Is ADHD a ‘real’ disorder?
MICHAEL QUINN and ANDREA LYNCH
In many western countries, attention deficit hyperactivity disorder (ADHD)
has achieved celebrity status, such that it probably no longer requires intro-
duction. The disorder is a global phenomenon, spreading rapidly as result of
the increasing dominance internationally of US psychiatric models, the need
for new markets for major pharmaceutical companies, increasing use of the
internet by parents and professionals and changing approaches to schooling.
There is a broad consensus among international experts and organisations
that ADHD is a genuine neurodevelopmental disorder based on empirical
research. However, many critics have questioned the legitimacy of ADHD.
This paper reviews the arguments for and against the ADHD construct. First,
the review examines the literature and research endorsing ADHD as a ‘real’
disorder. Second, the criticisms levelled against the ADHD construct are
Key words: ADHD, support, science, criticisms.
According to the American Psychiatric Association (2013), ADHD is a neurode-
velopmental disorder characterised by a persistent pattern of inattention and
hyperactivity–impulsivity. Symptoms of this nature persist into adulthood and
can cause several impairments in social, academic and occupational functioning
(Gapin et al., 2011). Globally, the disorder affects 5.3% of children (Polanczyk
et al., 2007). This figure was reported following a review of 102 prevalence
studies from seven regions, including North America, South America, Europe,
Africa, the Middle East, Asia and Oceania. The disorder is more commonly
diagnosed in males than in females in the general population, with a ratio of 2:1
in children (American Psychiatric Association, 2013). In the United States, and
increasingly in Europe, psychostimulants are first-line treatments for ADHD
(Singh, 2008) and since the 1950s, medications for ADHD have been used
In many western countries, ADHD has achieved celebrity status, such that it
probably no longer requires introduction (Graham, 2010). It is a global phenom-
enon, spreading rapidly as result of the increasing dominance internationally of
US psychiatric models, the need for new markets for major pharmaceutical com-
panies, increasing use of the internet by parents and professionals and changing
approaches to schooling (Stead et al., 2006). Campbell (2000) asserts it is safe
to argue that we likely know more about ADHD than any other childhood con-
dition. Yet, despite the existing plethora of research and skyrocketing increases
in the number of persons diagnosed with ADHD, it is clear that this topic is
highly misunderstood (Kewley, 1999).
Support for ADHD
The symptoms of ADHD do not represent a new phenomenon (Goldstein and
Goldstein, 1998): the British physician George Still made reference to a disorder
we now recognise as ADHD in 1902 (Cooper and Bilton, 2002). Descriptions of
inattention, impulsive and hyperactive behaviour in childhood have appeared in
texts as old as the Bible (Goldstein and Goldstein, 1998). Many international
experts and organisations have endorsed ADHD as a valid medical disorder (e.g.
Barkley, 2013; DuPaul and Stoner, 2014; Mash and Wolfe, 2015; Tannock,
1998; Kewley, 2011; Goldstein and Goldstein, 1998; American Psychiatric
Association, 2013; National Institute of Mental Health, 2008; British Psycholog-
ical Society, 2000; National Institute of Clinical Excellence, 2013). Many of
these organisations, among others, have published comprehensive guidelines
that provide evidence-based recommendations for the diagnosis and treatment of
ADHD. In 2002, Professor Russell Barkley and a consortium of medical practi-
tioners and researchers published an International Consensus Statement on
ADHD (Barkley et al., 2002). This document is significant in the context of the
current article because it confirmed the status of the scientific findings
60 Support for Learning Volume 31 Number 1 2016 V
concerning the validity of the disorder, and its adverse impact on the lives of
those living with ADHD.
Science and ADHD
Findings from genetic and neurological studies have given weight to the argu-
ment that ADHD is a valid disorder. For example, Tannock (1998) reviewed
several studies and identified the following findings which support a genetic
basis for ADHD:
Over the past 30 years, numerous family-genetic studies have reported a
higher prevalence rate of psychopathology, particularly ADHD, in parents
and other relatives of children with ADHD.
