Pharmacological therapy

Pharmacological interventions are recommended by clinical guidelines for ADHD as part of a comprehensive treatment programme (including a behavioural therapy component) when remedial measures prove insufficient.1-5 The decision about which medication should be used to treat ADHD depends on a range of factors, including: presence of comorbidities; side effects of the medication; individual compliance needs; potential for drug diversion; and the personal preference of patients and their caregivers.1-5 The section below contains an overview of the pharmacological treatment options available for the treatment of ADHD outside of the US.

Types of pharmacological treatment

Stimulants (e.g. methylphenidate, dexamfetamine and lisdexamfetamine dimesylate) and non-stimulants (e.g. atomoxetine and guanfacine) are two types of medication for the treatment of ADHD.1 Both stimulant and non-stimulant medications can be associated with side effects, and patients receiving medication for ADHD should be closely monitored for both physical and psychiatric adverse events.1-5

Mechanism of action

Although the mechanism of action of ADHD medications is not fully understood, they appear to alleviate ADHD symptoms by inhibiting the reuptake of dopamine and/or noradrenaline, thereby increasing the intrasynaptic concentrations of these neuromodulators.6-12

Response to pharmacological treatments

Clinical guidelines recommend methylphenidate as the first-line pharmacological treatment option for ADHD, however there are certain situations where other medications would be considered as treatment options.1,2 Treatment response in patients receiving medication for ADHD should be regularly monitored.1-4 For patients who do not respond well to a certain medication, adjustment to the dose or type of medication may improve their response.1,2 The presence of comorbidities should also be considered when evaluating treatment response.1

Treatment adherence

Treatment adherence is an area of particular concern in ADHD as many patients fail to adhere to treatment regimens.13,14 Choice of medication can play a role in this; for example longer continuity of treatment has been associated with once-daily extended-release formulations, compared with immediate-release formulations that require multiple doses per day.14


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  1. NICE (2008) Attention Deficit Hyperactivity Disorder: Diagnosis and Management of ADHD in Children, Young People and Adults. NICE clinical guideline 72. Available at www.nice.org.uk/CG72 [NICE guideline]. Last accessed May 2015.
  2. Taylor E, Döpfner M, Sergeant J, et al. European clinical guidelines for hyperkinetic disorder – first upgrade. Eur Child Adolesc Psychiatry 2004; 13 (Suppl 1): I7-30.
  3. Graham J, Banaschewski T, Buitelaar J, et al. European Guidelines Group. European guidelines on managing adverse effects of medication for ADHD. Eur Child Adolesc Psychiatry 2011; 20: 17-37.
  4. Canadian ADHD Practice (CAP) Guidelines. 3rd Edition. 2011. Last accessed May 2015.
  5. Guías clínica para el trastorno por déficit de atención e hiperactividad. 2010. Last accessed May 2015.
  6. Wilens TE. Effects of methylphenidate on the catecholaminergic system in attention-deficit/hyperactivity disorder. J Clin Psychopharmacol. 2008; 28(3 Suppl 2): S46-53.
  7. Hodgkins P, Shaw M, McCarthy S, et al. The pharmacology and clinical outcomes of amphetamines to treat ADHD. CNS Drugs 2012; 26: 245-268.
  8. Rang HP, Dale MM, Ritter JM. Central nervous system stimulants and psychotomimetic drugs in: Pharmacology. Edinburgh: Churchill Livingstone, 2009; 603-613.
  9. Bymaster FP, Katner JS, Nelson DL, et al. Atomoxetine increases extracellular levels of norepinephrine and dopamine in prefrontal cortex of rat: a potential mechanism for efficacy in attention deficit/hyperactivity disorder. Neuropsychopharmacology 2002; 27: 699-711.
  10. Wang M, Ramos BP, Paspalas CD, et al. Alpha2A-adrenoceptors strengthen working memory networks by inhibiting cAMP-HCN channel signaling in prefrontal cortex. Cell 2007; 129: 397-410.
  11. Ji XH, Ji JZ, Zhang H, et al. Stimulation of alpha2-adrenoceptors suppresses excitatory synaptic transmission in the medial prefrontal cortex of rat. Neuropsychopharmacology 2008; 33: 2263-2271.
  12. Yi F, Liu SS, Luo F, et al. Signaling mechanism underlying alpha2A-adrenergic suppression of excitatory synaptic transmission in the medial prefrontal cortex of rats. Eur J Neurosci 2013; 38: 2364-2373.
  13. Barner JC, Khoza S, Oladapo A. ADHD medication use, adherence, persistence and cost among Texas Medicaid children. Curr Med Res Opin 2011; 27: 13-22.
  14. Marcus SC, Wan GJ, Kemner JE, et al. Continuity of methylphenidate treatment for attention-deficit/hyperactivity disorder. Arch Pediatr Adolesc Med 2005: 159: 572-578.

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