Shoulder Pain

To Operate or Not to Operate?

Jeremy Lewis, Eric J. Hegedus, Mark A. Jones

Appointment 1

Alison was referred by a sports and exercise medicine consultant for assessment and management of a recalcitrant right shoulder problem. Alison is a 48-year-old high school teacher who is married and has three teenage children. She was educated to university level, having obtained an undergraduate degree in history. She reported that she sits for approximately 8 hours per day (in total), and until the recent episode of pain, participated in exercise an average of three to four times each week. Her exercises consisted of cardiac and strength training at the gym, walking, gardening, occasional outdoor bicycling and a passion for playing social tennis.

Area and Behaviour of Symptoms

Alison described that she experienced symptoms as per the body chart (Fig. 17.1).

No paraesthesia or numbness was experienced in either the upper or lower limbs. No headaches, scapular or cervicothoracic region symptoms were reported. Deep and occasionally sharp pain in the lateral region of the right shoulder was constant but varying between 3 and 4 out of 10 on a numerical pain rating score (NPRS), where 10 was defined as the worst pain imaginable. Pain would increase up to a maximum of 6–7/10 during activities involving shoulder elevation, dressing (including hand behind back) and driving (especially turning to the left). Alison reported that repeated movements of her right shoulder as may be required during the initial assessment could lead to a substantial increase in resting pain that may settle in minutes or hours or possibly longer. Although she preferred to be a ‘side-to-side’ sleeper, at present, sleeping was confined to lying on her back or left side (both with one pillow under the head) and supporting her right arm on a folded pillow when on the left side (as she had been previously recommended).

History

On the first visit, Alison reported that she had been suffering from recurring shoulder pain for more than 2 years. Prior to this episode there was no history of any cervical or shoulder symptoms. She was unable to specify any specific macro-trauma event prior to onset, but Alison associated her initial shoulder pain with a period when she and her partner spent a number of days stripping wallpaper and repairing and painting walls and ceilings in a house that they were renovating. Following this activity, she described experiencing twinges in her right (dominant side) shoulder when performing activities such as blow drying her hair (an activity that might take 10–15 minutes), where the dryer was held in her left hand and brush in her right, and occasionally when elevating her arm such as when reaching to a high shelf or writing on the whiteboards at school. She described these symptoms as very mild and as an annoyance, and she did not take any medications or seek treatment.

A few weeks after the home renovations, she reported playing tennis on an outside court. Leading up to this match, where she was competing against a more experienced player, she had not played tennis for more than 4 months. She considered this match physically demanding for her. She reported that she did not experience any symptoms on the day of the match, but upon waking the next morning, experienced substantial right shoulder pain. She did not remember if pain was present at rest but was certain it was felt during movement, such as when dressing and driving, describing that her first turn out of the driveway was to the left, and this was extremely painful. These symptoms continued for many days, and she eventually booked an appointment with her family physician, who diagnosed ‘subacromial impingement syndrome’ and prescribed a course of non-steroidal anti-inflammatory drugs (NSAIDs). During the initial treatment period of 3 to 4 weeks, Alison reported she was 20–30% better (she had also avoided provocative activities as much as she was able during this period), but no further improvement was made. As improvement had plateaued, her family doctor performed a landmark-guided injection of ‘steroids’, which hurt for a day or so but resulted in a substantial reduction in symptoms. Approximately 3 weeks later and feeling close to 100% reduction in pain, and being concerned that the protracted lack of use of her shoulder would result in a frozen shoulder (recently experienced by a friend), she went swimming. She had completed a ‘few laps’ (freestyle) of a 20-m pool and felt a sharp pain in her right shoulder on the commencement of the next lap just after her hand had entered the water. Concerned, she stopped swimming. and symptoms described as being ‘more or less’ identical to those after the tennis match started again. She was prescribed another course of NSAIDs, which had limited benefit, and was referred to physiotherapy, followed by a self-referral to osteopathy. Treatments were as follows: recommendations to rest and ice her shoulder, soft tissue techniques, taping, acupuncture and shoulder mobilization procedures.

