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Volume 3 - 2015
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psychotherapy. review process is at the total discretion of the editors and publisher.
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Table of Contents
Editorial . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 01
Pieter Rossouw
EDITORIAL TEAM
CHIEF EDITOR ADVISORY BOARD
Matthew Dahlitz
Pieter Rossouw, Ph.D. (Chair)
ASSOCIATE EDITOR Jack C. Anchin, Ph.D.
Richard Hill
Malek Bajbouj M.D.
MANAGING EDITOR Louis J Cozolino, Ph.D.
Geoff Hall Todd E Feinberg M.D.
Stanley Keleman, Ph.D. hc SK
Jeffrey J. Magnavita, Ph.D., ABPP
PUBLISHER Iain McGilchrist, M.D., MRCPsych
Dahlitz Media
Georg Northoff, M.D., M.A., Ph.D.
Allan N. Schore, Ph.D
Mark Solms Ph.D.
Paul G. Swingle, Ph.D.
Jonathan H. Turner, Ph.D.
David Van Nuys, Ph.D..
DISCLAIMER
The International Journal of Neuropsychotherapy (IJNPT) ISSN 2202-7653, is an open access online journal published by Dahlitz Media Pty
Ltd. The publisher makes every effort to ensure the accuracy of all the information contained in this publication. However, the publisher, and its
agents, make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the information
herein. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of, or endorsed
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publisher shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever
or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the information in this journal.
Our mission is to provide researchers, educators and clinicians with the best research from around the world to raise aware-
ness of the neuropsychotherapy perspective to mental health interventions.
For further information about this journal and submission details please go to
www.neuropsychotherapist.com/submissionscall/
We are excited to release this edition of the International Journal of Neuropsychotherapy as we enter our
third year since the launch. The global uptake of applied brain based research is in line with the post decade of
the brain phase as well as shifts in traditional treatment modalities like the shift towards the neural underpin-
nings in Cognitive Behavioural Therapies - the “fourth wave” of CBT; the focus on the neural basis of Accep-
tance and Commitment Therapy and focus on the neuroscience of analytical therapies to name a few.
The field of psychotherapy and psychological research has entered a phase that focuses on the interplay
between neuroscientific underpinnings and practical applications to enhance outcomes for the ever growing
demand to find workable strategies to effectively address patterns of unwellness.
One of the key variables that inform the development of a well-integrated person (neural system) is our
education systems. In this volume we discuss the pitfalls of a fear based education system and implications
of such an approach on individual neural development as well as societies in general and call for a stronger
research agenda to address this from neural perspective. We hope this will add to the debate and research in
this domain.
Neuroscience research should always be mindful of its ultimate focus – the wellness of societies and im-
provement of mental wellbeing. The words of Nobel laureate, Erik Kandel comes to mind:
Patient care is our most important responsibility. That is why we are here. Never let patient care take a sec-
ondary role. Patient welfare is the ultimate goal of biological science and it is the engine that drives the whole
scientific enterprise.
Neuroscience opens amazing new opportunities to benefit you clients – utilise it, do it justice and enjoy the
future!” (Kandel, E. R., 2006. In Search of Memory. The Emergence of a new Science of Mind. New York, NY:
W.W. Norton)
Pieter Rossouw
Chief Editor
Summer 2015
memory reconsolidation
understood and misunderstood
Bruce Ecker
Coherence Psychology Institute
Abstract
Memory reconsolidation is the brain’s natural, neural process that can produce transformational change: the
full, permanent elimination of an acquired behavior or emotional response. This article identifies and examines
10 common misconceptions regarding memory reconsolidation research findings and their translation into
clinical practice. The research findings are poised to drive significant advancements in both the theory and
practice of psychotherapy, but these benefits depend on an accurate understanding of how memory reconsol-
idation functions, and misconceptions have been proliferating. This article also proposes a unified model of
reconsolidation and extinction phenomena based on the brain’s well-established requirement of memory mis-
match (prediction error) for reconsolidation to be triggered. A reinterpretation of numerous studies published
without reference to the mismatch requirement shows how the mismatch requirement and mismatch relativity
(MRMR) model can account for diverse empirical findings, reveal unrecognized dynamics of memory change,
and generate predictions testable by further research.
