The Neuroscience of Talking Therapies: Implications for Therapeutic Practice
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For many years, the role of counselling has been a central focus of scientific study and discourse, which has benefited significantly more in recent times from the unique insights of neurobiological research into the effect of enriched environments on the brain—environments such as structured talking and counselling therapy, for example. In fact, the positive effects of talking therapies—not only on behaviour, thought patterns, and feelings, but on neurochemical shifts, neural activity, and even neurostructural changes, as well—have been clearly demonstrated ever since Nobel laureate, Eric Kandel, proposed a new intellectual framework for psychiatry and psychotherapy. In this paper I set out the recent findings in neuroscience and explore how these findings may shape the future of talking therapies.
Neurobiological findings have generated several new perspectives on the therapeutic process. Some of the most profound aspects are:
- The emerging paradigm in understanding neural functioning.
- The changing paradigm in brain studies, which have demonstrated a shift from a focus on the brain as an electrochemical system to the brain as a neural network, thereby shifting the focus from chemical interventions as baseline therapy to enriched environments, with talking therapies a key component.
- Neuroplasticity and the effect of talking therapies on changing brain functioning and brain structure; closely linked to these findings are new indicators concerning the role of antidepressant medication on neural function.
- The role of mirror neuron systems on the effects of counselling: discoveries have opened new perspectives on our understanding of what shapes human behaviour.
- The role of right-brain-to-right-brain activation linked to attachment and control patterns to facilitate change.
These new perspectives have profound implications for talking therapies. In the following sections, the implications of these findings, and how counselling has become a catalyst for effective therapeutic outcomes, will be explored.
A Decade after the Decade of the Brain
During the past 100 years, significant scientific discoveries have facilitated paradigm shifts in our way of being. First, Einstein’s theory of relativity demonstrated that time and space (entities that traditionally were seen as totally separate) are part of the same fabric (Einstein, 1954). Then, Louis de Broglie demonstrated that all matter (not just photons and electrons) has quantized wave/particle duality. This has led to a new understanding of the interaction between the physical brain and the mind, the effect of the mind on the brain, and the brain on the environment; in other words, the brain’s ability to command the environment and, for that matter, the universe (De Broglie, 1960).
Such paradigm shifts were properly recognised when, in 1990, the US Congress designated the 1990s the Decade of the Brain, and President George H. W. Bush proclaimed, “A new era of discovery is dawning in brain research”. During the ensuing decade, scientists greatly advanced our understanding of the brain: as Eric Kandel claimed, “We are in the midst of a remarkable scientific revolution, a revolution that is about to change the way we think about the brain and the mind” (Kandel, 1998, p. 467). In this paper, Kandel referred to possible neurochemical, neural structural, and neural network changes facilitated by—talking therapies! He also referred to possible changes in neural hardware that may occur due to neural machinery in the therapist’s brain acting on the client’s brain (Kandel, 1998). These were profound statements, especially as they had not (yet) been demonstrated in research findings. With good reason, Kandel’s article is often referred to as the most significant paper on the nature and future of psychotherapy published since Freud’s abandoned project—A Project for a Scientific Psychology (Freud, 1895/1953). Kandel made a significant contribution to the understanding of memory at the neurocellular level, and opened the field of cellular neuroscience to the field of psychotherapy. In 2000 he was awarded the Nobel Prize in Medicine and Physiology for his work
Kandel’s work (cf., Kandel, 2006; Kandel, Schwartz, & Jessell, 2013) sparked researchers like Wayne Drevets (2001), Richard Davidson (2010), Richard Davidson and Susan Begley (2012), Olaf Sporns (2011), James Schwartz (Kandel et al., 2013), and many others, who have contributed to facilitating this paradigm shift in understanding the brain: a shift from seeing the brain as an electrochemical system to viewing it as a network combining the social properties of the brain—the interconnectedness of “us” (Rossouw, 2011b).
