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ADHD & stimulants

Uni of Notts, Neurobiology of disease, second year, topic 2

TermDefinition
ADHD main diagnostic criteria (2) Inattention: difficulty & avoidance sustaining attention, distracted, disorganised, bad listener & forgetful Hyperactivity: Fidgeting, restlessness, excessive talking & volume, poor social filter & intrudes on social settings
Clinical diagnostic requirements: Children >6 symptoms of any category before age 12. Need to be present in at least 2 settings of: School, Home, or social life. Symptoms must be developmentally inappropriate for age groups
Clinical diagnostic requirements: Adolescents & adults >/=5 symptoms from either category. Diagnoses are more difficult & adults are usually just diagnosed as combined type (inattentive & hyperactive)
Possible link between ADHD & criminals 20% of inmates are diagnosed. ADHD patients deeply rooted in present, impaired future prediction causing disconnect between actions & consequences
Genetic:environmental cause ratio 4:1 genetic:environmental. 80% of the condition is heritable in twins
Environmental factors (neonatal & postnatal) Neonatal hypoxia, maternal toxins (tobacco, alcohol, lead etc.) & premature birth Encephalitis, seizure disorder, & acquired brain trauma
Neuroanatomical differences are in ADHD Smaller right frontal lobe, smaller basal ganglia (normalising by ~18), & smaller cerebellum. Reduced striatal metabolism & hyperactive sensory cortex
Volumetric differences & correlation to severity Reductions correlate with symptom severity & appear early in life. Implicated brain regions have smaller volumes & poorer synaptic connectivity
Key brain regions implicated in ADHD Dorsolateral prefrontal cortex, caudate, & putamen (fronto‑striatal circuits)
Role of DAT in ADHD neurobiology Higher DAT density in the striatum reduces synaptic dopamine from radiolabelled proteins showing higher frequency than control group
DRD4 7‑repeat allele & its importance 48‑bp Variable Number Tandem Repeat variant of a D4 receptor associated with ADHD, linked to inattention, novelty seeking & reduced AC coupling. 1.9:1 pooled odds ratio
DAT1 480‑bp repeat variant High‑risk allele of gene 5015.2 associated with elevated DAT expression and reduced dopamine signalling in the striatum. 1.16:1 pooled odds ratio
Effects of methylphenidate on DAT expression 4 weeks of treatment significantly reduces DAT ligand binding however, after 12 months neuroplasticity upregulates DAT until it can combat the drug
Therapeutic benefits of psychostimulants on ADHD They restore dopamine signalling in fronto‑striatal circuits, improving attention, working memory, & behavioural inhibition; & inhibit glutamate signalling
Glutamatergic signalling in ADHD Many NMDA receptors in fronto-striatal & reward pathways are implicated with ADHD behaviours by causing under or overexcitability & further dysregulating dopamine
Mechanism of non‑stimulant ADHD medications Inhibiting NET increases NE in the prefrontal cortex. Less addictive but less effective
Newer ADHD treatments Combining α‑adrenoceptor agonists (e.g., guanfacine, clonidine) & tricyclic antidepressants or antagonising NMDA receptors
Prevalence & comorbidities of ADHD Affects 3–5% of the population; more likely to be diagnosed with hyperkinetic disorder, epilepsy, anxiety, depression, opposition defiance disorder, tics, conduct disorders, mood disorders. 31% chance of appearing on its own
Gender differences with ADHD Males 2-3x more likely to be diagnosed & show more hyperactivity & conduct disorders; females show weaker emotional regulation & self-esteem. Both usually have exceptional creativity & intelligence but suffer academically
Created by: Denny12
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