Task 7 Flashcards
(21 cards)
What is ADHD?
ADHD is a neurodevelopmental childhood onset disorder characterized by inattentiveness and/or hyperactivity/impulsivity.
What are the subtypes of ADHD?
- Inattentiveness = 9 symptoms (2 selective attention, 2 memory, 5 executive functions)
- Hyperactive/impulsive = 9 symptoms
- Combined
What are the 5 executive function-related symptoms of ADHD?
- Difficulty to sustain attention
- does not seem to listen
- Fails to finish
- Has difficulty to organize tasks
- Avoids sustained effort
What are the two selective attention-related symptoms of ADHD?
- Fails to attend to detail
- is distracted by extraneous stimuli
What are the two memory-related symptoms of ADHD?
Loses things
is forgetful
What are the 9 symptoms of ADHD - hyperactive/impulsive type
- Blurts out answers
- Difficulty waiting turn
- Interrupts or intrudes
- Talks excessively
- Fidgets with hands or feet
- Leaves seat in classroom
- Runs about or climbs
- Difficulty playing quietly
- Motor excess
How is ADHD diagnosed in children?
at least 6 symptoms in more than two setting from age 7 – 12, for at least 6 months
How is ADHD diagnosed in adolescence and adults?
Adolescents & adults: at least 5 symptoms present from age 17.
What are 4 theories about about the causes of ADHD?
- Executive function dysfunctions (lack of inhibitory control)
- Motivation (reward) & delay aversion: immediate gratification due to lack of inhibitory control
- Dysfunctions in the Dynamic interplay between bottom-up and top-down that limits bottom-up processes and allows for control by the top-down.
- Dual pathway model: delay aversion (frontostriatal) & impulsivity (temporal).
How does ADHD differ from other comorbid disorders (e.g. ODD, CD, ADD, ASPD)?
- Trait impulsivity is the common trait in comorbid disorders (e.g. ODD, CD, ADD, ASPD)
- However, the environment (e.g. parenting, coercive family, deviant peer affiliations & neighbourhood risks) plays a greater role in its expression (i.e. if it develops into a more severe externalizing disorder
How does ADHD differ from the sluggish cognitive tempo disorder?
Distractability is exeternal for ADHD (e.g. deficient executive functions) & internal for SCT (daydreaming, mind wandering)
Executive function deficits: only planning and problem solving is affected in SCT but all executive functions are impaired in ADHD.
SCT is more associated with internalizing symptoms compared to ADHD
SCT has less social problems.
ADHD has greater academic impairment while SCT has deficits mostly in mathematics but this is not really researched.
SCT is more related to psychosocial adversity.
How does the demographics of ADHD & SCT differ?
ADHD - Symptoms decline with age, SCT has later onset
ADHD is greater in boys
SCT is associated with SES: e.g. lower parent education, lower annual income
What are some symptoms of SCT?
- Daydreaming,
- trouble staying alert,
- mentally foggy,
- stares a lot,
- spacey, lethargic,
- underactive,
- slow moving,
- inaccurate processing,
- drowsy,
- apathetic and withdrawn,
- lost in thoughts,
- slow to complete tasks,
- lacks initiative
Which brain structures are involved in ADHD?
- PFC & DL PFC, ACC: Executive functions, sustained attention, selective attention
- Posterior Parietal association areas: the how/where pathway + orienting of attention
- Inferior temporal & occipital cortex: the what pathway
- Cerebellum: regulation of movement
Which pathways are involved in ADHD?
- Where/how/what pathway
- Direct pathway: desired movement (D1 receptors -Excitor)
- Indirect pathway: prevents involuntary movements (D2 receptors: inhibition).
- Dopamine pathway/frontostriatal: VTA to PFC (mesocortical) & VTA to striatum (mesolimbic).
- Norepinephrine pathway: from spinal cord > locus ceruleus > dorsal adrenergic bundle > parietal and cerebellum
Which cathecholamines are involved in ADHD?
- DA – cog. impulsivity
- NE- attention
Which receptors are involved in ADHD?
- D1: excitatory
- D2: inhibitory
- NE: A1, A2, B1
- A2 Binding: enhanced activity
- B1 Binding: inhibitory – reduced activity
What are the neural causes of ADHD?
- Lack of DA in PFC needed for executive functions
- Increased DA in striatum associated with impulsive/hyperactive behaviours
- Insufficient amount of NE.
- hyperactivity/impusibity is modulated by too much DA in direct exciter pathway, and too little the indirect inhibitory pathway
- Structures involved: DA: VTA > striatum, VTA > PFC. NE: spinal cord > locus cereleus > PFC, Parietal cortex.
What are the treatments of ADHD & how do they work?
- Stimulants -indirect agonist : methylphinidate – increase DA by blocking DA reuptake by inhibiting NET & DAT
- direct agonist binds to receptors and activate it. E.g. if it binds to a2 receptors then it enhances the negative feedback loop - clonidine
- Non-stimulant (ATX) – increase DA in PFC not striatum through selective inhibition
What are some side effects of methylphenidate?
Loss of appetite
Difficulty falling asleep
Nervousness
Irritability
What is the role of trait impulsivity in early development of ADHD?
Trait impusivity in early life is due to low levels of DA in the mesolimbic system (which mayures before PFC). This leads to irritability and reward-seeking behaviour. Reward seeking behaviours produces DA. Trait anxiety and environment mediate the outcome of Trait impusivity (e.g. if it will develop into further externalizing behaviours). Environment also affects PFC development.
Since in early life the PFC is still developing, it cannot regulate the mesolimbic activities. Thus DA produced from reward seeking behaviour further stimulates the D1R in the nucleus accumben, thus producing DA, which produces impulsive/hyperactive behaviours (similarly to high doses of cocaine and amphetamine).
Although the PFC matures, its development is different from TDC because there are lower levels of DA which is needed to inhibit the actions of the mesolimbic system.
