IJPS April 2011
IJPS October 2011
IJPS April 2012
IJPS October 2012
IJPS April 2013
IJPS October 2013
IJPS Apirl 2014
IJPS October 2014
IJPS Apirl 2015
IJPS Apirl 2016
IJPS October 2016
IJPS Apirl 2017


Netranee Anju Ramdinny-Purryag

Consultant,St. Jean Pharmacy, Mauritius


ADHD is the most commonly studied and diagnosed psychiatric disorder in children, affecting about 3 to 5 percent of children globally1 and diagnosed in about 2 to 16 percent of school aged children.2 It is a chronic disorder 3 with 30 to 50 percent of those individuals diagnosed in childhood continuing to have symptoms into adulthood.4,5

ADHD has been recognised under different names for more than a century. In the earliest reports, behavioural abnormalities similar to ADHD were described as a complication of encephalitis after the influenza epidemic of 1918. ‘Organic driveness’ was a term used to describe the behaviour after epidemic encephalitis and damage to the brainstem was suggested as the cause. This description of behavioural symptoms caused by encephalitis or brain damage was followed by a variety of reports linked to brain dysfunction and described by various terms including minimal ‘brain dysfunction’ in 1966 and ‘hyperkinetic reaction of childhood or adolescence’ in 1968.

Theories of ADHD

Organic theory:

A cortical-striatal circuit has been proposed to explain the heterogeneous nature of ADHD.6 A decrease in the volume of the right anterior frontal region and loss of normal left to right striatal asymmetries have been shown on MRI studies. These findings support the involvement of the frontal lobes and striatal connections in the pathophysiology of ADHD. A temporal lobe arachnoids cyst-ADHD syndrome has also been described in a patient with coincidental learning and language disabilities.7

Genetic theory:

Genetic factors account for approximately 80% of the etiology of ADHD.8

Family, twin and adoption studies support the theory that ADHD is a highly heritable disorder, with the majority of patients having a first or second degree relative with a history of ADHD or learning disorder.9

Environmental theory:

Pregnancy and birth related risk factors include maternal smoking, exanthema, maternal anemia, breech delivery, prematurity, low birth weight, hypoxic-ischaemic encephalopathy, small head circumference, cocaine/alcohol exposure and iodine/thyroid deficiency.

Of all the factors implicated during pregnancy, maternal smoking has attracted the greatest attention in recent literature.

Childhood illnesses associated with occurrence of ADHD include viral infections, meningitis, encephalitis, otitis media, anaemia, cardiac disease, thyroid disease, epilepsy, autoimmune and metabolic disorders. Other causative factors include head injury involving the frontal lobes, toxins/drugs and nutritional disorders (eg food additives, food allergies, sucrose, gluten sensitivity and fatty acid/ iron deficiencies).

Brain Insult theory:

The hypothesised brain damage may potentially be associated with circulatory, toxic, metabolic, mechanical or physical injuries to the brain during infancy caused by infection, inflammation and trauma. Children with ADHD exhibit non focal (soft) neurological signs at higher rates than those in the general population.

Neurochemical theory:

. The peripheral sympathetic system is of more importance in ADHD. Thus a dysfunction in the peripheral system which causes norepinephrine to accumulate peripherally could potentially feedback to the central system and set the locus ceruleus at a lower level.

Neurophysiological theory:

The human brain usually undergoes major growth spurts at several ages: 3 to 10 months, 2 to 4 years, 6 to 8 years, 10 to 12 years and 14 to 16 years. Some children have a maturational delay in the sequence and manifest symptoms of ADHD that appear to normalize by 5 years of age. A physiological finding is a number of electroencephalographic correlates which normalize by the age of 5 years in few cases. For instance, increased beta band percentage or decreased delta band percentage is associated with increased arousal.

Studies using positron emission tomography have found lower cerebral blood flow and metabolic rates in the frontal lobe areas of children with ADHD than controls. PET scans have also shown that adolescent females with the disorder have globally lower glucose metabolism than both normal control females and males with the disorder.

Psychosocial theory

Prolonged emotional deprivation may explain the overactivity and poor attention spans in ADHD such as in children who are placed in institutions. These children tend to normalize as the deprivational factors are removed.