Over time (possibly a few months), her symptoms had settled, but she continued to feel pain in the right shoulder, especially when she elevated her arm (she again providing washing and drying her hair and school activities as examples). During this period, Alison avoided tennis and swimming but still continued to attend her gym on average two to three times a week for static bike cycling or cross training (holding the static grips on the cross trainer, as arm movement was sometimes painful), uphill walking on the treadmill and mat exercises, but no arm weight exercises or push-ups. She would work in the garden but would avoid heavy and above-shoulder activities. Over time, she felt her shoulder symptoms were improving. Approximatively 2 months prior to attending the physiotherapy our clinic, she again played tennis for about 30 minutes. She reported purposely playing a friend who understood she had a ‘weak’ shoulder, and they would play gently, with no serving, just gentle backhand and forehand shots. She reported that it was cold when they played and that the court was damp, and the ball possibly slightly wet. The day following the tennis match, she again experienced substantial pain, worse this episode than anything previously. She was angry with herself for playing and frustrated as she had played ‘gently’, although she expressed that playing when it was cold may have contributed to the increased symptoms. Pain was constantly present and would increase on movement and cause her to wake at night if she rolled onto her right side. She would typically take more than 15–30 minutes to return to sleep, and she would need to find a comfortable position to do so. She again returned to her family physician, and although she commenced another course of NSAIDs, she was not keen on another injection and discussed onward referral. She was referred to a consultant orthopaedic surgeon who referred her for an ultrasound (US) scan and radiograph. The radiograph showed an acromial spur (Type II), and the US scan showed bursal effusion and diffuse tendinosis of the right supraspinatus tendon, as well as a bursal-side partial thickness tear of the tendon. On the basis of the protracted history of symptoms; her limited response to the injection, therapy and other non-surgical management; the imaging findings; and the clinical findings of a positive Neer sign, Hawkins test and Jobe test, an arthroscopic subacromial decompression with probable rotator cuff repair was recommended by the surgeon. Unwilling to ‘rush’ to surgery, she again tried osteopathy. Shortly thereafter, a friend recommended she see a sports and exercise medicine consultant, who then referred Alison to our physiotherapy clinic.

Physical Characteristics and Medical History

Alison reported her height as 1.72 m and weight as 58 kilos (body mass index [BMI] 19.6). Her weight was stable, and she had never smoked cigarettes. She drank one to two glasses of wine on average once a week, reported no allergies and ate a balanced diet.

Alison reported no comorbidities or other health concerns and had recently had a negative test for thyroid disease. Alison was still having regular menses. She had never had surgery, and with the exception of about 1 month of ‘quite severe’ back pain after the birth of her youngest child, she reported no other significant musculoskeletal problems. There was no family history of rheumatoid arthritis. Her father (a builder) had a protracted history of shoulder pain, but she was unsure of the diagnosis, suggesting possibly a ‘frozen shoulder’.

Alison reported rarely taking medications, which included occasional paracetamol for her shoulder pain, and although she had taken omega-3 supplements in the past, she was no longer taking them or any other supplements.

Patient Perspectives

Alison did not see herself as anxious or depressed, just very frustrated and concerned about her right shoulder and the ongoing impact this was having on her life. Although uncertain that physiotherapy could help (due to the previous poor response), she wanted to ‘try everything possible’ before considering surgery. When asked what she was hoping to achieve from the initial and possibly subsequent physiotherapy treatments and what she would consider a positive outcome, her stated aim was ‘understanding what was going wrong’ and ‘relief of shoulder pain and return to full shoulder activity’.

Questionnaires

Alison was requested to complete the Shoulder Pain and Disability Index (SPADI) (Roach et al., 1991), and her initial score was 68%, where 100% represents maximal pain and disability.

