Neuroplasticity: Transforming the brain

Neuroplasticity is a concept that’s taken the world by storm over the past years – take a look at this Google graph of the growth in searches for the term!Capture


The idea behind using the brain’s ongoing neuroplasticity is that we can influence the connections between neurones by doing and thinking differently. Great idea, and definitely one we can use. There have been many discussions about how much we can influence plasticity – or not (this post refers to education and neuroplasticity, this to an old discussion about Norman Doidge’s book – and some of the points that have been omitted). Whatever the real situation, there’s no doubt that our brains do continue developing, forming and reforming connections between synapses and generally responding to our world and the interactions we have with our world via our bodies.

Pain researchers have been particularly enraptured by the idea that the brain can develop new connections, driven it seems by a greater understanding that our experience of pain is an integration of information from the body, modulated at every step of the way by both ascending and descending influences, right until that information is processed by various parts of our brain and, in combination with past experience, expectations, beliefs, predictions for the future, current goals and priorities and in our sociocultural context, produces what we know as pain. Long, long sentence – but you know what I mean!

So, the reasoning seems to go, if pain is an output of our nociceptive system and produced via all these interactions, then neuroplasticity should mean painful experiences can be reversed using the same principles. And yes! Lo and behold! In some cases this happens – vis all the research produced by Moseley and crew in Adelaide, and promoted by the NOI group, and others.

While Lorimer’s group has produced probably the most consistent body of work in relation to therapy based on neuroplasticity, with NOI promoting many of these approaches, it’s not the only group to do so.  Today I’m taking a look at Michael Moskowitz and Marla Golden’ book Neuroplastic Transformation: Your brain on pain, and the accompanying website.

I’ve been asked to take a look at this by a follower, and it’s been an interesting and fun project to work on.

The book is a spiral bound, colour printed A4 sized book with large print (yay!) and gorgeous illustrations of brain sections and neurones and other beautiful diagrams relevant to understanding the brain. The principles underpinning the book are that if we can understand a bit more about the brain, we can harness the functions so we can train our brain to be a little more settled and out of pain. The three neuroplastic rules are: What is fired is wired; What you don’t use you lose; When you make them you break them; when you break them you make them.  The premise is that it’s possible to reverse the changes that occur when a person is experiencing persistent pain – “treathment that uses the basic principles of neuroplasticity to change the brain pathways back to normal function and anatomy”. The authors discuss using thoughts, images, sensations, memories, soothing emotions, movements and beliefs to modify the experience.

The process of treatment involves four phases: Rescue, Adjustment, Functionality and Transformation, or RAFT. Rescue involves generating hope that pain can be changed by providing information about neuroplasticity, and developing a partnership between clinician and person living with pain. Adjustment involves “stabilising” the pain disorder – using a multi-modal approach including medications, injections, and psychosocial treatments to increase activities while reducing pain – emphasising that adjusting to the pain disorder is not the end goal. Functionality involves the person, every time he or she experiences pain, challenging the experience with non-painful stimuli. In other words, every time the person becomes aware of his or her pain, they need to use thoughts, beliefs, images, sensations, movements and emotions to “reverse the neuroplastic processes that cause persistent pain”. Finally, Transformation involves using the experience of overcoming pain to establish new ways to give pleasure.

What I like about this approach is that it is explained and illustrated very well, using up-to-date information and illustrations. It strongly supports self-management or the person being as much part of the treatment as any clinician. That’s good – because, as any of us who have ever tried to change a habit know very well, change is hard! And that’s probably one of the three main concerns I have about employing this approach as a core pain treatment.