Cite as: Ecker, B. (2015). Memory reconsolidation understood and misunderstood. International Journal
of Neuropsychotherapy, 3(1), 2–46. doi: 10.12744/ijnpt.2015.0002-0046
2004 Pedreira et al. Crab Contextual fear Reactivated learned expectation of visual threat must be
memory sharply disconfirmed for memory to be disrupted by cy-
cloheximide.
2005 Frenkel et al. Crab Contextual fear New experience modifies memory expression only if preced-
memory ed by a memory mismatch experience.
2005 Galluccio Human Operant condi- Memory is erased only by being reactivated along with a
tioning novel contingency.
2005 Rodriguez- Rat Taste recognition Novel taste following reactivation allows memory disruption
Ortiz et al. memory by anisomycin.
2006 Morris et al. Rat Spatial memory Reactivation allows disruption of original memory by aniso-
of escape from mycin only if learned safe position has been changed, creating
danger mismatch of expectation.
2006 Rossato et al. Rat Spatial memory Reactivation allows disruption of original memory by aniso-
of escape from mycin only if learned safe position has been changed, creating
danger mismatch of expectation.
2007 Forcato et al. Human Declarative Memory of syllable pairings learned visually is destabilized
memory and impaired by new learning only if, after reactivation by
presentation of context, presentation of a syllable to be paired
does not occur as expected, creating mismatch.
2007 Rossato et al. Rat Object recogni- Memory is disrupted by anisomycin only if reactivated in
tion memory presence of novel object.
2008 Rodriguez- Rat Spatial memory Reactivation allows disruption of original memory by aniso-
Ortiz et al. of escape from mycin only if learned safe position has been changed, creating
danger mismatch of expectation.
2009 Forcato et al. Human Declarative Memory of syllable pairings learned visually is labilized and
memory lost only if reactivation is followed by learning revised novel
pairings.
2009 Pérez-Cuesta Crab Contextual fear Reactivated learned expectation of visual threat must be
& Maldonado memory sharply disconfirmed for memory to be disrupted by cy-
cloheximide.
2009 Winters et al. Rat Object recogni- Memory is disrupted by MK-801 only if reactivated in pres-
tion memory ence of novel contextual features.
2010 Forcato et al. Human Declarative Memory of syllable pairings learned visually destabilizes and
memory incorporates new information only if, after reactivation, the
expected opportunity to match syllables does not occur, creat-
ing mismatch.
2011 Coccoz et al. Human Declarative Memory of syllable pairings learned visually destabilizes,
memory allowing a mild stressor to strengthen memory, only if, after
reactivation, the expected opportunity to match syllables does
not occur, creating mismatch.
2012 Caffaro et al. Crab Contextual fear New experience modifies memory expression only if preced-
memory ed by a memory mismatch experience.
2012 Sevenster et Human Associative fear Reactivated fear memory is erased by propranolol only if
al. memory (classical prediction error is also experienced.
conditioning)
2013 Balderas et al. Rat Object recogni- Only if memory updating is required does reactivation trig-
tion memory ger memory destabilization and reconsolidation, allowing
memory disruption by anisomycin.
2013 Barreiro et al. Crab Contextual fear Only if memory reactivation is followed by unexpected, mis-
memory matching experience is the memory eliminated by glutamate
antagonist.
2013 Díaz-Mataix Rat Associative fear Reactivated fear memory is erased by anisomycin only if pre-
et al. memory (classical diction error is also experienced.
conditioning)
2013 Reichelt et al. Rat Goal-tracking Target memory reactivated with prediction error was destabi-
memory lized and then disrupted by MK-801, but not if brain’s predic-
tion error signal was blocked.
2013 Sevenster et Human Associative fear Reactivated fear memory is destabilized, allowing disruption
al. memory (classical by propranolol, only if prediction-error-driven relearning is
conditioning) also experienced.
2014 Exton- Rat Instrumental Memory for lever pressing for sucrose pellet was disrupted by
McGuinness memory (operant MK-801 only if the reinforcement schedule during reactiva-
et al. conditioning) tion was changed from fixed to variable ratio, creating predic-
tion error.
