Lumbar Herniation,Achilles Tendinopathy, Neck Injury, VMO dysfunction

From the editorThe number one concern for injured athletes is getting back to training as soon as possible. This can be challenging for clinicians; sometimes a more aggressive intervention is appropriate but at other times, patience and extended rehab is what’s needed.

In our first article, Chris Mallac argues that lumbar spine disc herniation can fall into the former category, especially for elite athletes requiring a speedy return to competition. Chris outlines the likely signs and symptoms associated with disc herniation, and the selection criteria for micro-discectomy surgery in athletes.

Fol lowing this , Lachlan Wilmot cons iders midsubstance Achi l les tendinopathy. Lachlan explains that this is a condition where extended conditioning and rehab in the latter stages of recovery are absolutely essential for a satisfactory long-t e r m o u t c o m e , a n d p r o v i d e s a comprehensive programme for doing so.

In our third article, Kay Robinson looks at

the mechanics of neck injury and assessment techniques for the clinician. Although these injuries are less common in athletes, Kay presents evidence that they are on the rise – worrying because of the risk of associated concussion and spinal injuries.

Meanwhile I’ve been looking at the r e c e n t e v i d e n c e o n t h e u s e o f fluoroquinolone antibiotics and the (considerable) risk of tendon rupture in a t h l e t e s . H o w s h o u l d c l i n i c i a n s differentiate their treatments for athletes that have recently used these antibiotics so that risk is minimised, and how should any rehab programme be adapted?

Our final article revisits the VMO. Following on from his part 1 article Chris Mallac provides evidence that VMO dysfunction and PFPS are related; therefore strength and control exercises for the VMO are needed to fully rehabilitate the PFPS affected athlete – exercises which Chris goes onto provide.

Enjoy the contents and we’ll look forward to seeing you next month.

Andrew Hamilton BSc Hons MRSC ACSM (commissioning editor)

Low back pain is a reasonably common complaint in both the young college age athlete and professional athlete, and it has been estimated that more than 30% of athletes complain of back pain at least once in the career(1). The cohort of back injuries that can affect the athlete include disc degeneration, disc bulge/herniation, facet j o i n t a r t h r o p a t h y , s p o n d y l o s i s , spondylolisthesis, muscle spasm and stress fractures.

Lumbar spine disc herniation is one type of lumbar injury that can not only cause debilitating low back pain, but can also compress nerve roots and create radicular referral of pain into the lower leg with associated sensation changes and muscle

weakness. This injury will not only affect the short-term competition ability of the athlete, but may also reoccur and become chronic possibly resulting in a career ending injury.

Managing disc herniation in the athlete usually begins with conservative treatment and if this fails, surgical options are considered. However, often elite athletes will request a faster resolution to their symptoms to minimise time away from competition. Therefore, providing the criteria for lumbar spine surgery are indicated, the conservative period will often be compressed, and surgery will be sought earlier. The favoured surgical procedure for the athlete with a disc herniation is the lumbar disc micro-discectomy.

Anatomy and biomechanicsThe lumbar spine intervertebral discs play an important biomechanical role within the spine, allowing for motion between the spinal segments whi le dispersing compressive, shear, and torsional forces(2). These discs consist of a thick outer ring of fibrous cartilage termed the annulus f ib ros i s ( ak in to the on ion r ings surrounding the core of an onion), which surrounds a more gelatinous core known as the nucleus pulposus, which is contained within the cartilage end plates inferiorly and superiorly.

The intervertebral disc is composed of cells and substances such as collagen, proteoglycans, and sparse fibrochondrocytic

Disc herniation

Lumbar disc herniation: when is discectomy required?In the first of a 2-part article, Chris Mallac looks at the lumbar spine disc herniation. What are the likely signs and symptoms associated with disc herniation, and what are the selection criteria for micro-discectomy surgery in athletes?

diagnosis • treatment • rehabilitation • prevention

ISSN: 2397-6640 Issue 153 AprIl 2016

In this issueLumbar spine disc herniation: when is surgery appropriate? 1

Midsubstance Achilles tendinopathy and end stage rehab 4

Mechanics of neck injury, and assessment techniques for the clinician 8

Fluoroquinolone us in athletes: differentiating treatments to reduce tendon rupture risk 11

VMO dysfunction: strength and control exercise for the PFPS affected athlete 14

2 SPORTS INJURY BULLETIN No 153

can also damage the internal structure of the disc. This can occur as a result of a fall or strong muscular forces developed during tasks such as heavy lifting.

Athletes are commonly exposed to high loading conditions. Examples of this include:1. World-class power lifters, where the calculated compressive loads on the spine are between 18800 Newtons (N) and 36400N acting at the L3-4 motion segment(11). 2. Elite level football linesmen who have been shown to present time-related hypertrophy of the disc and changes in vertebrae endplate in response to the repetitive high loading and axial stress(12).3. Long distance runners have been shown to undergo significant strain to the intervertebral disc, indicated by a reduction in disc height(13).

Herniations can be classified based location such as central, posterolateral, foraminal, or far lateral as defined by Fardon and Milette (2001) (14). The herniation morphology can also be classified as protrusion, extrusion, or sequestered fragment. Finally, herniations are also identified based on level, with most herniations occurring at the L4/5 and L5/S1 intervertebral disc level; these can then in turn affect the L5 and S1 nerve roots leading to cl inical sciatica (15). Upper level herniations are less common, and when they do occur with radiculopathy, they will affect the femoral nerve. Finally, the prevalence of disc injury increases progressively caudally, with the greatest numbers at the L5/S1 levels(16).

Herniation in athletesThe offending movements implicated in creating disc herniation and the sports involved are usually sports with combined trunk flexion and rotation(17). The 20-35 age group are the most common group to herniate a disc, most likely due to the fluid nature of the nucleus pulposis and due to behaviour(18). This age group are more likely to be involved in sports that need high loads of flexion and rotation and/or are reckless with their postures and positions during loading.

The sports most a t r isk of d isc herniation are:

Hockey Wrestling Football Swimming Basketball Golf

radicular pain may be generated along with neurological symptoms such as numbness and paraesthesia.

The pain associated with lumbar radiculopathy occurs due to a combination o f n e r v e r o o t i s c h e m i a ( d u e t o compression) and inflammation (due to neurochemical inflammatory mediators released from the disc) . During a herniation, the nucleus pulposus places pressure on weakened areas of the annulus, and proceeds through the weakened sites in the annulus where it ultimately forms a herniation(6). It follows from this that some form of disc degeneration may exist before the disc can actually herniated(7).

In comparison to other musculoskeletal t i ssues , d iscs have a tendency to degenerate earlier in life, with some studies showing adolescents presenting signs of degeneration between the ages of 11 to 16(8). With increasing age, there is further degeneration of the intervertebral discs. Powell et al (1986) observed that more than one third of normal healthy subjects aged 21-30 years had degenerated discs(9).

While the disc may be at risk of injury in all fundamental planes of motion, it is particularly susceptible during repetitive flexion, or hyperflexion, combined with lateral bending or rotation(10). Traumatic events such as excessive axial compression

cells, which allow transmission and absorption of forces arising from body weight and muscle activity. To do this, the disc relies largely on the structural condition of the nucleus pulposus, annulus fibrosis and the vertebral endplate. If the disc is structural ly normal and is functioning optimally, forces are spread across the disc evenly(3).

However, disc degeneration (cell degradation, loss of hydration, disc collapse) can decrease the ability of the disc to withstand extrinsic forces, as forces are no longer transmitted and distributed evenly. Tears and fissures in the annulus can result, and with sufficient external forces, the disc material may herniate. Alternatively, a large biomechanical force placed on a healthy, normal disc may lead to extrusion of disc material as a result of catastrophic failure of the annular fibres – examples include a heavy compression type mechanism due to a fall on the tailbone, or strong muscle contraction such as very heavy weight lifting(4).

