A patient with de Quervain's tenosynovitis: a case report using an Australian approach to manual therapy.

Phys Ther. 1994;74.-314-326.]

Key Words: De Quervain's tenosynovitis, Maitland, Manual therapy, Mobilization, Neural tension.

According to the Bureau of Labor Statistics, reporting of cumulative trauma disorders quintupled from 1977 to 1989.[1] De Quervain's disease, an inflammatory disorder that can be caused by cumulative injury, is one of the most commonly diagnosed problems seen by hand surgeons.[2] Carpal tunnel syndrome (CTS), also thought to be caused by cumulative trauma, is a major cause of lost workdays and workers' compensation in the United States.[3] De Quervain's disease and CTS can occur singly or in combination.[4-6] Common clinical presentations and diagnostic tests for de Quervain's disease and CTS will be briefly described in this case report. The purpose of this case study is to illustrate the interrelationship among examination, assessment, and treatment response in the Australian approach to manual therapy as pioneered by Maitland in the management of de Quervain's disease and CTS.[7]

Review of the Literature

Clinical Signs, Symptoms, and Pathophysiology of De Ouervain's Disease

De Quervain's tenosynovitis is classically associated with localized tenderness and swelling in the region of the styloid process of the radius and wrist pain radiating proximally into the forearm and distally into the thumb.[8.9] Other findings may include decreased abduction range of motion (ROM) of the carpometacarpal joint of the thumb, palpable thickening of the extensor sheath and of the tendons distal to the extensor tunnel, and crepitus of tendons moving through the extensor sheath.[5]

Pathophysiology and Diagnostic Tests

The abductor pollicis longus and extensor pollicis brevis tendons pass through the first dorsal compartment of the wrist beneath the extensor retinaculum and can angle sharply when the wrist is deviated radially.[10] Various repetitive pronation and supination movements of the forearm, ulnar and radial deviation of the wrist, and abduction/extension of the thumb have been described as movements that create stress on tendons passing through the extensor retinaculum.[9,11] Muckart[12] concluded that firm grip (eg, wringing a cloth) or finger-thumb grip combined with radial deviation of the wrist creates the greatest stress on the structures of the first dorsal compartment. This position causes the taut abductor pollicis longus tendon to apply a tensile force to the fibrous extensor retinaculum. The extensor retinaculum thickens to resist the strain, resulting in more pain and pressure.[11,12]

Determination of whether a patient has de Quervain's tenosynovitis is based on the location of the patient's pain and the presence of swelling in the hand and decreased hand function. Finkelstein's test[11] is also frequently used in the diagnosis. The patient is asked to place the thumb inside his of her closed fist. if the test is positive, passive or active ulnar deviation of the wrist then produces pain over the styloid process of the radius.

With de Quervain's tenosynovitis, there is potential for upper-extremity symptoms other than those involving the tendon.[13] These symptoms can result from the close proximity of the nerves, tendons, tendon sheaths, and fascia of the forearm to the site of inflammation. According to MacKinnon and Dellon,[13] when there is entrapment, tethering, or inflammation of the superficial radial nerve, a sensory nerve, an incorrect diagnosis of de Quervain's tenosynovitis can be made. In the forearm, the superficial radial nerve lies beneath the brachioradialis muscle. The superficial radial nerve courses between the forearm musculature and runs subcutaneously from the midportion of the forearm to an area adjacent to the styloid process of the radius. Rask[14] has indicated that inflammation of the tendons of the first dorsal compartment can result in superficial radial neuritis because of the close proximity of these structures. This results in pain, paresthesias, and numbness of the radial aspects of the hand and wrist. Rask[14] reported that as the tenosynovitis resolves, so will the radial neuritis, but at a slower rate.

The superficial radial nerve passes between the dense fascia of the forearm and the tendons of the brachioradialis and extensor carpi radialis longus muscles. The tendons can press on the nerve in a scissor-like fashion when the forearm is pronated, causing a proximal tethering, according to MacFinnon and Dellon,[13] on the distal segment of the nerve at the wrist. This tethering can lead to entrapment of the superficial radial nerve, causing pain patterns that can be mistaken for CTS or de Quervain's tenosynovitis. This condition may require surgery.[13]

Clinical Signs, Symptoms, and Pathophysiology of Carpal Tunnel Syndrome

Carpal tunnel syndrome is often seen as the cause of progressive numbness or paresthesia of the fingers in the median nerve distribution, nocturnal burning pain or hypesthesia, weakness of the hand, decreased dexterity, and numbness or pain that can radiate proximally.[15] The pathophysiology of CTS remains unknown, although mechanical and vascular factors are believed to play a major role.[17] Nine flexor tendons (four each from the flexor digitorum profundus and superficialis muscles and one from the flexor pollicis longus muscle) and the median nerve pass through the carpal tunnel under the transverse carpal ligament.[16] Alterations in the size of these structures such as occurs with inflammation, edema, or fascial scarring can affect the perineural vasculature. According to Sunderland,[17] this inflammatory process can result in a self-perpetuating cycle of hypoxia, impaired nerve fiber nutrition, and leakage of edema from damaged capillary endothelium. Fibroblastic proliferation secondary to chronic edema may result in intraneural fibrosis of the median nerve.

Several clinical tests are used to confirm the diagnosis of CTS. Tinel's sign is elicited by repeated light tapping over the carpal tunnel. Tinel's sign consists of a tingling in one or more digits in the median nerve distribution.

