A.D.H.S. Anhang 8
http://ir.dut.ac.za/bitstream/handle/10321/35/Lottering_2006.pdf?sequence=26&isAllowed=y
[John-John Brian Lottering theories for ADHS]
The relative efficacy of Advanced Brain Food® and a Homeopathic Complex
(Quietude®
in the management of Attention Deficit Hyperactivity Disorder (ADHD) in
males between the ages of 8 and 13 years.
ADD/ADHD is one of the most commonly diagnosed disorders of childhood
development (Kendall and Hammen, 1995; Venter, 1996).
It is believed to affect between 3 - 5% of all children of school age
and although it also affects adults and adolescents, the figures here are not
available (DSM-IV, 1994).
The values for females are often under reported due to the fact that
they go undiagnosed as their symptoms are attributed to emotional problems
common in young girls (Kendall and Hammen, 1995/Berkow et al. 1992) and they
are less aggressive and active than boys, which makes them less noticeable
(Picton, 1997).
The diverse and conflicting opinions about ADHD have resulted in
confusion for families, care providers, educators and policy makers (NIH
Consensus Statement, 1998).
The controversy raises questions concerning the literal existence of
this disorder, whether it can be reliably diagnosed and, if treated, what
interventions are most effective (NIH Consensus Statement, 1998/American
Psychiatric Association, 1994).
ADD/ADHD characterised predominantly by developmental inappropriate
inattention +/o. impulsivity and/or hyperactivity (Woods and Ploof, 1997).
Children with ADD/ADHD usually have functional impairment across
multiple settings including their home, school and peer relationships (NIH
Consensus Statement, 1998/Breggin, 2003).
The symptoms characteristic of this disorder namely hyperactivity, short
attention span and impulsiveness are thought to suggest central nervous system
involvement (Castellanos et al. 1996/DSM-V, 1994).
Diagnosis is a problem as it has been shown that many children are not
identified or otherwise falsely identified by their paediatrician or doctor for
a number of reasons (Breggin, 2003/Richardson, Hamley and Sassone, 2000).
Testing of children is often limited and not comprehensive enough, case
histories may not be detailed enough and often the influence of a teacher or
school is enough to encourage a doctor to prescribe stimulant medication (NIH
Consensus Statement, 1998; Picton, 1997/Oltmanns
and Emerly, 1995). The most commonly used diagnostic method is from the
Diagnostic and Statistical Manual-IV (1994).
Attention Deficit Hyperactivity Disorder is a heterogeneous behavioural
disorder with multiple possible aetiologies.
These may be classified into the following causations: environmental
factors, central nervous system (CNS) insult, genetic origins and,
neurochemical/neuroanatomical factors (Goldman, 1998).
2.2.1
Neuroatomic
The brain consists of modules specialised for processing specific
data. These modules are autonomous to a
degree in both function and neural representation (Frei et al. 2001).
The outermost layer of the brain represents the cerebral cortex. The cortical (frontal) section of the brain
is related to learning and thinking.
The layer underneath, the sub-cortex, comprises a relay system that is
involved in sending messages to the processing and memory parts of the brain
(Rapoport, 1995)
This sub-cortical system consists of the brain stem‘s reticular
activating system, thalamus, hypothalamus and basal ganglia (Guyton,
1989/Rapoport, 1995).
Laufer et al. (1957), who proposed that the symptoms of ADHD were caused
by ―diencephalic dysfunction, reported the first anatomical-based
hypothesis for the cause of hyper-kinesis.
Recent research suggests that ADHD children generally have impaired
functioning in the cortical and subcortical areas (Hynd et al. 1993). In particular, frontal lobe and prefrontal
lobe dysfunction have been suggested (Hynd et al. 1991).
Anatomic neuro-imaging studies are converging in revealing differences
in children with ADHD, compared to age-matched controls (Castellanos, 2000;
Greenhill et al. 2002).
ADHD children notably have a smaller brain volume (4% decrease from
normal), as well as a smaller caudate nucleus, globus pallidus, anterior
frontal cortex and sub-region of the cerebellar vermis (Castellanos,
2000). These volumetric differences
appear early and are not secondary to stimulant medication.
In the early 1990s, many functional imaging techniques were used in a variety
of clinical settings to image the brains of ADHD patients in comparison to
normal control subjects.
Swanson et al. (1998) integrated the findings across multiple studies
and calculated the standardised effective size.
It was found that there is a consistent moderate reduction of about 10%
of the size in healthy controls in the frontal lobes (dorsolateral prefrontal
cortex and anterior cingulate), basal ganglia (caudate nucleus and globus
pallidus), and some regions of the corpus callosum (rostrum and splenium),
which link frontal and parietal brain regions (Swanson et al. 1998/Castellanos,
2000).
A recent study done by the National Institute of Mental Health found
that three structures in the right brain-prefrontal cortex, caudate nucleus and
globus pallidus were affected by ADHD (Castellanos, 2000).
These areas were smaller than those of children without ADHD, thus ADHD
is thought to be rooted in an inability to inhibit thoughts.
Furthermore, ADHD children exhibit smaller frontal lobes and less
activity in the striatum, which is a major dopamine-rich supply for the frontal
lobes (Castellanos, 2000).
The majority of ADHD children exhibit decreased perfusion in the
pre-frontal cortex with intellectual stress (Amen et al. 1997).
Brain scans have identified a clear-cut chemical abnormality in people
with attention deficit-hyperactivity disorder, a problem that makes life
difficult for an estimated 3 to 5% of US school children
scientists say (New York Times Syndicate - December 16, 1999).
With the development of imaging and isotope scanning techniques, studies
of anatomy and glucose metabolism of ADHD children have been made possible
(Swanson et al. 1998).
Positron emission tomography (PET) scan studies have shown reduced brain
glucose utilisation, particularly as related to the right frontal lobe, in ADHD
children (Zametkin and Rapoport, 1987).
Furthermore, ADHD children show decreased blood flow in the frontal
lobes (Hynd et al. 1993).
In a recent study, it was shown that the rate at which the brain uses
glucose, its main energy source, is lower in subjects with ADHD than in
subjects without ADHD (Zametkin et al. 1990).
Analysis of electroencephalograms (EEGS) of boys with ADHD has found
increased slow-wave activity in the frontal regions (Hynd et al. 1991).
Although this research suggests frontal lobe dysfunction, some
researchers believe the neurological basis for ADHD should not be limited to
frontal immaturity or abnormality (Baizier, 2001). They believe ADHD is related
to more widespread dysfunction in the brain (Benson, 1991).
These results suggest that ADHD may have an organic basis and that
dysfunction can be localised to cortical and striatal regions in the brain
(Woods and Ploof, 1997; Castellanos 2000).
2.2.2
Neurochemical hypotheses are based on the effects of neurotransmitters
(Zametkin et al. 1990).
These are chemicals that relay messages from one neuron to another
through synapses (Castellanos, 2000).
The neurotransmitters that function within the attentional system are
the catecholamines, which function in the neural circuits that control
motivation and motor behaviours, including activity level, restlessness, and
responsivity (Ballard et al. 1997).
The neurochemical theories postulate that behaviours seen in ADHD are
due to a dysfunction in the neurotransmitter system.
Supporting this theory is the beneficial effect that certain
medications, which have a direct effect on the neurotransmitters in the body,
have on the disorder (Bazier, 2001).
ADHD is a neurobiological disorder with anatomic and functional
impairments in the brain, leading to monoamine dysregulation and frontostriatal
alterations in neural circuitry (Herscu, 1995).
There is strong evidence that the catecholamines, dopamine and
norepinephrine are important in the pathophysiology of ADHD (Castellanos,
2000).
Dysfunction of dopaminergic and noradrenergic systems are constantly
implicated in ADHD (Baizier, 2001; Holford, 2001).
Dopamine and norepinephrine are important neuromechanisms governing focused
attention (Castellanos, 2002).
2.2.2.1
Dopamine is a neurotransmitter in the
catecholamine family that functions in the brain. Hypothesis is based on an
animal model of hyperactivity, biochemical and on clinical pharmacological
studies with ADHD subjects (Castellanos, 2000/Smalley et al. 2000/Zametkin and
Rapoport, 1987).
Some evidence suggests there is a reduction in cerebral turnover of
dopamine and decreased dopamine activity (dopaminergic dysfunction) within the
brain of an ADD and hyperactive subject (Smalley et al. 2000).
The models of dopaminergic dysfunction cannot account for the findings
that dopamine agonists have not proven efficacious when compared to stimulant
treatments, nor have dopamine-blocking agents been deleterious (Zametkin and
Rapoport, 1987).
More recent studies reveal that hyperactivity and possible poor motor
impulse control, in ADHD may result from excess dopaminergic activity in the
striatum +/o. nucleus accumbens (Castellanos et al. 1996).
According to Harvard Medical School, current research strongly suggests
that ADHD is caused in part by a deficiency of norepinephrine in the ascending
reticular activating system, and is thought that stimulant medications, such as
Ritalin®, increase the levels of norepinephrine in that part of the brain, as
well as probably increasing dopamine levels in the frontal lobes (Breggin,
2000; Rapoport, 1995).
Recent reports suggest that DNA variants of the dopamine D4 receptor
gene are associated with the personality trait of Attention Deficit
Hyperactivity Disorder (Paterson, 1999).
Boys with a low dopamine D4 receptor gene concentration exhibit
significantly more symptoms of ADD/ADHD than boys with normal dopamine D4
receptor genes (Castellanos, 2000).
Many dopamine agonists that stimulate postsynaptic dopamine receptors
have been given to patients and were ineffective.
The models of dopaminergic dysfunction cannot account for the findings
that dopamine agonists have not proved efficacious when compared to stimulant
treatments, nor have dopamine blocking agents been deleterious, unless other
hypotheses are put forth (Zametkin and Rapoport, 1987).
2.2.2.2
Serotonergic Theory
Although serotonin has been studied less thoroughly in the neurobiology
of ADHD, its role in the pathophysiology of this disorder has recently become
an area of intense investigation. Considerable evidence suggests a role for
this neurotransmitter in the aetiology of behavioural disorders characterised
by disinhibition including alcohol abuse, suicide, bulimia, antisocial
personality disorder, conduct disorder and aggression (Castellanos, 2000).
As ADHD is a behavioural disorder largely characterised by deficits in
inhibition and is a well-known precursor for many adult disorders of impulse
control, a role for 5-Hydroxytryptothan (5-HT) in ADHD has been
hypothesised.
Indeed, there is mounting evidence from both human and animal studies
that serotonergic neurotransmission is necessary for mediating several of the
behaviours present in ADHD (Schoenthaler et al. 1999).
A recent study of a mouse model of ADHD provided evidence which linked
serotonin to the control of hyperactive behaviour (Gainetdinov et al. 1999).
All of the studies done have used L-tryptophan, the amino acid precursor
to serotonin, and Fenfluramine®, an appetite suppressant that acutely increases
and then depletes brain serotonin (Zametkin and Rapoport, 1987).
No significant behavioural changes were seen in any of the ADHD patients
tested, decreasing the likelihood of the veracity truth of this hypothesis.
In conclusion, there is accumulating neurobiological evidence pointing
towards the role of the serotonin system in ADHD.
The strongest support from existing data suggests that serotonin is
responsible, at least in part, for mediating the hyperactive and impulsive
components of ADHD behaviour
(Hanna, Ornitz and Hariharan, 1996; Leary, 1994).
2.2.2.3
Noradrenergic Theory
Norepinephrine is another neurotransmitter in the catecholamine
family.
Kornetsky first proposed this hypothesis in 1970, stating that
amphetamine may act as an inhibitor of either norepinephrine synthesis or
turnover, or it may block the release
of norepinephrine in the over aroused organism.
This was hypothesised in response to the observations that amphetamine,
a sympathomimetic amine, causes a release of norepinephrine and most likely and
increase in the rate of turnover. Therefore, ADHD could result from an increase
in norepinephrine and amphetamine that may competitively bind to postsynaptic
norepinephrine receptors, reducing noradrenergic neuro-transmission (McGough
and McCracken, 2000).
Since then, studies have shown that some drugs, proven effective for
ADHD, actually alter noradrenergic turnover and may argue for a pathological
hyper-functioning of the noradrenergic system in ADHD subjects. Animal studies
have shown the opposite effects.
These studies lead to the hypothesis that animal hyperactivity is caused
by norepinephrine depletion (Zametkin and Rapoport, 1987).