My concerns:

  1. Reversing or altering cortical pathways is truly difficult – and it’s perhaps not possible to completely reverse, especially if the problem has been present for a long time. Here’s why: can anyone remember learning to ride a bike? Remember all that falling off, the wobbling, the stopping and starting, the weaving all over the place? How many hours did it take to learn to do that successfully, smoothly and to the point where you were safe to ride in traffic? Now, for some of you, it will have been YEARS since you jumped on a bike. Do you forget how to ride? No. You might wobble a bit, but you don’t actually forget. Similarly, in phobic states, pathways associated with avoiding the feared stimulus remain “wired together” even when new pathways associated with approaching the stimulus are developed. What this means is that it’s possible for a spider phobic to remain somewhat jumpy around a spider even after treatment has reduced the screaming heebie-jeebies. When we think about pain and the myriad associations between the experience, context, interoception (internal body feeling-sense), memories, emotions, language, treatment visits, investigations – there are so many connections that become wired together as a result of experiencing persistent pain that to completely reverse it is an almighty monumental challenge requiring hours or dedicated practice.
  2. While the principles of a neuroplastic approach are well-known, there are some differences in the approach depicted in this book that I’m not aware of being tested formally in pain research. For example, while it’s nice to have a pleasant smell or memory brought to mind, I’m not aware of studies showing that doing this changes memory for pain (or pain intensity). I may well be wrong about this and I’d love someone even more geeky than me to bring some studies to my attention.
  3. My third reservation relates to the well-established research showing that persistent pain is not easily changed, and meanwhile, in the pursuit of pain reduction, many people lose out on good things in life. While people are sitting in waiting rooms, spending time with therapists, monitoring and checking on pain intensity, it becomes very difficult to carry on with valued actions. There are many ways to make space to have your pain and live as well. This doesn’t mean you need to give up hope of pain reduction, but it does mean the focus moves from this as a life focus and on to the things that make life of any kind worthwhile. Maybe the two approaches can go hand in hand, but to my mind the very intensive nature of the approach within this book means that attention must be shifted away from valued actions and towards doing the things that this book argues will reverse pain.

Overall I like the approach within this book – I like that it’s person-centred, positive, uses underlying principles and encourages the person to be actively involved in his or her treatment. There’s no way you can be a passive recipient with this approach! I would love to see some more in-depth study of the effects of this treatment, even in a series of single-subject experiments. I think it could be very helpful, but I’m a little concerned at the focus on pain reduction as the primary goal, and the time and energy this approach demands.

The OOV – Fabulous or familiar?

I love gadgets! New, innovative, groovy – I feel special when I have a new toy to play with. I justify my pleasure by saying “Oh it saves me SO much time”, or “I can do SO much more” – but really, it’s the wow factor that gets me every time. So it is with new and groovy treatments for pain. It used to be all “leg length discrepancy” and “muscle imbalance”, now it’s “neuroplasticity” and “educational neurophysiology”. So I think I’ve stumbled upon the Next New Thing. The OOV.  I attended a one day fundamentals workshop – incidentally, paid for by the University Department in which I work, so this is an unbiased review.

The OOV is a neat foam device shaped somewhat like a goose (if you use your imagination), or perhaps like an insect thorax. It’s curved side to side and from front to back on the bottom, while the top has two concave and one convex curve roughly approximating the curves of the spine.OOV1OOV2Designed by an osteopath, there are several principles the inventor and educators indicate underpin the rationale for the OOV. These are:

  • Functional movement training
  • Developing stability via the pelvis and deep “core” muscles, with joint mobility where this is needed (shoulders and hips)
  • Developing motor control
  • Establish endurance
  • Refine balance
  • Relaxed performance

The exercises performed on an OOV are therefore carried out slowly (almost meditatively), in time with breathing (deep diaphragmatic breathing), and with control.

Training also requires attending to feedback from using the device itself – use it with inefficient motor control and you fall off. Use it with fluid control and, over time, develop strength. The materials included in the training manual state that motor control learning requires a “closed loop feedback” process of attending to sensory information as new movements are learned. After the movements are mastered, then and only then is speed acquired. Exercises focuses on using eccentric contractions to keep movements slow and smooth – and “allows for kinetic chain sequencing to improve”, “increases cross bridge connection between muscle fibres thereby increasing strength, activates the deep muscles, stimulates the low threshold slow twitch fibres building stamina, lengthens the fascia due to long, slow and sustained load”.

The training manual also discusses myofascial slings and suggests that by training the deep core muscles (transverse abdominis, multifidus and the pelvic floor – and don’t forget the diaphragm), and the superficial units (posterior oblique, deep longitudinal, anterior oblique and the lateral muscular slings) coordination and recruitment patterns will allow for stability, strength and speed as forces generated by limbs are transmitted through the body.