Phalen's test is performed by having the patient actively maintain maximal wrist flexion for 1 minute. Reproduction of paresthesia or hypesthesia along the median nerve distribution is considered diagnostic of CTS.[18] When symptoms have been present for several weeks or several months, electrodiagnostic testing may be used to differentiate CTS from other entrapment neuropathies and to assist in staging the disease.[19] Despite its common clinical use, nerve conduction velocity (NCV) testing has not shown consistent correlation with clinical findings of CTS.[20] Some patients with symptoms requiring surgery have been found to have normal NCVs.[21]

Consequences of Chronic Nerve Injury

Carpal tunnel syndrome is frequently associated with cervical spine disorders.[19,22,23] Upton and McComas[24] coined the term "double crush syndrome" to describe a process in which proximal compression of a nerve, involving disruption of the axoplasmic flow, could have an additive effect on the nerve, lessening its ability to withstand a more distal injury. Lundborg[25] described a "reverse double crush" that occurs when the distal injury occurs first. The association of de Quervain's tenosynovitis with superficial radial nerve entrapment[13] and their coexistence with more proximal syndromes such as tennis elbow6 lend support to the notion that a proximal or distal entrapment of a nerve may make the nerve more susceptible to subsequent injury.[24,25] Butler[26] argues that with any neuro-orthopedic disorder such as CTS, it is impossible to have only one structure injured or only one segment of a nerve injured. This may explain the confusing array of symptoms in patients with long-standing symptoms.

In order to assess the contribution of the cervical nerve roots and peripheral nerves to upper-extremity pain, Elvey[27] developed what he called the "brachioplexus tension test," later called the "upper-limb tension test (ULTT)."[28] The ULTT is designed to place tensile stress on the cervical nerve roots and their associated peripheral nerves by using a "longitudinal traction force."[28] With the patient lying supine, the ULTT consists of a series of joint movements applied to the shoulder girdle and upper limb. These movements will be described in detail in the case report. Butler[26] asserts that the ULTT assesses the mobility of neural tissues in relation to other "mechanical interfaces" (eg, the adjacent muscles, ligaments, bones, fasciae, and vascular tissues). Tendinous swelling, fascial scarring, or edema may constitute a "pathological mechanical interface" that could hamper the mobility of a peripheral nerve.[26]

Brieg[29] and Butler and Gifford[30] contend that nerve fibers can move in relation to their surrounding connective tissues (epineurium, perineurium, endoneurium), Intraneural movement, for example, could be affected by intraneural fibrosis or edema. Elvey[31] uses the term "adverse neural tissue tension" to describe restrictions in intraneural and extraneural mobility. There are no data relating test findings to the mechanism we have described, though the concept often guides clinical practice.

Theoretical Basis for the Use of Upper-Limb Tension Tests in Examination and Treatment

DeBuermann,[32] in 1884, demonstrated "marked nerve stretch" of the sciatic nerve in cadavers during a straight leg raise (SLR) and concluded that stretching of the nerve tissue was the cause of pain in the SLR. Other studies have attempted to measure excursion of the lumbosacral roots in cadavers when the trunk is flexed[33] and/or or during an SLR.[33.34]

Fajersztajn,[35] in 1896, suggested sensitizing or provoking further symptoms of sciatica by adding ankle dorsiflexion at the end of SLR in order to place additional traction or tension on the sciatic nerve. More recently, Brieg and Troup[36] suggested adding medial (internal) rotation of the hip to increase tension on the lumbosacral plexus.

The ULTTs of Elvey[27] and Butler[37] are designed to be tests for neural mobility, much like the SLR test for restriction of the sciatic nerve. Cadaver studies by Elvey[27] have confirmed movement of the brachial plexus when the ULTT is applied to the upper limb. Other studies[38-40] have demonstrated longitudinal sliding of median nerve and cervical nerve roots when the upper limb is moved. These studies provide support for the use of ULTTs in examination and treatment.

We believe the clinical findings of CTS and de Quervain's tenosynovitis reinforce the need for careful examination of cervical nerve roots and peripheral nerves because these neural structures traverse the fibrous retinaculum, pass through the deep fascia, and cross between muscles, and as a result decreased mobility of nerves[13] can occur. There are multiple sites in the upper quarter in which nerves can be susceptible to mechanical irritation or "friction fibrosis."[41]

Description of Upper-Limb Tension Tests

The radial nerve dominant test is a ULTT that is designed to place tensile stress on neural tissues of the upper limb along the course of the radial nerve. With the patient lying supine, the therapist applies the following motions sequentially to the patient's upper limb: shoulder girdle depression with approximately 10 degrees of shoulder abduction, elbow extension, medial rotation of the shoulder, pronation of the forearm, wrist and finger flexion, and ulnar deviation and further shoulder abduction.[26]

The median nerve dominant test is a ULTT that involves the application of shoulder girdle depression, shoulder abduction in the coronal plane to approximately 110 degrees, forearm supination, wrist and finger extension, shoulder lateral (external) rotation, and elbow extension. in applying each motion for the ULTT, the therapist is supposed to move the patient's limb through its available ROM until the therapist perceives tissue resistance and/or there is reproduction of the patient's symptom limiting the ROM that the limb can be moved through. Each position must be maintained while the next motion is applied.[26]

Kenneally et al[28] have suggested that the positions of the upper limb for the different tests place tensile stress on particular nerve structures. Butler26 argues that the complexity of the anatomy and joint axes of the upper limb prevents these ULTTs from being mutually exclusive from each other. For example, when the radial nerve dominant test is applied, nerve trunk, soft tissue, and joint structures are also having forces applied to them.