2.2.2.4
Non-specific
Catecholamine Theory
Each of the specific neurotransmitter hypotheses above have led to
either inconclusive or disproving results (World Health Organization,
1999).
Therefore, since the stimulants used to treat ADHD affect multiple
transmitters, it was thought that perhaps a dysfunction in the catecholamine
neurotransmitters as a group was to blame (Amen et al. 1997/Castellanos et al.
1996).
A series of studies were performed using a group of drugs that also
affect multiple neurotransmitters.
They all had immediate and positive behavioural effects on children with
ADHD (Castellanos, 2000).
However, the close relationship between the transmitter systems affected
and the fact that so many were affected does not illustrate that one was more
important that any of the others. Clearly, though, the array of effective
agents has served to put to rest any single neurotransmitter hypothesis
(Castellanos, 2000/Zametkin and Rapoport, 1987).
2.2.2.5
The Hypoarousal Theory
Alertness and directed attention depends on the normal functioning of
the reticular activating system (RAS) in the brainstem. Incoming sensory
stimuli are filtered and sorted before neural impulses are - despatched to the
cerebral cortex. Stimuli not relevant to immediate functioning are at this
point blocked from conscious awareness (Holford, 2001).
It has been postulated that children with ADHD are continuously in a
state of hypo-arousal and are therefore unable to filter out irrelevant and
distracting sensory input from their external surroundings (Hanna, Ornitz and
Hariharan, 1996). Research has shown that ADHD children have significantly less
alpha activity on electroencephalogram (EEG) readings as compared to normal
peers (Castellanos et al. 1996/Zametkin et al. 1990).
Genetics
Goodman and Poillion (1991) have indicated that the majority of causes
of ADHD are attributable to organic problems.
Their research indicated that genetics is the only presumed cause of
ADHD; sited by 48% of the authors they investigated. However, no specific gene responsible for
ADHD has as yet been isolated. There is evidence
that ADHD-type behaviours tend to recur in families (in first- and
second-degree relatives of ADHD children (Barkley et al. 1990).
In a recent study, 55% of families presenting with an ADHD child had at
least one parent with a lifetime diagnosis of ADHD. The frequency of ADHD in at least one
parent was higher in families with at least one affected girl than in
families with only affected boys (Faraone, Biederman and Monuteaux,
2000/Smalley et al. 2000).
The gender sex difference in prevalence of ADHD is consistent in a model
of inheritance in which girls require a greater loading of family influences to
develop ADHD (Zametkin, 1995). The lack of familial clustering of ADHD suggests
that hyperactive and inattentive symptoms reflect common familial underpinnings
and not unique familial effects (Smalley et al. 2000).
A molecular genetic study suggests a possible relation to the D4
receptor gene (Levy, 1997). Increasing evidence suggests that ADHD is an
inherited condition.
If one identical twin has symptoms of ADHD, the other twin has a 75 -
91% chance of sharing the same trait (Swanson, Lerner and Williams, 1995).
Children who have ADHD are likely to have one close relative who also
has ADHD.
1/3 of all fathers who had ADHD when they were young have children who
have ADHD (Swanson, Lerner and Williams, 1995).
Adoption studies provide evidence of a genetic link to ADHD: biological
children of parents with ADHD have a far higher chance of having ADHD than
adoptive children of parents with ADHD (Cantwell, 1996; Levy, 1997).
The parents of children with ADHD show an increased incidence of
hyperkinesis, sociopathy, alcoholism and hysteria.
Monozygous twins are more alike than dizygous twins of same sex in
measures of hyperactivity and inattention. Concordance for ADHD has been found
to be much lower for half siblings than for full siblings, whether they are
brought up by their mothers or are fostered (Kaplan and Sadock, 1988/Leary,
1994). These findings indicate that there may be a genetic link to ADHD.
2.2.4
Congenital Factors
Retrospective accounts suggest numerous congenital factors may be
related to ADHD.
However, there is no compelling evidence for specificity of perinatal or
congenital factors (Cantwell and Hanna, 1989).
Maternal substance abuse during pregnancy may be associated with ADHD
(Engel et al, 1992). Substances such as
cocaine and nicotine may induce ADHD-related symptoms (Holford, 2000).
2.2.5
Familial Factors
These are very difficult to separate from genetic factors but the
concept of parent and child temperament may be important (Tannock, 1998).
Several studies suggest that interaction between parents and children
may lead to an exacerbation of predisposed attention deficit behaviour (Safer
and Malever, 1995).
Hyperactivity and poor impulse control can also occur in response to
significant familial stress. Children
who have experienced a divorce, a move, and a change in school or other significant
life events may display impulsive behaviour, forgetfulness and
absentmindedness, which may be misdiagnosed as ADHD (Holford, 2001; Safer and
Malever, 1995).
2.2.6
Parental Behaviour
Parents of ADHD children have often been shown to be unresponsive to the
child‘s demands. The child‘s hyperactivity may merely be an attempt to elicit a
response from the parent (Biederman, 1996).
2.2.7
Temperament
Children who have been active from birth are likely to remain so. The
child‘s temperament and personality play an important part in the development
of this ADHD (Biederman, 1996; Graham, 1986).
2.2.8
Central nervous system injury
2.2.8.1
Head Injury
One of the first theories was that minor head injuries or undetectable
damage to the brain (due to early infection or birth complications) caused all
attention disorders and learning disabilities. There has been no substantial
evidence for this theory and thus it was dismissed (Tannock,. 1998).
Subtle brain damage may be found in some children that may result from
circulatory, toxic, metabolic, or other disorders during critical periods of
prenatal development.
In the early years of life, trauma, fever or inflammation can also cause
subtle central nervous system (CNS) damage.
These stresses may cause a range of disorders such as cerebral palsy,
seizure disorder, and mental retardation (Woods and Ploof, 1997). The less
severe forms of damage
may produce a variety of learning disabilities including ADHD (Kaplan
and Sadock, 1988; Tannock, 1998).
2.2.8.2
Environmental risk factors
While ADHD behaviours may be precipitated by deleterious social factors,
with the exception of head injury occurring at a young age, there is no
evidence of a single environmental agent causing ADHD (Paterson, 1999).
2.2.9
Diet
Feingold advocated foods containing additives, colourants and
salicylates as the cause of ADHD in children (Feingold, 1973).
Although his diet has gained widespread popularity and offered an
accessible alternative to ADHD management, numerous controlled studies have not
yet validated his theory (Leary, 1994/Walker, 1983/Mattes and Gittelman, 1981).
Dietary supplements have been studied extensively over the last decade
to understand the efficacy of dietary supplements for improving the symptoms of
ADHD.
A number of these studies have found strong positive correlation between
the use of certain supplements and ADHD (Schoenthaler, 2000).
In 1982, a conference was held to discuss the theory of what effect a restricted
diet can have on the symptoms of ADHD.
The data showed that the restricted diet only helped five percent of
children with ADHD, and these were mostly young children or those with food
allergies (Schoenthaler, 2000).
2.2.9.1
Refined Sugar and Food Additives
A later theory on the causes of ADD or ADHD suggested refined sugar and
food additives attributed to making children hyperactive and inattentive
(Holford, 2001).
This theory however was dismissed after it was found that there was no
statistical validity for such a claim (Schoenthaler, 2000).
2.2.9.2
Colourants and Flavourings
The Lancet published a study in 1985, which reported that 79% of
hyperactive children improved when certain foods were eliminated from their diets,
only to become
worse again when the foods were reintroduced. Artificial colourings and
flavourings were the most serious culprits; sugar was also found to have a
noticeable effect.
Additives included: Artificial flavours and colour ants
Preservatives included: Butylated Hydroxyanisole (BHA) and Butylated
Hydroxytoluene (BHT).
Sugars included: Sucrose, Fructose, Corn syrup,
Mannitol, Sorbitol and other Sweeteners.
An experimental study done in New York confirmed that during a 4 year
period, after eliminating food additives and colourants from t he diet, there
was a marked increase
in academic performance in ADHD children (Schoenthaler et al. 1986).
2.2.10
Minerals
Vitamin and mineral deficiencies have been implicated in mental
performance (Muller, 1995).
Mineral status among those with ADHD has been the subject of several
published clinical trials.
ADHD children are deficient in certain minerals (Holford, 2000).
These deficiencies can affect both behaviour and school performance. The
effect of vitamin and mineral supplements on academic performance and
children's behavioural problems is well documented and although it currently
seems unlikely that ADHD is caused solely by nutrient deficiencies, addressing
such deficiencies can significantly improve ADHD symptoms (Holford, 2002;
Muller, 1995).
2.2.10.1
Magnesium Deficient Diets
Magnesium deficiency is the most common of the mineral deficiencies
associated with ADHD (Starobrat-Hermelin, 1998).
In one study, magnesium deficiency was identified in 95% of ADHD
children examined (Kozielec, 1997).
The conclusion from the investigations is that magnesium deficiency occurs
more frequently in children with ADHD than in healthy children.
Analysis of the material indicated a correlation between increasing levels
of magnesium and freedom from distractibility (Schoenthaler et al. 1998).
2.2.10.2
Iron Deficiency
Iron plays a role in the regulation of dopaminergic activity
(Schoenthaler and Bier, 2000).
The frequent occurrence of ̳restless
leg syndrome‘ in children with ADHD may be associated with iron deficiencies
(Sever et al. 1997). Some studies have
shown
a clear relationship between low iron status and ADHD symptoms (Benton,
Haller and Fordy, 1995).
2.2.10.3
Zinc is required for the conversion of essential fatty acids (EFA‘s) to
prostaglandins (Black, 1998). In a recent study it was shown that zinc
supplementation reduced the incidence of symptoms that with which ADHD children
might present with (Stevens et al. 1995).
2.2.11
Vitamin Status
The Vitamin B-complexes includes all of the known essential
water-soluble vitamins (except vitamin C), including thiamine (vitamin B1),
riboflavin (vitamin B2),
niacin (vitamin B3), pantothenic acid (vitamin B5), pyridoxine (vitamin
B6), biotin, folic acid and the cobalamins (vitamin B12).
For the management of ADHD symptoms, the B-vitamins work together in the
brain for the production of the various neurotransmitters (dopamine, serotonin,
5-Hydroxytryptophan (5-HTP) and norepinephrine (Holford, 2001).
2.2.11.1
Vitamin B3 (Niacin/Nicotinamide)
Vitam in B3 is part of the vitamin B complex, which is considered by
many to be the single most important set of factors needed for the body's
proper maintenance
of the nervous system, proper functioning of cells and energy metabolism
(Holford, 2002).
Niacin deficiency or imbalance plays a role in the symptoms of mood
disorders.
Observational and experimental studies have shown an association between
niacin and aggression, anxiety, ADHD, bipolar disorder and depression
(Strohle,2003).
Clinical research has demonstrated that vitamin B3 supplementation may
help to reduce peripheral breakdown of L-Tryptophan.
As a result, L-Tryptophan will not be used up for niacin production in
the peripheral parts of the body, thus allowing it to be transported into the
central nervous system
where it can be converted to serotonin (Holford, 2002).
It subsequently leads to an increased production of serotonin, a
deficiency of which might lead to ADHD (Chouinard et al. 1999).
2.2.11.2
Vitamin B5 (Pantothenic Acid)
Pantothenic acid is responsible for helping to synthesize a
neuro-chemical called Co-enzyme A (CoA) which combines with choline in the
brain to produce the neurotransmitter Acetylcholine (Castellanos, 2000).
Although supplementation with pantothenic acid has not been proven as a
treatment option for attention deficit disorder, it most definitely affects
production of the neurotransmitter acetylcholine that may play a role in the
development of ADD/ADHD (Holford, 2001).
In a recent clinical study involving older adults with cerebral
disorders researchers found evidence that increasing levels of choline by way
of supplementation helped to improve memory and cognitive function (Fioravanti
et al. 2004).
2.2.11.3
Vitamin B6 (Pyridoxine)
The main function of pyridoxine is to convert amino acids into
serotonin.
It forms an integral part in the metabolic pathway for the manufacture
of brain chemicals, and an imbalance that can cause symptoms such as depression
and ADHD
(Holford, 2001).
Vitamin B6 is an important coenzyme for the biosynthesis of
neurotransmitters. These neurotransmitters are required for optimal brain
functioning.
Researchers in Spain observed a clinical improvement in behaviour and
school performance when patients were supplemented with vitamin B 6 and folic
acid
(Fioravanti et al. 2004).
