Chapter | 26 |

Tendinopathies of the wrist and handC Joseph Yelvington, Ellen J Pong

CHAPTER CONTENTS

Introduction 335

Definition of tendinopathy 336

Aetiology 336

Anatomy of the tendon 336

Basic components 336

Blood and nerve supply 337

Patho-anatomy 337

Tendon injury 338

Tendon healing 338

Tendinopathy classification 338

Tendinosis 339

Tendinitis 339

Paratendinitis 339

Combined paratendinitis and tendinosis 339

Examination and diagnosis 340

Clinical tests 340

Diagnostic imaging and invasive testing 341

Tendinopathic entities of the hand and wrist 341

Flexor carpi ulnaris 341

Testing 341

Differential diagnosis 341

Extensor carpi ulnaris 341

Testing 342

Differential diagnosis 342

Extensor carpi radialis longus and brevis(distal tendons) 342

Testing 342

Differential diagnosis 342

Extensor indicis proprius 343

Testing 343

Differential diagnosis 343

Extensor digiti minimi 343

Testing 343

Differential diagnosis 343

Abductor pollicis longus and extensorpollicis brevis 343

Testing 343

Differential diagnosis 344

Extensor pollicis longus 344

Testing 344

Differential diagnosis 344

Flexor carpi radialis 344

Testing 344

Differential diagnosis 344

Treatment and prognosis 345

Conservative treatment 345

Non-conservative treatment 347

Prognosis 347

Conclusion 347

INTRODUCTION

A large proportion of hand and wrist tendinopathiesoccur in individuals who perform highly repetitive andforceful jobs (Elder & Harvey 2005). The Department ofLabor, Bureau of Labor Statistics (1999), reported inci-dence of hand and wrist tendinitis (tendinopathy not

335© 2011 Elsevier Ltd.

DOI: 10.1016/B978-0-7020-3528-9.00026-1

specified) as 3.66% of upper extremity workplace injuriesrecorded in 1999, resulting in a mean of 6 lost work daysfor all hand/wrist injuries.

Patients and practitioners had discovered that once ten-dinopathy is established resolving symptoms can be diffi-cult. Treatment typically consists of resting in a splint,modifying activities for ergonomic correction, takingnon-steroidal anti-inflammatory medications (NSAIDs),and receiving corticosteroid injections; often with positiveresults (Fredberg & Stengaard-Pedersen 2008). Deep tissuefriction massage (DTFM), effleurage, connective tissuerelease and Rolfing have been utilized on tendons withthe premise that it will release scar tissue restrictions andallow improved collagen alignment. However, studies donot reliably confirm the positive benefit of these conserva-tive treatments (Brousseau et al 2002). This demonstratesa typical problem: randomized clinical trials of manualtherapy to the tendons of the hand and wrist are scarcely,if at all, available.

Investigators have continued to look more closely attendons, discovering processes that may explain why out-comes are not more positive. Adequate animal models forin vivo studies have only recently been developed(Soslowsky et al 2000). Tendinopathy has been classifiedand redefined. Current studies attempt to explain whyrepetitive motion and strain cause tendon pathologies(Backman et al 2005). This developing knowledge of ten-don pathology has shed new light on treatment rationale(Khan et al 2000).

This chapter follows the trend of current studies andexpanding knowledge, including a review of the tendino-pathy process from a molecular level. This review providesa knowledge base for the ensuing discussion of exam-ination, diagnosis, categorization of tendinopathy, andtreatment.

DEFINITION OF TENDINOPATHY

The lack of more positive results with conservative treat-ment may be due to mislabeling tendinosis as tendinitis(Khan et al 2000). Tendinitis must be qualified. Studiesare now consistently showing what was normally diag-nosed as tendonitis may represent only one classificationof tendinopathy (Futami & Itoman 1995). Tendinopathyrepresents histological findings that differ significantlyfrom the generally accepted condition of tendonitis. Thisis due primarily to the lack of evidence of inflammatory pre-cursors and cells in the tendon itself (Gabel et al 1994, Yuanet al 2003, Curwin 2005, Fredberg & Stengaard-Pedersen2008). Khan et al (2006) supported Bonar’s classificationof tendinopathy, which defined four classifications,each with distinct histological findings. Clinicians haveyet to apply this knowledge to support specific conserva-tive treatment use (Cannon 2001). A fourth edition

manual of upper extremity rehabilitation printed in2001 did not use the words tendinosis or tendinopathy,but used the terms tendinitis and paratendinitis for allrelated conditions of upper extremity pain caused bytendon pathology (Cannon 2001).

One reason for the continued consideration of tendonpathologies as tendonitis may be the initially positive out-comes with corticosteroids in symptomatic tendons(Fredberg & Stengaard-Pedersen 2008). The presence of an-itis or inflammation in the form of neurogenic inflamma-tion may also support persistence of the old terminology.Fredberg & Stengaard-Pedersen (2008) concluded that somecombination of classic inflammation and neurogenicinflammation does mean that tendonitis is not a completemisnomer. It is the histological difference in tendinopathiesstemming from tendinitis, tendinosis, and paratendinitisthat may dictate different treatments; particularly in manualtherapy.

There continue to be areas of needed research into thissubject. Findings from animal studies and from tendonstudies performed on other areas of the body will be usedin this chapter to provide data which may be extrapolatedto apply to the hand and wrist, despite differencesbetween weight bearing versus positional tendons (Smithet al 1997).

AETIOLOGY

Researchers report that knowledge of the aetiology of ten-dinopathy is evolving (Sharma & Maffulli 2005, Fredberg& Stengaard-Pedersen 2008). Many factors contribute totendinopathy, both intrinsic and extrinsic (Riley 2004).Renstrom & Hach (2005) summarized extrinsic factorsas: malalignments, reduced flexibility, muscle weaknessor imbalance, overuse and excessive body weight. Hartet al (2005) added genetics, gender, and fitness level,while Hammer (2007a) reported biomechanical faults.Intrinsic factors that affect apoptosis can lead to tendondegeneration. This process of programmed cell death canbe exacerbated by intrinsic oxidative or mechanical stres-ses (Yuan et al 2003, Sharma & Maffulli 2005). Theorieson tendon rupture have been separated into two cate-gories: vascular and mechanical (Riley 2004). The readeris encouraged to read the work of Riley (2004) to explorethis topic further.

ANATOMY OF THE TENDON

Basic components

The tendon is the attachment site of a muscle to bone. It isdesigned to transfer tension from the muscle to the bone,thereby causing motion to take place (Kannus 2000).

