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I have just about recovered form the build up, and full on 3 days at the conference, so just wanted to say a huge thankyou to all our speakers and delegates for making it such a success and such a vibrant and truly international event. Really enjoyed the whole event, and cant wait for Edinburgh 2013!

Huge thanks to the team and to Rachel for her relentless blogging-she needs to get out more for sure!

What a great event! 21 Key note and guest speakers, 51 oral presentations, 40 posters and 650 delegates from 15 countries. Edinburgh gave a stunning backdrop for the conference and also a superb venue, which had a welcoming circular structure!! The lectures gave us all much to think about, the sponsored interactive sessions were busy and the parallel clinical seminars all had standing room only!! Tea and coffee was always a welcome break giving the opportunity to socialise and view the varied exhibition stands, the most popular being the bouncing kangaroo shoes!!

Clinically the key message to come out of the conference was about sub-grouping of patients for targeted interventions. A great message for future developments in appropriate patient management and clinical research.

John Fearn, Reading Football Club, UK

Incidence is very prevalent.   But we must keep an open mind when examining the area.  Associated with:

• activity or load
• specific location of pain
• am pain and stiffness
• eases with activity
• local tenderness
• functional impairments

Clear diagnosis requires a complete history.  Imaging can help but beware there are many abnormal images that aren’t painful and vice versa.   There are many intrinsic and extrinsic aetiological factors.  Genetics and cholesterol are important intrinsic factors.

The continum of thae pathology that occurs in tendon pathology:

• causative event
• proliferative reactive tendinopathy
• tendon dysrepair
• degenerative tendinopathy
• … rupture?

It is important to treat patient sindivdually especially considering intrinsic factors.  Main aims are to reduce symptoms and resotre normal function.  sparse evicendce for treatment.  few comparing RDTs and none comparing conservative and surgical.

Rehabilitation isses. Needs to look at :

• whole kinetic chain – address mvt dysfunction issues and modify training loads.
• ensure target local tissues
• progressive loading
• eccentric training – don’t introduce too early
• extracorporeal shock wave therapy is effective, ultrasound is not.
• NSAIDs useful in early phase
• injection therapy were discussed
• other suggested protocols – GTN patches, DTF/SSTM, night splints, acupuncture, heel raises, cryotherapy
• surgical options
• other options for the future……

John discussed all of these interventions at length (and too quickly for me to keep up – sorry!!)

Differentiate into two areas proliferative/reactive phase and degenerative type require different management protocols.

Read Jon Fearn’s biography

View abstract on conference website

Abstract

This lecture will review rehabilitation strategies involved in managing Achilles Tendonopathy (AT). A brief overview of current evidence is given initially to update delegates on the latest physiology, pathology, assessment and diagnosis of AT. The core of the lecture will discuss the many suggested aetiological factors, both extrinsic and intrinsic, and go onto discuss options for conservative intervention. Areas that will be discussed in more detail include load management, exercise progression, eccentric training methods, manual therapy techniques, electrotherapy and scrutinise the numerous injection therapies available to the clinician. Treatment strategies for the two fundamental types of AT, Proliferative and Degenerative, will be suggested.

The author’s background in the rehabilitation of elite athletes allows him to offer some useful practical rehabilitation guidelines from early to late stage, stressing the essential aspect of the functional demand of the target tissue and of the athlete.

Jon Fearn. Rehabilitating Achilles Tendonopathy Manual Therapy, 2009 Oct; 14(5):S1-S54

Dirk Jan Veeger, University of Amsterdam, The Netherlands

Why model the MSK system?  Helps us to understand it on a mechanical basis, how things go wrong and how they can be changed. In shoulder modelling it is difficult to model the GH joint due to structural instability.  The scapula is a stable base.  Modelling scapula motion is essential in studying disorders.

Modelling procedures involves inputting kinematics and external forces, and the output is muscle forces.  Modelling applications include:

1. potential moment vectors – describe motion of muscles during a movement, useful to evaluate a muscle at a given position
2. looking at tendon and muscle transfers – to investigate effectiveness of procedures

The modelling of the transfer of LatMAj and TMajor to a rotator cuff site was discussed.

MSK modelling gives us an insight into mech constraints, are useful for education but what if we could model interventions?  There are a lot of challenges to this.  From general to to specific models, physiological responses to mechanical loading and control i.e. reflexes.