When ULTTs are administered, patients will normally demonstrate full joint ROM. The patients may report mild tingling along a nerve distribution (eg, along the radial nerve distribution for the radial nerve bias test). in general, reports of pain and comparing joint ROM with the opposite side are done with the ULTT in the same fashion as they are with the SLR.[28]

A tension test is considered positive if (1) it reproduces the patient's symptoms, (2) there is tissue resistance or a decrease in the ROM on one side of the body as compared with the other, (3) the patient's responses are different from what is expected for asymptomatic subjects, and (4) the test responses can be altered by a sensitizing maneuver that provokes an increase in symptoms. An example is when the patient's symptoms are worsened by movements that are generally away from the site of symptoms or restriction (eg, lateral flexion of the neck away from a limb on which the ULTT is being applied). Lateral flexion of the neck increases the tension on the cervical nerve roots and peripheral nerve trunks of the upper limb.[26]

The use of ULTTs in musculoskeletal examination is relatively new to physical therapists. Studies on the validity of ULTTs[42] and normative data on ULTT subjective responses[28,43] have been described, but largely in symposium proceedings. The ULTTs are also used to treat problems of restricted mobility of neural tissues by selectively utilizing components of the ULTT that provoke the patient's pain.[44,45]

Research studies that include patient groups and research designs for testing the reliability and validity of the findings of ULTTs are needed. The literature is currently devoid of such research.

Case Study

In the following case study, we will demonstrate how we used theoretical knowledge and clinical experience to develop an effective treatment plan for a patient who initially had de Quervain's tensynovitis and symptoms that later progressed proximally to involve other structures in the upper quarter.

Interview Data

The patient was referred for physical therapy with the diagnoses of possible left de Quervain's tenosynovitis and possible left CTS. Symptoms started 6 years previous to the referral as a dull pain in the palmar aspect of the patient's left wrist, with occasional numbness in her fingers. The patient was a 41-year-old right-handed bookkeeper. At work in the morning, she sat at a desk and rotated her upper trunk toward a table on her left to count bills and receipts with her left hand. This task required repetitive pronation and supination movements of her left hand. In the afternoon, she used a computer keyboard. She had no hobbies, but did routine housework and cooking for herself and husband. We believe that this routine indicated that the patient's symptoms were work-related.

The patient was asked to describe her symptoms. Maitland[46] describes the "subjective examination" as the patient relating his or her account of his or her complaints and previous history through the therapist's interview. The use of the term "subjective" by Maitland is different from that generally agreed on by measurement experts.[47] The area, depth (superficial versus deep), and constancy of symptoms (ie, pain, tightness, and paresthesia) were represented on a body chart (Fig. 1). Her symptoms were an occasional ache and tightness over the left scapula, a band of pain near the deltoid insertion, sharp shooting pain from the wrist and thumb into the left forearm, and numbness and tingling in the fingers. The body chart is used by the therapist to describe the patient's problems and enables the therapist to formulate an initial working hypothesis as to the most probable cause(s) of the patient's symptoms. This working hypothesis enables the therapist to frame further questions regarding how the "behavior of symptoms" relates to the patient's activities and positions (eg, arm movements, sleeping, sitting). The therapist notes what aggravates and eases the patient's symptoms in addition to the onset, intensity, and location of the symptoms (ie, whether pain is local or referred.)

We believe that by determining how symptoms change over a 24-hour period, we can decide whether there are musculoskeletal components that can be treated with manual therapy. The severity (intensity of symptoms) and the irritability of the condition are also evaluated, Irritability, according to Maitland,[46] is the amount of activity required to provoke symptoms. Irritability also reflects the intensity of those symptoms and the time it takes for the symptoms to return to the resting or nonaggravated level. Severity and irritability set limits on how much physical examination and treatment a patient can tolerate in a session. The assessment of severity and irritability is based on the therapist's interpretation of the patient's report or perception of his or her symptoms. In our view, information regarding symptom behavior establishes a level with which progress can be measured.

The patient in this case study complained of a constant, deep left wrist pain that radiated anteriorly up the forearm to the cubital fossa. After flipping and filing pages or counting bills with her left hand for half an hour, her wrist would throb and give occasional sharp, shooting pains to the cubital fossa. There was intermittent sharp, shooting pain at the carpometacarpal joint of the thumb, radiating proximally along the lateral aspect of the radius of the mid-forearm. She reported needing to stop for 5 to 10 minutes to alleviate the shooting pain. She needed to stop every half hour for relief of symptoms.

There was an intermittent band of throbbing pain approximately 2.5 cm (1 in) wide around one half the circumference of her arm laterally at the level of the deltoid muscle insertion. At work, the band of pain occurred when the wrist pain increased and radiated up the forearm. The patient reported experiencing no decreased mobility of the shoulder girdle except a sensation of "tightness" over the supraspinous fossa and across the base of the left scapula when putting her arm behind her back to fasten her bra in the morning. Her shoulder pain also occurred in the afternoon while she was at the computer, especially when she had a busy schedule. She did not report pain or restriction of cervical movements.

The patient reported a reduction in symptoms when she did not use her arm or after she took Naprosyn[R]* (275 mg). She had worn a splint at night for 3 years prior to her being seen by a physical therapist. The splint appeared to reduce the wrist pain. The patient reported a throbbing sensation in her entire upper extremity before she fell asleep. She stated she would awaken every night between midnight and 1 am with tingling and numbness in her hand, but that she was able to return to sleep within 15 minutes after shaking her hand and fingers for a few minutes.

The patient reported that in the morning her only symptom was the constant, deep wrist pain radiating up to the cubital fossa. She did not describe any sensation of stiffness in the shoulder girdle and upper extremity. She said that by the end of most afternoons her shoulder girdle and upper extremity ached. The patient also reported that her wrist ached on weekends, when she was inactive. She complained that her hand and arm felt "weak" when gripping pot handles.

Previous History

Maitland[46] contends that by collecting information about the onset of different symptoms during the latter part of the interview, the physical therapist can determine the sequence in which structures became involved in the clinical presentation. This information, according to Maitland, contributes to a further understanding of the pathology of the condition and its stage (ie, whether the condition is acute, chronic, stable, or deteriorating).