Herniations represent protrusions of disc material beyond the confines of the annular lining and into the spinal canal (see Figure 1)(5). If the protrusion does not invade the canal or compromise nerve roots then back pain may be the only symptom. However, if the extruded disc material contacts or exerts pressure on the thecal sac or lumbar nerve roots, then

Figure 1: schematic representation of herniated lumbar disc


ImagingMRI remains the preferred method of identifying lumbar spine disc herniation, as it is also very sensitive for detecting nerve root impingements(23). However, abnormal MRI scans can occur in otherwise asymptomatic patients(25); hence, clinical correlation is always essential prior to any surgical consideration. Furthermore, patients may present with clinical signs and symptoms that suggest the diagnosis of acute herniated disc, and yet lack evidence of sufficient pathology on MRI to warrant surgery.

Therefore it has been proposed that a volumetric analysis of a herniated disc on MRI may be potentially valuable in assessing the suitability for surgery. Several authors have already cited the potential value of volumetric analysis of herniated disc on MRI as part of the selection criteria for lumbar surgery(26).

In a study conducted at Michigan State University, it was found that the size and location of the herniated disc determined the likelihood for surgery with what researchers referred to as ‘types 2-B’ and ‘types 2-AB’ being the most l ikely candidates for surgery(27).

The MRI protocol for the lumbar spine consists of (see Figure 2):

1. Sagittal plane echo T1-weighted sequence2. Sagittal fast spin echo proton density sequence3. Sagittal fast spin echo inversion recovery sequence4. Axial spin echo T1-weighted sequence

SummaryDisc herniations are not a common complaint in athletes, but they do occur in

athlete include: Low back pain with pain radiating down one or both legs Positive straight leg raise test Radicular pain and neurological signs consistent with the nerve root level affected Mild weakness of distal muscles such as extensor hallucis longus, peroneals, tibialis anterior and soleus. These would fit with the myotome relevant for the disc level MRI confirming a disc herniation Possible bladder and bowel symptoms Failed conservative rehabilitation.

Typically, the elite athlete has a shorter time span in which to allow conservative rehabilitation to be effective. In the general population, medical practitioners will most likely prescribe a minimum 6-week conservative period of treatment with a review at 6 weeks as to whether to extend the rehabilitation a further 6 weeks or to seek a specialist opinion. The specialist may then attempt more medically orientated interventions such as epidural injections.

The athlete however will have these time frames compressed. They may be more willing to undergo an epidural very early in the conservative period to assess the effectiveness of this procedure. If no signs of improvement are evident in two weeks then they may opt to have an immedia te lumbar sp ine mic ro -discectomy.

Tennis Weightlifting Rowing Throwing events.

These are the sports that involve either high loads or high exposure to combined flexion and rotation mechanisms. Furthermore, those who participate in longer and more intense training regimes appear to be at higher risk of spinal pathologies, as do those involved in impact sports.

Signs and symptoms indicating discectomyThe efficacy of management plans for lumbar spine disc herniation – in terms of t h e d e c i s i o n t o o p e r a t e o r t r e a t conservatively – will be discussed in greater depth in part two of this series. However, the decision to operate in an athlete is usually driven by the motivation and upcoming goals that the athlete has set themselves. They may in fact prefer a relatively simple micro-discectomy rather than waiting for symptoms to abate t h r o u g h a n e x t e n d e d p e r i o d o f rehabilitation.

T h i s c o n s e r v a t i v e p e r i o d o f management may involve medication therapy, epidural injections, relative rest and trunk muscle rehabi l i ta t ion, acupuncture , os teo/chi roprac t i c interventions. However, the typical presenting signs and symptoms that indicate a significant disc herniation that may require surgical intervention in the

Various radiographic techniques reveal that athletes present with more cases of disc degeneration than the general population. For example:

In a study on 24 male elite gymnasts and 16 non-athletes it was found that gymnasts were at a higher risk of disc degeneration than non-athletes(19).

Herniation accounts for 43% of lumbar injuries in tennis players(17).

Elite level female gymnasts are at greater risk of experiencing disc degeneration(20).

The prevalence of lumbar intervertebral disc degeneration was greater in Olympic athletes when compared to the normal population. Various degrees of disc displacements were found in 18 out of 31 Olympic subjects(16).

Magnetic resonance imaging (MRI) revealed that 28 of 33 adolescent tennis players presented clinical symptoms, ranging from disc degeneration, disc herniation, pars lesions, and facet joint arthropathy(21).

Interestingly it has been found that that female flamenco and ballet dancers had a lower prevalence of disc degeneration as measured by MRI when compared to age matched non-athletic controls(22). This suggests that the type of physical activity influences the prevalence of disc degeneration in an athletic population.

High load sports such as weightlifting were associated with greater incidence of degenerative discs than runners(23).

Athletes and disc degeneration: the evidence

Figure 2: MRI lumbar spine disc herniation at L5/S1

Image on left is a sagittal T1 weighted image; image on right is a sagittal weighted T2 image


sports that involve high loads or repetitive flexion and rotation movements. Sufferers of a disc herniation will usually feel focused low-back pain, possibly with referral into the lower limb with associated neurological symptoms if the nerve root has been compressed. MRI still remains the gold standard for identifying disc herniation’s and associated nerve root impingement.

Managing a disc herniation in an athlete is somewhat different to the general population as often the risk of a protracted failed rehabilitation period is bypassed for the more secure and low risk micro-discectomy procedure. In the second instalment in this series, we will discuss the exact surgical options involved and how to rehabilitate the elite athlete fo l lowing a lumbar sp ine micro -discectomy.

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It’s human nature to associate pain with a problem, and for the most part, the absence of pain with health and function. F o r t h i s v e r y r e a s o n , e n d - s t a g e rehabilitation can often be accelerated or overlooked. While there is an ever-growing body o f ev idence a round in i t i a l tendinopathy treatment – something we’ll touch on by discussing phase 1 and 2 progressions - the focus of this article will be based around the later phase 3 and 4 progressions.

These progressions are of particular importance, as during these stages the tendon may often be only minimally painful, therefore reducing motivation levels to continue diligently following the program. And while this article is based on exercise prescription for midsubstance Achilles tendinopathy (tendinopathy symptoms that occur around the central part of the tendon, as opposed to insertional tendinopathy that occurs at the insertion of the Achilles tendon), the concepts and philosophies covered within this article can be adapted and tailored for tendinopathies occurring in various sites.

Tendinopathy overviewTendinopathy can be a frustrating

condition, particularly for those who compete in sports with little opportunity f o r r e s t o r r e c o v e r y p e r i o d s . Tendinopathies have previously been associated with repetitive and overuse activities(1),although the repetitive activity itself may not necessarily be the only underlying issue.

In the presence o f movement dysfunction, this may be the case, but more recently tendinopathies have been linked to sudden spikes in loading that exceed the tendons tolerance(2). Sudden increases in loading, regardless of the modality, can severely disrupt the tendons ability to heal (3). For the most part, tendons are capable of maintaining equilibrium, and adapting to increases in loads. However, if the rate of loading is greater than the tendons adaptive r e s p o n s e , a n a c u t e e p i s o d e o f tendinopathy may occur.

Current Evidence-Based TreatmentsA common misconception in treating tendinopathies is to cease all activities involving the tendon and unload the limb in an attempt to improve the condition. Unfortunately, this method does not aid in

the repair of the tendon, nor does it help build tendon resilience. Cessation of all activity for an athlete often sets them up for future flare-ups and can decrease the load resilience of the tendon(4).

Tendons are capable of tolerating loads even in the acute phases of rehabilitation. In fact, recent studies have shown isometric contractions for tendinopathies can have a positive effect on reducing pain(1,4,5). Once the painful flare up has subsided, eccentric loading can be used to build tendon resilience providing pain levels do not exceed a score of 3 out of 10(3).

When referring to the rating of 3 out of 10 pain, this is based on a traditional pain scale where 0 refers to being pain free and 10 refers to unspeakable pain -the worst pain ever experienced. When using the rating of 3, this will usually refer to pain that is noticeable or distracting, but can be managed and often adapted to throughout the session. It should not c h a n g e m o v e m e n t m e c h a n i c s . T h e r e f o r e , t h e m a n a g e m e n t o f tendinopathies should be based around correct exercise prescription and loading principles rather than complete cessation of activity.

Achilles rehabilitation

Midsubstance Achilles tendinopathy: what’s the endgame?

