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BIOL3025 - Neuropharmacology of CNS Disorders > VP - ADHD > Flashcards

VP - ADHD Flashcards

1
Q

What is ADHD?

A

Attention-Deficit/Hyperactivity Disorder
A neurodevelopmental disorder characterized by impairing levels of inattention, impulsiveness, and hyperactivity.

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2
Q

What are the two main domains and three presentations of ADHD?

A

Domains:
1. Inattention
1. Hyperactivity/impulsivity

Presentations:
1. Inattentive
1. Hyperactive/Impulsive
1. Combined

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3
Q

What are the inattentive symptoms of ADHD? (9)

A
  • Often fails to pay attention to details or makes careless mistakes.
  • Often has difficulty concentrating
  • Often does not seem to listen when spoken to directly.
  • Often does not follow through on instructions and fails to finish tasks.
  • Often has difficulty organizing daily activities.
  • Tends to procrastinate, especially tasks that require mental effort.
  • Often loses things.
  • Is often easily distracted by external stimuli.
  • Is often forgetful in daily activities.

At least 6/9 symptoms in childhood; 5/9 in adulthood

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4
Q

What are the impulsivity-hyperactivity symptoms of ADHD? (9)

A
  • Often fidgets.
  • Cannot stay seated for long.
  • Feels restless.
  • Tends to be loud.
  • Talks excessively.
  • Has more energy than others.
  • Often has difficulty awaiting turn.
  • Often says things without thinking.
  • Often interrupts others.

At least 6/9 symptoms in childhood; 5/9 in adulthood

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5
Q

What is the prevalence and demographic differences of ADHD? (4)

A
  • Affects 4-6% of children and 2-3% of adults.
  • Higher prevalence in males (2.5:1 male-to-female ratio in children and young people).
  • No significant differences between low- and high-income countries
  • ADHD often persists into adolescence (50-80%) and adulthood (30-50%). (tends to get better with age)
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6
Q

How does ADHD impact everyday life? (4)

A

Negative effects on:

  • Academic performance and employment: Poor grades, failure, low self-esteem.
  • Health: Obesity, vision disorders, allergies, asthma, diabetes, somatic issues.
  • Risk behaviors: Addictions, unhealthy eating/drinking habits, higher risk of accidents.
  • Social and emotional issues: Bullying, criminal behaviors, emotional problems.
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7
Q

What are the key diagnostic criteria for ADHD? (3)

A
  • Age-inappropriate levels of hyperactive-impulsive and/or inattentive symptoms for at least 6 months
  • Symptoms appear in multiple settings (e.g., home, school) and impact daily life.
  • Some symptoms present in early to mid-childhood.
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8
Q

How is ADHD diagnosis conducted? (4)

A
  • Psychiatric interviews.
  • Rating scales (e.g., Conner’s Rating Scales).
  • Collateral information (e.g., from school).
  • NO objective markers
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9
Q

What are the factors that contribute to the development of ADHD? (3)

A

Liability threshold model: Genetic and environmental factors accumulate until a threshold is crossed.

Genetic factors: Polygenic risk, familial patterns, and broader psychiatric vulnerabilities.

Environmental factors: Toxins, maternal substance use during pregnancy, nutrient deficiencies, stress, infections, poverty, and trauma.

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10
Q

What brain networks are associated with ADHD (3) and how do they contribute to ADHD?

A

Fronto-striatal networks

Crucial for:

  • executive functions
  • attention
  • reward processing.

Parietal connections

Involved in:

  • spatial awareness
  • attention
  • sensory integration.

Cerebellar connections

Related to:

  • motor control
  • balance
  • cognitive functions.

Abnormalities/disruptions in these networks are implicated in ADHD.

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11
Q

What modulates the activity within these networks?

A

Dopaminergic and noradrenergic pathways

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12
Q

What is dopamine’s role in the brain’s catecholaminergic pathways? (3)

A
  • Dopamine (DA) is synthesized in the substantia nigra pars compacta (SNc) and ventral tegmental area (VTA).
  • DA regulates movement via the nigrostriatal pathway
  • Mesocortical and mesolimbic pathways influence executive functions and affect regulation.
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13
Q

What is norepinephrine’s role in the brain? (2)

A
  • Originates in the locus coeruleus (LC) and connects with cortical regions like the prefrontal cortex (PFC).
  • Modulates attention and arousal state.
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14
Q

What are cortico-striatal loops? (2)

A
  • GABA-glutamatergic circuits, regulated by dopamine,
  • Link the cortex, basal ganglia, and thalamus
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15
Q

What are the three main loops and how do they contribute to ADHD?

A
  • Motor loop: Sensorimotor cortex-striatum-thalamus for motor planning.
  • Cognitive loop: Prefrontal cortex-striatum-thalamus for planning and learning.
  • Limbic loop: Emotion-related movements (e.g., smiling).
  • These circuits contribute to executive functions and affect regulation, which can be impaired in ADHD.
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16
Q

How do dopamine and norepinephrine optimize PFC function?

A

Dopamine (D1 receptors): Reduces ‘noise’ in glutamatergic circuits by increasing cAMP (helps suppress irrelevant neural activity).