2014 Sevenster et Human Associative fear Reactivated fear memory is destabilized, allowing disruption
al. memory (classical by propranolol, only if prediction-error-driven relearning is
conditioning) also experienced, and termination of prediction error termi-
nates destabilzation.
for destabilisation and subsequent reconsolidation of occurs when the blue light is turned off with no shock
a memory” (p. 375). That is the research finding that having been experienced. Only then are perceptions
translates into major advances for the psychotherapy discrepant with what the target learning “knows.”
field (Ecker, 2011; Ecker et al., 2012, 2013a,b). Now the synapses encoding the target learning unlock
For those advances to materialize, it is necessary for into a modifiable state, because now it is definite that
clinicians to understand well what the brain regards as no shock occurred as expected while the blue light
an experience of mismatch or prediction error. Mis- was on.
conceptions abound on this point as well. The follow- Understanding the mismatch requirement allows
ing example shows the meaning of mismatch at the us to interpret correctly the results of various studies
basic level of classical conditioning in the laboratory, that were misinterpreted by the researchers because
as demonstrated by Pedreira et al. (2004) and other they analyzed their studies without reference to the
studies listed in Table 1. Clinically relevant learnings mismatch requirement. The simple logic of the situa-
are often far more complex, and the guiding of mis- tion, as stated by Agren (2014), is that “the studies that
match experiences in psychotherapy looks very differ- have shown effects of reconsolidation . . . must some-
ent, as a rule, from the laboratory instances described how have induced a prediction error” (p. 80). Ecker et
in this article, but the principles of mismatch are use- al. (2012) articulated the same principle: “Whenever
fully clarified at this basic level. the markers of erasure of a learning are observed, both
Consider a target learning that was created by sev- reactivation and a mismatch of that learning must
eral repetitions of turning on a blue light and deliver- have taken place, unlocking its synapses, or erasure
ing a mild electric shock several seconds later, during could not have resulted. This logic can serve as a use-
the last half-second of the light being on. Subsequent- ful guide for identifying the critical steps of process in
ly, if the blue light is turned on again, the learned both the experiments of researchers and the sessions
expectation of the shock is reactivated immediately, of psychotherapists” (p. 23).
along with fear and the physiological expressions of Therefore, identifying the presence or absence of
fear, such as a mouse’s freezing or a human’s change mismatch in each of the many published studies of
of skin conductance. However, this reactivation does reconsolidation that lacks consideration of the mis-
not deconsolidate and destabilize the memory circuits match requirement is an exercise necessary for bring-
of this learned association of light and shock, because ing the field of reconsolidation research to maturity
no mismatch experience has occurred as yet. While from its present fragmented condition. The remain-
the blue light stays on without any shock being deliv- der of this section begins that unifying exercise by
ered, a mismatch or prediction error has not occurred describing several key studies, analyzing the presence
because the shock might still occur. The target learn- or absence of mismatch in them, and reinterpreting
ing is in a state of expectancy of the shock. Mismatch their results accordingly. This analysis of mismatch in
Misanin, J. R., Miller, R. R., & Lewis, D. J. (1968). Pérez-Cuesta, L. M., & Maldonado, H. (2009). Memo-
Retrograde amnesia produced by electroconvul- ry reconsolidation and extinction in the crab: Mu-
sive shock following reactivation of a consolidated tual exclusion or coexistence? Learning & Memory,
memory trace. Science, 16, 554–555. doi:10.1126/ 16, 714–721. doi:10.1101/lm.1544609
science.160.3827.554 Phelps, E. A., Delgado, M. R., Nearing, K. I., & LeDoux,
Monfils, M.-H., Cowansage, K. K., Klann, E., & J. E. (2004). Extinction learning in humans: Role of
LeDoux, J. E. (2009). Extinction-reconsolidation the amygdala and vmPFC. Neuron, 43, 897–905.
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Morris, R. G., Inglis, J., Ainge, J. A., Olverman, H. J., Pine, A., Mendelsohn, A., & Dudai, Y. (2014). Uncon-
Tulloch, J., Dudai, Y., & Kelly, P. A. (2006). Mem- scious learning of likes and dislikes is persistent,
ory reconsolidation: Sensitivity of spatial memory resilient, and reconsolidates. Frontiers in Psychol-
to inhibition of protein synthesis in dorsal hip- ogy, 5(1051), 1–13. doi:10.3389/ fpsyg.2014.01051
pocampus during encoding and retrieval. Neuron, Pittenger, D. J., & Pavlik, W. B. (1988). Analysis of the
50, 479–489. doi:10.1016/j.neuron.2006.04.012 partial reinforcement extinction effect in humans
Myers, K. M., & Davis, M. (2002). Behavioral and using absolute and relative comparisons of sched-
neural analysis of extinction. Neuron, 36, 567–584. ules. American Journal of Psychology, 101, 1–14.
