Download Towards an integrated theory on adult ADHD and Substance Abuse

Towards an integrated theory of ADHD (and
substance abuse)
Alban Burke
November 2010
[The brain] ...is bound together in a dynamic system of systems
that does millions of different things in parallel. It is probably so
complex that will never succeed in comprehending itself. Yet it will
never cease to try. (Carter, 1998, p.8)
1
Introduction
• Attention Deficit /Hyperactivity disorder (ADHD) is a complex and
common disorder with a great variation in its clinical presentation.
• It has been historically classified primarily as a childhood disorder
and has core symptoms associated with hyperactivity/ impulsivity
and inattention.
• Research evidence suggests that this disorder has strong
neurobiological and genetic underpinnings.
• The symptoms associated with ADHD are clinically significant
impairment in the social and academic functioning of children with
this disorder.
2
S
O
Stimulus
C
F
I
A
O
-
M
Organism
E
I
C
L
O
Y
N
O
Response
M
I
C
Cognitive
Footer
Emotional
Behavioural
Physiological
3
Stimulus
• This involves both internal and external events that start a
recursive process.
• External events are quite self-explanatory, however internal
events are often ignored, especially in some quarters of
Psychology.
• These internal events are important in our ultimate model and
they include cortical and sub-cortical hyper- or hypo-arousal as
well minor or major physiological events.
Footer
4
Organism:
•Due to the fact that research on cortical and sub-cortical structures is not
limited to humans, we decided on this term as it allows flexibility in
accommodating various animal studies.
•Various themes are included here, e.g.:
Genetics
Cortical arousal
Sub-cortical structures
Temperament / “personality”
Coping and survival strategies
Perceptual processes
Information processing and memory
Selective and sustained attention
Psychomotor abilities
Executive functions
Footer
5
Response:
• Typically, and erroneously, responses are often equated to
behaviour only, however, it is argued that all responses have
conscious or unconscious behavioural, emotional, cognitive and
physiological responses.
• In this model it is imperative that one investigates, and
understands, all responses to an event.
• It is maintained that all responses, and their outcomes, are
monitored. In effect a response is not a final outcome, but rather a
continuous process of reassessment which either results in the
maintenance or adjustment of the response hierarchy.
Footer
6
Always late, poor sense of time
Interrupts others
Anxious
Irritable
Preference for jobs involving verbal skills,
such as salesman
Argumentative
Likes risky sports
Preference with jobs involving working
with the hands
Bored easily
Loses train of thought
Preference for self-employment
Cannot keep checkbook balanced
Low frustration tolerance
Problems with alcohol and drug abuse
Chronic fatigue
Low self-esteem
Procrastinates
Compulsive and impulsive spending
May have been arrested or spent some
time in jail
Racing thoughts
Daydreaming
Rage attacks
Depression
May verbally or physically abuse spouse
or children
Difficulty with authority figures
Mood swings
Disorganized
Muscle tics
Reading problems (dyslexia)
Restless -- cannot sit still, cracks
knuckles, bites nails, jiggles feet
Short or hot temper
Failed to finish high school
Narcissistic
Talk excessively
"Foot-in-mouth" disease -- says
inappropriate things before thinking
Overreactive
Unable to finish high school or college
Poor concentration
Forgets things
Unmotivated
Poor in math in school
History of multiple jobs
Unstable personal relationships
Poor short-term memory
Impulsive
Vocal tics
Poor with spatial concepts
Insomnia
Footer
7
History of cADHD and aADHD
Year
Public / Social event
Scientific event
1950’s
1968
Diagnostic event
Diagnostic labels included:

Minimal Brain Dysfunction (MBD)

Hyperactive Syndrome

Hyperkinesis

Hyperactive Disorder of Childhood
The terms Hyperactivity and MBD were most
commonly used. (see Conrad 1975)



Child's behaviour, especially at school, main
criteria.
Emphasis on hyperactive and disruptive
behaviours (Conrad 1976).
Well known, due, in part, to publicity it received
concerning controversies about drug treatment.



