ADHD Flashcards

Learn the basics of ADHD

1
Q

Describe the symptoms of ADHD?

A

Developmentally inappropriate levels of

  • Inattentiveness
  • Impulsivity
  • Hyperactiviy
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2
Q

What factors must exist to be diagnosed?

A

Diagnosed in childhood:

  • Persistent for six months
  • Be present before age 7
  • Functional impairment: executive function deficit most characteristic.
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3
Q

What is hyperactivity?

A

Excessive fidgetiness or talking

- Peak at age 8 and then decline.

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4
Q

What is impulsivity?

A

Difficulty taking turns; blurt out answers

- Peaks at age 8, but does not decline.

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5
Q

What is inattention?

A

Forgetfulness, distractibility

- Does not appear until age 8 or 9.

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6
Q

Describe the prevalence.

A

Estimates range from 2-18%

  • Most estimates are 5-10% in school age children.
  • Roughly 4x more common in boys (may reflect referral bias)
  • 30-70% of individuals continue to show symptoms into adulthood
  • Adult prevalence ~4%
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7
Q

Explain ADHD with other disorders.

A

Often comorbid with other disorders

  • ODD, CD, Anxiety, Depression, Learning disabilities
  • Primary deficit appears to be dysregulation of NE and DA in prefrontal cortex.
  • ~70% of children successfully treated with pharmacotherapy.
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8
Q

Describe the relevance of environmental factors.

A

Diet: food additives, refined sugars, food sensitivity, deficiency in fatty acids, Fe/Zn deficiency.

  • premature birth/low birth weight
  • prenatal alcohol exposure
  • head trauma
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9
Q

Describe Adult ADHD.

A
Disinhibition characteristic
- Poor self-regulation
- Poor goal-directed behavior
- Appear disorganized and hectic. 
Some people have late-onset
- Suggestion to remove diagnostic creteria of beofre age 7.
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10
Q

Explain the genetic significance of ADHD.

A
Monozygotic concordance: 92%
Dizygotic convergence: 33%
Implicate genes:
DRD1, Drd2, DRD4, DRD5
- 5-TH transporter gene 
- 5-HT 1B receptor
- SNAP 25
- Metabotropic glutamate receptor (GRM5), 
- Increased number of CNA's (15 vs 7%)
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11
Q

What are the differences in noradernergic system?

A

Modulates cortical functipns:- attention, alertness, vigilance, executiee

  • Imbalance between NE and DA results in pathology.
  • Small changes can have large impact on PFC function.
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12
Q

The effects of Norepinephrine.

A

Increases the signal strengthens connectivity of input to cells.

  • acts on alpha2A receptors on dendritic spines.
  • antagonize alpha2A receptors to miimic ADHD.
  • Agonize alpha 2A rectors to improve function.
  • High levels impair PFC function.
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13
Q

The effects of Dopamine.

A
  • Acts on D1 receptors
  • Weaken irrelevant inputs to cells.
  • Transporter density increased in patients
  • High levels weaken too many connections and inhibit firing.
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14
Q

Describe the effects of too little NA and DA.

A

The PFC abilities drops (distracted, disorganized, forgetful, and impulsive) and the levels of catecholamine release involved in the arousal state is low (fatigued).
- LOW pfc abilities and FATIGUED

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15
Q

Describe the effects of NA alpha1, beta1, and excessive D1.

A

Person is: STRESSED and has LOW PFC abilities.

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16
Q

Describe the effects of NA alpha2A and moderate D1.

A

Person is: ALERT and has HIGH PFC abilities (Focused, Organized, and Responsible)

17
Q

Children who are ambidextrous were:

A

Twice as likely to have some form of ADHD.

18
Q

Tie in socioeconomic status into ADHD prevalence.

A

Children that had parents with LOWER education and welfare had higher chances of having ADHD.
- Divorce rates also increase.

19
Q

What is SNAP-25?

A

Protein: Synaptosomal associated protein
Gene: gene of interest encodes a protein component that interacts with syntaxin and VAMP to form SNARE complex.

20
Q

Why is SNAP-25 important?

