Lateral Elbow Pain With Cervical and Nerve-Related Components

Robert J. Nee, Michel W. Coppieters, Mark A. Jones

Initial Examination

Patient Profile and Reported Symptoms

Henry (age 46) reported to physical therapy with a physician diagnosis of ‘tennis elbow’. He worked as a safety engineer consultant for the navy. His job involved computer and desk work interspersed with on-site ship inspections at the naval base. He enjoyed golf, gardening and home improvement projects.

Henry’s main problem was right (dominant-limb) lateral elbow pain that limited his ability to perform computer work (keyboard and mouse) and power-grip activities (Fig. 7.1). He took frequent breaks from the computer to complete his work duties. He had no ship inspections at the time of the initial examination, but he thought that pain with gripping handrails would make it difficult to negotiate steep stairwells to reach the different levels of a ship. Henry also took frequent breaks to complete weekly gardening activities and did not start any new gardening or home improvement projects because of his symptoms. Although he liked to golf two or three times a week, he could not play because his elbow pain did not allow him to grip and swing a golf club.

Fig. 7.1 Body chart showing Henry’s symptoms at the initial examination. Check marks indicate areas where Henry denied the presence of any symptoms.

Henry also reported having right-sided headaches, right low cervical and upper trapezius area symptoms and a ‘falling asleep’ feeling in his right arm since a motor vehicle accident (MVA) 25 years ago (Fig. 7.1). He stated these symptoms had not changed since his lateral elbow pain started approximately 1 year ago.

Behaviour of Symptoms

Henry’s computer work was limited to 20 minutes because of achiness in his lateral elbow and forearm. Symptoms settled in 10 minutes with resting the arm by his side, and he could then repeat another 20 minutes of computer work. The lateral elbow and forearm did not get more sensitive with repeated 20-minute sessions of computer work throughout the day.

Power-grip activities (e.g. gardening tools, other tools) also aggravated the lateral elbow and forearm symptoms. The ‘ache’ increased to a ‘sharp pain’ when objects were heavier or required a larger grip. Henry was able to continue the activity as long as the object was not too heavy (i.e. <5 kg). The ‘sharp pain’ always settled immediately, but the time required for the ‘ache’ to settle varied from a few minutes to as long as 60 minutes depending on how hard he pushed the activity. Power-grip activities in elbow extension or in greater degrees of forearm pronation or supination were more painful and took closer to 60 minutes for the ‘ache’ to settle. The issues with elbow extension and forearm pronation/supination prevented Henry from gripping and swinging a golf club. The ‘sharp pain’ created by the impact of hitting the golf ball was also problematic. Henry modified power-grip activities to make sure that the ‘ache’ settled within 60 minutes.

In addition to taking more frequent breaks and modifying activities, Henry used an over-the-counter non-steroidal anti-inflammatory drug (NSAID) that helped keep the lateral elbow and forearm ‘ache’ intermittent, rather than constant. He also occasionally iced his lateral elbow and forearm to help ease his symptoms.

Henry reported no problems sleeping, but his right elbow was generally stiff (lateral side > medial side) when waking in the morning. Gentle flexion and extension movements helped reduce the stiffness in 20 minutes, but if he did not move the elbow, the stiffness lingered for 60 minutes. Even with pacing activities during the day, the lateral elbow and forearm felt more ‘tired’ and ‘achy’ at the end of the day, but these feelings were gone by the next morning.

Henry also stated that using his right arm to brush his teeth or reach overhead caused his arm to ‘fall asleep’. This feeling settled immediately after stopping the activity. He considered this to be more of a nuisance than a real problem because it had been present since his MVA 25 years ago. As noted previously, the feeling of his arm ‘falling asleep’ had not changed since his lateral elbow pain started about 1 year ago.

The impact that Henry’s symptoms had on his daily function was quantified with the Patient-Specific Functional Scale (PSFS) (Hefford et al., 2012; Stratford et al., 1995). Computer work, gardening and swinging a golf club were the activities Henry nominated for the PSFS at the initial examination (Table 7.1).