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The basic building block of the tendon, tropocollagen, isformed by fibroblasts (O’Brien 2005). These are assem-bled into fibrils which are arranged into fibres, which areorganized into fascicles and bound together with a looseconnective tissue called endotendon (endotenon) (Kannus2000, Sharma & Maffulli 2005). The endotendon is thepathway for blood vessels, nerves, and lymphatics (Riley2004). Bundles of fascicles are bound together by anotherlayer of connective tissue called the epitendon (epitenon)which is continuous with the endotendon (Kannus2000) (Fig 26.1).

Synovial tendon sheaths, also called paratendon (parate-non), are found in areas subjected to increased mechani-cal stress, such as the tendons of the hands and feet,where efficient lubrication is required (Sharma & Maffulli2005). Fibre bundles are predominantly aligned withthe long axis of the tendon and these are responsible forthe tensile strength of the tendon (Riley 2004). A smallproportion of fibres run transversely, and there are evenspirals and plait-like formations (Kannus 2000). Thiscomplex ultrastructure provides resistance against trans-verse, shear, and rotational forces acting on the tendon(Riley 2004).

Blood and nerve supply

Tendon vascular support comes from three sources: at themyotendinous junction, the osteotendinous junction, andthe extrinsic system through the paratendon (Benjamin &Ralphs 1996, Sharma & Maffulli 2005, Scott et al 2007).Innervation accompanies vascular pathways through theparatenon (Hart et al 2005). The nerve receptors that sup-ply tendons can terminate in the vicinity of mast cells,where neuropeptides are involved in normal tendon regu-latory control (Hart et al 2005).

Patho-anatomy

Tenocytes and tenoblasts are the cells involved in tendonhealing (Sharma & Maffulli 2005, 2006). Tenocytes aresparse in tendon tissue but have extensions that createan extensive network inside the matrix (O’Brien 2005).They are responsible for maintenance of matrix and colla-gen (Harley & Bergman 2008). Tenocytes are cruciallyresponsive to environmental conditions. Mechanicaldemands placed on tendon tissue will promote changesin the microarchitecture of the tissue (Magra et al 2007).Strain applied to a tendon can change its structure; thesechanges can be damaging or they can be reparative ifappropriately and purposefully applied in treatment.

Scott’s research (Scott 2007) evidenced that it is stimu-lation of the tenocyte that is associated with tendinosis,rather than intrinsic inflammation. Alterations in cellactivity lead to tendon changes from mechanical stressrather than the converse (Riley 2004). The local stimula-tion of tenocytes, which is a load-driven cellular response,rather than inflammation or apoptosis, is the true mecha-nism in tendinosis (Scott et al 2007). Apoptosis plays arole later in the tendinopathic process (Scott et al 2007).Localized hypoxia from vigorous exercise can lead to teno-cyte death (Sharma & Maffulli 2005) and tendinopathicchanges.

Tenocyte metabolism is regulated partly by mechanicalstimulation (Maeda et al 2009). Maeda et al (2009)showed that cyclic strain will change gene expression intendon cells. Force applied to a tendon changes cellularprocess via mechano-transduction, the process in whicha cell converts biomechanical stimuli into chemical sig-nals (Maffuli & Longo 2008). Mechano-transduction uti-lizes gap junctions, stretch activated channels (Wall &Banes 2005), voltage operated calcium channels (VOCC)and tandem pore domain potassium channels (TPDPC)

Tropocollagen fibrilTropocollagen fibre

Tendon

Fascicle

Fascicle bundles

Endotendon

Epitendon

Fig 26.1 Basic tendon structure.

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to communicate with adjoining tenocytes (Wall & Banes2005, Magra et al 2007). Tension on surface proteins,called integrins, embedded in the cell membrane is trans-mitted to the cell’s cytoskeleton. This force is transmittedvia the intracellular network to the nucleus of the celland can alter protein expression (Chiquet 1999). Huanget al (2004) observed that mechanical loading is essen-tial for homeostasis of the bone, cartilage, and skin.Additionally, external forces are capable of producingchanges in intracellular reactions. Tenocytes are respon-sible for changing structure in response to demand byaltering, ‘gene expression patterns, protein synthesisand cell phenotype’ (Maffulli & Longo 2008). This alter-ation is suspected of being the link to overuse and tendi-nopathic changes (Scott et al 2007). Importantly from amanual therapy perspective, Maffulli & Longo (2008)supported that an alteration of mechanical forces mayaugment the healing process. Conversely, understimula-tion can cause tendinopathic changes (Arnoczky et al2006).

The tendon matrix is responsible for maintenance ofthe tendon. Its damage, according to Riley (2004), is theleading event in tendinopathy. The ground substance ofthe extracellular matrix network surrounding the collagenand the tenocytes contains proteoglycans, glycosamino-glycans, glycoproteins, as well as several other small mole-cules (O’Brien 2005). Water makes up 60–80% of theground substance (O’Brien 2005). Proteoglycans arestrongly hydrophilic, enabling rapid diffusion of water-soluble molecules and the migration of cells (Sharma &Maffulli 2005). They, along with glycoproteins, have arole in organization of collagen into fibrils and fibres(O’Brien 2005). When repetitive damage becomes exten-sive it overwhelms the ability to heal (Riley 2004).Arnoczky et al (2007) credited extracellular matrix degen-eration as a precursor of tendon weakness. Riley (2004)described the possibility that changes in cellular activityin the matrix due to mechanical strain can influence thestructural properties of tendons.

Tendon injury

Riley summarized overuse tendinopathy as the phenome-non caused by repeated strains below the failure thresholdthat outstrips the cell’s ability to heal (Riley 2004). Tissueinjury from repetitive strain is thought to be a cellularevent (Arnoczky et al 2006). Recent studies in animalmodeling have produced results of tendinopathy that cor-respond those found in non-experimental tendinopathiesin humans. Soslowky’s model of repetitive motion identi-fied tendinopathic changes in supraspinatus tendons inrats (Soslowky et al 2000). These changes mimic whathas been found in idiopathic tendinopathies in humans,including reduced mechanical properties (Lavagninoet al 2006, Arnoczky et al 2007). Glazebrook et al(2007) found similar changes in rats after overuse

induced by repetitive running. Backman et al (2005) pro-duced similar results with rabbits.