Lachlan Wilmot explains the importance of end-stage rehab for midsubstance Achilles tendinopathy and provides a framework to help build tendon resilience across high-end movements


pain with activity and the ability to perform 10 calf raises per leg with no more than a 4 out of 10 pain score. Performed correctly, phase 1 will reduce a large amount of the acute pain in the tendon and build some low-level tendon resilience.

Phase 2 – load IntroductionPhase 2 is focused on building strength in the tendon while still reducing pain levels. If tendons fail to tolerate a load well, it may take as long as 72 hours post exercise, to become painful – unlike traditional delayed onset of muscle soreness (48 hours). Being mindful of this window, it is therefore important to avoid large loadings within 3

Isometric exercises such as single leg holds off a step are an effective way to reduce pain levels and provide an easy position to start adding load to as a progression. Isometric holds are to be built up to 20 seconds each leg initially, ensuring no pain above a score of 3 out of 10 is experienced. The aim is to complete 3 sets, 3-4 times per day as tolerated, and slowly building the hold time up to 40 seconds using the same guideline of no more than a 3 out of 10 pain score. As the set-rep times increase, the frequency of daily sessions can be reduced down to 1 or 2.

P r o g r e s s i o n o n t o p h a s e 2 i s characterised by a marked reduction in

Loading phases (see Tables 1 and 2 for phase descriptions and definition of terminology)

Phase 1 – acute/protectiveThe length of an initial phase can vary in time because some athletes respond better and their pain levels subside quickly, while others take longer to respond. The key focus in this phase is about pain relief, which is often achieved through the use of isometric exercises and the administration of Non Steroidal Anti-inflammatory Drugs (NSAIDs) under the guidance of an a p p r o p r i a t e l y q u a l i f i e d m e d i c a l practitioner.

Table 1: 4-phase progression of Achilles tendon loading

Phase Focus CharacteristicsTime

Frame

Key Strength Modality Frequency Prescription Example

Ph

ase

1

Acute/Protective

Pain/Stiffness upon wakening

Pain on palpation

Pain during activity

Difficulty performing 10 calf raises

0-2 Weeks Isometrics Daily

Single leg Isometric Hold (heel off step) – Body weight x 20-40 sec x 3 sets

Progress to loaded holds

Ph

ase

2

Load Introduction

Pain/Stiffness upon wakening

Pain on palpation

Reduced pain during activity

Pain below a 4/10 when perfoming 10 calf raises

2-5 Weeks

Isolated Resilience

Controlled Eccentrics

Daily to every

second day (the heavier

the load, the longer recovery

time between sessions)

Single Leg Calf Raises (heel off step) x (build up to 20 reps) x 3 sets

Eccentric Heel Lowers (heel off step) – 2 legs up, 1 leg down x 10 reps x 3 sets

Progress to loaded eccentrics and loaded calf raises

Ph

ase

3

Strength Accumilation

Pain free upon wakening

Reduced pain on palpation

Minimal/zero pain with activity

Can perform 10 loaded calf raises

4-10 Weeks

Strength Resilience

Reactive Stiffness

Every 2-3 days

Slow Prowler Push x 20 steps x sets

BB Step Up – Double Box x 6 reps x sets

Mini Tramp Jog x 40 sec ON: 20 sec OFF x 5 sets

Knee Drive Hold on BOSU x 20 sec hold x 4 sets

Ph

ase

4

Elastic Tolerance

Pain free upon wakening

Reduced pain on palpation

Pain free with activity

Jump rope pain free

10+ Weeks

Reactive Stiffness

Ballistic Stiffness

Every 2-3 days

Linear hop and stick; 6 reps x 4 sets

Lateral hop and stick; 6 reps x 4 sets

Linear hurdle and hop; 6 reps x 3 sets

Lateral hurdle and hop; 6 reps x 3 sets

Note: Time frame is only a guide, there is large variation in this within each individual

Table 2: Definition of terminology

Isometrics Exercises characterised by no concentric/eccentric movement – designed to relieve tendon pain and build low level resilience (eg Iso Holds – off step)

Controlled Eccentrics Exercises characterised by a significantly higher load on the tendon during the eccentric portion – designed to build tendon strength and resilience (eg Heel Lowers)

Isolated Resillience Exercises characterised by an isolated loaded or unloaded concentric/eccentric movement – designed to build tendon strength and resillience (eg Calf Raise)

Strength Resillience Exercises characterised by a loaded concentric/eccentric movement – designed to accumulate the strength capacity of the tendon (eg Prowler Push)

Reactive Stiffness Exercises characterised by low level instability and/or low level stretch-shortening cycle – designed to build low level tendon stiffness/elasitcity (eg Mini Tramp Jumps)

Ballistic Stiffness Exercises characterised by high level instability and/or high level stretch-shortening cycle – designed to build high level tendon stiffness/elasitcity (eg Hurdle hop)


The Achilles tendon was designed to be used as a contributor to stiffness of the ankle joint allowing for elastic energy to be utilised. Strength resilience exercises are utilised to further increase the strength capacity of the tendon and allow loading of the tendon in a dynamic yet controlled environment. The use of a slow prowler push (Figure 3) is a great way to pre-stretch the Achilles tendon by dorsiflexing the foot prior to foot contact. This removes muscle slack in preparation for generating force into the ground. This allows the Achilles tendon to be utilised in a semi-isometric state, while promoting force transfer prior to toe-off.

A double box step up (Figure 4) is another global exercise that allows the Achilles to aid in force transfer within the functioning system. Both of these exercises are great examples of integrating the Achilles tendon into global strength movements, whilst still having the focus placed heavily on the Achilles tendon. Phase 3 requires key exercises to integrate the Achilles tendon back into the global system via its contribution via the soleus/gastrocnemius complex through stiffness. Maximal to near-maximal loads should be utilised in this phase to allow the tendon to experience a high amount of tension and force transfer.

Also beginning in phase 3 are some lower-level reactive stiffness exercises. These exercises allow the tendon to be i n t r o d u c e d t o a m o r e d y n a m i c environment while keeping forces low and

and therefore is often assumed to have returned to optimal function. With the tendon relatively pain free, higher-end strength capacity becomes the focus along with introducing some reactive stiffness.

days of each other.Building strength while reducing pain

levels can be achieved through isolated resilience exercises such as single leg calf raises (Figure 1) and controlled eccentric training. Look to build single leg calf raises up to 20 reps per set while keeping pain scores to below 3 out of 10. Once the client has built up to 3 sets of 20 reps each side for calf raises, you can look to add loading, always monitoring any pain levels at the time and for subsequent days.

The introduct ion of control led eccentrics within the same session is permitted once the client has achieved 3 sets of 10 unloaded calf raises. A good example of this is a double-leg calf raise up, then lowering for 5 seconds on 1 leg (Figure 2), gradually building up to 10 reps each side. Load can also be added to the controlled eccentric reps once 3 sets of 10 reps have been achieved. Progression on to phase 3 can be characterised by minimal to zero pain with activity and the ability to perform 10 loaded calf raises pain free.

Phase 3 – strength accumulation Phase 3 is an important phase that is commonly overlooked or neglected as the tendon presents with minimal to no pain,

Figure 1: Single-leg calf raise

Figure 2: Eccentric heel lowers (2-legged calf raise up, 1 leg lowers down)

Figure 3: Slow prowler push

Figure 4: BB step up – double box


controlled. Mini tramp jogging (Figure 5) is perfect for this type of exposure. The trampoline has enough elasticity to allow the impact forces to be low, yet causes the tendon to act with stiffness, to create a series of stretch-shortening cycles (SSC) with the soleus/gastroc complex.

The use of the SSC is not the only stimulus that needs to be addressed in Phase 3 of rehabilitation. While the knee drive hold on a BOSU (Figure 6) does not require the use of the SSC, it forces the tendon to respond to a changing environment under the foot. While the forces are low level, it makes for the perfect introduction to a reactive environment while integrating the entire posterior chain. A plate held in different positions is used to manipulate the environment and force the body to continually react to ma in ta in pos ture and s t i f fness . Progress ion in to phase 4 can be characterised by being pain free on palpation, pain free with activity and specifically being able to jump a rope pain free for approximately 2 minutes.

