777 final ADHD Flashcards
Attention Deficit Hyperactivity Disorder
Persistent pattern of inattention and/or hyperactivity-impulsivity that interferes with functioning or development
Hyperactive-impulsive type
Inattentive type
Combined type
ADHD
Neurodevelopmental disorder
Preschooler, children, adolescents, and adults
Characterized by a pattern of diminished sustained attention and increased impulsivity
Clear evidence to support a biological basis for ADHD
DSM-5 Changes
ADHD symptoms present by age 12 rather than 7
Inattentive and hyperactive subtypes replaced by 3 specifiers
1. Combined presentation
2.Predominantly inattentive presentation
2. Predominantly hyperactive/impulsive presentation
Comorbid ADHD and ASD
Fewer criteria for adolescents 17 and older and adults
Epidemiology
5% of children, 2.5% of adults
Most frequent psychiatric disorder in childhood
Most cultures
More frequent in males by 2:1 ratio in children and 1.6:1 in adults
Females more likely to have inattentive features
Diagnostic Features
Persistent pattern of inattention and/or hyperactivity-impulsivity
Interferes with functioning or development
Begins in childhood
Manifestations of the disorder present in more than one setting
Symptoms vary depending on setting
Associated Features
Mild delays in language motor or social development
Low frustration tolerance
Irritability
Mood lability
Impaired academic or work performance
Increased risk of suicide esp when co-morbid with mood, substance or conduct disorders
Development and Course
Toddler and preschoolers: excessive motor activity
School age: inattention more prominent
Hyperactivity less obvious in adolescence and adulthood, restlessness, impatience, poor planning feeling like one is driven by a motor, impulsivity
Attention Difficulties
Inattention Lacking persistence Difficulty sustaining attention Disorganization Hyperactivity Excessive motor activity Excessive restlessness, fidgeting, tapping talkativeness Adults wearing others out with activity Impulsivity Hasty actions and decisions with high harm potential and without forethought and consideration for long-term consequences Desire for immediate reward Inability to delay gratification Social intrusiveness
Sustained Attention Deficiencies in ADHD
Executive dysfunction
Inability to sustain attention and solve problems
Hypothetically linked to inefficient information processing in the dorsal lateral prefrontal cortex (DLPFC)
DLPFC activated by the n-back test
Selective Attention Deficiencies in ADHD
Difficulty with selective attention
Inability to focus
Hypothetically linked to the dorsal anterior dorsal anterior cingulate cortex (dACC)
dACC can be activated by the Stroop test
Risk Factors
Environmental Genetic Neurochemical Neurophysiological Neuroanatomical Psychosocial
Environmental Factors
Very low birth weight (< 1500 grams 3.3 pounds) 2-3X the risk Maternal smoking ETOH exposure in utero Lead exposure Dietary: food coloring, additives Disorganized chaotic households Poverty Head trauma
Genetic
Substantial heritability
Increased concordance in monozygotic twins
2-8 times the risk if a sibling or parent has ADHD
Association of dopamine transporter gene (DAT1) with ADHD
Neurotransmitters and ADHD
DA and NE dysregulation prevents normal tuning of pyramidal neurons in the PFC
DA and NE imbalances hypothetically cause inefficient information processing in prefrontal circuits
Hypothetically associated with excessive signaling in prefrontal DA and NE pathways
Neurobiology of Attentional Disorders
ADHD as a disorder of the prefrontal cortex
Trio of symptoms
Inattention
Difficulties with sustained and selective attention
Hyperactivity
Modulated by a cortico-striato-thalamo-cortical loop from PFC to the putamen to the thalamus and back to the PFC
Impulsivity
Hypothetically linked to the orbitofrontal cortex (OFC)
Neurodevelopment and ADHD
Classic: onset by age 7
Formation of synapses and the selection of synapses for removal in the PFC occur in childhood
May be a disruption causing prefrontal abnormalities
Some children compensate and “grow out of the ADHD”
Neurodevelopment and ADHD (continued)
Hypotheses
Abnormal synapse formation
Abnormal synaptic neurotransmission
Genes involved are linked to DA neurotransmission
Genes under investigation are linked to a2A adrenergic receptor, serotonin receptors
Synaptogenesis and Development
Age 1: working memory emerges
3-4 years: minimal capability to sustain attention
6-7 years: sustained attention and planning
Synaptic pruning taking place
Comorbidity
Oppositional defiant disorder Conduct disorder Learning disorders Disruptive mood dysregulation disorder Anxiety Depression Substance use