1970’s



Footer
The major treatments for hyperactivity were stimulant
medications, especially Ritalin.
While there was no solid evidence of biological causation,
there was an assumption that there was some type of
organic pathology.



DSM-II identified "minimal brain
damage" and "hyperkinetic reaction"
The disorders, thus, were defined by
both hyperactivity and inattention
Although mainly childhood it also
allowed for the possibility of persistence
into adolescence.
Most common childhood psychiatric problem (Gross and
Wilson 1974)
No methodologically sound epidemiological studies but it
was estimated that 3-5% of elementary school students
were hyperactive (occasionally estimates were as high as
10%).
Several cohort studies were published which followed
children who had been originally diagnosed with
hyperactivity a decade or more earlier and traced their
development into adulthood. These studies established that
for some hyperactive children, the symptoms persisted into
adolescence and even into adulthood.
Thus emerged the notion of what we call "adult
hyperactives,"
8
1980

Footer
Varuous books and popular media

reports aimed at the lay market
were published:
o Paul Wender (1987), The
Hyperactive Child, Adolescent
and Adult
o
Frank Wolkenberg (1987)
wrote a first-person account

in the New York Times
Magazine about his discovery
that he had ADHD This highly
visible testimony of someone
not previously diagnosed with
ADHD as a child put the idea
of "ADHD Adults" into the

public realm.
o
Clinics for adults with ADHD
were established at Wayne
State University in 1989 and
two years later at the
University of Massachusetts
in Worcester (Jaffe 1995).
A major shift in psychiatric thinking
occurred with the publication of DSMIII in 1980, when the largely
psychoanalytic orientation was
abandoned and replaced with an
avowedly bio-medical and categorical
approach to diagnosis.
The "diagnostic project" was now
heralded as a scientific endeavor, a
claim that has increased with the
publication of DSM-IV (1994), a
revision that identifies nearly 400
distinct medical diagnostic entities
(Conrad & Potter, 2000).
Researchers investigated the
persistence of symptoms into
adulthood (e.g., Biederman, et al.,
1996) to further identify what they
believed to be confounding factors
(such as co-morbidity with other
disorders).



The scientific studies
found their way into
diagnostic systems.
Any diagnosis of Attention
Deficit Disorder (ADD, as
the diagnosis was
renamed) was found only
among adults whose
disorder persisted from
childhood and, thus, was
not a disorder that was
either "missed" during
childhood or was of adult
onset.
All ADD adults were
hyperactive children
grown-up.
9
1990’s

Popular media continues, with an
increasing focus on adult ADHD:

Lynn Weiss (1992) A.D.D. and
Creativity
Tapping Your Inner Muse: Attention
Deficit Disorder

Kelly and Ramundo (1993) You Mean
I'm Not Lazy, Stupid or Crazy?

Thom Hartmann (1994), Attention
Deficit Disorder : A Different
Perception

"20/20," Catherine Crier attributed
ADHD to a "biologic disorder of the
brain" in adults (September 2, 1994).

Dr. Timothy Johnson on "Good
Morning America" (March 28, 1994)

Newsweek, for example, described a
38-year old security guard who held
more than 128 jobs since leaving
college after being enrolled in the
academic institution for 13 years
(Cowley and Ramo 1993).

Ladies' Home Journal (Stich 1993)

Edward Hallowell and John Ratey
(1994), Driven to Distraction

Hallowell and Ratey (1994), Driven to
Distraction

The cover of July 18, 1994 Time
Footer magazine issued a clarion call for
ADHD adults: "Disorga-nized?
Distracted? Discombobulated?



Zametkin et al (1990)used positronemission tomography (PET)
scanning to measure brain
metabolism and demonstrated
different levels of brain activity in
individuals with ADHD compared to
those with-out the disorder, providing
new evidence for a biologic basis for
ADHD.
November 1998, NIH convened a
Consensus Conference on the Diagnosis and Treatment of Attention
Deficit Hyperactivity. While little new
emerged from the conference, two
papers explicitly focused on adults
with ADHD. Overall, the conference
report affirmed the validity of ADHD,
although recognizing scientific
controversies, the need for more
basic and longitudinal research, and
a lack of consensus on optimal
treatment
It is clear that by 1994, the clinical
diagnosis of ADHD had expanded to
include adolescence and adulthood
and had become institutionalized in
psychiatry and medicine.