Phase 4 – elastic tolerance Phase 4 is focused on introducing the SSC in a more dynamic environment . Plyometrics are introduced and form the foundation of this phase. A good starting point is the linear and lateral hop and stick (Figures 7 & 8). These exercises allow both a linear and lateral component to the initial program by adding an explosive component, whilst not overloading the tendon with an aggressive SSC. These reactive stiffness exercises are essential prior to progressing in to ballistic stiffness exercises.

Ballistic stiffness exercises begin to add more of a SSC component, along with higher landing forces, which are usually continuous in nature. These higher landing forces build stiffness in the tendon and therefore contribute to more efficient and effective tolerance to explosive movements. Linear and lateral hurdle hops (Figures 9 & 10) are perfect to start this progression, and to retrain the Achilles tendon to utilise elastic energy.

ConclusionEnd stage tendinopathy rehabilitation is commonly overlooked or neglected. This article attempts to layout some of the end-stage options available to help safeguard the Achilles tendon against higher-end load exposure. There are numerous exercise options and variations for each category; the exercises listed here are just the tip of the ice berg, but act as a

Figure 5: Mini-tramp jog

Figure 6: Knee drive hold on BOSU

Figure 7: Linear hop and stick

Figure 8: Lateral hop and stick


good starting point. When it comes to rehabilitation, Achilles tendinopathy is never a linear progression. It will flare up some days and feel great other days. The most important thing is to manage and periodise the tendon’s exposure to loads.

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Figure 9: Linear hurdle hop

Figure 10: Lateral hurdle hop

Key points Isometric exercises act as pain relief across all stages of rehabilitation

3 out of 10 pain on the tendon site is acceptable during training

Isometrics and isolated resilience exercises must be maintained during a weekly training program on an ongoing basis. Once in Phase 3 they can be completed 3 times per week

Never remove all load from tendon, simply regress if needed

Periodising loading is key – avoid sudden spikes in load

Neck injury

Neck assessment and screening

Kay Robinson looks at the mechanics of neck injury and assessment techniques for the clinician

Nearly half the population will experience neck pain at some point during their lives, and with sport accounting for around 10% of all neck injuries(1), the cervical spine is an area that warrants more focused attention than it currently gets. The prevalence of neck injuries in sport is thought to be r is ing , and this i s u n q u e s t i o n a b l y p a r t l y d u e t o improvements in injury reporting and monitoring. However the increase in the physicality of sport and the growth of ‘extreme sports’ are leaving untrained necks at greater risk of injury.

Working in the sport of skeleton (where athletes sprint on ice and then hurtle head first down the icy, often bumpy track at speeds in excess of 130kph) opened my eyes into the importance of neck training. Neck injuries are common in skeleton, and so an obvious motivation is to prevent this. However, neck training isn’t just about injury-risk mitigation; in a sport where the gold medal can be decided by a single hundredth of a second, training aimed at strengthening the neck so that it can keep the athlete’s chin off the ice, can be the difference between the standing on

the podium or applauding from the stands.

In order to reduce the risk of injury, the neck needs to be specif ical ly and strategically trained to ensure its tolerance is greater than the loads that it is exposed to. However, prior to this training program being implemented, it is necessary to accurately evaluate the cervical spine in a comprehensive assessment and screening process. It is this that will be the focus of the first article of this two-part series on neck injury and the cervical spine.


Much of the research in this area has been carried out by military air forces, monitoring the effect of G-force on fighter pilots. The symptoms are thought to arise due to a combination of reduced blood flow to the head, visual disturbances and high loads placed on the musculature of the neck(5).

G force should also be considered in contact sports, where collisions between players may expose athletes to forces equivalent of those experienced in a car collision(6). Long term exposure to G-force is suggested to leave athletes at increased risk of vertebral disc degeneration, therefore exposure should be monitored closely(7). This is already commonplace in the world of cccupational health and safety, where machinery operators have limitations on time exposed to vibrational forces to minimise long-term damage.

Assessing the neckIn all sporting environments, basic neck range and strength should be assessed to provide baselines, and to aid return to sport planning – exactly as we would use following any other peripheral joint injury.

Cervical movement and musculature is complex (see Figure 1), with vertebral levels contributing to varying degrees of overall neck motion. The change of orientation of the cervical vertebral bodies of the mid to lower cervical spine allow for rotation, flexion and extension. However, this also isolates lateral flexion to the upper portion of the cervical spine. When determining baseline range of movement it is important to recognise that this commonly decreases with age therefore ‘normal’ range will vary between athletes and is likely to change over an athlete’s career.

irritation of the nerve roots – most commonly of the 7th cervical level(3). Clinicians need to have a high index of suspicion of spinal cord injury following any compression or distraction injury, and this serious consequence and needs to be cleared by a thorough on-field assessment prior to the athlete being moved.

‘Whiplash Associated Disorders’ (WAD) are commonly seen in the general population. However, they can frequently occur in sports involving sudden acceleration and deceleration, and can also occur following a blow to the trunk or head(4). A combination of neck pain, headaches, temporal mandibular d y s f u n c t i o n a n d r e f e r r e d p a i n /neurological symptoms are the result of the forces transferred to the neck causing sudden, uncontrolled movement, which results in damage to the anterior and posterior structure of the cervical spine.

The cervical spine is not just prone to acute injuries however. Chronic force exposure from maintained static positions (such as in sports like archery) or repetitive exposure to gravitational (G) or vibration forces are often implicated in the development of overuse symptoms. As with any area of the body, athletes that are unable to attenuate the forces they are exposed to through their neck will be at a greater risk of injury or dysfunction.

The side effects of chronic G-force exposure include dizziness, disorientation, altered vision, reduced co-ordination, as well as neck pain(5). Any of these side effects can not only reduce performance, but also put athletes and opponents at risk, particularly when travelling at high speeds!

How do necks get injured?Neck injuries are unsurprisingly most common in motorsports, as well as high impact, collision sports such as rugby. The reasons for this injury profile include:

Acute force exposure through axial loading (compression and distraction) Direct blows Sudden acceleration/deceleration

Let’s look at the first mechanism. Compression, or axial loading, is the primary mechanism of neck injuries in sport, and most commonly occurs when load is applied, and the neck’s natural lordosis is lost – usually due to excess flexion causing energy dispersal to be compromised(2). Acutely, the increased loading can cause severe cervical spine trauma, but chronic exposure can also have a cumulative effect. Situations where this can arise include collapsed scrums in rugby, falls from heights and mistimed manoeuvers in combat sports.

Another neck injury that can arise from axial forces are ‘stingers’ or ‘burners’, which are the frequent result of brachial plexopathy injury or irritation. These can be either compressive or distractive in nature and are most common in tackling sports, or as a result of a fall from a height where the neck is laterally flexed and the shoulder girdle depressed.

Stingers are a result of a downward traction force on the shoulder girdle while the neck is contra-laterally flexed, or the result of compressive forces that close down the ipsilateral posterior elements of the vertebra. Symptoms are often consistent with a ‘dead arm’ and include temporary altered sensation and weakness due to the

Figure 1: Cervical musculature


to minimise assessor bias. Decisions on which ranges should be tested should remain consistent and accommodate for sport specific positions if required.

To ensure data is normalised the following considerations should be made:

Torso stabilised Minimised lower limb involvement (eg

feet on wobble cushion) Set appropriate ranges that strength will

be measured at/through Standardised warm up and testing

protocols

The neck does not function in isolation. Strong correlations have been found between neck pain and shoulder dysfuction and vice-versa; therefore the entire kinetic chain should also be considered in neck assessment. With swimmers in particular, shoulder dysfunctions commonly lead to hypertonicity of the cervical muscles, resu l t ing in musc le imbalances , dysfunction and pain, all of which predispose the athlete to further neck injury(13).

Neck injuries and concussionClinicians should have a high level of suspicion of concussion when treating acute neck injuries due to the high forces translated between the areas. It follows from this neck assessment should be carried out in all athletes following

neck rehabilitation to regain stability. Postural assessment is a lso a key component of neck assessment. The primary purpose of the neck is to optimise head position and equal displacement of the weight of the head (3-6kg) is important in minimising overload to the stabilising muscles. Segarra et al describe a battery of reliable tests to aid assessment of cervical movement control dysfunctions including neck function in four point kneeling and with upper limb movement(11).

