Attention Deficit Disorder (ADHD)

What is Attention Deficit Disorder (ADHD)?

Attention-deficit hyperactivity disorder (ADHD) is a chronic and highly common neurobehavioral condition afflicting children between 6 and 17 years of age, although symptoms may persist into adulthood in 50% of cases.

Three subtypes of ADHD are now recognized:

• Predominantly hyperactive impulsive

• Predominantly inattentive

• A combined type, characterized by a combination of the first 2 subtypes

Psychological and biological symptoms of ADHD

Because of impulsive behavior and altered information processing abilities, children and adolescents with ADHD often perform poorly academically and are more likely to drop out of school.

Impulsiveness is also associated with a higher risk for motor vehicle accidents and casual sexual encounters, which may explain the higher rates of pregnancies and incidence of sexually transmitted diseases in adolescents with ADHD.

Children and adolescents with ADHD are often diagnosed with lower self-esteem, which may lead to challenges in social relationships, increases the likelihood for substance abuse, and has also been associated with greater tendency for criminal offence.

In addition, ADHD often presents with one or more other conditions such as oppositional defiant disorder (ODD), major depressive disorder (MDD), and anxiety disorders, which add further challenges to the life of these individuals.

As adults, the challenges exhibited at earlier stages of life may be associated with inferior job performance, lower socioeconomic status, and marital/relationship problems.

What causes ADHD?

Research suggests that the symptomatology of ADHD reflects complex interactions between genetic and non-genetic factors.

Magnetic resonance Imaging (MRI) studies, for example, indicate that ADHD is associated with reduced volume or functionality of grey and white matter in the brain, which may play a role in deficits in cognitive processing, attention, motor planning, and speed of processing responses.

Several studies have reported that dopamine (DA) receptor density in several brain regions of ADHD patients is lower than normal and polymorphisms for the genes that encode for DA have also been shown.

Other research has demonstrated altered functionality of norepinephrine (NE) transmission in ADHD.

Altogether, the hypothesis for an altered DA and NE in ADHD is in perfect agreement with the mechanisms of action of the medications used to treat the disorder.

Diagnosis of ADHD

Although several neuroimaging studies have revealed that ADHD is associated with both volumetric and functional changes in the brain, definitive results still await confirmation, mainly because of the complexity of the disorder itself.

Clinicians usually follow the criteria outlined by the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-V) for diagnosing ADHD. However, given that there are 3 subtypes of ADHD, each subtype exhibiting different symptomatology, it is required that at least 6 symptoms must be presented by children (5 for subjects older than 17 years) for at least 6 months in order to be diagnosed with a particular subtype of ADHD.

Comorbidities such as ODD, MDD, and anxiety disorders can complicate the diagnosis of ADHD because of the symptoms these disorders share with ADHD.

The DSM-V scale for ADHD however, still fails to address gender differences. For example, males are 3 folds more likely to have ADHD than females and mostly exhibit the hyperactive or combined subtype, are more aggressive and are more likely to abuse the law. On the other hand, females tend to exhibit the inattentive subtype, often showing cognitive impairment and eating disorders.

Clinicians must consider these sexual and developmental differences between individuals to avoid the over or underdiagnosis of the disorder. For this reason, the diagnosis of ADHD must be done by trained professionals, carefully keeping into account the repeated observations and reports from parents, teachers or other caregiver, also controlling for other disorders like ODD and MDD that may potentially act as confounders and lead to a misdiagnosis of ADHD.

Treatments for ADHD

Treatments for ADHD include medications (e.g., methylphenidate, more commonly known by brand names such as Ritalin, amphetamine and atomoxetine) and non-pharmacological interventions such as behaviour support, skills training, individual and family therapy and, more recently, neurofeedback.

One of the primary difficulties with ADHD medications is their range of adverse effects, which include loss of appetite, increased blood pressure and mood swings. In adults with ADHD, treatment with medication can be even more complex given the range of drug interactions, and the likelihood of the individual having other conditions being treated with medications.

Published research shows the benefit of drug therapy for children with ADHD, but with significant drawbacks due to the adverse effects. There have been continuing calls to increase research into non-pharmacological interventions.

Neurofeedback has shown particular promise in this regard, with studies showing reduced impulsivity and distractibility as well as increased organisation ability.

A recent review has shown the effects of neurofeedback training to be similar to those of medication, without side-effects. More specifically, neurofeedback training had long-term effects of on inattention, impulsivity and hyperactivity. Another study of 104 school-age children with ADHD showed that those who underwent neurofeedback training, when compared to those who underwent other cognitive remediation training or no intervention, made more prompt and greater improvements in symptoms at a six-month follow up.

Overall, research indicates that neurofeedback can help individuals with ADHD feel more in control of their day-to-day lives, often reducing anxiety and stress around getting things done on time and being organised.

If you are wondering if your child has ADHD, you can read this article. You can read more about ADHD in Ireland here.

As with all of our interventions, we personalise all our plans on the basis of a formulation by one of our psychology team, alongside the acquisition of electroencephalographic (EEG) data from the brain.

