This paper is largely made up of a summary of one major review article on the current state of play in ADHD, with some emphasis upon the reality of the condition as highlighted by brain imaging and activation studies. 

A brief subsequent section reflects the current interest in dietary issues, citing advice about what should be avoided and what should be included within a diet associated with positive functioning.



M.J.Connor                                                                                                    May 2005





The general summary, completed by Voeller (2004), was based upon the recognition of the many changes in approaches both to diagnosing and in managing ADHD that have arisen over the recent past, largely as a result of increasing data about the genetics involved or of insights gained from neuro-imaging methods.


It is noted that a genetic basis can be recognised in the majority of cases, with a number of different genes implicated; and that the remaining cases represent some environmental assault upon neurological development and functioning. 

Some individuals may experience problems from both sources.


The author holds that the ideal management strategies involve a combination of medical and behavioural elements, with early recognition and action necessary if secondary emotional or psychiatric difficulties are to be minimised or averted; and there is a need for the close involvement of family members along with school staff to provide consistency of handling and expectation.


The frequent comorbidity of ADHD with learning difficulties highlights the significance of optimal school planning and action.  




ADHD is now seen as a relatively common neurological disorder with up to 10% of school aged children estimated to be affected to at least some degree. 

However, there is no specific test by which unarguably to confirm the presence or absence of ADHD.

Instead, the identification is a matter of ratings by which to match the observed behaviour of a child (ideally according to different raters – at least school staff and parents in the settings of school and home) against the criteria set down in DSM-IV which lists 9 behavioural patterns for the inattentive type and a similar number for the hyperactive/impulsive type.


The problem is that to determine whether an individual does meet certain behavioural criteria may rely on subjective interpretation of terms like “ often has difficulty in organising tasks and activities ”.  There is no guarantee that different observers will interpret concepts like “often” or “difficulty” or “organising” in the same way.

There may be disagreement between the two parents whether behaviour is indicative of hyperactivity and impulsiveness or of simply having loads of energy; and parents and teachers may disagree whether the child has a significant disorder with attention or is simply failing to make any effort.


Meanwhile, ADHD is seen as falling into one of three categories … largely inattentive, largely hyperactive/impulsive, or combined. 
Debate continues whether it is appropriate to talk in terms of discrete categories when it may be more reasonable to regard the various elements of ADHD as falling somewhere along a continuum. 

For example, a child displaying 5 of the 9 DSM characteristics would not be formally diagnosed with ADHD, while a child who displays 6 of the characteristics would be diagnosed.  However, the day to day difficulties displayed by the two children might not be very different (and the ratings may have been more or less severe according to when they were completed).


Further, some children who might well be described as having a form of ADHD are those who seem under-aroused, and whose attention is variable, and have been categorised as showing a “sluggish cognitive” style.  However, this kind of behaviour has not been included in DSM-IV on the grounds that its presence might well predict inattention and the associated difficulties, but its absence does not predict no problems with inattention. 


Much review data indicate that the existing DSM subtypes differ in age of onset, the ratio of boys to girls, and the pattern of comorbid conditions including (specific) learning difficulty.


Age of Onset


Observations and experience have indicated that the signs and symptoms of ADHD are apparent in most cases before the age of 7 years, with the median age of evident impairment of functioning occurring as the child approaches 4 years.


The hyperactive/impulsive type emerges earlier than the combined type, and significantly earlier than the inattentive type.    Children categorised with either of the first two types of ADHD will have shown a typical age of onset at between 4 and 5 years; while the inattentive type will have shown a mean age of onset of around 6+ years, and would not have been clearly identifiable before around 7 years.

There is a concern that many individuals who experience the inattentive type of the condition may not be diagnosed at all, and many adults will have struggled with these difficulties without their being recognised as indicative of a specific problem.


Early identification is seen as important, and it is not surprising that symptoms can be observed in the preschool child given the strongly genetic nature of the disorder.  Later diagnosis of ADHD may be predictable from disorganised attachment behaviour during infancy. 


