Dr Tanya Mackenzie presenting at The Arm Clinic educational evening on Friday 27th May 2016

1. Atraumatic/MDI –
physiotherapy principles and
management
Tanya Anne Mackenzie

2. Research – does the evidence
help?
what do we want to know from research?
In the MDI Sh:
• What are the kinematics – know normal - what occurs in the MDI sh?
• What are the M activation patterns in the MDI sh?- influence on rehab?
• Leading to best conservative intervention?

3. problems with interpreting research
Discrepancies in the precise definition, classification & pathogenesis of MDI?
• occurs in multiple directions with insignificant trauma
• classification is based on the acronyms as in TUBS & AMBRI
• Generalised looseness of the sh
• Abnormal excursion of the HOH in the glenoid in all directions
• Instability in 2 direction
• Instability in 3 directions
• Instability inferiorly with one of either anterior or posterior instability
• Polar types on Stanmore triangle – still a spectrum
(Warby, Pizzari, Ford, Hahne, & Watson, 2014) (Longo et al., 2015)

4. problems with interpreting research
Differing diagnostic criteria for MDI for inclusion in the study?
Heterogeneity of populations
MDI mixed with traumatic unidirectional & traumatic + MDI
(Warby, Pizzari, Ford, Hahne, & Watson, 2015) (Longo et al., 2015)

5. problems with interpreting research
Hx of trauma are more likely to have a structural lesion
Pts with a structural lesion have better outcomes after Sx
In studies:
• No differentiation subjects who had trauma with those that had no trauma
• no imaging to rule out a structural lesion
• Therefore, studies include subjects with MDI who also have also co-pathology in sh
(Warby, Pizzari, Ford, Hahne, & Watson, 2015) (Longo et al., 2015)
Will influence outcomes

6. problems with interpreting research
Outcome measures (OM) – scoring not specific to this condition.(CONSTANT/ASES/ROWE etc )
OM used across all of the included studies were
• impairment-only OM
• OM not specific to measuring changes in the instability population.
• Therefore, OM that were insensitive to clinical changes in the instability population
(Warby, Pizzari, Ford, Hahne, & Watson, 2015) (Longo et al., 2015)

7. problems with interpreting research
Interventions:
• lack of standardisation of the rehab interventions
• Only a brief summary of their programmes – unable to replicate
• When comparing to conservative to Sx intervention – In Sx group -Variation in
Sx done within same study studies.
(Warby, Pizzari, Ford, Hahne, & Watson, 2015) (Longo et al., 2015)

8. Quantitative…… Qualitative….

9. pathomechanics - drivers
challenge = find the driver
(Warby, Pizzari, Ford, Hahne, & Watson, 2014) (Barrett, 2015)
non-traumatic
sh instability
(MDI)
secondarypsychological
emotional &cognitive factors
anatomical or neural defects
acquiredor genetic
redundantanteriorcapsule
bonyand capsulolabral anatomy
mechanosensitivity
neural tissue
Motor development
poor muscle tone
poor sensoryintegration
Hyperlaxity
generalisedor
congenital syndromes
Pain
peripheral (somatic)
central sensitisation(neuropathic)
changesinsensoryandmotor cortical representation
Movementdysfunction
neuromuscularcontrol
scapulakinematics
atypical patternsof muscularactivation
Proprioceptionloss
microtrauma

10. Complex patients and complex conditions to
unravel

11. pathomechanics – drivers
challenge = drivers out of
physio control
(Warby, Pizzari, Ford, Hahne, & Watson, 2014) (Barrett, 2015)
non-traumatic
sh instability
(MDI)
secondarypsychological
emotional &cognitive factors
anatomical or neural defects
acquiredor genetic
redundantanteriorcapsule
bonyand capsulolabral anatomy
mechanosensitivity
neural tissue
Motor development
poor muscle tone
poor sensoryintegration
Hyperlaxity
generalisedor
congenital syndromes
Pain
peripheral (somatic)
central sensitisation(neuropathic)
changesinsensoryandmotor cortical representation
Movementdysfunction
neuromuscularcontrol
scapulakinematics
atypical patternsof muscularactivation
Proprioceptionloss
microtrauma

