Neurological aspects - Introduction

This section looks at ADHD from a neurological perspective.

Various cortical and subcortical brain regions are involved in ADHD.¹

Neurological aspects

• Neurotransmitters in ADHD
  • Dopamine
    1. Control ranges through dopamine
    2. The 5 dopaminergic systems of the brain
    3. Interactions of the dopaminergic brain areas
    4. Dopamine formation and storage
    5. Dopamine release
    6. Tonic / phasic / extracellular dopamine
    7. Dopamine effect on receptors
    8. Dopamine reuptake, dopamine degradation
    9. Regulation of dopamine
    10. ADHD - Disorders of the dopamine system
    11. Dopamine and stress
    12. Autism as a dopaminergic Disorder
    13. Depression as a dopaminergic Disorder
    14. Parkinson’s - another Disorder of the Dopamine System
    15. Measurement of dopamine
  • Noradrenaline
  • Cannabinoid system
    • Cannabinoids
    • Cannabinoid receptors
    • Other receptors to which cannabinoids bind
    • Cannabinoid reuptake and degradation
    • What is regulated by cannabinoids
      • Cannabinoids regulate dopamine
      • Cannabinoids also regulate appetite and food intake via dopamine
      • What regulates cannabinoids
    • Cannabinoids for ADHD and stress
    • Dopaminergic disorders with endocannabinoid involvement
  • Adenosine
  • Traceamine
  • Serotonin
  • Glutamate
  • GABA
  • Glycine
  • Acetylcholine
  • Histamine’
  • Opioids
• Hormones for ADHD
  • CRH
  • ACTH
  • Cortisol
    • Cortisol and other stress hormones in ADHD
    • Cortisol and stress axis changes in other disorders
  • Vasopressin
  • DHEA
  • Aldosterone
  • Oxytocin
  • Orexin / Hypocretin
  • Alpha-amylase
  • BDNF
• Neurophysiological correlates of ADHD symptoms
  • Aggression in ADHD - neurophysiological correlates
  • Drive problems in ADHD - neurophysiological correlates
  • Arousal and activation in ADHD - neurophysiological correlates
  • Attention problems in ADHD - neurophysiological correlates
    • The dopaminergic and noradrenergic attention centers
  • Thinking blocks and decision-making problems in ADHD - neurophysiological correlates
  • Emotional dysregulation - neurophysiological correlates
  • Frustration intolerance in ADHD - neurophysiological correlates
  • Hyperactivity in ADHD - neurophysiological correlates
  • Impulsivity in ADHD - neurophysiological correlates
  • Learning problems in ADHD - neurophysiological correlates
  • Motivation in ADHD - neurophysiological correlates
  • Organizational and executive function problems in ADHD - neurophysiological correlates
  • Sleep problems in ADHD - neurophysiological correlates
  • Social phobia - neurophysiological correlates
• Eyes and vision with ADHD
• Gender differences in ADHD
• ADHD in animal models
  • ADHD animal models with reduced extracellular dopamine
  • ADHD animal models with increased extracellular dopamine
  • ADHD animal models with unknown dopamine alteration
  • Animal models that inadequately represent ADHD
• Brain networks and connectivity in ADHD
• Brain hemispheres
• People with ADHD affected brain regions

Some sections of the article ⇒ could also be useful for understanding neurological correlations 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 the cause of ADHD
    • 4.2.1 Dopamine levels too low
    • 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 Reduced tonic dopamine release increases phasic dopamine release
  • 4.3. ADHD as a developmental disorder of dopaminergic brain pathways
    • 4.3.1 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 peaks and epileptoform EEG abnormalities