2.2.11.4
Vitamin B12 is essential for normal nervous system function and red
blood cell production.
Scientists at Baylor University Medical Centre reported that vitamin B
12 and folic acid deficiencies could alter neurotransmitter function and
contribute to neurologic and psychiatric pathologies (Fioravanti et al.
2004/Holford (2002) demonstrated that Vitamin B12 accelerates the learning
process and is important for the health of the brain cells.
2.2.11.5
Folic Acid
Folic acid has a protective function in the brain.
It protects the brain from chemicals like food additives and
preservatives additives (Holford, 2002).
2.2.12
Amino Acids
Assays of amino acid metabolism have generally revealed imbalances of
these essential nutrients in ADHD. Serum
amino acid levels as well as other nutrient cofactors may influence synthesis
pathways for certain inhibitory and excitatory neurotransmitters (Kolesnichenko
et al.1999).
Vitamin B6 is an important coenzyme for the biosynthesis of
neurotransmitters.
These neurotransmitters are required for optimal brain functioning.
Researchers in Spain observed a clinical improvement in behaviour and
school performance when patients were supplemented with vitamin B6 and folic
acid (Fioravanti et al. 2004).
2.2.11.4
Vitamin B12
Vitamin B12 is essential for normal nervous system function and red
blood cell production.
Scientists at Baylor University Medical Centre reported that vitamin B
12 and folic acid deficiencies could alter neurotransmitter function and
contribute to neurologic and psychiatric pathologies
(Fioravanti et al. 2004).
Holford (2002) demonstrated that Vitamin B12 accelerates the learning
process and is important for the health of the brain cells.
2.2.11.5
Folic Acid
Folic acid has a protective function in the brain.
It protects the brain from chemicals like food additives and
preservatives additives (Holford, 2002).
2.2.12
Amino Acids
Assays of amino acid metabolism have generally revealed imbalances of
these essential nutrients in ADHD. Serum
amino acid levels as well as other nutrient cofactors may influence synthesis
pathways for certain inhibitory and excitatory neurotransmitters (Kolesnichenko
et al. 1999).
Research in the area of amino acids and ADHD points to a defect in
metabolism o./+ synthesis of neurotransmitters.
Simply loading the amino acid precursors to neurotransmitters appears to
be of limited clinical effect, perhaps owing to the failure of such therapies
to address the und erlying errors of metabolism involved (Kolesnichenko et al.
1999).
2.2.13
Essential Fatty Acids (= EFA’s)
A deficiency in EFA‘s is being singled out by some as a cause of ADHD.
EFA‘s influence ADHD primarily in two ways: they influence gut
permeability and are needed for the proper development of brain tissue (Burgess
et al. 2000).
It is important to remember that a simple deficiency of EFA‘s due to
decreased/insufficient intake is unlikely (Holford, 2003). Studies have shown that in many cases the
child diagnosed with ADD/ADHD has siblings who are not affected, yet they
adhere to the same basic diet (Middle borough, 2001).
There are three postulated reasons given for this deficiency:
a) ADD/ADHD children could have an inherent intestinal problem which
leads to difficulty with absorption of EFA's.
A large-scale survey by the New York Institute for Childhood Development
found that these children may be incapable of absorbing carbohydrates
normally;, therefore a problem with fat absorption
would not be unlikely (Medical Hypothesis, 1981).
b) ADD/ADHD children could have a metabolic requirement for higher
levels of EFA's than normal due to a genetic difference (Medical Hypothesis,
1981;
They fail to give close attention to detail, their work tends to be
messy and they often make careless mistakes in schoolwork and other tasks.
ADHD individuals have great difficulty sustaining attention in tasks
often shifting from one incomplete activity to another (Berkow et al. 1992).
They are easily distracted by irrelevant stimuli and frequently
interrupt ongoing tasks to attend to trivial noises and events usually, and
easily, ignored by others (American Psychiatric Association, 1991).
Impulsivity manifests as impatience, difficulty in delaying responses,
frequently interrupting or intruding on others and making comments out of
turn.
They may grab things from others and touch things they are not supposed
to.
This picture often results in ADHD children being regarded as the -
classroom clown.
They engage in reckless activities with little consideration of possible
consequences (American Psychiatric Association, 1991).
They can exhibit overreaction to stress, have low frustration tolerance
with catastrophic reactions of rage and outbursts, which subject them to
continuous censure and rejection overtly or covertly (Breggin, 2001/Smith,
1983).
Hyperkinesis may be manifested by fidgetiness or squirming in one‘s
seat, by excessive running or climbing in situations where it is inappropriate,
or by talking excessively.
ADHD symptoms vary greatly with the individual‘s age and needs to be
cautiously diagnosed, especially in toddlers and preschoolers, in whom symptoms
can be variable and inconsistent (American Psychiatric Association, 1991).
Mood swings are common (Swanson, Lerner and Williams, 1995) and it is
estimated that up to 25% of ADHD children suffer from depression (Berkow et al.
1992).
Wong (1985) found that 40% of children with learning disabilities scored
in the depressed range on the Roberts Apperception Test for Children.
A study conducted in Los Angeles County over a three-year period found
that 50% of the children under the age of fifteen who committed suicide had
been identified as having a learning disability,
as compared to 5 – 8% in the general population (American Psychiatric
Association, 1994/Peck, 1985).
2.4
DIAGNOSIS OF ADHD
Attention-deficit hyperactivity disorder (ADHD) is a common,
heterogeneous disorder, conservatively estimated to affect 3% to 5% of
school-age children (American Psychiatric Association, 1994/Anderson et al.
1987/Shaffer et al. 1996).
Attention Deficit Disorder (ADD) or Attention Deficit Hyperactivity
Disorder (ADHD) is a collection of symptoms or criteria, rather than a true
diagnostic entity (Borak, 2002).
There are no laboratory tests or specific features that have been
established as diagnostic in the clinical assessment of ADHD (American
Psychiatric Association, 1991).
Although ADHD is more prevalent in boys than in girls, little doubt
exists that it is also an important cause of psychiatric disability in
girls.
While the exact prevalence of the disorder in females remains unclear it
may not be minor (American Psychiatric Association, 1991).
ADHD is a common psychiatric disorder that significantly hampers
psychosocial adaptation (Biederman, 1996/Tannock, 1998).
Precise guidelines and criteria for the clinical diagnosis of ADHD in
children are not universally accepted (Reichenburg-Ullman, 1996); this may
account for the large variances in ADHD statistics in different countries.
In a trainee survey on residents at seven Ohio paediatric programmes it
was found that 30% of children evaluated for ADHD were not given that diagnosis
(the majority were considered to have
behavioural problems due to family dysfunction (Stancin et al.1990).
Further confusing the picture is that the concern the child raises in a
social environment also varies according to family expectations and societal
attitudes (NIH Consensus Statement, 1998).
Health care providers, such as paediatricians or child psychologists can
diagnose ADHD with the help of standard guidelines from the American Academy of
Paediatrics (DSM–IV-TR, 2000).
The diagnosis involves gathering information from several sources,
including school, caregivers and parents.
The health care provider will consider how a child's behaviour compares
with that of other children the same age.
The primary ADHD signs are behavioural and an accurate diagnosis is best
made by an experienced health care professional.
Medical histories, school reports, rating scales, and checklists are
essential for diagnosis (Mathews, 2000).
Due to the lack of specific organic signs in ADHD, if a diagnosis is
made, it remains a clinical one (NIH Consensus Statement, 1998).
Examination
2.4.1.3
Physical Signs
Minor physical anomalies such as hypertelorism (developmental defect
characterised by an abnormally wide space between two organs or parts) (Glanze,
1986/Rapoport, 1995),
highly arched palate and low set ears, may occur at a higher rate than
in the general population (American Psychiatric Association, 1991).
Waldrop and Goering (1971) found an increased incidence of head
circumference out of the normal range in ADHD children. Also noted were higher rates of epicanthus
(vertical fold
of skin from upper eyelid), widely spaced eyes, curved 5th
finger, absence of ear lobes and widened spaces between the 1st and
2nd toes.
4.1.5
Soft Neurological Signs
On examination EEG abnormalities may be detected while
neuropsychological testing sometimes shows non-localised soft neurological
signs (minor neurological abnormalities) and
frontal lobe dysfunction (Sierles, 1993).
Neurological soft signs
(NSS) may be defined as minor abnormalities in the neurological
examination in the absence of other features of fixed or transient neurological
disorders (American Psychiatric Association, 1991).
Wender (1971) found an incidence of 50% of children suffering from ADHD
to exhibit soft neurological signs such as:
Visual perception impairment
Auditory perceptual impairment
Poor motor co-ordination
Mild reflex asymmetries
Poor balance
Clumsiness
Strabismus
Mild choreoform movements.
Neurological signs and minor physical anomalies cannot independently exclude
or confirm a diagnosis of ADHD (NIH Consensus Statement, 1998).
2.4.1.6
Diagnostic and Statistical Manual of Mental Disorders Criteria
The DSM-IV classification has grouped two main symptom categories,
firstly inattention and secondly hyperactivity/impulsiveness.
In each of the categories, six of the nine listed traits must be present
for at least six months to warrant a diagnosis of ADHD.
A)
1) Six (or more) of the following symptoms of inattention have persisted
for at least 6 months to a degree that is maladaptive and inconsistent with
developmental level:
Inattention
a) often fails to give close attention to details or makes mistakes in
schoolwork, work or other activities
b) often has difficulty sustaining attention in tasks or play activities
c) often does not seem to listen when spoken to directly
d) often does not follow through on instructions and fails to finish
schoolwork, chores, or duties in the workplace (not due to oppositional
behaviour or failure to understand instructions)
e) often has difficulty organising tasks and activities
f) often avoids, dislikes, or is reluctant to engage in tasks that
require sustained mental effort (such as schoolwork or homework)
g) often loses things necessary for tasks or activities (e.g. toys,
school assignments, pencils, books or tools)
A)
2) Six (or more) of the following symptoms of hyperactivity-impulsivity
have persisted for at least 6 months to a degree that is maladaptive and
inconsistent with developmental evel.
Hyperactivity
a) often fidgets with hands or feet or squirms in seat
b) often leaves seat in classroom or in other situations in which
remaining seated is expected
c) often runs about or climbs excessively in situations in which it is
inappropriate (adolescents or adults, may be limited to subjective feelings of
restlessness)
d) often has difficulty playing or engaging in leisure activities
quietly and is often "on the go"
e) often acts as if "driven by a motor"
f) often talks excessively
Impulsivity
g) often blurts out answers before questions have been completed
h) often has difficulty awaiting turn
i) often interrupts or intrudes on others (e.g. butts into conversations
or games)
B)
Some hyperactive-impulsive or inattentive symptoms that caused impairment
were present before age 7 years.
Formatted:
Bullets and Numbering
C)
Some impairment from the symptoms is present in two or more settings
(e.g. at school [or work] and at home).
D) There must be clear evidence of clinically significant impairment in
social, academic, or occupational functioning.
E) The symptoms do not occur exclusively during the course of a
Pervasive Developmental Disorder, Schizophrenia, or other Psychotic Disorder
and are not better accounted for by
another mental disorder (e.g. Mood Disorder, Anxiety Disorder,
Dissociative Disorder, or a Personality Disorder).
Because the criteria require symptoms to be present for at least six
months in multiple settings, diagnosis of ADHD is not possible at a clinical
visit, yet medical doctors promote the
idea of office diagnosis (Patricelli, 1994).
Because of the unreliability and subjectivity of measurement tools, no
single objective measure can diagnose ADHD (McBurnett, Lahey and Pfiffner,
1993).
Assessment should include a network of parents and professionals using
multiple methods in multiple situations, along with a thorough review of school
records (Hunt, 1988; McKinney,
Montague and Hocutt, 1993).
Assessment instruments should be used to detect learning disabilities
and emotional-behavioural disorders, which can co-occur with ADHD (McKinney,
Montague and Hocutt, 1993).
Likewise, testing must include sensitivity to other DSM-IV disorders
which may co-occur with ADHD, preclude a diagnosis of ADHD, or which need to be
considered as alternative
explanations before a diagnosis of ADHD is made (DSM-IV).
2.4.1.7
Assessment Scales for ADHD Diagnosis
There are a number of assessment scales used to diagnose ADHD and
measure the effectiveness of ADHD therapies such as the Conner's/CADS Scale,
the Swanson, Kotkin, Atkins,
M-Flynn, and Pelham (SKAMP) scale, and Clinical Global Impression
(CGI-I) scales.