By 1994, DSM-IV reflected the growing
consensus that adults could be diagnosed with
ADHD, provided they had exhibited symptoms
as children before the age of seven.
Two (out of the five) diagnostic criteria were
clearly relevant to adults:
o
DSM-IV required that "some
impairment must occur in at least 2
settings." While for children, these
settings usually mean school and home,
the range of settings may be greater for
adults and include home, school, work,
and other vocational or recreational
settings.
o
Secondly "there must be clear evidence
of interference with developmentally
appropriate social, academic, or
occupational functioning."
o
The inclusion of work environments in
the criteria section of the manual
reflected the central and relatively
uncontroversial position that the
diagnosis of ADHD in adults now
occupied."
10
2000










Footer
The expansion of the hyperactivity diagnosis to adults is not,
primarily, the result of new scientific discoveries as findings have
been varied.
Several social factors appear to have contributed to the
diagnostic expansion. Conrad and Potter describe these as
being:
o
The Prozac Era
o
The Medicalization of Underperformance
o
A New Disability
Studies have shown that the interaction of lay and professional
claims-makers, rather than "medical imperialism," typically
underlies the medicalization process.
The case of adult ADHD indicates that popularization may also
play a part in diagnostic expansion.
Media, including TV, popular literature, and now the Internet,
spread the word quickly about illnesses and treatment.
This popularization of symptoms and diagnoses can create new
"markets" for disorders and empower previously unidentified
sufferers to seek treatment as new or expanded medical
explanations become popularly available.
The widespread popular acceptance of entities as illnesses
suggests a feedback loop among professionals, claims-makers,
media, and the public in terms of the creation, expansion, and
application of illness categories.
Medical diagnoses can penetrate the public consciousness and
become "taken-for-granted as an objective natural entity" in the
public sphere (Horwitz forthcoming).
Such medical diagnostic entities are often accepted without
recognizing their history and with an assumption of their
universal categorical significance regardless of cultural context.
Within an increasingly medically aware public reside individuals
who take identified "symptoms" as revealing an underlying
disease condition and, in cases like adult ADHD, may seek to
attain their diagnosis of choice.





Genetics is the rising paradigm in medicine and an
increasing number of human problems are being
attributed to genetic associations, markers, or
causes (Conrad 1999).
Some experts have long believed that there is a
genetic component to ADHD and its predecessor,
hyperactivity, but to date, evidence is only
suggestive, even though the claims of inheritance
date back at least 25 years (Cantwell 1975; Wender
1971; Wood, et al. 1976).
Recent research has focused on a genetically
induced imbalance of dopamine. Researchers posit
a potential link between ADHD and three genes: D4
dopamine receptor gene, the dopamine transporter
gene, and the D2 dopamine receptor gene (Faraone
and Biederman).
The thinking is that people who carry the gene
overproduce dopamine, which impairs self-control.
Despite the research and much published testimony
the genetic nature of ADHD is still contested.