Prime moversCervical prime mover strength can be assessed in a number of ways including the u s e o f i s o k i n e t i c a n d i s o m e t r i c dynamometers, and can be combined with measuring muscle activity using EMG studies to increase validity. Cervical extension is stronger than flexion in general population studies, while lateral side flexion is commonly coupled with extension with a bias towards the subject’s dominant side. In athletes who rely on a dominant side bias (eg racquet and throwing sports) for performance advantage, this asymmetry should be recognised but not necessarily be seen as detrimental.

In the athletic environment without access to isokinetic and EMG equipment, baseline strength can be determined using a handheld dynamometer, ideally mounted

The gold standard for measuring cervical range of movement is radiological examination; however due to expense, this is technique is unlikely to be feasible in the sporting environment. Many clinicians commonly ‘eyeball’ neck motion, but there are in fact a number of more reliable and inexpensive tools that can be used and increase intra-rater reliability. These include the full-circle goniometer, or simply a tape measure to record the distance between anchor points, which can be easily replicated (see Table 1).

The primary stabilisers of the neck are collectively known as the deep neck flexors (DNFs – longus capitus, longus colli, rectus capitis anterior and rectus capitis lateralis(8). These are difficult to isolate without using EMG resources, but are most active through the commonly prescribed ‘chin tuck’ (craniocervical flexion). The most common assessment used to measure the activation and endurance of the DNFs is the craniocervical f lex ion test and assessed using a biofeedback device (see Figure 2). This assessment is a useful baseline test, and can recognise weakness and movement control dysfuntions. One drawack however is that it lacks normalised data(9).

Research tells us that the activity of the stabilisers is significantly decreased and delayed in anyone with neck pain(10), and therefore this is a great starting point in all

Table 1 – Anchor points used to assess Cx range of movement using tape measure

Flexion Extension Lateral Flexion Rotation

Anchor point 1 Tip of chin Tip of chin Tragus of ear Tip of chin

Anchor point 2 Manubrium Manubrium Acromion process Acromion process

Cranio-Cervical Flexion Test (Jull et al. 2008) Patient supine, crook lying with neck in neutral position. Uninflated pressure sensor placed behind neck so that it borders the occiput.

Cuff is inflated to 20mmHg Movement is described as ‘a slow head nodding action’ Patient attempts to sequentially target five 2mmHg progressive pressure increases, with 10sec holds.

Compensation strategies to observe

Pressure loss of > 2 mmHg Began using superficial neck flexors (palpation) Jerked chin down Loss of cervical lordosis through retraction.

Figure 2: Cranio-cervical flexion test(12)


2008. 1(3-4) 175 – 179

2. Clinical Sports Medicine 2003. 22 (427-443)

3. Clinical Sports Medicine 2003. 21:493–500

4. British Journal of Sports Medicine 2012

46(9):662-663

5. Aviat Space Environ Med 2005. 76:496–500

6. Int J Sports Physiol Perform. 2015.

Sep;10(6):681-6

7. Aviat Space Environ Med 2013. 84:734–8

8. Physical Therapy 2005. 85:1349-1355

9. Physiotherapy Research Int 2010. 15; 144-149

10. Spine 2004. 29(19):2108-14

11. Manual Therapy 2015. 20: 570-579

12. J Manip Physiol Ther 2008. 31:525-533

13. Journal of Orthopaedic & Sports Physical

Therapy 2012. 42(6):552-558

14. Journal of Primary Prevention 2014. 35:

309-319

out severe spinal injury and concussion, and also include range of movement measurement and deep neck flexor and prime mover strength assessment. Consideration should also be made for the rest of the kinetic chain – in particular the shoulder girdle – due the high correlation between dysfunctions of the two areas.

In the next article, we’ll discuss management ideas for neck injuries and the phases of rehabilitation, whether it’s to return players to the field post injury or address any dysfunctions found in assessment and screenings.

References1. Current Review Musculoskeletal Medicine

concussion or head trauma. As research into concussion grows there is more focus on the association with neck strength. Collins et al concluded that neck strength was a significant predictor of concussion amongst a large sample of high school athletes and although further research is needed, showed positive outcomes in reducing concussion risk from adopting neck strengthening programs(14).

SummaryCervical injuries can occur in a range of sporting environments from the result of acute trauma through axial loading, prolonged position exposure, whiplash and external forces such as vibrations and G forces. All cervical assessments should rule

Tendon rupture and antibiotic use

Fluoroquinolones and injury

Previous research reported by SIB suggested that fluoroquinolone antibiotics could pose a potential threat to tendon health in sportsmen and women. Andrew Hamilton looks at more recent research on fluoroquinolones and explore the implications for clinicians...

The development of antibiotics is without doubt one of mankind’s greatest scientific achievements, saving countless millions of lives since their introduction. However, notwithstanding the current concerns about ‘superbug’ resistance, not everything is rosy in the antibiotic garden. A few years ago, we reported on growing evidence that one particular group of antibiotics – fluoroquinolones – might be implicated in rapid-onset tendon degeneration, exposing sportsmen and women to an increased risk of tendonitis or even tendon rupture. In the intervening years, more research into this topic has been carried out, providing a useful insight for clinicians dealing with athletes who may have athletes in their care who are either taking or have taken fluoroquinolone antibiotics.

Fluoroquinolone anatomyFluoroquinolones are effective, broad-spectrum antibiotics first developed in the 1970s, which play an important role in the treatment of serious bacterial infections such as pneumonia, typhoid, diarrhoea, kidney/urinary tract infections and many other stubborn and virulent infections. Indeed, some of the more recent iterations of fluoroquinolones are particularly effective against bacteria such as S t a p h y l o c o c c u s A u r e u s a n d

Staphylococcus Pneumoniae, which have become res i s tant to many o ther antibiotics.

The fluoroquinolones (see Figure 1) are a subgroup of the larger quinolone family of antibiotics. All quinolones work by preventing bacterial DNA from unwinding and duplicating. Examples of commonly used fluoroquinolone antibiotics include ciprofloxacin, levofloxacin, norfloxacin and gemifloxacin. All the fluoroquinolones

share the same essential chemical structure (shown in Figure 1 below). The ‘F’ denotes the fluorine atom (giving rise to the ‘fluoro’ in fluoroquinolones), while the ‘R’ denotes the chemical side group – it’s the different R groups that produce the different types of fluoroquinolone antibiotics.

Fluoroquinolone concernsHailed by some as ‘wonder antibiotics’,

Figure 1: Fluoroquinolone structure

R R

ROO

HO

R

F

N

NB: ‘F’ represents the fluorine atom common to all fluoroquinolones while the blue ‘R’ group is the side chain of atoms determining the exact type of antibiotic that results


tendon may require surgical repair. Tendinitis and tendon rupture in the rotator cuff, the hand, the biceps, and the thumb have also been reported. Tendon rupture can occur during or after completion of fluoroquinolone use; cases occurring up to several months after completion of therapy have been reported. Fluoroquinolones should be discontinued if the patient experiences pain or inflammation in a tendon (symptoms that may precede rupture of the tendon), or tendon rupture. Patients are advised, at the first sign of tendon pain, swelling, or inflammation, to stop taking the fluoroquinolone, to avoid exercise and use of the affected area, and to promptly contact their healthcare provider about changing to a non-fluoroquinolone antimicrobial drug.”

Recent evidenceWhat does the recent science say about fluoroquinolone use and tendinopathy/rupture? In terms of aetiology, compelling evidence suggests that fluoroquinolones can rapidly affect the chemical composition of tendon structure by depleting levels of glycosaminoglycans (GAGs – compounds vital to the elasticity and integrity of structural tissue) in the tendon.

In a study published earlier this year, researchers used a technique known as sodium magnetic resonance imaging (sodium MR) to study pathological changes and changes in GAG levels in the Achilles tendons in the 14 ankles of 7 men who took 500ms of Ciprofloxacin twice a day for 10 days(11). As figure 2 shows, after 10 days, there was a marked reduction in the GAG content of the Achilles tendon, which though reversible, still hadn’t fully recovered 5 months after ending the Ciprofloxacin course.