Stressful psychic events, disruption of family equilibrium and other anxiety inducing factors contribute to the initiation and perpetuation of ADHD.

Predisposing factors include child’s temperament, genetic familial factors and the demands of society to adhere to a routinized way of behaving and performing.

Clinical Features of ADHD

Predominantly inattentive types include:

1.       Being easily distracted, missing details, forgetting things and frequently switching from one activity to the other

2.       Having difficulty focusing on one task

3.       Becoming bored with a task after only few minutes

4.       Having difficulty in organising and completing a task or having difficulty in learning something new and often losing things (eg pencils, toys, assignments)

5.       Not seeming to listen when spoken to

6.       Daydreaming

7.       Having difficulty in processing information as quickly and accurately as others

8.       Struggling to follow instructions

9.       Predominantly hyperactive-impulsive type symptoms include:

10.   Fidgeting and squirming in their seats

11.   Talking persistently

12.   Being constantly in motion, touching or playing with anything and everything in sight

13.   Having difficulty in sitting still during dinner, school and story time

14.   Having difficulty in doing quiet tasks or activities

15.   Manifestations of impulsivity are primarily:

16.   Being very impatient

17.   Blurting out inappropriate comments, showing their emotions without restraint and to act without regard for consequences

18.   Having difficulty waiting for things they want or waiting for their turns in games

19.   A 2009 study found that children with ADHD move around excessively because it helps them stay alert enough to complete challenging tasks.10

Differential diagnosis of ADHD

ADHD may accompany other disorders such as anxiety or depression. Such combinations can greatly complicate diagnosis and treatment. Where a mood disorder complicates ADHD, it would be prudent to treat the mood disorder first but parents of children who have ADHD often wish to have the ADHD treated first because the response to treatment is quicker.11

To make the diagnosis of ADHD, a number of other possible medical and psychological conditions must be excluded.

Medical Conditions

1.       Hypothyroidism

2.       Anaemia

3.       Lead poisoning

4.       Chronic illnesses

5.       Hearing or vision deficits

6.       Substance abuse

7.       Medication side effects

8.       Sleep impairment & Child abuse 12

9.       Cluttering (tachyphemia)

There is substantial empirical evidence from a neuroanatomic standpoint to suggest that there is considerable overlap in the central nervous system centres that regulate sleep and those that regulate attention/arousal.13 There are multilevel and bidirectional relationships among sleep, neurobehavioural functioning and the clinical syndrome of ADHD.14

Behavioural manifestations of sleepiness in children range from the classic ones (yawning, rubbing eyes) to externalising behaviours (impulsivity, hyperactivity, aggressiveness), to mood liability and inattentiveness.14,15

Children with ADHD should be regularly and systematically assessed for sleep problems.

Management of ADHD

Combined medical management and behavioural treatment is the most effective ADHD management strategy, followed by medication alone, and then behavioural therapy. 16


The most common stimulant medications are methylphenidate (Ritalin), dextroamphetamine (Dexedrine) and mixed amphetamine salts(Adderall). Atomoxetine (Strattera) is currently the only non-stimulant drug approved for the treatment of ADHD. Stimulant medication is an effective treatment for Adult ADHD although the response rate may be lower for adults than children.17

Stimulants used to treat ADHD raise the extracellular concentrations of the neurotransmitters dopamine and norepinephrine which causes an increase in neurotransmission. The therapeutic benefits are due to the noradrenergic effects at the locus coeruleus and the prefrontal cortex and the dopaminergic effects at the nucleus accumbens.18

A metaanalysis of clinical trials found that about 70% of children improve after being treated with stimulants in short term but this conclusion may be biased due to the high number of low quality clinical trials in the literature. There have been no randomized placebo controlled clinical trials investigating the long term effectiveness of methylphenidate beyond 4 weeks. Thus, the long term effectiveness of methylphenidate has not been scientifically demonstrated. Serious concerns of publication bias regarding the use of methylphenidate for ADHD has also been noted.18

Higher rates of schizophrenia and bipolar mood disorders as well as increased severity of these disorders occur in individuals with a past history of stimulant use for ADHD in childhood.19

Although under medical supervision, stimulant medications are considered safe, the use of stimulant medications for the treatment of ADHD has generated controversy because of undesirable side effects, uncertain long term effects and social and ethical issues regarding their use and dispensation.20 The United States FDA has added black box warning to some ADHD medications while the American Heart Association and the American Academy of Paediatrics feel that it is prudent to carefully assess children for heart conditions before treating them with stimulant medications.