In terms of diagnostic expansion,
the ADHD case is not unique.
We can point to other cases
where medicalized categories,
which were originally developed
and legitimated for one set of
problems, were extended or
reframed to include a broader
range of problems.
11
Current status of research: Genetics
• Nadder , Silberg, Rutter, Maes and Eaves (2001) did a study in which
they explored the phenotypic and genetic interrelationships underlying
ADHD.
• The ADHD symptomatology was assessed by various instruments in a
sample of 735 male and 819 female same-sex twin pairs, aged 8 to 16
years. Multivariate analyses were applied to parental and teacher ratings
from an investigator-based interview, the CAPA, and three
questionnaires (the CBCL and the Rutter Parent and Teacher Scales).
• Results from patterns of intercorrelations and factor analyses of
maternal measures suggested that at the phenotypic level, these
assessed the same underlying behavioural construct, which differed from
other emotional and behavioural constructs.
Footer
12
• Genetic analyses, however, showed that in addition to a common
factor underlying the expression of ADHD as assessed across the
range of measures, additional genetic factors were identified that
were method- and rater-specific.
• The findings suggest that although the investigator-based
interview and the behavioural checklists tap similar aspects of
ADHD behaviour, there is additional rater-specific variance.
• In line with this, Sharp, McQuillin and Gurling (2009) describe
ADHD as a clinically and genetically heterogeneous syndrome
which is comorbid with childhood conduct disorder, alcoholism,
substance abuse, antisocial personality disorder, and a wide array
of affective disorders.
Footer
13
• The common denominator seems to be the dopamine transporter
gene (DAT1). Remarkably, and for the first time in psychiatry,
genetic markers at the DAT1 locus appear to be able to predict
clinical heterogeneity because the non-conduct disordered
subgroup of ADHD is associated with DAT1 whereas other
subgroups do not appear to be associated.
• The second most well replicated susceptibility gene encodes the
DRD4 dopamine receptor and many other dopamine related
genes appear to be implicated.
• It is becoming increasingly clear that genes causing bipolar mania
overlap with genes for a subtype of ADHD.
• The key to understanding the genetics of ADHD is to accept very
considerable heterogeneity with different genes having effects in
different families and in different individuals.
Footer
14
Current status of research: Neurology,
Neuropsychology and Neurophysiology
Frontal lobe
Decrease in size in the prefrontal cortex region part of the frontal lobe and Attention Deficit
Disorder children show excessive slow brainwave activity (theta and alpha ranges) compared
to non- ADD ADHD activity. The slow brainwave activity indicates a lack of control in the cortex
of the brain. Response inhibition and working memory impairments in ADHD may stem from a
common pathologic process rather than being distinct deficits. Such pathology could relate to
right frontal-cortex abnormalities in ADHD, consistent with prior reports, as well as with the
demonstration here of a significant association between SSRT and SWM in right frontal
patients. Smaller white matter volume in ADHD is distributed bilaterally in frontal lobes.
Parietal
Smaller white matter volume in ADHD bilaterally in parietal lobes
Occipital
Although some research shows decreased volume in left, more research necessary
Temporal
Smaller white matter volume in ADHD was distributed bilaterally in temporal lobes
Footer
15
Right putamen
An overall reduction in gray matter in ADHD compared to controls
Globus pallidus
An overall reduction in gray matter compared to controls.
Caudate nucleus
combines with the putamen and globus pallidus to form a larger brain region called the
corpus striatum
Basal ganglia
This region has often been found to be underactive in ADHD and similar disorders and
overactive in obsessive compulsive or anxiety-related disorders.
Limbic system
If the limbic system is over-activated, a person might have wide mood swings, or quick
temper outbursts. He might also be "over-aroused," quick to startle, touching everything
around him, hyper-vigilant.
Reduced volume, more significant in posterior areas
Corpus Callossum
Cerebellum
Footer
Several studies in ADHD in childhood and adolescence
have shown structural cerebellar impairment . Indeed, the most marked neuroanatomical