The Brain as an Electrical System
In 1902, the brilliant electrophysiologist, Julius Bernstein, discovered that nerve cells have steady potentials (electrical charges) and that—even in a resting state—there is a difference in voltage between the inside and the outside of the nerve cell. This discovery was one of the first indicators of the brain as an electrical system, and was later confirmed by Alan Hodgkin and Andrew Huxley, who linked the process to memory systems. This led, in 1938, to the discovery of electroconvulsive therapy by Ugo Cerletti and Lucio Bini (Shorter, 2007). Electroconvulsive therapy subsequently gained widespread use as a form of treatment, and is still used as a treatment mode for many disorders today (Rossouw, 2013).
Focus on Chemical Processes
Research by Henry Dale and colleagues indicated that the chemical acetylcholine acts as a transmitter of signals, hence it appears the basic operating system of the brain is not purely electrical activation but, rather, electrochemical. The Hungarian-American neurophysiologist, Stephen Kuffler, and John Eccles, the Australian neurophysiologist, were the first to demonstrate how the release of acetylcholine gives rise to, and fully accounts for, all phases of action potentials. Their work facilitated a paradigm shift in understanding the function of the brain—it was the birth of the chemical model towards the understanding and treatment of the human brain, often referred to as the “medical model”. Eccles was awarded the Nobel Prize in Physiology or Medicine in 1963.
These discoveries changed the nature of the treatment of the brain, and were followed by a huge number of studies looking at chemical interventions to enhance neural functioning. The most important of these for mental health was the discovery of the properties of a compound that acts as an inhibitor of serotonin. The scientists Bryan Molloy and Robert Rathbun, working in collaboration with Eli Lilly, found that the antihistamine diphenhydramine showed some antidepressant-like properties. Later, another Lilly scientist, David Wong, worked on derivatives to inhibit only serotonin and, in May 1972, Jong-Sir Horng tested a compound that seems to be the most potent inhibitor of serotonin. This compound was later called fluoxetine (Prozac). The first paper on fluoxetine was published in 1974 (Wong, Horng, Bymaster, Hauser, & Molloy 1974); a twenty-year follow-up study was published in 1995 (Wong, Bymaster, & Engleman, 1995). The drug appeared on the Belgian market in 1986. Final approval was given in 1987. Within a year, sales in the USA alone reached $350 million.
Since 1978 a large number of related drugs have been introduced to the market, with annual sales of U.S. $11 billion in 2008. At the same time, thousands of research papers have been published indicating that the primary mode of intervention for people suffering from anxiety and/or depression is an anti-depressant, a Selective Serotonin Reuptake Inhibitor (SSRI). Therefore, as a result of outcome-based evidence, the medical model—the focus on the brain as a chemical system—became the preferred mode of delivery of psychiatric care (Rossouw, 2013).
The guidelines in health circles were clear: that the first-line intervention for people suffering from baseline illnesses (i.e., all diseases with primary or co-related symptoms of depression and/or anxiety) is a chemical intervention—antidepressant medication.[Content protected for subscribers only]
The Long-Term Benefits of Chemical Interventions: Questions
A number of research studies have recently questioned the established view that chemical interventions are helpful for the brain, without detrimental effects. One group of medications, which is widely used in many disorder presentations, is the antidepressant group—the second-generation antidepressants, the SSRIs in particular. This group has been identified as being possibly not as beneficial for neural processes as previously thought. A recent study by Paul Andrews and colleagues, for example, states that the present medical model of prescribing antidepressant medication as a first-line treatment modality for an array of conditions needs to be re-evaluated against current neuromolecular evidence (Andrews, Thomson, Amstadter, & Neale, 2012). The processes of regulating serotonin are described by the authors of this study in relation to one of the key principles of molecular science—that disruptions of evolved adaptations degrade biological functioning (Andrews et al., 2012). As Kandel had shown, the key role of serotonin in adaptation processes has been clearly established and accepted in neuroscience (Kandel 1976, 2001, 2005; Kandel et al., 2013); any disruption to the role of serotonin, therefore, may have adverse health effects because inhibition of neurobiological actions (i.e., serotonin reuptake) causes morphological changes to neural structure, resulting in higher risk of apoptosis, or neural death. This means relapse rates will increase with prolonged intake of serotonin inhibition.