Norepinephrine (α2A receptors): Enhances ‘signal’ by reducing cAMP production (strengthening specific synaptic connections).

17
Q

What are the roles of the direct (3) and indirect (3) pathways in motor control?

A

Direct pathway:

  • Facilitates movement via D1 receptor stimulation,
  • Involves the striatum, internal globus pallidus, and thalamus
  • thalamus disinhibited and subsequent motor cortex activation

Indirect pathway:

  • Inhibits unwanted movements via D2 receptor stimulation
  • Involves the striatum, external globus pallidus, subthalamic nucleus, and internal globus pallidus
  • Thalamic inhibition, supressing unwanted movements
18
Q

What is the inverted U curve in ADHD pathophysiology?

A

Both excessive and insufficient catecholamine release negatively affect PFC functions, leading to suboptimal brain activity.

19
Q

What evidence supports catecholaminergic dysfunction in ADHD? (4)

A
  • Candidate gene studies
  • Animal models.
  • Efficacy of stimulants.
  • PET/SPECT studies showing greater striatal DAT binding in ADHD.

Note: DAT removes dopamine from the synapse

20
Q

What challenges exist in DAT binding studies for ADHD?

A

Inconsistent findings may stem from:

  • Effects of previous stimulant treatment.
  • Adaptive responses to chronic treatment causing persistent DAT blockade.
21
Q

What are medications for moderate/severe ADHD? (2)

A
  • Stimulants e.g. methylphenidate (Ritalin, Concerta) are first-line treatments.
  • Other options include lisdexamfetamine, atomoxetine, and guanfacine.
22
Q

What are the common side effects and precautions for stimulant medications in ADHD? (5)

A
  • Increased blood pressure
  • Increased heart rate.
  • Decreased appetite.
  • Sleep disturbances.

Precautions:
* Monitor blood pressure, heart rate, height, and weight before and during treatment.

23
Q

How is ADHD managed for different age groups (NICE guidelines)?

A

Preschoolers (< 5 years)

  • ADHD-focused group parent training.
  • Specialist advice and medication if severe.

Children and adolescents (≥5 years):

  • Group-based ADHD-focused support.
  • Medication progression: Methylphenidate (first line) Lisdexamfetamine/ dexamphetamine (second line), Atomoxetine/Guanfacine (non stimulants)
  • CBT if symptoms persist.

Adults:

  • Medications in order: Methylphenidate, Lisdexamfetamine/dexamphetamine, Atomoxetine.
  • Supportive psychological interventions if requested or medications ineffective.
24
Q

What is the difference between Ritalin and Concerta?

A
  • Ritalin: Short-acting; ideal for children.
  • Concerta: Long-acting; better suited for adolescents and adults.
25
Q

How does methylphenidate (MPH) work in ADHD treatment? (3)

A
  • Exists as enantiomers: d-threo-MPH and l-threo-MPH. The d-enantiomer is primarily responsible for the therapeutic effects.
  • Blocks dopamine (DA) and norepinephrine (NE) transporters, increasing DA and NE levels in the synaptic cleft.
  • Involves allosteric binding to transporters.
26
Q

How does Amphetamine work in ADHD treatment? (3)

A
  • Also exists as Enantiomers: d-isomer more potent for DAT but equally potent for norepinephrine transporters (NET) binding
  • Competitive inhibitor of DAT and NET
  • Reverses the direction of these transporters at higher doses, releasing stored neurotransmitters
27
Q

What is lisdexamfetamine, and how does it differ from other stimulants? (2)

A
  • A long-acting d-amphetamine prodrug hydrolyzed in the blood to active form.
  • Provides therapeutic effects for up to 13–14 hours.
28
Q

How do acute stimulant doses affect brain activity/functional connectivity? (3)

A
  • Shift activity in ADHD brains towards patterns seen in neurotypical peers.
  • Enhance connectivity in task-related networks (fronto-striatal/parietal).
  • Suppress activity in the default mode network (DMN).

Note: Prolonged stimulant treatment might not translate into long-lasting changes of brain anatomy/activity, although this may require further investigation.

29
Q

What are the roles of non-stimulants like atomoxetine and guanfacine in ADHD treatment? (4)

A

Atomoxetine:

  • Selective norepinephrine reuptake inhibitor.
  • Acts on the prefrontal cortex (PFC)
  • Safer use in addiction (Lower levels of NET in the n. accumbens - reduces the risk of abuse).

Guanfacine (children only):

  • Selective α2A receptor agonist, mediating NE effects in PFC.
  • Weaker sedative and hypotensive effects than clonidine.
30
Q

What are some predictors of ADHD treatment response?

A
  • Individuals with a smaller left superior longitudinal fasciculus (SLF I) may respond less to methylphenidate (MPH).
  • Combined biological and clinical characteristics increase prediction accuracy for treatment response.
31
Q

What did MRI studies reveal about brain alterations in ADHD non-responders? (2)

A
  • ADHD non-responders show more brain alterations than responders.
  • Cortical differences are enriched for biologically plausible genes, such as those involved in noradrenaline transport, a target of methylphenidate

BIOL3025 - Neuropharmacology of CNS Disorders (17 decks)

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