anomaly in ADHD has been described in the cerebellum,with volume changes more marked
than in the prefrontal cortex (Castellanos et al. 2002). In children, reductions in right
cerebellar hemisphere and vermis volume have been reported
16
Nigrostriatal
This dopaminergic pathway normally improves attention by increasing focus and on-task
behaviour and cognition. It is thought that in ADHD there may be underactivity which
leads to impaired selective and sustained attention.
Frontostriatal
White matter abnormalities in motor/ premotor circuits are responsible for the persistence
of overflow movements in patients with ADHD. The effect of MPH on myelin/
oligodendrocyte-related genes in a mature oligodendrocyte explains the improvement or
resolution of overflow movements in children with ADHD (D'Agati, Casarelli, Pitzianti, &
Pasini, 2010).
Anterior cingulate
Hypoactive and compensates by using lateral prefrontal cortex, insular cortex, as well as
unilateral activation of the caudate, putamen, thalamus and pulvinar (Schneider, Retz,
Coogan, Thome, & Rösler, 2006).
Posterior cingulate
Volume reduction in right hemisphere in children with ADHD (Schneider, Retz, Coogan,
Thome, & Rösler, 2006).
Footer
17
Glutamate
Too little dopamine or norepinephrine is a problem, and too much is a problem. And the importance of
glutamate in PFC functioning is beginning to come to the forefront in research. small doses of
methylphenidate actually impact the effects of norepinephrine in the pre-frontal cortex more than it impacts
the effects of dopamine in the PFC. This research has also shown that when the a2 receptors in the prefronatal cortex are blocked that the symptoms of ADHD can be created in a subject, including lack of selfcontrol, impulsivity, and hyperactivity (Berridg et al, 2006)
Norepinephrine
Too much or too little of either neurotransmitter decrease cognitive functions, both in terms of the
performance of brain cells, and in the real world. But when the ratios and relationships are just right,
performance is improved.
Dopamine
If ADHD involves altered reward processing, then alterations in dopamine function may underlie some of
the symptoms of ADHD.
Creatine and NAcetylaspartate (NAA)
It is also likely that metabolic differences in the globus pallidus play a role in ADHD. Individuals with ADHD
had an abnormally low ratio of NAA to creatine. Creatine supplements, often used by exercise enthusiasts,
have been shown to boost levels of this nutrient to the brain as well, which can decrease the NAA to
Creatine ratio (i.e., more creatine and less NAA), however creatine supplementation can possibly actually
exacerbate some of negative effects of ADHD.
Footer
18
• Imaging data are often confounded by small numbers of patients
and sometimes contradictory results. However, recent findings
have shown similarities in adult ADHD and ADHD in children,
such as the impairment of cerebello-striato-frontal networks.
• Consistent imaging findings are in the dysfunction of striatal brain
structures and anterior cingulated cortex (Schneider, Retz,
Coogan, Thome & Rösler, 2006).
• Although the prefrontal cortical structures also seem to play a
pivotal role in ADHD psychopathology, these findings are not
unique or specific to ADHD.
Footer
19
• Given that ADHD symptomatology undergoes changes with
adulthood in terms of decline of hyperactivity and impulsivity,
while disorganization and emotional dysregulation come to the
fore, a more focused approach to understanding emotional
dysregulation in adult ADHD should reveal insights into the
pathophysiology of this condition.
• It is important to bear in mind that comparison of results between
young children and adults with ADHD could be confounded by
maturational or developmental effects with increasing age
(Schneider, Retz, Coogan, Thome & Rösler, 2006).
Footer
20
• Finally, in animal models emerging evidence suggests that
methylphenidate alters the dopaminergic system with long-term
effects beyond the termination of treatment (Grund, Lehmann,
Bock, Rothenberger, & Teuchert-Noodt, 2006).
• On the other hand, longterm treatment did not show functional
differences after termination of medication compared to
treatmentnaïve ADHD patients (Pliszka, Glahn, SemrudClikeman, Franklin, Perez, Xiong & Liotti, 2006).
• Whether stimulant medication has long-term influence on brain
morphology or neuroregenerative effects is not clarified.
• Thus, controversies between structural and functional results