Contrary to the widely-held belief that antidepressants promote production of brain-derived neurotrophic factor (BDNF), or neurogenesis, Andrews et al. (2012) argue that the method used to detect this—5-bromo-2’-deoxyuridine (BrdU), which detects DNAsynthesis—interprets this synthesis as an indication of neurogenesis. They point out, however, that DNA synthesis often occurs during apoptosis, and is most likely part of cyclic-related cell death (Herrup, Neve, Ackerman, & Copani, 2004). More recently, sophisticated studies have found no evidence that antidepressants trigger neural growth (Kobayashi, 2010); to the contrary, Kobayashi (2010) found that fluoxetine caused mature neurons to take on immature functional characteristics. Thus, constant serotonergic input is needed to maintain the mature state of neurons, the implication being that long-term inhibition of serotonin uptake may lead to a much greater risk of relapse when inhibition discontinues (discontinuation of medication). This leads to a vicious cycle where neural maturation is compromised, both when medication continues and when it is discontinued (the double loose loop).
Networks: The Emerging New Paradigm
The discovery of brain “wiring” was made during the 1940s by Donald Hebb. He suggested that “When an axon of cell A is near enough to excite cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A's efficiency, as one of the cells firing B, is increased” (Hebb, 1949, 1961). This phrase is often referred to as “Hebb’s law” and was popularised in the catchphrase, “neurons that fire together, wire together” (Grawe, Donati, & Bernauer, 1994)—in other words, the more neurons fire in a specific sequence, the stronger the neural connections become. This process is known as up-regulation of neural activity, which is an important process in brain development and assists with streamlining neural communication. The same principle applies to “looping”, where the formation of powerful (unhelpful) loops of neural firing occurs.
Kandel’s research on sea slugs (aplysia californica) demonstrated how neural communication can be explained on a cellular level. He also demonstrated how “hardwired” systems can change the direction of neural activation via activation from the environment. This work has assisted the understanding of how genes express through interaction with the environment. The implications are clear: the environment changes the brain. Kandel also demonstrated that the essence of neural functioning is not chemical but rather a network of connections. Thus, while Freud’s hypothesis that the subconscious (or memory) is situated in the space between two neurons was in principle correct, recent research indicates it is a bit more complex; in fact, as Kandel showed, memory consists of a series of communication networks between neurons. These networks are constituted as patterns of behaviour, feelings, and thoughts—a complex pattern of firing that defines the “self”. Experiences, good or bad, change these patterns and lead to new patterns of activation.
The key question is: Can this process and the formation of neural loops change? Or is the sufferer of trauma or some pathology doomed to experience the symptoms of discomfort forever, due to the existence of these loops? An answer to these questions lies in the neurobiological research, which has demonstrated that new, effective neural pathways can indeed be established (Rossouw, 2010, 2012). Neural imaging scans have shown how cortical blood flow shifts, and new firing patterns emerge when, for example, a client is given specific instructions to focus on, or asked to write down his or her thoughts and consider possible solutions to the worries. These actions subsequently activate the left pre-frontal cortex, shifting cortical blood flow into these regions, and in the process establishing new neural firing activity. This does not mean a single intervention changes neural firing, but it does activate new firing patterns. The difficulty is that the old firing patterns become the default patterns, therefore—unless the new pattern is actively activated—the client will constantly drift back into the old firing patterns in day-to-day life.
To establish these new firing patterns and to assist these patterns to become stronger, ongoing activation is needed over a period of time. When new patterns are activated for a period of time (6-8 weeks), the same Hebbian principle applies—neurons that fire together, wire together—and a new neural pattern is established. This is the aim of the neuropsychotherapeutic process. The network principle of neural functioning has recently been demonstrated by Sporns (2011), Davidson (2012), Schore (2012), and Siegel (2010, 2012), among others.
An essential aspect of the neural network theory is the role of avoid-and-approach patterns in neural firing to facilitate behaviour. These patterns interact in close proximity of each other as an integral part of the limbic mirror neuron system (more about the mirror neuron system later). Both avoid-and-approach patterns play a major role in motivation, but the outcomes are significantly different: healthy development of these patterns forms an essential cornerstone towards mental wellness (Spielberg et al., 2012), whereas overactivation of fear responses (especially during the first 10 months post birth), facilitates high activity in anterior cingulate areas, resulting in excessive patterns of avoidance and the foundation of the anxious brain. The questions then arise: Does this mean that the brain is hardwired to remain anxious, or can change be facilitated? And if yes, how?