12. pathomechanics - drivers
Brain wave drivers
(Warby, Pizzari, Ford, Hahne, & Watson, 2014) (Barrett, 2015)
non-traumatic
sh instability
(MDI)
secondarypsychological
emotional &cognitive factors
anatomical or neural defects
acquiredor genetic
redundantanteriorcapsule
bonyand capsulolabral anatomy
mechanosensitivity
neural tissue
Motor development
poor muscle tone
poor sensoryintegration
Hyperlaxity
generalisedor
congenital syndromes
Pain
peripheral (somatic)
central sensitisation(neuropathic)
changesinsensoryandmotor cortical representation
Movementdysfunction
neuromuscularcontrol
scapulakinematics
atypical patternsof muscularactivation
Proprioceptionloss
microtrauma

13. Growing Evidence
When compared MDI with controls
• Change in threshold corticospinal response in LT and In Spin
• ↓feedback mechanism
• Altered neural control
(Alexander CM 2007
Hundza & Zehr 2007)

14. Changes in cortical representation - Cortical
drivers
Physio challenge to reverse the arrows

15. Manifests in complex patients
Cortical re-organisation
• Anxiety and emotional regulation
• Fear net work – neurotags
• Loss of precision
• Disrupted mvt motor control
• Changes in sensory function
• Alteration in perception of body part
• ? Hx Neurodevelopment delay
• Yamaoto et al., 2015; Safran et al., 2010; Milgrom et al 2014)

16. Neurodevelopment & altered body
perception = alarm bells avoid Sx
• Reciprocal limitations on tasks / rhythm/separate each side of the
body/ coordination/ R hand L hand judgement
• Two point discrimination (4.5cm =C/ 8.5cm in MDI)
• Pain/ catastrophising scores
• Ask developmental milestones
(Mosley et al, 2012, Howard et al, 2015)

17. How we influence the neurotags-Negative
reinforcement vs positive reinforcement
• Lack of Support
• Misunderstood
• Attentions seeking behaviour
• Disengaged with normal activities
• Significant emotional issues
• Frequent AnE visits
• Beliefs re diagnosis
• Beliefs re Previous Tx
• Previous failed interventions
• How does physio alter neuro tags: what we say, how we listen, reverse the process via physical
intervention and rehab

18. How can physio modalities help?
Focused sensory discrimination
Motor imagery ( L/R judgement tasks)
Mirror visual feedback
Body perception re-education
visual input to increase somato-senory cortex response
Cross midline
Neuro dev – crawling, rolling
(Serino er al, 2007; Mosley et al 2008, 2009.)

19. How can physio modalities help?
• Visual targets (lazer/ spots on a wall etc/Ha2Ha )
• Feedback, such as visual cues, tactile cues, tape and demonstration,
• Boundary setting is a useful tool.
• Clear rehabilitation parameters communicated.
• The patient should be given achievable ‘homework’
• Modify activity/technique/ergonomics/nb the gym
• key is that the patient is taking responsibility
for self as a condition of ongoing treatment
(Serino er al, 2007; Mosley et al 2008, 2009.)

20. pathomechanics - drivers
Drivers local to the shoulder
(Warby, Pizzari, Ford, Hahne, & Watson, 2014) (Barrett, 2015)
non-traumatic
sh instability
(MDI)
secondarypsychological
emotional &cognitive factors
anatomical or neural defects
acquiredor genetic
redundantanteriorcapsule
bonyand capsulolabral anatomy
mechanosensitivity
neural tissue
Motor development
poor muscle tone
poor sensoryintegration
Hyperlaxity
generalisedor
congenital syndromes
Pain
peripheral (somatic)
central sensitisation(neuropathic)
changesinsensoryandmotor cortical representation
Movementdysfunction
neuromuscularcontrol
scapulakinematics
atypical patternsof muscularactivation
Proprioceptionloss
microtrauma

21. Mainstay Physio tool remains change
biomechanical drivers at shoulder
• RC timing issues
• Scap dyskinesia
• ↓proprioception
• ↓fatigue resistance
• Balance issues( KC)
• Posture (KC)
• JPS
• FIRST SESSION change their symptoms = confidence, trust, belief system
alters etc

22. atypical patterns of scapular muscular
activity as the driver
• A review
• MDI no clear pattern scapulothoracic M activity compared to healthy controls
• contradictory results on scapulothoracic M activity patterns.
• no consensus was found on M recruitment timing.
(Struyf et al., 2011)

