A closer look at the brain differences of people with ADHD. A cognitive neuroscience review of The aetiology of ADHD

ADHD is the most common neurodevelopment disorder of childhood and has a strong persistence throughout the individual’s lifespan. ADHD is characterised by age-inappropriate behaviour is thought to affect between 3% and 5% of all school-aged children (Buitelaar, 2002) age-inappropriate behaviour typically characterises it.

ADHD is a lifelong disorder which can increase morbidity, including impaired academic results; unable to maintain a job successfully; relationship failures; increased rates of substance abuse; persistent neuropsychological impairments (Biederman, 2004; Vos et al., 2005). Therefore, it is clear how vital determining the neural substrate of ADHD is.

People with ADHD display a persistent pattern of inattention, impulsivity and hyperactivity that interferes with functioning or development (Buitelaar, 2002). Inattention in this instance refers to the inability to direct and maintain attention to relevant tasks. Impulsivity refers to acting without thought of the consequences, such as shouting out answers in class. Hyperactivity refers to excessive motor activity.

This review will aim to use a reductionist approach to introduce phenomenology and conceptualisations of ADHD.  The essay will begin by investigating the neuroanatomical features of ADHD, looking at predominantly functional studies, laying foundations about neural systems that are associated with ADHD and how behaviours are manifested.  Finally, concluding with some self-reflection practice as a teacher.

Affected areas of the brain in ADHD

Looking at data from neuroimaging, neuropsychological, and neurochemical studies, they have mostly indicated frontostriatal differences which contribute to ADHD (Bush et al., 2005; Durston et al., 2003; Vaidya and Stollstorff, 2008).

The frontostriatal is a neural pathway connecting the frontal lobe region to the basal ganglia; these areas are often impaired in people with ADHD (Cherkasova & Hechtman, 2009).  Cognitive skills controlled by this area include decision making, memory and attention.

(Image Retrieved from- Introduction To The Basal Ganglia. (2018). https://kevinbinz.com/2016/01/17/basal-ganglia-introduction)

Neuroimaging studies can help to identify the pathophysiology of ADHD, as it searches for abnormalities of brain regions that are usually involved in the symptoms of ADHD; attention, cognition, executive function, motor control, response inhibition, working memory, and motivation.

In a positron emission tomography (PET) study, a tracer (glucose) is emitted into the body, and then an imaging technique is used to observe metabolic processes in the body. Results found in adults with ADHD glucose metabolism was reduced significantly compared to the control groups values.  In 30 out of 60 regions of the brain, the most significant reduction was found in the premotor cortex, which are associated with motor activity and controlling attention (Zametkin et al., 1990).

Imaging studies on people with ADHD show altered patterns of activity in the dorsal anterior midcingulate cortex (daMCC), dorsolateral prefrontal (DLPFC) and ventrolateral prefrontal cortices (VLPFC), parietal, and cerebellar regions.  These areas have been identified as regions associated with attention and cognition (Nigg and Casey, 2005: Bush, 2011).

Volumetric abnormalities were found in the basal ganglia which comprise the caudate (Stark et al., 2011), primarily responsible for motor control. Results show a decrease in caudate volume using MRI in those with ADHD compared to the control group (Castellanos et al., 2008), in contrast, other research found no volume differences in people with ADHD (Hill et al., 2003).  The striatum is nuclei in the subcortical basal ganglia (that facilitates voluntary movement, Schultz, 2006), the dorsal striatum consists of the putamen, caudate and nucleus accumbens.  It is frequently reported that the putamen and caudate are larger in people with ADHD compared to those without (Valera et al., 2007). If this area is linked to voluntary movement and if there is damage to this area, it’s clear to see why people with ADHD have hyperactivity.

Imaging studies on people with ADHD show altered patterns of activity in the dorsal anterior midcingulate cortex (daMCC), dorsolateral prefrontal (DLPFC) and ventrolateral prefrontal cortices (VLPFC), parietal, and cerebellar regions. These areas have been identified as regions associated with attention and cognition (Nigg and Casey, 2005: Bush, 2011).  Many PET and fMRI (functional magnetic resonance imaging; measures brain activity by detecting changes associated with blood flow) studies have reported hypofunction in the daMCC in people with ADHD using a variety of cognitive tasks and techniques (Zametkin et al., 1990; Bush et al., 1999).  Such dysfunction in these areas could lead to inattention as the target cannot be detected, it may lead to hyperactivity by not reducing motor activity that is not in line with the individual’s target, or by failing to modify the behaviour by using reward and error feedback. Impulsivity could be as a result of damage to the area which encodes information insufficiently, resulting in displaying behaviour characterised by little or no forethought, reflection, or consideration of the consequences.