References

1. Berger, I., Diagnosis of attention deficit hyperactivity disorder: much ado about something. Isr Med Assoc J, 2011. 13(9): p. 571-4.

2. Childress, A. C. and Berry, S. A., Pharmacotherapy of attention-deficit hyperactivity disorder in adolescents. Drugs, 2012. 72(3): p. 309-25.

3. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed. Washington, DC: American Psychiatric Association; 2013.

4. Cortese, S., The neurobiology and genetics of attention-deficit/ hyperactivity disorder (ADHD): what every clinician should know. Eur J Paediatr Neurol. 2012;16:422-433.

5. Dopheide, J., A., ASHP therapeutic position statement on the appropriate use of medications in the treatment of attention deficit/hyperactivity disorder in pediatric patients. Am J Health Syst Pharm. 2005;62:1502-1509.

6. Maul, J., Advokat C., Stimulant medications for attention deficit/hyperactivity disorder (ADHD) improve memory of emotional stimuli in ADHD-diagnosed college students. Pharmacol Biochem Behav. 2013;105:58-62. 7.

7. Modesto-Lowe V., Meyer A., Soovajian V. A clinician’s guide to adult attention-deficit hyperactivity disorder. Conn Med. 2012;76:517-523.

8. Biederman, J., Faraone, S. V., Spencer, T. J., Mick, E., Monuteaux, M.C., Aleardi, M., Functional impairments in adults with self-reports of diagnosed ADHD: A controlled study of 1001 adults in the community. J Clin Psychiatry. 2006;67: 524-540.

9. Arnsten, A.F., Pliszka SR. Catecholamine influences on prefrontal cortical function: relevance to treatment of attention deficit/hyperactivity disorder and related disorders. Pharmacol Biochem Behav. 2011;99:211-216.

10. Kesner, R. P., Churchwell, J. C., An analysis of rat prefrontal cortex in mediating executive function. Neurobiol Learn Mem. 2011;96:417-431

12. Arnsten, A.F., Catecholamine and second messenger influences on prefrontal cortical networks of “representational knowledge”: a rational bridge between genetics and the symptoms of mental illness. Cereb Cortex. 2007;17(suppl 1):i6-i15.

13. Arnsten, A. F., Paspalas, C. D., Gamo, N. J., Yang, Y., Wang, M., Dynamic network connectivity: a new form of neuroplasticity. Trends Cogn Sci. 2010;14:365-375.

14. Pliszka, S. R., The neuropsychopharmacology of attention deficit/hyperactivity disorder. Biol Psychiatry. 2005;57: 1385-1390.

15. Robbins, T. W., Dopamine and cognition. Curr Opin Neurol. 2003;16(suppl 2):S1-S2.

16. Bowton, E., Saunders, C., Erreger, K., et al. Dysregulation of dopamine transporters via dopamine D2 autoreceptors triggers anomalous dopamine efflux associated with attention-deficit hyperactivity disorder. J Neurosci. 2010;30:6048-6057.

17. Wang, M., Ramos, B. P., Paspalas, C. D., et al. Alpha2A adrenoceptors strengthen working memory networks by inhibiting cAMP-HCN channel signaling in prefrontal cortex. Cell. 2007;129:397-410.

18. Baumeister, A. A., Hawkins, M. F., Incoherence of neuroimaging studies of attention deficit/hyperactivity disorder. Clin Neuropharmacol. 2001;24:2-10.

19. Bush, G., Neuroimaging of attention deficit hyperactivity disorder: can new imaging findings be integrated in clinical practice? Child Adolesc Psychiatr Clin N Am. 2008;17:385-404.

20. Bush G., Valera, E. M., Seidman LJ. Functional neuroimaging of attention-deficit/hyperactivity disorder: a review and suggested future directions. Biol Psychiatry. 2005;57:1273-1284.

21. Perlov, E., Philipsen, A., Matthies, S., et al. Spectroscopic findings in attention-deficit/hyperactivity disorder: review and meta-analysis. World J Biol Psychiatry. 2009;10:355-365.

22. Durston, S., Converging methods in studying attention-deficit/ hyperactivity disorder: what can we learn from neuroimaging and genetics? Dev Psychopathol. 2008;20:1133-1143.

23. Zimmer L., Positron emission tomography neuroimaging for a better understanding of the biology of ADHD. Neuropharmacology. 2009;57:601-607.

24. Kehoe, W. A., Treatment of attention deficit hyperactivity disorder in children. Ann Pharmacother. 2001;35:1130-1134.

25. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 4th ed, text rev. Washington, DC: American Psychiatric Association; 2000.

26. Trent, S., Davies, W., The influence of sex-linked genetic mechanisms on attention and impulsivity. Biol Psychol. 2012;89:1-13.

27. Rader, R., McCauley, L., Callen. E. C., Current strategies in the diagnosis and treatment of childhood attention-deficit/hyperactivity disorder. Am Fam Physician. 2009;79:657-665.

28. Sharma, A. and Couture, J., A review of the pathophysiology, etiology, and treatment of attention-deficit hyperactivity disorder (ADHD). Ann Pharmacother, 2014. 48(2): p. 209-25.