ADHD Flashcards
Learn the basics of ADHD (37 cards)
Describe the symptoms of ADHD?
Developmentally inappropriate levels of
- Inattentiveness
- Impulsivity
- Hyperactiviy
What factors must exist to be diagnosed?
Diagnosed in childhood:
- Persistent for six months
- Be present before age 7
- Functional impairment: executive function deficit most characteristic.
What is hyperactivity?
Excessive fidgetiness or talking
- Peak at age 8 and then decline.
What is impulsivity?
Difficulty taking turns; blurt out answers
- Peaks at age 8, but does not decline.
What is inattention?
Forgetfulness, distractibility
- Does not appear until age 8 or 9.
Describe the prevalence.
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%
Explain ADHD with other disorders.
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.
Describe the relevance of environmental factors.
Diet: food additives, refined sugars, food sensitivity, deficiency in fatty acids, Fe/Zn deficiency.
- premature birth/low birth weight
- prenatal alcohol exposure
- head trauma
Describe Adult ADHD.
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.
Explain the genetic significance of ADHD.
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%)
What are the differences in noradernergic system?
Modulates cortical functipns:- attention, alertness, vigilance, executiee
- Imbalance between NE and DA results in pathology.
- Small changes can have large impact on PFC function.
The effects of Norepinephrine.
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.
The effects of Dopamine.
- Acts on D1 receptors
- Weaken irrelevant inputs to cells.
- Transporter density increased in patients
- High levels weaken too many connections and inhibit firing.
Describe the effects of too little NA and DA.
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
Describe the effects of NA alpha1, beta1, and excessive D1.
Person is: STRESSED and has LOW PFC abilities.
Describe the effects of NA alpha2A and moderate D1.
Person is: ALERT and has HIGH PFC abilities (Focused, Organized, and Responsible)
Children who are ambidextrous were:
Twice as likely to have some form of ADHD.
Tie in socioeconomic status into ADHD prevalence.
Children that had parents with LOWER education and welfare had higher chances of having ADHD.
- Divorce rates also increase.
What is SNAP-25?
Protein: Synaptosomal associated protein
Gene: gene of interest encodes a protein component that interacts with syntaxin and VAMP to form SNARE complex.
Why is SNAP-25 important?
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
Describe SNAP-25 gene application.
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
Explain the trends in ADHD brain morphology.
Overall decreased brain volume - Caudate nucleus - Prefrontal cortex (white matter) - Corpus callosum - Cerebellar vermis By late adolescence these differences tend to disappear
SNAP-25 gene study.
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
What is involved in the Dopaminergic systems?
VTA, striatum, PFC
DAT1, dopamine receptors (esp. D2, D3, D4)