The prolonged period of disrupted t e n d o n p a t h o l o g y f o l l o w i n g fluoroquinolone administration may be aggravated by impaired tendon healing

Canadian study of 98 case studies from the scientific literature found that pefloxacin and ciprofloxacin were most frequently implicated, but tendon injury had been reported with most fluoroquinolones(8). The median duration of fluoroquinolone treatment before the onset of tendon injury was eight days, although symptoms occurred as early as two hours after the first dose and as late as six months after treatment was stopped. Up to one-half of patients experienced tendon rupture, and of these, almost one third had also received long-term corticosteroid therapy before or during fluoroquinolone use.

As concern over the association between fluoroquinolone use and tendonitis/tendon rupture grew, the US FDA issued a ‘prescribing warning’ followed in 2008 by a more general alert on the risks of fluoroquinolone use stating(9): “Tendinitis and tendon rupture most frequently involves the Achilles tendon, and rupture of the Achilles

fluoroquinolone use by physicians increased dramatically towards the turn of the century. In the late 90s however, evidence began to emerge l inking fluoroquinolone antibiotic use with structural changes at the cellular level to connective tissue in the body – particularly to collagen, a major and vital component of tendon tissue.

Many of the initial findings came about as a result of studies on rats (see Table 1)(1-6). However, studies on human cell samples seemed to indicate that by causing a decrease in essential components of tendon tissue such as collagen type I, elastin, fibronectin and proteoglycan, fluoroquinolone-induced degenerative structural changes to tendon tissue were also possible in human tendon tissue(7).

Around about the same time, a growing number of tendonitis and tendon rupture cases were being observed among patients taking fluoroquinolone antibiotics. A 2003

Table 1: Structural and biochemical changes in tendon cells induced by fluoroquinolones(1-6)

Fluoroquinolones Structural changes

Ciprofloxacin, Enrofloxacin Fleroxacin, Garenoxacin Gemifloxacin, Ofloxacin Pefloxacin

Swelling and dilatation of cell mitochondria and endoplasmic reticulum Multiple vacuoles and large vesicles Densified nuclei and clumped chromatin Decrease of fibril diameter Increase of distance between collagenous fibrils Cell detachment from extracellular matrix Hyalinization of collagen bundles

Ciprofloxacin & Levofloxacin Reduction of cytoskeletal and signaling proteins

Ciprofloxacin & Pefloxacin Inhibition of collagen synthesis Decrease of elastin and fibronectin Inhibition of proteoglycan synthesis

Fluoroquinolone-induced tendinopathy/rupture tends to manifest itself somewhat differently from ordinary tendon pathology. Signs that clinicians should be aware of include:

An abrupt onset and sharp pain that occur spontaneously upon walking or palpation;

Tendon rupture is almost always preceded by spontaneous pain at the bony insertion 2 to 3 centimetres above the insertion point, believed to be correlated with diminished vascularisation at this anatomic site;

Pain, swelling, or inflammation is commonly observed in the tendon area for up to two weeks before rupture occurs;

With Achilles involvement, patients can experience difficulty to perform plantar flexion of the foot (Thompson’s sign).

Bilateral pathology is extremely common – in up to 50 percent of cases;

The weight-bearing Achilles tendon is most commonly affected, occurring in over 90% percent of cases (although other tendons such as biceps brachii, supraspinatus, and extensor pollicis longus, can also be affected).

Box 1: Clinical manifestations of fluoroquinolone-induced tendinopathy/tendon rupture(10)


However, whether this protective effect is significant in humans undergoing fluoroquinolone treatment is unknown and the best option by far is for athletes to avoid fluoroquinolones altogether if possible.

Rehab and fluoroquinolone-induced tendinopathyGraduated eccentric training regimes, in which muscle tendons are subjected to increasing loads during muscle elongation, have proved both popular and effective for treatment and rehab of tendinopathy – and this approach is supported by the literature(24). For sportsmen and women, eccentric training programmes have been shown to be particularly effective, resulting in a success rate of around 90% in those with tendinopathy(25) – a significantly better outcome than for the (more sedentary) population as a whole(26).

However, while loading tendon with eccentric exercise may be appropriate for treating tendinopathy most athletes, this approach should not be used for treating f luoroquinolone- induced tendon conditions, at least in the early stages of symptoms. In study on this topic, Greene i l l u s t r a t e d t h a t p a t i e n t s w i t h fluoroquinolone-related tendinopathy should be rehabilitated using a 2-phase approach (see Box 2)(27):

An initial phase of bracing and support to allow the tendon to recover from the chemical injury caused by the fluoroquinolone

A second phase, consisting of progressive loading

increases the production of enzymes known as’matrix metalloproteinases’, some of which can adversely alter the structure of the extracellular matrix of tendons(15).

W e a l s o k n o w t h a t l o w - d o s e corticosteroids in isolation can increase the risk of Achilles tendon rupture, and evidence suggests that combined use of corticosteroids with fluoroquinolones potentiates this adverse effect(16,17). Indeed, studies suggest that over 50% of patients with fluoroquinolone-related tendon rupture had received systemic or inhaled corticosteroids(18), and that patients prescribed both fluoroquinolones and corticosteroids have a 46-fold greater risk of Achilles tendon rupture than those taking neither medication(19)!

Given these facts, a recent review of fluoroquinolone use among athletes has recommended that athletes should not be prescribed fluoroquinolones and should be given alternative antibiotics whenever possible(20). This is particularly true in the light of the added risk of corticosteroid treatment; asthma is common among sportsmen and women(21), many of whom may be using corticosteroid medication. Fluoroquinolone use in such athletes could therefore be very hazardous.

When fluoroquinolone antibiotics are the only option for an athlete, there’s some evidence from cell culture studies that the co-ingestion of vitamin E could help to alleviate some of the harmful effects(22,23). This might occur due to the ability of vitamin E to help prevent of free-radical damage in biological membranes.

capacity. A recent study on mice looked at tendon healing capacity in those treated with Fleroxacin before rotator cuff surgery(12). Compared to control mice who received no Fleroxacin, the treated mice showed significantly less fibrocartilage and poorly organized collagen at the healing enthesis. Moreover, the treated mice had a significantly reduced tendon cross-sectional area and the researchers concluded that the fluoroquinolone treatment had negatively influenced tendon healing, which could have implications for patients undergoing tendon surgery/repair in the months following a course of fluoroquinolones.

Recent risk dataIn terms of the r isk of part icular fluoroquinolone drugs, recent research has suggested that Ciprofloxacin, Fleroxacin, Pefloxacin and Ofloxacin present the greatest threat to tendon health(13). While o t h e r f l u o r o q u i n o l o n e s s u c h a s Trovafloxacin and Levofloxacin may present less of a risk, they are not risk free. For example, Levofloxacin has been implicated in Achilles tendon rupture in some case studies(14), while for other fluoroquinolones, there may simply not be enough data to determine safety one way or the other.

More worryingly is that the recent evidence suggests that when it comes to tendonitis or tendon rupture, athletes and fitness enthusiasts may be especially v u l n e r a b l e t o t h e e f f e c t s o f fluoroquinolones. There are a number of reasons why this is the case. Firstly, excessive loading of tendons during physical training is regarded as a major p a t h o l o g i c s t i m u l u s f o r t e n d o n degeneration. This is because exercise

The approach advocated by Green consists of an overlapping 2-phased intervention. The first phase consisted of techniques to protect the tendon from overload stresses, and the second phase consisted of graduated loading of the tendon and muscle.

In the early stages of treatment, the tendon is likely to overload easily, causing inflammation. To protect the tendon from overloading forces, techniques should used initially to unload the tendon during weight-bearing activities – eg use of crutches and heel lifts for the purpose of decreasing tendon loading. During the third week of therapy, a counterforce Achilles tendon brace (a non-elastic constraint with a tension strap that crosses the Achilles tendon) can be used during functional weight-bearing activities, excluding specific exercises. The theory behind the tendon brace is pressure from the tension strap either broadens the musculotendinous attachment or limits muscle expansion at the time of contraction resulting in decreased stress within the tendon.

