March 27 - Attention Deficit Hyperactivity Disorder Flashcards
What are common results of ADHD?
Individuals with ADHD tend to have more injuries, lower grades, poor driving record, high drug abuse, be more antisocial, poor job status and performance
How is ADHD diagnosed?
Diagnosed required thorough assessment by a highly skilled practitioner and a global approach (hasty initiation of medication is a bad idea)
What are common comorbidities of ADHD?
Tourette’s disorder, learning disability, oppositional or conduct disorder, anxiety, depression, enuresis (night time bed wetting)
For the sake of objectivity, ADHD symptoms are differentiated into two clusters. What are they?
Inattentive cluster
Hyperactive cluster
What are symptoms of the inattentive cluster?
Distractibility Forgetfulness Poor organization Impersistence Mistake-prone Work avoidance
What are symptoms of the hyperactive cluster?
Fidgetiness Intrusiveness Restlessness Noisiness Talkativeness Inappropriate activity
Describe the course of ADHD
It’s variable
Usually onset by 12 years old (what prompts diagnosis is when the child cannot comply with the structure of school and symptoms become more noticeable)
Between the ages of 12 and 20, 20% of patients will remit, 60% will have partial remission (they are better but not great)
Hyperkinesis usually presents first; inattention presents later and is least likely to remit
Describe adult ADHD
Roughly 50% of children with ADHD continue to manifest significant symptoms in adulthood (around 8% of children have ADHD, 3-5% of adults have ADHD)
Symptoms often move away from the hyperactive domains and the distractibility and inattention may predominate (affects driving record, drug abuse/dependency effects)
Describe the etiology of ADHD
Genetics (perhaps 80% responsible)
Right-sided “hypofrontality” (decision centre is not as metabolically active)
Locus ceruleus “underperforms”
Children born in the fall (linked to a virus in utero; only a theory)
Worsened by stressors
More evident in routinized setting (school)
Describe the neuropathophysiology and neuroimaging in ADHD
Small increase in cerebrum growth (10%) at age of 1-3 years
Reduced numbers of cerebellar Purkinje neurons (approx 30%)
Reduced cell size and increased cell density in the limbic areas of the brain
Modified genes/proteins impairing the balance of excitatory vs inhibitory synaptic signalling in local and extended circuits (theory)
What increases the risk of ADHD
There’s a 4-8x higher risk if a first-degree relatives has ADHD
Risk increases with fetal alcohol syndrome, lead poisoning, meningitis, obstetric adversity, maternal smoking, adverse or absent parent-child relationship
Imaging and D4 allele abnormalities
It all boils down to is response inhibition and/or arousal regulation deficits
What are triggers of ADHD (not in every patient)
Artificial colours, flavours, additives Refined sugar, sodas, caffeine Food allergy or intolerance Essential fatty acid deficiency Iron and zinc deficiency
How is ADHD treated?
Multimodal approach
Behavioural (involving the parents, family, classroom, teacher, establishing a pattern of consistent reward and privileges with structure, checklists and attainable goals)
Avoiding triggers, if known
Chiropractic approach
When medication is required, ensure combination treatment. Drugs without support usually ends in poor outcomes
What are the treatment goals of ADHD?
Collaborative: support system and school
Realistic, achievable, measurable, 3-6 items (they can change over time)
May include relationship factors, academic performance, rule following
Clarity, immediacy, predictability, consistency, responsibility are vital
What are deficits associated with ADHD?
Inhibition of the ability to control behavoir, resist distractions, develop an awareness of space and time
Arousal dysregulation - insufficient alertness alternating with overarousal
Under performing neurotransmitters