After the onset of this patient's symptoms (ie, dull wrist ache and numbness in the fingers, which developed 6 years previous to seeing a physical therapist), she worked her normal hours for 3 months. Because the patient's condition was not improving, she went to a physician, who told her that she had a "wrist sprain." The prescribed treatment was to again wear a neutral-position splint at night, to take 275 mg of Naprosyn[R] as needed, and to take 2 days off work. In addition, the sitting position of turning to the left to count money and flip pages was adjusted to enable her to work directly in front of herself As a result of following this regimen, she became essentially symptom-free.

Three years after being given the splint, the patient's symptoms recurred. At that time, she reported having a constant, deep ache in her wrist and numbness and tingling in her fingers. The pain was worse than in the previous episode. Another physician diagnosed her condition as CTS and muscle strain, and she was given the same type of splint. This splint held her wrist in a neutral position. She was instructed to use the splint as, needed on the job. All symptoms decreased, although she was not symptom-free. During busy weeks at work, however, her symptoms throughout the upper extremity would return.

The patient continued working as a bookkeeper. A year before the patient went to a therapist, her wrist pain had increased to the point at which it radiated proximally to the elbow. An ache at the deltoid muscle insertion was felt and was diagnosed as "arm strain" by another physician. She was given a sling and told to wear it for 2 weeks. This led to a decrease in all arm symptoms. The patient could not describe the sling but said that while wearing it, she developed severe neck pain that spread over her scapula. She was unaware of any restriction in cervical spine movements during that period.

The patient remained without treatment until her employer referred her to an industrial orthopedist nearly 1 1/2 years later. The orthopedist examined her neck, shoulder, elbow, and arm. Nerve conduction velocity tests were within normal limits. She was referred to physical therapy for stretching and strengthening of the upper quarter.

Physical Examination Data

At the completion of the interview, our working hypotheses for this woman's symptoms were (1) a wrist problem, including possible degenerative changes (early osteoarthrosis) at the wrist, thumb pathology, and CTS, and (2) a superimposed cervical component, possibly from wearing the sling. The band of pain around the deltoid muscle insertion could have been from a glenohumeral problem[46] or interrelated with the other symptoms. Based on data from the interview, initial working hypotheses were generated. These hypotheses are summarized in Table 1.

[TABULAR DATA 1 OMITTED]

Because the patient demonstrated a complex array of symptoms, multiple areas of the upper quarter were examined. We used what Maitland[46] calls "comparable movement signs" to monitor the patient's progress during treatment. Abnormal active, passive, or functional movements that reproduce the patient's complaints or appear to be related to the patient's symptoms are referred to as comparable signs. Abnormal movements can be loss of physiological or accessory ROM because of pain, stiffness, or muscle spasm in a structure that appears related to the patient's symptoms.

Range-of-motion measurements for selected extremity joints were taken by one therapist, using a universal goniometer. Readings were taken to the nearest 5-degree increments. Reliability of goniometric ROM readings was not assessed. Cervical ROM was determined by visual inspection. Mobility assessments included the assessment of "end-feel" or the resistance of tissues at the end of the available passive range of motion (PROM).

Sitting posture. The patient had a slight head-forward posture, an increased kyphosis at C-7/T-1, and rounded shoulders. The general impression was one of tightness (adaptive muscle shortening) and inability to relax the cervical spine and shoulder girdle with the left upper trapezius muscle elevated. The patient's symptoms in this position were minimal wrist and scapular ache.

Cervical range of motion. The patient was unable to complete axial extension of the cervical spine to neutral (dorsal glide) because of a sensation of "stiffness" and central C-7 pain over the spinous process. Active cervical rotation to the left was 70 degrees according to visual inspection. When overpressure[7] (firm pressure producing oscillatory movements at the limit of ROM) was applied passively, the left rotation remained at 70 degrees with a stiff end-feel. There was no change in the symptoms when the patient was resting. Rotation to the right was pain-free according to the patient, and there was full ROM as determined by visual inspection and overpressure.

Shoulder. Active shoulder abduction, flexion, and rotation were pain-free according to the patient, and there was full ROM as observed by the examiner. In response to the glenohumeral quadrant maneuver on the left, the patient reported a "pulling sensation" at the elbow. This glenohumeral quadrant maneuver is described by Maitland[46] as a passive movement test designed to maximally stress the shoulder girdle to reveal minimal signs (ie, abnormality of movement, pain, or stiffness), The arm is placed in approximately 130 degrees of abduction and flexion, with the forearm in 90 degrees of elbow flexion. The arm is then rotated medially and laterally to reproduce pain or assess limitation of movement comparable to the patient's complaints (Fig. 2). Routine isometric tests- for the rotator-cuff musculature (shoulder abductors, medial and lateral rotators, and biceps) were pain-free.

Elbow. All active ranges of motion (AROMs) were considered full as determined by visual inspection with overpressure.

Wrist. The left wrist displayed weakness throughout the range of flexion and extension based on a manual muscle test (MMT)[49] grade of 4/5 for both movements.

There was increased pain across the carpal joints when the patient gripped the therapist's middle three fingers. Active wrist flexion with overpressure was 60 degrees and extension was 50 degrees of ROM, and a sharp pain in the region of the carpal bones was reproduced at the end-range of these tests. Tests of accessory movements of the carpal bones, especially the lunate and capitate, resulted in crepitus and decreased mobility. The patient's wrist ache was reproduced.

Phalen's test was not performed because of the patient's limited wrist ROM. Finkelstein's test elicited a sharp, shooting pain that radiated proximally along the radius from the carpometacarpal joint of the thumb. Deltoid and biceps brachii muscle strength were both diminished to an MMT grade[49] of 4/5. Deep tendon reflexes (ie, biceps brachii, triceps brachii, and flexor digitorum longus) and sensation in the upper limb were intact, Tinel's testing at the left wrist elicited a tingling sensation into the hand.