Psychotherapeutic Approaches

There are a variety of psychotherapeutic approaches employed by psychologists and psychiatrists: the one used depends on the patient and patient’s symptoms. The approaches include psychotherapy, CBT, support groups, parent-training, meditation and social skills training. If psychotherapy fails to bring improvement, medications can be considered as an add-on or alternative.21 Improving the surrounding home and school environment can improve the behaviour of children with ADHD.22

The different educational interventions for the parents jointly called Parent Management Training Techniques include operant conditioning: a consistent application of rewards for meeting goals and good behaviour (positive reinforcement) and punishments such as time outs or revocation for failing to meet goals or poor behaviour.22Classroom management is similar to parent management training. Strategies include increased structuring of classroom activities, daily feedback and token economy.22

Working memory training

Many of the problems shown by children with ADHD can be traced back to deficits in working memory (or short term memory). By training and improving this memory, some of the other symptoms may decrease as well. In a study by Klingberg et al., a computerised training program has shown good results in working memory, even if the generated effect to behavioural symptoms was not as clear.

Massage therapy

For children and adolescents with ADHD, paediatric massage therapy has been found to improve mood and increase on task behaviours while reducing anxiety and hyperactivity.23,24

Art therapy

Some psychologists feel that cutting down on the time spent on television, video games or violent games, or violent media can help some children. One study indicated a correlation between excessive TV time and a child with higher rates of ADHD symptoms.25 Some psychologists feel Art therapy may be one of the most effective therapies to help children to concentrate, slow down and stabilize.

Other therapies

Other therapies that have been effective for some have been positive changes in diet, such as low sugar, low additives and no caffeine. Children, who spend time outdoors in natural settings (dubbed Green Therapy) such as parks, seem to display fewer symptoms of ADHD.

Dietary Supplements

Omega-3 supplements (seal,fish or krill oil) may reduce ADHD symptoms for a subgroup of children and adolescents with ADHD characterised by inattention and associated neurodevelopmental disorders.26 A meta-analysis has found that dietary elimination of artificial food colouring and preservatives provides a statistically significant benefit in children with ADHD.27 Other more recent studies agree with these conclusions.28

Future Directions

1.       Different diagnostic criteria need to be established for children, adolescent and adult ADHD respectively.

2.       More data regarding the long term effects of the methods of treatment that have been in use for several decades need to be established, as well as the long term outcomes of children who have not been treated.

3.       Psychotropic medications which are safer and more effective need to be developed for ADHD alone.

4.       Studies in areas of prevention/early intervention that target known risk factors need to be conducted.

5.       Further evaluation for rapidly evolving technology of brain imaging techniques as a possible tool in the diagnosis and subsequent management of ADHD.


1.        Zametkin AJ, Rapoport JL. Neurobiology of ADHD. J Am Acad Child Adolesc Psychiatry 1987; 26(5): 676-616.

2.        Sookup VM, Patterson J, Trier TT, Chen JW. Cognitive improvement despite minimal arachnoid cyst decompression. Brain Dev. 1998; 20(8):589-593.

3.        Biederman J, Faraone SV. Current concepts on the neurobiology of ADHD. J Atten Disord 2002; 6(1):S7-S16.

4.        Mayes SD, Calhoun SL, Crowell EW. Learning disabilities and ADHD: overlapping spectrum disorders. J Lear Disabil 2000; 33(5):417-424.

5.        Nair J, Ehimare U, Beitman BD, Nair SS, Lavin A. Clinical review: evidence-based diagnosis and treatment of ADHD in children. Mo Med 2006; 103 (6):617–21.

6.        Rader R, McCauley L, Callen EC. "Current strategies in the diagnosis and treatment of childhood attention-deficit/hyperactivity disorder". Am Fam Physician 2009; 79 (8): 657–65.