Image adapted from- Bush, G. (2010). Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/19759528

Moving out of the forebrain and frontal lobe of the brain, the parietal cortex that has key roles in processing sensory information and attention allocation (Culham, 2002) is enlarged in individuals with ADHD (Bush, 2009).  Moving down to the hindbrain, (responsible for motor coordination) findings using magnetic resonance imaging (MRI) have reported smaller cerebellum volumes in people with ADHD (Bledsoe et al., 2009).

In this brief review, there has been a focus on imaging studies.  There are many other methods to measure brain activity with ADHD such as neuropsychological, genetics, and neurochemical studies.  It must be noted that neuroimaging studies are still controversial, they are expensive, so sample sizes tend to be small.  Neuroimaging studies have been criticised for being oversimplified and having experimental limitations (Lee and Cohen, 2003).

The affected areas of the brain and the skills associated give an insight into the behaviour that is manifested by people with ADHD, and these skill impairments contribute to the three key ADHD symptoms.  When cogitating the aetiology of the disorder, the intricacy of ADHD needs to be understood, and the complex interplay of different risk factors need to be considered.

Future studies should focus on a deeper understanding of these brain regions, and continuous technological advancements will improve imaging techniques to help with a more increased understanding.

Brain Chemistry

In addition to functional and structural abnormalities in the brain, neurotransmitters in the brain are considered to contribute to the symptoms of ADHD.  The neurotransmitter, dopamine is responsible for feelings of pleasure and reward, it helps regulate emotional responses and takes actions to achieve specific rewards.  Neurotransmitters surround the frontostriatal pathway, so changes in the levels of neurotransmitters explains why there is an effect on prefrontal function. Research has shown lower levels of dopamine are linked to symptoms of ADHD (Swanson et al., 2007).

Dopamine contributes to the functioning of the prefrontal cortex and basal ganglia. Therefore, minimal amounts of dopamine in these areas restrict inhibition movement; producing hyperactivity; reducing impulse control which will result in deficits in working memory (Spencer et al., 2005). Dopamine deficiency impairs the functioning of the basal ganglia, resulting in hyperactivity in people with ADHD (Curatolo et al., 2010). A recent study in adults with ADHD shows lower dopamine levels in the caudate, hippocampus and amygdala, which is associated with inattention (Volkow et al., 2009).

Neurons in the brain and nervous system have higher concentrations of proteins called dopamine transporters, these prevent dopamine from moving onto the next cell, reducing the effect of dopamine.

The concentration of these proteins is known as dopamine transporter density (DTD).  There was a 70% increase in DTD in adults with ADHD compared to typical controls (Dougherty, 1999).  This was supported Campo et al., (2011), that also found people with ADHD have an increased DTD in cortical areas meaning that dopamine levels were not at optimal levels.  However, the researchers argue the use of participants who take no medication compared to participants using stimulants to control ADHD symptoms, make it difficult to establish cause and effect (del Campo et al. 2011).

Other research shows lower levels of dopamine transporters in the left brain in participants that had ADHD (Volkow et al., 2007).  Results in this area are conflicting, it’s difficult to establish if higher levels of DTD and lower levels of dopamine indicate ADHD.  However, research is showing an association suggesting that dopamine could be a possible treatment for ADHD.  Further studies need to investigate dopamine’s role in ADHD before any firm conclusion can be made.

Grey matter

Studies of cortical or grey matter thickness using MRI have approximately 3-4% thinning of the cortex in all four lobes in people with ADHD (Castellanos et al. 2002). Shaw et al. (2007) conducted a study on the developmental trajectory of cortical maturation.  The results showed children with ADHD had a three-year delay in attaining peak thickness in the cerebrum and regions controlling attention affected, (ADHD reached at 10.5 years, while control group reached peak cortical thickness at 7.5 years).  The prefrontal cortex functions are associated with suppressed thoughts, executive control of attention, high order motor control and working memory.   This suggests ADHD is characterised by a delay in cortical maturation rather than deviance.  However, Vaidya and Stollstorff (2008) argue the increase in grey matter may be due to areas have to compensate for reduced prefrontal activity in cognitive tasks.  Research has supported this, a meta-analysis of 55 fMRI studies concluded areas have to compensate for the functional deficiencies (Cortese et al., 2002).  There is little other research that supports this theory of delay in cortical maturation in ADHD.  However, trajectories of brain development based on neuroanatomic data is providing an understanding of ADHD, which may guide future research.