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neuropsychotherapy:
defining the emerging paradigm of
neurobiologically informed psychotherapy
Matthew Dahlitz
Abstract
Over the past two decades, the theoretical basis and application of psychotherapy has been undergoing a
paradigm shift from a focus on higher cortical/cognitive processes to a new and growing appreciation of
affective phenomena as the locus of behaviour change. The move has been prompted by breakthroughs
in neuroscience that show bottom-up, left-hemisphere neural processes to underpin behaviour, validat-
ing affectively focused clinical practices. This paper examines the theoretical basis of this paradigm shift,
with an emphasis on Klaus Grawe’s consistency theory as central to its early description, and identifies
the specific neural underpinnings for an effective clinical application of psychotherapy as established by
contemporary neuroscience.
Cite as: Dahlitz, M. J. (2015). Neuropsychotherapy: Defining the emerging paradigm of neurobiologi-
cally informed psychotherapy. International Journal of Neuropsychotherapy, 3(1), 47–69. doi: 10.12744/
ijnpt.2015.0047-0069
A) Amino Acid Neurotransmitters (the major neu- 1.1.2 Activation Patterns and Neural Systems
rotransmitters)
A single neuron does not produce much informa-
1) Glutamates are excitatory neurotransmitters. tion on its own through its binary function of either
Receptor sites are either fast-acting ionotropic firing or not. Firing entails a certain rate, intensity
types (AMPA), which primarily activate or inhibit, and resulting neurotransmitter output at the synapse.
or slower-acting N-methyl D-aspartate (NMDA) A single neuron does not on its own “perceive” any-
types, which facilitate a strengthening of the syn- thing—perception is a group task in the world of neu-
aptic connection called long-term potentiation rons—but rather responds to specific input from oth-
(Grawe, 2007, pp. 32–40). Glutamates bind with er neurons, or directly from the environment in the
activating receptors, namely Alpha-amino-3-hy- case of sensory cells. To make sense out of the flow
droxy-5-methylisoxazole-4-proprionic acid of information coming from our sensory organs, our
(AMPA), resulting in fast activation of the postsyn- neural system is organised into a hierarchy of increas-
aptic neuron (as described above). ingly complex networks. Individual neurons, boast-
2) Gamma-aminobutyric acid (GABA) is an in- ing, on average, 10,000 connections to other neurons,
hibitory neurotransmitter. It is fast acting, binding together contribute to broader “neural net profiles”
with GABA receptors to cause an inhibiting effect that represent an aspect of brain function (such as
on the postsynaptic cell. GABA and AMPA inter- perceiving a particular sound), and these profiles in-
actions are seen across the brain and result in much tegrate with many others to form various functions of
of the fast action of our neural processes—much of our nervous system, some of which are concentrated
our thought processes and sensory input/process- in different areas of the brain (Siegel, 2012). Klaus
ing, for example. Grawe (2007) describes as a hierarchical model of in-
formation processing, based primarily on the work of
neurophysiologists David Hubel and Torsten Wiesel
B) Biogenic Amines (monoamines, more localised in (1959, 1962, 1968), who demonstrated that neurons
distribution than the amino acids and known to be could have specific activation patterns in response to
released also from non-synaptic sites) specific stimuli.
1) Catecholamines trigger physiological changes The hierarchy of our neural system is organised
to prepare the body for physical activity such as the from sensory input to the perception of complex ob-
“fight-or-flight” response. jects/understandings to even more complex cognitive
Dopamine has many functions, including mo- and affective processes. For example, the “raw” visu-
tivation. Most dopaminergic neurons are in the al data streamed from the sensory input of the reti-
midbrain and hypothalamus. na is recognised by neurons in a fragmented fashion
whereby individual parts of the scene are processed
Norepinephrine acts as a hormone and a neu-
by neurons tuned to “recognise” small, specific ele-
rotransmitter. It increases heart rate and acts as
ments. These fragments are then assembled by more
a stress hormone affecting the amygdala.