Post-injury disuse of a tendon, through immobilizationor compensation, can also have detrimental effects. Theconcept of stress shielding can be applied to tendons. Anexample of this in terms of bone is application of Wolff’slaw with reduced bone density following fracture immobi-lization. Woo et al (1981) observed that after fracture heal-ing, reapplied weight bearing will increase bone density.Kannus & Jozsa (1991) showed that under-stimulationof tendon cells post-injury produced degenerative findingsin investigation of tendinopathy. DeBoer et al (2007)supported this with his demonstration of tendon proteinsynthesis rates decreasing progressively through 10 daysof immobilization. Lavagnino et al (2006) inducedmechanical injury in rat tail tendons, followed by immobi-lization, which revealed an upregulation of collagenasemRNA and protein synthesis in this damaged area. Evenundamaged fascicles showed similar upregulation duringthe immobilization portion of this study. In an earlierstudy they found that these adverse effects could be con-trolled, in vitro, with cyclic stretching (Lavagnino et al2003). Screen et al (2005) reported similar results withcyclic stretching in non-injured tendon fascicles. In regardto treatment of tendinopathy, attempting to immobilize atendinosis via splinting or casting thus appears to bedetrimental.

Tendon healing

The phases of tendon healing following injury resemblethat of other connective tissues in the body. The phasesare: (1) acute inflammatory, lasting 1–2 days; (2) repair-regeneration or proliferative phase, lasting up to 6 weeks;and (3) maturation or remodelling phase, lasting 3 weeksto a year (Leadbetter 1992, Sharma & Maffulli 2005).Each of these phases in tendinopathy has unique cellularprogression that should be considered when preparing atreatment plan. Tenocytes begin new collagen synthesisaround day 5 post-injury and continue synthesis for 5weeks (Maffulli & Moller 2005). Intrinsic tenocytes beginproliferating at week 4 and are involved in remodellingthrough week 8 (Maffulli & Moller 2005). Applying stan-dard but specific treatments in a global fashion to alltendinopathies without addressing the stage of healingcould be ineffective. Cook & Purdam (2009) recom-mended that interventions should be tailored to the sus-pected pathology.

TENDINOPATHY CLASSIFICATION

Tendinopathy actually represents several different, mixedand sometimes overlapping degenerative processes.Histologically there are mixed findings. Absence ofinflammatory cells, increased ground substance, increased

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vascularity and cellularity with collagen disorganization,are evidenced (Khan et al 2006). Each of these can disruptsome tendon fibres and weaken the remaining fibres(Maffulli & Moller 2005). The role of the tenocyte in ten-don changes has already been discussed. Murrell (2002)stated that apoptosis, or programmed cell death, mayhave a roll in tendinopathy. Oystein et al (2007) showedapoptosis was enhanced in patellar tendinopathy biopsiescompared to controls.

Inflammation is partially controlled by a neurogenicprocess. Substance P and calcitonin-related gene peptide(CRGP) are sensory neuropeptides (Hart et al 2005).These, among other substances, are found in symptomatictendons (Andersson et al 2008) and directly stimulatenociceptor endings (Ueda 1999). Hart et al (2005)hypothesized that neuropeptides are involved via mastcells in tissue in normal tendon regulatory control; also,a dysfunctional regulatory loop produces an inadequaterepair response. This differs from classic inflammation.Riley (2004) observed, ‘. . .nerve endings and mast cellsmay function as units to modulate tendon homeostasisand mediate adaptive responses to mechanical strain. Healso stated that ‘excessive stimulation as a result of overusemay result in pathological changes to the tendonmatrix’ (Riley 2004, p 137). There is a growing body ofevidence that pain associated with tendinopathy may beneurogenic.

Tendinopathy severity is graded according to histologi-cal features distinguished under light microscopy(Maffulli et al 2008). Various scales have been proposed.Two early scales were originally developed for lowerextremity research. The Movar scale and the Bonar scalehave since development each been applied successfullyto research of the upper extremity (Maffulli et al 2008).Each scale considers the microscopic appearance of fiveto seven factors; each factor is given a grade ranging fromlowest number (normal tendon), to highest number(markedly abnormal tendon). The sample is gradedcumulatively with combined scores from each factor(Maffulli et al 2008). Scott et al (2007) used a modifiedBonar scale to specifically assess tendinosis. The modifiedscale considers five histological changes: (1) tenocytemorphology; (2) tenocyte proliferation; (3) collagenchanges; (4) glycosaminoglycans (GAG), and (5) neovas-cularization (Scott et al 2007).

A lack of common description of these histologicaltissue changes which vary from scale to scale to modi-fied scale has limited a clear classification and under-standing of tendinopathy with its underlying causes.Kahn et al (2006) cited Clancy as having initially madea classification of tendinopathy types that was latermodified by Bonar and now includes: tendinosis, tendini-tis (tendonitis) or partial rupture, paratenonitis (paraten-donitis/paratendinitis/tenosynovitis/tenovaginitis) andparatenonitis with tendinosis. The following sections pro-vide details.

Tendinosis

Tendinosis is defined by Maffulli et al (2003a) as intra-tendinous degeneration typical with aging or devasculari-zation. It is characterized by fibre disorientation, hypercel-lularity, and focal necrosis and calcification (Maffulli et al2003a). Kraushaar & Nirschl (1999) defined the threefindings in tendinosis as fibroblastic hyperplasia, hyper-vascularity, and abnormal collagen production with theformer being the first response. Kannus & Jozsa (1991)examined 891 spontaneously ruptured tendons in theupper and lower extremity. Histopathologic examinationshowed that 97% of these had degenerative changes.These were sub-classified into hypoxic degeneration(44%), mucoid degeneration (21%), tendolipomatosis(8%), and calcific tendinopathy (5%) (Kannus & Jozsa1991) There is multiple cell/tissue involvement and thismay be difficult to discern from other classifications.

Tendinitis

Tendinitis and partial rupture are grouped together inthis classification. An active inflammatory response,symptomatic degeneration and true vascular disruptionare characteristic findings (Kahn et al 2006). Lympho-cytes and neutrophils are seen (Kraushaar & Nirschl1999). It has similar characteristics to tendinosis buthistopathologically will also demonstrate fibroblasticproliferation, haemorrhage and granulation tissue (Maffulliet al 2003a). Hammer (2007a) stated that isolated activeinflammation is not common but is usually associatedwith some degree of rupture, which implies that this classi-fication is falsely over-diagnosed.

Paratendinitis

Paratendinitis, also termed tenosynovitis, is evidenced asfrank inflammation of the outer layer of the tendon(Kahn et al 2006). Microscopically this will reveal infil-trate possibly including fibrin deposition, exudate, andareolar tissue degeneration which could explain the palpa-ble crepitation at certain stages of its progression (Kahnet al 2000, Maffulli et al 2003a).

