Putting It All Together:
A Neuroanatomical/Neurochemical Model for ADHD

Multiple neuroanatomic models have been postulated for AD/HD. I will present one model to exemplify how the available research data can be used to design a model and how such a model may help conceptualize future research endeavors (34).

Clinicians agree that they anecdotally experience subtypes of AD/HD. Some children have more aggressive/aroused behaviors that result in cognitive difficulties due to stimulus overload. Other children have prominent inattention with increased off task activity. A third population has been proposed of children who are primarily disinhibited. Their cognitive difficulties and high activity level arises from an inability to think before acting. These subtypes of AD/HD may reflect disorders of different attention mediating CNS pathways and neurotransmitters.

Several anatomic locations in the brain contain pathways which modulate cortical motor and cognitive output. At each anatomic location a different neurotransmitter is used primarily.

  • Dopaminergic pathways exist at the cortical and subcortical level (with in the right cerebral hemisphere, prefrontal cortex, hippocampus and nucleus accumbens) which when impaired prevent appropriate sensory filtering and cognitive processing. Deficiencies in these Dopaminergic pathways are most closely related to the inattentive form of AD/HD.

  • Arousal level is mediated in the brain stem by the reticular formation and locus coeruleus. The primary neurotransmitter is norepinephrine. Disorder in this pathway result in the hyper aroused AD/HD.

  • The prefrontal cortex modulates behavior inhibition and serotonin is the predominant central inhibiting neurotransmitter. Defects in this pathway lead to AD/HD like behaviors secondary to impulsivity.

Click here if you would like to view a graphic representation of this model.

These concepts remains to be evaluated in a controlled fashion. However, such a model may ultimately prove useful in choosing the best therapeutic agent for a given child, predicting comorbid disorders, aid in defining prognosis and in designing better case specific behavioral interventions.