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
- ✓
