Neurodevelopment - ADHD Flashcards

(44 cards)

1
Q

ADHD Clinical Features + Diagnoses #1

A

Persistent inattention and/or hyperactivity-impulsivity

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2
Q

ADHD Clinical Features + Diagnoses #2

A

Symptoms must be developmentally inappropriate and impair functioning

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3
Q

ADHD Clinical Features + Diagnoses #3

A

Symptoms present in 2 or more settings for 6+mos

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4
Q

ADHD Clinical Features + Diagnoses #4

onset?

A

Onset must be before age 12

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5
Q

ADHD Clinical Features + Diagnoses #5

A

Interferes with social, academic, or occupational functioning

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6
Q

ADHD Clinical Features + Diagnoses: best practice assessment requires…

A
  • Collateral information (e.g., teacher interviews, report cards)
  • This makes retrospective adult diagnosis more complex and challenging
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7
Q

ADHD - common byproducts

A
  • Fidgeting, tapping
  • Difficulty listening
  • Making mistakes
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8
Q

3 ADHD types

A
  1. Hyperactive (talk a lot, always “on the go”)
  2. Inattentive (daydream a lot, has to use reminders)
  3. Combined
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9
Q

ADHD Prevalence - Children vs. Adults

A
  • (Children): ~7-8%
  • (Adults): ~4.5%
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10
Q

Gender & Diagnosis: Childhood - who is more diagnosed than who?

A
  • Boys diagnosed 2-3x more often than girls
  • Historical diagnostic models were based on hyperactive boys + move overt
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11
Q

Gender & Diagnosis: Female Presentation often missed due to…

A
  • Predominantly inattentive symptoms (“daydreamy”)
  • Symptoms are internalized (anxiety, low self-esteem) vs. externalized (disruptive)
  • Masking: tendency to suppress H/I behaviours due to societal expectations (e.g., perfectionism, people-pleasing)
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12
Q

ADHD Course & Outcomes

A
  • About 2/3 of children continue to have impairing symptoms into adulthood
  • Hyperactivity may lessen, but inattention & executive dysfunction often persist
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13
Q

ADHD Course & Outcomes - risk if left untreated

A
  • Includes poor job fit, academic underachievement, and relationship issues
  • Higher risk for accidents, injury, substance misuse, and comorbidities (anxiety, depression)
  • Associated with an average 7.5-year reduction in life expectance
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14
Q

ADHD Course & Outcomes - benefits of treatment

A
  • Medication is highly effective and mitigates risks.
  • Associated with a reduced risk of death (~19%), overdose (~50%), and motor vehicle accidents (~38%)
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15
Q

ADHD Comorbidities - Sensory Oversensitivity

A
  • Common to have more intense reactions to sights, sounds, textures
  • Can exacerbate distractibility & emotional reactivity
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16
Q

ADHD Comorbidities - Emotional Dysregulation

A
  • Higher than in the general population
  • Central feature or consequence?
  • Not a DSM criterion but distinct from (though may be amplified by) comorbid mood disorders
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17
Q

ADHD Comorbidities - Differential Diagnoses: vs ODD

A

Defiance (“I won’t”) vs inability to sustain effort (“I can’t”)

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18
Q

ADHD Comorbidities - Differential Diagnoses: vs anxiety

A

Inattention due to internal worry vs external distraction

19
Q

ADHD Comorbidities - Differential Diagnoses: vs ASD

A

Social issues from disengagement vs impulsivity; tantrums from broken routines vs poor self-control

20
Q

ADHD Causes: Biological & Genetic

associated with _ system genes?

