Movement management of low back pain Dr Neil Langridge DClinP MSc MMACP MCSP

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1 Movement management of low back pain Dr Neil Langridge DClinP MSc MMACP MCSP

2 What underlies LBP?

3 MRI Disc degeneration = 91% Loss of disc height = 51% Disc bulges = 64% Disc protrusion = 32% Annular tear = 38% Prevalence of MRI findings in people without LBP

4 Pain Nociceptive Inflammatory Neuropathic Functional Over 50% is insidious Mechanical v non-mechanical

5 Motor Control Reflex model sensory input / movement outputs/sensation is necessary Hierarchical Central programmes, top down patterns of movement clear difference in voluntary and reflex. Systems Task orientated links the two

6 Protective and equilibrium reactions Righting reactions Tonic reflexes Primitive reflexes

7 Considerations Activity of muscle Control of segment Patterns Accommodations Context Anticipation Environment

8 Mechanical Non-Mechanical Clear proportionate response to mech stimuli Disproportionate Clear location Movement hyper-sensitivity Linked to posture, loading Note = MIXED pictures No clear anatomical Wide spread hyperalgesia Pressure Temperature Anxiety, fear, stress

9 MRI Poor use can lead to; Poor perceived prognosis Higher disability Greater chance of being off work More likely to have surgery Depression is a stronger indicator as a indicator of LBP

10 Pain behaviours to address Grimacing Moaning Propping Holding breath Braces/sticks Limping

11 Body schema Anticipation does not match actual Discrepancies between real and virtual Over concern = EMG All driven by beliefs Also consider sleep and obesity = independent variables

12 Other physical factors Balance Speed Quality Proprioception Breathing All need to be addressed

13 Specific Movement training Normalise faulty patterns Discourage pain behaviour Target pain provocative tasks Goal orientated Breakdown the task Reduce the threat

14 Specific changes Beliefs Self efficacy Provide hope Provide confidence Provide CONTEXT

15 Imagery Distorted Increases performance Feeling of swelling Increase power Inhibits the lateral side of the somato-sensory cortex Reduces threat Helps set the pattern Practice the context Difficult to distinguish normal Lack of tactile acuity

16 Motor cortex Stored patterns Stored expectation Stored control

17 Creating the action and sensing the change Pain will affect the input system At the spinal cord. Inappropriate input from sensory cortex Poorly informs cerebellum Starts to create a change in patterns At the cortex

18 Theories to consider Vicious Cycle Theory A stereotypical increase in muscle firing/activity. Ischeamic response - metabolite change PH raised. Muscle spindle activity raised. Spasm / Pain / Spasm Lack of movement further soft tissue changes Increased nociceptive barrage more pain and it continues.

19 Mechanisms Direct nociceptive afferents on motoneurons. Inhibitory/facilitatory inter-neurons at spinal cord and brain-stem Heightened muscle spindle activity Reduced inter-neural activity can reduce but also lead to separate compensatory activity changes.

20 Adaptation to input. Mechanisms to consider for rehabilitation.

21 Humans either cope or fail Postural Failure Post trauma failure As therapists we analyse and look to optimise loading, and balance across the spine. Many of these extreme postures are therefore continually either under or over stimulating the natural proprioceptive input to the nervous system.

22 Theories to consider Vicious Cycle Theory A stereotypical increase in muscle firing/activity. Ischeamic response - metabolite change PH raised. Muscle spindle activity raised. Spasm / Pain / Spasm Lack of movement further soft tissue changes Increased nociceptive barrage more pain and it continues.

23 Pain Adaption Theory Movement or action of a muscle then becomes uniformly inhibited. The antagonist is facilitated. This inappropriate balance then further aggravates the painful movement. Proposed to be controlled at sub-cortical level, reflex-like in nature.

24 MOST COMMON DYSFUNCTIONS

25 Flexion. TES and upper abdo acivity. Inability to differentiate ant pelvic tilt. Extension involves upper spine. Inability to control lordosis in forward postures. Squatting, sitting with knee ext/hip fx. Poor repositioning sense. Poor breathing control-apical

26 Extension-Active. High levels of ES activity-increased lordosis. Increased movement at hip 1:3. Loss of reverse lordosis-flexion-relax. Hyperextend at segment. Ant pelvic rotation. Squat increased ext. Sitting hyper lordotic. Sit Stand maintained hyper lordosis.

27 Lateral. Strategy asymmetry, ql activity. Flexing causes lateral dev and flexion. Single leg stand lateral shift of thorax. Squat, sit, sit to stand all increased flexion/lat dev.

28 Extension. Passive. Upper Ra,EO,IO activity. Thorax post to pelvis. Increased segmental lordosis. Sway back extend at segment. Excessive pelvis sway. Change C of G.

29 This Morning Consider how to assess movement disorders Consider how to create new patterns Consider other factors Consider exercise programmes

30 TITLE AND CONTENT LAYOUT WITH Chart

31 Two content layout with table First bullet point here Second bullet point here Group 1 Group 2 Class Class Class Third bullet point here

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The Proprioceptive Lumbar Spine & The role of manual therapy. Dr Neil Langridge DClinP MSc MMACP BSc (Hons) Consultant Physiotherapist

The Proprioceptive Lumbar Spine & The role of manual therapy Dr Neil Langridge DClinP MSc MMACP BSc (Hons) Consultant Physiotherapist What do we do? Manual therapy Pain control Movement Re-educate Muscular