Re:건병증 치료를 위한 통증성 원심성 트레이닝 - 극상근 건병증의 치료

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정리해보자

The supraspinatus tendon

Anatomy

The rotator cuff consists of four separate muscles: the subscapularis, the supraspinatus, the infraspinatus and the teres minor muscle. They all arise from the scapula and are inserted into the tuberosities of the humerus (Fukuda, et al. 1990). The supraspinatus has a fleshy origin in the fossa supraspinatus, and inserts into the greater tuberosity (Fig. 7). Its tendinous insertion fuses with the infraspinatus posteriorly, and the coracohumeral ligament anteriorly. Because of its anatomical position, confined above by the acromion and the coracoacromial ligament, and below by the humeral head, the tendon is at risk for compression and attrition. The rotator cuff is considered to have three functions, to provide the gleno-humeral joint with stability, movement, and nutrition (Fukuda, et al. 1990). 

 Tendon structure

The rotator cuff tendons are surrounded by an epitenon. This is the outermost layer, as the rotator cuff tendons do not have a paratenon. Near the insertion of the supraspinatus tendon into the great tuberosity, a five layer complex has been described, that details the density and organisation of collagen and its associated elements (Malcarney, et al. 2003). It has been suggested that this intratendinous variation of collagen fibre density and orientation, may create shear forces within layers and lead to intrasubstance tears (Soslowsky, et al. 2000). Such variations in fibre orientation within the cuff/capsule complex, from superficial to deep, affect the biomechanical properties. In a complex way, the five-layer collagen complex can redirect the intratendinous strain in the rotator cuff during abduction (Fig.8). This

may mask a tear during joint abduction. This also explains why partial thickness tears may propagate into larger, full-thickness tears (Bey, et al. 2002). 

 Circulation

The rotator cuff receives its blood supply from several different branches of the axillary artery, for example the anterior and posterior circumflex humeral arteries, the thoracoacromial artery, and the suprascapular artery. The anterior circumflex humeral artery runs along the inferior border of the subscapular muscle, supplying the anteriosuperior rotator cuff (Rathbun, et al. 1970;Malcarney, et al. 2003).

 Innervation

The supraspinatus muscle is innervated by the suprascapular nerve (C4-6).

The innervation patterns of the rotator cuff have not been clearly described.

An electrophysiological experiment by Minaki et al. showed that there are

nociceptors receiving pain sensation, and proprioceptors receiving position

sense in the supraspinatus muscle-tendon unit (Minaki, et al. 1999). The

subacromial bursa is positioned in very close proximity to the tendon. The

bursa is innervated by the suprascapular nerve posteriorly and anteriorly by

the lateral pectoral nerve (C5, 6), and they provide the bursa with

proprioception and nociception (free nerve endings) (Ide, et al. 1996).

Biomechanics

Due to the anatomical structure, it is difficult to measure strain forces of the

supraspinatus tendon in vivo. In vitro strain tests of the supraspinatus

tendon during different angles of arm abduction have been reported. The

cross-sectional area of the tendon fibres has been shown to be smaller on the

joint side compared to the bursal side of the tendon, leading to a reduced

ability to withstand strain at the joint side (Nakajima, et al. 1994). It seems

that the strain is higher at the joint side, near the insertion of the tendon,

compared to the bursal side (Bey, et al. 2002). The strain at the joint side

increases in higher angles of arm abduction. There is also a difference in

strain between the joint and bursal side during static loading and abduction

of the humerus, implying a shearing effect between the two parts. It has been

stated that this initiates intratendinous tears at the joint side (Reilly, et al.

2003;Huang, et al. 2005;Seki, et al. 2008). The tensile strength and stiffness

of the supraspinatus tendon decreases with age. However, a specimen from a

65 year old human can still demonstrate a maximum tensile strength of

about 900 newton (N), and is not necessarily ruptured or degenerately

altered (Rickert, et al. 1998). 

Supraspinatus tendinopathy

Definitions

Intrinsic supraspinatus tendinopathy is defined as tendon pathology that originates within the tendon, usually as a consequence of overuse or overload (including compression) (Lewis 2009). Hashimoto et al. have described similar degenerative changes as in other tendinopathies (Hashimoto, et al. 2003).