A
  • Strong genetic heritability (one of the highest in psychiatry)
  • Runs in families; associated with dopamine system genes
21
Q

ADHD Causes: Neurobiological influences (3)

A
  • Slightly smaller total brain volume
  • Delayed cortical maturation, especially in frontal regions (responsible for executive functions; e.g., planning, inhibition)
  • Impaired function in brain networks for attention and self-control
22
Q

ADHD Causes/Exacerbating Factors: Sleep & Cognition

A
  • Sleep problems are common especially in children with ADHD
  • Inattention and hyperactivity worsen with poor sleep (bidirectional relationship)
  • Sleep-focused interventions show promising results
  • Working memory and inhibitory control often most impaired
23
Q

ADHD Causes: Environmental Risk Factors

A
  • Prenatal exposure to smoking and alcohol
  • Maternal stress and low birth weight
  • Family conflict and parenting style may exacerbate symptoms
  • Food additives and toxins NOT strongly supported
24
Q

Classic ADHD Theories - #1

A

Traditional Executive Function (EF) Models (e.g., Barkley)

25
1. Traditional Executive Function (EF) Models (e.g., Barkley): **type of model? primary deficit?**
* A **"Top-Down"** failure model * **Primary Deficit: Behavioral Inhibition**
26
Traditional Executive Functional Models - **cascades into other deficits**
1. Working memory 2. Self-regulation 3. Problem solving + planning
27
Traditional Executive Function Models - **brain links?**
**Prefrontal-Striatal Circuits (Dopamine system)**
28
Classic ADHD Theories - #2
Attention/Arousal Dysregulation Models (e.g., Sergeant)
29
Attention/Arousal Dysregulation Models (e.g., Sergeant) - **type of model? primary deficit?**
* A **"Bottom-Up"** failure model * Primary Deficit: **Poor regulation of Arousal, Alertness, & Activation**
30
Attention/Arousal Dysregulation Models - **leads to...**
**"Unstable cortical arousal":** * **Under-Aroused** → **Inattention** * **Compensating** → **Hyperactivity & Sensation-seeking**
31
Attention/Arousal Dysregulation - **brain links?**
**Brainstem/Locus Coeruleus** (Norepinephrine system)
32
Classic ADHD Theories - #3
Dual Pathway Models (e.g., Sonuga-Barke)
33
Dual Pathway Models (e.g., Sonuga-Barke) - **integrates? explains**
* Integrates classic models * Explains heterogeneity (diversity/variability)
34
Dual-Pathway Models - **pathway 1:**
* **"Cool"** * **"Top-down"** * **Cognitive pathway** * **Executive Function deficits**
35
Dual-Pathway Models - **pathway 2**
* **"Hot"** * **"Bottom-up"** * **Motivational pathway** * **Delay Aversion** (preference for immediate rewards)
36
Classic ADHD Theories - #4
Reinforcement Learning Models
37
Reinforcement Learning Models - **builds on which pathway? explores why...?**
* Builds on the **"hot" motivational pathway** * Explores why **reward sensitivity and decision- making are atypical**
38
Reinforcement Learning Models - **focus on atypical...**
atypical **dopamine signaling** (how the brain learns from rewards and consequences)
39
Reinforcement Learning Models - **ADHD is WHAT?**
ADHD is **heterogeneous**; it is not one thing and can result from multiple, overlapping pathways
40
The Relatability Problem (What ADHD Isn’t)
"Relatable" symptoms can confuse common traits with a clinical disorder
41
ADHD Treatment: Core Modalities
1. Stimulants 2. Psychosocial interventions
42
Medications (Stimulants):
* First-line treatment (e.g., Ritalin, Adderall, Dexedrine) * Function: **Increase availability of dopamine & norepinephrine** * Effect: **Highly effective at reducing core symptoms** (inattention, hyperactivity, impulsivity) * Side effects: **appetite loss, sleep issues, irritability**
43
Psychosocial Interventions:
* Parent training in behavior management (for younger children) * Classroom-based behavioral programs Executive Function Skills Training: * Uses strategies to improve core deficits like working memory, planning, & inhibition * Real-world practice is crucial for transferring skills to daily life
44
ADHD Treatment: overview of what medication vs psychosocial can do?
* Medication → Manages core neurobiological symptoms; Helps the brain focus * Psychosocial → Builds real-world skills & functioning; Teaches what to do with that focus