Read Dirk Jan Veeger’s biography

View abstract on conference website

Abstract

The structure of the shoulder is an ingenious compromise between stability and mobility that allows the hand to be moved within almost 2/3 of a sphere. In addition to the truly three-dimensional mobility of the upper extremity, the hand is capable of exerting forces in almost any direction. This versatility is enabled by mobile joints and controlled by mono-, bi- and tri-articular muscles. Given the 3D structure of the shoulder, muscles will not only generate joint moments to meet external forces, but will also generate considerable undesired joint moment components, which must be compensated by other muscles. Also, the mechanical effect of each muscle is highly dependent on arm posture and can even change sign completely.

We developed a musculoskeletal model of the shoulder and elbow to aid understanding the working of the upper extremity. The model comprises the thorax, scapula, clavicle, humerus and forearm and all muscles controlling these. The model uses musculoskeletal parameters from one specimen and works on the assumption of the existence of a general control principle (or cost function) based on the minimization of energy cost.

The model can, and has been used for several clinical applications, of which a selection will be discussed:

1. prevention of muscle overload: to be able to prevent overload injuries in wheelchair users the magnitude of muscle strains and joint loading should be quantified so that decisions on training and overuse prevention can be made (Van Drongelen et al, 2005 );
2. “what if”: The decision on what tendon transfer to perform to restore function is dependent on its functional gain, f.i. in terms of Activities of Daily Living (Magermans et al, 2004), on the newly constructed moment balance around a joint (Veeger et al., 2004).
3. understanding muscle control in pathological cases: in patients sometimes muscle activation patterns can be seen that conflict with their primary function (Steenbrink et al., 2006) Understanding this requires insight in the mechanical balance of the system, including all interactions between muscles;

Any modeling result is only as good as the model itself. Recently, the model has been validated with the use of an instrumented endoprosthesis (Asadi Nikooyan, 2008). Validation has included the effect of scaling, but still two issues remain, namely the extent to which patient data can be related to model results in which a general control principle is assumed and second, to what extent models can, or should be individualized.

References

1. Van Drongelen et al, Archives of Physical Medicine & Rehabilitation 2005; 1434-1440
2. Magermans et al, Clinical Biomechanics 2004; 116-122
3. Veeger et al., Journal of Hand Surgery 2004; 259-264
4. Steenbrink et al., Manual Therapy 2006; 231-237
5. Asadi Nikooyan et al, 2008, Proceedings 16th ESB Conference, Lucerne, Switzerland

Dirk Jan (H.E.J.). Veeger. “What if”: the use of biomechanical models for understanding and treating upper extremity musculoskeletal disorders Manual Therapy, 2009 Oct; 14(5):S1-S54

Alison Grimaldi, University of Queensland, Australia

Alison started by talking about the hip abductor synergy and layers of control that the muscles provide.

The superficial system (TFL, UGM with ITB, GMax and VL):

• torque production
• there is some correlation between VL and poor abductor strength, clinically we see increase VL bulk and activity

The intermediate system (GMed) :

• ant and post are deep to middle or ‘lateral’ portion – implications for EMG
• deeper parts more involved in joint production, superficial parts involved in torque production

The deep system (GMin):

• strong attachments to joint capsule which:
• prevents impingement of capsule with abduction
• resists sup, lat and ant migration of humeral head common in OA
• active in all directions except adduction when capsule on maximal strain

Alison described how GMin and GMed were active in normal and functional movements.

In hip pathology(OA)  there are contrdictory reports of strength in the abductors.  Why?  Related to stage of OA or methods used in the studies i.e. testing the entire abductor synergy does not take account for compensatory mechanisms.  Looking at EMG data also shows discrepancy. Alison showed us the figures and disussed changes that occur with OA.

• In early pathology – increase adduction, increase superficial abductors and GMed hypertrophy
• Advanced pathology  – decrease GMed activity GMed & Min atrophy and changes in fibre types

Unloading leads to muscle deficits with atrophy of antigravity muscles, slow twitch muscle fires and intrinsic stabilisers at the hip and knee.  Alison’s 8 week bed rest lying only study showed no effect on size in UGM and TFL, the deeper abductors showed insignificant change but there were significant changes were shown in GMin.  But there was a recovery of size from week 2 to finish.  Implications for muscle function lends to a stability function of GMin. The recovery from week 2 indicates an incomplete elimination of gravity during bed rest ie. GMin may have been stimulated in lying to increase fast fibres and decrease slow fibres.