Upper-limb tension test. The median and radial nerve dominant ULTTs described by Butler[26] were used to assess the mobility of neural structures in the patient's left arm. In the median nerve dominant test (Fig. 3), the patient was restricted to 45 degrees of elbow extension, with wrist extension limited to 45 degrees. The application of this ULTT requires the therapist to use both hands to maintain all components of the test; therefore, goniometric measurements were not taken and angles were estimated. When the patient's head was laterally flexed to the right (presumably adding tension to the neural tissues from the cervical spine to the upper limb), she experienced an increase in sharp pain in her left wrist. The pain was relieved by left lateral neck flexion. This change in distal symptoms produced by the patient's head movements suggested to us that there may be impaired mobility of neural tissues. We believe this provides the therapist with a justification to examine areas with structures capable of referring pain into that area.26

When the radial nerve dominant test was applied to the patient's left upper extremity, the test was modified by placing the shoulder girdle and elbow in the normal test positions, with the patient's hand in the Finkelstein's test position (Fig. 4). The maneuver resulted in a positive test result. The thumb pain increased sharply, and pain in the deltoid muscle also occurred. Both thumb pain and deltoid muscle pain became worse when the patient attempted to laterally flex her head to the right. The pain was relieved by left lateral flexion. A positive response in this test position (ie, increased pain and restriction of movement) suggested to us that the patient, in addition to having a problem tendon at her wrist, also had decreased mobility of neural tissues that contributed to her symptoms.

Palpation. The patient found it difficult to relax her cervical and upper thoracic musculature because of a sensation of "tightness" in these areas. Central posteroanterior (PA) accessory intervertebal movements with the thumb tips over the spinous processes[7] of C-5 to T-6 showed that these segments were prominent (posterior to the expected normal lordosis of the cervical spine) and demonstrated marked resistance to thumb pressure. Left unilateral pressures[7] over the apophyseal joints at these levels also were painful and indicated that there was resistance to movement. The right side was asymptomatic.

Our conclusions at the end of the examination supported our initial working hypotheses, and we expanded the hypotheses (Tab. 2). The structures that appeared to be involved were (1) the carpal bones of the left wrist, (2) the tendons of the first dorsal compartment (suggesting de Quervain's syndrome), (3) the flexor tendons and retinaculum of the wrist (suggesting possible CTS), (4) the glenohumeral joint, (5) the C-5 to C-7 spinal segments, and (6) the neural tissues. We believe there was strong evidence of extra neural and intraneural components to the problem, as suggested by the positive response to the ULTTs.

The patient's functional limitations were that she was working with pain, and at home she was unable to vacuum and lift heavy pots. She needed to work for financial reasons, and she appeared to be stoic and have good pain tolerance. Her employer was cooperative and helped with ergonomic changes in her work situation. Her work space was changed so that she no longer had to rotate her trunk to count bills, and her keyboard position was adjusted to support her wrists.

An assessment of her overall prognosis needed to be made so that a realistic treatment plan could be formulated. The patient had the problem for 6 years, and the condition appeared to have worsened over this period to incorporate many interrelated structures. She had continued to work with limited physical therapy intervention. Because we believed her problem was multifactoral and because her symptoms continued to be aggravated by activities at work, treatment over several months was anticipated. We expected that the patient's symptoms would be exacerbated by excessive activity.

Treatment Plan

The physical therapy goals were (1) to decrease wrist and deltoid muscle pain, (2) to increase cervical and thoracic mobility, and (3) to restore mobility of neural tissues. The overall functional goal of the physical therapy was to enable the patient to be pain-free at work.

There were two options at the beginning of treatment. One option was to begin treatment distally at the hand and focus treatment on the individual signs and understood pathology: Finkelstein's test and the decreased mobility at the wrist. The other option was to look for patterns of symptoms in the musculoskeletal system and treat several bony or soft tissue structures in one area, starting in the vertebral column to determine how groups of symptoms change.

A "pattern-recognition" approach is the foundation of the Australian approach to manual therapy. By beginning treatment centrally (ie, at the cervical and thoracic spines) to restore mobility to the dorsal glide and left rotation restriction, the therapist would anticipate changes in some distal signs and symptoms (eg, band of pain at the deltoid muscle insertion, wrist problem). This approach will provide information to the therapist as to what portion of the patient's symptoms can be changed by treating centrally and what portion will require treatment of peripheral structures. Thus, after treating the cervical and thoracic spine, the plan was to add treatments to other symptomatic areas: the wrist and thumb, the tight muscles in the upper quarter, and finally the neural tissues throughout the upper quarter.

Treatment

The patient was treated three times in the first week with mobilization (both central and left unilateral PA accessory movements)[7] to the lower cervical (C-5 to C-7) and upper thoracic (to T-6) spines. She reported a decrease in the general arm ache and stated her left wrist pain that radiated anteriorly up the forearm was absent for up to 4 hours per day. The intermittent numbness in her thumb and fingers was no longer present. The sharp local pain in the thumb returned while working but did not radiate proximally along the lateral radius. There was no pain at night, and she reported no longer wearing the splint.

Based on our visual inspection, we noted left cervical rotation increased to 90 degrees and the patient was able to dorsal glide her cervical spine to neutral. There was decreased tightness and less pain with the glenohumeral quadrant maneuver. There was minimal change in findings with the ULTTs. Finkelstein's test reproduced local pain only. The patient's deep wrist pain, which radiated anteriorly to the cubital fossa, was no longer present. Wrist flexion and extension ROM improved to 70 and 60 degrees, respectively, with goniometric measurements. The PA accessory movements of the lunate and capitate were less restricted.