Combined paratendinitisand tendinosis

This fourth classification (Kahn et al 2006), originallydescribed by Clancy, includes characteristics of both ten-dinosis with an overlying paratendinitis as describedabove. Most clinicians, including primary care physicians,would not be able to differentiate which of these weremost prominent in a patient presenting with generalhand/wrist pain, as the signs and symptoms are similarto isolated paratendinitis.

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Of the above categories, only tendinitis and paratendi-nitis have an inflammatory component and would con-ceivably respond to an anti-inflammatory regimen, andlikewise would logically not respond to deep tissue fric-tion massage.

EXAMINATION AND DIAGNOSIS

A comprehensive assessment is the most important step todetermining appropriate treatment of most musculoskele-tal disorders. History, clinical tests, and imaging will con-tribute to a differential diagnosis. The reader is referred toChapters 2–4 for discussion of history taking, physicalexamination, and pertinent imaging. Clinical testing fortendinopathy can include palpation, selective tissue test-ing, and provocation testing. It is theorized that clinicaltests will help to differentiate the structure involved, yetreliability and validity are still in research. Indeed, this isonly one part of the diagnostic equation. Identifying thetype of tendon involvement and stage of pathology isanother factor of greater difficulty.

The diagnosis of tendinopathy will be the result from acomprehensive examination, but distinguishing betweentendinosis and tendinitis can be difficult (Khan et al2000). Maffulli et al (2003a) identified tendinopathy clin-ically as localized tendon swelling and pain with impairedfunction. Curwin (2005) stated that we must assume thelevel of tendon involvement can be correlated withthe level of dysfunction and pain. Per Curwin (2005),the degree of injury cannot be ascertained acutely. Elder& Harvey (2005) maintained that acutely the specific areais usually easy to isolate. Leadbetter (1992) defined acuteinjury as having a sudden specific onset followed by grad-ually decreasing pain. Identifying an acute onset duringhistory taking should help differentiate a current stage ofacute or subacute inflammatory process from a chronicstage when inhibiting pain occurs during activity or after-ward (Leadbetter 1992), and will help guide treatment.

One complicating factor in isolating a specific involvedstructure is that most tendons to be identified will haveanatomic variations or supernumerary insertions. Thesevary too much for inclusion here. Another complicationis the possibility that a trigger point is responsible for allor a portion of the symptoms. Trigger points in the upperquarter can refer pain to the wrist area. The subscapularis,biceps brachii and brachialis are some of the muscles thatcan refer pain to the wrist (Finando & Finando 2005).Lack of clearing these points/areas of potential contribu-tion will delay appropriate treatment. It cannot be over-emphasized that suspected trigger points should becleared as part of the initial examination. The reader isreferred to Chapter 32 of this text for additional informa-tion on referred pain from muscle/myofascial triggerpoints (TrPs) in arm pain syndromes.

Clinical tests

Regarding general palpation, oedema and hyperaemia ofthe paratenon may be evidenced clinically. A fibrinousexudate accumulates within the tendon sheath, and crepi-tus may be felt on clinical examination (Kahn et al 2000,Sharma & Maffulli 2005). This may be important in dif-ferentiating paratendinitis from tendinopathy; however,the presence of crepitis to palpation does not prove thatparatendinitis is present (Kahn et al 2000, Sharma &Maffulli 2005).

Palpation for tenderness is a common tool for clinicaldiagnosis and differential testing in tendinopathy. Cooket al (2001) assessed the value of palpation to identifypatellar tendinopathy in a group of 326 young athletes.Intra-rater reliability was good at 82%. Palpation of ten-dons in patients with symptoms resulted in sensitivity of68% and specificity of 9% (Cook et al 2001). However,applicability to the wrist is limited since the patellar ten-don is larger than those of the hand/wrist.

Maffulli et al (2003b) found a high positive predictivevalue in palpation, when combined with the RoyalLondon Hospital test and a painful arc sign to determineAchilles tendinopathy. The painful arc sign is theorizedto differentiate pathology within the tendon itself versuspathology of the paratendon. If the pathology is confinedto the tendon structure, a palpable area of thickness andtenderness will move with the tendon as the ankle ismoved; if the painful, thickened area stays in a fixed posi-tion regardless of ankle movement then the pathology iswithin the paratendon (Easley & Le 2009). The sensitivityand specificity of this test was 52% and 83% (Maffulliet al 2003b). The Royal London Hospital test identifiestendinopathy by eliciting local tenderness with palpationof the tendon in neutral or slightly on slack. The test ispositive if the tenderness decreased significantly or disap-pears with the tendon on stretch. The sensitivity and spec-ificity of this test was 54% and 91%. The sensitivity andspecificity of direct palpation was 58% and 74%. Whenthe three tests were combined, sensitivity was 58% andspecificity was 83% (Maffulli et al 2003b). There is adearth of evidence-based research application of theseclinical tests to tendons of the wrist and hand.

Cyriax supported selective tissue tension testing (STT)(Hammer 2007b). Selective tissue tension testing is uti-lized to compare non-contractile to contractile tissueinvolvement (Hammer 2007b). The tendon is isolated asmuch as possible based on planes of motion performed,either isolated or overlapped with other tendons. Theexaminer attempts to administer a minimal isometricforce to the tendon/muscle while the patient resists. Elici-tation of pain is a positive test (Hammer 2007b). Han-chard et al (2005) found agreement (0.71–0.79, kappaand 95% confidence interval) among Cyriax-trained asses-sors using STT combined with clinical history when asses-sing tendinopathy of the rotator cuff. Reliability has yet to

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be established for any upper extremity tendon application(Stasinopoulos & Johnson 2007).

Provocation tests (special tests) are used with varyingevidence-based support of reliability, sensitivity, and spec-ificity. These tests are included, as available and relevant,in the outlined discussion of tendinopathies unique tospecific tendons of the wrist and hand following diagnos-tic imaging and invasive testing.

Diagnostic imaging and invasivetesting

Due to the difficulty in reliably diagnosing tendinopathy,Fredberg & Stengaard-Pedersen (2008) recommendedultrasound (US) or magnetic resonance imaging (MRI) ifthere is no response to conservative treatment or if radicu-lar pain is present. Fredberg & Stengaard-Pedersen (2008)described the efficacy of ultrasound versus MRI. Theseinclude more detailed visualization of tendon microstruc-ture, better tendon border definition, and its interactivenature. A focal thickening, visualized with ultrasound, isassociated with tendonitis in tendons without sheaths. Thismay correspond to angiofibroblastic areas associated withmicro-ruptures (Daenen et al 2003). Furthermore, the ten-don or tendon sheath, as viewed via ultrasound, will bethickened on more chronically involved tendons (Daenenet al 2003). Ultrasound can be performed directly over thesubjectively painful area and even during range of motion(Fredberg & Stengaard-Pedersen 2008). McNee & Teh(2007) considered ultrasound the ‘investigation of choice’in tendon pathology. Beddi & Bagga (2007) stated that ultra-sound is the gold standard for tendon examination.

