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• dsm5 - neurodevelopmental disorders characterized by developmental deficits or differences in brain processes- lead to impairments of personal, social, academic or occupational functioning. Neurodiversity= umbrella term.
• -‘Neurodiversity’ is considered "...a concept that implies thatneurological difference is best understood as an inherent andvaluable part of the range of human variation, rather than apathological form of difference".(p. 168. Dyck & Russell, 2019)-The neurodiversity movement primarily differs from the Autisticadvocacy movement in its greater breadth, extending beyondautism to capture multiple domains of neurodevelopmentaldifference(Schuck et al, 2021)
• Autism Spectrum Condition - Persistent difficulties with social communication, social interaction, restricted & repetitive behaviours,activities, interests since early childhood, that limit and impair everyday functioningAutism Spectrum Disorder = diagnosis
• DSM - Criteria A subcategory 1includes inattentive traits.According to the DSM, inattentioncriteria are met if: "Six (or more)of the following symptomshave persisted for at least 6months to a degree that isinconsistent withdevelopmental level and thatnegatively impacts directly onsocial andacademic/occupationalactivities." [Note for people 17and older only five traits have tobe present to meet the criteria]
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• Barriers to thriving include high anxiety where neurodiverse students feel excluded,have a reduced sense of belonging, struggle to negotiate campus life This impacts on wellbeing (Hamilton & Petty, 2023)DSM 5 highlights sensory challenges for many students with autism - in HE there are increased sensory inputs, lack of accommodation in physical environments(Waisman et al, 22)
• Biopsychosocial model – Clinical intervention alleviates symptoms, psychosocialsupport and understanding can reduce anxiety and increase social inclusion(Doyle, 2020)A shift toward a context that allows all learners to thrive is growing but does requirecareful navigation
• ADHD hallmark symptoms- Inattention, Impulsivity, and Hyperactivity

  Its a neurodevelopmental fronto-striatal (inc frontal cortex and striatum) condition

  Diagnosis should be made before 7 y/o (peak onset 3-4)

  4x more present in boys

  Impulsivity is considered most significant / disruptivesymptom
• ADHD proper – hyperactivity, distractibility, dyscontrol (problemscontrolling behaviours).• This variant seems to be more common in boys.• Problems with selective attention may involve pre-frontal structures(dorsolateral prefrontal cortex and orbitofrontal cortex)

  ADD (without hyperactivity) – withdrawn, passivity, failure toengage)• This variant seems to be more common in girls.• Problems with sustained attention may involve additional posterior parietalinvolvement.• This variant is less associated with later conduct disorder.
• Both variants may have co-morbidity with other conditions such asanxiety, depression, and learning problems.• Complex heterogenous condition
• DSM-5 diagnostic criteria

  A persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development.

  Symptoms presenting in two or more settings (e.g. at home, school, or work; with friends or relatives; in other activities).

  And negatively impacts directly on social, academic or occupational functioning.
• Aetiology of ADHD

  
• Aetiology of ADHD - Genetics

  Strong Genetic Component

  •ADHD is one of the most heritable mental health conditions.

  •High heritability  ~ 74%

  •Evidence from family and adoption studies (genetic vs environment) and twin studies (monozygotic vs dizygotic).

  •Concordance rates MZ twins ~ 66%

  •Concordance rates DZ twins ~ 28%

  •ADHD unlikely to be caused by a single gene, likely to be the result of combination of genes.
• Aetiology of ADHD - Genetics

  •Genome-Wide Association Studies (GWAS) – looks at entire genome to detect common genetic variants within groups of individuals with ADHD.

  •Dopamine transporter gene (chromosome 5) – responsible for DA depletion (linked to problems with attention, hyperactivity).

  •D4 dopamine receptor gene (chromosome 11) – responsible for blunted response to DA (linked to novelty seeking, impulsivity, excitability). D4 receptors can be found in the striatum and dorsolateral prefrontal cortex.
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  •Genetic vulnerability – genes turned ‘on’ and ‘off’ during development (with some protective factors that influence expression of genes involved).
• Aetiology of ADHD – Environmental Factors

  •Premature birth (increases with degree of prematurity) and low birth weight are associated with ADHD.

  •Brain injury

  • Even mild brain injury is associated with development of ADHD (Adeyemo et al., 2014).

  •Prenatal exposure to substances such as alcohol and tobacco
• •Chemical contamination – there is an association between exposure to lead and ADHD (Donzelli et al., 2019).

  •Iron deficiency – low iron levels are associated with ADHD (Wang et al., 2017).

  •Pathogenesis (i.e., cause and development of a disease) of ADHD remains unclear.

  •Pre-, peri-, and early post-natal period of neurodevelopment is likely to be a sensitive time for ADHD.
• Development of ADHD Brain

  •Cortical areas in ADHD individuals may not reach peak thickness (full development), until some years after typically developing controls.

  •Frontal cortex (inc., PFC) shows the greatest delay (Shaw et al., 2007). Delayed myelination, reduced signalling.
• At 10 years of age, around 80% of cortical areas have reached peak thickness in typically developing children. This is compared with just 30% in children with ADHD.

  
• Development of ADHD brain

  Maturation of the brain, as reflected in the age at which a cortex area attains peak thickness, in ADHD (left) and typical development (right) (Shaw et al., 2007).

  •PFC develops more slowly and shows reduced volume and activity, which means that signalling will also be slower.

  •These changes are correlated with symptoms and severity of ADHD

  •Medication can normalise PFC activity.
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• Neurotransmission Imbalance

  •Main brain regions implicated in ADHD development:

  •Prefrontal cortex (PFC).