We believe the identified changes confirmed our hypothesis that there was a central cause for the patient's constant deep wrist pain that radiated anteriorly to the cubital fossa and for the decreased wrist mobility. The sharp pain in the thumb was only partially related to cervical structures. The presence of de Quervain's tenosynovitis became evident. Similarly, we believed that the decreased wrist mobility was also related to degenerative changes at the wrist. The cause of the band of pain around the deltoid muscle insertion remained unclear,

After the initial improvement in the patient's symptoms following 1 week of treatment applied to the cervical and thoracic spines, the therapist added treatment to other areas. At week 2, mobilization of the carpal bones utilizing PA and anteroposterior accessory movements on the capitate and lunate were incorporated; this treatment brought wrist fiexion and extension to full ROM. Gentle transverse friction[48] Was applied to the abductor pollicis longus and extensor pollicis brevis tendons. The superficial radial nerve at the wrist was mobilized by gently pulling a thumbnail across the region where the nerve passed. Following this combination of treatment to the wrist area, Finkelstein's test was no longer positive in the wrist area, indicating that de Quervain's tenosynovitis had resolved.

The tightness in the patient's upper-quarter musculature was treated by stretching the upper trapezius, scalenus, biceps brachii, and triceps brachii muscles with hold-relax techniques, Soft tissue massage techniques were applied to muscles along the course of the median and radial nerves in an attempt to restore normal mobility between interfacing neural and muscular tissue.[26] To increase the vigor of the treatment, these muscle groups were stretched utilizing the ULTT positions.

Treatment was directed toward mobilizing the interfaces between muscles and nerves by the therapist pulling her index finger pad across the region of the nerve at easily accessible sites (ie, the distal axilla, the spiral groove in the humerus, the cubital fossa, and the forearm above the wrist). When the radial nerve was mobilized along the spiral groove of the humerus, the patient had an exacerbation of wrist symptoms and severe deltoid muscle pain for 5 days. In our view, this outcome confirmed the hypothesis that the deltoid muscle pain was related to the neural tissues. Furthermore, this result led us to eliminate any possibility of glenohumeral involvement.

When the patient's deltoid muscle and wrist symptoms returned to their resting level, neural tissues of the upper quarter were mobilized in the ULTT positions and a self-mobilizing program[26] was designed for her to carry out at home. With the patient's arms by her side, the therapist instructed her to depress her shoulder girdle, then gently flex and extend her elbows and wrists. For ease of coordination, this movement was performed bilaterally. Later, when able to tolerate this activity without symptoms, these stretches were progressed to the shoulders, with the shoulders abducted to 90 degrees. This movement was done in a pain-free ROM and to tolerance. Later, strengthening exercises for the interscapular musculature were included to help her postural endurance while sitting at work. These exercises were cervical and scapular retraction while the patient was positioned supine over a green "Gymnastik Ball." The exercises were performed morning and night in groups of 10 repetitions and were only partially successful because repetition with light resistance exacerbated her arm ache.

Results of Treatment

The patient was treated three times per week for 3 months, two times per week for 2 months, and once weekly for 1 month. A physician reviewed the patient's progress every 6 weeks and prescribed continuation of physical therapy because of the favorable responses to treatment. Despite the extended period of physical therapy, the therapist considered intervention to be cost effective because the patient was able to continue uninterrupted full-time employment while her symptoms improved. The rate and progression of treatment were governed by the fact that structures involved in the upper quarter could not tolerate aggressive treatment.

Over the 6-month period of treatment, the patient's symptoms varied, but she reported improvement over time rather than at each treatment session. Table 3 summarizes the status of the patient's signs and symptoms before and after treatment. When discharged, she reported having no pain at night, no wrist and hand pain, no numbness, and no sharp pain in the thumb or radiating pain up the lateral aspect of the radius. The pain in the deltoid muscle remained the most resistant to change, with exacerbations occurring for no identifiable reason. The patient reported she was still unable to vacuum or lift heavy pots because of weakness.

[TABULAR DATA 3 OMITTED]

After the first week of treatment, active cervical rotation to the left was pain-free and full. The glenohumeral quadrant, which is used to assess end-range shoulder girdle mobility, remained tight. Wrist flexion and extension were full, with a springy, tight end-feel. This finding suggested to us a secondary change resulting from a chronic problem, Accessory movements of the carpal bones were full and pain-free.

The ULTT, radial nerve dominant test was pain-free, with tightness and a pulling sensation radiating from the deltoid muscle down the patient's arm at end-range. The previous sharp thumb pain was now gone. The ULTT, the median nerve dominant test was 30 degrees of elbow extension, with a pulling sensation to the wrist. This residual restriction in ULTT was expected because of the chronicity of the patient's problems and involvement of soft tissue structures throughout the upper quarter.

Discussion

Physical therapists frequently treat patients who have a diagnosis of de Quervain's tenosynovitis or CTS. The importance of this case study lies in the therapists' analysis of signs and symptoms to implement treatment and to obtain a response that dictated the direction of future treatments.

After the patient interviews, the initial working hypothesis was that the patient had a wrist problem, a cervical problem, and a possible glenohumeral problem. By focusing treatment on the cervical spine, information was gained on the relationship between the cervical area, the shoulder girdle, and the wrist-thumb complex.

We believe the improvement in cervical ROM, the decrease in arm ache, the presence of periods without wrist and thumb pain, and the increase in carpal joint mobility supported the effectiveness of cervical treatment and the hypothesis of a cervical component of the patient's problem. We contend that loss of mobility of carpal bones was partially reduced by treatment of the cervical spine. The residual stiffness decreased further following treatment involving carpal accessory movements. After treatment of the cervical region, numbness and tingling in the fingers also disappeared, which suggested to us that the carpal tunnel symptoms were from structures other than those under the flexor retinaculum. We therefore rejected the hypothesis of possible CTS.