Isolated identification of the involved structure can beassessed by removing sensation from specific areas,continuing until the patient’s symptoms are resolved.Selective anaesthetic injections, usually with lidocaine,are supported by Elder & Harvey (2005) as ‘the best diag-nostic test’ for tendinopathy of the hand and wrist, butthey offer no studies to back up this recommendation.

TENDINOPATHIC ENTITIES OF THEHAND AND WRIST

This section will describe common areas of tendon painin the wrist. Areas of rare involvement are not included.

Flexor carpi ulnaris

Pathology of the flexor carpi ulnaris (FCU) muscle (Fig26.2) may include tendinitis, tendinosis, or a combina-tion of these two. This is the most common wrist flexortendinopathy (Elder & Harvey 2005) and often occurs inthose who play racquet sports and golf (Rettig 2001).The FCU inserts into the pisiform, the hook of the

hamate, and the fifth metacarpal (Moore 1992). It is notheld in place by the flexor retinaculum, but instead relieson its own tendon sheath (Elder & Harvey 2005).

Testing

• Characterized by painful palpation of the pisiformand the FCU tendon, presence of angiofibroblastichyperplasia is often evidenced by palpable swellingand thickening in symptomatic FCU tendons (Budoffet al 2005)

• Pain with resisted wrist flexion and ulnar deviation

• Shuck test if pisotriquetral involvement is suspected(Rettig 2001)

• Passive wrist extension and radial deviation willprovoke symptoms (Elder & Harvey 2005)

Differential diagnosis

Rettig (2001) recommended the pisotriquetral grind test toimplicate the pisotriquetral joint painover a FCU tendinopa-thy. Campbell (2001) and Burke (1996) describe the test asgrasping the pisiform and compressing it onto the trique-trum and rotating the pisiform under pressure. Palpationalone may implicate the tendon with pain and crepitus,whereas painwith compression implicates the pisotriquetraljoint. Pisotriquetral compression syndrome (Rettig 2001),arthritis, calcific tendonitis and ulnar neuritis, pisiform liga-ment complex syndrome, pisotriquetral arthrosis (Rayan2005), and Guyon’s canal syndrome (Elder & Harvey2005) are additional differential diagnoses.

Extensor carpi ulnaris

Tendinopathy of the extensor carpi ulnaris (ECU) (Fig26.3) may commonly include a tendinitis, tendinosis, or

Flexor carpiradialis

Flexor carpiulnaris

Fig 26.2 Tendiopathic entities: flexor tendons.

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these in combination. It is also subject to subluxation(Elder & Harvey 2005). Activities such as racquet sportsand baseball batting will cause rapid and repetitive supina-tion, flexion, and ulnar deviation, which have been cited aspromoting factors (Elder & Harvey 2005, Hammer 2007c).Rettig (2001) noted that ECU tendinopathy often involvedthe non-dominant hand in tennis players who used a two-handed backhand stroke. Futami & Itoman (1995) foundthat of 155 patients with dorsal wrist pain, 53 had painpossibly caused by tenovaginitis (paratendinitis) of theECU induced by overuse. Bencardino & Rosenburg(2006) associated sub-luxations of the ECU with tenosyn-ovitis and recommended testing supination and volarflexion for ulnar sub-luxation of the tendon. Montalvanet al (2007) studied 28 clinical cases of ECU related painwith three clinical patterns described: (a) acute traumaticinstability of the ECU in the fibro-osseus groove (12 cases);(b) tendinopathy (14 cases); and (c) complete ECUrupture (4 cases).

Testing

• Symptoms are provoked by combined activesupination and wrist extension (Elder & Harvey 2005)and combined resisted ulnar deviation and extension(Elder & Harvey 2005, Young et al 2007)

• Dislocation can be reproduced by a clicking onsupination and extension actively, not passively (Elder& Harvey 2005)

• Tenderness to palpation over sixth dorsalcompartment (Rettig 2001) at the ECU tendon andulnar head (Elder & Harvey 2005)

Differential diagnosis

Rupture, sub-luxation, dislocation, triangular fibro-cartilagecomplex (TFCC) pain, triquetrum-lunate ligament lesion,

pisiform-lunate joint pain, and fractures of the lunate, tri-quetrum and pisiform are differential diagnoses (Futami &Itoman 1995). Additional diagnoses to be excluded areextensor digiti minimi tenosynovitis, TFCC tears (Elder &Harvey 2005), and stenosing tenosynovitis in the ulnar wrist(Rettig 2001).

Extensor carpi radialis longusand brevis (distal tendons)

A common combined pathology of the extensor carpiradialis longus (ECRL) and brevis (ECRB) tendons (Fig26.3) distally is known as intersection syndrome. This isalso termed peritendinitis crepitans (Young et al 2007),crossover tendinitis, and squeaker’s wrist (Rettig 2001). Thesyndrome may include tendinitis, tendinosis, and/or bur-sitis. It is common among racquet players, weight lifters,and canoeists (Hammer 2007c). Ski pole and hammerusage can also provoke this particular syndrome (Elder& Harvey 2005).

Intersection syndrome is associated with friction fromthe crossing of the first dorsal compartment abductorpollicis longus (APL) and the extensor pollicis brevis(EPB) over the second dorsal compartment (ECRL andECRB) (Young et al 2007). It is a paratendinitis (teno-synovitis) that can result in stenosis of the affectedtendons.

Cvitanic (2007) noted a natural foramen between theextensor pollicis longus (EPL) and ECRB in cadavers atthe site of the intersection. This could explain the areasof multiple symptoms in the dorsal forearm and couldmake differential diagnoses more complicated. Inflamma-tory conditions of the ECRB and ECRL at their insertionsmay be associated with bony protuberances at the capi-tate, second or third metacarpals, or trapezoid (Daenenet al 2003).