Next, the manual describes several postural types. There is the so-called “ideal posture”, kyphotic-lordotic posture, flat back posture, and sway back posture – and of course, we must correct the variants so we can achieve the ideal. I’ll leave you to draw your conclusions as to the rationale for this.

Finally, there are the four pillars of movement:

  1. Axial elongation – for efficient spine articulation, the “safest” environment for movement, preventing compression and shearing forces, and providing the optimal position for the core muscles to work. Just by lying on the OOV, the spine is placed in this wonderful position, provided of course that you lie with your lumbar region in the right spot, which can be just an inch or so from where you may really want to lie.  Efficient breathing – Axial elongation allows for diaphragmatic breathing, with the head lower than the hips which apparently inhibits the secondary respiratory muscles.
  2. Hip mobilisations – to develop correct posture and proper alignment begins with the feet, by dissociating the lower half of the body from the upper half, the stationary half provides stability and support so that forces are directed towards the moving half.
  3. Shoulder and thoracic spine mobilisation – to enhance, strengthen and extend the fluid range of movement at the shoulder which, because of our terrible working environments, seems to produce faulty movement patterns.
  4. Core control – as the manual says “not enough can be said about the importance of a strong core. But strength means nothing if all the muscles that make up the core are not working efficiently during movement”.

OK, so far so good. Training is based on the principles above, with the addition of balance and proper alignment, interspersing new exercises with a balance position, adding new movement patterns to increase the challenge to the nervous system (yes! neuroplasticity!), practice to develop complex movement patterns, and finally repeated practice using weights, increased repetition etc. And if you perform a new set poorly, step back a bit, reduce the demands until motor control develops.

I spent a day using the OOV. With my sensitive nervous system letting me know three days later that I’ve been using muscles I don’t usually demand so much from, I think it does what it says it does – you definitely work a range of muscles more intensely than in everyday life. It’s fun, and because of the slow pace where control is the aim, it’s achievable even for people who wouldn’t ordinarily want to “do exercise”.

What do I think of it? Well, I predict there will be classes for OOV training in many gyms in New Zealand and the world. During the workshop I heard that performance athletes (yes! the Australian swim team!) are using it, that you can rehabilitate sore backs, shoulders, hips, whatever; I learned that you must be SO careful with your back because the discs can be smashed; that posture patterns are dysfunctional; that the reason we have back pain is because of poor core stability, that we can have an unstable pelvis; that this is the way of the future. Even 70 year old women with osteoarthritis can now manage things she couldn’t do before.

Warning: I am skeptical of any new thing. After seeing so many variations over the years I’ve worked in pain management, particularly within the musculoskeletal world, I guess I’m a bit wary of fads. Here’s the thing: While I think the OOV functions well as an option for exercise, and novelty can be a good thing to maintain motivation, let’s not inflate the potential. Buzz words like “motor control”, “neuroplasticity”, “core strength” are going to have grab. The exercises, many based on Pilates, will be familiar and yet challenging on the unstable platform of the OOV. BUT the basic assumptions that:

  • there is one ideal posture and lordosis is associated with back pain and disc degeneration (Been & Kalichman, 2014; Murray, Dixon, Hollingworth, Wilson & Doyle, 2003; Nourbakhsh & Arab, 2002)
  • backs are fragile and must be coddled, particularly the discs  (Bakker, Verhagen, van Trijffel, Lucas & Koes, 2009; Claus, Hides, Moseley & Hodges, 2008; O’Sullivan, O’Keefe, O’Sullivan, O’Sullivan & Dankaerts, 2012);
  • core stability and motor recruitment are at fault in back pain, therefore they need to be retrained ( Laird, Kent, & Keating, 2012)
  • that myofascia can be effectively stretched (Scleip, Dureselen, Vleeming, Naylor, Lehmann-Horn, Zorn et al, 2012; Turrina, Martinez-Gonzalez & Stecco, 2013)

are, I think, arguable. I particularly dislike the language associated with the reasons for developing core stability – that backs are easily damaged, that great care must be taken to avoid damage, and that a critical reason for back pain is either lack of core stability or pelvic instability. While these notions are logical from a biomechanical viewpoint, they don’t accommodate natural bony, ligamentous and muscular variations (how many clavicle variations have been identified?), they omit the nervous system, and they fail to include the active, dynamic and ever-changing, self-regulating, homeostatic human systems involved.