This may have implications for therapy.  We need to:

• be specific  which muscle are recruited and how they are recruited
• consider stage and pathology of OA and associated functional patterns
• re-establish correct balance of hip abductors
• target the superficial system

Read Alison Grimaldi’s biography

View abstract on conference website

Abstract

The lateral stability mechanism of the hip consists of a complex arrangement of muscles with variable function and differing responses to the presence of joint pathology, or to unloading in the absence of pathology. Clearer understanding of the function and dysfunction of this system will be important for the development of more specific and effective management programmes not only for hip pathologies, but for optimal alignment and function of the lumbopelvic region and the whole lower kinetic chain. The hip abductor synergy primarily responsible for lateral stability can be divided into 3 layers – the superficial layer consisting of the tensor fascia lata muscle, the upper portion of the gluteus maximus muscle, and their connections with the iliotibial band, the intermediate layer including the piriformis and the gluteus medius muscles, with the gluteus minimus muscle the deepest member of the abductor synergy. This presentation will provide evidence from recent research to suggest that our approach to assessment and therapeutic exercise prescription for lateral pelvic stability may need to be re-evaluated. Exercise prescription should address all parts of the abductor synergy in a manner consistent with their normal functional role. Real time ultrasound in assessment and re-education of the hip abductors may be a valuable tool, while higher level exercise progressions should consider the importance of weightbearing stimulus and pelvic-femoral alignment for optimal muscle balance within the abductor synergy.

Alison Grimaldi. Understanding the Lateral Stability Mechanism of the Hip & Pelvis Manual Therapy, 2009 Oct; 14(5):S1-S54

Wayne Diesel, Tottenham Hotspur Football Club, UK

Injury is caused by alterations to the muscular, nervous or articular systems.  Pre-season screening uses two movement patterns: overhead squat and single leg squat to assess movement dysfunction.  Movement dysfunctions must then be broken down to investigate problems in the muscular, nervous or articular systems.  The dynamic movement assesssment is also used in pre & post intervention assessment.

Need to follow corrective exercise continuum based on dynamic movement screening: inhibiy, lengthen,  activate, integrate.

1. Inhibit overactive muscles – self myofascial release with foam roller
2. Lengthen overactive muscles – stretching
3. Active underactive muscles – isolated strengthening
4. Integrate into dynamic movement pattern – low load then progress

Take home messages

• Dynamic compliment screening should compliment isolated joint muscle screening
• generic injury prevention programme do work
• corrective exercise continuum used to re-establish normal movement patterns
• self directed

View abstract on conference website

Abstract

Traditionally pre-season physiotherapy screening exams of footballers have in the main revolved around joint specific clinical tests.  However, more recently medical staff at Tottenham Hotspur Football Club has started looking at screening tools that are functional; require little or no equipment; don’t take long to complete and hopefully prevent either the onset or recurrence of intrinsic injuries.  The National Academy of Sports Medicine’s [NASM] approach to functional screening met all of these objectives. The functional movements used include an Overhead Squat [OHS] and Single–Legged Squat [SLS]; requires only a postural grid; digital camera and can be completed inside of 15 minutes.

Overactive muscle groups that require inhibition and lengthening as well as underactive muscle groups that need isolated strengthening can then easily be identified and incorporated into the player’s individual Injury Prevention [IP] programmes. Historically all players, irrespective of differing movement dysfunction patterns, participated in identical IP programmes.

Finally, in the event of injury thought to result from dysfunction in their movement patterns, the restoration of correct movement patterns will follow a specific sequence of events. The NASM have developed a Corrective Exercise Strategy that will be discussed during the presentation.

Wayne Diesel. Pre-Season Screening of Professional Footballers – The Role Of Movement Assessment Manual Therapy, 2009 Oct; 14(5):S1-S54

Nadine Foster, Keele University, UK

Subgrouping in back pain is the holy grail of back pain research. guidelines at the moment recommend a diagnostic triage. Despite this approach there has been no reduction in prevalence. Clear trends in high quality RCTs that there is mild effect with no difference between interventions. When we comparewhat we have to offer patient sthere are no differences and when we compare what we do with normal GP care there are small improvements.Why? Simply the natural course of these conditions, available treatments are simply not very good, heterogeneity of patients and treatment effects.