2.4.1.7.1
Conner‘s/CADS Scale
Various Conner Rating Scales Revised (CRS-R)
versions offer flexible administration options while also providing the
ability to collect varying perspectives on a child‘s behaviour from parents,
teachers, caregivers and the child or
adolescent (NIH Consensus Statement, 1998).
There are three versions -parent, teacher and adolescent self-report-
all of which also have a short and long form available. In addition, there are
three screening tools that offer
the option of administering a 12-item ADHD Index or the 18-item DSM-IV
Symptom Checklist or both.
These instruments also offer versions for parents, teachers, and
adolescents.
Two formats are included for self-report ratings and observer
ratings.
Both the self-report and observer forms provide multimodal assessments
of the same behaviours and problems and contain an identical set of scales,
sub-scales and indexes.
Conner‘s Abbreviated Assessment Rating Scale (CAARS) forms are available
in long, short, and screening versions.
2.5
DD:
Attentional difficulties and excessive motor activity are non-specific
responses of the organism that can commonly be seen in completely unrelated
disorders (Breggin, 2000).
The most common cause of these two symptoms in children can be anxiety
or depression (Kaplan and Sadock, 1988/Tannock, 1998).
Attention Deficit Hyperactivity Disorder (ADHD), sometimes inaccurately
referred to as ADD (there is no clinical term by this name) is a disorder
usually first diagnosed in
infancy, childhood or adolescence (American Psychiatric Association,
1994/Holford, 2001/NIH Consensus Statement, 1998).
There are 4 recogniszed types of ADHD.
They are:
I. Predominantly Inattentive type;
II. Predominantly Hyperactive-Impulsive type;
III. Combined type (inattention and hyperactivity-impulsivity);
IV. ADHD- Not Otherwise Specified.
There is a high level of correlation between children with ADHD and
other psychiatric illnesses. This
includes illnesses ranging from behavioural, mood, family, anxiety, cognitive,
social to school functioning, with the greatest increase in those with
the ADHD combined subtype (Fletcher, 1999).
ADHD needs to be distinguished from other learning disabilities such as
environmentally based underachievement (e.g. children with anxiety, phobias,
depression or other
psychiatric functional disorders) and mental retardation with uniform
and broad deficiency in academic performance (American Psychiatric Association,
1991).
When an impulsive, inattentive and hyperactive child also exhibits
considerable aggressive and antisocial behaviour, differentiation between conduct
disorder and ADHD may be
difficult (NIH Consensus Statement, 1998).
Following is a brief outline of possible differential diagnosis‘s
(Biederman, 1991):
Epidemiology: Associated Conditions
A.
Language and Learning Disability (10 - 15%)
Usually less hyperactive and more inattention
B.
Tourette's Syndrome
(70% with tics have ADHD)
C.
Oppositional Defiant Disorder (33% of ADHD patients)
D.
Conduct Disorder (25 - 50% of ADHD patients)
E.
Major Depression (20% of ADHD patients)
F.
Anxiety Disorder (25% of ADHD patients) should not be diagnosed if
presenting symptoms are better accounted for by other mental disorders such as:
Mood disorder
Anxiety disorder
Dissociative disorder
Personality disorder
Personality change due to general medication
Substance related disorders
Oppositional behaviour (American Psychiatric Association, 1991)
A misdiagnosis can easily be made in cases of suspected ADHD.
This has practical consequences because treatment with psychostimulants
is contraindicated in most of the above mentioned disorders (Bazier,
2001/Breggin, 1999/Kaplan and Sadock, 1985).
Webb and Latimer (1993) discuss another condition which can complicate
ADHD diagnosis: Giftedness.
Traits of gifted children which may lead to false ADHD diagnosis include
off task behaviour, less need for sleep, questioning of rules and traditions,
power struggles and resistance to repetitive tasks.
2.6
EVALUATION OF TREATMENT
Once a child has been diagnosed with ADHD, and the appropriate dose
level for the prescribed drug has been identified, continued monitoring of
response to treatment is essential. Several questionnaires
used in the initial evaluation can be completed regularly by the parent
and teacher of the ADHD child to establish the degree of change in hyperactive behaviours
(NIH Consensus Statement, 1998).
In addition to this, the child on the medication should have a follow-up
clinical examination every 6 - 8 months.
During this time height, weight, blood pressure, and heart rate should
be recorded to determine potential side effects (Biederman, 1996).
2.7
MANAGEMENT
Current management of ADHD is multifactorial, often involving
medication, behavioural counselling and dietary control.
For some children behavioural modification and educational support is
sufficient. Some children require only
one form of therapy to improve while others respond with a combination of
therapies.
In some instances the parents of ADHD children can attend parent
counselling. This supports the theory
that ADHD is multifactorial (Breggin, 2000/Holford, 2001).
Cerebral stimulants are the most widely used drugs for the management of
ADHD.
However, the results of several long-term follow-up studies have
indicated minimal improvement beyond those obtained at the onset of treatment
(Biederman, 1991/Breggin,1998).
It is still unclear whether stimulants do in fact improve long-term
academic achievement (Breggin, 1999).
Children with ADHD do not outgrow their problems.
Therefore, long-term use of stimulants is often required needed, while
of which the effects are limited in scope as well as in time (Whalen and
Henker, 1991).
2.7.1
Behavioural Modification
Behaviour modification is a technique used to modify behavioural
patterns in children with ADHD.
According to Green and Chee (1997), the basic law of behaviour
modification states:
"A behaviour which pays off for the child will be repeated - a
behaviour that brings no advantage to the child will disappear.
This means that if the right behaviour is rewarded, it should happen
more frequently, while ignoring what is undesired means it should disappear
(Green and Chee 1997).
The key concepts of behaviour modification in the management of ADHD are
immediacy and consistency in as many areas of the child's environment as
possible (home, school and if possible,
during leisure activities) (Woods and Ploof, 1997).
These concepts must be present in all forms of behaviour
modification.
As with other skills, consistency and immediacy need to be practiced and
reinforced before they become automatic (Woods and Ploof, 1997).
The secret of behaviour modification is reinforcement with small,
frequent rewards (Green and Chee, 1997).
To encourage the best behaviour, hard, soft or cumulative rewards can be
used.
A hard reward is something tangible such as money, food or a special
privilege.
Soft rewards are praise, enthusiasm or a show of parental pride.
Cumulative refers to the collection of stars, stamps or tokens, each
given for a small period of good behaviour, and eventually adding up to a major
prize (Green & Chee, 1997).
As the child learns acceptable behaviour, so the rewards should be
gradually decreased (Warner-Rogers, 1998).
Parents and teachers need to initially give material rewards, along with
praise, to reinforce appropriate behaviour and subsequently they may use praise
alone to maintain the behaviour (Green and
Chee, 1997/Warner-Rogers, 1998).
Therefore rewarding positive behaviours not only reinforces that
behaviour but also provides the child with desperately needed success, which in
turn builds their self-esteem (Green and Chee, 1997).
The basic strategies for parenting a child with ADHD include:
a) providing a high degree of positive attention and consequently no
complaining about bad behaviour
b) developing clear, concise and consistent expectations for behaviour;
c) utilising non-physical negative consequences for problem behaviours
in a non-punitive fashion (Warner-Rogers, 1998).
A disorganised, unstable home environment can promote the development of
symptoms more readily than one that is more structured and stable (Green and
Chee, 1997).
If the parents can learn to become more organised and structured at
home, the child with mild symptoms may make gains without medication.
The need for structure is substantially more important in the ADHD child
who likes to have a fixed framework to direct their day.
They wake at a certain time, put their pyjamas under their pillow,
straighten the duvet, get dressed, have breakfast, etc.
If their equilibrium is thrown by anything different their ADHD symptoms
may worsen (Green and Chee, 1997).
Parents need to understand that the lack of a structured front within
the home will only exacerbate the child's difficulties due, for example, to the
obvious failure to provide needed
consistency (Green & Chee, 1997/Woods and Ploof, 1997).
An important aspect of behaviour modification is in communication.
Parents and teachers are advised to be very direct and explicit in
communicating directions and feedback.
They should make eye-to-eye contact, use a clear, distinct voice and use
simple terms.
This is often the only way to maintain the child's attention while
relating significant information (Green and Chee, 1997/Woods and Ploof, 1997).
Parents and teachers are advised to exaggerate the level of praise for
the child's behaviour even in academic tasks (Green and Chee, 1997/Woods and
Ploof, 1997).
This is accomplished through the use of exaggerated facial expressions,
gestures and an emotional tone of voice.
The benefits of an exaggerated praise approach are twofold.
First, it might help to activate the reinforcement systems of the
brain.
Secondly, ADHD children have an almost constant need for personal attention
because of the failure of their own reward and punishment systems, leaving them
with an intense awareness of an
internal emptiness that can only be relieved through the overt
expression of feeling from others (Green and Chee, 1997/Woods and Ploof, 1997).
2.7.2
Psychosocial Treatments
Ness and Price (1990) believe that "the best non-medical
interventions (for ADHD) are practical, common sense adjustments to an
impulsive and disorganised style.
They also go on to state that those suffering from ADHD will be more
frustrated, apathetic and pessimistic than others about psychosocial
treatments, decreasing the probability of success.
Thus, the important first step in the treatment of a person with a
learning disability is the gaining acquisition of their participation, and
helping them to becoming active participants in their treatment.
Two of the first obstacles that must be overcame initially in order to
do this are the common feelings of denial and under-confidence (Ness and Price,
1990).
According to Barton and Fuhrman (1994), the four problems that are
brought into the therapeutic setting by the ADHD client are stress and anxiety
resulting from struggles to meet life's demands,
low self-esteem, and feelings of incompetence, grief over lack of accomplishments
and helplessness.
Another factor that can be added here is social skills.
Up to 20% of children and adults with ADHD will not respond to
medications, and many more will experience only partial remission of their
symptoms.
Additionally, a significant portion of the impairment from ADHD comes
from or its secondary impact on self-esteem and social skills deficits.
These are the targets of psychotherapeutic interventions (Clinical
Practice Guideline, 2001).
2.7.3
Occupational Therapy
Another intervention that forms part of the multidisciplinary approach
to ADHD is the work of occupational therapy.
The occupational therapist works on the child's sensorimotor skills
through the use of tactile, kinaesthetic, motor planning and motor accuracy skills
as well as verbal and visual cues (Kleinman and
Stalcup, 1991).
This may include such simple skills as tying shoelaces, throwing a ball
straight, catching a ball or moving smoothly (Green and Chee, 1997).
Their visual perception is targeted through the use of figure-ground
discrimination, parts-to-whole-relationships and spatial relationships.
Their cognitive skills are enhanced with sequencing skills, number
concepts and measuring skills (Kleinman and Stalcup, 1991).
Many ADHD children have problems with hand writing and it is the
occupational therapist that helps with their pencil grip, organisation of
letters and the flow from word to word (Green and
Chee, 1997).
Occupational therapists work with children with Sensory Integration
Dysfunction. They use sensory integration and recreational activities to build
up their basic sensory and motor skills (Kranowitz,
1998).
2.7.4
Orthodox Pharmaceutical Intervention
Since medication is frequently used in the treatment of ADHD, it is important
to have reasonable expectations regarding its effectiveness and to be aware of
potential side effects.
2.7.4
(A) General Medication Information
Each person responds uniquely to medication.
Medications are very safe.
More studies have been done about on children taking stimulant
medications than any other medications, including non-prescription drugs.
Medication should be prescribed in minimal doses.
Individuals do not have a physical craving for medication.
When medication is out of the blood stream, the individual goes back to
exhibiting full-blown ADHD symptoms.
Both hyperactive and non-hyperactive individuals can benefit from
medications.
Medication is effective for 54% of non-hyperactive children and 80 - 90%
of hyperactive children.
Medication does not cause psychosis but can precipitate a psychosis in
susceptible individuals (NIH Consensus Statement, 1998).
2.7.4
(B)
Medication Does Not:
Teach the ADHD individual how to cope and compensate for difficulties.
Imply a - magic pill".
Just treat hyperactivity.
Medication also helps with impulsivity and attention difficulties.
Lead to aggressive, dangerous behaviour.
Cause seizures or Tourette‘s Syndrome (Karen et al. 1997/NIH Consensus
Statement, 1998).
2.7.4
(C)
Medication Does:
Treat ADHD symptoms.