complex neural networks involving higher-order cells
2) Indolamine is the family of neurotransmitters that recognise the assembly of the parts. At the top
that includes serotonin and melatonin (derived of the hierarchy are cells and networks in the cortex
from serotonin). that recognise the whole picture. Once this broader
5-HT (Serotonin) is involved in the regulation perception is realised, further cognitive/affective pro-
of mood, appetite, and sleep, as well as memory cesses can occur as a result of this input. The flow of
and learning. It is a major antidepressant. information is not serial but a complexity of parallel
processing that utilises feedback from various brain
C) Acetylcholine is used by only a few cell groups and regions. There is no neuron that can recognise the
is the major neurotransmitter in autonomic ganglia. complexities of an object like a chair. Only the sum-
D) Peptides form a large and diverse group of trans- mation of complex networks, with experience (neural
A well-known division of the human brain is that The brain has to attend to the world in two com-
described by neurologist Paul MacLean as the triune pletely different ways, and in so doing to bring
brain (MacLean, 1990). This evolutionary view of the two different worlds into being. In the one [that
brain describes three main regions in an evolution- of the right hemisphere], we experience—the
ary hierarchy: the primitive “reptilian” complex (the live, complex, embodied world of individu-
brainstem), the “palaeomammalian” complex (the al, always unique beings, forever in flux, a net
limbic system), and the “neomammalian” complex of interdependencies, forming and reforming
(the cortex). The reptilian complex is fully developed wholes, a world with which we are deeply con-
at birth, while the palaeomammalian complex is part- nected. In the other [that of the left hemisphere]
ly developed and continues to develop during early we “experience” our experience in a special way:
childhood, and the neomammalian complex is mostly a “re-presented” version of it, containing now
underdeveloped at birth and is the last part of the tri- static, separable, bounded, but essentially frag-
une brain to develop (The Neuropsychotherapy Insti- mented entities, grouped into classes, on which
tute, 2014c). The implications of the model are that the predictions can be based. This kind of attention
survival instincts of the palaeomammalian complex isolates, fixes and makes each thing explicit by
(the limbic system) are significantly developed during bringing it under the spotlight of attention. In
the early years of life, distinct from the later-develop- doing so it renders things inert, mechanical,
ing cognitive processes of the neomammalian com- lifeless. But it also enables us for the first time
plex (Rossouw, 2011). More sophisticated contempo- to know, and consequently to learn and to make
rary models of the brain and behaviour do not fully things. This gives us power. (McGilchrist, 2014,
support MacLean’s evolutionary model; however, the p. 31).
“bottom-up” perspective of development remains in- Allan Schore explains that the early-maturing right
structive for a corresponding bottom-up therapeutichemisphere is the locus of attachment formation and
approach (Rossouw, 2011). This bottom-up approach, essentially the gateway to affect regulation later in
as distinct from a top-down, cognitive approach, life—so much so, indeed, that developing an expanded
looks to establish safety through down-regulation of
capacity for right-hemisphere processing (an empha-
sympathetic over-arousal and activation of a state of
sis on right-brained affective skills rather than a left–
parasympathetic security, resulting in increased cor-
cognitive bias) is central to clinical expertise (Schore,
tical blood flow to the left frontal cortex for effective
2012). In a similar vein Badneoch (2008) warns ther-
activation of cognitive abilities, and limiting “looping”
apists to be grounded in right-brain engagement with
activity within the limbic system (Rossouw, 2011, p. 4)
clients or run the risk of being disengaged from the
to allow for effective new learning. regulating and integrating influence of right brain-
Iain McGilchrist, in his noteworthy book The to-right brain connection with clients. She further
Master and His Emissary: The Divided Brain and the encourages therapists to widen their window of tol-
erance (see section 1.1.6.1), be conscious of implicit
51 INTERNATIONAL JOURNAL OF NEUROPSYCHOTHERAPY Volume 3 Issue 1 (2015)
vulnerabilities, and develop mindfulness to be present alised, non-verbal, implicit yet highly meaning-mak-
with both the client and self. There is a place for left- ing memories of this type that shape foundational
brain focus when thinking about specific interven- understandings of self and the world and determine
tions, but as McGilchrist admonishes, the left should how we anticipate the future.
remain servant to the master right hemisphere.