In twin and adoption studies, reports have consistently shown a much
greater incidence of ADHD among identical monozygotic (MZ) twins than
among non-identical dizygotic (DZ) twins. Passmore (2014) also adds that
MZ twins share 100 per cent of their genes, whereas DZ twins only share
50 per cent of their genes: ‘Scientists have found that if one twin has
symptoms of ADHD, the risk that the other will have the disorder is as
high as 75-90%’ (Barkley, 2013).
In the dopamine system, molecular genetic research has identified genetic
abnormalities. Dopamine is one of many neurotransmitters found in the
brain and is essential for attention among other things (Ratey and Hager-
There have also been suggestions that ADHD may have its roots in neurological
causes (Buckley et al., 2009; Barkley and Murphy, 2006; Jacobs and Wendel,
2010). Neurotransmitter chemicals such as dopamine, norepinephrine and sero-
tonin play a vital role in regulating human behaviour (Reynolds et al., 2012;
Parker, 1998). These neurotransmitters carry messages between brain cells dur-
ing mental tasks – rather like workers moving around and putting things together
in a factory (Munden and Arcelus, 1999). Ratey and Hagerman (2008) explain
why these particular neurotransmitters are so important in the case of children
with ADHD. First, the neurotransmitter dopamine is essential for attention,
among other things. Second, norepinephrine affects arousal, alertness, attention
and mood. Third, serotonin regulates many functions, including mood, impulsiv-
ity, learning and self-esteem. Professionals maintain that children with ADHD
have a deficiency in these neurotransmitter chemicals (Barkley, 2013; Ratey and
C2016 NASEN Support for Learning Volume 31 Number 1 2016 61
Hagerman, 2008; Reiff and Tippins, 2004). Studies have discovered particularly
low levels of activity in the neurotransmitters located in the frontal lobes of the
brain (Wheeler, 2007). Findings from various studies support the argument that
neurological factors are a key contributor to ADHD. Neuro-imaging studies
involving children with ADHD have shown a decreased size of the prefrontal
cortex (e.g. Mostofsky et al., 2002), resulting in expected deficits in certain pre-
frontal executive functions, such as response inhibition and working memory
(Barkley, 1997; Tannock, 1998). In the United States, one study that deserves
particular attention was carried out at the National Institute of Mental Health by
Zametkin et al. (1990). This study has been described as a landmark piece of
research (Ratey and Hagerman, 2008). Using a type of brain scan referred to as
Positron Emission Tomography (PET) scans, the study focused on the rate at
which the brain uses glucose, which is the brain’s main energy source. Results
illustrated that during an attention test, participants with ADHD displayed 10
per cent less brain activity than the control group. The largest deficit was within
the prefrontal cortex, an area of the brain which plays a crucial role in regulating
behaviour, and is also prone to positive reinforcement through physical activity
(Ratey and Hagerman, 2008).
Medicalising ‘annoying’ behaviour
Some critics of the ADHD construct question the possibility that ADHD is per-
haps nothing more than an example of the ‘medicalisation’ of behaviours in
children which are the most annoying and problematic for adults to control. As
Bromfield proclaims, the condition is implicated in ‘all sorts of abuses, hypoc-
risies, neglects, and other society ills that have nothing to do with ADHD’
(Bromfield, 1996, p. 3; cited in Conrad and Potter, 2000, p. 570). Indeed, those
who are critical of ADHD as a medicalised construct often cite ADHD as ‘a
means of labelling and controlling children who exhibit difficult behaviours’
(Mather, 2012, p. 19). Child neurologist Fred Baughman has been one of the
most outspoken critics of ADHD, calling it a ‘fraud’. As Baughman (2006)
‘Virtually all the symptoms of ADHD relate to classroom behaviour. Children
who don’t do homework, fidget, squirm, interrupt, and are forgetful and disor-
ganized are assumed to have a biochemical imbalance in their brain. These chil-
dren can be difficult to control in a classroom and in many cases are more
62 Support for Learning Volume 31 Number 1 2016 V
compliant when drugged. However, there is absolutely no scientifically valid
evidence that compliant –drugged students learn faster.’ (2006, p. xiii)
He goes on to conclude: ‘ADHD is a disorder manufactured to match our times.