TABLE 7.1

PATIENT-SPECIFIC FUNCTIONAL SCALE (PSFS) SCORES AT THE INITIAL EXAMINATION *
Activity	Initial Exam
Computer	4
Gardening	4
Swing golf club	0
Average	2.7

^*Each activity nominated by the patient is rated from 0 (unable to perform the activity) to 10 (able to perform activity at ‘pre-injury’ level).

History

Approximately 1 year ago, Henry was pulling a heavy bookcase across the floor and felt a ‘twinge’ in his right lateral elbow. He thought nothing of it at the time and continued his activities without problems. One week later he performed a ship inspection that required a lot of power-grip activities to use the handrails to ascend and descend steep stairwells to reach different levels of the ship. He also had to lift thick and heavy safety manuals to look at information required for the inspection. The inspection lasted 1 week, and during this time, he noticed a gradual onset of the lateral elbow ache. At the end of the week, the lateral elbow ache had increased to the point that he could no longer perform power-grip activities, and he also noticed the sharp pain.

Henry saw his physician 2 months later (10 months ago) because the symptoms had not improved. He received a cortisone injection to his lateral elbow that provided some relief. However, 4 months after the cortisone injection (6 months ago), he was still having symptoms and was referred to physical therapy. Henry reported that physical therapy treatment focused on stretching and strengthening exercises for the common wrist extensors. After 2 months of treatment with no change in his symptoms, he received a second cortisone injection (4 months ago). The second injection led to some additional improvement, but his symptoms had plateaued at his current level of function for the past 2 months.

Henry had no significant medical history, no medical ‘red flags’ and no symptoms suggestive of potential cervical arterial dysfunction. He was involved in a ‘head-on’ MVA 25 years ago. He did not lose consciousness and drove his vehicle from the scene. The right-sided headaches and right low cervical and upper trapezius area symptoms started a few days later. He saw a physician shortly after the MVA. Radiographs of his neck were negative, and the physician prescribed pain medication for his symptoms, but it did not help very much. He did not recall how soon after the MVA that the ‘falling asleep’ feeling started in his right arm. Henry had not pursued any other treatment for these symptoms.

During the patient interview, Henry expressed some frustration with the lack of improvement in his lateral elbow symptoms and not being able to golf. He also wondered whether his neck and arm symptoms from the MVA might partly explain why his elbow symptoms had not responded to previous treatment. A more formal assessment of psychosocial status was not pursued because, other than this frustration, Henry did not convey any overt yellow flags during the patient interview.

Reasoning Question:

1. What were your hypotheses and reasoning at the end of your patient interview regarding dominant ‘pain type’ (nociceptive, neuropathic, nociplastic), possible ‘sources of symptoms’ and specific ‘pathology’?

Answer to Reasoning Question:

The findings from the patient interview related to Henry’s main problem of lateral elbow pain were consistent with lateral epicondylalgia (Coombes et al., 2015). Signs of central sensitization have been documented in lateral epicondylalgia (Coombes et al., 2015) and after MVAs (Sterling, 2014). However, peripheral sensitization of non-neural and neural tissues at the lateral elbow was thought to be the primary contributor to Henry’s pain experience. This hypothesis would be consistent with a combination of nociceptive and peripheral neuropathic pain types. Peripheral sensitization of non-neural tissues was likely because the lateral elbow symptoms were relatively localized and consistently aggravated by activities that apply mechanical forces to the common extensor origin and the humero-ulnar, humero-radial and proximal radio-ulnar joints (Coombes et al., 2015; Gifford & Butler, 1997; Smart et al., 2010). Peripheral sensitization of neural tissues was likely because studies show that neurodynamic tests often reproduce symptoms in patients who have lateral epicondylalgia (Berglund et al., 2008; Coombes et al., 2014; Waugh et al., 2004; Yaxley & Jull, 1993). Furthermore, sensitization of upper limb neural tissues can be relatively common in patients who have experienced an MVA (Sterling et al., 2002). Although the ‘falling asleep’ feeling in the right arm had not changed with the onset of lateral elbow pain, it suggested that neural tissues may have already been sensitized. Impairments in the middle and lower cervical spine were also likely contributing to peripheral sensitization of nociceptive and non-nociceptive pathways associated with lateral elbow and neural structures (Berglund et al., 2008; Cleland et al., 2005; Coombes et al., 2014; Waugh et al., 2004).