It is the heterogeneity of patients and treatment effects that Nadine will talk about.  Lots of high quality RCTs  but which person will get better with which treatment is unanswered.  arguments for subgrouping: current system of diagnostic triage is inadequate, we know clinicians believe in subgroups, promising early data, been identified as a research priority.  There several approches to subgroupng:

1. To provide more homogeneous groups: pathology, prognosis, treatment responsiveness
2. Statistical approaches
3. Clinical judgement approaches

Irrespective of these approaches the idea of sugrouping is a form of measurement.

Arguments about subgrouping:

• subgroups are not supported by data
• casual homogenetiy does not imply prognostic homogenity or treatment responsiveness
• recent guidelines for LBP do not recommend subgrouping patients with NS-LBP.  Why? Due to lack of evidence.

What are the key features of a robust approach to subgrouing?

• Plausible
• Exhaustive
• Mutually exclusive in classification
• Reliable
• Clinically useful
• Simple

What study designs and analyses are the most appropriate? (Hancock et al, 2009)

• investigate treatment effect modifiers in RCT
• limit the analyses to small number of subgroups
• use tests of interactions
• use larger sample sizes
• treat the findings with caution if the main effect of treatment is small
• externally validate (again and again …)

Nadine has been researching subgrouping for LBP in primary care.  Her investigations include the development of the STarT Back Screening Tool and trials studying this.  They are now working on the IMPACT Back study.

Subgrouping approaches have along way to go  and we need well designed clinical studies and programmes.

Read Nadine Foster’s biography

View abstract on conference website

Abstract

Low back pain is a common, disabling condition with high personal and economic costs. Despite available guidelines for practice, there have not been tangible reductions in the population prevalence of back pain or its serious long-term consequences. One reason for this, that has received increasing research attention, is that the ‘one size fits all approach advocated by many guidelines fails to target treatments at patients who might benefit from them most, thus diluting their potential benefits.

Systematic identification of key obstacles to recovery in primary care back pain patients from high quality epidemiological studies can inform the development of early, targeted interventions. Indeed, maximising the potential for optimally targeted interventions is predicated on better understanding of the prognostic factors that are causally related to clinical outcome and identifying which are a) most predictive of outcome and b) most likely to be modifiable in primary care. Only then can closer matching of treatments to patient characteristics be a clinical reality.

Using specific examples drawn from recent research within the Arthritis Research Campaign National Primary Care Centre at Keele University in the UK, and other studies, this presentation will provide an overview of subgrouping approaches under investigation, provide new evidence about the predictive strength of obstacles to recovery and share experience from studies that focus on translating subgrouping approaches into workable sytems in primary care clinical practice.

Clinical Take Home Messages:

1. Although many factors are suggested to be important obstacles to recovery, only a few are clearly distinctive, in that they independently predict back pain-related disability in primary care consulters.
2. The results challenge some assumptions regarding the key obstacles to recovery in this population and will help focus future targeted interventions.
3. The challenge is to translate this knowledge about the most predictive obstacles to recovery in primary care into workable subgrouping approaches for busy primary care practice, targeted interventions and improved outcomes for patients.

Acknowledgements: Research support from the Arthritis Research Campaign (arc), the National Institute of Health Research (NIHR) and the Health Foundation. Nadine Foster is funded by a Primary Care Career Scientist Award from the NIHR in the UK.

Nadine E Foster. Subgrouping patients with low back pain in primary care: are we getting any better at it? Manual Therapy, 2009 Oct; 14(5):S1-S54

Lorimer Moseley, Prince of Wales Medical Research Institute, Australia

Lorimer will talk about the work that he has been doing which have great potential clinical implications but have not yet be fully tested.

Treatment aims should be to get patients pain free.  Three arms of our approach to chronic pain: cognitive, behavioural, brain changes.  Today we will focus on changes in the brain when we have pain for a long time.  For this we are interested in the changes that occur in the somatotopic representations in the primary sensory cortex. Can we estimate the changes clinically?  We can by looking at tactile acuity.  In chronic pain intracortical inhibition is lost.  Two point discrimination threshold is larger in patients with pain.  Does tactile acuity relate to lumbopelvic control?  Yes, they are associated.  Can we train somatotopic representations? Yes, if we do a treatment aimed at the primary sensory cortex.  What is the effect of the visual system on tactile acuity? Looking at the skin of the area touched fosters inhibition and enhances tactile acuity.  What are the effects of focusing the attention?  Attending spatially to the area is likely to also increase tactile acuity.

