Ben Wand

The University of Notre Dame Australia

MALADAPTIVE NEURAL PLASTICITY AND CHRONIC LOW BACK PAIN

In 2000 this appeared (Grachev et al. 2000)

Particularly Interesting Because

Current treatment for CLBP is not very effective

Maybe we are missing some important part of the problem?

A fair amount of research since then has demonstrate significant alterations in brain structure and function

Maybe the brains contribution to the CLBP experience is the thing we have been missing?

Lots of structural alterations have been shown

Altered neurochemical profiley DLPFC, OFC, ACC, Insula, Thal, S1(Grachev 2000, 2002, 2003, Siddall 06, Gussew 2010, Sharma 2011)

Altered grey matter density/volumey DLPFC, Thal, A/MCC, PPC, S1, midbrain, MTL, MC

y Putamen, Thal, insula(Apkarian 2004, Schmidt-Wilcke 2006, Buckalew 2008, Gussew 2010, Seminowicz 2011, Ruscheweyh 2011)

Decreased white matter volumey Insula, MCC(Buckalew 2008, Gussew 2010)

Altered white matter connectivityy Splenium of corpus callosum(Buckalew 2010) – disabled v non disabled CLBP

Lots of functional differences as welly Altered sensory representation (Flor 1997a, Lloyd 2008)

y Altered response to nociception(Flor 1997, Diers 2007, Giesecke 2004, 2006, Kobayashi 2009)

y Altered response to non-noxious & verbal stimuli(Flor 1997a, Flor 1997b, Lloyd 2008)

y Altered motor representation(Tsao 2008, Tsao 2011)

y Altered activation with movement(Jacobs 2010)

y Altered corticospinal drive(Strutton 2005)

y Altered resting state(Baliki 2008, Buckalew 2010, Tagliazucchi 2010, Balenzuela 2010)

There are some problems

y The data are preliminary

y The studies are all small

y Often analysed uncorrected

y Opioids are a confounder

y Not always controlled

y Patient diversity

y Most data are cross-sectional

y Consequence or Cause?y Symptom or disease

y Temporal relationship

y Strength of association

y Consistency

y Experiment

y Other explanations

y Plausibility/Coherence

Enhanced nociceptive efficiencyy Degeneration of antinociceptive areas

y Implicated in placebo analgesiay Failed activation of antinociceptive areas

y Local hyperalgesia (Giesbrecht 2005, Kobayashi 2009, Blumenstiel 2011)

y Remote hyperalgesia (Giesecke 2004, Giesbrecht 2005, O’Neill 2011)

y Not in community CLBP people (Blumenstiel 2011)

y Enhanced remote sensitisation (O’Neill 2007, Kleinbohl 1999)

y Spontaneous pain linked to cortical activation abnormalitiesy Different to peripherally evoked pain (Baliki 2006)

y Multi modal sensitivity (Small 2006, Fann 2005)

y Sensitised system – top downy Maybe contribute to failure of MT

Psychological problems

y Degeneration frontal areasy DLPFC activity inversely related to catastrophisationy DLPFC activity inversely related to unpleasantness

y Emotional decision making poorer (Apkarian 2004)

y Memory and mental flexibility impaired (Weiner 2006, Lorenco 2009, Buckalew 2008)

y Related to catastrophisation

y Same pain intensity rated as more unpleasant (Kobayashi 2009)

y Left sided LBP more depressed, worse mood than right sided (Wasan 2010)

y Maybe contribute to failure of psychological Rx

Attentional processingy DLPFC involved in maintaining goal relevant priorities

y Avoid interference from goal irrelevant informationy Maintain attentional load and attentional sety Prevent attentional capture and interference by painful stimuli

y Reciprocal connections with the cingulate cortex

y Difficulty disengaging from threat pictures (Roelofs 2005)

y Attentional bias to pain related words (Haggman 2010)

y Distraction seems less analgesic in CLBP (Johnson 1997, Goubert 2004)

y Worse at digit span task, working memory, stroop (Gijsen 2011)

y Functioning with pain more difficulty Attentional capture greatest when pain intense, novel & threatening

y Failure of Rx approaches emphasise function despite pain

Altered body perception/awarenessy Degeneration S1, MCy Reorganisation of S1y Reorganisation of M1y Altered biochemistry S1

y Decreased sensory acuity(Luomajoki 2011, Moseley 2008, Wand 2010)

y Poorer graphaesthesia (Wand 2010)

y Sensory thresholds intact

y Altered proprioception(Brumagne 2000, Gill 1998, Lee 2010, O'Sullivan 2003, Taimela 1999)

y Poorer laterality recognition (Bray 2011)

Altered body perception/awarenessy Smaller than really isy Midline shifty Miss bits out (Moseley 2008)

y Neglect that sidey Body and space (Moseley under review)

y Certainly move differentlyy Altered muscle recruitment

y Motor control related to acuity (Luomajoki 2011)

y Qualitative study (Smith & Osborn 2008)

y ‘Not part of me’y ‘Not controlled automatically’y ‘Doesn’t belong’