Testing

• Pain to palpation and visible swelling may beevidenced in the tendons proximal to the firstcompartment (Plancher et al 1996, Benicardino &Rosenburg 2006)

• Thickening and interstitial fluid collection aroundboth tendons approximately 4 to 6 to 8 cm proximalto Lister’s tubercle will show on MRI (Benicardino &Rosenburg 2006, Plancher et al 1996)

• Crepitation between the APL/EPB and ECRL/ECRBwith wrist flexion or extension may be palpable(Elder & Harvey 2005)

Differential diagnosis

Finkelstein’s test will be positive but in a more proximalregion of the dorsal forearm than would be the case in

Extensor digiti minimi

Extensor carpi ulnaris

Extensorindicis proprius

Extensor carpiradialis brevisand longus

Fig 26.3 Tendiopathic entities: extensor tendons.

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DeQuervain’s tenosynovitis (Elder & Harvey 2005, Younget al 2007).

Extensor indicis proprius

Pain and swelling over the fourth dorsal compartment isthe most common finding in extensor indicis proprius(EIP) (Fig 26.3) syndrome (Plancher et al 1996). This syn-drome involves an irritation of the tenosynovium near theextensor retinaculum (Elder & Harvey 2005). Plancheret al (1996) attributed symptoms of EIP tendinopathy tooveruse hypertrophy, or to synovitis secondary to overuse.The former could lead to the latter if symptoms were notaddressed in a timely fashion. Anatomic variations (75%)are common, complicating the exact structure involved(Plancher et al 1996, Soejima et al 2002).

Testing

• Pain and swelling are evidenced in fourth dorsalcompartment distal to ulnar head with supination(Plancher et al 1996)

• Resisted index extension (Hammer 2007c) with wristfully flexed (Elder & Harvey 2005) provokessymptoms

Differential diagnosis

Extensor digitorum communis (EDC) or extensor pollicislongus (EPL) tenosynovitis, dorsoradial ganglion, Kle-bock’s disease, extensor digitorum communis tendinopa-thy, and fourth-compartment syndrome are diagnoses tobe excluded (Elder & Harvey 2005).

Extensor digiti minimi

The extensor digiti minimi (EDM) (Fig 26.3) occupies thefifth dorsal compartment. The pathology most often occur-ring here is a tenosynovitis (Elder & Harvey 2005). Duplica-tion of the tendon is common complicating implication ofthe proper structure (Young et al 2007). Elder & Harvey(2005) stated that continuous hand usage such as handwrit-ing will provoke symptoms. Hammer (2007c) reported alack of pain with resisted testing, which is unusual for tendi-nopathy, but no reason for this phenomenon was given.

Testing

• Grip is painful (Elder & Harvey 2005)

• Limitation in fifth digit extension is seen (Elder &Harvey 2005)

• Wrist flexion after fist closure or flexing a fist is painful(Elder & Harvey 2005)

• Tenderness to palpation is present just distal to ulnarhead (Plancher et al 1996)

Differential diagnosis

Extensor carpi ulnaris (ECU) tenosynovitis, TFCC pathol-ogy, ulnar impaction should be ruled out (Elder & Harvey2005).

Abductor pollicis longusand extensor pollicis brevis

Together the abductor pollicis longus (APL) and extensorpollicis brevis (EPB) (Fig 26.4) contribute to De Quer-vain’s tenosynovitis. These tendons normally passtogether through a single fibro-osseous tunnel to inserton the first metacarpal and first proximal phalanx respec-tively (Plancher et al 1996). De Quervain’s tenosynovitisoften results from excessive pinching or radial deviation(Hammer 2007c). This syndrome is a common occur-rence in golf, racquet sports and fishing (Rettig 2001).

Testing

• Finkelstein’s test (Fig 26.5A). Ahuja & Chung (2004)detailed the true test and variations, as the test ismisrepresented vigorously in the literature.The original test Finkelstein (1930) described wascompletely passive: the clinician grasps the patient’sthumb and quickly pulls the wrist into ulnardeviation via the thumb. A positive result isreproduction of pain at the ulnar styloid. Thesurgeon Eichhoff described a test for de Quervain’sdisease that is often mistaken for Finkelstein’s test(Fig 26.5B). His test consisted of the patient activelyplacing the thumb into the palm and folding thefingers down, holding the thumb in place while theclinician passively moves the wrist into ulnardeviation. A positive test is the same as describedfor Finkelstein’s test. This test, which many believeto be the Finkelstein test, has been criticized asgiving false-positive results. Brunelli described a testin 2003 that he claimed was more accurate than thetrue Finkelstein’s test. Brunelli criticizedFinkelstein’s test for false-positive results due to the

Abductor pollicis longus

Extensor pollicis brevis

Extensor pollicis longus

Fig 26.4 Tendiopathic entities: thumb tendons.

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stretch of the radial collateral ligament, thescaphotrapezial ligament, or the thumbcarpometacarpal ligament caused by the APL andEPB tendons being moved away from the pulley.Brunelli described a test in which the wrist is heldin radial deviation while forcibly abducting thethumb (Ahuja & Chung 2004). Psychometricproperties of these tests have not been established(Elder & Harvey 2005).

• The EPB entrapment test identifies separatecompartments and resulting stenosis; this test wasreported to have sensitivity of 81% and specificity of50% (Alexander et al 2002)

• Tenderness on palpation and swelling over the radialstyloid (Elder & Harvey 2005) and first dorsalcompartment (Rettig 2001) are present

• Resisted thumb extension is painful (Elder & Harvey2005)

Differential diagnosis

Intersection syndrome (Elder & Harvey 2005), scaphoidfracture, flexor carpi radialis (FCR) tendinopathy, first car-pometacarpal (CMC) joint arthritis, and Wartenburg’ssyndrome (Plancher et al 1996) are differential diagnoses.

Extensor pollicis longus

The extensor pollicis longus (Fig 26.4) often exhibits atenosynovitis common to racquet sports players. Historyof repetitive trauma like racquet sports, pain, crepitus,and swelling around Lister’s tubercle will narrow the list

of suspected diagnoses (Plancher et al 1996). Triggeringof the thumb may be seen in severe cases.

Testing

• Pain, swelling, and crepitus along the EPL tendon atthe third dorsal compartment (Plancher et al 1996),and at Listers tubercle (Elder & Harvey 2005) areevidenced

• Pain is elicited with resisted thumb extension orpassive flexion (Elder & Harvey 2005)

• Passive interphalangeal joint flexion can reproducethe pain (Elder & Harvey 2005)

Differential diagnosis

Differential diagnoses have not been established as neces-sary for this tendon pathology.