Epidemiology

Disorders of the shoulder rotator cuff are very common in the general

population and in overhead athletes. The incidence of shoulder pain in the

general population ranges from 6.6–25 cases per 1,000 persons, with a peak

incidence in those aged 45–64 years (van der Windt, et al. 1995). The annual

preval‎ence in the adult population in different countries is reported to range

between 20% and 51% (Hasvold, et al. 1993;Pope, et al. 1997). The

preval‎ence in swimmers has been shown to increase with the number of

swimming years, ranging from 3% up to 65% (Kennedy 1974;Bak 1996).

Recently, a study on elite swimmers showed that 69% suffered from

supraspinatus tendinopathy (Sein, et al. 2008). Questionnaire studies by

Fahlstrom et al. reported that among recreational and competitive

badminton players, 52% had previous or present shoulder pain on the

dominant side. Furthermore, the studies showed that persisting shoulder

pain during the playing season was found among 20% of competitive players

and among 16% of recreational players (Fahlstrom, et al. 2006;Fahlstrom, et

al. 2007).

Aetiology

Rotator cuff disease is the most common cause of shoulder pain, and is often explained by chronic overuse. However, the aetiology to rotator cuff injuries has not been clarified and appears to be multifactorial, related to primary changes within the tendon (intrinsic cause) and other structures in its environment (extrinsic causes) (Uhthoff, et al. 1997).

Intrinsic risk factors

 Age, joint laxity, and bony impingement due to the shape of acromion, have been linked to supraspinatus tendinopathy and subacromial

impingement (Neer 1972;Kannus 1997).  Muscle weakness of the rotator cuff muscles and pathological changes in the supraspinatus tendon due to overload (Nirschl 1989). Ogata et al, suggested that degeneration is the primary aetiological factor contributing to partial supraspinatus tears (Ogata, et al. 1990).

Extrinsic risk factors

 Overuse, such as excessive physical activity in high arm positions, and with high loads, is an important factor contributing to the development of tendon injury (Stenlund, et al. 1993). In a recently published study on swimmers, Sein et al. found that more than 15 hours of swim training per week increased the risk of developing supraspinatus tendinopathy (Sein, et al. 2008).

 Underuse or stress-shielding has lately been discussed as an aetiological

factor in supraspinatus tendinopathy. There is ongoing remodelling in the

normal tendon with degradation and rebuilding of tendon tissue. This

process is believed to be mediated by matrix metalloproteinases (MMPs) and

tissue inhibitor metalloproteinases (TIMPs). It has been suggested that

underload possibly causes the development of supraspinatus tendinopathy

by altering the remodelling process. Decreased expression‎ of MMP3, TIMP2,

and TIMP3 may contribute to tendon degeneration in sedentary individuals

(Lo, et al. 2004).

Pathogenesis

Two main theories, one vascular and one impingement theory, have been

used to explain why the supraspinatus tendon seems prone to degenerative

changes. The vascular theory suggests that a compromise of the vascular

supply may cause degeneration. Codman described a theory of a critical

zone in the supraspinatus tendon, near the distal end of the tendons

insertion into the humerus (ruptures were often seen in this area) (Codman

1934). Later, Rathbun reported poor vascularity in this critical zone, and

hypothesised that this could be the reason for degenerative changes

(Rathbun, et al. 1970). Other authors have supported this theory and also

suggested that the vascularity is poorer on the joint side compared to the

bursal side of the supraspinatus tendon (Lohr, et al. 1990).

It has been proposed that the high incidence of supraspinatus tendinopathy

could be a result of impingement in and around the critical zone of the

vascular supply (Luo, et al. 1998). Further, it has been suggested that this is

the primary cause of tendinopathy in the shoulder (Neer 1983). In the

shoulder, it is thought that the supraspinatus tendon impinges under the

anterior acromion during forward flexion of the shoulder, leading to  degeneration. The shape of the acromion has been linked to impingement of

the supraspinatus tendon. Three types of anatomical variations have been

described (Bigliani 1986): type I (flat), II (curved) and III (hooked), where

type III has been shown to be related to a high incidence of cuff tears (Neer

1972). The impingement theory has been challenged, Hyvonen et al.

suggested that acromioplasty does not prevent the progression of the

impingement syndrome into rotator cuff tears (Hyvonen, et al. 2003).