Baer, R. A., Smith, G. T., Hopkins, J., Krietemeyer, J., Dahlitz, M. J. (2013). Klaus Grawe. The
& Toney, L. (2006). Using self-report assessment Neuropsychotherapist, 2, 128-129.
methods to explore facets of mindfulness. Assess- Dahlitz, M. J., & Rossouw, P. J. (2014). The consist-
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Maria I. Kostyanaya
Introduction
From the late 20th century until the present time, researchers in the broad field of psychological science have
been noting the need for refined intellectual frameworks to arise (Homskaya, 2010; Kandel, 1998, Rossouw,
2011; Rossouw, 2014). Western views that are presented in the following pages refer to “…the dawn of the
mental health renaissance.” (Rossouw, 2011, p. 3), which was heralded by the “…new intellectual framework
in psychiatry” (Kandel, 1998, p. 457) and the corresponding technological advances in the neurosciences. As
a result, the emerging field of brain-based care is rapidly gaining momentum - a neuroscientifically informed
therapy or neuropsychotherapy (Grawe, 2007, Rossouw, 2014).
In the early years of 20th century a group of academics in the field of psychology in Russia formed a new
school, which during the restricted times of Soviet regime received insufficient recognition on a global scale
(Kostyanaya & Rossouw, 2013). The investigators aimed at developing an “objective” approach to understand-
ing the connection between mind and brain with latest research focussed on the problem of personality, its
neural correlates and the impact of society on human mental functioning (Homskaya, 2010; Luria, 1979). Due
to the opening of the iron curtain and present-day globalisation more literature on Soviet psychological devel-
opments is being translated and is becoming available for a broader audience (see, for example multiple works
of Akhutina (2003), Akhutina & Pylaeva, 2012; Leontiev (2005a, 2005b, 2012, 2013), published in English).
This new state of affairs allows the comparative analysis of Soviet paradigms and the contemporary Western
paradigms which is the general aim of this paper.
In the first part of the paper a neuropscyhotherapeutic framework is presented, starting with an outline of
its roots and most current conceptualisations of neuropsychotherapy as a research field. The second part of the
report focuses on the development of Soviet school of psychology and its main postulates. The third part of
the report includes the comparative analysis of the two paradigms as well as a consideration for future analytic
inquiry in this area. The final part of the paper closes with a succinct conclusion.
Cite as: Kostyanaya, M. I., (2015). Russian psychology and neuropsychotherapy: Comparative analysis.
International Journal of Neuropsychotherapy, 3(1), 70–88. doi: 10.12744/ijnpt.2015.0070-0088
Contemporary state of
neuropsychotherapy as a
research field
Present-day authors define
neuropsychotherapy as a field of ap-
plied research which tries to: identify
neural mediators and functional tar-
gets of psychotherapeutic effects, to de-
termine new therapeutic routes using
neurotechnology, and to design psycho-
frontal lobes. In such cases, the neural activation of therapeutic interventions on the basis of
survival initiates the onset of patterns of avoidance. neuroscientific knowledge (author’s emphasis) (Walter
This short-term enhancement of survival can compro- et al., 2009). The main trajectory of the field is seen in
mise thriving in the long-term, leading to the onset of its potential to provide investigators with “reliable sur-
psychopathology. Rossouw (2014) postulates that fear rogate markers” (Walter et al., 2009, p. S180) or clini-
based neural activation when it become the default ac- cal indicators of causal factors for the development of
tivation pattern leads to psychopathology developing mental disorders, useful for diagnosis, prognosis and
from the bottom to the top. prediction of psychotherapeutic changes. This course
Rossouw (2014) describes particular principles of becomes possible with the integration of neuroscience
bottom up neuropsychotherapy derived from the out- into psychotherapeutic education, research and prac-
lined theoretical framework, which are also support- tice.
ed by a number of case studies presented in the book. With regard to identification of the neural mediators
The major trajectory of neuropsychotherapeutic work and functional targets of psychotherapeutic effects, the
implies the priority of facilitating safety experiences most clearly marked examples refer to the research on
(on physical and emotional levels) for clients, through the neural substrate underlying dysfunctional emo-
down-regulation of their stress responses by means of tional regulation (Beauregard et al., 2001; Davidson et
the Rogerian principles (Rodgers, 1961) and thereby al., 2000; Grawe, 2007; Ochsner et al., 2004; Rossouw,
addressing basic human needs. Here the robust ther- 2012; Walter et al., 2009). Even though anxiety and de-
apeutic alliance ensures “integrative relationships” pression are functionally different (Grawe, 2007), the
Kaptelinin, V., & Nardi, B.A. (2006). Acting with Leontiev, A. N. (1983). Izbrannye psikhologicheskie
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Karpov, Y. V., & Haywood, H. C. (1998). Two ways to pean Psychology, 43(3), 8-69.