Tendinopathy at the common extensor origin was the tissue pathology most likely related to Henry’s lateral elbow symptoms (Coombes et al., 2015). Despite recent debate about the nature and amount of any inflammatory process (Rees et al., 2014), tendinopathy is characterized by a dysfunctional healing response to repetitive microtrauma that reduces the load-bearing capabilities of the tendon complex (Coombes et al., 2015; Scott et al., 2013). However, there is no direct relationship between pathology and reports of pain or other symptoms (Chourasia et al., 2013; Coombes et al., 2015; Scott et al., 2013). We therefore thought that treatment should focus on reducing signs of sensitivity in lateral elbow and neural structures, rather than trying to change tendon pathology (Coombes et al., 2015).

Clinical Reasoning Commentary:

Deductive reasoning, based on recognition of accepted criteria, has elicited a diagnostic hypothesis of lateral epicondylalgia, potentially involving multiple local non-neural and neural tissues, with tendinopathy considered the most likely pathology. As discussed in Chapter 1, clinical patterns incorporate enabling or predisposing factors, pathobiological and psychosocial processes and the resulting consequences or disability:

• Enabling conditions: conditions or constraints under which a disease or problem occurs, such as personal, social, medical, hereditary and environmental (e.g. load and ergonomics) factors
• Fault: the pathobiological and psychosocial processes associated with any given disease or disability
• Consequences of the fault: signs and symptoms of the particular problem, as well as its functional impact on the patient’s life

Although pattern recognition has been shown to be the dominant mode of reasoning of expert clinicians confronted with familiar, straightforward presentations, musculoskeletal clinicians are frequently presented with more complex presentations requiring more thorough assessment and deductive analysis (i.e. ‘slow thinking’ discussed in Chapter 1). Musculoskeletal diagnostic reasoning has been made more challenging with the increasing knowledge of pain science highlighting the influence that ‘pain type’ and mechanisms of peripheral and central sensitisation can have on local tissues.

Tendinopathy is hypothesized as the most likely ‘pathology,’ and research demonstrating the lack of relationship between pathology and symptoms has guided the proposed plan of management. The limitations of pathology-focused reasoning are discussed in Chapter 1, with the suggestion for a balance between pathology- and impairment-oriented reasoning being needed.

Reasoning Question:

2. What were your hypotheses and reasoning regarding potential ‘contributing factors’ to the development and onset of his pain and disability and ‘precautions to your physical examination and management’?

Answer to Reasoning Question:

The onset of Henry’s lateral elbow pain appeared to be related to a gripping and traction injury when pulling the heavy bookcase, followed by a large amount of power-grip activity during the ship inspection 1 week later. As mentioned previously, pre-existing cervical and neural tissue sensitivity from the MVA might have contributed to the development of the lateral elbow symptoms. However, pulling a heavy bookcase and a substantial power-grip activity could lead to similar lateral elbow symptoms in an individual who has no history of neck pain or injury. The relationship between pulling the heavy bookcase and the onset of symptoms suggested that ergonomic issues for computer work, gardening and golf were not likely to be related to the development of Henry’s lateral elbow pain. Any ergonomic advice for these activities during treatment would aim to provide relative rest for sensitive tissues, rather than trying to change movement patterns that might have contributed to the initial onset of symptoms.

There were no specific precautions for the physical examination or management. Henry’s lateral elbow symptoms were low on the irritability scale (Maitland, 1991), there were no medical ‘red flags’ and there were no concerns about cervical arterial dysfunction. Despite Henry’s previous MVA, upper cervical stability testing was not planned for the physical examination because the middle and lower cervical spine would be the target for testing and any initial treatment. Furthermore, initial cervical spine treatment was not likely to involve high-velocity thrust techniques.