A

SNARE complex holds vesicles at the presynaptic membrane to regulate neurotransmitter exocytosis.
- SNAP-25 promotes axonal growth, dendritic spine formation and synaptic plasticity.
EG. reduction of SNAP-25 expression => morphologically immature dendritic spines

21
Q

Describe SNAP-25 gene application.

A

The Model for ADHD: Coloboma mouse w/ a deletion in SNAP-25
What is observed:
- increased norepinephrine in striatum and nucleus accumbens
- Increasing copies of risk haplotype reduces SNAP-25 expression

22
Q

Explain the trends in ADHD brain morphology.

A
Overall decreased brain volume
- Caudate nucleus
- Prefrontal cortex (white matter)
- Corpus callosum
- Cerebellar vermis
By late adolescence these differences tend to disappear
23
Q

SNAP-25 gene study.

A

The Study:
- Dense SNP mapping across SNAP-25 gene in families with and without ADHD
- PCR of SNAP-25 transcripts in inferior frontal gyrus
What they found:
- increased AAC (risk haplotype) => decreased expression of SNAP-25 in IFG tissue
- increased GTC (protective haplotype) => increased expression of SNAP-25 in IFG tissues

24
Q

What is involved in the Dopaminergic systems?

A

VTA, striatum, PFC

DAT1, dopamine receptors (esp. D2, D3, D4)

25
Q

What is involved in the Noradrenergic system?

A

DLPFC, locus coeruleus

- Some evidence for serotoninergic and cholinergic systems.

26
Q

What are some other observed abnormalities?

A
Cortical thinning
Alterations in structural connectivity
Parietal/temporal lobes
PFC and striatum
Alterations in functional connectivity
Asymmetry in caudate
Decreased blood flow to putamen
Aberrant and/or delayed cortical development
Hypoactivation of networks related to executive function, cognition, emotion, sensorimotor functions.
27
Q

Explain the Dopamine-Transfer Deficit (DTD) Theory.

A

Plasticity in DA cells during learning suggest that behavioral reinforcers can gradually be transferred to previously neutral cues that predict eventual reward
- In normal children, positive reinforcement is gradually transferred to predictors of reward
Leads to continuous anticipatory DA signaling
- In ADHD children this transfer is disrupted
In absence of continuous behavior reinforcement, the DA anticipatory signaling is weak or absent

28
Q

What is sustained attention?

A

The ability to maintain goal-directed focus in the absence of exogenous or external cues.

  • reciprocal interaction between cortical and subcortical areas
  • triggers locus coeruleus to release norepinephrine in the cortex
  • right hemisphere dominant
29
Q

What is the temporal explanation?

A

ADHD symptoms result of impaired timing functions

- inferior and orsolateral PFC, cerebellum, and parietal lobe implicated

30
Q

What is the default mode network (DMN) explanation?

A

ADHD symptoms result from intrusion of DMN activity during cognitive tasks.
- Ventromedial PFC, posterior cingulate gyrus, and lateral parietal cortex implicated

31
Q

How has the DSM V changed?

A

Examples added to show symptoms are various ages/developmental periods.

  • Comorbid diagnosis with autism is allowed
  • Cross situational requirement increased
  • Onset criteria change
32
Q

What is TOVA?

A

Test of Variables of Attention

  • Can be used in combination with other interviews and psychological evaluations to diagnose ADHD.
  • Could identify non-hyperactive ADHD 84% of the time and hyperactive ADHD 90% of the time.
33
Q

What is NEBA?

A

The NEBA system is a brain can test approved by FDA to diagnose ADHD.

  • Involves non-invasive EEG recording
  • Measures the ratio between theta and beta waves.
  • Significantly higher ratio in those with ADHD.
34
Q

What are some behavioral therapies?

A

Limiting distractions
Sports
Positive reinforcement

35
Q

What are the stimulants of Pharmacotherapy?

A
Methylphenidate (Ritalin)
Amphetamines
- Adderall
- Dextroamphetamine
- Vyvanse
36
Q

What are non-stimulants of Pharmacotherapy?

A

Norepinephrine

  • Reuptake inhibitors
  • Alpha-2-adrenergic agonists
  • Antidepressants
37
Q

What do amphetamines do?

A

First used as a therapy for child behavior disorders in 1937.

  • Increase synaptic dopamine levels
  • Very similar structure to DA
  • May cross plasma membrane