Quantitative assessment of self reported disturbances in body

perception - FreBAQNever Rarely Occasional

ly

Often Always

Not part of the rest of my body 56 15 19 7 4Focus all my attention on my back to make it move 22 22 30 19 7Back moves involuntarily, without my control 48 19 19 15 0I don’t know how my back is moving 44 22 11 15 7I don’t know where my back is in space 52 33 4 4 7I can’t perceive the exact outline of my back 41 30 19 11 0My back feels like it is swollen 26 22 22 22 7My back feels like it has shrunk 78 11 7 0 4My back feels lopsided (asymmetrical) 19 19 26 22 15

Mislocalisation of sensory information

y 24 CLBP patients and 24 healthy controlsy 672 stimulations in total per groupy Referred and Mislocalised sensations

y Referred sensations y 5 patients - 3 controlsy 26 stimulations for patients - 5 for controls

y Mislocalisation y 16 patients - 5 controlsy 41 stimulations for patients – 8 for controls

Altered body perception might influence the clinical condition in a number of ways

Might cause painy Virtual back ���������y Sensori-motor incongruence

y Discordance generates painy Some experimental supporty All movement patterns faulty if the

brain doesn't know what happening

Likely to change way movey Reason for motor problems

y Another pain generatory Extra challenge for Retraining

Might affect tissue healthy Disrupt homeostasisy Cooling with disownership y Perception changes swelling

Might contribute to fear/worryy Feels wrong/strange/peculiar y Unexpected mvts and sensationsy Loss of controly Extra challenge for cognitive

treatments

Is chronic LBP a problem of perception of the back?

Maladaptive cognitive perceptiony Amount degeneratedy Fragility /robustnessy Reversibility of the problemy Controllability of problemy Prognosis of the problem

Maladaptive self perceptiony How the back feelsy The size y The outline y When it is and isn’t

moving y How much movingy Position in spacey Ownership and controlAnd these two issues are likely to be strongly interactive

and mutually reinforcing

The maladaptive perceptions model

What does this mean for management

Biopsychosocial rehabilitation which has normalisation of

cognitive perception and self perception as its goal

Cognitive perception

y Provide a coherent understanding of the problemy Explains all of what they feel, including treatment failure

y Outline a clear path to resolutiony Reduce anxiety about condition and future course

y Disavow lumbar pathoanatomical basis y Emphasise robustness of the spiney Emphasis controllable, reversible, amenable to treatmenty Plausible reasons to engage in activities been avoidingy Additional reasons why fearful and avoidant

I think a cortical perspective makes these things easier

What about self perception?

Treatment of other pain problems directed

towards self perception has helped

y MVF for PLP and CRPSy GMIP for CRPS and PLPy Sensory discrimination for PLP

and CRPSy Magnifying hand made worse -

minifying it made better in CRPSy Simulated walking for SCI

A lot of what we currently do may positively influence self perception of the back

y Massage, mobilisation, dry needling, TENSy Sensory awareness

y Specific muscle activation trainingy Motor awarenessy Often without movement so may minimise incongruence

y Dissociation trainingy Sharpen up delineation between areasy Again without moving

y And these things are a bit helpfuly Maybe better if done with explicit aim of improving perception

MIRROR VISUAL FEEDBACKCross-over experiment

Standardised range, speed and reps – 60 repsmoving with vision v without vision

With visual

feedback

mean (SD)

Without visual

feedback

mean (SD)

Mean

difference

(SD)

95% CI p

value

pain intensity 7.75 (11.92) 17.00 (14.61) 9.25 (18.50) 1.44-17.06 .022

Time to ease 48.50 (56.09) 97.38 (80.17) 48.88 (69.50) 19.53-78.22 .002

Graded cortical retrainingProgressive engagement of

sensory areasy Localisation of stimulusy Localisation and type of stimulusy Graphaesthesia trainingy Lettersy Wordsy Sums y Size y Orientationy Speed y Lateralityy Overlap

Graded cortical retrainingProgressive engagement of motor

areasy Laterality recognitiony Recognise©

y Imagined movementsy Small range then large

y Isometric local muscle activationy Inner unit contractiony with dissociation exercises

y Movements with feedback optimisedy Small range movementsy Large range movements

Meta-analysis rTMS: Pain short term

Low frequency <5Hz

High frequency ��+]

SMD= -0.32 95% CI -0.51 to -0.13 (p=0.0009)

I2 = 71%

Corrected n=267

Meta-analysis rTMS: Pain short term: Subgroup: High frequency motor cortex stimulation

Single dose studies

SMD= -0. 40 95% CI -0.54 to -0.26 (p=0.00001)

I2 = 36%

Multiple Dose Studies

On a 0-100mm VAS scale:

9.3mm (95% CI 6.2 to 12.5mm)

15% (95% CI 10% to 20%)

Corrected n= 184

Meta-analysis tDCSAll studies Subgroup: Motor

cortex studies

SMD -0.5995% CI -1.10 to -0.08p=0.02I2 = 45%

n = 83

n = 73

Questions?Acknowledgements: Neil O’ConnellProf. Lorimer Moseley

Thank You