Consider the OOV as an adjunct, a toy, a nice way to introduce movement to people who are fearful of movement. Use it to vary an exercise routine. Have fun with it. But please don’t base your back pain rehabilitation on the idea that this device is the bees knees.

Quick addendum: GREAT critical questions about a ten-year follow-up of strengthening vs flexbility exercises with or without abdominal bracing –; the original article is


Bakker, E. W., Verhagen, A. P., van Trijffel, E., Lucas, C., & Koes, B. W. (2009). Spinal mechanical load as a risk factor for low back pain: a systematic review of prospective cohort studies. Spine, 34(8), E281-293.

Been, E., & Kalichman, L. (2014). Lumbar lordosis. Spine Journal: Official Journal of the North American Spine Society, 14(1), 87-97.

Claus, A., Hides, J., Moseley, G. L., & Hodges, P. (2008). Sitting versus standing: does the intradiscal pressure cause disc degeneration or low back pain? Journal of Electromyography & Kinesiology, 18(4), 550-558.

Kirilova, M., Stoytchev, S., Pashkouleva, D., & Kavardzhikov, V. (2011). Experimental study of the mechanical properties of human abdominal fascia. Medical Engineering & Physics, 33(1), 1-6.

Laird, R. A., Kent, P., & Keating, J. L. (2012). Modifying patterns of movement in people with low back pain -does it help? A systematic review. BMC Musculoskeletal Disorders, 13, 169.

Murrie, V. L., Dixon, A. K., Hollingworth, W., Wilson, H., & Doyle, T. A. (2003). Lumbar lordosis: study of patients with and without low back pain. Clinical Anatomy, 16(2), 144-147.

Nourbakhsh, M. R., & Arab, A. M. (2002). Relationship between mechanical factors and incidence of low back pain. Journal of Orthopaedic & Sports Physical Therapy, 32(9), 447-460.

O’Sullivan, K., O’Keeffe, M., O’Sullivan, L., O’Sullivan, P., & Dankaerts, W. (2012). The effect of dynamic sitting on the prevention and management of low back pain and low back discomfort: a systematic review. Ergonomics, 55(8), 898-908.

Schleip, R., Duerselen, L., Vleeming, A., Naylor, I. L., Lehmann-Horn, F., Zorn, A., . . . Klingler, W. (2012). Strain hardening of fascia: static stretching of dense fibrous connective tissues can induce a temporary stiffness increase accompanied by enhanced matrix hydration. Journal of Bodywork & Movement Therapies, 16(1), 94-100.

Turrina, A., Martinez-Gonzalez, M. A., & Stecco, C. (2013). The muscular force transmission system: role of the intramuscular connective tissue. Journal of Bodywork & Movement Therapies, 17(1), 95-102.

It’s really all about the brain
Neuroscience is such a geeky area to study. And I have to say I didn’t really study the brain all that well in my undergraduate training all those years ago – but oh, how the worm has turned! It’s so exciting to see how basic science directly influences treatments that we can use for people who don’t have many pharmacologic options for their pain.

While I don’t have really up-to-date papers today, I think the 2008 paper by Herta Flor presages some of the approaches we’re starting to use in clinical settings now, a scant three years later. Flor’s work has always been impressive – she has often looked at what happens when brains are deprived of their normal feedback because of trauma or amputation, and (really exciting!) she is coming to Australia for NOI’s Conference 2012.
I came across this 2008 paper while compiling some readings for students enrolling in the Postgraduate papers in Musculoskeletal Medicine through University of Otago (distance taught papers for health professionals interested in pain and pain management).

BTW it’s not too late to enrol for MSMX 704 (Pain) and MSMX 708 (Pain Management) – papers suitable for medics, nurses, occupational therapists, physiotherapists, psychologists, social workers – anyone working in the area of pain.