Spatial representation (the space that the affected area resides in) can also be affected in affected body parts.

Perceptual representation (body image) may also be disrupted.  Could distorted body image be contributing to symptoms?  Yes it could.  What about in back pain? We know that cortical representation is changed. What about the percept when the cortical representation is increased?  This changes but in opposite ways to in CRPS patients.  Perceptual representation is also important for motor control.

Lorimer talked extensively about studies that they have completed to investigate all that is mentioned above.  The take home messages were:

• Chronic pain is characterised by facilitation and inhibition
• We can train inhibition and subdue facilitation
• Mind affects body and body affects mind – need to treat both.

See Lorimers other clinical seminar notes and his website www.bodyinmind.com.au

Read Lorimer Moseley’s biography

View abstract on conference website

Abstract

In this lecture, I will outline some important developments in the way chronic pain is understood and treated. I will present fundamental research that has clear implications for the treatment of people in pain – for example, studies that show a two way relationship between the state and regulation of our body and the way our body feels, and studies that show high-order cognitive processes have implications for blood flow, brain processing of sensory input, immune function and immune-related tissue inflammation. These exciting findings are more exciting than they are intimidating – I will contend that we can harness the complexity of the human brain to help people in pain. I will provide examples of the use of visual input to trick and train the brain of people with chronic painful disorders. I will discuss studies that are at the forefront of this new line of enquiry and suggest that we are obliged as clinicians to begin integrating these new findings within our current clinical reasoning paradigms.

Lorimer Moseley. The eyes have it – recent developments in training the brain for chronic pain Manual Therapy, 2009 Oct; 14(5):S1-S54

It’s day three here in Edinburgh. We have a great line up of keynotes and guest lectures today to keep us all amused until it’s time to go home. The messages so far have been around sub-classification and targeted interventions. I’m suspecting that this theme will continue today and hopefully be extrapolated upon.  Chris McCarthy chairs this mornings session.

Again like yesterday there are three parallel sessions each with 4 presentations (15 minutes each). Unfortunately I can’t be in three places at once (as much as I wish I could) so I am not able to cover these sessions (not to mention that I honestly can’t keep up with the speakers at these!!). The programme of these sessions can be found here and the abstracts can be found in Manual Therapy, Vol 14, Supp 1 (Oct 2009).

OK, we’re going to be tweeting this afternoon. I will be floating around the clinical seminars and bringing snippets from a plethora of the sessions taking place this afternoon. You can follow my travels here:

Mark Comerford, Kinetic Control, UK

A lot of pressure to keep athletes fit and well.  Does screening really work? There is good evidence for Hx of previous injury leading to reinjury, stretching does not prevent injury, ligamentous injury increases risk for injury, musclse strengthening does not prevent injury.  No reliable evidence to support screening for physical factors to prevent injury and reduce risk of injury.

How then do we screen? Asses ‘real’ not isolated function and assess the control of ‘real’ function.

Identifying uncontrolled movement is important and classification methods needs to be developed.  Mark talked about the importance of dentifying and subclassifying uncontrolled movement. He discussed:

• the reliability in identifying uncontrolled movement,
• the links between uncontrolled movement and pain,
• factors related to identifying risk for developing MSK injuries related to uncontrolled movement,
• that battery of tests are more reliable and more valid in diagnosis
• and new screening tools which include a battery of tests

Read Mark Comerford’s biography

View abstract on conference website

Abstract

Screening of athletes for musculo-skeletal factors is commonplace in elite, professional and competitive sport. This screening is promoted as part of an injury risk management strategy to prevent recurrence of pain or re-injury. To date, musculo-skeletal screening has focused on testing joint range, muscle strength (both power and endurance) and testing muscle extensibility (Bennell et at 1998 1999, Garrick 2004, Leetun et al 2004, Gabbe et al 2005, Kibler et al 2006). Assessing these parameters invariably tends to isolate the individual joints or muscles in non-functional ‘standard’ situations.