Flexor carpi radialis

Flexor carpi radialis (FCR) (Fig 26.2) tendinopathy iscommon in people who play racquet sports, golf andbaseball (Rettig 2001). Elder & Harvey (2005) reportedan often insidious onset without known trauma. A pri-mary symptom is pain near the proximal aspect of the tra-pezium (Gabel et al 1994). This is often a result ofoveruse with repeated flexion of the wrist, of complicationafter scaphoid fracture or distal radius fracture, or of otherdirect trauma (Gabel et al 1994). The FCR is subject totraumatic injury due to its position. The FCR lies in directcontact with the roughened surface of the trapezium. Itsinsertion onto the trapezium is only 20% of the entireinsertion. Additional insertions include the second andthird metacarpals (Bishop et al 1994) and the joint cap-sule of the trapezio-scaphoid joint itself (Schmidt 1987).The tendon occupies 90% of the fibro-osseous tunnel,making it vulnerable to compression (Bishop et al 1994,Elder & Harvey 2005). FCR tendinopathy is also asso-ciated with scaphotrapezial joint osteoarthritis, malunionof the trapezium, or scaphoid cyst (Soejima et al 2002).

Testing

• Symptoms are exacerbated by resisted flexion and radialdeviation of the wrist (Elder & Harvey 2005, Rayan2005) and with resisted flexion (Rettig 2001); wristhyper-extension or resisted wrist flexion with radialdeviation can reproduce symptoms (Young et al 2007)

• Pain andnotable swelling are evidenced at the level of thedistal wrist crease along its course (Elder &Harvey 2005)and near the fibro-osseous tunnel (Young et al 2007).

Differential diagnosis

Differential diagnoses include osteoarthritis of the firstCMC joint, scaphoid cysts, fractures, ganglion cysts,

A

B

Fig 26.5 (A) Finkelstein’s test: The clinician grasps the patient’sthumb, uses it to quickly and passively place the wrist intoulnar deviation, causing pain at the radial styloid process.(B) Eichhoff test: The patient actively grips the thumb in the fistand then the clinician passively places the wrist into ulnardeviation, which causes pain at the radial styloid process

(after Ahuja & Chung 2004).

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DeQuervain’s syndrome, and Lindburg’s syndrome (Elder& Harvey 2005).

TREATMENT AND PROGNOSIS

Conservative treatment

Conservative treatment for tendinopathy includes modal-ities such as ultrasound, electric stimulation, ice, and laser(Curwin 2005); as well as injections and splinting(Plancher et al 1996). Konijnenberg et al (2001) attempteda meta-analysis of outcomes of repetitive strain injuries.Many body areas were included in the analysis. They foundno strong evidence for any conservative treatment option(Konijnenberg et al 2001). Conservative treatmentsincluded physiotherapy involving multiple types of inter-ventions, but none included the hand or wrist.

Manual therapy, in particular deep tissue friction mas-sage (DTFM), is a conservative treatment for tendinopathythat is utilized by some clinicians; however efficacy hasnot been proven. This could be due at least in part to studydesign. DTFM for tendon pain was first popularized byJames Cyriax. Cyriax did not perform outcome studies, butstudies done by Stasinopoulos & Johnson (2007) concludedthat effectiveness of DTFM for lateral epicondylitis could notbe assessed from the studies they reviewed. Stasinopoulosdid not study outcomes of the wrist.

Cyriax techniques of DTFM for treatment of soft tissuelesions are performed with direct pressure on the painfularea. The clinician’s finger rubs firmly transversely to thefibres of the tissue, which includes tendon. Recom-mended duration and frequency are 20-minute sessionsfor 6–12 treatments with at least 48 hours between treat-ments (Cyriax 1983). Cyriax (1983) theorized that thetreatment eroded scar tissue between muscle fibres viaabrasive contact; in tenosynovitis the rolling was theo-rized to smooth roughened synovial surfaces. More recentwork has specified the optimal time of application for ten-don strain based on the previously discussed stage ofpathology. Research by Zeichen et al (2000) subjectedfibroblasts to strain for varying times, monitoring for pro-liferation of fibroblasts as a response to a biaxial strainover subsequent hours. The results showed that 15minutes of strain resulted in increased proliferation overcontrols at 6 and 24 hours (Zeichen et al 2000).

The 48 hours of recommended minimum acceptedtime frame between treatments roughly equals the endingof the acute stage of inflammation, when remodellingbegins (Leadbetter 1992). The harder pressure, as recom-mended by Cyriax (1983) may be justified by a Gehlsenet al study (1999) showing that firmer pressure had morepositive effects.

Hammer (2007d) applied soft tissue mobilization withgreater precision regarding stage of tendon pathology.While he generally concurred with treatment in the 5–15

minute duration twice/week lasting 2 weeks to 2 months,Hammer (2007d) recommended no manual treatmentuntil the proliferative phase, which was described as7–14 days after original injury. Treatment during acutephase when rest is recommended should be light, ‘aidingfibroblastic proliferation and breaking down of immaturecollagen’. The maturation phase could be treated morevigorously to reduce fibrosis (Hammer 2007c).

Kahn (2009) and Kraushaar & Nirschl (1999) theorizedthat mechanical disruption may transform a failed intrin-sic healing into a therapeutic extrinsic healing mecha-nism. Brousseau et al’s (2002) research on DTFM andtendinitis (not tendinosis) considered cross friction treat-ment as only cross friction and not other techniques,including a stroke along the muscle. This could be oneexplanation for the lack of more positive outcomes:improper or non-uniform direction of force. Another rea-son could be lack of proper selection of subcategory oftendinopathy as classified earlier in this section. Someclassifications, such as acute inflammation, theoreticallycannot be affected by manipulation.

Despite the lack of randomized controlled trials of ten-don pain and DTFM, other research is emerging. Thesestudies provide, on a small scale, a patho-anatomic linkbetween manual therapy and reversal of tendinopathicchanges. Meltzer & Standley (2007) demonstrated that amodelled indirect osteopathic manipulative technique(IOMT) significantly reduced pro-inflammatory secretionscompared to controls 24 h after application, concludingthat the modelled IOMT can reverse some of the effectsof repetitive strain (Meltzer & Standley 2007). Standley& Meltzer (2008) studied the effect of modelled manualtherapy on cellular response. Improved range of motion,reduced analgesic requirements and decreased oedemapost-myofascial release was theorized as a result of anti-inflammatory cytokines from strain inducement of myo-fascial release (Standley & Meltzer 2008).