After three weeks, a progressive exercise program consisting of graduated loading of the tendon begins. The patient’s feedback in these early stages is important and the progression in loading needs to be very gradual and patients should be encouraged to keep a daily log of exercise performed and their responses to it. Ancillary exercise such as deep water walking, gentle stretching and stationary cycling (with the arch of his foot contacting the pedal to decrease the force on the Achilles tendon) can also be useful. This phase may take 3 months or more before full functionality is restored.

Box 2: A two-phase approach for rehab of fluoroquinolone-induced tendinopathy(27)

Figure 2: GAG levels in the Achilles tendon after 10 days of Ciprofloxacin

Left = pre-Ciprofloxacin, middle = after 10 days of Ciprofloxacin, right = 5 months later.Red/orange areas indicate high GAG levels in the tendon; green = lower levels


Summary and recommendationsEvidence continues to mount suggesting that fluoroquinolone antibiotics are harmful for sportsmen and women, who seem particularly vulnerable to their effects. Not only do they adversely affect the chemical composition and structural integrity of tendons, their use seems to inhibit the normal repair mechanisms that bring about recovery from tendon injury. Worse, the risk of fluoroquinolone-induced tendinopathy is further increased when corticosteroid medication is being used, which is the case in many athletes with asthmatic conditions. In the light of the above, clinicians should follow the recommendations below when dealing with athletes who are or who have in the past 6 months been on fluoroquinolone antibiotics.

Practical recommendations

Athletes should avoid all use of fluoroquinolone antibiotics unless no alternative is available. This is especially true if corticosteroid medication is also used.

If a fluoroquinolone antibiotic has been prescribed and no alternative is available, athletes should immediately reduce high-intensity and ballistic activities and total training volume. These reductions should remain throughout the duration of the antibiotic course and athletes made aware of the increased risk for the development of musculoskeletal complications for up to 6 months following antibiotic treatment. Co-administration of vitamin E supplements might provide some protective effect.

Oral or injectable corticosteroids should never be administered while an

athlete is taking fluoroquinolones. If the athlete has no symptoms after

completing the full course of the antibiotic, then a graduated return to full activity under direct medical supervision should be initiated, with close monitoring for the development of musculoskeletal symptoms.

If any pre-rupture symptoms (see Box 1) are noted, all athletic activity should cease immediately and fluoroquinolone should be discontinued if possible.

Clinicians treating fluoroquinolone-induced tendinopathy should be aware that tendons may not respond well to the usual rehab protocols (eg eccentric training), and that an extended period of force unloading may be required before a very gradual programme if eccentric training begins.

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Vastus Medialis Obliquus: Part 2In part one of this series, Chris Mallac explained the anatomy and complex biomechanics of the VMO and its role in relation to the patellofemoral joint. In part 2, he argues that regardless of cause and effect of the VMO on patellofemoral pain, VMO dysfunction in the presence of pain is very real, and thus exercises to rehabilitate the function of this muscle are necessary...

patella stability

By and large, the majority of the research suggests that VMO is an important patella stabiliser for the knee, as it moves during flexion and extension movements. However, many of these findings relate the role that VMO plays on the patella in a non weight-bearing situation, and the function of not only the patellofemoral joint, but also the VMO, may change as we assume a weight bearing position.

In weight bearing the limb is subject to so many more kinetic variables such as pelvic position, hip joint f lexion/adduction, hip rotation postures, valgus

knee collapse, foot pronation postures as well as inherent tibial torsions, femoral anterversions and genu valgus postures. These all impact on the patellofemoral alignment and thus may possibly play a bigger role in patella dysfunction rather than VMO dysfunction.

VMO dysfunction in the presence of knee painAtrophy of the quadriceps is a common observable clinical feature following injury to the knee(1) (PFPS included), particularly atrophy of the VMO(2). Atrophy of the

VMO, imbalance of the VMO/vastus lateralis (VL) strength, and altered neuromuscular timing of the different parts of the quadriceps muscle have all been described in patellofemoral pain (PFP) syndrome(3). The exact mechanisms that cause a morphological change in the muscle during atrophy is still a subject of debate. It may be either a decrease in muscle fibre diameter/area (atrophy) and/or a decrease in the numbers of muscle f ibres (hypoplasia)(4,5). Furthermore, it is unclear whether atrophy of the VMO precedes a


5. Biofeedback awareness6. Stable vs. unstable surfaces7. Concurrent adductor contraction with quadriceps activation

However, in a systematic review of the literature on exercise therapy in the conservative management of PFPS, Bolga and Boling (2011) found no difference in pain response and exercise therapy if it incorporated quadriceps electrical stimulation, biofeedback, or simultaneous hip adductor activation with exercise(21). Indeed, all these approaches provided no additional benefit over quadriceps exercise alone. However, they did not elaborate whether or not the interventions shown in these studies demonstrated greater VMO activation compared with a control exercise. Although the interventions may n o t c h a n g e t h e r e s p o n s e a n d improvements in pain, they may in fact be more selective in activation of the VMO.

What needs to be considered in the selection of exercises are the following points;1. Patellofemoral joint stress is minimised from 90 to 45 degrees of knee flexion during non-weight bearing exercises(22). 2. PF stress is minimised from 45 degrees to 0 degrees of knee flexion when the limb is weight-bearing(22).3. EMG feedback can increase a client’s

on the affected side that was not correlated to CSA loss. It may be that PFPS leads to greater loss of strength in the quadriceps compared with loss of CSA.

Finally, some researchers believe that delayed activation of the VMO is possibly the more significant variable rather than gross muscle strength loss of the VMO(10-12). Therefore, the muscle may look the same as the unaffected side (CSA), it may be as strong or close to the same strength, but it may activate in a different manner, or have delays in activation, in a similar way that transversus abdominus has been found to have a delayed activation in patients with low back pain (13,14) (see activation ratios above).

Retraining VMO functionThe selection of effective exercises to strengthen and activate the VMO has also received widespread attention in the form of research into the ‘best’ exercises and positions to produce ‘VMO firing’. The variables that can be considered and manipulated, and which have been the subject of greatest research are:1. Weight bearing vs. non weight bearing exercises.2. Hip rotation position – external vs. internal vs. neutral3. Knee joint angles of flexion4.Facilitation with electrical stimulation

patella injury or develops secondarily as a consequence of pain inhibition and physical inactivity following recurrent injuries(6).

Clinically, what is observed is that the PFPS patient presents with a painful knee, usually some swelling and observable atrophy of the VMO or inability to activate the VMO. However, this is not to suggest conclusively that the lack of VMO has caused the PFPS. All that can be said for certain is that in the presence of PFPS some manner of morphological change and alteration in activation in the VMO co-exists.

Final ly , the exact cause of this morphological change is also debatable. The most common explanation is that the quadriceps atrophy is caused by reflex inhibition leading to loss of muscle contractility and thus muscle size over time(1). This phenomenon is commonly referred to as ‘autogenic muscle inhibition’ or AMI(7).

AMIAMI is described as a reflexive ‘shut down’ of the musculature surrounding a joint. It is initially designed to protect an injured joint; however the inability to fully activate the muscles may still persist after the acute stage of the injury, leading to barriers in the rehabilitation process. It has been suggested that the cause of the AMI is altered afferent input from the joint mechanoreceptors that then modulates the outgoing efferent output from the spinal motor neurones to the muscle. This alpha motorneurone modulation (inhibition) results in an inability to fully activate the muscle(8).

Cross sectional area (CSA)Very few studies have measured the actual CSA of the quadriceps under imaging. However it has been found that after traumatic injury resulting in an inability to weight bear, quadriceps atrophy is more pronounced than in sufferers of more chronic knee pain who have been full weight bearing(1,9). This suggests that even modified weight bearing has some benefits in maintaining muscle mass.

However, the actual effect of knee pain on quadriceps atrophy and CSA may not be as significant as once thought. Callaghan and Oldham (2004) found only a small 3.38% difference in CSA of the quadriceps between affected and non-affected limbs in patients with chronic PFPS. Interestingly, the same researchers did find a more pronounced loss of peak extension torque

Many studies have shown the inhibiting effects of a knee injury on muscle activation. Muscle activation patterns can be measured using muscle stimulation and evaluating central activation ratio of the muscle being tested. In a thorough systematic review, Hart et al (2010) have collated the data from many studies on the central activation ratios and have concluded that activation deficits in the VMO existed in knees having suffered ACL injury, in ACL reconstructed knees and also in knees with anterior knee pain(15). These deficits are commonly observed on both the injured and uninjured sides, highlighting the importance of central activation of the motor neurone pools bilaterally following knee injury.