Reasoning Question:

1. On the basis of Alison’s clinical presentation thus far, please discuss your hypotheses regarding the dominant ‘pain type’ (nociceptive, neuropathic, nociplastic), possible ‘sources of symptoms’ and ‘pathology’ and likely ‘contributing factors’ to the development and continuation of her pain and disability. Also, you appear to undertake significant screening of personal/lifestyle details (e.g. BMI, cigarette and alcohol consumption, allergies, diet, education, sitting/activity pattern and general health, including menstrual status and perception of psychological health). Would you also please briefly highlight how information acquired through these inquiries assists your analysis?

Answer to Reasoning Question:

Due to the duration and presentation of symptoms, the possibility of nociplastic pain (Coronado et al., 2014; Paul et al., 2012), and cortical changes (Ngomo et al., 2015) must be considered, although definitive clinical methods of testing such hypotheses remain uncertain due to a paucity of research evidence. However, we felt the pain type was primarily nociceptive, primarily based on previous clinical experience (Lewis, 2010; McCreesh and Lewis, 2013; Lewis, 2014a; Lewis and Ginn, 2015) and because the pain was worse on movement and localized, and there were definitive aggravating and easing factors (Smart et al., 2011). Other potential sources of symptoms were assessed, such as the cervical spine and acromioclavicular joint region, and although we could not be certain, the most likely sources of nociception were the subacromial bursa and rotator cuff tendons.

Neural elements have been identified within the rotator cuff tendons, biceps tendon and sheath, transverse humeral ligament and the subacromial bursa. A significantly richer supply of free nerve fibres has been reported in the subacromial bursa compared with the aforementioned tissue (Soifer et al., 1996). Additional research has implicated subacromial bursal tissue as a potential source of shoulder pain. In this research, patients diagnosed with subacromial pain syndrome were randomized to acromioplasty and bursectomy or to bursectomy alone, with equivalent results reported in both groups (Henkus et al., 2009). Another study reports that injections targeting the subacromial bursa in isolation were associated with a significant reduction in shoulder pain (Henkus et al., 2006). It is acknowledged that confounding factors may have influenced reported findings in these studies. Additional research has identified a host of substances in the subacromial bursa in people with subacromial pain, such as substance P and pro-inflammatory cytokines (IL-Iβ, TNF-α, VEGF) in higher concentrations than in people without subacromial pain, as well as an association between higher concentrations of substance P and the subjective experience of pain (Gotoh et al., 1998, 2002, 2001; Sakai et al., 2001; Yanagisawa et al., 2001; Voloshin et al., 2005).

The main contributing factor for Alison’s pain was felt to be overload of the rotator cuff at a level beyond the tissues’ physiological capacity to meet the demands of the imposed load. Overload of the rotator cuff muscles can cause fatigue, and especially when coupled with pain, this can inhibit the rotator cuff, thus producing a superior migration of the humeral head leading to compression of the subacromial bursa and rotator cuff tendons (Sharkey and Marder, 1995; Keener et al., 2009; Deutsch et al., 1996; Chen et al., 1999). Possible intrabursal and intra-fascicular tendinous friction may result in a release of nociceptive substances (Backman et al., 2011a, 2011b; Blaine et al., 2005). However, currently, there is no certainty as to the cascade of events that had occurred within the tissues that resulted in Alison’s symptoms.

In our opinion, questions pertaining to lifestyle factors are essential and should be considered a mandatory component of the information acquisition from the patient. Lifestyle factors in relation to musculoskeletal conditions have recently been reviewed in detail (Dean and Söderlund, 2015a, 2015b). Increased adiposity and a high-cholesterol diet may be associated with a greater risk for tendinopathy (Gaida et al., 2009; Beason et al., 2014). Cigarette smoking also has a detrimental impact on tendon tissue (Galatz et al., 2006; Baumgarten et al., 2010; Carbone et al., 2012), as may oestrogen deficiency (Frizziero et al., 2014). Extended periods of sitting and inactivity pose a significant health risk, including risk for heart disease, diabetes, cancer and death (Blair, 2009; Weiler et al., 2010; Lee et al., 2012; Biswas et al., 2015). The size of rotator cuff tears, degree of retraction and number of tendons torn have not found to correlate with pain, but the number of comorbidities and education level are correlated (Dunn et al., 2014; Unruh et al., 2014).