In this paper, Flor summarises some of the changes that occur along the neuraxis following amputation, and spends time expanding on the mechanisms of maladaptive neuroplasticity and from this, discusses therapies that might directly influence this plasticity.  She notes that the majority of current therapies (particularly pharmacological) don’t address this at all.  Sadly, most of these therapies have limited effect on people, and a large number of unpleasant side effects.

Let’s take a look at some of the mechanisms thought to play a role in phantom limb (and note the similarities between phantom limb, complex regional pain syndrome and post-spinal cord injury pain).  Also please note that I’ve simply abridged notes from Flor’s paper – no reinventing the wheel!

Peripheral mechanisms

  • Structural changes in neurons and axons – terminal swelling and regenerative sprouting of the injured axon end occurs and neuromas form, giving rise to abnormal afferent input to the spinal cord with upregulation, and altered trafficking, of voltage-sensitive sodium channels and decreased potassium channel expression, as well as altered transduction molecules for mechano-, heat and cold sensitivity in the neuromas.
  • Ectopic impulses – these occur in the DRG and can summate with ectopic activity from neuromas in the stump, which can lead to the depolarization and activation of neighbouring neurons, significantly amplifying the overall ectopic barrage.
  • Ephaptic transmission – this refers to transmission of nerve impulses without the need for a neurotransmitter, developing from non-functional connections between axons.
  • Sympathetic–afferent coupling – in some patients sympathetic dysregulation in the residual limb is apparent, and spontaneous as well as triggered sympathetic discharge can elicit and exacerbate ectopic neuronal activity from neuromas as well as at the level of the DRG
  • Down- and upregulation of transmitters – novel receptors in the neuroma that are sensitive to cytokines, amines and so on, may enhance nociceptive processing, while ‘setpoints’ at which the nerve may fire are lowered, requiring less input for the nerve to respond
  • Selective loss of unmyelinated fibres – following trauma, axotomized afferent neurons show retrograde degeneration and shrinking, primarily involving unmyelinated neurons

Central changes

  • Unmasking – Inhibitory GABA(γ-aminobutyric acid)-containing and glycinergic interneurons in the spinal cord could be destroyed by rapid ectopic discharge or other effects of axotomy, or might change from having an inhibitory to an excitatory effect under the influence of brain-derived neurotrophicfactor (BDNF) released from microglia at the spinal cord level, leading to a loss of the normal inhibitory responses.  Downregulation of opioid receptors, on both primary afferent endings and intrinsic spinal neurons can add to this disinhibition due to reducing the normal inhibitory GABA and glycine activity.
  • Sprouting – nerve growth factors can be released in part because of activation of previously quiescent pathways that become functionally strengthened.
  • General disinhibition – previously quiescent, or low-threshold afferents can become functionally connected to ascending spinal projection neurons that carry nociceptive information to supraspinal centres, leading to an increase in the amount of information flowing upwards to higher centres.
  • Map remodelling – reorganization of the spinal map of the limb,could be due to the unmasking of previously silent connections, is also reflected in brainstem and cortical remapping – this is experienced as increased sensitivity in areas adjacent to the original area of damage.
  • Loss of neurons and neuronal function
  • Denervation
  • Alterations in neuronal and glial activity
  • Sensory–motor and sensory–sensory incongruence – the effect of illusions, such as the perception of body ownership of a rubber hand originally demonstrate the speed at which the SI cortex and also frontal and parietal areas respond to visual and sensory incongruence.  It’s this aspect of brain function that is particularly targeted when we start to incorporate mirrorbox or other visual feedback into treatments for phantom limb pain.

I get all excited when I read about this kind of research.  It opens up a whole range of treatment strategies that, for some clinicians, has previously been thought of as ‘purely psychological’, as if there was no ‘real’ (ie ‘organic’, ‘we can image/detect it’) effect.  As we go further into how the neuromatrix works, it starts to provide us with both new ways for treating this kind of pain – but it also goes to explain why some of our treatments work the way they do.

Let’s take, for instance, hypnosis.  One of the effects of hypnosis in chronic pain management can be to provide a person with post-hypnotic analgesia.  An interesting factoid to consider is that hypnosis can also produce post-hypnotic pain, with the right kind of  suggestion.  How can that be?