Neuroresearcher, Michael Merzenich, demonstrated another principle in molecular science, “neurons that fire apart, wire apart” (Bao, Chang, Woods, and Merzenich, 2004). This principle demonstrates that, when neurons stop firing together (that is, they are not activated in a specific sequence), they “lose interest” in each other and align themselves separately. Then synaptic strength becomes less, and neurons that used to attach eventually become detached. The implications of this are significant. For people suffering from depression and/or anxiety, and experiencing significant neural loops, it means that they can be assisted to establish new neural firing patterns and new neural activity. When those patterns are established and regularly activated, not only will the old firing patterns become the less preferred patterns but, based on the principle “neurons that fire apart, wire apart”, they will also slowly start to deconstruct, resulting in less risk of relapse into the default patterns. Greater changes to the neural firing patterns occur when the new neural patterns are effectively established and continuously activated.
Over the last decade, due to the introduction of talking therapies, a significant number of studies have demonstrated changes in brain functioning, cortical blood flow and/or structural changes. In 2001, Arthur Brody and colleagues identified metabolic changes in patients with depression when treated with interpersonal therapy (Brody et al., 2001), while, in the same year, Stephen Martin and colleagues identified blood-flow changes in depressed patients treated with interpersonal therapy (Martin et al., 2001). Then, in one of the most profound studies on neural change, Thomas Furmark and colleagues demonstrated significant lasting changes in cerebral blood flow in patients with social phobia treated with cognitive-behavioural therapy in comparison to Citalopram (Furmark et al., 2002). At this time, many studies were demonstrating, in particular, the effectiveness of cognitive behaviour therapy (CBT). For example, Goldapple and colleagues demonstrated the effect of CBT on cortical-limbic pathways for patients with major depression (Goldapple et al., 2004); Jan Prasco and colleagues demonstrated changes in the regional brain metabolism of sufferers of panic disorder through treatment with CBT (Prasco et al 2004); Kim Felmingham and colleagues identified changes in the anterior cingulate cortex and amygdala regions (after CBT), for sufferers of post-traumatic stress disorder (Felmington et al 2007); and, in a study using neuroimaging, Sidney Kennedy and colleagues demonstrated differences in brain glucose metabolism due either to CBT or chemical interventions, showing that the two approaches activate distinct neural regions (Kennedy et al., 2007). Similarly, in a study on clients presenting with borderline disorders using fMRI scans, Knut Schnell and Sabine Herpertz demonstrated significant changes in the right prefrontal cortical regions as result of dialectic-behavioural-therapy (Schnell & Herpertz, 2007). Julie Maslowsky and colleagues also used fMRI scans to identify the effects of CBT on the neural systems of adolescents presenting with generalised anxiety disorder (Maslowsky et al., 2010), and Manfred Beutel and colleagues demonstrated changes of brain activation in fronto-limbic patterns as a result of short-term psychodynamic inpatient psychotherapy (Beutel, Stark, Pan, Silbersweig, & Dietrich, 2010). In recent studies, increased cortical inhibition has been facilitated in problematic perfectionists through group CBT (Radhu et al., 2011), and multiple metabolite effects have been recorded with MRSI (magnetic resonance spectroscopic imaging) arising from CBT interventions in paediatric obsessive-compulsive disorder (O’Neill et al., 2012).
Although many of the studies described here used cognitive therapies as a mode of service delivery, there are ample indications that all talking therapies—interpersonal therapy, dialectic behavioural therapy, short-term psychodynamic therapy, behavioural activation therapy, and others—facilitate neurochemical and neural network changes. The reason for this is clear: all these therapies share a common denominator—being a talking therapy conducted in a safe (enriched) environment (Rossouw 2011a, 2012). And right now, studies are being conducted to compare the efficacy of these various modes of delivery.