Clinical Reasoning Commentary:

Although validation of clinical assessment criteria for pain type is still not definitive, as discussed in Chapters 1 and 2, there is increased agreement on the clinical patterns of nociceptive, neuropathic and nociplastic pain types. The criteria for pathological neuropathic pain have been revised, and new measures of CNS sensitization are becoming available. The significance of hypothesizing about pain type, as put forward in this answer, is its implications for other hypothesis categories such as management and prognosis.

Specific sources of symptoms (nociception in this case) and pathology also cannot be definitively confirmed by clinical examination alone. This highlights the importance of having a balance in reasoning between sources of symptoms and pathology on the one hand and impairments in body function or structure on the other. Known pathology must be seriously considered and unknown pathology cautiously hypothesized for their implications for safety (in physical examination and management, as with a structural instability) and for the associated research evidence supporting therapeutic management options (e.g. tendinopathy).

Hypotheses regarding potential contributing factors similarly significantly inform management and prognosis. Attention to likely contributing factors not only alleviates many patients’ persistent symptoms and disability but logically also reduces the likelihood of recurrence. However, because the relevance of contributing factors also usually cannot be definitively confirmed, care is needed to avoid the confirmation-bias error of simply attending to predetermined potential contributing factors. This can be achieved by systematic ‘testing’ of different factors through procedures such as the shoulder symptom modification procedure (SSMP), discussed later in this case, and through targeted interventions with careful re-assessment.

The screening of lifestyle factors, highlighted here as essential, concurs with the discussion of ‘screening’ in Chapter 1 as a strategy to ensure that relevant information is not missed (e.g. other symptoms, other aggravating factors, comorbidities, etc.) that may have further implications for management and prognosis, as discussed in this answer.

Physical Examination

Posture

In standing, posture was examined from the front, back and sides. The only significant finding was that the right shoulder girdle was observed to be substantially lower than the left. The angle made by the clavicle, measured by placing an inclinometer on the clavicle, was 12 degrees on the left (reference lateral end of clavicle to horizontal plane) and 2 degrees on the right. Minimal muscular atrophy was observed in the right infrascapular fossa. Palpation was unremarkable with the exception of tenderness over the region of the right long head of biceps tendon in the intertubercular sulcus. However, this region was also sensitive on the left asymptomatic side.

Active and passive range-of-movement (ROM) assessments are presented in Table 17.1. Passive accessory joint movement was not tested. Internal rotation was not tested in isolation but as part of the combined functional movement of hand behind back. Scapular dyskinesis was not assessed during active movements at this stage, but the influence of scapular posture was assessed later during the assessment. The muscle strength assessment is presented in Table 17.2.

TABLE 17.1

APPOINTMENT 1 RANGE-OF-MOVEMENT IMPAIRMENT MEASUREMENTS
	Left Shoulder			Right Shoulder
	Active ROM	NPRS /10	Passive ROM	Active ROM NPRS/10 \| Base Pain ~ 3/10	Passive ROM
Flexion (LLv)	178°	0		60° (P1 – 6/10) \| NI* (no attempt at further AROM)	From 60° ~ + 10° (P ~7/10)
Flexion (SLv)				82° (P1 – 4/10) \| NI
Abduction (POS) (LLv)	178°	0		70° (P1 – 5/10) \| Parc to 110° (P↑ 7/10) \| NI	P↑ with attempted PROM
Abduction (POS) (SLv)				76° (P1 – 4/10) \| Parc to 100° (P↑ 6/10) \| NI
External rotation (with arms by the side)	38 cm	0		24 cm (P1 – 3/10)	~ + 6 cm (P↑ ~4/10)
Hand behind back	Mid-thorax	0		Lat buttocks (P1 – 6/10) \| NI
Extension	45°	0		15° (P1 – 3/10) \| NI	From 15° + 8° (P↑ ~4/10)
Horizontal flexion	Fingers to CL post acromion	0		Not tested because symptoms reproduced with other movements
Horizontal extension				Not tested because symptoms reproduced with other movements