We didn’t really know how hypnosis worked until fMRI started being used in research.  When someone is given a hypnotic suggestion of analgesia, the cerebellum, anterior midcingulate cortex, anterior and posterior insula and the inferior parietal cortex are all activated to a greater extent than when a suggestion of analgesia is given without hypnosis.

Another form of so-called psychological treatment, cognitive behavioural therapy including biofeedback (EMG and temperature modalities), also activates ‘higher centres’, providing people with structured feedback on what their bodies do in response to their own coping efforts.  When these approaches are monitored with fMRI, lo and behold, once again those same areas of the cerebellum, anterior midcingulate cortex, anterior and posterior insula and the inferior parietal cortex are affected.  This applies when people use ‘coping self statements’ like “I can manage”, “I’ll be OK”, and diaphragmatic breathing as well.

Where this leads me to is that over the next 5 – 10 years, I predict that there will be increasing recognition for pain management strategies that have been demonstrated to be effective for some people, in that the neurobiological basis for this treatment response will be imaged.  It’s a shame that “seeing is believing” rather than looking at longitudinal outcome results within RCT ‘s for treatments that are not biomedical to be accepted, but there you have it.

Tomorrow – some more approaches that have been found useful for phantom limb, post spinal cord injury pain, and CRPS pain.   Not just mirrorbox!

Flor, H. (2008). Maladaptive plasticity, memory for pain and phantom limb pain: review and suggestions for new therapies Expert Review of Neurotherapeutics, 8 (5), 809-818 DOI: 10.1586/14737175.8.5.809

Flor, H., Nikolajsen, L., & Staehelin Jensen, T. (2006). Phantom limb pain: a case of maladaptive CNS plasticity? Nature Reviews Neuroscience, 7 (11), 873-881 DOI: 10.1038/nrn1991

Derbeyshire, S., Whalley, M., Oakley, D. (2009). Fibromyalgia pain and its modulation by hypnotic and non-hypnotic suggestion: An fMRI analysis. European Journal of Pain, 13(5), Pages 542-550 doi:10.1016/j.ejpain.2008.06.010

Travel to interesting places online!

Today’s post is about some of the interesting links you can find online.  Mostly links to do with brains, psychology and pain – but not all!

Genes to Cognition Online – featuring the 3-D brain, lovely interactive graphical interface to burrow down into really interesting topics like cognitive processes, disorders, research approaches and neuroimaging research, you can lose yourself for hours.

Deric Bownds’ MindBlog is full of brain and music information.  It’s in-depth material that can challenge and intrigue – some great podcasts available, and loads of links.

If you’re ever in need of some stimulating discourse on neuroplasticity and things to do with the nervous system, head to Neurotonics: a PT team blog.  The above two links are courtesy of the contributor’s fascination with brain stuff – and as ever, thought-provoking discussion about the meaning of new discoveries about the brain.

For a huge collection of brain information, BrainMeta is a place to browse. You can link to BrainMaps which is an interactive brain atlas – they have human brains, cat brains, rat brains and others – great for comparative analysis, with some excellent downloadable desktop tools to use to view the images.

Challenging our minds is for kids – a cognitive training programme online that adults can also have fun with.  If you don’t mind the rather computerised voice of ‘Al’, the exercises are good for anyone.  Free registration, and it can be used for months so you can see results before any financial investment is needed.

PsyBlog has been around a while, but never fails to surprise with posts about understanding your mind.  The post on why thought suppression doesn’t work starts like this: It sometimes feels like our minds are not on the same team as us. I want to go to sleep, but it wants to keep me awake rerunning events from my childhood. I want to forget the lyrics from that stupid 80s pop song but it wants to repeat them over and over again ad nauseam.’ – hmm, feel familiar?  A great post on what not to do to forget.

Finally today, a collection of podcasts on ‘ideas worth spreading’ from TED.  I’m only hoping the place where I work will let me open them up (YouTube is not allowed) – so many excellent clips from great speakers including Dan Gilbert discussing Happiness.

Have a great day!