Mirror Neurons, the Brain, and Talking Therapies
Mirror neurons are a class of neurons that were originally discovered by researchers at the University of Parma, Italy. They were found in the ventral premotor cortex of macaque monkeys, where the neurons discharged in association with movement (Gallese, Fadiga, Fogassi, & Rizolatti, 1996; Rizolatti, Fadiga, Gallese, & Fogassi, 1996). Subsequent research has found mirror neuron systems in different parts of the brain, and in the human brain (Bastiaansen, Thioux, & Keysers, 2009; Cattaneo & Rizolatti, 2009; Kilner, Friston, & Firth, 2007; Yuan & Hoff, 2008). Research has also indicated the role of these systems in imitation, empathy, mind reading, and predicting actions (Cataneo & Rizolatti, 2009; Iacoboni, 2009). Many mental health disorders are directly linked to the mirror neuron system (MNS) (Iacoboni, 2009; Yuan & Hoff, 2008).
Initial models used to explain the MNS adopted a simplistic causality approach where a perceived action is followed by a motor action—that is to say, motor actions can be triggered by perceived actions. This model seems to answer the question: Is it possible to understand the intentions of other people by simply observing their actions? It is the classical mirror effect: we smile at a baby, the baby smiles back; the actions of one person are mirrored by the actions of another. This insight into the MNS builds on the brilliant observations of William James who, more than a century ago, asserted that “every mental representation of a movement awakens to some degree the actual movement which is its object” (James, 1890, p. 526).
Soon it became clear that the real question still remained: How can intentions be inferred through action observation? This gave rise to more sophisticated investigation into the MNS. Take as an example a picture of someone in an operating theatre holding a scalpel. We know—because our MNS predicts the future—that a cut will be made on the skin of a patient as part of an operation to heal. Now take the example of Dr Jekyll and Mr Hyde: it is the same scene but, in the first instance, the scalpel is in the hand of Dr Jekyll and, in the second, the scalpel is in the hand of Mr Hyde. If the observer has no knowledge of the narrative of Dr Jekyll and Mr Hyde, the MNS fires the same in both scenes regardless. But if the observer has a clear knowledge of the narrative of this one person with two personalities, the MNS fires in different ways. Intent seems to play a role.
To understand intent, Rizolatti and Craighero (2004) proposed the following explanation, which is rather simple but certainly non-trivial in terms of implementation:
Each time an individual sees an action done by another individual, neurons that represent that action are activated in the observer’s premotor cortex. This automatically induced, motor representation of the observed action corresponds to that which is spontaneously generated during active action and whose outcome is known to the individual. Thus the mirror neuron system transforms visual information into knowledge. (p. 172)
The authors further proposed that visual information is transferred from deeper (limbic) regions towards the higher cortical regions, and predictive coding runs in a bottom-up mode through at least two MNSs—the premotor MNS residing in the parietal lobe and premotor cortex, and the limbic MNS in the anterior mesial frontal cortex. Evidence of these systems was found in a number of neurophysiological investigations using electroencephalography, magnetoencephalography, and transcranial magnetic stimulation (Rizolatti & Craighero, 2004).
Understanding intention coding is a vital component of various aspects of MNS functioning, including the hierarchical process of coding, predictive coding (goals, meaning and future), and understanding pathology (prediction error). These aspects hold significant implications for the psychotherapeutic process.
Activation of the two MNSs occurs in a hierarchy, indicating the superiority of one system over the other. The more primitive limbic MNS is a robust system organised to enhance survival. This predictive coding network is established based on minimising prediction error, where each level of the hierarchy predicts representations on the level below. On a neural level this resonates with the theoretical framework of Maslow—that fulfilment of basic survival needs supersedes higher cortical needs. Activation of the limbic MNS is not purely a genetic predisposition, however, because the interaction of the infant with its environment also sets the tone for the expression of genetic indicators. The implications are clear: the infant needs an enriched, safe environment to express an effective circuitry for predictive coding. Hence, violation of basic needs—primarily attachment and safety, which are key components for down-regulating any ongoing fear-based activations—facilitates a fear-based predictive coding framework. The limbic MNS interprets external cues both in relation to prior coded activations, and within the (pathological) predictive coding framework, and responds to secondary MNSs in such a way as to minimise error. This is survival coding. The result is a neural system that maintains (and strengthens) its pattern of pathology (see Figure 1).