Eccentric exercise is a more recently applied form ofconservative treatment with the theory of reversing degen-eration via specific load application. This treatment hasshown positive outcomes (Ohberg et al 2004). Eccentricexercise involves contraction of a muscle to control ordecelerate a load while the muscle and tendon are length-ening or in a lengthened position. Eccentric exercises havebeen proven effective at changing ultrasonic findings oninvolved Achilles tendons within 12 weeks (Ohberg et al2004). Follow-up showed reduction in tendon diameterand return of normal tendon structure in a majority (19of 26) of tendons. The unchanged tendons had undefinedresidual defects (Ohberg et al 2004).

Woodley et al (2006) reviewed 11 studies of eccentricexercises that met inclusion criteria of methodologicalquality and levels of evidence. They covered both upperand lower extremity tendinopathies. Eccentric exercisewas more effective than other treatments that includedfrictions, stretching, splinting and ultrasound in treating

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tendon pain and improving patient satisfaction andreturn to work outcomes (Woodley et al 2006).

Curwin (2005) outlined an eccentric programme thatconsisted of warm up activities, stretching, 3 sets of 10eccentric exercises, repeated stretching, and icing. Thiswas continued for 6 weeks unless symptoms resolved first.The protocol was performed by 200 patients with chronictendinopathy that failed conservative therapy. Marked orcomplete relief of symptoms was reported in 90% ofpatients who completed the programme. Despite the largesample size there was no control group or randomization(Curwin 2005).

Knobloch (2008) supported eccentric training on thewrist as equally effective as that on the Achilles tendonin decreasing abnormal capillary tendon flow (angiogene-sis) seen in tendinopathy. Kahn et al (2009) promoted

the theory that effects of eccentric muscle contraction onthe tendon appear to stimulate tissue healing.

The research by Kannus & Josza (1991) illuminatedhow stress reduction can lead to degenerative changes intendon including reduction in mechanical properties.That may be why eccentric exercises are effective in somecases in reducing the effects of immobilization. Soft tissuemobilization along the tendon could also reduce theeffects of immobilization, but only to a localized portionof that tendon. Any force, including eccentrics, will notaffect the tendon equally. Undamaged fascicles will acceptand transmit that force normally, while damaged fascicles,according to Arnoczky et al (2007), will not transferthat force to all fascicles, which leads to degenerationof the involved fascicles. This will be a necessary subjectof future studies. An algorithm (Fig 26.6) outlines a

Fibre weakening

Rupture

Normal tendon tissue

Repetitive strain Submaximal strain

Matrix/cell changes

Fibre damagestress shielding

Conservativetreatment:

rest, ice, immobilization

Symptom reduction

Eccentrics

No relief

Manual tendonrelease

Treatment

No treatment

No treatment

Surgery

Excessiveintensity

Excessiveduration

Excessivefrequency

Fig 26.6 Selected treatment algorithm.

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proposed pathway of manual treatment and eccentrics intendinopathy.

Non-conservative treatment

Reviewing the recent literature on surgeries for wristtendinopathy reveals a consistent use of the termstendinitis and tenosynovitis in surgical cases. This use istherefore continued in the report of surgical interventions.

DeQuervain’s tenosynovitis that does not respond toconservative therapy may undergo surgery. This involvesdecompression of the first dorsal compartment and isnot without risks (Plancher et al 1996). Rettig (2001)reported that after 7–10 days of splinting, return to sportscan be expected in 6–9 weeks.

Flexor carpi ulnaris surgery often involves excision ofthe pisiform (Rettig 2001). The expected return to sportsaverages 8 weeks (Rettig 2001).

As the flexor carpi radialis occupies 90% of theavailable space in its synovial tunnel, surgery hereinvolves decompression of the tunnel (Plancher et al1996).

Plancher et al (1996) stated that extensor carpi ulnarissub-luxation does not always respond to conservativecare. The sixth dorsal compartment is released in extensorcarpi ulnaris tendinitis. Due to chance of sub-luxationsome authors recommend release of the fibro-osseus tun-nel it occupies (Plancher et al 1996). Rettig (2001)reported that after 4–6 weeks of casting return to sportsrequired a minimum of 8 weeks.

Surgery for intersection syndrome, according to Plan-cher et al (1996), involves release of the second com-partment with synovectomy. Rettig (2001) mentionedbursectomy between the involved tendons. Release ofthe third dorsal compartment is also performed on non-responsive cases of extensor pollicis longus tendinitis.

Prognosis

Prognosis with conservative treatment for specific tendi-nopathies or syndromes is not widely available in evi-dence-based studies. Regarding conservative treatmentfor DeQuervain’s tenosynovitis, Harvey et al (1990)reported 80% resolution of symptoms with injectionsalone. Lane et al (2001) concluded that classifying thesepatients before conservative treatment was initiated

improved outcomes; 17 of 18 patients with classified mildsymptoms improved with splinting and non-steroidalanti-inflammatory medications. Patients with symptomsclassified as moderate to severe responded most favour-ably to injections (76%) (Lane et al 2001). Richie & Bri-ner (2003) reviewed seven descriptive studies comparingconservative treatments for DeQuervain’s tenosynovitis.They reported an overall cure rate of 83% for injectionalone, 61% for injection and splint, 14% for splint alone,and 0% for treatments that consisted solely of non-steroi-dal anti-inflammatory medications and rest. Tendinopa-thies of the other structures of the wrist have not beenas widely studied.

CONCLUSION

While muchmore is now known about tenocyte and matrixdysfunction, successful application of these concepts fortreatment of tendinopathy in the wrist and hand has notbeen proven. Studies continued to be hampered by samplesize, lack of meaningful outcomes, small populationselection, and lack of randomization. Adequate studiesregarding conservative treatment of non-inflammatorytendinopathies do not appear to exist currently.

Eccentrics show promise for treating tendinopathy in amajority of weight bearing tendons. Successful applica-tion of this into tendinopathies of the upper extremityhas yet to be accomplished.

Manual therapy’s place in treatment of wrist tendinopa-thy has not been established. If the efficacy of manualapplied eccentrics or what some authors call ‘activerelease’ could be likewise established in the upper extrem-ity, they could easily be performed adapting Curwin’s(2005) guidelines for eccentric exercises. A study thatreveals the effects of manual therapy on tendinopathy willrequire the following: (1) selection of appropriate tendonpathology, which will pose its own difficulties; (2) soft tis-sue mobilization such as ‘active release’ along the tendonfibres; (3) continued self-range of motion routinely for 48hours, to reduce the effect of immobilization; and (4) therepetition of criteria (2) every 48 hours for up to 6 weeksuntil function has returned. A design incorporating thesefactors may be able to discern the true worth of DTFMin tendinopathy.

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Part | 5 | The wrist and hand regions

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