It is a quick catch-all diagnosis with a magic bullet treatment’ (2006, p. xiii).
Other critics view ADHD as a social construct which is the result of our
performance-driven cultures and societies, citing the prolific increase of Ritalin
and other stimulants to ‘treat’ ADHD as nothing more than a method of perform-
ance enhancement. According to Lawrence Diller (1998), the ADHD label is ‘sal-
vation’ for some, allowing them to avoid feelings of ‘failure’ as they blame their
behaviour and related issues on brain functioning or genetics, rather than accepting
personal responsibility for their problems. The same author contends that the
increased numbers of those diagnosed with ADHD has led to the development of
supportive communities which provide a sense of belonging to people whose
behaviour has otherwise made them outsiders in the dominant culture.
Disagreement on how to ‘define’ ADHD
A review of literature shows there is no consensus on an agreed definition for the
disorder. For the example, in the Diagnostic and Statistical Manual of Mental Dis-
orders, Fifth Edition (DSM-5) published by the American Psychiatric Association
(2013), ADHD is defined as a ‘neurodevelopmental disorder’, and the Interna-
tional Classification of Diseases and Related Health Problems refers to it as a
‘hyperkinetic disorder’ (World Health Organization, 1992). ADHD is also defined
in a wide variety of ways within the research literature, and each definition can
give some insight into the author’s philosophical position concerning the nature of
ADHD. It is not uncommon to see ADHD defined as a neurobiologic condition
(Quinn, 2008), a neurodevelopmental disorder (Mrug et al., 2012), a mental disor-
der (Benkert et al., 2010) and a heterogeneous condition (Newcorn et al., 2001;
Faraone and Biederman, 1998). In addition, the following terms have also been
historically applied to ADHD: ‘attention deficit disorder (ADD), hyperkinetic dis-
order (HKD), hyperkinesis, minimal brain dysfunction, minimal brain damage
(MBD), and disorder of attention, motor control, and perception (DAMP)’ (Carr,
2006, p. 421). Regardless of the kind of term used, children with ADHD continue
to present with severe and pervasive symptoms of inattention, hyperactivity and
C2016 NASEN Support for Learning Volume 31 Number 1 2016 63
Lack of a biological marker and unknown etiology
Despite copious amounts of medical and psychological research, science has yet
to discover a biological marker or characteristic for ADHD. Unlike other medi-
cal conditions which have clear and identifiable markers that indicate the pres-
ence of disorder, in the case of ADHD, ‘No biological marker is diagnostic’
(American Psychiatric Association, 2013, p. 61). Also, there are no objective
medical ‘tests’ which can detect the presence of ADHD (Timimi and Taylor,
2004). Science remains unable to identify the exact causes or etiology of
ADHD, and prominent researchers like Faraone and Biederman admit that we
have yet to achieve this goal (Faraone et al., 1995). The inability to conclusively
identify causes of ADHD calls into serious question the legitimacy of ADHD as
a medical disorder (Visser and Jehan, 2009). Not surprisingly, several theories
exist concerning the causes of ADHD in the individual.