Image from- Shaw, P., et al. (2007). Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2148343/figure/F1/

Genetics and the Environment

The abnormalities in the function and structure of the brain are complemented by genetic studies, which demonstrate the inheritability of ADHD’s pathogenesis, focusing of gene abnormalities including the dopamine system (Poelmans et al., 2011).  The research found 40% of children with ADHD have a parent with the disorder (Faraone et al., 2000; Chen et al., 2008).  Also, twin studies show there is a high chance of inheriting ADHD (Faraone et al., 2005).  Adoption studies show children have more similarities to their biological relatives than their adoptive relatives (Faraone et al., 2005).

The nature versus nurture debate is often studied when investigating the cause of ADHD. Research shows there is a complex interplay of genes and the environment.  Faraone et al. (2000) argue that twin studies have shown genes cannot be the sole cause of ADHD, as the rate would be 100%, so environmental factors must be an attributable factor.  But, there is little research conducted on causal environmental factors (Thapar, 2009).


People with ADHD have a debilitating disorder, that can lead to social, academic and mental health problems. The whole debate of ADHD is mired in adversity; from conceptualisations, treatment, assessment to comorbidities. Due to the brief nature of this essay, all the neurological findings on ADHD cannot be captured. Since ADHD is a heterogeneous condition, a simple neurobiological basis is not possible and research has been unable to identify a distinctive aetiology. The majority of research uses neuroimaging, but this technique has questionable probative value.  Advancements in neuroimaging techniques will give an enriched understanding of regions of the brain associated with ADHD.  The cardinal symptoms of ADHD are not unique to the disorder, and there is strong comorbidity with other mental health conditions.  Although much research has been conducted, there is still a lack of clarity to the cause and the variation of symptoms.  Behavioural manifestations of ADHD are thought to be produced by dysfunctions in brain circuits, which are attributed to cognitive functioning.  The research discussed shows there are multiple abnormalities in circuitry, chemistry and structure.  Dopamine levels have been identified as a crucial factor in the disorder, methodological issues in the research still cloud the findings of the studies. Research findings into ADHD being a delay rather than deviance gives a new understanding of the cause of ADHD and improvements in imaging techniques are a stepping stone to getting closer to finding the aetiology of the disorder.


An Introduction To The Basal Ganglia. (2018). Fewer Lacunae. Retrieved 20 January 2018, from https://kevinbinz.com/2016/01/17/basal-ganglia-introduction/

Buitelaar, J.K. (2002) “Epidemiology: What have we learned over the last decade?”. In Hyperactivity and attention-deficit disorders, 2nd ed., Cambridge: Cambridge University Press.

Biederman. J. (2004). Impact of comorbidity in adults with attention-deficit/hyperactivity disorder. J Clin Psychiatry 65(Suppl 3): 3–7.

Bledsoe, J., Semrud-Clikeman, M., & Pliszka, S. (2009). A Magnetic Resonance Imaging Study of the Cerebellar Vermis in Chronically Treated and Treatment-Naïve Children with Attention-Deficit/Hyperactivity Disorder Combined Type. Biological Psychiatry65(7), 620-624. http://dx.doi.org/10.1016/j.biopsych.2008.11.030

Bush, G., Frazier, J., Rauch, S., Seidman, L., Whalen, P., & Jenike, M. et al. (1999). Anterior cingulate cortex dysfunction in attention-deficit/hyperactivity disorder revealed by fMRI and the counting stroop. Biological Psychiatry45(12), 1542-1552. http://dx.doi.org/10.1016/s0006-3223(99)00083-9

Bush, G. (2009). Attention-Deficit/Hyperactivity Disorder and Attention Networks. Neuropsychopharmacology, 35(1), pp.278-300.

Bush, G. (2010). Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/19759528

Bush, G. (2011). Cingulate, Frontal, and Parietal Cortical Dysfunction in Attention-Deficit/Hyperactivity Disorder. Biological Psychiatry69(12), 1160-1167. http://dx.doi.org/10.1016/j.biopsych.2011.01.022

Castellanos, F. (2002). Proceed, with caution: SPECT cerebral blood flow studies of children and adolescents with attention deficit hyperactivity disorder. J Nucl Med 43: 1630–1633.