All have been relatively unsuccessful at predicting risk of re-injury or recurrence of pain. There is almost no reliable evidence base to support the use of screening for these physical factors to either predict risk of injury to prevent re-injury in the systematic review or meta-analysis databases (Chalmers 2002, Wingfield et al 2004).

Currently, the research and review evidence points to a history of previous injury being the single most consistent and reliable predictor of high risk of re-injury (Van Mechelen et al 1992 1996, Watson 2001, Locke 2003, Reed 2004, Joy et al 2004, Fuller & Drawer 2004). If this is the case, then clearly there is a problem in the way that we are managing the original or previous injury. It seems that the acceptable outcomes of asymptomatic function, normal range of joint motion (isolated testing) and normal muscle strength (isolated testing) are not adequate rehabilitation end points to prevent recurrence.

The process of assessing the control of ‘real’ function, that is, the influence of the multiple muscle interactions acting on multiple joints in functionally orientated tasks has not be promoted because it has universally been put in the ‘too hard basket’. This is the missing piece of the screening puzzle.

Mark Comerford. Recurrence of Injury and Pain in Sport – What’s Missing Manual Therapy, 2009 Oct; 14(5):S1-S54

Chad Cook, Duke University, USA

In reality we use tests not just for diagnosis (triage, ruling out and confirmation), we also use them for prognosis, to assess disability status and to direct treatment.

The focus today is diagnosis.  Diagnostic accuracy studies are case controlled designs where bias must be controlled and large samples used.  Findings often change with a spectrum of patients.  Reliability, sensitivity, specificity and the likelihood ratios are essential for establishing the accuracy of diagnostic tests.  Likelehood ratios can influence decsion making regarding tests.

Chad has looked at any tests and accumulated the best diagnostic tests for spinal dysfunction.

To be included each test had to meet the following requirements:

• sensitivity >90%
• positive liklehood ratio <5
• negative liklehood ratio <5
• Quadas score >10

Cxsp

• ULTT helps to rule out the presence of cervical raiculopathy if used eatly in exam
• canadian cxspine rules good to identdy who should get an xray
• palpation side glide test – helps to rule out or rule in presense of block or restriction
• clinical prediction rule for cervical myelopathy – helps to rule in and rule out myelopathy
• invereted supinator sign – most sensitive test for myelopthay
• hoffmans sign -
• babinski
• spurlings test and cervical distraction test – help to rules in cervical radiclopathot  buta strong tes
• PA of Cx spine – good to rule out presence of Cx spine dysfunction
• flexion rotation test – usefull in ruling out Cx headache at C1/2

Txsp

• has no studies that meet the bench mark for testing dysfunction in Txsp

Lxsp

• percusiion test – good to rule out presencr of disc dysfunction
• SLR helps to rule out the presence of lumbar radiculopathy. not diagnostic
• centralisation – good at identifying discogenic dysfunction anf radiculopathy
• PA – good for rule in presence of lack of hypomobility
• PPIVMS – appropriate to rule in hypomobiliyt

Chad also mention some studies on clusters of tests that were suitable for all three areas of the spine.

What is missing?

• Sharps purser
• Alar ligament
• Any Tx OS test
• VBI
• Slump test
• Prone instability test
• Well leg raise
• DTR’s, MMT, and sensory testing

Read Chad Cook’s biography

View abstract on conference website

Abstract

In clinical practice, physical therapists use spine-related tests and measures daily and frequently associate all tests equally. Use of diagnostic accuracy values such as sensitivity, specificity, and positive likelihood ratios has improved our ability to discriminate tests’ strengths. Recent advances in diagnostic accuracy research have allowed physical therapists to progress beyond simple unadjusted accuracy measures; to categorize tests and measures based on the tests’ strengths in the spectrum of differential diagnosis. Differential Diagnosis is designed to provide the beginning and experienced physical therapist with parameters for analyzing elements of differential diagnosis and Prognosis (e.g. diagnostic accuracy values, checklists for quality scores for tests and measures, and guidelines for accuracy of prognosis studies). The foci of this presentation include essential parameters for effective screening, differentiation, and confirmation of spine-related tests and measures, used by physiotherapists. Strengths and weakness of each test and measure are discussed and tests are either vilified or advocated depending on each test’s value. Upon completion, the learner will have knowledge of a battery of useful diagnostic tests (as well as those that have limited use) but most importantly, will have knowledge on how to critique study designs to determine future values of tests and measures.

