ADHD: Diagnostic Concepts, Neurobiology, and Evolutionary Perspectives

Comprehensive practice flashcards detailing diagnostic definitions, disease models, cross-cultural empirical findings, neurocognitive and neuroimaging mechanisms, genetics, and evolutionary perspectives on ADHD.

What are the core diagnostic requirements for symptom duration and pervasiveness in ADHD according to diagnostic classification systems?

Symptoms of inattention and/or hyperactivity-impulsivity must persist for at least $6\text{ months}$ and be pervasive across multiple settings (such as home, school, work, or the playground).

By what age do ADHD symptoms typically onset according to diagnostic guidelines?

Symptoms typically begin during early childhood, usually by age $12$.

What specific clinical presentation subtypes are designated under the ICD-11 code $6\text{A05}$ for ADHD?

$6\text{A05.0}$ (Predominantly inattentive presentation), $6\text{A05.1}$ (Predominantly hyperactive-impulsive presentation), $6\text{A05.2}$ (Combined presentation), and $6\text{A05.Z}$ (ADHD, unspecified).

What proportion of typically developing children exhibit the behavioral profile of ADHD?

Approximately $5\%$ (or $1\text{ in }20$ children).

What historical significance does the Ebers Papyrus ($1550\text{ BC}$) hold in the context of disease classification?

Originating in ancient Egypt in $1550\text{ BC}$, it represents one of the earliest recorded disease classification systems and contains the first known written documentation of symptoms of type $1$ diabetes.

In the modern biomedical disease model, what three elements are informed once a diagnosis is established from observed symptoms?

Pathogenesis (pathogen/underlying mechanism), prognosis (expected future course), and treatment.

Why is cystic fibrosis contrasted with ADHD regarding the application of the biomedical disease model?

Cystic fibrosis has a definitive biological marker ($CFTR$ gene mutation on chromosome $7$) and an established pathogenic cascade, allowing confirmatory testing, whereas ADHD currently lacks definitive biomarkers.

What is the documented prognosis for individuals with pervasive childhood hyperactivity and inattention in the absence of treatment?

An increased risk for academic underachievement, occupational underachievement (failing to meet intellectual potential), and involvement in the criminal justice system (criminality).

What is the reported acute response rate of psychostimulant medications for treating ADHD symptoms?

An acute response rate between $70\%$ and $80\%$.

In the cross-cultural study by Bruce Morton and Ronald Magiste, what participant samples were recruited from Canada and Trinidad & Tobago?

Canada: $n = 177$ ($65$ teachers [$62$ female] and $112$ parents [$105$ female]); Trinidad & Tobago: $n = 203$ ($55$ teachers [$41$ female] and $148$ parents [$104$ female]).

How did ADHD knowledge scores compare between Canadian participants and Trinidad & Tobago participants in the Morton and Magiste study?

Knowledge was substantially higher in Canada ($63.1\%$ for teachers, $61.7\%$ for parents) than in Trinidad & Tobago ($43.9\%$ for teachers, $35.6\%$ for parents), despite Trinidadian public school teachers being required to hold a Master's degree.

How did attitudes toward ADHD compare between participants in Canada and Trinidad & Tobago?

Attitudes were largely commensurate across both countries, with Canadian participants having slightly more favorable scores (teachers $91.2$, parents $88.5$) compared to Trinidad and Tobago (teachers $83.5$, parents $82.3$).

When presenting behavioral vignettes without the ADHD label, which attributions did participants in Trinidad & Tobago endorse significantly more strongly than Canadian participants?

They more strongly endorsed "low motivation" and "disciplinary issue" as explanations for the child's behaviors.

What happened to the cross-country differences in behavioral attributions when Morton and Magiste statistically controlled for knowledge of ADHD?

The country differences in perceptions and attributions disappeared completely, indicating that differing interpretations were driven by access to medical information rather than deep-seated cultural attitudes.

What cognitive mechanism does the Stop-Signal Reaction Time (SSRT) task assess?

Behavioral inhibition, specifically the latency required to cancel or suppress a motor response that has already been initiated.

Why do executive function tasks that yield large effect sizes ($d = 0.5$ to $1.0$) between ADHD and control groups fail as standalone diagnostic tools?

