systematising = men; empathising = women
- Explains higher prevalence of autistic traits among scientists and engineers
- No good evidence
Cognitive theories of ASD
Weak Perceptual Priors theory
- Reduced reliance on prior knowledge and experience which makes it very overwhelming and draining to process info around you
- Explains perceptual differences and sensory sensitivity
What are some interventions for ASD?
- Early Intensive Behavioural Intervention - for children 5 yrs or younger for improvement in language, play and social communication
↪ small to medium effect sizes - Naturalistic Developmental Behavioural Intervention
- CBT for related psychological difficulties such as anxiety or depression
- Pharmacotherapy - for co-occurring psychiatric conditions such as emotion dysregulation and ADHD
↪ Adverse effects: changes in appetite, weight, sleep