^*In the context of these physical findings, NI (not irritable) indicates the movement did not increase resting pain after its assessment.

~, Approximately; ↑, increase; AROM, active range of movement; CL, post, contralateral posterior; Lat, lateral; LLv, long lever; NI*, not irritable; NPRS, numerical pain rating scale; P, pain; P1, first increase in pain; Parc, painful arc; POS, plane of scapula; PROM, passive range of movement; ROM, range of movement; SLv, short lever (i.e. elbow flexed to 90 degrees).

Notes: Flexion and abduction movements led with thumb facing up toward ceiling.

TABLE 17.2

APPOINTMENT 1 MUSCLE STRENGTH IMPAIRMENT MEASUREMENTS USING A HAND-HELD DYNAMOMETER
	Left Shoulder			Right Shoulder
	MVC–B	Reps to Pain	Reps to Fatigue	MVC–M	Reps to Pain	Reps to Fatigue
10° abduction	86 N			36 N	1	NT
External rotation (with arms by side)	45 N		SL (5 kg) \| 10	18 N	1	NT
Internal rotation (with arms by side)	72 N			66 N	NT	NT
Elbow flexion at 90°	108 N			112 N	1	NT
Full can test	NT			NT	NT	NT
Empty can test	56 N			NT	NT	NT
External rotation at 80° abduction	NT			NT	NT	NT
Other:

MVC–B, Maximum voluntary contraction – break; MVC–M, maximum voluntary contraction – make; N, Newton); NT, not tested; reps, repetitions; SL, side-lying.

Tests (e.g. full or empty can) performed as described in Magee (2014).

Cervical spine active movements appeared full and did not reproduce any local or referred shoulder symptoms. The same finding was recorded after passive end-range testing (overpressure) of the cervical physiological movements and during movements combining right cervical rotation with cervical flexion, and cervical extension with left and right cervical side-flexion. Active thoracic spine extension, flexion, rotation and side-flexion were equally unremarkable. A neurological examination (sensation, reflexes, vibration sense and muscle power) was not conducted because there did not appear to be any clinical evidence of a neurological deficit. Special orthopaedic tests, such as the Neer impingement sign, Hawkins test and O’Brien active compression test (Magee, 2014), were not included in the assessment, due to repeated concerns and evidence suggesting the orthopaedic tests lack the ability to differentiate the intended anatomical structure(s) of interest (Lewis and Tennent, 2007; Lewis, 2009; Hegedus et al., 2012).

Following palpation and motion and strength measurements, the SSMP (Lewis, 2009) was applied. Because Alison had indicated that repeated movements aggravated her symptoms, resulting in substantial irritability, and because resting pain had increased to approximately 4/10 on the NPRS following the limited shoulder impairment assessment, a clinical decision was made to test components of the SSMP on resting pain and not as a response to movement. Each position was held for approximately 20–30 seconds. Table 17.3 summarizes the SSMP response on right shoulder resting pain.