With age, ADHD becomes linked with deficits in executive functioning, such as poor working memory, inefficient planning, shifting attention, and an intolerance for any delay in response or reward.  The implications for school progress can be significant, and one notes the value of clinical rating scales by which to identify, during the pre-school period, the children who are likely to have these problems.

It is noted, however, that it is the hyperactive/impulsive type which may be readily recognised. 

There is also some evidence that ADHD follows a developmental pathway where the earliest signs are or hyperactive behaviour, and the child may subsequently show signs of the combined type of disorder during the early years at school; and the inattentive type of disorder evolves after the overt behavioural signs have lessened but as the demands for independent social and scholastic functioning become greater.


ADHD – Gender Effects


In all surveys, it is consistently noted that more boys than girls are identified.  The statistics from various specialist centres indicate that the ratios may vary between 6:1 and 12:1.


However, the above figures relate to individuals who are actually referred for specialist assessment and intervention.  Epidemiological samples suggest that the actual boy-girl difference in incidence is lower … more like 3:1. 

The implication is that girls who experience a form of ADHD may well be undiagnosed, possibly because they tend not to display the overtly disruptive behaviours that are more common among boys.  Girls have around half the rates of conduct disorder or oppositional defiance that are observed among boys, but they do have significant social problems.  They are more likely to have emotional pressures, are more prone to depression, and to have a low self esteem along with feelings of minimal control over events. 

The important issue is that the girls may experience problems, including the impairments of executive functioning, but do not manifest their needs in an overt way which will impact upon the day to day working of other people.




There is a consensus that it is rare for a child to display a “pure” form of ADHD with  no signs of any other emotional or learning difficulty.  Instead, ADHD is associated with a range of such difficulties, and a comorbid learning difficulty is very common, particularly dyslexia or dyscalculia. 

Executive function deficits will be greater in those individuals who experience both ADHD and a learning disability.


Conduct disorder, oppositional defiance, depression or bipolar disorder, anxiety including obsessive-compulsive disorder, and Tourette Syndrome are all conditions frequently observed alongside ADHD. 

Language disorder is another common category of problem that may be linked to ADHD.


Teenagers with ADHD are at enhanced risk for substance abuse.


Motor difficulties may prove an early marker for the child who is identified subsequently as having ADHD; and a separate syndrome has been identified – Deficits in Attention, Motor Control, and Perception (DAMP) – to describe a subgroup of individuals with ADHD-type and associated difficulties.


Meanwhile, ADHD may be a common comorbid condition in the case of individuals whose “primary” need is (severe) learning difficulty, autistic spectrum disorder, and non-verbal learning disability.


Neuropsychological Profiles


Studies of children with ADHD have indicated a pattern of cognitive weaknesses consistent with pre-frontal executive function deficits … inattention, poor self regulation, weak response inhibition (impulsiveness), restlessness and hyperactivity, or apathy in some cases.


The inattentive dimension, but not the hyperactive/impulsive dimension, is associated with a significant neurological impairment. 

Further, it has been suggested that both sets of symptoms can be linked to the underlying trait of “disinhibition” with inattention related to cognitive performance and the hyperactive/impulsive symptoms related to behavioural performance; and that the two types of difficulty show differences in heritability. Twin studies have indicated that a high level of inattention was heritable regardless of the degree of hyperactive and impulsive behaviour; while the hyperactive symptoms were closely linked to the number of inattention symptoms shown by the twin diagnosed with ADHD.


In other words, it is possible that the basic dysfunction in ADHD involves inattention and disorganisation rather than hyperactivity or impulsivity as has been assumed; and that these behavioural dimensions result from some other factor.


Behaviourally, ADHD involves a failure of self-regulation which reinforces the view of the condition as a dysfunction of the frontal-subcortical system.

Evidence exists for consistent differences in the brains of children with ADHD compared to those of normal controls, and the differences may be summarised as follows …….


Total cerebral or intracranial volume is smaller in ADHD … the difference is in the order of 5% which is large enough to be significant.

In particular, the grey matter in the right prefrontal cortex and left occipital cortex is reduced in individuals with ADHD and in their non-ADHD siblings with the implication that the changes in cerebral volume has to reach a critical level before observable symptoms arise.  The evidence further supports the genetic basis of ADHD.