23. Evidence for scapular kinematic
as a driver
MDI = high % Scap dyskinesia (Kibler et al., 2013)
The patterns tends to be:
• ↑ upward rotation (Longo et al., 2015)
• ↓ upward rotation (Warby, Pizzari, Ford, Hahne, & Watson, 2015)

24. atypical patterns of GHJ muscular
activity as the driver
Morris et al. (2004) (Barden et al., 2005) (Illyés et al., 2009) (Struyf et al., 2011) (Labriola, Lee, Debski, & McMahon, 2005)
-Dynamic M activity –concavity compression- resistance to translation

25. EMG vital to understanding the RC
• M activity levels MVC
• Patterns of m activity with in the RC
• Patterns of m activity between RC and other Ms
• Timing of onset of m activity
• Broadness of contraction
Reporting all = interpretation complicated
BUT not reporting all O Measures = simplifies interpretation & skews interpretation
Care with interpretation or reporting of EMG studies:
what can we glean from EMG?...simply put

26. Led to the

27. To date research has illustrated that the
dynamic cuff:
RC Ms perform diff functn roles during dynamic motion (Wattanaprakornkul, Halaki, Boettcher, Cathers, & Ginn, 2011)
Eccentric to concentric strength ratios in the RC Ms are relevant (David et al., 1999)
RC activity is influenced by:
• Plane of motion (Alenabi, Dal Maso, Tétreault, & Begon, n.d.) (Tardo, Halaki, Cathers, & Ginn, 2013)
• Range (arc) of motion (Alenabi, Dal Maso, Tétreault, & Begon, 2015)
• Velocity of motion
• Fatigue (Teyhen et al., 2008.)
• Presence of symptoms & pathology (Reddy et al., 2000),.
Therefore, when rehabbing the RC take all into account
Hawkes, D. H., Alizadehkhaiyat, O., Fisher, A. C., Kemp, G. J., Roebuck, M. M., & Frostick, S. P. (2012).

28. atypical patterns of muscular activity as
the driver
Morris et al. (2004) (Barden et al., 2005) (Illyés et al., 2009) (Struyf et al., 2011) (Labriola, Lee, Debski, & McMahon, 2005)
Infraspinatus & supraspinatus
• But in MDI = premature deactivation just before the end of
ER at 65°
• Concl: compromise the RC - stability to GHJ at a critical point

29. atypical patterns of muscular activity as
the driver
Morris et al. (2004) (Barden et al., 2005) (Illyés et al., 2009) (Struyf et al., 2011) (Labriola, Lee, Debski, & McMahon, 2005)
Posterior Deltoid
• Controls = eccentric posterior deltoid onset 46° before end IR
• MDI = only 12° before the end IR

30. atypical patterns of muscular activity as
the driver
Morris et al. (2004) (Barden et al., 2005) (Illyés et al., 2009) (Struyf et al., 2011) (Labriola, Lee, Debski, & McMahon, 2005)
Pectoralis major
In flex/ext & abd/add & IR/ER
• MDI = maintained low levels of activity throughout mvt
• Control subjects = distinct patterns of activation &
deactivation in separate phases.

31. SO does rehab change scapular kinematics &
atypical M pattering
Biomechanical analysis of the effect of Ex alone has shown that significant alterations in
kinematic parameters in Pts with MDI cannot be completely normalized by Ex.
(Nyiri, Illyés, Kiss, & Kiss, 2010)
Atypical patterns of M activation in Pts with MDI may not be sufficiently restored with
Ex alone
(Illyés, Kiss, & Kiss, 2009)(Barden, Balyk, Raso, Moreau, & Bagnall, 2005)
In MDI Shs Physios
They optimise them

32. Considerations when planning successful cuff
rehab programs
 Which RC M/ Ms need to be targeted in rehab?
aim to create synergy bet the RC Ms (balance)
aim to create synergy bet the RC & other sh girdle Ms
aim to alter RC timing – onset of m activation (latency)
aim to broaden or shorten time of RC contraction
What type of contraction (concentric or eccentric) needs rehab

33. Considerations when planning successful cuff
rehab programs
what range of the M (inner, outer, or middle) needs rehab
What range/ plane of physiological motion needs rehab

34. Making the complex simple
• Simply change body position: supine, Prone, Standing, whatever
• Simply alters where gravity is by altering body position and retest
(alters the function of the RC i.e. mover or stabiliser, alters type of
contraction ie eccentric or concentric, alters range of muscle and
physiological range)
• Simply add manual or a form of resistance to alter length of
contraction, alter timing and create synergy or to bias a specific RC m.
• then add to the functional movement