Furthermore, if impingement itself is causing rotator cuff tears at the later

stage of the disease, why do the majority of tears occur intrasubstance

and/or on the joint side when the compression occurs on the bursal side

(Ogata, et al. 1990).

Histology

 The histopathology of chronic painful supraspinatus tendinopathy is similar

to that of other insertional tendinopathies. The tendon shows mucoid

degeneration and fibrocartilaginous metaplasia, along with loss of the

characteristic parallel collagen bundles with separation and disorganisation

(Fukuda, et al. 1990;Hashimoto, et al. 2003). Hypervascularity and

neovascularisation of the degenerative rotator cuff have been reported by

Chansky et al, who concluded that the hypervascularity was an attempt to

repair or regenerate the lesion in the suprapinatus tendon (Chansky, et al.

1991).

Pain mechanisms

 Pain in the shoulder often decreases shoulder strength and causes impaired

function. The rotator cuff and subacromial bursa (SAB) are considered to be

the primary pain-producing structures. The SAB reduces friction during

shoulder movement and has been shown to provide the shoulder with

kinesthetic sense and mechanoreception (Ide, et al. 1996). Individuals with

pain during shoulder elevation have been shown to have high concentrations

of inflammatory, pain-mediating and matrix-modifying proteins, in the

bursa. This could have a catabolic effect on collagen (Voloshin, et al. 2005).

Also, a high concentration of SP in the bursa has been shown to be

correlated with pain (Gotoh, et al. 1998;Gotoh, et al. 2001;Yanagisawa, et al.

2001;Voloshin, et al. 2005). Using US and CD, high blood flow was found in

chronic painful, but not in pain-free, supraspinatus tendons. Pain relief has

been achieved from sclerosing polidocanol injections in the region with high

flow (bursa wall just outside the tendon) (Alfredson, et al. 2006). 

 Clinical symptoms

Patients with supraspinatus tendinopathy often describe the onset of their

pain symptoms as gradual. Pain after activity, especially overhead activity,

weakness, and fatigue in the shoulder muscles are common complaints. The

pain is usually dull and aching, commonly located at the anterior aspect of

the shoulder, and sometimes laterally in the upper humerus.

 Clinical examination

Based on the patient’s medical history, a physical examination should help to

clarify the diagnosis. It is important to also examine the neck carefully in

order to exclude abnormalities such as degenerative disease or nerve

entrapment. Examination should include an inspection of the scapular

motion and position (winging). Test of the active and passive range of

motion of the shoulder in all planes, as well as palpation of the rotator cuff,

the acromioclavicular joint (Ac-joint) and sternoclavicular joint (Sc-joint)

should always be included. Specific strength tests of the rotator cuff muscles

should be carried out. The examination can disclose pain and weakness but

also scapulothoracic dysfunction. Neers and Hawkins tests are examples of

traditionally used subacromial impingement sign tests (Hawkins, et al.

1980;Neer 1983).

 Differential diagnoses

Osteoarthrosis in the Ac-joint could cause similar pain symptoms as

subacromial impingement. Palpation of the joint and a cross-body adduction

test meant to provoke could reproduce pain in this area. Injection of a local

anaesthetic into the joint is helpful when trying to trace the pain. Cervical

radiculitis should be ruled out by using provocative tests and nerve stretch

tests. A superior labral anterior to posterior (SLAP) lesion could lead to

secondary impingement. One important difference is that the symptoms

often arise acutely, often following a trauma to the shoulder. Tests that are

commonly used include the O'Brien and the biceps load II test (O´Brien

1998;Kim, et al. 2001). Biceps pathology could be tested using Speed’s biceps

test (Bennett 1998). Glenohumeral instability is common in overhead

athletes and could lead to secondary impingement. Tests commonly used to

provoke instability include the apprehension and relocation tests (Speer, et

al. 1994;Tennent, et al. 2003). The Sulcus Sign for inferior instability is a

general laxity test and posterior instability is eval‎uated using the posterior

subluxation test (Tennent, et al. 2003). Partial or total ruptures of the

supraspinatus tendon are not uncommon in traumatic falls in middle-aged

and elderly individuals. These patients experience weakness and/or pain

during abduction of the shoulder. An US or MRI confirm‎s the clinical  diagnosis (Frost 2006). Adhesive capsulitis due to chronic inflammation and

fibrosis in the subsynovial layer of the shoulder capsule reduces the passive

and active range of motion (Frost 2006). Calcific tendonitis is a deposition of

calcium salts within the intact supraspinatus tendon. The patients have

severe pain anterolaterally, and movement of the shoulder joint aggravates

the pain. A plain radiography (x-ray) is useful to confirm‎ this diagnosis

(Frost 2006).