Frontal lobe volume is smaller among cases of ADHD.  Brain regions involved in self regulation can be differentiated from those of controls in that the frontal lobes or subregions of the lobes are consistently smaller in the ADHD cases.


Various regions of the basal ganglia have been reported to be smaller in children with ADHD.  It appears that the children concerned start off with smaller volume of basal ganglia, particularly the caudate nucleus, although differences may be less evident over time.


Right hemisphere structures are more affected than those on the left.

In normally developing individuals, the right frontal area is larger than the left frontal area; and given  the significance of the right hemisphere in regulating attention, a reduction in size here would have been anticipated among cases of ADHD.  This finding has been made in a number of studies, albeit not consistently.


The cerebellum shows a relative decrease in size, and this becomes significant given the role played by the cerebellum in regulating executive functions and given its reciprocal connections to the prefrontal cortex.


It is emphasised that these reductions in various brain areas are not the result of psychostimulant treatment since the findings were equally observable among children with ADHD who had not been given any such treatment.


In summary, the author highlights the small but significant changes in brain volume among children with ADHD, notably the brain regions associated with the regulation of attention and other executive functions.  The implication is that the behaviours seen in children with ADHD reflect a real dysfunction, and are not the result of environmental circumstances nor linked to some distortion of judgement on the part of teachers or parents.


This conclusion is supported by evidence emerging from functional neuro-imaging studies which have revealed anomalies in the working of the prefrontal-subcortical system, particularly in the right hemisphere.


One study of adolescent girls with ADHD showed that cerebral glucose metabolism was 15% lower than in control girls, and nearly 20% lower than in boys with ADHD. The brain regions in which this lower activity was observed were the right frontal premotor cortex and right temporal cortex.

A study of adults with ADHD demonstrated that global cerebral glucose metabolism was reduced in females with ADHD, but not in men with ADHD or in controls. However, females with ADHD showed better performance on auditory attention tasks with increasing age.


Such evidence would suggest a complicated interaction between gender, hormonal effects, and age.


In a further study of adolescents, controlled for the effects of sexual maturation, the ADHD cases showed signs of a higher level of dopamine synthesis in the right midbrain compared to controls, with the implication that ADHD is associated with some dysfunction in the dopaminergic system.


Evidence goes on to highlight that, when children  are presented with tasks which place demands upon executive functions, those with ADHD show atypical patterns of brain activation.

Children with ADHD do not activate frontostriatal networks to the same extent as seen in control children, but demonstrate a more diffuse activation pattern suggesting that there is some delay in the development of neural connectivity in these areas.

Further, there is some evidence that children with ADHD activate frontal areas to a greater extent than controls, with the possible implication that tasks involving executive function place enhanced demands upon these children and that more effort has to be expended.


Some studies have identified decreased activity involving the temporal lobe and cerebellum in samples of children with ADHD, supporting the hypothesis that the dysfunction in ADHD involves not only the frontal-subcortical circuits, but also the integration of temporal lobe and cerebellar functions in emotion, cognition, and motor planning.


EEG studies among children with ADHD have revealed an excess of slow wave activity consistent with decreased alertness and underarousal.

However, it is held that, even with some clear differences between EEG patterns of children with ADHD and controls, the heterogeneity among the AHD samples limits the diagnostic significance of findings in this area.


In any event, the EEG patterns suggest reduced cortical differentiation and neurological specialisation among the ADHD children, more prominently demonstrated in the children with the hyperactive/impulsive type than those with the inattentive type. 

Further, the children with the inattentive type of ADHD were found commonly to show two different EEG patterns … one consistent with underarousal, reflecting the “sluggish” type, and one consistent with a maturational lag.


Here, too, the summary suggests that electrophysiological studies of children with ADHD indicate atypical brain wave patterns, suggesting dysregulation of arousal and attention.


Causal Pathways


Voeller notes from converging evidence that ADHD is a highly heritable condition; but it can also be “acquired”.  Some individuals have a combination of genetic and acquired ADHD. 


In the majority of cases, ADHD is of familial origin, with evidence indicating that parents with ADHD have a greater than 50% chance of producing a child similarly affected; and about 25% of children with ADHD have parents who meet the formal diagnostic criteria for ADHD.  Twin studies estimate the heritability of ADHD at around 80%.