35. Finally: Train into controlled position
of vulnerability
Normalization of active ROM with special attention
to end ROM & critical vulnerable positons

36. references
• An, Y. H., & Friedman, R. J. (2000). Multidirectional instability of the GHJ Jt. The Orthopedic Clinics of North America, 31(2), 275–285.
• Barden, J. M., Balyk, R., Raso, V. J., Moreau, M., & Bagnall, K. (2005). Atypical Sh M activation in multidirectional instability. Clinical Neurophysiology: Official Journal of the International Federation of Clinical
Neurophysiology, 116(8), 1846–1857. http://doi.org/10.1016/j.clinph.2005.04.019
• Barrett, C. (2015). The clinical physiotherapy assessment of non-traumatic Sh instability. Sh & Elbow, 7(1), 60–71. http://doi.org/10.1177/1758573214548934
• Bateman, M., Smith, B. E., Osborne, S. E., & Wilkes, S. R. (2015). Physiotherapy Tx for atraumatic recurrent Sh instability: early results of a specific exercise protocol using pathology-specific outcome measures. Sh &
Elbow, 1758573215592266. http://doi.org/10.1177/1758573215592266
• Burkhead, W. Z., & Rockwood, C. A. (1992). Tx of instability of the Sh with an exercise program. The Journal of Bone & Jt Sx. American Volume, 74(6), 890–896.
• Illyés, Á., Kiss, J., & Kiss, R. M. (2009). Electromyographic analysis during pull, forward punch, elevation & overhead throw after conservative Tx or capsular shift at patient with multidirectional Sh Jt instability. Journal of
Electromyography & Kinesiology, 19(6), e438–e447. http://doi.org/10.1016/j.jelekin.2008.09.008
• Kiss, J., Damrel, D., Mackie, A., Neumann, L., & Wallace, W. A. (2001). Non-operative Tx of multidirectional Sh instability. International Orthopaedics, 24(6), 354–357.
• Labriola, J. E., Lee, T. Q., Debski, R. E., & McMahon, P. J. (2005). Stability & instability of the GHJ Jt: The role of Sh Ms. Journal of Sh & Elbow Sx, 14(1, Supplement), S32–S38. http://doi.org/10.1016/j.jse.2004.09.014
• Longo, U. G., Rizzello, G., Loppini, M., Locher, J., Buchmann, S., Maffulli, N., & Denaro, V. (2015). Multidirectional Instability of the Sh: A Systematic Review. Arthroscopy: The Journal of Arthroscopic & Related Sx, 31(12),
2431–2443. http://doi.org/10.1016/j.arthro.2015.06.006
• Merolla, G., Cerciello, S., Chillemi, C., Paladini, P., Santis, E. D., & Porcellini, G. (2015). Multidirectional instability of the Sh: biomechanics, clinical presentation, & Tx strategies. European Journal of Orthopaedic Sx &
Traumatology, 25(6), 975–985. http://doi.org/10.1007/s00590-015-1606-5
• Misamore, G. W., Sallay, P. I., & Didelot, W. (2005). A longitudinal study of Pts with multidirectional instability of the Sh with seven- to ten-year follow-up. Journal of Sh & Elbow Sx, 14(5), 466–470.
http://doi.org/10.1016/j.jse.2004.11.006
• Nyiri, P., Illyés, A., Kiss, R., & Kiss, J. (2010). Intermediate biomechanical analysis of the effect of physiotherapy only compared with capsular shift & physiotherapy in multidirectional Sh instability. Journal of Sh & Elbow
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• Struyf, F., Nijs, J., Baeyens, J.-P., Mottram, S., & Meeusen, R. (2011). Scapular positioning & movement in unimpaired Shs, Sh impingement syndrome, & GHJ instability. Sc&inavian Journal of Medicine & Science in
Sports, 21(3), 352–358. http://doi.org/10.1111/j.1600-0838.2010.01274.x
• Warby, S. A., Pizzari, T., Ford, J. J., Hahne, A. J., & Watson, L. (2015). Exercise-based management versus Sx for multidirectional instability of the GHJ Jt: a systematic review. British Journal of Sports Medicine, bjsports–
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