Castellanos, F., Margulies, D., Kelly, C., Uddin, L., Ghaffari, M., Kirsch, A., Shaw, D., Shezad, Z., Di Martino, A., Biswal, B., Sonuga-Barke, E., Rotrosen, J., Adler, L. and Milham, M. (2008) Cingulate-precuneus interactions: a new locus of dysfunction in adult attention-deficit/hyperactivity disorder. Biol Psychiatry 63:332–337.

Cherkasova, M. V., & Hechtman, L. (2009). Neuroimaging in attention-deficit hyperactivity disorder: Beyond the frontostriatal circuitry.  The Canadian Journal of Psychiatry, 54(10), 651-664.

Cortese, S., Kelly, C., Chabernaud, C., Proal, E., Di Martino, A., Milham, M., & Castellanos, F. (2012). Toward Systems Neuroscience of ADHD: A Meta-Analysis of 55 fMRI Studies. American Journal Of Psychiatry169(10), 1038-1055. http://dx.doi.org/10.1176/appi.ajp.2012.11101521

Chen, W., Zhou, K., Sham, P., Franke, B., Kuntsi, J., Campbell, D., Fleischman, K., Knight, J., Andreou, P., Arnold, R., Altink, M., Boer, F., Boholst, MJ., Buschgens, C., Butler, L., Christiansen, H., Fliers, E., Howe-Forbes, R., Gabriëls, I., Heise, A., Korn-Lubetzki, I., Marco, R., Medad, S., Minderaa, R., Müller, UC., Mulligan, A., Psychogiou, L., Rommelse, N., Sethna, V., Uebel, H., McGuffin, P., Plomin, R., Banaschewski, T., Buitelaar, J., Ebstein, R., Eisenberg, J., Gill, M., Manor, I., Miranda, A., Mulas, F., Oades, RD., Roeyers, H., Rothenberger, A., Sergeant, J., Sonuga-Barke, E., Steinhausen, HC., Taylor, E., Thompson, M., Faraone, SV., and Asherson, P. (2008) DSM-IV combined type ADHD shows familial association with sibling trait scores: A sampling strategy for QTL linkage. Am J Med Genet B Neuropsychiatr Genet.

Culham, J., Cavina-Pratesi, C., & Singhal, A. (2006). The role of parietal cortex in visuomotor control: What have we learned from neuroimaging?. Neuropsychologia44(13), 2668-2684. http://dx.doi.org/10.1016/j.neuropsychologia.2005.11.003

Curatolo, P., D’Agati, E., & Moavero, R. (2010).  The neurobiological basis of ADHD.  Italian Journal of Pediatrics, 36(1), 79-85.

Del Campo, N., Chamberlain, S. R., Sahakian, B. J., & Robbins, T. W. (2011).  The roles of dopamine and noradrenaline in the pathophysiology and treatment of attention-deficit/hyperactivity disorder.  Biological Psychiatry, 60  (e145-e157). Doi: 10.1016/j.biopsych.2011.02.036

Dougherty, D., Bonab, A., Spencer, T., Rauch, S., Madras, B., & Fischman, A. (1999). Dopamine transporter density in patients with attention deficit hyperactivity disorder. The Lancet354(9196), 2132-2133. http://dx.doi.org/10.1016/s0140-6736(99)04030-1

Durston, S., Van Belle, J., & de Zeeuw, P. (2011). Diifferentiating frontostriatal and fronto-cerebellar circuits in attention-deficit/hyperactivity disorder.  Biological Psychiatry, 69, 1178-1184.

Ernst M, Zametkin AJ, Matochik JA, Pascualvaca D, Jons PH, Cohen RM(1999). High midbrain [18F]DOPA accumulation in children with attention deficit hyperactivity disorder. Am J Psychiatry 156: 1209–1215.

Faraone SV, Biederman J, Monuteaux MC. (2000) Attention-deficit disorder and conduct disorder in girls: evidence for a familial subtype. Biol Psychiatry.  Jul 1;48(1):21–9.

Faraone SV, Perlis RH, Doyle AE, Smoller JW, Goralnick JJ, Holmgren MA, Sklar P. (2005)  Molecular genetics of attention-deficit/hyperactivity disorder. Biol Psychiatry.  Jun 1;57(11):1313–23. Epub 2005 Jan 21.

Hill, D. E., Yeo, R. A., Campbell, R. A., Hart, B., Vigil, J., & Brooks, W. (2003). Magnetic resonance imaging correlates of attention-deficit/hyperactivity disorder in children. Neuropsychology, 17(3), 496-506.