It was also important to examine Henry’s cervical spine from a psychosocial and management perspective. First, he wondered whether his neck and arm symptoms might partly explain why his lateral elbow pain had not responded to previous treatment. Examining the cervical spine was necessary to help answer his question. Second, previous physical therapy treatment had apparently focused on musculotendinous tissues at the elbow and was not successful, and Henry was frustrated by the lack of improvement in his symptoms. Examining factors not addressed during previous treatment, such as the cervical spine and upper-quarter neural tissues, could reveal different treatment options that might lead to better outcomes. Even if the result of examining these other factors indicated that treatment should still target the musculotendinous tissues at the elbow, the examination process and subsequent explanation of the results might strengthen the therapeutic alliance with Henry and change the context surrounding any local elbow treatment (O’Keefe et al., 2016; Pinto et al., 2012; Stenner et al., 2018). A stronger therapeutic alliance between the patient and clinician is associated with better outcomes (Hall et al., 2010).

Clinical Reasoning Commentary:

Judging the relevance of potential intrinsic and extrinsic contributing factors to the development and maintenance of a patient’s problem(s) is challenging given that these, like pathology, do not correlate well with symptoms and signs (or pathology). Because extrinsic factors, such as excessive tissue load and poor ergonomics, and intrinsic factors, such as impaired muscle length and motor control/strength, do not necessarily result in symptoms, skilled clinical reasoning is needed to identify historical and other relationships between potential factors and patient symptoms to generate hypotheses regarding which factors are likely relevant in the individual patient’s clinical presentation. Ultimately, all such hypotheses must then be ‘tested’ in the management phase through targeted interventions and outcome re-assessment.

Information regarding irritability of symptoms and screening for red flags has contributed to the reasoning concerning precautions for physical examination and treatment. See Chapter 1 for further discussion of this important hypothesis category and examples within the range of information that can inform these clinical decisions.

A biopsychosocial approach is evident in the consideration of Henry’s queries regarding the possible relevance of his neck and arm symptoms and his frustration with the failure of previous treatments to the physical examination planned, despite no significant psychosocial yellow flags being present.

Physical Examination

Henry showed no relevant postural deviations. Active right elbow extension with the forearm supinated was limited by lateral elbow stiffness at 25 degrees from full extension (full extension on left). Active right elbow flexion with the forearm supinated was limited by lateral elbow stiffness at 115 degrees (130 degrees on left). With the elbow in 90 degrees of flexion, active right forearm supination was limited by lateral elbow stiffness at 65 degrees (85 degrees on left). Active right forearm pronation was full range with no symptoms.

Passive physiological movements were consistent with active movements. Passive right elbow extension (forearm supinated) was much stiffer than other movements and reproduced Henry’s lateral elbow pain. Passive elbow flexion was stiff and provoked lateral elbow pain that was not as intense as with elbow extension. Passive forearm supination (elbow flexed 90 degrees) was stiff and provoked stiffness in the lateral elbow region but not pain. Restrictions in passive forearm supination were greater when the elbow was near full extension. Passive forearm pronation was unremarkable.

Passive accessory movement testing focused on the head of the radius with the elbow extended and forearm supinated (Kaltenborn et al., 1980). Anterior-posterior (A-P) and posterior-anterior (P-A) glides of the radial head were very stiff and provoked lateral elbow pain. However, A-P glides were stiffer and more painful.

A dynamometer was not available for measuring grip strength. Therefore, large power grip was tested by having Henry squeeze the distal portion of the examiner’s forearm. When tested in 90 degrees of elbow flexion, grip pressure was moderately decreased on the right compared to the left and provoked lateral elbow pain. When tested in elbow extension, there were greater reductions in grip pressure on the right with provocation of more intense lateral elbow pain (De Smet & Fabry, 1996; Dorf et al., 2007).

Resisted isometric wrist extension (Coombes et al., 2015; Cyriax, 1982) showed findings similar to large power grip. Weakness and provocation of lateral elbow pain were more evident during testing in elbow extension than during testing in 90 degrees of elbow flexion.

The shoulder complex was screened with a combination of active movements and resisted isometric tests (Maitland, 1991). Active abduction and hand-behind-back had full range of movement and were pain-free with passive overpressure. Resisted isometric abduction with the shoulder abducted to 30 degrees was full strength and pain-free (Cyriax, 1982).