have still to be resolved.
Footer
21
Footer
22
Sensation seeking: Mediating factor in
substance abuse
• A study by Faraone, Kunwar, Adamson and Biederman (2009)
provides some evidence that those who have been diagnosed
with AADHD show specific personality traits such as novelty
seeking, harm avoidance, reward dependence, persistence, selfdirectiveness, cooperativeness and self-transcendence (Faraone
et al., 2009).
• These personality traits manifest, according to Faraone et al
(2006) as follows:
Footer
23
Sensation seeking: Mediating factor in
substance abuse
– High novelty seeking:individuals high in novelty seeking are quick-tempered,
curious, easily bored, impulsive, extravagant, and disorderly.
– High harm avoidance: People high in harm avoidance are fearful, socially
inhibited, shy, passive, easily tired, and pessimistic even in situations that do
not worry other people. Although the higher harm avoidance of ADHD
subjects is consistent with ADHD’s comorbidity with anxiety disorders and
depression (Biederman et al. 2006; Kessler et al. 2006), the group differences
Faraone et al (2006) observed were not accounted for by these disorders,
which suggests that this personality subscale may tap subclinical traits.
– Low persistence: Tendency to give up easily when frustrated, less likely to
strive for higher goals, unlikely to persevere at tasks and associated deficits in
executive functioning. Low persistence is consistent with the executive
functioning deficits seen in many patients with ADHD (Biederman et al. 2007).
– Low reward dependence: Practicality, tough-mindedness, social insensitivity
and indifference.
Footer
24
Sensation seeking: Mediating factor in
substance abuse
– Low self-directedness: Less responsible, reliable, resourceful, goal-oriented
and self-confident than other adults and they find it difficult to define, set and
pursue meaningful internal goals.
– Low cooperativeness: Self-absorbed, intolerant, critical, unhelpful, and
opportunistic and inconsiderate of other people’s rights or feelings. These
traits are consistent with ADHD’s co-morbidities with ODD and conduct
disorder.
• The extreme of normal personality traits, as suggested by the
aforementioned study, not only describe a pattern of disruptive
behaviour, but also raises many other questions and alternative
perspectives on AADHD.
• One personality trait which was not investigated by Faraone et al
(2003) but may also be related to AADHD, is sensation seeking
(the tendency to seek out novel experiences).
Footer
25
Sensation seeking: Mediating factor in
substance abuse
• Research on the neurological and neurophysiological aspects of
sensation seeking has yielded some interesting results.
• One of these is where brain images showed that when high
sensation seekers viewed emotionally arousing photographs,
there was increased activity in the brain region known as the
insula (See Figure 1a).
• This brain structure acts in part as a gateway where visceral
signals from the body are first received and interpreted by the
brain. In contrast to this, when low sensation seekers looked at
arousing photographs, there was increased activity in the frontal
cortex area of the brain (See Figure 1b).
Footer
26
Sensation seeking: Mediating factor in
substance abuse
• Regardless of whether the pictures were pleasant (e.g., mild
erotica) or unpleasant (e.g., a snake poised to strike), the highsensation seekers showed early and strong activation in the
insula. (See Figure 1a).
• In contrast, in the low-sensation seekers, insula activity barely
rose above baseline levels. (See Figure 1b.)
• Instead, there was pronounced early activity in the anterior
cingulate, a part of the cortex strongly linked to the regulation of
emotions (and many other things).
• In high-sensation seekers, anterior cingulate activation was
delayed in relation to the lows, though it eventually reached a
similar peak.
Footer
27
Sensation seeking: Mediating factor in
substance abuse
Footer
28
Sensation seeking: Mediating factor in
substance abuse
• However, not only is there increased activity in certain areas but, in a
further study, using urine samples and spinal taps, it was found that high
sensation seekers had a significant deficit in levels of a byproduct of the
brain chemical norepinephrine.
• The findings of the aforementioned study should be viewed together with
findings on brain structures, as the two are not mutually exclusive.
• Often researchers make the mistake of viewing the causes of pathology
