ADHD background

In this section I do not intend to cover the different perspectives, views, opinions and experiences on the subject of Attention Hyperactivity Disorder. There are on going debates as to the validity of the disorder, its aetiology and its pharmaceutical treatments that are published in professional journals and public media ( ses BMJ is it valid, Bremner Radio 4, Singh) which will not be reviewed here in depth. My intention in this research is not to ignore dissenting or alternative voices to the main scientific proposition, and in the next chapter I will explore and critique the concept of medicalisation that is often used to discuss this contested terrain. But for now I wish to briefly map the present scientific theses that are actively called upon by clinicians, patients and scientists in the context of the diagnostic process. To do this I will respond to four of the most frequently asked questions in relations to adult ADHD found on a patient support group leaflet (AADD-UK)

1. Is ADHD a modern problem? 2. What are the causes of ADHD? 3. How do people know they have ADHD 4. What is it like to have ADHD

1. Is ADHD a modern problem?

Recently historians of medicine and psychiatrists have been examining the antecedents of the present ADHD diagnostic. A number of articles published from 1988 onwards (Barkley 1990 , Historical development, Klaus W. Lange 2010, Conners 2000) articulate a common chronology for the historical development of the scientific concept of ADHD which is now established and used in manuals (Ascherson 2011, Barkley 2006), presented to experts in congresses ( UKAAN Sept 2011) as well as Patient Organisations conferences ( ADDISS Oct 2011). Typically the birth of the concept starts with the 3 Goulstonian Lectures of Sir George Frederic Still in 1902 that provided descriptions of children with impulsive behaviours, sometimes accompanied with inability to focus attention but most notably who were not brain injured or damaged. Previous descriptions are mentioned, in particular Crichtons morbid alterations of attention in 1798 causing distractibility, impulsivity and restlessness ( Early description) or the childrens tales of Struwwelpeter by Heinrich Hoffmann published in Germany in 1845 ( Eric taylor 2011. But Stills moral defect of control ( 1902) is presented as the precursors of a scientific development that led to other nomenclature, such Minimal Brain Damage ( Tredgold 1908) , Minimal Brain Dysfunction (Bax & Mackeith 1963) and Attention Deficit Disorder with or without Hyperactivity ( DSM 1980). It is worth noting the change from the moralistic conception associated with ADHD symptoms to a concept of brain damage, then brain dysfunction and finally brain disorder which could be said to have

taken place in parallel with a change in the wider societal interest and perception of childhood in the UK

2. What are the causes of ADHD?

Whilst ADHD is one of the most researched psychiatric disorder, its causes remain uncertain; nevertheless the consensus in the scientific community is that it is a multi factorial disorder with genetic, neurobiological and psychosocial factors which the following research is exploring ( ADHD in Lancet,, consensus 2010, understanding ADHD).

In the last decade molecular genetics research has moved from investigating the heritability of ADHD (is it genetic) to functional studies (what do the genes do?) These functional studies concentrate on the identification of the genes involved with dopamine transmission and the candidates predominantly investigated are a receptor ( DRD4), a transporter (DAT1) and a trigger ( SNAP25) ( Ascherson 2004 and 2010, Biederman and Faraone 2005). As well as twin studies and family studies animal models, ie: rats and mice, have been investigated as they provide the opportunity to experiment the interactions between gene, behaviour and environment(Thome and Reddy 2009). All studies also point out that ADHD is a multifactoral

disorder and that any particular gene involved may only add 1% to 3% risk of developing it. A range of factors may adversely affect the brain development in children such as the foetus exposure to nicotine, alcohol, causing premature delivery, low birthweigth ( ADHD in lancet). Neuroimaging technologies are involved in exploring the neuroanatomy of ADHD by studying static maps of the brain (structural imaging) and dynamic maps of the neural activity (functional imaging). ADHD Structural studies, using MRI (Magnetic Resonance Imaging), concentrate principally on brain volume reduction in specific area such as the cerebellum, frontal lobe, corpus callosum and basal ganglia and are positing that altered size reduction causes circuitry malfunction in these sections of the brain. One recent hypothesis is that rather than an abnormal size volume, individuals with ADHD have a maturational lag in brain volume development which may eventually normalise( Rubia 2011).Whilst there are very few MIR studies of adults with ADHD (Seidman, Valera, and Makris 2005), proponents of a life long disorder model are pointing out that the delay in growth may not resolve itself, hence the persistence of symptoms in the adult population. ADHD Functional studies using PET (Positron Emission Tomography) but more frequently fMRI, focus on measuring the deficit in neural mechanism of executive functions associated with the prefrontal cortex. Whilst there are no tests to differentiate

specific ADHD brain activity from any normal control subjects, ultimately the aim of such research is to provide diagnostic tools in support of other clinical interventions, just as Xrays are used to distinguish between bronchitis and pneumonia (Bush 2005). This diagnostic move is tentatively considered a possibility in the next 5 to 10 years. (UKAAN 2011) Cognitive research has linked environmental factors such as disrupted or discordant family relationship to childrens difficulty in acquiring four major executive functions, working memory, internalised speech, motivational appraisal and behavioural synthesis ( Barkley 1997). The impact is an impairment of social intelligence, a lesser ability to self regulate in relationship with others, control responses and cope with interferences that would disrupt mental processing. This theory has been very influential in highlighting the possibility of having a high IQ but poor academic results. Dietary factors have also been noted, in regards to intake of food colouring additives and sugar in and their potential impact on brain development. ( NICE)