Deep tendon reflexes and sensory testing of dermatomes were normal. Myotomal testing was negative except for C6. Resisted isometric elbow flexion was weak and provoked lateral elbow pain. As noted previously, resisted isometric wrist extension was also weak and painful. Testing for the C6 myotome was therefore considered inconclusive because it was unclear whether the weakness reflected a neurological impairment or pain inhibition from sensitive structures in the elbow complex (Cyriax, 1982).

The median nerve upper limb neurodynamic test (ULNT_MEDIAN) on the right provoked lateral elbow and forearm pain at 40 degrees from full elbow extension (ULNT_MEDIAN range of motion on left to 20 degrees from full elbow extension and pain-free) (Fig. 7.2). Side-bending the neck away from the tested limb increased the lateral elbow pain (structural differentiation) (Butler, 2000; Elvey, 1997; Nee et al., 2012). The radial nerve test (ULNT_RADIAL) on the right was modified to accommodate Henry’s lack of full elbow extension (Butler, 2000; Elvey, 1997; Nee et al., 2012) (Fig. 7.3). Passive wrist/finger flexion during ULNT_RADIAL provoked lateral elbow and forearm pain. However, structural differentiation by altering the amount of shoulder girdle depression or side-bending the neck away from the tested limb did not change these symptoms.

Fig. 7.2 End position of the median nerve neurodynamic test (ULNT_MEDIAN). Testing sequence involves the following: shoulder girdle stabilization, shoulder abduction, wrist/finger extension, forearm supination, shoulder lateral rotation and elbow extension. Side-bending the neck away from the tested limb or releasing wrist extension can be used for structural differentiation (Butler, 2000; Elvey, 1997; Nee et al., 2012.)

Fig. 7.3 End position of the radial nerve neurodynamic test (ULNT_RADIAL). Testing sequence involves the following: shoulder girdle depression, elbow extension, shoulder internal rotation and forearm pronation, wrist/finger flexion and shoulder abduction as needed. Side-bending the neck away from the tested limb, releasing shoulder girdle depression, or releasing wrist/finger flexion can be used for structural differentiation (Butler, 2000; Elvey, 1997; Nee et al., 2012.)

Active cervical flexion had full range of movement and was pain-free with passive overpressure. Extension was limited by stiffness at 55 degrees (measured with inclinometer) with poor segmental motion in the low cervical spine. Passive overpressure provoked right low cervical discomfort. Right rotation was limited by stiffness at 55 degrees (measured with goniometer) and passive overpressure provoked right low cervical discomfort similar to extension. Left rotation was significantly less stiff at 75 degrees (measured with goniometer), and passive overpressure did not provoke any discomfort. Combined extension, side-bending and rotation to the right (low cervical quadrant) (Maitland, 1986) had 50% less motion than to the left and provoked right low cervical discomfort. Cervical movements and passive overpressures did not provoke lateral elbow or forearm symptoms.

Palpation examination of the cervical spine involved unilateral A-P pressures and caudal pressures on the first rib in supine as well as central and unilateral P-A pressures in prone (Hengeveld & Banks, 2014; Maitland, 1982). Unilateral A-P pressures from C5 to C7 were significantly stiffer on the right and provoked Henry’s symptoms in the right low cervical and upper trapezius area but no elbow symptoms (C6 stiffest and most sensitive). Caudal pressures on the first rib were also significantly stiffer on the right but only provoked local discomfort. Central and right unilateral P-A pressures from C5 to C7 were also very stiff and provoked right low cervical and upper trapezius area symptoms but no elbow symptoms (C6 stiffest and most sensitive). Central P-A pressures were stiffer and more sensitive than right unilateral P-A pressures. Overall, unilateral A-P pressures were stiffest and provoked the most intense symptoms in the low cervical and upper trapezius area. Central and right unilateral P-A pressures at C1 and C2 were also significantly stiff and provoked local discomfort.