TABLE 17.3

PATIENT RESPONSES TO SELECTED MOVEMENTS OF SHOULDER SYMPTOM MODIFICATION PROCEDURE (SSMP)
SSMP	Right Shoulder Resting Pain
Thoracic component Active • Extension • Flexion Taping procedure	No change NT NT
Scapula component (Passive repositioning prior to active movement) • Elevation • Depression • Protraction • Retraction • Posterior tilt • Anterior tilt Combined: Elevation and posterior tilt	Slight ↓ P for a few seconds then returned ISQ ↑ P No change No change Slight ↓ P for a few seconds then returned ISQ ↑ P As for individual tests
Humeral head component • Active depression in standing • Active and passive depression in supine lying • Active depression (abduction) • Active depression (flexion) • AP glide • PA glide • AP glide with superior inclination	NT No change NT NT Slight ↓ P for a few seconds then returned ISQ Worse Slight ↓ P for a few seconds then returned ISQ
Pain modulation component • Spinal mobilization with arm movement (Mulligan, 1999) to lower cervical spine, with pressure applied from both sides of the spine (with arm at rest and during one movement of right shoulder flexion) • In left side-lying (right side uppermost with arm supported on pillow), combinations of the following pressure/touch techniques: • Cervical region mobilization techniques directed to right lower cervical region (equivalent to a Maitland [1986] Grade III pressure) • Upper to mid-thoracic region mobilization techniques from midline and to right of midline (equivalent to a Maitland Grade III pressure) • Supra- and infrascapular fossae regions soft tissue techniques	Reduced resting pain for a few minutes post-procedures to ~1–2/10 but then returned to 4/10

~, Approximately; ↓, decrease; ↑, increase; AP, anteroposterior; NT, not tested; PA, posteroanterior; ISQ, in status quo or no change; P, pain.

Reasoning Question:

2. Please discuss your analysis of Alison’s physical examination findings with respect to your previous hypotheses regarding ‘pain type’, ‘sources of symptoms’, ‘pathology’ and ‘contributing factors’, highlighting those features that support your primary hypotheses.

Answer to Reasoning Question:

The physical examination was restricted primarily due to Alison’s descriptions of irritability and clinical uncertainty as to how her shoulder would respond to a more comprehensive physical assessment. Following the limited physical examination, we continued to hypothesize that the pain type was primarily nociceptive and local to the shoulder. There was no evidence of referred pain from the cervical region, neuropathic pain or overt signs of nociplastic pain. Although there was constant pain, symptoms were provoked in the physical examination with movement in a mechanical and consistent manner, and this presentation is consistent with descriptions of nociceptive pain (Smart et al., 2011). In addition, when the load was purposely reduced during the examination of shoulder movement from long-lever shoulder flexion and abduction to short-lever movements, combinations of less pain and greater movement were recorded, reinforcing the hypothesis that nociceptive pain was the primary pain type and was associated with tissue overload (i.e. longer moment arm resulted in a greater weight imposed on the local shoulder tissues during movement).

The main aim of the examination was not to identify a structure or structures as specific sources of symptoms but to instead identify techniques that would reduce or alleviate her symptoms. Morphologically, it is unlikely that it is possible to differentiate a particular rotator cuff tendon from the others and also from other local tissues (Clark et al., 1990; Clark and Harryman, 1992), and because of this, tests such as the Jobe test (Jobe and Moynes, 1982) (colloquially known as the ‘empty can’ test and designed to test the structural integrity of the supraspinatus tendon) are probably incapable of specifically testing this tendon with certainty. In addition, needle electromyographic (EMG) investigations of the full and empty can tests have demonstrated, respectively, that eight and nine other muscles are as equally activated as the supraspinatus (Boettcher et al., 2009). It is also inconceivable that these tests do not stretch and compress the overlaying subacromial bursa (Lewis, 2011).