The biological theory of impaired brain functioning is perhaps the most widely
accepted of all theories (Tidefors and Strand, 2012), as it suggests that ADHD is
the result of malfunction in brain processes and/or structures (Qiu et al., 2011;
Castellanos et al., 2002; Taylor, 1999). Genetic factors have also been strongly
linked to ADHD causation (Tannock, 1998; Hawi et al., 2013; Park et al., 2010;
Thapar et al., 2007; Faraone and Biederman, 1998), as have ‘deficits’ in the
individual, such as deficits in executive functioning (Shoemaker et al., 2012), in
executive inhibition (Nigg, 2001) and in behavioural inhibition (Barkley, 1997).
ADHD has also been linked to a host of sources outside of the individual, such
as conditions before, during and after gestation, psychosocial influences and
environmental factors (Thapar et al., 2013; Taylor and Sonuga-Barke, 2008).
The existing body of research is not without its critics. Researchers such as
Ongel (2006) take a more sceptical view of such studies, warning us that associ-
ation between variables (such as abnormal behaviour and brain abnormalities)
does not automatically signify causation.
Diagnosis of ADHD: subjectivity and checklists
The subjective nature of the ADHD diagnosis is another cause for criticism.
Senior (2009) argues that ADHD is so contested precisely because of the subjec-
tive nature of the diagnostic process. ADHD diagnosis is based largely on the
characteristic criteria established in the DSM-5 (American Psychiatric Associa-
tion, 2013) and the International Classification of Diseases and Related Health
64 Support for Learning Volume 31 Number 1 2016 V
Problems (World Health Organization, 1992), and is subjectively identified by
medical professionals through use of behavioural checklists and rating scales
(Stead et al., 2006). There is no one standardised checklist in use for ADHD
diagnosis; rather, there are at least two dozen, if not more (Cohen, 2006). Often,
whether a person obtains a diagnosis of ADHD can be a matter of degree and
Over-diagnosis and use of psychotropic drugs in children
Critics of the ADHD construct also question the ever increasing diagnosis of
ADHD along with skyrocketing rates of psychostimulant drug usage in children.
It is estimated that in the UK during the ten-year period from 1994 to 2004, the
prescription of methylphenidate increased by an astonishing 7,600% (Cohen,
2006). As Cormier (2008) explains, we should be extremely concerned regard-
ing the ever increasing numbers of pre-schoolers who are diagnosed with
ADHD, as well as the ‘sevenfold’ increase in the prescription and use of stimu-
lant medications in children. Statistics such as this raise questions regarding the
possibility of the ‘over-diagnosis’ of ADHD. In their research, Bruchmuller
et al. (2012, p.128) determined that therapists commonly fail to diagnose in
strict accordance with manuals and that ‘overdiagnosis of ADHD occurs in the
clinical routine’. However, others argue against the concept of overdiagnosis,
claiming this is a misperception which has simply taken hold in public percep-
tion and media coverage (Sciutto and Eisenberg, 2007).
Questions have also been raised regarding the influence and motives of the phar-
maceutical industry in the race to ADHD diagnosis (Conrad and Bergey, 2014;
Ongel, 2006). While much of the research literature strongly asserts the efficacy
of psychostimulant drugs in treating and controlling symptoms associated with
ADHD (Benkert et al., 2010; Forness et al., 1999), questions must be raised
regarding the potential for bias, especially in cases where pharmaceutical com-
panies are backing research into the efficacy of pharmacological treatments for
ADHD. One example of such research is the Survey of ADHD in Irish Children
(Fitzgerald, 2007) which was directly supported by the pharmaceutical company
Eli Lilly and Co. (Ireland) Ltd. Interestingly, many of the questions in this ‘sur-
vey’ of parents of children with ADHD highlight strongly positive outcomes
reported by parents when their children were on medication, as opposed to
when they were not.