Response After Physical Examination

After palpation examination of the cervical spine, active and passive extension of the right elbow (forearm supinated) were only 15 degrees from full extension with noticeably less stiffness, and Henry reported significantly less lateral elbow pain. A-P and P-A glides of the radial head were less stiff and less painful. Large power-grip pressure (elbow extended) was noticeably improved and significantly less painful. ULNT_MEDIAN still provoked lateral elbow pain, but symptoms were not provoked until the elbow was 30 degrees from full extension.

Reasoning Question:

3. Please discuss your interpretation of these physical examination findings with respect to whether they supported or did not support your previous hypotheses regarding ‘pain type’, ‘sources of symptoms’ and ‘pathology’.

Answer to Reasoning Question:

The physical examination findings supported earlier hypotheses that Henry had lateral epicondylalgia with cervical and nerve-related components. Painful decreases in force production during grip testing and resisted isometric wrist extension were consistent with lateral epicondylalgia, especially because these impairments were worse in elbow extension (Coombes et al., 2015; Cyriax, 1982; De Smet & Fabry, 1996; Dorf et al., 2007). Passive stretching of the common extensor origin was incorporated into the ULNT_RADIAL. Passive wrist/finger flexion with the elbow extended at the end of the ULNT_RADIAL provoked Henry’s lateral elbow and forearm pain, but structural differentiation did not change these symptoms. This response to the ULNT_RADIAL suggested that the provocation of lateral elbow and forearm pain was related to stretching sensitized musculotendinous tissues at the common extensor origin, another finding that was consistent with lateral epicondylalgia (Cyriax, 1982; Waugh et al., 2004). Limited motion and provocation of lateral elbow pain/stiffness with passive elbow extension, passive forearm supination and radial head glides were relevant ‘articular’ signs that are present in many individuals who have lateral epicondylalgia (Waugh et al., 2004). The humero-radial joint was likely involved because symptoms were at the lateral elbow, deficits in forearm supination were worse when tested in elbow extension and radial head glides were restricted when tested in elbow extension and forearm supination (Kaltenborn et al., 1980; Maitland, 1991).

The cervical and nerve-related components of Henry’s problem were supported by the physical examination and re-assessment immediately after cervical palpation examination. Provocation of lateral elbow pain during the ULNT_MEDIAN and changing this pain with structural differentiation suggested that Henry’s elbow symptoms were at least partly related to increased nerve sensitivity (Nee et al., 2012). The fact that the lateral elbow pain provoked during the ULNT_RADIAL did not change with structural differentiation was unexpected because the ULNT_RADIAL is the neurodynamic test that typically provokes symptoms in patients who have lateral epicondylalgia (Berglund et al., 2008; Coombes et al., 2014; Waugh et al., 2004; Yaxley & Jull, 1993). The inability to achieve full elbow extension during testing was thought to be the likely reason for the ‘negative’ response to the ULNT_RADIAL. Impairments in motion from C5 to C7 during cervical palpation examination were consistent with data showing that many patients who have lateral epicondylalgia also have cervical spine findings (Berglund et al., 2008; Coombes et al., 2014; Waugh et al., 2004). The cervical spine findings were thought to be relevant to Henry’s lateral elbow pain because re-assessment showed immediate improvements in passive elbow extension, radial head A-P and P-A glides, grip pressure and ULNT_MEDIAN range of motion.

The proportional responses to mechanical testing of tissues supported the hypothesis from the patient interview that peripheral sensitization of lateral elbow and neural structures was the main contributor to Henry’s pain experience (Gifford & Butler, 1997; Smart et al., 2010). However, categorizing the peripheral sensitization of these structures into specific pain types can be challenging. The impairments in grip pressure, resisted isometric wrist extension and physiological and accessory movements at the elbow supported the previous hypothesis of a nociceptive pain type (Gifford & Butler, 1997; Smart et al., 2010). The physical examination did not definitively support the previous hypothesis of peripheral neuropathic pain because Henry did not exhibit signs of hyperesthesia or hypoesthesia that are needed to diagnose this type of pain clinically (Finnerup et al., 2016; Treede et al., 2008). Although clinicians feel that positive responses to the ULNTs can help diagnose peripheral neuropathic pain (Smart et al., 2010), we are not aware of any data showing that the ULNTs can diagnose this type of pain in patients who have lateral epicondylalgia (Nee et al., 2012). Even though we could not apply a definitive label of peripheral neuropathic pain to Henry’s symptoms, we thought that the increased nerve sensitivity identified during the ULNT_MEDIAN needed to improve during treatment because it was associated with the provocation of his lateral elbow pain.

