Neurological aspects

In this section, ADHD is considered from a neurological perspective.

In ADHD, different cortical and subcortical brain regions are involved.¹

Neurological aspects

• Neurotransmitters in ADHD
  • Dopamine
  • Norepinephrine
  • Serotonin
  • GABA
  • Glycine
  • Glutamate
  • Acetylcholine
  • Histamine
• Hormones in ADHD
  • CRH
  • ACTH
  • Cortisol
    • Cortisol and other stress hormones in ADHD
    • Cortisol and stress axis changes in other disorders
  • AVP - Vasopressin
  • DHEA
  • Aldosterone
  • Oxytocin
  • Orexin / Hypocretin
  • BDNF
  • Alpha-amylase
• Neurophysiological correlates of ADHD symptoms
  • Neurophysiological correlates of working memory problems in ADHD
  • Neurophysiological correlates of attention problems in ADHD
    • The dopaminergic and noradrenergic attentional centers
  • Neurophysiological correlates of hyperactivity in ADHD
  • Neurophysiological correlates of inhibition problems and impulsivity in ADHD
  • Neurophysiological correlates of drive and motivation problems in ADHD
  • Neurophysiological correlates of delay aversion, pleasure inability, and recovery inability in ADHD
    • Where does aversion to mindfulness come from in ADHD and procrastination?
  • Neurophysiological correlates of thinking blocks and decision problems
  • Neurophysiological correlates of aggression in ADHD
  • Neurophysiological correlates of arousal and activation
  • Neurophysiological correlates of learning problems in ADHD
  • Neurophysiological correlates of emotional dysregulation
  • Neurophysiological correlates of sleep problems in ADHD
  • Neurophysiological correlates of stress
• Gender differences in ADHD
• High Sensitivity - Contributory Cause and Consequence of Early Childhood Stress Injury
• Research topic: ADHD in animal models

For the understanding of neurological correlations, some sections of the article ⇒ may further be ADHD - different explanatory models in the past and today May be helpful. The following headings link directly to the respective sections:

• 4. Cause-oriented descriptions
  • 4.1. nutritional consequences / food intolerances
  • 4.2. dopamine as a cause of ADHD
    • 4.2.1 Too low dopamine level
    • 4.2.2 Tonic and phasic dopamine
      • 4.2.2.1 The dynamic development theory
        • The mesolimbic dopamine branch
        • The mesocortical dopamine branch
        • The nigrostriatal dopamine branch
      • 4.2.2.2 Decreased tonic dopamine release increases phasic dopamine release
  • 4.3. ADHD as developmental disorder of dopaminergic brain pathways
    • 4.3.1 The maturation of the dopaminergic pathways
    • 4.3.2 Post-maturation of the brain?
  • 4.4. dysfunction in the anterior cingulate cortex
• 5. More complex neurological models
  • 5.1. cognitive-energetic model according to Sergeant (2000)
  • 5.5. 2 or 3 - causes model according to Sonuga-Barke (Dual-Pathway / Triple-Pathway)
  • 5.2. 3-Endophenotypes according to Castellanos and Tannock
  • 5.3. 4-category model according to Hunt
  • 5.4. reduced inhibition / overactivity of the default mode network (DMN)
  • 5.5. Rolandic wave spikes and epileptoform EEG abnormalities