Influence long-term progress and prognosis of ADHD children when
utilised in conjunction with treatment modalities specific for ADHD.
Stimulate the attention centre of the brain to function more normally.
Affect impulsivity, attention, and behaviour positively. More specifically, stimulants can increase
attention span, concentration, and compliance; improve handwriting and fine
motor skills
and allow improved peer relationships.
In addition, a decrease in impulsivity, aggressiveness,and hyperactivity
can occur. (Karen et al. 1997).
2.7.4.1
Psychostimulants Introduction
Many clinicians treating ADHD believe that greater harm - emotionally
and socially occurs to untreated ADHD patients than could possibly come from
the side effects of the medications.
Not everyone agrees, however, and many parents are concerned about the
side-effects of medications.
Nevertheless, the usefulness of psychostimulants in the treatment of
ADHD has been established and is the standard of care in mainstream medicine
(Greenhill et al. 2002).
Stimulants have been widely prescribed by physicians for more than 40
years for a variety of disorders including Parkinsonism, depression, fatigue
states, narcolepsy, asthma, obesity and
hyperactivity in children (Karen et al. 1997).
They are widely prescribed as adjuncts to other remedial measures
(psychological, educational and social) in ADHD management. Stimulants should
only be prescribed for ADHD after remedial
measures such as psychological and sociological intervention as well as
appropriate educational placement have been proven to be insufficient alone
(Borak, 2002).
There are many styles for the use of medication in ADHD.
Some clinicians increase the medicine's dose until the desired effect is
achieved or too many undesirable side effects [jitteriness, stomach (aches) or
headaches] occur and do not subside
after several weeks (Breggin, 1999/Holford, 2001).
Some clinicians use other medications to treat the side effects of the
psychostimulants, an approach that becomes even more problematic for parents
already concerned about the
consequences or long-term effects of medication use (Karen et al. 1997).
Mechanism of Action
The exact mechanism by which psychostimulants benefit ADHD children has
not yet been identified.
They are known to facilitate dopamine and noradrenalin release by
inhibiting the action of monoamine oxidase (MAO) (Leary, 1994/Lawson-Wending,
1981).
The calming action is non-specific and has been reported in normal
children as well (Karen et al. 1997/Spencer et al. 1996).
Beneficial Effects
Many controlled studies using both subjective and objective criteria to
judge response, indicate that psychostimulants are beneficial in children with
ADHD when used for one
to three months (Caroll and Rounsaville, 1993; Swanson et al. 1995).
When properly prescribed, stimulants have a paradoxical calming effect on
hyperactive children, and will
facilitate their educational and social development (Caroll and
Rounsaville, 1993/Karen et al. 1997).
Stimulants have been shown to improve short-term learning by prolonging
attention span; improving goal directed activity, concentration and classroom
behaviour and reducing
impulsiveness, hyperactivity, and aggressive behaviour in children. The
behaviour of treated children was found to be organised in a more efficient and
effective manner, with
better processing of incoming stimuli and better planned responses (Frei
et al.2001/Kaplan and Sadock, 1985/Karen et al. 1997).
Benefits were particularly seen in ratings of behavioural functioning,
lowered activity levels, and improved attending skills (Levin and Kleber,
1995).
Side Effects and Contraindications
Side effects commonly seen include decreased appetite, insomnia,
increased heart rate or blood pressure, stomach-aches (Holford, 2001),
withdrawal symptoms and irritability
(Swansone al. 1991).
Long-term use of the psychostimulants may limit linear growth and
weight, most likely due to appetite suppression, decreased food intake, and
altered secretion of growth
hormone (Holford, 2001/Wilens et
al. 1997). Children with a
history of tics, Tourette's disorder, thought disorder, or psychosis should not
receive stimulants as they have been
alleged to precipitate the symptoms of such disorders (Bazier,
2001/Breggin, 2000/Lowe, 1982).
Loss of spontaneity and apathetic withdrawal are signs of overdosage
(Leary, 1994).
Special Prescriber‘s Points
Occasional - drug holidays‖ over weekends and holidays restores
sensitivity to the stimulants and allows the dosage to be decreased when
therapy is reinstated
(Caroll and Rounsaville, 1993/Swanson et al. 1995).
As many as 20% of children who respond poorly to one stimulant are
believed to show a positive response to a second one.
It is generally recommended to begin stimulant medication with Ritalin®,
followed by Cylert® if a poor response to Ritalin® develops (Karen et al.
1997).
Determining when it is safe to discontinue medication is a controversial
topic. Barkley (1981) has found that as many as 26% of the children can
discontinue the
medication because of improved self-control after two years of
treatment.
He does state that this is not because the children are cured or have
outgrown their disorder, but because their problems are not severe enough to
warrant the continued use
of stimulants.
2.7.4.1.1
Methylphenidate HCL (Ritalin®) and sustained-release preparations
(Ritalin-SR®, Concerta®, Metadate CD®):
Methylphenidate is said to affect as much as a 70% improvement in those
affected with ADHD.
Methylphenidate is supposed to induce hyper-perfusion [increase blood
supply] to the frontal lobes of the brain (Greenhill et al. 2002). Of all the
ADHD medications,
Ritalin® is the most inconsistently absorbed (Caroll and Rounsaville,
1993). Some adults and children absorb as much as 80 - 90% of the medication,
whereas others only
absorb 30 - 40% of a medication dose (Karen et al. 1997).
Since 1990, prescriptions for Ritalin have increased by 500% in the USA
(Holford, 2001/Breggin, 1999/Baizer, 2001/Wilens et al. 1997).
In South Africa there is considerable evidence that methylphenidate is
being over prescribed (Cotton, 1988/Middleborough, 2001/Strauss, 2000).
Methylphenidate is derived from the same family as cocaine and increases
blood flow to the basal ganglia and decreases flow to frontal and motoric
regions (Bazier, 2001).
Cerebral studies in persons with ADHD have shown cerebral hypo-perfusion
in the frontal lobe and decreased blood flow to the caudate nucleus (Zametkin
and Rapoport, 1987).
Methylphenidate hydrochloride (Ritalin®), a piperidine derivative of
amphetamine, is the drug of choice when it comes to stimulant treatment of ADHD
children (Holford, 2002).
Mechanism of Action
The mode of action of methylphenidate hydrochloride in man is not
completely understood, but methylphenidate presumably activates the brain stem
arousal system and cortex
to produce its stimulant effect (Castellanos, 2000).
There is neither specific evidence that clearly establishes the
mechanism whereby methylphenidate produces its mental and behavioural effects
in children, nor conclusive evidence
regarding how these effects relate to the condition of the central
nervous system (Spivak et al. 1999).
Methylphenidate hydrochloride in extended-release tablets is more slowly
but as extensively absorbed as in the regular tablets (Karen et al. 1997).
Bioavailability of the methylphenidate hydrochloride extended-release
tablet was compared to a sustained-release reference product and an
immediate-release product (Karen et al. 1997/
MD Pharmaceutical Inc., 2002).
The extent of absorption for the three products was similar, and the
rate of absorption of the two sustained-release products was not statistically
different (Karen et al. 1997).
Methylphenidate is an indirectly acting sympathomimetic agent (a drug
that stimulates the sympathetic nervous system) that releases dopamine and
noradrenalin inhibits MAO
and probably acts directly on catecholamine and serotonin receptors
(Spivak et al. 1999).
As compared to the other amphetamines, Ritalin acts more directly on
dopamine release (Strohle, 2003/Zametkin and Rapoport, 1987).
Beneficial Effects
In numerous comparative studies, Ritalin® proved to be statistically
superior to dextroamphetamine (Dexedrine®) and magnesium pemoline (Cylert®) in
several measurements
of improvement. Behavioural improvement appeared to be sustained for at
least two years as judged by subjective criteria (Baizer, 2001/Paterson,
1999/Spivak et al. 1999).
Approximately 35 % of children with ADHD show a dramatic improvement on
Ritalin®, while another 35% show only moderate improvement (Safer and Allen,
1976/Zametkin, 1995).
25 - 30% of children are poor responders and need alternative treatment
(Leary, 1994/Berkow et al. 1992/Greenhill et al. 2002).
Methylphenidate has been reported to increase attentiveness, reduce
distractibility, enhance concentration and decrease motor restlessness and
hyperactivity in ADHD patients (Barkely
et al. 1990/Paterson, 1999).
Methylphenidate is reliably associated with a short-term enhancement in
sustained attention, impulse control and reduced activity levels (Levin and
Kleber, 1995/Strohle, 2003).
Positive behavioural effects include increased compliance, independent
play and responsiveness to social interactions with parents, teachers (peers
(Mino and Ohara, 1991/Whalen et a
l. 1991).
However Buhrmester et al. (1992) found that stimulants had a general
dampening effect on social behaviour, significantly reducing social engagement
and increasing dysphoria
[an emotional state characterised by depression, restlessness, and
malaise] (Greenhill et al. 2002).
Side Effects and Contraindications
Undesirable side effects such as nervousness, sleep disturbances,
appetite suppression, anxiety, high blood pressure and headaches are common
(Holford, 2001/Karen et al. 1997).
These side effects are largely dose dependant and spontaneously remit
once the medication is discontinued (Karen et al. 1997/Levin and Kleber, 1995).
Prolonged therapy may result in anorexia, weight loss and growth
retardation (South African Medicines Formulary, 1995). Decreased growth rates
are only temporary. Once
the medication is stopped the child catches up with his peers with no
long-term growth problems (Kozielec, 1997).
Less commonly seen side effects include dizziness, dyskinesia, rashes,
nausea, abdominal pain, hypertension, hypotension, palpitation, tachycardia and
arrhythmias, and headache.
(Holford, 2001; Breggin, 2000).
Other reactions
Induce hypersensitivity (including skin rash, urticaria, fever,
arthralgia, exfoliative dermatitis, erythema multiforme with histopathological
findings of necrotizing vasculitis, and
thrombocytopenic purpura); anorexia, nausea, dizziness, palpitations,
headache, dyskinesia; drowsiness, blood pressure and pulse changes, both up and
down;
tachycardia; angina; cardiac arrhythmia; abdominal pain; weight loss
during prolonged therapy (Holford, 2002). Rare reports of Tourette's syndrome
(Baizer, 2001).
The drug has also been shown to inhibit certain drug metabolising liver
enzymes, causing a prolongation of the half-life of certain anti-epileptic
drugs, tricyclic antidepressants
and MAO inhibitors (Karen et al. 1997).
This may result in an elevation of therapeutic doses to toxic levels.
Acute episodes of psychosis and hallucinations have been reported with
Ritalin (Lambert and Hartsough, 1998/NIH Consensus Statement, 1998).
Methylphenidate is contraindicated in patients with marked anxiety,
tension, thyrotoxicosis, tachyarrhythmias, agitation, or glaucoma.
Should be used cautiously in epileptic and hypertensive patients
(Bazier, 2001/Karen et al. 1997).
Drug Interactions
Methylphenidate may decrease the hypotensive effect of guanethidine.
It should be used cautiously with pressor agents and MAO
inhibitors.
Human pharmacologic studies have shown that methylphenidate may inhibit
the metabolism of coumarin anticoagulants, anticonvulsants (phenobarbital,
phenytoin, primidone),
phenylbutazone, and tricyclic anti-depressants (imipramine,
clomipramnine, desipramine).
Downward dosage adjustments of these drugs may be required when given
concomitantly with methylphenidate (Karen et al. 1997)
Special Prescriber‘s Points
Abuse and dependence on the amphetamine-type drugs (e.g.,
methylphenidate) are common (Clarke, 1986/Bazier, 2001).
Although there have been no reports of psychic dependence with
methylphenidate use in ADHD children, the possibility for drug abuse needs to
be acknowledged
(Barkley, DePaul and Connerors, 1999/Biederman, 1996).
A recent study showed that children with learning disabilities
(including ADHD) display a higher proportion of chemically dependant traits
when compared to children without any
learning disabilities (Karacostas, 1993).
Kavale (1985) completed an extensive review of the research done on the
efficacy of methylphenidate in ADHD management.
He could not draw any conclusions on methylphenidate‘s benefit on
ADHD.
This was mostly due to methodological flaws in studies completed on
methylphenidate‘s efficacy (NIH Consensus Statement, 1998).
Long-term follow-up studies indicate that children on methylphenidate may
continue to have difficulty in school, exhibit behavioural disorders and have
poor self-esteem into
adolescence, which may persist as personality-trait disorders into
adulthood (Bazier, 2001/Holford, 2001/Karacostas, 1993/Milman, 1979).