Based on Alison’s history, the main factor contributing to her protracted symptoms appeared to be cumulative mechanical loading of the rotator cuff and surrounding tissues at a physiological level beyond the structures’ abilities to cope and restore homeostasis. The episode that had most recently exacerbated her symptoms was playing ‘gentle’ tennis on a wet court. It is highly probable that ‘gentle’ was her perception of how she was playing, but the imposed load was beyond the physiological limit of her shoulder tissues, and a wet ball would have further increased the load due to increased weight and the force required to effectively return the ball to the opposite side of the court. If drying and brushing her hair exacerbated her shoulder pain, then it is highly probable that even ‘gentle’ tennis subjected her shoulder tissues to a load beyond their physiological capacity. It is not possible to implicate any one tissue or combination of tissues with certainty because imaging and clinical tests cannot identify the specific source of symptoms with confidence (Lewis, 2009; Hegedus et al., 2008, 2012; Lewis and Tennent, 2007). However, research – albeit with risk of high levels of bias and identifiable confounding factors – has implicated the subacromial bursa as a potential source of nociception (Santavirta et al., 1992) for people experiencing constant, irritable and nocturnal pain, as Alison described.

The purpose of the SSMP (Lewis, 2009) is to systematically assess the influence of potential contributing factors, including (1) central (spinal) posture, (2) scapular position and (3) humeral head position, as well as (4) pain neuro-modulation procedures and (5) combinations of these on symptoms associated with movements, postures and activities. Examples of these physiological movements or activities include routine shoulder movements such as shoulder flexion and hand behind back and higher-level functional activities such as swimming strokes, push-ups and high-speed, explosive throwing movements or activities such as hammering or throwing. However, for people whose symptoms would be exacerbated during repeated movement testing, the effect of SSMP procedures 1–5 may be assessed on static baseline symptoms. In this instance, the SSMP failed to meaningfully reduce Alison’s symptoms.

Reasoning Question:

3. On the basis of Alison’s findings from both the subjective and physical examination, and supporting research evidence, please outline your plans and associated rationale for ‘management’.

Answer to Reasoning Question:

The primary initial aim of management was to reduce Alison’s shoulder pain, especially the irritability she was experiencing, to allow rehabilitation and restoration of function to progress effectively without detrimentally exacerbating symptoms. Patient education and tissue load management are key priorities to achieve this.

Numerous clinical methods aimed at controlling pain have been advocated. Commonly these include soft tissue massage, passive mobilization procedures, acupuncture, acupressure, trigger point therapy, taping and electrotherapy modalities. The majority of these techniques sit within Section IV of the SSMP (i.e. the pain neuro-modulation procedure component). The clinical effectiveness of these procedures has not been unequivocally proven, and it has been challenged in many cases. Although many therapists find these techniques helpful, there may be an element of survivor bias, and research investigating the efficacy of these procedures is either non-existent or frequently short term, subject to high levels of risk of bias, equivocal and fail to report important information such as Numbers Needed to Treat. As such, clinical practice is commonly fraught with difficulty as to which techniques and procedures should be selected to control pain. In this specific case, all four sections of the SSMP failed to reduce Alison’s resting pain and pain associated with her shoulder movement. In this situation, anecdotal experience has suggested that isometric muscle contractions in the direction of pain provocation may help to reduce pain (Parle et al., 2016). The use of this is described later in this case.

Clinical Reasoning Commentary:

The lack of research supporting some common therapeutic interventions for musculoskeletal pain, in part related to limitations in research design, as highlighted in the previous answer, underscores the importance of skilled and critical clinical reasoning in treatment selection and progression. Lack of evidence of statistically significant and clinically meaningful effects should be heeded when backed by high-level and high-quality studies which have been replicated with similar findings. This is especially the case when the patient’s clinical presentation is clearly consistent with the inclusion/exclusion criteria for participants in these studies. Similarly, the proposed intervention needs to be consistent with that investigated in these studies, with relevant factors such as the skill level of the treating practitioner, dosage and the use or lack of use of commonly associated modalities (e.g. the prescription of simple pain-free range of motion or functional home exercises following passive joint mobilization) considered in the weighting of the research evidence.

When the quality of existing research is limited, management must be guided by the best available evidence, including the individual clinical experience of the practitioner as well as the collective professional craft knowledge, and by the critical appraisal of treatment effectiveness through thorough re-assessment and monitoring of outcomes.

Only gold members can continue reading. Log In or Register to continue