Links with the Emotions
Observation seems to activate a mosaic—of the motor and somasensory neural systems, and the affective systems too. This is why we feel like crying when we see a loved one in distress. And why we wince when we see someone hurting him or herself. We know these affective systems play a vital role in social functioning, including empathy, social learning, and psychotherapy. The evidence for MNSs in emotions was demonstrated by Bastiaansen, Thioux, and Keysers in 2009.
The emotions of disgust and pain are primitive emotions that are closely related to the sensation of distaste; they can be clearly identified via connections from the basal ganglia, amygdala, anterior cingulate, anterior insula and orbitofrontal cortex. The function of these systems is, again, closely linked to the survival response. Predictive coding to minimise error is highly active, and sets the tone for the establishment of key neural processes in the first 10 months after birth. Violations of basic needs such as malnutrition or other forms of abuse—actions that compromise the quality of the ideal, enriched environment—trigger neural patterns of protection. The mirror effect of predictive coding strengthens this process, resulting in strong (albeit unhelpful) patterns, to minimise error, based on the need to survive.
The Mirror Neuron System and Therapy
Based on the above, the question is: What are the implications of MNSs for therapy? In other words, we need to ask to what extent therapists should be mindful of the role of the MNS in a clinical context, and whether the MNS can in any way help to facilitate change.
The example of Dr Jekyll and Mr Hyde is useful here: the mirror neuron stimulus of a scalpel in the hand is interpreted in terms of intention or, to simplify, the perceived outcome of an event is affected by the neural representation of prior experience, in relation to prior activation. Thus, the first handshake and smile of the therapist meeting his or her client for the first time are, in general, interpreted as friendly gestures intended to facilitate safety and the start of a good therapeutic relationship. However, in cases of violated neural systems, the smile and reaching out of a hand may be interpreted as the mirror representation of not being safe. The reality is that a clinician’s intent and a client’s mirror activation may not resonate the same response—precisely because the intent of the action will activate different pathways in limbic alertness, depending on the expression of pathways relative to prior experience, especially that which occurs during early brain development.
The notion that neural structure is a fixed entity, which merely deteriorates over time, has been disproved by many researchers over many decades. The opposite view is neural plasticity, which is linked to how synaptic potentials activate—where neural connections are driven by the Hebbian principle of neural activation (neurons that fire together, wire together), or deactivation (neurons that fire apart, wire apart). Many factors play a role both in neural activation, and changes in neural activation. And neural plasticity is the facilitator.
It has recently been demonstrated that environmental factors have the most important role in neural plasticity, and contribute to shaping neural activation patterns that adjust to maximise survival in the face of these forces (Davidson & McEwan, 2012). The human brain responds on all levels, from meeting the most essential survival needs—oxygen, food, water, reproduction, and shelter—to the most complex—such as enjoying a relaxing evening with family—through a tightly-woven network of neural connections. And if any of those needs, on any level, are compromised or violated, the connections change and new patterns of firing are formed. By far the most significant body of neural pathways are established prenatally and during the first 10 months following birth. The environmental needs of control and attachment have been identified as the most essential of all the environmental variables to facilitate well-functioning neural patterns.
Although neural plasticity operates throughout one’s life, until death, the quality of plasticity decreases with age. It can also be compromised by poor nutrition, lack of exercise, smoking, disturbed sleep patterns, and many drugs; all these factors inhibit the essence of the plasticity, and encourage neural rigidity. Further, any violation of basic needs (such as trauma) up-regulates the fear response system and, using the same plasticity, generates neural patterns of protection. These are the looping neural connections, clearly demonstrated in fMRI and PET images, which maximise immediate survival and minimise problem solving.
The implications for therapeutic work are significant. Clearly, if neural plasticity is so powerful, and neural systems can change their connection patterns via synaptogenesis and synaptoplasticity, we need to ask: Are there evidence-based indicators that maximise neural plasticity and facilitate neural activation that is strong and effective.
Neuroscience, Talking Therapies and the Future: Indicators for Evidence-Based Practice
We are now in the midst of the era following the decade of the brain. While neural science continues to ask ever more profound questions, and continues to present new worlds of information on a daily basis, we are at the same time experiencing the era of applied neuroscience. No longer is this an isolated world of scientists locked in laboratories; we can now see that neuroscience has come full circle in its interaction with its environment, where the focus is to promote wellness in our society.