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Pieter Rossouw
Abstract
Attention deficit hyperactivity disorder (ADHD) is one of the most common childhood disorders,
affecting approximately 7% of the population, the exact cause of which is unknown. It is widely recog-
nized as a non-curable neurobiological behavior disorder, characterized by inattention, hyper¬activ-
ity, and impulsivity, and is routinely treated using stimulant medication and behavior modifica¬tion
techniques.
New research indicates a positive correlation between ADHD symptoms and physiological changes
associated with the increased release of the stress hormones norepinephrine, epinephrine, and corti-
sol, and a corresponding reduction in neurotransmitter levels of dopamine and serotonin. It is sug-
gested that these physi-ological changes in children may be directly attributed to prolonged exposure
to stress in early childhood, both in care facilities and the compulsory school system.
Ongoing research has linked bullying with similarly fluctuating neurotransmitter levels. Bullying
is a complex and subjective behavior pattern, destructive by nature, pervading every aspect of society,
and thought to affect 20% of the population. Given that bully behavior is characterized by morbid so¬-
cial behavior, hyperactivity and/or hyper-reality, and impulsivity, and predominates in the compulsory
school system, the parallel with ADHD is observed, making the choice of the label, social deficit hy-
perac-tivity disorder (SDHD), appropriate.
The authors believe that the impact bullying has on learning and working environments cannot be
quantified until SDHD is first recognized and accepted as a neurobiological behavioral disorder with
determinate criteria. Classification of SDHD would facilitate research into the hypothesis that ADHD
and SDHD are comorbid conditions and give the condition the attention it deserves.
Cite as: Laurens, S. D., & Rossouw, P. J. (2015). Social deficit hyperactivity disorder (SDHD): A sibling of
ADHD? International Journal of Neuropsychotherapy, 3(1), 92–100. doi: 10.12744/ijnpt.2015.0092-0100
5 Self-actualization Identity
text of other causes implicated by reduced serotonin Notwithstanding the significance of a possible
and dopamine levels. Lack of sufficient sleep, lack of ADHD gene and nicotine involvement, the learned
physical activity, insufficient exposure to sunlight, and
behavior option is of particular interest in the context
nutritional deficiencies are all considered contributing
of this article. Just as a child learns to speak English in
factors in ADHD behavior. an English-speaking family, so too does a child learn
Another factor, genetic predisposition to ADHD, anxiety-reducing methods by imitating the same
suggests: methods used by the family members. Suffice to say,
if a child is not exposed to chronic stress prematurely,
An individual was born with presumed ADHD there should be no need for their survival instinct to
genes, thereby predisposing that individual to ADHD manifest—thereby eliminating or reducing a child’s
through genetic transference. need to experiment with or implement learned stress
An individual was exposed as a foetus to nico- management techniques.
tine, thereby predisposing the individual to ADHD The possible causes of ADHD and links to reduced
through environmental factors (National Institute for neurotransmitter levels are outlined in Table 4.
Mental Health, 2014)
Whilst ADHD is considered a neurobiological
An individual was born into a family where at least behavioral disorder, there is an equivalent social dis-
one parent/primary caregiver is diagnosed as having order that deserves recognition and consideration.
ADHD, thereby predisposing the individual to ADHD Social deficit hyperactivity disorder (SDHD) is the
through learned behavior. name we have given to what is commonly referred to
22. Often intrudes on others (e.g., Impatient/ impulsive Serotonin Nonverbal Kinetic
butts into games)
23. Often has difficulty waiting in line Impatient/ impulsive Serotonin Nonverbal Kinetic
or awaiting a turn in games or
group situations
24. Often interrupts others (e.g., butts Impatient/ impulsive Serotonin Verbal Auditory
into conversation)
25. Often blurts out answers before Impatient/ impulsive Serotonin Verbal Auditory
questions have been completed
Table 5:
Elaborate Interpretation of Suggested Diagnostic Criteria for the Evaluation of Social Deficit Hyperactivity
Disorder (SDHD)
Note. The information in Table 5 was compiled from the following sources: REACHOUT.com, Australia’s leading online youth
mental health service; beyondblue (2014); State Government of Victoria Department of Education & Training (2014); McGrath and
Noble (2006); and Porter (2007); and Robinson (n.d.).