2.7.4.1.2
Pemoline (Cylert®): ranks third in sales for the treatment of ADHD (NIH
Consensus Statement, 1998).
Unlike other stimulant medications, Cylert ® has an onset of action of
about an hour and must be taken for 1-2 weeks before improvement occurs.
Cylert® is more expensive than Ritalin® or Dexedrine® (Bazier, 2001).
Important points about Cylert®:
Liver enzyme changes have occasionally been noted in patients taking
Cylert®.
Baseline liver enzymes (tests?) are recommended with follow-ups at 3 – 6
months.
Persons using alcohol are at higher risk with this medication.
Patients with either liver or kidney compromise should not take this
medication.
SSRI‘ (Selective Serotonin Reuptake Inhibitors) affect the use of
Cylert® due to their effects on the liver P450 isoenzymes.
Cylert® is a useful alternative for patients with cardiovascular
disease, as it has no effect on this system.
Cylert® may cause insomnia, appetite suppression, and tics (American
Academy of Paediatrics Committee on Children with Disabilities, 1996; Bazier,
2001).
Mechanism of Action
Cylert® (Pemoline) has a pharmacological activity similar to that of
other known central nervous system stimulants, however, it has minimal
sympathomimetic effects.
Although studies indicate that Pemoline may act in animals through
dopaminergic mechanisms, the exact mechanism and site of action of the drug in
man is not known
(Spivak et al. 1999).
There is neither also no specific evidence, which clearly establishes
the mechanism whereby Cylert® produces its mental and behavioural effects in
children, nor conclusive evidence
regarding how these effects relate to the condition of the central
nervous system (NIH Consensus Statement, 1998).
Pemoline (Cylert®) is metabolized by the liver.
Cylert® is excreted primarily by the kidneys with approximately 50%
excreted unchanged and only minor fractions present as metabolites (Spivak et
al. 1999).
Cylert ® (Pemoline) has a gradual onset of action. Using the recommended
schedule of dosage titration, significant clinical benefit may not be evident
until the 3rd of 4th week of
drug administration (Pelham et al. 2001).
Side Effects and Contraindications
Common adverse affects to Cylert® include insomnia, anorexia and weight
loss (weight gain occurs after three to six months of continued
administration). Less frequently occurring
side effects include dizziness, drowsiness, headache, depression,
hallucinations, rashes, nausea and gastrointestinal distress (Karacostas,
1993/Pelham et al. 2001).
Most of these reactions were, however, reversible on withdrawal of the
drug (Karacostas, 1993/Spivak et al. 1999).
Hepatic dysfunction has occurred in a few patients with elevated hepatic
enzyme levels. One case of fatal hepatic
dysfunction has been reported (NIH Consensus Statement, 1998).
2.7.4.2
Second-line Therapy - When Stimulants Cannot Be Used
2.7.4.2.1
Antidepressant Medications
Anti-depressant medication is often prescribed for persons with ADHD who
cannot tolerate or show no signs of improvement on stimulants, or for those who
have mood
sequealae (Karen et al. 1997).
Dosage levels, while there are guidelines, are essentially determined on
a case-to-case basis.
Because ADHD persons are often poor self observers it may be helpful to
enlist a person with whom the ADHD person is close in order to note any
improvement or deterioration in
Behaviour following medication changes (Spivak et al. 1999).
It should be strongly emphasised that treatment of ADHD with
anti-depressants does not necessarily imply that the patient is depressed.
Antidepressants are often used to enhance the control of the patient's
symptoms, rather than as treatment of primary depression (Spivak et al. 1999).
Some clinicians feel that the SSR I's (Selective Serotonin Re-uptake
Inhibitors) have superior benefits, especially with children, for the mooded
aspects of ADHD because
they cause less side-effects than older generation anti-depressants such
as the tricyclics (Imipramine®, Nortriptyline®, Amitryptyline®, Desipramine®).
Desipramine® has become less prescribed due to some unexplained sudden
deaths which appeared to be related to heart conduction patterns (Bush et al.
1999).
2.7.4.2.2
Busiprone (BuSpar®) in Treating ADHD is a relatively new anti-anxiety
medication which shows some promise in treating ADHD when psychostimulant
medications are not effective
or their side effects cannot be tolerated (Bush et al. 1999/Spivak et
al. 1999).
It can also "potentiate" benefits of the serotonergic
antidepressants.
The side-effects of Busiprone are often tolerated better than those of
other medications used for ADHD (Pelham et al. 2001).
It should always be remembered that, for reasons still not fully
understood, every individual responds differently and uniquely to a specific
medication. The effective administration of a specific medication for any
psycho-neurological condition will still -and most likely will for quite some
time- remain an art, rather than a science (Spivak et al. 1999).
2.7.4.2.3
Imipramine Tofranil® is a tricyclic antidepressant that has a marked
sedative action in children.
Beneficial results however, have not been consistent (Pelham et al
2001).
These drugs should only be considered as alternatives in patients who
cannot tolerate or do not respond to Dexedrine®, methylphenidate, and Cylert®
(Karen et al. 1999).
Mechanism of Action
This drug acts pharmacologically by blocking the re-uptake of
noradrenaline and serotonin into the presynaptic neuron and indirectly modifies
their rate of release. To some extent,
it also inhibits dopamine re-uptake (McCracken, 1991).
Beneficial Effects
Tricyclic antidepressants have been shown to effectively increase
attentiveness and reduce distractibility in children and adults.
Tofranil® has been identified as being superior to a placebo in inducing
school return and in global therapeutic efficacy in 40 - 85% of ADHD cases (Huessy and Wright, 1970/Karen
et al. 1997/
Waizer et al. 1974/Wiener, 1977/Winsberg, et al. 1972).
It was found to decrease hyperactivity, aggression, defiance, and
inattentiveness. In a comparative study between methylphenidate and Tofranil®,
all rating measurements favoured Tofranil®
(Karacostas and Fisher, 1993/Wiener, 1977).
Other investigators have found that, although Tofranil® may initially
control ADHD, thereafter the child‘s behaviour deteriorates over a 2 - 3 month
period (Katzet al. 1975/Karen et al 1997/
Bazier, 2001).
Side Effects and Contraindications
The main side effects of Tofranil® include nausea, weight loss,
insomnia, dry mouth, constipation, drowsiness, gastric upset and difficulty
with micturition.
Syncope and seizures may be precipitated (South African Medicines
Formulary, 1995).
Special Prescriber‘s Points
2 - 3 weeks of therapy are required in order to see a therapeutic
response to the tricyclic antidepressants (Wiener, 1977).
2.7.4.2.4
Fluoxetine (Lorien®; Lilly-Fluoexetine®; Nuzak®; Prozak®) one of a group
of new generation antidepressants, which selectively inhibits serotonin re-uptake
(Karen et al. 1997).
Mechanism of Action
It selectively blocks serotonin re-uptake at the pre-synaptic neurons.
Beneficial Effects
A positive response may only be seen after two to three weeks of
continued therapy.
Side Effects and Contraindications
Common side effects include headache and gastrointestinal disturbances.
CNS effects include nervousness, drowsiness, and confusion.
Fluoxetine should be used with caution in patients with hepatic or renal
impairment and epilepsy (Pelham et al. 2001).
Special Prescriber‘s Points
Safe-use in children has not been established (South African Medicines
Formulary, 1995).
2.7.5
COMPLEMENTARY/ALTERNATIVE TREATMENTS FOR ADHD
2.7.5.1
Biochemical Tissue Salts
William Schuessler, a German physician, identified 12 different mineral
salts in 1873 which are essential for human life. He postulated that the
balance of these 12 mineral salts were essential
for building and maintaining health, and that they could also be used to
treat disease (Boericke and Dewey, 1984).
The Schuessler system is based on 12 remedies prepared according to the
homoeopathic law to D6 potency (1:1 000 000) (Goodwin, 1980).
According to Schuessler‘s theory, symptoms presented by an ADHD child
are indicators of various mineral deficiencies.
Subsequently, administration of these minerals to the ADHD child should
result in an improvement in his/her overall condition (Fisher, 1978).
A study conducted by Muller (1996) showed that mineral therapy was
effective in decreasing the overall hyperactivity exhibited by an ADHD child.
She advocates the use of mineral therapy as alternative to cerebral
stimulants (such as Ritalin®) in some cases, or as a reinforcing treatment in
others (Muller et al. 1996).
2.7.5.2
Homoeopathic Treatment
With regards to brain function, Niacin has significant benefits in
reversing schizophrenia.
As early as 1957 Dr. Humphrey Osmond and Dr. Abram Hoffer from
Saskatchewan in Canada proved that supplementing with niacin normalised
behaviour in those diagnosed
with schizophrenia. Dr. Hoffer, who has now treated over 5000
schizophrenic patients, claims an 80% success rate using niacin and other
connector nutrients.
Niacin and niacinamide doubled the two-year recovery rates from this
mental disease after just five weeks (Holford, 2002).
Gingko Biloba
As one of the most well researched herbs, gingko has been shown to
improve short-term and age related memory loss, slow thinking, depression,
circulation and blood flow
directly to the brain (Holford, 2001).
A review of ten studies testing gingko‘s effects on people with
circulation problems, carried out at the University of Limburg in the
Netherlands, found significant improvement in
memory, concentration, energy and mood (Holford, 2003).
It appears that by increasing cerebral blood flow, and therefore oxygen
and glucose utilisation, gingko offers relief of the presumed ―side
effects‖ of aging and may offer
significant protection against their development (Crook et al. 1992).
In addition, experimental and clinical studies show that gingko
increases the rate at which information is transmitted at the nerve cell. It has also been shown to normalise the
acetylcholine receptors in the hippocampus of aged animals, to increase
cholinergic transmission and to address many of the other elements of
Alzheimer‘s disease
(Cenacchi et al. 1993/Holford, 2001).
Vitamin B12
Although cobalamin, as vitamin B12 is technically termed, appears in all
animal foods and can be manufactured by beneficial bacteria in the
gastrointestinal tract, a deficiency
and its health consequences are never far away, especially in
vegetarians (Holford, 2002).
Absorption depends entirely on a healthy intestinal supply of ―intrinsic
factor which is a substance made in the stomach that latches onto B12 and draws
it into the bloodstream.
With age we generate less and less intrinsic factor, one of the reasons
anyone older than fifty is vulnerable to a deficiency (Fioravanti et al. 2004).
A broad range of emotional and cognitive abilities relies on an optimal
amount of Vitamin B12. In cognition
tests of elderly people, for instance, those who had the poorest
scores had the lowest blood measurements of cobalamin (Holford, 2002). People diagnosed with depression had low
levels of cobalt, the mineral that forms the centre
of the vitamin B12 molecule.
Restoring a healthier blood concentration relieves symptoms of dementia
and confusion for many people (Holford, 2001).
It also contributes to minimising the mental deterioration that occurs
in AIDS.
Folic acid
Research at King‘s College Hospital and the Institute of Psychiatry in
London found that a third of all patients with either severe depression or
schizophrenia were deficient in
folic acid (Fioravanti et al. 2004).
Supplementing folic acid for six months made a big difference in their
symptoms and ability to relate (Holford, 2002).
Folic acid, together with B12, is needed to convert the amino acid
L-tryptophan into serotonin and tyrosine into dopamine (Holford, 2002).
Pantothenic acid (vitamin B5) is essential to convert choline, such as
phosphatidylcholine, into the neurotransmitter acetylcholine, the key memory
molecule (Holford, 2002).
Without this vitamin, supplementation of choline of any kind would be of
little value (Engel et al. 1992).
Pantothenic acid is involved in the breakdown of carbohydrates, fats and
protein and in the production of various enzymes, pantothenic acid is needed by
the adrenal cortex for
the secretion of glucocorticoids (Fioravanti et al. 2004).
Pyroglutamate (2-oxo-pyrolidone carboxylic acid, or PCA) is an amino
acid found in vegetables, fruits, dairy products and meats (Holford, 2001).
Arginine is a non-essential amino acid and is abundant in protamines and
histones, which are both proteins associated with nucleic acids and was first
isolated in 1895 from
animal horn 100 (Kolesnichenko et al. 1999/Murray et al. 1998).
Pyroglutamate is also present in large amounts in the human brain, cerebrospinal
fluid and blood (De Freudis, 1998).
A key brain chemical in enhancing memory and mental function is the
amino acid pyroglutamate and its derivatives.