C2016 NASEN Support for Learning Volume 31 Number 1 2016 65
The authors of this paper reviewed the literature and research supporting ADHD
as a valid disorder. They also explored the many criticisms levelled against the
ADHD construct. Research literature on both sides of the ADHD argument
presents clear and compelling evidence for their theories and positions and it is
clear that the debate surrounding the legitimacy of ADHD as a medical condi-
tion is far from over. Although the ADHD construct has been scientifically
explored, it has gathered limited medical support, and admittedly, serious gaps
in knowledge remain unanswered. This highlights the need for further research
and exploration of this controversial and contested condition, with which many
of our children and students continue to be diagnosed and labelled in the present
AMERICAN PSYCHIATRIC ASSOCIATION (2013) Diagnostic and Statistical Manual of
Mental Disorders (DSM-5) (5th ed.). Washington, DC: American Psychiatric Association.
BARKLEY, R. (2013) Taking Charge of ADHD: The Complete Authoritative Guide for Parents.
New York: Guilford Publications, Inc.
BARKLEY, R. et al. (2002) International consensus statement on ADHD. Clinical Child and
Family Psychology Review, 5, 2, 89–111.
BARKLEY, R. (1997) Behavioral inhibition, sustained attention, and executive functions:
constructing a unifying theory of ADHD. Psychological Bulletin, 121, 1, 65–94.
BARKLEY, R. and MURPHY, K. (2006) Attention-deficit Hyperactivity Disorder: A Clinical
Workbook (3rd ed.). New York: The Guilford Press.
BAUGHMAN, F. (2006) The ADHD Fraud: How Psychiatry makes ‘Patients’ of Normal
Children. Victoria, BC: Trafford Publishing.
BENKERT, D., HENNING-KRAUSE, K., WASEM, J. and AIDELSBURGER, P. (2010)
Effectiveness of pharmaceutical therapy of ADHD (Attention-deficit/hyperactivity disorder) in
adults—health technology assessment. GMS Health Technology Assessment, 6, 1–12.
BRUCHMULLER, K., MARGRAF, J. and SCHNEIDER, S. (2012) Is ADHD diagnosed in
accord with diagnostic criteria? Overdiagnosis and influence of client gender on diagnosis.
Journal of Consulting and Clinical Psychology, 80, 1, 128–138.
BUCKLEY, S., GAVIN, B. and MCNICHOLAS, F. (2009) Mental Health in Children and
Adolescents: A Guide for Teachers. Drogheda, Ireland: Mulberry Publications.
CAMPBELL, S. (2000) Attention-deficit/hyperactivity disorder: a developmental view. In
Sameroff, A., Lewis, M. and Miller, S. (eds), Handbook of Developmental Psychopathology
(2nd ed.), pp. 383–401. New York: Kluwer Academic/Plenum Publishers.
CARR, A. (2006) Attention and over-activity problems. In Carr, A. (ed), The Handbook of Child
and Adolescent Clinical Psychology: A Contextual Approach (2nd ed.), pp. 421–460. London:
66 Support for Learning Volume 31 Number 1 2016 V
CASTELLANOS, F., LEE, P., SHARP, W., JEFFRIES, N., GREENSTEIN, D., CLASEN, L.,
BLUMENTHAL, J., JAMES, R., EBENS, C., WALTER, J., ZIJDENBOS, A., EVANS, A.,
GIEDD, J. and RAPOPORT, J. (2002) Developmental trajectories of brain volume
abnormalities in children and adolescents with attention-deficit/hyperactivity disorder. Journal
of the American Medical Association, 288, 14, 1740–1748.
COHEN, D. (2006) Critiques of the ADHD enterprise. In Lloyd, G., Stead, J. and Cohen, D.
(eds.) Critical new perspectives on ADHD, pp. 12–44. London: Routledge.
CONRAD, P. and BERGEY, M. (2014) The impending globalization of ADHD: notes on the
expansion and growth of a medicalized disorder. Social Science & Medicine, 122, 31–43.
CONRAD, P. and POTTER, D. (2000) From hyperactive children to ADHD adults: observations
on the expansion of medical categories. Social Problems, 47, 4, 559–582.