Neurotransmitter Communication
Suggested Diagnostic Criteria for the evaluation of Social Symptom of reduced
Deficit Hyperactivity Disorders (SDHD) neurotransmitter levels involvement preference
1. Repeatedly engages in behavior intended to be hurtful or Inability to feel pleasure Dopamine Nonverbal
cause distress to another person
2. Often abuses position of power (or perceived power) to Inability to feel pleasure Dopamine Nonverbal
exert control over another person
3. Often uses extortion to obtain money, food, possessions, Inability to feel pleasure Dopamine Nonverbal
or sexual gratification from another person
4. Often uses extortion to force a person to commit antiso- Inability to feel pleasure Dopamine Nonverbal
cial or illegal acts, including theft, vandalism, sexual acts
5. Often uses threats to expose shared confidences Inability to feel pleasure Dopamine Nonverbal
6. Often uses threat of exposed shared confidences to ob- Inability to feel pleasure Dopamine Nonverbal
tain favors, including sexual favors
7. Often discriminates against a person based on ethnic or Inability to feel pleasure Dopamine Nonverbal
gender bias, subjecting that person to repeated harass-
ment
8. Often discriminates against a person with a physical Inability to feel pleasure Dopamine Nonverbal
handicap, cognitive impairment, emotional vulnerability,
or who is socially disadvantaged, subjecting that person
to repeated harassment
9. Often uses exclusion tactics to socially isolate a person, Inability to feel pleasure Dopamine Nonverbal
including conditional or restrictive tactics
10. Often uses public exclusion tactics to socially isolate a Inability to feel pleasure Dopamine Nonverbal
person, including huddles, loud gangs, or hiding away
11. Often leaves anonymous notes or phone messages for Inability to feel pleasure Dopamine Nonverbal
another person
17. Fails to acknowledge that antisocial behavior is inappro- Lack of remorse Dopamine Nonverbal
priate
Hyperactivity/Hyperreality
18. Often involved in aggressive physical behavior with in- Aggressive Serotonin Nonverbal
tent to oppress another person, including pushing, shov-
ing, punching, hitting, bashing, kicking, tripping, hair
pulling, and clothing pulling, with or without a weapon
19. Often uses loud, aggressive language with intent to em- Aggressive Serotonin Verbal
barrass, humiliate, threaten, or oppress another person,
including screaming and swearing
20. Often involved in destructive behavior with intent to Aggressive Serotonin Nonverbal
steal or destroy another person’s property
21. Often makes unsolicited sexual advances toward another Aggressive Serotonin Nonverbal
person, including kissing and touching
22. Repeatedly and intentionally stalks another person OCD behavior Serotonin Nonverbal
23. Often uses technology to sabotage another person’s iden- OCD behavior Serotonin Nonverbal
tity and wellbeing
24. Often uses stares, disparaging looks or rolling eyes to Inability to feel pleasure Dopamine Nonverbal
embarrass or intimidate another person
25. Often calls another person derogatory names Inability to feel pleasure Dopamine Verbal
26. Often gossips or spreads malicious rumors about another Inability to feel pleasure Dopamine Verbal
person
27. Often tells lies about another person Inability to feel pleasure Dopamine Verbal
28. Often verbally insults or ridicules another person, in- Inability to feel pleasure Dopamine Verbal
cluding the use of taunts or sarcasm
29. Often engages in negative verbal teasing of another per- Inability to feel pleasure Dopamine Verbal
son including telling jokes about that person
30. Often engages in negative physical teasing of another Inability to feel pleasure Dopamine Nonverbal
person, including playfully pulling hair or clothing,
intentionally bumping or crowding
31. Often uses code names for a person or whispers about Inability to feel pleasure Dopamine Verbal
another person behind their back
Impulsivity
32. Often intrudes on others (butts into games or activities) Impatience/impulsivity Serotonin Nonverbal
33. Often actively attempts to spoil a game or activity of Impatience/impulsivity Serotonin Nonverbal
another person
34. Often interrupts another person (butts into a conversa- Impatience/Impulsivity Serotonin Verbal
tion)
35. Often taunts or provokes another person already in- Impatience/Impulsivity Serotonin Verbal
volved in a conversation
99 INTERNATIONAL JOURNAL OF NEUROPSYCHOTHERAPY Volume 3 Issue 1 (2015)
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