Because the distribution of scores for children with ADHD and typically developing children heavily overlaps, preventing the selection of any cut-off score that avoids high rates of false negatives or false positives.

Which brain region is highlighted here that is classically associated with cognitive control, executive functioning, and higher-order goal regulation?

The dorsolateral prefrontal cortex (dlPFC).

Which two dopaminergic midbrain and striatal structures are highlighted here in relation to reward anticipation and impulsivity?

The ventral tegmental area (VTA) and the nucleus accumbens (NAcc).

In the mega-analysis of $9,647$ individuals ($1,533$ with ADHD), what was found regarding cortical thickness on the lateral cortical surface?

There was a complete absence of neuroanatomical differences on the lateral surface (dlPFC), and where differences were found, the cortex was thicker in ADHD (thinner in controls), contradicting predictions of dlPFC thinning or brain defects.

What did the meta-analytic review by Plichta and Scheres demonstrate regarding ventral striatum responsiveness during reward anticipation in ADHD?

Individuals with ADHD exhibited hypo-responsiveness (hypo-activation) of the ventral striatum compared to healthy controls, rather than the intuitive hyper-activation.

How do the Task-Positive Network (TPN) and Default Mode Network (DMN) typically interact during normal cognitive functioning?

They operate in an anti-correlated trade-off: when external demands activate the TPN, the DMN is suppressed; when external engagement drops and internal mind-wandering occurs, the DMN activates and the TPN is inhibited.

In the ABCD study sample of $7,979$ children analyzed by Kelly Duffy and Nathaniel Helwig, what functional connectivity pattern predicted higher Child Behavior Checklist (CBCL) attention problem scores?

A reduction in the anti-correlation between the task-positive and default-mode networks (DT-DLA functional connectivity), indicating an inability of the task-positive network to sufficiently suppress the default mode network.

What is the estimated heritability of ADHD based on twin study literature?

Between $70\%$ and $80\%$ (heritability coefficient of approximately $0.7$ to $0.8$).

What major conclusion regarding ADHD genetic architecture emerged from the GWAS meta-analysis of $20,183$ ADHD individuals and $35,191$ controls?

It identified $12$ genome-wide significant risk loci and demonstrated that ADHD is polygenic, linked to many common genetic variants each exerting a diminishingly small effect.

How is an ADHD diagnosis clinically established in practice given the absence of definitive biomarkers?

It is established as a consensus decision (a social construction) agreed upon by psychometrists/diagnosticians, teachers, and caregivers based on observed behavior across contexts.

How does the neurodiversity perspective conceptualize neurodevelopmental profiles such as ADHD, ASD, and dyslexia?

As examples of natural phenotypic variation within the human population rather than intrinsic medical pathologies or disease defects.

How did the lecture use the population distribution of handedness to argue against pathologizing ADHD?

$10\%$ of the population is left-handed and $90\%$ is right-handed; being at an extreme end of the distribution represents a natural variation rather than a medical pathology.

Where is the polymorphic variable number of tandem repeats (VNTR) located in the $DRD4$ receptor gene, and what traits are linked to the $7$-repeat allele ($DRD4\text{-R7}$)?

It is located in exon $3$, encoding the third intracellular loop of the dopamine D4 receptor; the $7$-repeat allele is associated with increased novelty-seeking, impulsivity, vigilance, and distractibility.

What evolutionary relationship is illustrated in this scatter plot from Chen et al. (1999) regarding the $DRD4$ gene?

As macro-migration distance from ancestral East Asia increases along migratory routes into and across the Americas, the proportion of $DRD4$ long alleles ($7$-repeat) increases from near $0\%$ to over $70\%$.

What does a delay discounting task assess, and what does a steeper discounting curve reflect?

It assesses how an individual values a reward as a function of delay interval (e.g., choosing between smaller immediate cash versus larger delayed cash); steeper discounting reflects greater impulsivity and preference for immediate rewards.

According to Sweitzer et al. (2012), how does childhood socioeconomic status (SES) interact with the presence of the $DRD4$ $7$-repeat allele in predicting delay discounting?

Individuals carrying the $7$-repeat allele exhibit differential susceptibility: they show markedly higher discounting in low childhood SES environments, but lower discounting in high childhood SES environments compared to non-carriers.