or behaviour as being either brain structure, or neurotransmitter based.
• However, in this instance we are not considering structural deficits, but
rather functional deficits.
• Brain activity, in essence, relies on neurotransmitter release.
• If one considers that the noradrenergic pathway runs through the frontal
and prefrontal cortex (see Figure 2), then altered norepinephrine must
have an effect on the activity in these areas.
Footer
29
Noradrenergic
Footer
Serotonergic
Dopaminergic
30
Case study
• 28 year old female, childhood diagnosis of ADHD, no formal diagnosis of aADHD,
no medication.
– 15-16 years very anti-drugs, then had boyfriend who smoked cigarettes and
maijuana
– Started using on weekends out of curiosity, first experience, no effect, thereafter
euphoric, and heightened sensation (“supersonic hearring”)
– Used it once before school day for the thrill of it
– Went to raves where she started using Ecstasy. First experience was total
euphoria, thereafter never the same experience and used more to try and regain
that first experience
– Also reports that her thoughts seemed to be more focussed
– Stopped because she became bored of it
– Used cocaine a few times, but according to her it had no effect
– Anti-smoking and anti-alcohol (father an acloholic)
– Smoked Hookah pipe
– Now uses Bioplus and Vitamin B tablets because she discovered by accident that it
slows her down and helps with her attention and concentration
Footer
31
Integrated model
• We propose that ADHD children and adults are predisposed to
substance abuse.
• In our opinion, ADHD sufferers are aware that their behaviour is
unacceptable, and this awareness creates discomfort (e.g. 5year-old:”I don’t want to be like this”). i.e. the symptoms in
themselves do not create discomfort (as opposed to disorders
such as mood and anxiety).
• The patients themselves are not aware of the underlying
neurological causes
• According to Mowrer’s two factor theory we propose that initial
contact with a substance happens by chance and they ascribe
“feeling better” to the substance
Footer
32
• Subsequent use and “positive effects” are positively reinforced
(operant conditioning)
• Sensation seeking and resultant risk taking behaviour is a
predisposing risk factor
• We postulate that sensation seeking shares the same
neurological and substrates with ADHD which is why we assume
that it predisposes adults with ADHD to substance abuse
Footer
33
Future research
Adult
ADHD
Diagnostic
Self Report
Questionnaires
Neurocognitive
Neuropsychological signs
and symptoms
(CANTAB)
Psychodiagnostics
Neurological &
Neuropsychological
assessments
Footer
Cortical Arousal
(Biopac Evoked
potential)
Mental
HealthProfessionals'
perceptions
Sequelae
Clinical Picture
and
classification
Co-morbidity
Sensation
seeking and risk
taking behaviour
Substance abuse
Investigating the role
of dorsolateral,
prefrontal-subcortical;
anterior cingulatesubcortical;
orbitofrontalsubcortical (fMRI)
Career
34
Creativity
So what do we propose to do?
Degree
D.Litt et Phil
M.A (Psychology)
M.A (Clin Psych)
Footer
Student / Staff
Topic
Alban Burke
Investigating the neurodevelopmental theory of ADHD by means of DTI scans
Tracey-Lee Austin
Subcortical relationships between ADHD and Sensation seeking
Human, Werner
Neuropsychology of ADHD
Human, Wilmien
Comparison between ADHD and non ADHD
Cave, J
Comparison of attention, impulsivity and interpersonal relationships between ADHD and other disorders
Jordaan, E
Critical Psychological perspectives of ADHD
Sayce, S
Nicotene (Hubbly Bubbly) use and abuse in ADHD
Sklar, R
Hyperfocus in ADHD
Cilliers, M
Frontal cortical arousal in ADHD and sensation seeking
Weideman, A
Role of hormones in ADHD
Pumphrett, C
Career decision and ADHD
De Jongh, H
Comorbid conditions in aADHD
Bester, T
Ritalin: Risk or protective factor in ADHD and substance abuse
Spannidis, C
Lived experience of adults with ADHD
Erasmus, A
Alpha and Theta frontal wave activity in ADHD
Ferreira, Q
Comparison of alpha and theta frontal wave activity between anxiety and ADHD
35
Conclusion
• It seems unlikely to me that we will continue to punish people for
misconduct when the crossed wires that spark their behaviour
become as clear to see as a broken bone. Rather, I hope (and
expect) we will use our knowledge of the brain to develop
treatments for sick brains that will be infinitely more effective than
the long-winded, hit and miss psychological therapies we use
today. (Carter, 1998, p.334)
Footer
36