COOPER, P. and BILTON, K. (2002) Attention Deficit/Hyperactivity Disorder: A Practical
Guide for Teachers (2nd ed.) London: David Fulton.
CORMIER, E. (2008) Attention deficit/hyperactivity disorder: a review and update. Journal of
Pediatric Nursing, 23, 5, 345– 357.
DILLER, L. (1998) Running on Ritalin: A Physician Reflects on Children, Society, and
Performance in a Pill. New York: Bantam Books.
DUPAUL, G. J. and STONER, G. (2014) ADHD in Schools: Assessment and Intervention
Strategies (3rd ed.). New York: The Guilford Press.
FARAONE, S. and BIEDERMAN, J. (1998) Neurobiology of attention-deficit hyperactivity
disorder. Biological Psychiatry, 44, 10, 951–958.
FARAONE, S., BIEDERMAN, J., CHEN, W., MILBERGER, S., WARBURTON, R. and
TSUANG, M. (1995) Genetic heterogeneity in attention-deficit hyperactivity disorder
(ADHD): gender, psychiatric comorbidity, and maternal ADHD. Journal of Abnormal
Psychology, 104, 2, 234–345.
FITZGERALD, M. (2007) Survey of ADHD in Irish Children. [Online at http://positivecare.ie/
wp-content/uploads/2012/05/adhd-survey-ireland-parents.pdf]. Accessed 16/04/15.
FORNESS, S., KAVALE, K. and CRENSHAW, T. (1999) Stimulant medication revisited:
effective treatment of children with ADHD. Reclaiming Child Youth, 7, 4, 230–233.
GAPIN, J. L., LABBAN, J. D. and ETNIER, J. L. (2011) The effects of physical activity on attention
deficit hyperactivity disorder symptoms: the evidence. Preventive Medicine, 52, 70–74.
GOLDSTEIN, S. and GOLDSTEIN, M. (1998) Managing Attention Deficit Hyperactivity
Disorder in Children (2nd ed.). New York: John Wiley and Sons.
GRAHAM, L. J. (2010) (De)constructing ADHD: Critical Guidance for Teachers and Teacher
Educators. New York: Peter Lang.
HAWI, Z., MATTHEWS, N., WAGNER, J., WALLACE, R., BUTLER, T., VANCE, A., KENT,
L., GILL, M. and BELLGROVE, M. (2013) DNA variation in the SNAP25 gene confers risk
to ADHD and is associated with reduced expression in prefrontal cortex. PloS ONE,8,4.
JACOBS, C. and WENDEL, I. (2010) The Everything Parent’s Guide to ADHD in Children.
Avon, MA, U.S. Adams Media.
KENDALL, J., HATTON, D., BECKETT, A. and LEO, M. (2003) Children’s accounts of
attention-deficit/hyperactivity disorder. Advances in Nursing Science, 26, 2, 114–130.
KEWLEY, G. (1999) Attention Deficit Hyperactivity Disorder: Recognition, Reality, snd
Resolution. London: David Fulton Publishers.
KEWLEY, G. (2011) Attention Deficit Hyperactivity Disorder: What can Teachers Do? (3rd ed.).
London: David Fulton Publishers.
C2016 NASEN Support for Learning Volume 31 Number 1 2016 67
MASH, E. J. and WOLFE, D. A. (2015) Abnormal Child Psychology (6th ed.). Boston, MA:
MATHER, B. (2012) The social construction and reframing of attention-deficit/hyperactivity
disorder. Ethical Human Psychology & Psychiatry, 14, 1, 15–26.
MRUG, S., MOLINA, B., HOZA, B., GERDES, A., HINSHAW, S., HECHTMAN, L. and
ARNOLD, L. (2012) Peer rejection and friendship in children with attention-deficit/
hyperactivity disorder: contributions to long-term outcomes. Journal of Abnormal Child
Psychology, 40, 6, 1013–1026.