Scientific consensus has moved towards proposing that biology creates propensity for the development of ADHD and that genetic factors interact with psychosocial and environmental factors to influence neurological development. In other words the context in which ADHD symptoms develop is recognised as a crucial element in

the understanding of this disorder. ( Antecendents taylor, Understanding ADHD, Biology in context Singh)

3. How do people know they have ADHD?

According to the diagnostic criteria for ADHD, in the Diagnostic and Statistical Manual of Mental Disorders, 4th Ed, Text Revised (DSM-IVTR)(2004), the most common behaviours of ADHD falls into three categories which are inattention, hyperactivity, and impulsivity. An individual is diagnosed to have ADHD with the presence of either : 1) Having six or more symptoms of inattention, or 2) having six or more symptoms of hyperactivity-impulsivity. Symptoms for either condition must have persisted for at least 6 months to a degree that is maladaptive and inconsistent with developmental level (DSM-IV-TR, 2004). The symptoms and impairments of either condition must be present in two or more settings (school, work, home etc) and must have been present before the age of 7. This last feature is particularly distinctive of the diagnostic of adult ADHD; most psychiatric disorder in the DSM require that a symptomatic history is taken, that would typically record a first onset in teenage years for Personality Disorder, or early adulthood for Schizophrenia. In the case of adult ADHD symptoms must have been noted prior to 7 years old or even prior to 6 years old in the ICD10.

In addition there must be clear evidence that the symptoms cause significant impairment in social, school or work functioning and that they are not experienced as part of a psychotic disorder ( schizophrenia) nor are they better accounted for by another disorder (Mood Disorder, Anxiety Disorder, Dissociative Disorder, or a Personality Disorder).

Based on these criteria, three types of ADHD are identified: IA. ADHD, Combined Type: if both criteria IA and IB are met for the past 6 months IB. ADHD, Predominantly Inattentive Type: if criterion IA is met but criterion IB is not met for the past six months IC. ADHD, Predominantly Hyperactive-Impulsive Type: if Criterion IB is met but Criterion IA is not met for the past six months

Since 2004 clinicians have continued to debate these criteria, particularly in regards to adults with ADHD and pointing out amongst other things the following areas of uncertainties: that the hyperactivity threshold may be less relevant to adults, that there may be a gender bias in the criteria resulting in more boys being diagnosed that impulsivity is overrepresented and inattention under represented

that the age of onset at 7 is arbitrarily set that adults symptoms such as procrastination or insomnia are not considered.

Consequently the task force commissioned to update the criteria and publish the DSM5 due in 2013 (http://www.dsm5.org/ProposedRevisions/Pages/proposedrevision.asp x?rid=383#) , is suggesting a number of changes of which the lowering of the number of symptoms from 6 to 4 for adolescents and adults change the age of onset from 7 to 12 years adding a 4th sub-type of Inattentive Presentation

These points are particularly noteworthy as they are likely to increase the numbers of adults meeting the criteria for diagnosis.

4. What is it like to have ADHD?

There are many sources that describe and indentify symptoms for adult ADHD, including in the DSM, various rating scales used by diagnosticians, the NICE guidance, but also support groups websites, and clinician publications ( Weiss, Barkley, AADDUK, NICE , UTAH self report) Given the variety of diagnostic sub-types described above,

individual experiences are likely to be varied and combining a range of theme with various consequences such as;

Difficulties in organising daily activities, forgetfulness, difficulties in time management and procrastination may be experience through the inability to sustain employment, to meet deadlines, to pay bills

Physical and mental over-activity, to have many projects going simultaneously, intolerance of boredom which may lead to feeling of restlessness, of being unfocused and may cause insomnia and a feeling of exhaustion.

Impulsivity and impatience with a low tolerance for frustration is often experienced though argumentative behaviour in public spaces, speeding while driving, overspending through shopping.

Mood swings with faster and less pronounced cycles as with bipolar disorder, often experienced as being over anxious, depressed, low motivation, contrasted with periods of elated moods and being the life and soul of the party.

There are obvious differences in the way ADHD may be experienced by adults in comparison to children simply due to their different lifestyle and positions. There are circumstances specific to adults that affect the diagnosis and the treatment of ADHD such as the

development of coping strategies which may cause problems in their own right, the ability to refuse treatment with unpleasant side effects, difficulties in getting collateral reports from employers and other sources and they may be themselves carers of children and needing to control symptoms not only at work during the day but also at home in the evening when stimulants are unlikely to have been prescribed. This last point is often at the centre of negotiations between clinician and patient as the development of long lasting effect non-stimulant treatment is being promoted (see Obs Report and UKAAN 2011) to replace the fast acting stimulant treatments which can be associated with the potential for misuse.