It has been shown that individuals symptomatic for PFPS have lower VMO to Vastus Lateralis (VL) EMG activity ratios when compared with asymptomatic individuals. This has been found during isometric terminal knee extension(16), during stair-climbing movements(17), closed kinetic chain exercises(18,19) and in a variety of weight bearing functional movements as well as non weight bearing exercises(20).

In summary, those who suffer PFPS and other forms of knee pain do conclusively show delays in muscle activation of the VMO compared with the other quadriceps. This again does not imply causation — simply an association between knee pain and VMO dysfunction. Therefore, exercises designed to recruit the VMO will be necessary to correct not only the activation delays, but any atrophy and loss of peak strength that may persist in the VMO.

Activation ratios


awareness of VMO to VL activation within 5 days of biofeedback facilitated training(23).4. Resistance used in rehabilitation is also important. Leroux et al (1999) found when using electrical stimulation, the VMO contributed only 6.31% of the total torque produced during a maximum voluntary isometric knee extensor contraction(24). It is therefore likely that VMO will not respond to high load resistive exercises.5. Hip rotation positions seems to have no beneficial effect on VMO:VL activation(19,23).6. Strengthening work on the hip

abductors and external rotators has a positive effect on patients with PFPS, without any specific exercises for VMO(25).7. Squat exercises performed on unstable surfaces with high levels of instability can enhance the activity of the VMO, and that squatting exercises performed on foam surfaces with low levels of instability or hard surfaces are not as effective for the selective activation of the VMO(26). 8. Despite some landmark research many years ago demonstrating the interconnections between the VMO and adductor mass and the idea that hip adduction may preferentially activate the

VMO(27), the idea that hip adduction can preferentially activate the VMO has been refuted by many other studies(28,29).

VMO exercisesWith these above points in mind, below are some examples of exerc ises that incorporate the following parameters to preferentially activate the VMO and/or assist in the relief of PFPS. The key features of these exercises are: small ranges of movement in safe positions for the PF joint, unstable surfaces, high repetition and low load, external force to incorporate the hip external rotators and hip abductors, and EMG feedback used if available.

a. Stand on an unstable surface such as a BOSU ball or two foam pads. The lead foot on the unstable surface belongs to the VMO you wish to retrain.b. Place the other foot on a bench behind you. The focus is to hold as much of the weight as possible on the front foot. c. The distance between the front foot and hip joint needs to be reasonably small as to closely approximate the running posture. For sports that need greater lunge type positions such as hockey, the front foot can be placed further out in front.d. Place a theraband or powerband around the knee so that the direction of pull is from the front. This induces a

flexion moment on the knee that then requires the quadriceps to work harder to counteract. The band can be under slight tension when the knee is flexed and it will then stretch and create tension as the knee extends.e. Place another band around the upper shin (below the patella) so that the direction of pull attempts to pull the knee inwards, thus creating hip adduction/internal rotation. This will then activate the hip abductors and external rotators to counteract this force.f. Bend/flex the knee so that the knee follows the third toe and minimise the knee flexion to a maximum of 45 degrees. g. The direction of knee flexion should

be so that the patella is pushed forward towards the toes and the tibia creates a positive angle. If the tibia is kept upright, then this directs force away from the quadriceps and towards the hip extensors. The purpose of the exercise is to stimulate the quadriceps so the knee needs to be allowed to come forward. h. Perform three sets of 15 repetitions and light weight can be added as strength and control improves. This can be a barbell on the shoulders or holding two dumbbells in the hands. i. To further increase the stability challenge, the arms can be held above the head to increase the height of the centre of mass of the body (with or without dumbbells overhead).

An inside band provides a medially directed force

Front band provides an additional knee flexion force

Additional balance challenge with arms above head

1. Split Squat


a. Place a slant board on a foam mat. Stand on this slant board with the foot that belongs to the VMO you wish to retrain.b. The purpose of the slant board is that it encourages the knees to come forward during knee flexion, thus working the quadriceps over the hip extensors, and the slight plantarflexed position takes away passive tension of the soleus during dorsiflexion that can

‘steal’ force away from the quadriceps.c. The other foot is placed on a bench so that the hip is in flexion, abduction and external rotation.d. Place a band around the working knee and then stand on the band with the foot on the bench. Wrap the band over the thigh and hold onto it. This band creates an adduction and internal rotation force on the hip, requiring the hip abductors and external rotators to

work harder.e. Keeping the spine vertical, slowly bend the knee to no more than 45 degrees. If the trunk is allowed to come forward and create too much hip flexion, force will shunt away from the quadriceps and onto the hip extensors. f. Keep the kneecap tracking in line with the third toe.g. Perform three sets of 15 repetitions slowly.

a. Using the same slant board and foam block as in the ‘baby squat’, stand on this, with the foot belonging to knee with the affected VMO. b. The other leg is held up in hip flexion.c. Place the opposite shoulder in contact with the wall. d. Hold a light weight overhead on the stance leg side. The arm will be in vertical flexion. e. Slowly bend the knee and allow the opposite shoulder to slide down the wall. f. The bending knee again should follow the third toe. g. The opposite hip can now start drop out of full flexion. h. As the knee now extends straight during ascent of the body, the opposite shoulder will slide up the wall. Drive the opposite hip back into full flexion. This

will mimic the running action of the opposite leg during swing phase of running. i. The friction of the shoulder against the wall acts as a resistance. j. Perform three sets of 15 repetitions slowly.

Start position: Notice the band attempts to pull the knee in a medial direction

Finish position: Notice small range of knee flexion to minimise the patellofemoral joint compression

Finish position: Notice vertical trunk posture to ensure the movement becomes ‘quad loading’

2. Baby Squat

3. Wall slider squat

Start position

Finish position


SummaryInjuries to the knee are a common occurrence in sports. Ligament injuries, patellofemoral pain syndromes and meniscal tears can all create autogenic muscle inhibition, and this can shut down the excitability of the quadriceps muscles – particularly the VMO. The VMO has for a long time been thought to be the main controller of the patellar alignment in the trochlear groove and thus weakness in this muscle has been thought to be the causative factor in PFPS.

However, the majority of scientific opinion is still divided as to the exact role that the VMO plays in creating PFPS. It may be that VMO dysfunction is the consequence of PFPS, and other biomechanical and load variables can be implicated in the creation of PFPS.

Irrespective of the cause and effect of VMO dysfunction and PFPS, it is clinically observed (and the literature supports the notion) that VMO dysfunction and PFPS are related; therefore strength and control

exercises for the VMO will be needed to fully rehabilitate the PFPS affected athlete.

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Contributors to this issue

Chris Mallac has worked as Head of Performance at London Irish Rugby, Head of Sports Med at Bath Rugby and Head Physio at Queensland Reds Super 14. He is currently teaching globally on Rehab Trainer Courses.

Lachlan Wilmot is the Senior Athletic Performance Coach at the Greater Western Sydney Giants Australian Football League Team, specialising in strength and power development.

Kay Robinson is a physiotherapist specialising in young athlete development, the sporting neck and return to performance. She is also physiotherapist to the gold medal winning GB Skeleton team at Sochi2014.

Andrew Hamilton BSc Hons, MRSC, ACSM is a member of the Royal Society of Chemistry, the American College of Sports Medicine and a consultant to the fitness industry, specialising in sport and performance nutrition.

Sports Injury Bulletin is published by Green Star Media Ltd, Meadow View, Tannery Lane, Bramley, Guildford GU5 0AB, UK. Telephone +44 (0)1483 892894

Commissioning Editor Andrew Hamilton

Technical Editor Chris Mallac

Managing Director Andrew Griffiths

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To subscribe to Sports Injury Bulletin call Duncan Heard on +44 (0)1483 892894

Lumbar Herniation,Achilles Tendinopathy, Neck Injury, VMO dysfunction

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