Being on the receptor end of brain communication, pyroglutamate improves
learning, memory, concentration and the speed of reflexes (Holford, 2002).
Pyroglutamate is known to have a number of remarkable
cognitive-enhancing effects (Holford, 2002).
Toxicity and symptoms of high intake of Pyroglutamate: Although rare,
but symptoms of massive dosages may include skin thickening and coarsening of
the skin, weakness,
diarrhoea, nausea, as well as increasing the activity of some viruses.
For this reason people suffering from herpes should avoid high dosages.
Pregnant and lactating women and people suffering from schizophrenia
should also avoid high dosages (Kolesnichenko et al. 1999).
So-called ―smart drugs‖ have been developed based on slight
variations of this substance helping with learning and memory related problems
(Borak, 2002; Holford 2001).
Numerous studies using these ―smart drugs‖ have proven to
enhance memory and mental function, not only in those with pronounced
memory-decline but also people with
so-called normal memory function (Blokland et al. 1999).
2.8
PROGNOSIS
Although orthodox treatment may improve many aspects of general
behaviour in the ADHD child, studies have failed to show it to be effective in
improving school achievement
(NIH Consensus Statement, 1998).
Prognosis remains unchanged, whether the child is on allopathic drugs or
no medication (Karen et al. 1993/Safer and Allen, 1976).
Follow-up studies on children with ADHD have found that they do not grow
out of their difficulties (Biederman, 1996/Bird, 1996).
Long-term studies on ADHD children have indicated that only about 25% of
these children make good adjustments to adult life. Approximately 15% of ADHD
children become
psychotic at some stage during their adult lives and 40 - 60% continue
to have significant concentration and impulse control difficulties (Borak,
2002/Leary, 1994).
2.8.1
Adult ADHD
Although ADHD is primarily regarded as a childhood disorder, it is,
however, being increasingly identified that children with ADHD grow up to
experience various
psychological problems such as chronic depression, drug dependencies and
antisocial behaviour (Klein and Mannuza, 1991).
Morrison (1980) found an increased incidence of violence and legal
problems, less education and low work status in adults who were diagnosed as
suffering from ADHD
as children.
Subsequently Leary (1994) found that adolescents (with a history of
ADHD) showed increased aggressive behaviour and conduct disorder and as
adults. He found a higher
incidence of substance abuse, court summonses and involvement in motor
vehicle accidents (Leary, 1994).
ADHD problems that may persist into adolescence and adulthood may
manifest as
-
Formatted:
Line
spacing:
1.5
lines
102
Imp
ulsiveness and attention deficiency
Academic failure
Low self
-
esteem
Mood and anxiety disorders
Depressio
n and irritability (Haislip, 1996)
Drug use disorders
Antisocial personality disorders (25
%
percent
)
Impulsiveness (50
%
percent
) (Sierles, 1993).
2.9
CONCLUSION
ADHD is a socially and academically debilitating condition seen in 10 -
20% of school-aged children.
Inability to maintain concentration in the classroom environment is an
important factor resulting in academic maladjustment.
It has been shown that ADHD is not primarily a childhood disorder and
that symptoms do persist into adulthood (Strauss, 2000).
Ritalin®, the drug of choice, is effective in improving concentration,
memory, frustration and anger, but it is ineffective in up to 30% of suffers
(Picton, 1997).
Ritalin®, which physicians consider to have only short-term effects, may
initiate changes in the brain structure and function that remain after the
therapeutic effects have dissipated
(Baizer, 2001).
Methylphenidate does not make a difference in the long-term outcome of
ADD/ADHD (Breggin, 2001/Holford, 2001).
A recent study carried out at Montreal Children‘s Hospital discovered
that at the end of five years, hyperkinetic children who received stimulant
drugs (Ritalin® or Chlorpromazine®)
did not differ significantly from children who had not received these
drugs (Karen et al. 1997).
Although it appeared that hyperactive children treated with Ritalin®
were initially more manageable, the degree of improvement and emotional
adjustment was essentially identical at
the end of five years to that seen in a group of children who had received
no medication at all (Breggin, 2002/Holford, 2001).
Present drug management involves the long-term use of powerful drugs
which can lead to dependency, whilst the long-term effects are not yet
conclusive. There is no data to conclusively
demonstrate that these drugs improve learning over long periods (NIH
Consensus Statement, 1998).
Many parents are dissatisfied with the use of drug therapy due to the
adverse side-effects and lack of clinical response, and are thus therefore
seeking alternatives (Whalen and Henker, 1991/
Pooley, 1999).
7 - 10% of the children in America take some form of psychostimulants at
some point in their school career (Breggin, 2000; Holford, 2002). Data has
shown a 1000% increase in drug
abuse injury reports involving Ritalin in the 10 - 14 year age group
(Haislip, 1996).
Homoeopathy provides an alternative for many people seeking medication
without fear of dependency or undesirable side effects. Homoeopathic remedies
have minimal to no side
effects, should not produce dependency and are considered safe to use
for all age groups (Jouanny, 1993).
A homoeopathic alternative to drug therapy in ADHD has not yet been
extensively researched and may provide a relatively inexpensive and safe
substitute to drug therapy.
Advanced Brain Food® is a nutritional supplement formulated to meet the
needs of children with learning, concentration and behavioural
difficulties. According to research
done by Holford in the United Kingdom (1998), the individual nutrients
in Advanced Brain Food® have been shown to enhance neurologic function and
learning capabilities as well as
assisting in moderating blood sugar changes.
This combination of nutrients offers the perfect solution in assuring
that children receive the appropriate nutrients essential for growth (Holford,
2000).
The aim of the study was to evaluate the efficacy of the homoeopathic
combination preparation Quietude® and a nutritional supplement, Advanced Brain
Food® in the management of
ADHD in children. This study proposes to show that Quietude® +/o.
Advanced Brain Food® could be used as an alternative to methylphenidate
hydrochloride or other orthodox drugs
in the management of ADHD, with particular regard to concentration
abilities, hyperactivity and impulsivity.
CONCLUSION
Subjects taking Advanced Brain Food® during the trial performed better
than the group taking Quietude® with regards to conduct and impulsivity
according to the Student
Behaviour Log (SBL), with a significant difference\between groups only
being noticeable after four weeks of treatment.
The groups performed similarly regarding inattention, hyperactivity
and anxiety (no significant differences were seen at the four different
assessment periods).
Supplementation and treatment with Advanced Brain Food® cannot claim to
replace effective psychological interventions but merely help to correct
deficiencies. The fact
that an improvement was noted in this treatment group signifies that
further research is necessary to establish the exact role of such interventions
in the treatment of ADD/ADHD.
Quietude®
Hyoscyamus niger 3C HPUS
(contains less than 10-9 mg alkaloids per dose) - Relieves restless sleep
associated with nervousness
Nux moschata 4C HPUS -
Relieves restless sleep
Passiflora incarnata 3X HPUS -
Relieves sleeplessness associated with worries and exhaustion
Stramonium 6X HPUS (contains
less than 10-8 mg alkaloids per dose) - Relieves sleeplessness with
intermittent awakening
Advanced Brain Food®
Nutritional Information
Optimum Nutrition Formula Tablets (per daily intake 2 tablets)
Lithothamnion Calcareum, Calcium Citrate, Calcium Ascorbate (Preparation
with Hydroxypropyl Methylcellulose),
Magnesium Oxide, Magnesium Citrate, Magnesium Ascorbate:
Providing Calcium
Providing Magnesium
Providing Vitamin C
Vitamin E 135 i.u. (as D-Alpha Tocopheryl Succinate1)
Anti-Caking Agents (Magnesium Stearate, Stearic Acid & Silicon
Dioxide)
Pantothenic Acid (Vitamin B5 as Calcium Pantothenate)
Niacin (Vitamin B3 as Nicotinamide)
Iron (as Amino Acid Chelate)
Choline (as Bitartrate)
Thiamine (Vitamin B1 as Thiamine Hydrochloride)
Zinc (as Citrate)
Riboflavin (Vitamin B2)
Tablet Coating (Hydroxypropyl Methylcellulose)
Vitamin B6 (as Pyridoxine Hydrochloride / Pyridoxyl-5-Phosphate)
Vitamin A 5000 i.u. (as Acetate with Acacia Gum, DL Alpha Tocopherol,
Sucrose & Tricalcium Phosphate)
Inositol
Boron (as Amino Acid Chelate)
Vitamin D 600 i.u. (Preparation as Ergocalciferol with Maltodextrin,
Hydroxypropyl Methylcellulose & Tocopherols)
Manganese (as Citrate)
Biotin (Preparation with Dicalcium Phosphate)
Selenium (Preparation as L-Selenomethionine with Dicalcium Phosphate)
Iodine (Preparation as Potasssium Iodide with Dicalcium Phosphate)
Beta Carotene (Preparation with Alginate & Soya Protein1)
Vitamin B12 (Preparation as Cyanocobalamin with Dicalcium Phosphate)
Folic Acid (Preparation with Dicalcium Phosphate)
Vanadium (as Sulphate)
Vitamin K (Preparation with Acacia Gum & Sucrose)
Molybdenum (as Molybedenum Amino Acid Chelate)
Chromium (as Polynicotinate)
Copper (as Citrate)
Immune C (per daily intake 2 tablets)
Vitamin C
Black Elderberry Extract (4% total flavonoids)
Ginger
Bilberry Extract (2% anthocyanadins)
Zinc
Essential Omegas (per daily intake 2 capsules)
Fish Oil providing EPA
DHA
DPA
Borage Oil providing GLA
Brain Food (per daily intake 2 capsules)
Arginine Pyroglutamate
DMAE
Pantothenic Acid (Vitamin B5)
Trimethylglycine (TMG)
Phosphatidylcholine
Phosphatidylserine
Niacin (vitamin B3)
Folic Acid
Vitamin B12
[Thomas Struppe]
ADHS – eine fabrizierte Erkrankung?
Schreiende und tobende Kinder außer Rand und Band, verzweifelte Eltern, ohnmächtige Pädagogen: Keine andere Erkrankung des Kindes- und Jugendalters rückte in der Vergangenheit so stark in den Fokus der breiten Öffentlichkeit wie das sogenannte Aufmerksamkeitsdefizit-/Hyperaktivitätssyndrom, kurz ADHS.
Eine wahre Flut an ADHS-Diagnosen brachte das Fass vor einigen Jahren endgültig zum Überlaufen und erste kritische Psychiater und Psychotherapeuten meldeten sich zu Wort. Sie bemängelten nicht
nur die inkonsistenten Diagnosekriterien, sondern vermuteten auch einen nicht unerheblichen Anteil an Fehldiagnosen.
Damit lagen sie höchstwahrscheinlich richtig, denn Forscher der Ruhr-Universität Bochum konnten zeigen, dass es häufig zu Fehldiagnosen aufgrund der von Kinder- und Jugendpsychotherapeuten benutzten Faustregeln kommt. Die Experten verwenden zur Diagnosestellung also eher Heuristiken, anstatt sich an wissenschaftlichen Kriterien zu orientieren.
In einer weiteren Studie der Universität Köln legten die Forscher dar, dass auch ein Großteil der nicht an ADHS leidenden Jungen in bestimmten Entwicklungsphasen einzelne ADHS-Symptome zeigt, wodurch eine klare Differenzierung von der Norm noch erheblich erschwert wird.
Der „wissenschaftliche Vater“ des ADHS, der amerikanische Kinderpsychiater Leon Eisenberg, sprach 2009 von einem „Paradebeispiel für eine fabrizierte Krankheit“. Im Zuge dieser Kritik bezeichneten wichtige Wortführer ADHS als „gesellschaftliches Konstrukt“. Die Symptomatik wird dabei als Folge der aktuellen Lebensumstände verstanden, was gerade vielen Pädagogen aus dem Herzen spricht. Auch Eisenberg hatte kurz vor seinem Tod angemerkt, dass „die genetische Veranlagung für ADHS vollkommen überschätzt wird“ und „psychosozialen Aspekten mehr Beachtung geschenkt werden sollte“.
ADHS – eine gekaufte Diagnose?
Das Thema ist noch aus einem weiteren Grund so brenzlig, denn mit der Diagnose ADHS wird sehr viel Geld verdient: Das Nürnberger Pharmaunternehmen Novartis, welches das Medikament Ritalin herstellt, machte damit im Jahr 2010 einen weltweiten Umsatz von 464 Millionen US-Dollar.