  •Cerebellum.

  •Caudate.

  •Slower maturation /reduced volume of PFC and reduced volume/activation of caudate or cerebellum found in ADHD.

  •These brain regions can be linked to neurotransmitters (NTs) implicated in ADHD – dopamine, noradrenaline, serotonin.

  •Noradrenaline and dopamine – essential for typical brain function, important for executive function and attention.
• Dopamine (DA) Pathways

  Mesocortical pathway begins in the ventral tegmental area and projects to the frontal cortex.

  Mesolimbic pathway  begins in ventral tegmental area ànucleus acumbens and limbic structures (hippocampus and amygdala).

  Nigra-striatal pathway begins in the substantia nigra and ends in the striatum (includes caudate nucleus and putamen).

  
• ADHD and DA – DA Transporter Channel

  •Figure shows a synapse in the brain releasing neurotransmitter (NT) from the presynaptic neurone that binds to receptors on the postsynaptic neurone.

  •One gene that has been linked to ADHD is the gene that codes for the dopamine transporter channel.

  •This gene is known as SLC6A3, and it can exist in several forms which differ according to the number of times a specific part of the genetic sequence within the gene is repeated (these are known as ‘repeats’).
• figure: h

  
• figure t

  •Two forms of SLC6A3 gene are associated with ADHD (Bonvicini et al., 2016):

  •The nine-repeat form is associated with ADHD in adults.

  •The ten-repeat form is associated with ADHD in children.

  •Having these genes results in higher levels of the dopamine transporter channel within the brain (Madras et al., 2002).

  •Dopamine is removed from synapse before it has chance to bind to receptors.

  
• ADHD and Changes to DA Signalling

  •DA D4 receptor expression is influenced by gene DRD4

  •The longer version of DRD4 alters DA receptor functioning and reduces the neurone’s response to dopamine (i.e., D4 receptor sensitivity is reduced).

  •This means that the same amount of dopamine has less of an effect.

  
• Dopamine (DA) Theory of ADHD

  •ADHD results from a hypo-dopaminergic state (i.e., a deficit in dopamine function that results in less dopamine) (Levy, 1991).

  •Hypo-dopaminergic state à mesocortical pathway (implicated in attention, including selective attention).

  •BUT not all areas of the brain have reduced dopamine. Some are hyper-dopaminergic (Castellanos, 1997).

  •Hyper-dopaminergic state à nigrostriatal pathway (implicated in impulsivity and hyperactivity).
• Evaluation of Dopamine (DA) Theory

  + •Imaging – shows reduced activity in brain regions (frontal) that receive dopamine.

  •Genetics – variants of genes are increased in ADHD.

  •Treatment – medication works by acting on DA system to alleviate symptoms.

  • •Imaging – changes in brain activity are complex and may involve multiple brain systems.

  •Genetics – most robust finding is for DRD4, but this is only slightly more prevalent in ADHD.

  •Treatment – effective medication also acts on noradrenaline system.
• Cognitive Performance - Attention

  Endogenous attention – Top Down

  •Wilful attention to something based on our current goals.

  •Impairment might be expressed as difficulty in attending to the specific voice of a teacher because of disruption by intrusive thoughts.

  Exogenous attention – Bottom Up

  •Attention is drawn to a stimulus based on its characteristics (e.g. flashing light).

  •Impairment could be increased sensitivity to irrelevant but salient (most notable) stimuli, such as loud noises outside classroom.
• Selective Attention

  The ability to preferentially process one stimulus in the presence of other potentially distracting stimuli
• Managing ADHD

  •Medication is the last resort for preschool children –first approach is parent training, followed by personalised psychosocial interventions and finally medication.

  •Children and young people - first approach is parent support/ teacher training, then medication and CBT.

  •Adults – first approach is medication, then CBT.

  
• Managing ADHD - Medication

  •Psychostimulants – are methylphenidate and amphetamine.

  •Brand names:  Ritalin® and Adderall®

  •These work by increasing synaptic levels of dopamine, noradrenaline, serotonin.

  •Low doses can reduce movement and impulsivity, and improve cognitive function (e.g., sustained attention).

  •Methylphenidate reduces symptoms in ~ 57% of individuals (Newcorn et al., 2008).

  •Amphetamine reduces symptoms in ~ 82% of individuals (Dittmann et al., 2013).

  •Non-stimulant drugs – Atomoxetine.

  •Brand name: Strattera®

  •Works by increasing synaptic levels of noradrenaline.
• ADHD Medication - Methylphenidate

  •Blocks the reuptake channels / transporters.

  •Prevents dopamine from being removed from the synapse.

  •Increases the probability that dopamine will bind with receptors.
• ADHD Medication - Amphetamine

  Amphetamine enters through reuptake channels

  Dopamine is displaced from the vesicles

  Dopamine ‘leaks’ out through the reuptake channels (action is reversed)

  No action potential needed!

  Amphetamine also blocks the reuptake channels
• ADHD Medication - Atomoxetine

  Atomoxetine works by blocking the reuptake channels. This prevents noradrenalin from being removed from the synapse and increases the probability that it will bind to receptors. This increases noradrenalin activity at the level of the synapse.
• Summary

  ADHD is a neurodevelopmental fronto-striatal disorder.

  •Genetic and environmental factors are implicated in ADHD.

  •Research shows some changes in brain regions such as the pre-frontal cortex (implicated in problems with sustained attention).

  •Dopamine plays a major role in ADHD, but other neurotransmitters are implicated (noradrenaline, serotonin).

  •Medication involves psychostimulants and non-stimulant drugs that work by increasing dopamine and noradrenaline.