7.        Van Cleave J, Leslie. Approaching ADHD as a chronic condition: implications for long-term adherence. Journal of Psychosocial Nursing and Mental Health Services 2008; 46 (8):28–37.

8.        Bálint S, Czobor P, Mészáros A, Simon V, Bitter I. Neuropsychological impairments in adult attention deficit hyperactivity disorder: a literature review (in Hungarian). Psychiatr Hung2008; 23 (5): 324–35.

9.        Elia J, Ambrosini PJ, Rapoport JL. Treatment of attention-deficit-hyperactivity disorder. The New England Journal of Medicine 2009;340 (10):780–8.

10.     Rapport MD, Bolden J, Kofler MJ, Sarver DE, Raiker JS, Alderson RM. Hyperactivity in boys with ADHD: a ubiquitous core symptom or manifestation of working memory deficits? J Abnorm Child Psychol 2009;37(4): 521-534.

11.     Brunsvold GL, Oepen G. Comorbid Depression in ADHD: Children and Adolescents. Psychiatric Times 2008: 25(10).

12.     Smucker WD, Hedayat M. Evaluation and treatment of ADHD. American Family Physician 2001;64(5):817-829.

13.     Owens JA. The ADHD and sleep conundrum: a review. Journal of Developmental and Behavioural Pediatrics 2005; 26(4):312-22.

14.     Owens JA. Sleep disorders and ADHD. Current Psychiatry Reports 2008; 10(5): 439-444.

15.     Golan N, Shahar E, Ravid S, Pillar G. Sleep disorders and daytime sleepiness in children with ADHD. Sleep 2004;27(2): 261-6.

16.     Garcia JA, Glied S, Crowe M, Foster M, Hinshaw S, Vitello B et al. Cost Effectiveness of ADHD treatments: Findings from the Multimodal Treatment Study of Children with ADHD. American Journal of Psychiatry 2005; 162(9):1628-1636.

17.     Spencer T, Biederman J, Wilens T. Stimulant treatment of adult ADHD. Psychiatric Clinics of North America 2004: 27(2).

18.     Solanto MV. Neuropsychopharmacological mechanisms of stimulant drug action in ADHD: a review and integration. Behavioural Brain Research 1998: 94(1);127-52.

19.     Ross RG. Psychotic and Manic-like symptoms during stimulant treatment of ADHD. AJP 2006;163(7):1149-52.

20.     Stem HP, Stern TP. When children with ADHD become adults 2002: 95(9); 985-91.

21.     Greydanus DE, Pratt HD, Patel DR. ADHD across the lifespan: the child adolescent and adult. Dis Mon 2007;53(2):70-131.

22.     Clinical practice guideline: Treatment of the school aged child with ADHD. American Academy of Paediatrics. Subcomittee on ADHD and Comittee on Quality Improvement. Paediatrics 2001: 108; 1033-44.

23.     Field T, Quinhno O, Hernandez-Reif M, Koslovsky G. Adolescents with ADHD benefit from massage therapy. Adolescence 1998; 33: 103-108.

24.     Khilnani S, Field T, Hernandez-Reif M, Schanberg S. Massage therapy improves mood and behaviour of students with ADHD. Adolescence 2003; 38: 623-38.

25.     Zimmerman FJ, Christahis DA. Associations between content types of early media exposure and subsequent attentional problems. Paediatrics 2007; 120(5): 986-92.

26.     Johnson M, Ostlund S, Fransson G, Kadesjo B, Gillberg C. Omega3/Omega6 fatty acids for ADHD: A randomised placebo controlled trial in children and adolescents. Journal of Attention Disorders 2009; 12(5): 394-40.

27.     Schab DW, Trinh NH. Do artificial food colours promote hyperactivity in children with hyperactive syndromes? A meta-analysis of double blind placebo controlled trials. Journal of Developmental and behavioural paediatrics 2004; 25(6): 423-34.

28.     Zimmerman FJ, Christahis DA. Associations between content types of early media exposure and subsequent attentional problems. Paediatrics 2007; 120(5):986-92.