In 1998 Eric Kandel identified a revolution—saying we were in the midst of a remarkable scientific revolution, a revolution that was about to change the way we view our sense of being (Kandel, 1998). This revolution is indeed taking place in terms of the strategies being used to enhance wellness, which are based directly on neurobiological information as a psychotherapeutic tool.
Molecular neuroscience has demonstrated how talking therapies are the preferred strategies to facilitate neural change—that new patterns of neural activation can be facilitated via the unique qualities of talking strategies provided in an enriched environment. These new patterns of neural activation are facilitated by effective activation of the mirror neuron systems, enhancing cortical blood flow to empower solution-focused outcomes, and facilitating and strengthening new activation patterns, to enhance long-term patterns and reduce risk of relapse into default protection patterns. Current research indicates that many different talking therapies are effective in facilitating neural change. The meta-analysis provided by Klaus Grawe (2007) shows clearly that the common denominator for change through talking therapies is adherence to the key principles of neuroanatomy—namely, to facilitate limbic resonance by activating the primitive limbic mirror neuron system (LMNS); to facilitate safety to enable down-regulation of distress; to enhance cortical blood flow; to address risk factors that cause neural rigidity, such as various lifestyle factors; to strengthen neural activation networks, and facilitate healthy social interactions.
The human brain is not an isolated entity. It exists in relation to its environment; if all stimulation ceases, therefore, the brain dies. The new paradigm in our understanding of the brain indicates that neuroscience is not a reductionist approach but, rather, an inclusive approach. The mirror neuron system is one of the most profound indicators of the interconnectedness of “us” (Rossouw, 2011b). The human brain is a social entity, and its wellness depends on the quality of its connection with its environment. In this framework, talking therapies are seen to foster the microcosms of new, safe and secure social structures, which facilitate the building of new healthy neural pathways.
Talking therapies are not magic cures. To foster new neural pathways of thinking, feeling, behaving, and being, synaptoplasticity must be activated to facilitate communication among new neural networks. These networks are fragile, however, and can relapse to default patterns easily; therefore the challenge is to facilitate adequate activation towards new patterns of firing to cause default patterns to shift. This means a shift in glial activation in order to strengthen the new patterns—recall the Hebbian principle, neurons that fire together, wire together.
Cost-effective interventions are also key. In this regard, significant debates about the health care system have arisen, especially in countries like Australia where rebates are available for some services, but on a sliding scale. Unless new patterns of thinking, feeling, doing and being—as identified in therapy—are effectively facilitated, molecular neuroscience has shown that they are doomed to fail and relapse. Inevitably, this forces the health system further into a crisis management model where more resources are continuously channelled for less result.
Strengthening new neural patterns needs personal support and regular activation—that is, the mirror neuron effect and the homework effect. While internet-based interventions have been proposed to enhance therapeutic outcomes, a meta-analysis of such treatment models currently being undertaken at The University of Queensland demonstrates that almost all models aimed to reduce symptoms of pathology fail to facilitate lasting neural change in terms of the basic principles of neuroanatomy. Clearly, the exclusion of ongoing therapist–client interaction compromises the model.
At The University of Queensland, in conjunction with the Queensland Brain Institute and key neuroscientists around the world, we are working on internet-based models to enhance facilitation of neural pathways via clinician-based activation. This program will focus on strengthening the interventions used by practising clinicians through interactive internet-based activities that will be inclusive of the regular interventions of a therapist. The program is currently in the experimental phase, however, the early indicators are very promising and it is hoped clinicians nationwide will be introduced to these models in the near future.
In terms of psychotherapy, modern neuroscience suggests that the person of the therapist is more important than how much of a specialist he or she may be, and more important than the knowledge base or the insights into a bag of tricks. Recent research indicates instead that the therapeutic alliance, limbic mirror neuron effect, and facilitation of safety and control, are ultimately more crucial in facilitating effective neural change than any of the above-mentioned variables. These qualities will be enhanced more by a better understanding of neural processes and evidence-based practice than anything else.
Undoubtedly, mental health clinicians are in the midst of an exciting era post the decade of the brain, the era of neural application. This is indeed an exciting time where—more than ever—counselling has been identified as the fundamental catalyst to facilitate and enhance wellness.
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