Treatment

 Many different conservative treatment methods for patients with

supraspinatus tendinopathy are used, the purpose is usually to decrease pain

and improve activity. However, many of these methods have not been

studied in proper scientific studies (Almekinders, et al. 1998).

Rest  is commonly used to avoid activities that aggravate symptoms

(Almekinders, et al. 1998).

ESWT  has shown promising results in patients with calcifying tendinitis,

but not for supraspinatus tendinopathy (Gerdesmeyer, et al. 2003).

Ultrasound  is used but there are no evidence for beneficial effects in

randomised controlled trials (Robertson, et al. 2001).

Low-level laser  is used as a treatment method, but has not been shown to

be effective (Basford 1995).

Topical glyceryl trinitrate patches . A well designed double-blind study

by Paoloni et al. showed promising results in patients with supraspinatus

tendinopathy (Paoloni, et al. 2005).

Strength training  and exercise programs are the mainstay for the

conservative treatment of patients with supraspinatus tendinopathy.

However, there is a lack of high quality research to support this (Michener,

et al. 2004). Exercise programs may include the following interventions:

range of motion, stretching and flexibility, and strengthening exercises. The

general recommendation for rehabilitation exercise for cuff tendinopathy is

that the exercise should be performed with a low range of motion, primarily

focusing on the depressor muscles like the subscapularis, infraspinatus and

teres minor, endeavouring to avoid exercising the deltoideus and

supraspinatus muscles. The exercise should be carried out within a pain-free

range of motion (Brewster, et al. 1993;Litchfield, et al. 1993;Morrison, et al.

1997). Some randomised controlled trials have investigated the effectiveness

of exercises (Brox, et al. 1993;Conroy, et al. 1998;Bang, et al. 2000;Ludewig,   et al. 2003;Walther, et al. 2004;Haahr, et al. 2005;Senbursa, et al.

2007;Lombardi, et al. 2008). Results from these studies show that exercise

is effective as pain reduction in patients with impingement syndrome.

Furthermore, home-based exercise was comparable to supervised exercise.

The study protocols vary a lot as regards to frequency, duration, load, and

type of exercise (Brox, et al. 1993;Bang, et al. 2000;Ludewig, et al.

2003;Haahr, et al. 2005;Senbursa, et al. 2007). Unfortunately, the type of

strength training used is often not described in detail (Haahr, et al.

2005;Senbursa, et al. 2007). Most studies used elastic bands as a resistant

tool for strength training (Bang, et al. 2000;Ludewig, et al. 2003;Walther, et

al. 2004;Senbursa, et al. 2007).

US and CD-guided sclerosing polidocanol injections  targeting the

region with high blood in the subacromial bursa wall just outside the

supraspinatus tendon have shown promising results in a pilot study

(Alfredson, et al. 2006).

Surgical  reports from subacromial decompression (acromioplasty) therapy

for impingement syndrome have shown a success rate of 80–90% (Burns, et

al. 1992;Checroun, et al. 1998;Chin, et al. 2007). However, these results have

been questioned. When comparing acromioplasty with physiotherapy

exercises, surgery was not clinically beneficial at 6, 12 or 48 months (Brox, et

al. 1993;Haahr, et al. 2005;Haahr, et al. 2006). According to Hyvonen et al.

acromioplasty does not prevent from progression of impingement syndrome

to a rotator cuff tear (Hyvonen, et al. 1998). 

General aims

The general aims of this thesis were to eval‎uate and modify painful eccentric

training as a treatment method for different chronic tendinopathies;

 Achilles tendinopathy (study I-II)

 Patellar tendinopathy (study III-IV)

 Supraspinatus tendinopathy (study V)