Symptoms that did not respond to cervical mobilization were addressed directly. The treatment plan was progressed to focus on wrist joints and tendons and on the superficial radial nerve at the wrist and thumb. The patient's favorable response to treatment, in our view, confirmed the working hypothesis that pain was caused by involvement of the first dorsal compartment tendons and possible superficial radial neuritis.

The tightness and muscle guarding in the upper quarter and positive ULTT response were addressed first by muscle stretching and soft tissue massage, and finally by mobilizing the neural tissues, utilizing various components of the ULTTs. The positive responses to ULTTs at discharge suggested a mild residual restriction of neural tissue mobility. A self-mobilizing and strengthening program was given at discharge to assist the patient in maintaining the gains achieved.

Summary and Conclusion

The patient had a wrist problem, starting 6 years previous to our seeing her, that deteriorated over time to incorporate multiple structures throughout the upper quarter. When discharged, the patient achieved considerable reduction of symptoms but was not symptom-free. We contend that patients with multiple musculoskeletal problems may have diagnoses that sometimes can be inadequate or incorrect, causing the physical therapist to inadvertently limit the scope of the examination and treatment. The Australian approach to manual therapy we described provides, in our opinion, a systematic process for identifying the working hypotheses and using treatment to continually reassess and confirm or reject these hypotheses.

We believe that if the patient in this case study had been treated only for the de Quervain's syndrome, only some of her functional problems would have been addressed. In patients with chronic musculoskeletal problems, we contend that focusing on patterns of signs and symptoms throughout the upper quarter and responding to emerging data from the patient enable the physical therapist to develop an effective treatment strategy for addressing multiple structures.

The Australian approach we described is one of several manual therapy approaches to examination and treatment of patients with musculoskeletal dysfunction. Physical therapists should recognize that the efficacy of this approach still needs to be studied and compared with that of other manual therapy approaches.

[TABULAR DATA 2 OMITTED]