Clinical Reasoning Commentary:

A hypothesis-oriented approach to clinical reasoning, as evident here, is important to reduce the risk of bias from medical diagnosis (‘priming’ influence discussed in Chapter 1) and initial impressions formulated through the patient interview. It is essential that clinical reasoning is an evolving process of data gathering, analysis, ‘testing’ of hypotheses and hypothesis revision when supported by a synthesis of information. Here initial hypotheses from the patient interview regarding pain type, sources of symptoms and pathology are all supported by the physical examination. Although specific pathology associated with lateral epicondylalgia cannot be confirmed with the clinical examination, specific physical impairments can, and these are highlighted here with supporting research, thus providing options for impairment-targeted treatments and the ongoing re-assessment necessary for management progression. Re-assessment between key aspects of the physical examination (e.g. cervical palpation and elbow ‘articular’, isometric contraction and neurodynamic assessments) has provided support to hypothesized relationships between these different impairments and the patient’s symptoms. Although time consuming, these brief re-assessments enable evaluation of the influence of movement and/or adding load to one impairment on another that can assist treatment decisions while also ensuring that the progressive physical assessment is not worsening the patient’s signs and symptoms.

Reasoning Question:

4. Please also discuss the implications of the physical examination findings with respect to overall management plans and specific treatments considered.

Answer to Reasoning Question:

The cervical, neurodynamic and elbow ‘articular’ findings provided different options for management that might lead to better outcomes than Henry’s previous treatments. Clinical trial data support mobilizing the cervical spine in patients who have lateral epicondylalgia (Cleland et al., 2005; Hoogvliet et al., 2013). Evidence for mobilizing the elbow is variable, with less support for simply mobilizing the radial head and more support for a mobilization with movement (MWM) technique where a lateral glide of the proximal ulna is combined with repetitive pain-free gripping (Hoogvliet et al., 2013; Lucado et al., 2018; Mulligan, 1999). Prospective case series data support using radial nerve gliding techniques for patients who have lateral epicondylalgia (Arumugam et al., 2014; Ekstrom & Holden, 2002). Despite its lack of effect during previous treatment, evidence also suggests that therapeutic exercise for the common extensor origin should be part of the overall management of lateral epicondylalgia (Cullinane et al., 2014; Hoogvliet et al., 2013). Exercise for the common extensor origin might be more effective if cervical, neurodynamic and elbow ‘articular’ signs are also addressed during treatment (Hoogvliet et al., 2013; Lucado et al., 2018). The immediate improvements following cervical palpation examination suggested that it would be a good option to start treatment by mobilizing the cervical spine. The progression of treatment at future visits would be dictated by the results of re-assessment of physical examination findings and Henry’s report of changes in symptoms and function (Maitland, 1991). As stated previously, intervention needed to focus on techniques that reduced signs of sensitivity in the lateral elbow and neural structures and allowed Henry to perform computer work, gardening, golf and other power-grip activities without limitations (Coombes et al., 2015).

Clinical Reasoning Commentary:

Evidence-informed practice requires awareness of critically appraised research relevant to your patient’s clinical presentation that is then used as a guide to assessment and management. Here, the research-supported identified physical impairments commonly associated with lateral epicondylalgia and research-supported management strategies are highlighted. In the absence of definitive evidence for best management, significant improvement in signs and symptoms following cervical palpation examination is used to support initial treatment directed to the cervical spine. Most clinical problems present with a range of potentially relevant symptomatic and asymptomatic physical impairments and some mix of physical, environmental and/or psychosocial potential contributing factors, almost all of which can be linked to some level of research evidence supporting their attention in management. Although Henry’s treatment may have been differently commenced by some clinicians, what is essential is that the treatment options considered are evidence-informed, tailored to the patient’s particular presentation, and guided by ongoing re-assessment.

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