The condition can be categorised as a disorder of neurotransmitter functions, particularly in respect of the operation of the transmitter substances dopamine and norepinephrine. 
Dopamine is seen as crucial in the regulation of learning, as well as maintaining appropriate learned responses and goal-directed/motivated behaviours.  It is also implicated in working memory, and in responsiveness to external cues. 

The operation is principally within prefrontal and temporal cortices

Norepinephrine (noradrenaline) is involved in maintaining attention and alertness. The norepinephrine neurons are triggered by novel and significant stimuli.


Psychostimulant medication that increases the amount of central dopamine and norepinephrine is a common and effective method of intervention.


Behaviours typical of ADHD can also arise from environmental factors that interfere with normal brain growth, whether at a pre-natal, peri-natal, or post-natal stage.


One example of an environmental factor is foetal alcohol syndrome which is linked with subsequent inattention, hyperactivity, and impulsivity, and is linked with a reduction in the volume of the child’s prefrontal and temporal cortices … those areas linked to the regulation of attention and impulse control.


Maternal smoking has also been linked to ADHD.


It has been found that the dopamine system is highly sensitive to hypoxia, particularly at the pre-natal or neonatal stages of life, so that any events which disrupt the flow of blood and oxygen to the brain might be implicated in later symptoms of ADHD.

Iron deficiency has also been associated with deficits in dopamine functioning.


Jaundice in the neonatal period can evolve into symptoms of an ADHD type later in childhood, possibly because of an impact upon the functioning of the basal ganglia areas of the brain.


Any injury to the brain that involves the prefrontal and subcortical circuits can result in ADHD signs and symptoms.  Similarly, the impact of strokes which have an impact upon these brain areas can have these effects.

The longer term outcomes of meningitis and encephalitis, and autoimmune disorders,  are also associated with ADHD-like behaviours.


The author emphasises that the role of environmental factors should never be underestimated.  Early deprivation can result in ADHD symptoms in later childhood; and children who grow up in disorganised or chaotic circumstances do, themselves, show frequent problems in regulating attention, impulsivity, and emotionality.

The risk of ADHD is proportional to the number of adverse factors which are present.




Voeller organises the description of treatment approaches according to a series of principles ………


Principle 1

The treatment of ADHD involves the selection of an appropriate medication at an appropriate dose, in combination with behaviour therapy.


The implication is that medication alone does not cure the condition but provides an opportunity to establish consistent behavioural approaches.

Evidence demonstrates that the combination of medication and behavioural management is associated with a better longer-term outcome than medication alone or than behavioural approaches alone.


What are seen as significant elements of the behavioural management include …


What seems to matter is consistency over time and between the adults concerned, so that the child can recognise the link between his/her behaviours and the outcomes.


Principle 2

Adequate behavioural management requires intensive and prolonged parental involvement and cooperation with the teacher(s).


It is recognised that appropriate management of the child and positive long-term outcomes do require a great deal of parental time and energy in order to ensure a very high degree of structure and consistency.


Voeller suggest that the parents’ task is to take over the role of an “additional frontal lobe” in that they must learn how to recognise incipient problems and develop a tactful approach for managing them.


The example is given of the typical situation where a child does not get organised for school in the morning but gets side-tracked or simply delays events, putting pressure on the rest of the family.  The parental responsibility would include getting the child up that little bit earlier and checking that medication is taken, while monitoring the child’s progress in getting dressed.  There will have been time set aside the evening before to have books and other school materials ready to take to school. 
A consistent time for bed and a bed-time routine would also help to have the child  more calm and ready for sleep.


It is recognised that, while it may be unavoidable, having the child spend time in a range of environments … school … after-school club … child-minder … etc … can be disorganising for the child; and there is the further problem that the parents may well have some ADHD-type difficulties of their own which can decrease their capacity to set and stick to routines (with the implication that the parents may need direct support or intervention for themselves if they are to help their own children through setting routines and establishing a system of rewards for specific targeted behaviours).