Jeong, S., Choi, K., Lee, K., Kim, E., Kim, Y., & Joo, E. (2015). Association between the dopamine transporter gene (DAT1) and attention deficit hyperactivity disorder-related traits in healthy adults. Psychiatric Genetics25(3), 119-126. http://dx.doi.org/10.1097/ypg.0000000000000086

Jucaite A, Fernell E, Halldin C, Forssberg H, Farde L (2005). Reduced midbrain dopamine transporter binding in male adolescents with attention-deficit/hyperactivity disorder: association between striatal dopamine markers and motor hyperactivity. Biol Psychiatry 57: 229–238.

Leo, J., & Cohen, D. (2003). Broken brains or flawed studies? A critical review of ADHD neuroimaging research. Journal of Mind and Behavior, 24(1), 29-56.

Nigg, J., & Casey, B. (2005). An integrative theory of attention-deficit/ hyperactivity disorder based on the cognitive and affective neurosciences. Development And Psychopathology17(03). http://dx.doi.org/10.1017/s0954579405050376

Schultz, W. (2006). Behavioral Theories and the Neurophysiology of Reward. Annual Review Of Psychology57(1), 87-115. http://dx.doi.org/10.1146/annurev.psych.56.091103.070229

Shaw, P., Eckstrand, K., Sharp, W., Blumenthal, J., Lerch, J., & Greenstein, D. et al. (2007). Attention-deficit/hyperactivity disorder is characterized by a delay in cortical maturation. Proceedings Of The National Academy Of Sciences104(49), 19649-19654. http://dx.doi.org/10.1073/pnas.0707741104

Spencer TJ, Biederman J, Madras BK, Faraone SV, Dougherty DD, Bonab AA et al (2005). In vivo neuroreceptor imaging in attention-deficit/hyperactivity disorder: a focus on the dopamine transporter. Biol Psychiatry 57: 1293–1300.

Stark, R., Bauer, E., Merz, C., Zimmermann, M., Reuter, M., & Plichta, M. et al. (2011). ADHD related behaviors are associated with brain activation in the reward system. Neuropsychologia49(3), 426-434. http://dx.doi.org/10.1016/j.neuropsychologia.2010.12.012

Swanson, J., Kinsbourne, M., Nigg, J., Lanphear, B., Stefanatos, G., & Volkow, N. et al. (2007). Etiologic Subtypes of Attention-Deficit/Hyperactivity Disorder: Brain Imaging, Molecular Genetic and Environmental Factors and the Dopamine Hypothesis. Neuropsychology Review17(1), 39-59. http://dx.doi.org/10.1007/s11065-007-9019-9

Swanson, J., Baler, R. D., & Volkow, N. D. (2011). Understanding the effects of stimulant medications on cognition in individuals with attention-deficit hyperactivity disorder: A decade of progress.  Neuropsychopharmacology, 36,  207-226.

Thapar, A. (2009). An Overview on the Genetics of ADHD. Acta Psychologica Sinica40(10), 1088-1098. http://dx.doi.org/10.3724/sp.j.1041.2008.01088

Vaidya CJ, Stollstorff M (2008). Cognitive neuroscience of attention deficit hyperactivity disorder: current status and working hypotheses. Dev Disabil Res Rev 14: 261–267.

Valera EM, Faraone SV, Murray KE, Seidman LJ (2007). Meta-analysis of structural imaging findings in attention-deficit/hyperactivity disorder. Biol Psychiatry 61: 1361–1369.

Vos, T., Haby, MM., Magnus, A., Mihalopoulos, C., Andrews, G., and Carter, R. (2005). Assessing cost-effectiveness in mental health: helping policy-makers prioritize and plan health services. Aust NZ J Psychiatry 39: 701–712.

Volkow, N. D., Wang, G. J., Newcorn, J., Fowler, J. S., Telang, F., Solanto, M. V. et al. (2007). Brain dopamine transporter levels in treatment and drug naive adults with ADHD. Neuroimage 34: 1182–1190.

Volkow, N. D., Wang, G., Kollins, S. H., Wigal, T. L., Newcorn, J., Telang, F., & Swanson, J. (2009).  Evaluating dopamine reward pathway in ADHD: Clinical implications.  Journal of the American Medical Association, 302(10), 1084-1091.

Zametkin AJ, Nordahl TE, Gross M, King AC, Semple WE, Rumsey J et al(1990). Cerebral glucose metabolism in adults with hyperactivity of childhood onset. N Engl J Med 323: 1361–1366. Seminal large-scale PET study of ADHD adults that showed global and regional hypometabolism in ADHD adults.

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