ADHD Psy2003

Core features of ADHD

inattention, hyperactivity, impulsivity

DSM-5 ADHD

Symptoms must be present before age 12

Must occur in more than one setting

Must cause functional impairment

ADHD subtypes

Predominantly inattentive

Predominantly hyperactive-impulsive

Combined

1902

George Frederic Still described children with "moral control" deficits and poor sustained attention

1917-1928

Post-encephalitic behaviour disorders linked hyperactivity to brain injury

1940s-60s

Terms like "minimal brain damage" and "minimal brain dysfunction" were used

1968 DSM-II

"Hyperkinetic Reaction of Childhood"

1980 DSM-III

Introduced "ADD (with or without hyperactivity)"

1987 DSM-III-R

ADHD as a unified diagnosis

DSM-5 (2013)

Introduced "presentations" and clearer diagnostic criteria

Impact on Education

Higher odds of failing to achieve GCSE-equivalent qualifications (OR ~6.5 for boys, ~8.5 for girls)

Impact on Occupation

Adults diagnosed in childhood showed lower employment rates and income

Impact on Social Integration

Children with ADHD were more likely to be rejected by peers and less likely to be popular (Hoza et al., 2005)

Impact on Physical health

Higher accident rates: 23% in ADHD vs 15% in controls (Lange et al., 2016)

Impact on Mental Health

Increased rates of anxiety, depression, Tourette's syndrome, and substance dependence

Classical Theory 1

Frontal Cortex Dysfunction

Evidence for Classical Theory 1

ADHD symptoms resemble damage to frontal cortex (e.g., impulsivity, poor planning)

Barkley's "behavioural disinhibition theory" emphasises poor executive function

Classical Theory 1 Imaging

Structural imaging:

Reduced frontal lobe grey matter volume (MRI studies)

Functional imaging:

PET scans show lower glucose metabolism in frontal regions in ADHD teens

Classical Theory 2

Dopamine Dysfunction

Classical Theory 2 - medication

Stimulants like methylphenidate and amphetamine increase dopamine levels

Classical theory 2 evidence

Behavioural:

Disrupted learning under non-contingent reinforcement (Douglas & Parry, 1983)

ADHD children show delay aversion and reduced sensitivity to reward

Classical theory 2 imaging

SPECT imaging shows increased dopamine reuptake in ADHD brains

Limitaitons of classical theories

Frontal cortex dysfunction is non-specific (seen in many disorders)

Dopamine theories are challenged by new treatments (e.g., atomoxetine) targeting noradrenaline

ADHD is heterogeneous, suggesting no single "cause" or unified mechanism

Why focus on Distractibility

Distractibility is a central DSM-5 criterion: "Is often easily distracted by extraneous stimuli"

Has long been considered a core symptom (since Strauss in 1940s-50s)

New research suggests that focusing on neural substrates of distractibility may better explain ADHD

The Brain's 'Distractibility' centre

The Superior Colliculus (SC)

SC

Part of the subcortical visual system

Controls eye movements and shifts in attention

SC lesions

Collicular lesions reduce distractibility in animal studies (rats, cats, monkeys)

Gaymard et al. (2003): Human lesion study linked SC pathway damage to attention problems

SC animal models

Animal models (e.g., Clements et al., 2013) show SC hyper-responsiveness in ADHD-like behaviour

SC Human evidence

Panagiotidi et al. (2017): Adults with ADHD traits showed differences in multisensory integration tasks

ADHD linked to simultaneity judgement deficits, suggesting SC abnormality

SC treatment impact

Stimulants like amphetamine reduce SC hyperactivity (Gowan et al., 2008)

SC - Classical Theory 1

Frontal Cortex:

SC receives input from frontal regions;

SC dysfunction may explain apparent frontal deficits

(Bertram et al., 2014; Leriche et al., unpublished)

SC - Classical Theory 2

SC has direct projections (tectonigral pathway) to dopamine-producing neurons

Activation of SC leads to dopamine release in forebrain (Dommett et al., 2005)

Collicular theory summary

ADHD may involve hyper-responsivity in the superior colliculus, explaining:

Increased distractibility

Links to dopamine dysfunction

Connectivity to frontal cortex

Collicular theory implications

Suggests new, less addictive therapeutic targets (e.g., drugs modulating SC activity)

Moves beyond frontal/dopamine models to include sensory integration and attentional control