References

1. Cook C, Hegedus E. Orthopedic clinical special tests. Upper Saddle River; Prentice Hall: 2008.
2. Jaeschke R, Meade M, Guyatt G, Keenan SP, Cook DJ. How to use diagnostic test articles in the intensive care unit: diagnosing weananability using f/vt. Crit Care Med. 1997;25:1514-1521.
3. Garbuz et al. Classification systems in orthopaedics. J Am Acad Orthop Surg. 2002;10:290-297
4. Obuchowski et al. Ten Criteria for Effective Screening. Am J Roent. 2001;176:1357-62
5. Kleinstuck et al. Are structural abnormalities on MRI a contraindication to the successful conservative treatment of chronic nonspecific low back pain? Spine. 2006;31:2250-2257.
6. Jarvik et al. Three-year incidence of low back pain in an initially asymptomatic Cohort. Spine. 2005;30:1541-8.

Chad Cook. Diagnostic Utility of Clinical Tests for Spinal Dysfunction Manual Therapy, 2009 Oct; 14(5):S1-S54

Steve Harridge, Kings College London, UK

Read Steve Harridge’s biography

View abstract on conference website

Abstract

Our muscles are machines that allow us to convert the chemical energy stored in food into mechanical work, enabling us to undertake all the necessary activities for daily living. Our muscles are made up of hundreds and thousands of long cells, our fibres, and nature has produced a system by which differences in these fibres allow us to produce great feats of strength and power on the one hand and great feats of endurance on the other.

Fibres can crudely be classified on their basis of their colour (red or white), or on the basis of twitch contraction time (slow twitch and fast-twitch). There are however, traditionally considered to be three types of fibre which can be identified on the basis of their ATPase activity (type 1, type IIa and type IIx), their metabolic properties (slow oxidative, fast oxidative or fast glycolytic) or different isoforms of myosin, the molecular motors, (myosin heavy chain (MHC)-I, MHC-IIa and MHC-IIx). Whilst the nomenclature of these classifications is based on the specific characteristic measured, there is a general agreement between classifications. For example, slow oxidative fibres are those that normally contain MHC-I isoforms and are classified as type I by ATPase histochemistry. However, it should be noted that even these classifications are somewhat crude, in that fibres can also represent a continuum between types, with some containing more than one type of MHC isosform (i.e. they are hybrid). In contrast to type I fibres, type II fibres have a higher velocity of shortening and as a consequence have a greater potential for power generation than type I fibres. However, the compromise is the lesser ability of type II (particularly type IIx fibres) to sustain power over a prolonged period of time. In other words they fatigue more easily. Type I fibres are slow to contract, but are highly resistant to fatigue. Unlike some animal muscles, human muscles are not made up of exclusively one or other type, but are mixed with varying proportions of fast and slow fibres. However, it makes sense that muscles with a postural function, such as the soleus, are dominated by type I, fatigue-resistant fibres. It also comes as little surprise that athletes who excel in different events have muscles with compositions that reflect the demands of particular events. Sprinters tend to have a high proportion of high-power generating type II fibres, whilst endurance runners tend to have with a higher proportion of fatigue resistant type I fibres. The question is to what extent can, through changes in activity, a fibre be switched? We know from animal studies, that have used cross-innervation or chronic low-frequency stimulation techniques, that it is possible to effectively change fast muscles into slow muscles. However, under more normal physiological conditions, such as voluntary exercise, such a switch is difficult to demonstrate. This is the case in both humans and animals. In contrast to increased activity, we know that disuse, associated with prolonged bed rest or cast immobilisation, results not only in fibre atrophy, but also a switch towards the fast type. This is exemplified in the muscles of spinal chord injured individuals who demonstrate a dominance of type II fibres in the affected muscles distal to the sire of lesion.

This lecture will address the extent to which human muscles can alter their type within the context of athletic performance, rehabilitation and ageing. It will also address the question as to whether a drive towards making fibres become “type I”, is a desirable outcome. Indeed it may be preferable for fast fibres to be conditioned so as to increase their fatigue resistance, but retain their ability to generate power.

Stephen D.R. Harridge. Skeletal muscle fibres. What types have we got? Can we change them and does it matter? Manual Therapy, 2009 Oct; 14(5):S1-S54