Principle 3

Treatment of ADHD is not the same as treating a learning disorder. 

The two areas of difficulty may go together but the successful management of the ADHD symptoms are only the first element; there is also a need to provide support for the child in terms of identifying the nature of the learning problems and in providing consistent remediation.


Principle 4

Basic issues like ensuring that the child eats properly, gets enough sleep, and takes a reasonable amount of exercise are important parts of the overall intervention. 

The author emphasises the matter of (vigorous) exercise given not only the general health benefits but also because appropriate arousal is enhanced . 

A simple implication is that of avoiding long periods of sedentary working but allowing the child to move around after completing elements of a task.


Principle 5

Children should be encouraged to develop self awareness and enhanced autonomy.

Sharing with the children some information about the nature of ADHD in tangible terms can be helpful.  Discussion in general or vague terms is probably not very helpful.

This tangible issue, such as “not keeping track of your homework”,  can then be linked to some specific action or system agreed between teacher/parent/child by which to tackle it.

To talk in terms of “trying harder” is not very useful if the child does not have specific examples of what (s)he actually has to do to meet some given target.


Principle 6

The child can be helped to monitor his/her own behaviour when the target behaviours are clearly identified, and simple reminders or signals may be sufficient to keep attention focused.

Rewarding compliance to routines is more effective than punishing non-compliance, with the role of parent or teacher that of offering reminders to compensate for the child’s difficulty in anticipating events or making plans.


Principle 7

Teacher involvement is crucial. 

The situation is unlikely to be shifted positively if there is not regular feedback from the teacher; and ideally, the child should be able to see daily contact between home and school.  Parents and teachers can thus collaborate on particular targets and share the organisation of rewards for positive outcomes.


                            *          *          *          *          *          *


Diet and Symptoms of Learning or Behavioural Difficulty


It appears that what children eat has become a major issue once again … perhaps a function of the publicity surrounding what has been, compared to what should be, included within typical school lunches.


Dr. John Briffa (2005) has contributed a lengthy review article about what should be included in a healthy diet, and what should be avoided, and he concluded with a summary of how one might alleviate symptoms of ADHD.

The main points were as follows :


Demonstrating again the current interest in this field, a further article in the national press (Lawrence 2005) has highlighted a study linking deficiencies in vital nutrients with atypical brain functioning.


The evidence, produced by researchers at Oxford and based upon properly controlled and double-blind studies, has indicated that underachieving children (among whom there was also an element of disruptiveness) showed clear improvements in their functioning when given dietary supplements containing fish oils rich in omega-3 fatty acids .. which may be lacking in typical diets involving processed foods.


A significant proportion of he target sample of 5 to 12 year old children (normal ability, but underachieving and showing symptoms of dyspraxia which is commonly comorbid with ADHD and dyslexia) were shown to make dramatic improvements in literacy following the use of the supplements.  A control group, given a placebo substance, did not make this same progress.

The experimental group were differentiated from the control group by the mean 9 or 10 months’ improvement in reading and spelling ages over the three month period that was associated with the use of supplements … with the control group making improvements in literacy scores of just 3 months.

However, when the control children were switched from a placebo to the omega-3 supplements, they too made marked shifts in their rate of progress.  


The children who had shown symptoms indicative of ADHD no longer showed these symptoms after the 3-month usage of fish oils.


The lead researcher (Alexandra Richardson) concluded that food does indeed affect behaviour, and that dietary intervention could make a significant difference.


                                *          *          *          *          *          *




M.J.Connor                                                                                                May 2005




Briffa J.  2005   Doctor’s orders.  In “Hungry for Attention”  (By-Line Andrew Purvis) Sunday Observer  April 25th


Lawrence F.  2005   Children’s diet link to disorders.  Guardian 2nd May 2005.  Summary of the article by Richardson et al published in the May edition of the American journal “Pediatrics”


Voeller K.  2004   Attention deficit hyperactivity disorder (ADHD).   Journal of Child Neurology  19(10)  798-814


(nb   The above is a review article and makes many references to existing research studies.  The full set of references can be obtained from the present writer – MJC)


This article is reproduced by kind permission of the author.

© Mike Connor 2005.

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