MUNDEN, A. and ARCELUS, J. (1999) The ADHD Handbook: A Guide for Parents and
Professionals on Attention Deficit/Hyperactivity Disorder. London: Jessica Kingsley Publishers.
MOSTOFSKY, S. H., COOPER, K. L., KATES, W. R., DENCKLA, M. B. and KAUFMANN,
W. E. (2002) Smaller prefrontal and premotor volumes in boys with attention deficit/
hyperactivity disorder. Biological Psychiatry, 52, 8, 785–794.
NATIONAL INSTITUTE OF MENTAL HEALTH (2008) Attention Deficit Hyperactivity
Disorder (ADHD). Bethesda, MD: National Institute of Mental Health.
NATIONAL INSTITUTE FOR HEALTH AND CLINICAL EXCELLENCE (2013) Attention
Deficit Hyperactivity Disorder: Diagnosis and Management of ADHD in Children, Young
People and Adults. London: National Institute for Health and Clinical Excellence.
NEWCORN, J., HALPERIN, J., JENSEN, P., ABIKOFF, H., ARNOLD, E., CANTWELL, D.,
CONNERS, C., ELLIOTT, G., EPSTEIN, J., GREENHILL, L., HECHTMAN, L.,
HINSHAW, S., HOZA, B., KRAEMER, H., PELHAM, W., SEVERE, J., SWANSON, J.,
WELLS, K., WIGAL, T. and VITIELLO, B. (2001) Symptom profiles in children with
ADHD: effects of comorbidity and gender. Journal of American Child and Adolescent
Psychiatry, 40, 2, 137–146.
NIGG, J. (2001) Is ADHD a disinhibitory disorder? Psychological Bulletin, 127, 5, 571–598.
ONGEL, U. (2006) ADHD and parenting styles. In G. Lloyd, J. Stead and D. Cohen, Critical
New Perspectives on ADHD, pp. 115–127. London: Routledge.
PARK, J., WILLMOTT, M., VETUZ, G., TOYE, C., KIRLEY, A., HAWI, Z., BROOKES, K.,
GILL, M. and KENT, L. (2010) Evidence that genetic variation in the oxytocin receptor
(OXTR1) gene influences social cognition in ADHD. Progress in Neuro-Psychopharmacology
and Biological Psychiatry, 34, 4, 697–702.
PARKER, H. C. (1998) The ADD Hyperactivity Handbook for Schools: Effective Strategies with
Attention Deficit Disorders in Elementary and Secondary Schools. Florida: Specialty Press.
POLANCZYK, G., DE LIMA, M. S., HORTA, B. L., BIEDERMAN, J. and ROHDE, L. A.
(2007) The worldwide prevalence of ADHD: a systematic review and metaregression analysis.
The American Journal of Psychiatry, 164, 6, 942–948.
PASSMORE, S. (2014) The ADHD Handbook. New South Wales: Exisle Publishing.
QIU, M., YE, Z., LI, Q., LIU, G., XIE, B. and WANG, J. (2011) Changes of brain structure and
function in ADHD children. Brain Topography, 24, 3, 243–252.
QUINN, P. (2008) Attention-deficit/hyperactivity disorder and its comorbidities in women and
girls: an evolving picture. Current Psychiatric Reports, 10, 5, 419–423.
RATEY, J. J. and HAGERMAN, E. (2008) SPARK: The Revolutionary New Science of Exercise
and the Brain. New York: Little, Brown.
REIFF, M.I. and TIPPINS, S. (2004) ADHD: a complete authoritative guide. Illinois: American
Academy of Pediatrics.
68 Support for Learning Volume 31 Number 1 2016 V
REYNOLDS, C., VANNEST, K. and HARRISON, J. (2012) The Energetic Brain: Understanding
and Managing ADHD. San Francisco: Jossey-Bass.
SCIUTTO, M. and EISENBERG, M. (2007) Evaluating the evidence for and against the
overdiagnosis of ADHD. Journal of Attention Disorders, 11, 2, 106–113.