Nach der Neuauflage des Diagnose-Handbuchs der American Psychiatric Association kam ans Licht, dass mehr als die Hälfte der Autoren der ADHS-relevanten Kapitel Einkünfte von der Pharmaindustrie erhielt. Neben Novartis und weiteren Pharmaunternehmen verdient am ADHS eine ganze Industrie, die Literatur, spezielles Spielzeug und weitere Produkte an die Eltern betroffener Kinder vertreibt.
Doch selbst wenn die genetischen Veranlagungen nur eine untergeordnete Rolle bei der Genese des ADHS spielen sollten und die Pharmaindustrie bei der Verbreitung der populären Diagnose kräftig mitmischte, so bleibt dennoch ein hoher Leidensdruck bei den betroffenen Kindern und die Ohnmacht ihrer Eltern und Betreuer, denn die Verhaltensauffälligkeiten sind, kulturelles Phänomen hin oder
her, durchaus real.
Es ist nicht zielführend, dem ADHS seinen Stellenwert als Erkrankung abzusprechen und zu glauben, dass damit alle Probleme vom Tisch seien. Aktuell wird die Debatte auf dem Rücken der
Betroffenen ausgetragen, anstatt nach möglichen Lösungsansätzen zu suchen.
Von Anfang an standen, vor allem bei den Praktikern, bestimmte Ernährungsfaktoren im Verdacht, ADHS auszulösen bzw. dessen Symptome zu verstärken. Doch auch die wissenschaftliche Forschung widmete sich diesem brisanten Thema, welches immer wieder zu hitzigen Diskussionen führte.
Erste ernährungstherapeutische Ansätze
In den 1970er-Jahren entwickelte Dr. Ben Feingold, ein amerikanischer Kinderarzt und Allergologe, erstmals eine spezielle Diät zur Behandlung von ADHS-Symptomen. Die Methode beruht auf der Vermeidung von synthetischen Zusatzstoffen (Farb-, Geschmacks- und Konservierungsstoffe) sowie von synthetischen Süßstoffen (z.B. Aspartam). Erste Studien mit oft geringen Teilnehmerzahlen berichteten Erfolgsquoten von teilweise über 70% und rückten Dr. Feingolds Ansatz in den Fokus weiterer Forscher. Doch leider waren die Ergebnisse der folgenden Untersuchungen bei Weitem nicht so beeindruckend, wie die faszinierenden Fallberichte. Die Diät half also einzelnen Kindern auf ganz erstaunliche Weise und einige konnten sich sogar ihrer Medikamente entledigen. Doch dem größeren Teil konnte nicht geholfen werden.
Trotz des eher enttäuschenden Fazits konnten durch die durchgeführten Folgeuntersuchungen einige neue Erkenntnisse gewonnen werden. Die wissenschaftlichen Publikationen zu Feingolds Diätansatz gingen aber über die Jahre konstant zurück.
Interessanterweise schaltete sich 1974 die Nutrition Foundation of New York in die Diskussion ein, eine Organisation, der u.a. Coca Cola angehörte. Obwohl sie ebenfalls weitere Untersuchungen angekündigt hatte, erklärte die Nutrition Foundation schon wenige Tage später, dass es „keine Hinweise aus kontrollierten Studien gäbe, die auf einen Zusammenhang zwischen künstlichen Zusatzstoffen und Hyperaktivität schließen lassen“. Dieser Satz wurde lange und oft von den Medien wiederholt und bekam dadurch leider für viele Eltern, aber auch zahlreiche Ärzte und Wissenschaftler, einen Wahrheitswert.
Die Southhampton-Studie
Im Jahr 2007 griff ein britisches Forscherteam die Ideen von Dr. Feingold auf. Die Wissenschaftler untersuchten 300 Kinder ihrer Gemeinde. Ein Teil der Kinder bekam ein Getränk, welches synthetische Zusätze in Form von Farb- und Konservierungsstoffen enthielt, während der Rest nur eine Placebolösung trank. Die Kinder, welche die Zusatzstoffe konsumierten, wurden in den Urteilen von Eltern, Lehrern und zusätzlichen unabhängigen Beobachtern als deutlich hyperaktiver eingeschätzt. Die Art und Dosis der synthetischen Zusatzstoffe findet sich regulär in zahlreichen, vor allem bunten, „Kinderlebensmitteln“.
Doch die britischen Forscher ließen es damit nicht beruhen. 2010 publizierten sie einen Artikel, in dem sie sich mit der Genetik jener Kinder beschäftigten, welche in der Southampton- Studie besonders hyperaktiv reagiert hatten. Sie konnten dadurch nachweisen, dass diese Kinder Probleme mit der Regulation ihres Histaminhaushalts hatten. Es scheint also, als sei ADHS in vielen (aber nicht allen) Fällen eine Folge einer Lebensmittelallergie.
Spätestens die Publikationen dieser neuen Befunde sollten dem oben zitierten Fazit der Nutrition Foundation of New York den finalen Streich versetzen.
Die bahnbrechende INCA-Studie
Belgische Wissenschaftler, welche sich 2011 der Verbindung zwischen Ernährung und ADHS widmeten. Sie untersuchten insgesamt 100 Kinder, welche bereits in der Vergangenheit eine ADHS-Diagnose erhalten hatten. Die jungen Probanden aßen über 9 Wochen eine sogenannte Eliminationsdiät (weißer Reis, Fleisch, Gemüse und Birnen) oder eine „gesunde Kontrolldiät“ (u.a. Vollkorngetreide, Pflanzenöle, Milchprodukte, Nüsse und Samen, Obst und Gemüse). Ziel der Eliminationsdiät war es, alle Lebensmittel mit potenziell allergenen Eigenschaften aus dem Speiseplan der Kinder zu verbannen.
Die Ergebnisse der Studie waren im wahrsten Sinne des Wortes beeindruckend: Etwa 60% der Kinder zeigten mit der Eliminationsdiät enorme Fortschritte bei den ADHS-relevanten Verhaltensauffälligkeiten. Diese Fortschritte verschwanden, sobald sie wieder zu einer „gesunden Kontrolldiät“ zurückkehrten.
(Es gab auch eine „sanftere“ Form der Eliminationsdiät, welche geringe Mengen Getreide beinhaltete. Doch nach zwei Wochen hatten 41% der Kinder überhaupt keine Reaktion auf diesen Ansatz gezeigt und wurden somit der eigentlichen Eliminationsdiät zugeordnet.)
Der negative Einfluss von vor allem glutenhaltigem Getreide auf die Verbesserung der Symptome scheint nicht wirklich verwunderlich. So zeigten zahlreiche Studien in der Vergangenheit mögliche Zusammenhänge zwischen Weizen und Schizophrenie, den depressiven Störungen und Autismus.
ADHS-spezifische Mikronährstofftherapie
Neben den eigentlichen diätetischen Ansätzen gerieten in den letzten Jahren auch einige Mikronährstoffe in den Fokus der Wissenschaftler. Es wurde u.a. festgestellt, dass die Konzentration von langkettigen Omega-3-Fettsäuren in den Zellmembranen von ADHS-Betroffenen dauerhaft herabgesetzt ist. In der sogenannten Oxford-Durham-Studie erhielten Kinder mit Koordinationsproblemen ein Supplement mit einer hohen Omega-3- Konzentration. Die meisten Kinder zeigten eine deutliche Verbesserung der ADHS-Symptome, während die Kinder der Kontrollgruppe keine signifikante Linderung erfuhren. Auch die Buchstabier- und Lesefähigkeit verbesserte sich weitaus deutlicher in der Supplementgruppe.
In weiteren Studien konnte gezeigt werden, dass Kinder mit einem Zinkmangel mehr hyperaktives Verhalten zeigen. Eine Supplementation mit Zink ließ die benötigte Medikamentenmenge im Gegensatz zur Kontrollgruppe um ca. 30% sinken.
Des Teufels liebster Dämon? Der Zucker ...
Zucker stand schon frühzeitig bei Praktikern und Eltern im Verdacht, der Hauptschuldige am ADHS-Dilemma zu sein. Im Zuge der ersten Veröffentlichungen entspann sich eine der hitzigsten Debatten im Zusammenhang mit Ernährung und ADHS. Die gesammelten Erfahrungen tausender Eltern und Lehrer standen den statistischen Daten einiger Forschergruppen gegenüber. Zahlreiche Wissenschaftler verwiesen immer wieder darauf, dass Zucker in den durchgeführten Studien niemals konsistent zu aggressiverem oder hyperaktiverem Verhalten gegenüber Placebo geführt hatte.
Allerdings zeigen Kinder signifikante Änderungen im Elektroenzephalogramm und im Verhalten, wenn ihre Blutzuckerwerte rapide unter 75 mg/dl fallen. Dieses Phänomen, auch reaktive Hypoglykämie genannt, kann leicht durch eine zuckerreiche Mahlzeit provoziert werden. Es treten hierbei die für die Hypoglykämie typischen zentralnervösen Symptome auf, wie etwa Verwirrtheit, Konzentrationsund Koordinationsstörungen.
In einem wahren Mammutprojekt wurden Daten von über einer Million Schülern an öffentlichen New Yorker Schulen über sieben Jahre erfasst. Dabei wurde der Zuckerkonsum dieser Kinder stark reduziert und einige synthetische Farbstoffe aus der Ernährung verbannt, woraufhin sich die schulischen Testleistungen bedeutend verbesserten.
Weitere Unterstützung für die Eltern kommt durch Studien der Universitäten in South Carolina und Yale. Umso höher die zugeführte Menge an Zucker in den Untersuchungen mit ADHS-Kindern wurde, desto häufiger zeigten sie zerstörerisches bzw. aggressives Verhalten und Ruhelosigkeit. Auch der Grad der Unaufmerksamkeit stieg mit höherer Dosis an.
Ein weiteres Problem mit dem Zucker sind die vielen leeren Kalorien, welche dieser liefert. Mit anwachsendem Zuckerkonsum kommt es häufig zu einer mangelnden Zufuhr essenzieller Mikronährstoffe, u.a. auch den für die ADHS-Symptomatik so wichtigen Omega-3-Fettsäuren.
Ein Fazit und die brennende Frage: Was ist zu tun?
Dieser riesige Berg an Forschungsergebnissen scheint beinahe erdrückend. Doch nach dem Ordnen der Ergebnisse und Gedanken sollte eindeutig die Hoffnung überwiegen, dass eine Ernährungsumstellung vielen ADHS-Betroffenen helfen kann, ihre Symptome deutlich zu reduzieren – ganz ohne chemische Medikamente mit teilweise verheerenden Nebenwirkungen. Doch wo sollten Therapeuten und interessierte Eltern beginnen?
Inzwischen behandeln viele ADHS-Experten ihre Klienten mit Mischformen der oben vorgestellten Ansätze und das teilweise mit durchschlagendem Erfolg! Dr. Sandy Newmark z.B. empfiehlt eine zuckerarme Diät basierend auf unveränderten Lebensmitteln und unter Einbeziehung von Fischöl (Omega-3-Lieferant) und Zink.
Eine Weiterentwicklung der Specific Carbohydrate Diet, einer Diät zur Behandlung chronisch entzündlicher Darmkrankheiten, die sogenannte Gut and Psychology Syndrome Diet (GAPS), führt als eine Hauptindikation ADHS auf.
Entwickelt bzw. weiterentwickelt wurde dieser Diätansatz von Dr. Natasha Campbell-McBride. Interessanterweise eliminiert die GAPS-Diet alle gängigen und oben erwähnten negativen Einflussfaktoren, obwohl sie zeitlich vor den bedeutenden aktuellen Untersuchungen konzipiert wurde.
GAPS beruht auf unverarbeiteten Lebensmitteln, vor allem Gemüse, Obst, Nüssen und Samen, Olivenöl, Seefisch, Fleisch und Eiern. Der Diätansatz ist frei von Zucker und Getreide und liefert durch den Verzehr von fettem Seefisch wichtige Omega-3-Fettsäuren.
Obwohl zur Effektivität von GAPS in Bezug auf ADHS nur Fallberichte und keine klinischen Studien existieren, scheinen die oben aufgeführten Untersuchungen den Nutzen dieser Diät zu unterstreichen. Als besonders positiv kann natürlich auch das Vorhandensein von Literatur, Rezepten usw. gesehen werden, was den Einstieg und die praktische Umsetzung einer solchen Diät erheblich erleichtern kann.
Vorwort/Suchen Zeichen/Abkürzungen Impressum