References

[1] Bureau of Labor Statistics Reports on Survey of Occupational Injuries and Illnesses in 1977-1989. Cited in: Rempel D, Barnhardt S, Harrison R. Work-related cumulative trauma disorders of the upper extremity. JAMA. 1992;267: 838-842. [2] Otto N, Wehbe MA. Sleroid injections for tenosynovitis in the hand. Orthop Rev. 1986;15: 45-48. [3] Cummings K, Maizlish N, Rudolph L, et al. Occupational disease surveillance: carpal tunnel syndrome. MMWR. 1989;38:485-489. [4] Lipscomb PR. Tenosynovitis of hand and the wrist: carpal tunnel syndrome and de Quervain's. Clin Orthop, 1959;13:158-164, [5] Arons MS. De Quervain's release in working women: report of failures, complications, and associated diagnoses. J Hand Surg [Am]. 1987; 12:540-544. [6] Phalen GS. Stenosing tenosynovitis: trigger finger and trigger thumb, de Quervain's disease, acute, calcification in wrist and hand. In: Flynn JE, ed, Hand Surgery 3rd ed. Baltimore, Md: Williams & Wilkins; 1982:489-499. [7] Maitland GD, Vertebral Manipulation. London, England: Butterworth & Co (Publishers) Ltd; 1964, [8] Reid DAC, McGrouther DA. Surgery of the Thumb. London, England: Butterworth & Co (Publishers) Ltd; 1986:210-212. [9] Lamb DW, Hooper G, Kuczynski K. Practice of Hand Surgery. 2nd ed. London, England: Blackwell Scientific Publications Ltd; 1989. [10] Lapidus PW, Fenton R. Stenosing tenovaginitis at the wrist and fingers: report of 423 cases in 269 patients, Arch Surg. 1952;64:475-487. [11] Finkelstein H. Stenosing tendovaginitis at the radial styloid process. J Bone Joint Surg. 1930;12:509-540. [12] Muckart RD. Stenosing tendovaginitis of abductor pollicis brevis at the radial styloid (de Quervain's disease). Clin Orthop, 1964;33: 201-208 [13] MacKinnon EJ, Dellon AL. Surgery of the Peripheral Nerve. New York, NY: Thieme Medical Publishers Inc; 1988:149-166, 275-304, [14] Rask MR. Superficial radial neuritis and de Quervain's disease. Clin Orthop. 1979;131:176-178. [15] Ditmars DM, Houin HP. Carpal tunnel syndrome, Hand Clin. 1986;2:525-531. [16] Conolly WB. Color Allas of Treatment of Carpal Tunnel Syndrome. Oradell, NJ: Medical Economics Books; 1982:8-9. [17] Sunderland S. Nerve lesions in carpal tunnel syndrome. J Neurol Neurosurg Psychiatry, 1976;39:615-626. [18] Phalen GS. Spontaneous compression of the median nerve at the wrist. JAMA. 1951;145: 1128-1133. [19] Dawson DM, Hallett M, Millender LH. Entrapment Neuropathies. Boston, Mass: Little, Brown & Co Inc; 1983;20:36-37. [20] Spindler HA, Dellon AL. Nerve conduction studies and sensibility testing in carpal tunnel syndrome. J Hand Surg 1982;7:260-263. [21] Grundberg AB. Carpal tunnel decompression in spite of normal electromyography. J Hand Surg. 1983;8:348-349. [22] Hurst LC, Weissberg D, Carroll RE, The relationship of double crush to carpal tunnel syndrome (an analysis of 1,000 cases of carpal tunnel syndrome). J Hand Surg. 1985; 10:202-204. [23] Pfeffer G, Osterman AL, Double crush syndrome: cervical radiculopathy and carpal tunnel syndrome. J Hand Surg [Am]. 1986; 11:766. Abstract. [24] Upton AR, McComas AJ. The double crush in nerve entrapment syndromes. Lancet. 1973; 2:359-362. [25] Lundborg G. Nerve Injury and Repair, Edinburgh, Scotland: Churchill Livingstone; 1988. [26] Butler DS. Mobilisation of the Nervous System, New York, NY: Churchill Livingstone Inc; 1991:35-52, 65-68, 147-181, 185-210 [27] Elvey RL. Brachial plexus tension tests and the pathoanatoniical origin of arm pain, In: Glasgow EF, Twomey LT, eds. Aspects of Manipulative Therapy, Melbourne, Victoria, Australia: Lincoln Institute of Health Sciences; 1979:105-110 [28] Kenneally M, Rubenach H, Elvey RL. The upper limb tension test: the SLR test of the arm. In: Grant R, ed. Physical Therapy of the Cervical and Thoracic Spine. Edinburgh, Scotland: Churchill Livingstone; 1988. [29] Brieg A. Adverse Mechanical Tension in the Nervous System. Stockholm, Sweden: Almqvist och Wiksell Forlas; 1978, [30] Butler DS, Gifford L. The concept of adverse mechanical tension in the nervous system, part 1: testing for dural tension. Australian Journal of Physiotherapy, 1989:75:623-626. [31] Elvey RL. Treatment of arm pain associated with abnormal brachial plexus tension. Australian Journal of Physiotherapy, 1986:32:225-230. [32] DeBuermann. Cited in: Woodall B. Hayes G. The well leg raising test of Fajersztajn in the diagnosis of ruptured intervertebral disc. J Bone Joint Surg [Am). 1950;32:786-792. [33] Inman V, Saunders J, The clinico-anitomical aspects of the lumbosacral region, Radiology. 1942;38:669-678. [34] Goddard MD, Reid JD. Movements induced by straight leg raising in the lumbosacral roots, nerves and plexus and in the intrapelvic section of the sciatic nerve. J Neurol Neurosurg Psychatry. 1965;28:12-17. [35] Faiersztajn J. Cited in: Woodall B, Hayes G. The well leg raising test of Faiersztajn in the diagnosis of ruptured intervertebral disc. J Bone Joint Surg [Am]. 1950;32:786-792. [36] Brieg A, Troup J. Biomechanical considerations in the straight leg raising test, Spine. 1979;4:242-250. [37] Butler DS. Adverse mechanical tension in the nervous system: application to repetition strain injury. In: Proceedings of the Fifth Biennial Conference of the it Manipulative Therapists Association of Australia, Melbourne, Australia. 1987:247-270. [38] McLellan DL. Longitudinal sliding of the median nerve during hand movements: a contributory factor in entrapment neuropathy. Lancet. 1975;1:633-634. [39] McLellan DL, Swash M. Longitudinal sliding of the median nerve during movements of the upper limb. J Neurol Neurosurg Psychiatry 1976;39:566-570. [40] Wilgis EF, Murphy R. The significance of longitudinal excursion in peripheral nerves. Hand Clin. 1986;2:761-766. [41] Sunderland S. Nerves and Nerve Injuries. 2nd ed. London, England: Churchill Livingstone; 1978:151-157. [42] Selvaratnam P. The discriminative validity of the brachial plexus tension test. In: Proceedings of the Fifth Biennial Conference of the Manipulative Therapists Association of Australia, Melbourne, Australia. 1987:325-350. [43] Yaxley GA, Kull GA. A modified upper limb tension test: an investigation of responses in normal subjects, Australian Journal of Physiotherapy, 1991;37:143-152. [44] Butler DS. Adverse mechanical tension in the nervous system: a model for assessment and treatment. Australian Journal of Physiotherapy. 1989;35:227-238. [45] Elvey RL. Treatment of conditions accompanied by signs of abnormal brachial plexus tension. In: Proceedings of the Fourth Biennial Conference of the Manipulative Therapists Association of Australia, Brisbane, Australia. 1983:53-65. [46] Maitland GD. Peripheral Manipulation. 3rd ed. Boston, Mass: Butterworth-Heinemann; 1991. [47] Task Force on Standards for Measurement in Physical Therapy. Standards for tests and measurements in physical therapy practice. Phys Ther, 1991:71:589-622. [48] Cyriax JH. Textbook of Orthopaedic Medicine, Volume I.- Diagnosis and Soft Tissue Lesions. 7th ed. London, England: Bailliere Tindall; 1978. [49] Medical Research Council. Aids to the Investigation of Peripheral Nerve Injuries: War Memorandum No. 7 2nd rev ed. London, England: His Majesty's Stationary Office; 1943. [50] Grant R, Jones M, Maitland G. Clinical decision making in upper quadrant dysfunction. In: Grant R, ed. Physical Therapy of the Cervical and Thoracic Spine, New York, NY: Churchill Livingstone Inc; 1988:51-80.

M Anderson, PT, is Private Practitioner, Marin Orthopedic Rehabilitation, Mill Valley, CA 94941, a Senior Faculty Member, Kaiser Permanente-Hayward, Physical Therapy Residency Program in Advanced Orthopedic Manual therapy, 27400 Hesperian blvd, Hayward, Ca 94545.

CJ Tichenor, PT, is Director, Kaiser Permanente-Hayward, Physical Therapy Residency Program in Advanced Orthopedic Manual Therapy, 27400 Hesperian Blvd, Hayward, CA 94545 (USA). Address all correspondence to Ms Tichenor.

This article was submitted August 30, 1993, and was accepted November 8, 1993.