SENIOR, J. (2009) ADHD: inclusion or exclusion in mainstream Irish schools. In S. Drudy (ed),
Education in Ireland: Challenge and Change, pp. 89–103. Dublin: Gill & Macmillan.
SHOEMAKER, K., BUNTE, T., WIEBE, S., ESPY, K., DEKOVIC, M. and MATTHYS, W.
(2012) Executive function deficits in preschool children with ADHD and DBD. Journal of
Child Psychology and Psychiatry, 53, 2, 111–119.
SINGH, I. (2008) Beyond polemics: science and ethics of ADHD. Nature Reviews Neuroscience,
STEAD, J., LLOYD, G. and COHEN, D. (2006) Widening our view of ADHD. In G. Lloyd, J.
Stead and D. Cohen (eds), Critical New Perspectives on ADHD, pp. 1–11. Oxford: Routledge.
TANNOCK, R. (1998) Attention deficit hyperactivity disorder: advances in cognitive,
neurobiological, and genetic research. Journal of Child Psychology and Psychiatry, 39, 1,
TAYLOR, E. (1999) Developmental neuropsychopathology of attention deficit and impulsiveness.
Development and Psychopathology, 11, 3, 607–628.
TAYLOR, E. and SONUGA-BARKE, E. (2008) Disorders of attention and activity. In M. Rutter,
D. Bishop, D. Pine, S. Scott, J. Stevenson, E. Taylor and A. Thapar (eds), Rutter’s Child and
Adolescent Psychiatry (5th ed.), pp. 521–542. Oxford: Blackwell Publishing.
THAPAR, A., COOPER, M., EYRE, O. and LANGLEY, K. (2013) Practitioner review: what
have we learnt about the causes of ADHD. Journal of Child Psychology and Psychiatry, 54,
THAPAR, A., LANGLEY, K., OWEN, M. and O’DONOVAN, M. (2007) Advances in genetic
findings on attention deficit hyperactivity disorder. Psychological Medicine, 37, 12,
THE BRITISH PSYCHOLOGICAL SOCIETY (2000) Attention Deficit/Hyperactivity Disorder
(ADHD): Guidelines and Principles for Successful Multi-agency Working. Leicester: The
British Psychological Society.
TIDEFORS, I. and STRAND, J. (2012) Life history interviews with 11 boys diagnosed with
attention-deficit/hyperactivity disorder who had sexually offended: a sad storyline. Journal of
Trauma and Dissociation, 13, 4, 421–434.
TIMIMI, S. and TAYLOR, E. (2004) ADHD is best understood as a cultural construct. British
Journal of Psychiatry, 184, 8–9.
VISSER, J. and JEHAN, Z. (2009) ADHD: a scientific fact or a factual opinion? A critique of
the veracity of attention deficit hyperactivity disorder. Emotional and Behavioural Difficulties,
14, 2, 127–140.
WHEELER, L. (2007) Attention Deficit Hyperactivity Disorder (ADHD): Identification,
Assessment, Contextual and Curricular Variability in Boys at KS1 and KS2 in Mainstream
Schools. PhD thesis, University of Worcester in association with Coventry University.
WORLD HEALTH ORGANIZATION (1992) The ICD-10 Classification of Mental and
Behavioural Disorders: Clinical Descriptions and Diagnostic Guidelines. Geneva: World
C2016 NASEN Support for Learning Volume 31 Number 1 2016 69
ZAMETKIN, A. J., NORDAHL, T. E., GROSS, M., KING, A. C., SEMPLE, W. E. and
RUMSEY J, et al (1990) Cerebral glucose metabolism in adults with hyperactivity of
childhood onset. New England Journal of Medicine, 323, 20, 1361–1366.
School of Education
University College Dublin (UCD)
70 Support for Learning Volume 31 Number 1 2016 V