A 52-year-oldfemale accountant presented in clinic witha 6-week history ofelbow and neck pain. The cause of onset is unknown,however is aggravated whilst playing badminton. The pain has significantlyincreased in the last week.
Anti- inflammatory medication (NSAIDS) were takenby the patient, which initially resolved the pain. ‘Clinical reasoning’is the process by which a therapist works with a patient to gatherinformation to generate and test hypotheses and determine optimal diagnosis withan effective treatment plan (Jones, 1995). The most common form ofclinical reasoning within the physiotherapy profession is hypothetico-deductivereasoning. The clinician collects the necessary information regarding the patient’s problemwhich forms an initial diagnosis (Doody & McAteer, 2002). Furtherdata is collected during an objective assessmentwhich may confirm or contradict the diagnosis. This process may continue to occur during managementand reassessment.Frequent reflectionduring the assessment and monitoring phase is a valuable part of clinicalreasoning. It aids the therapist to recognise their strengths and weaknesses andfurther develops their clinical reasoning skills (Jones,1995).
Miss Lionel presented with immediate pain along the extensor carpiradialis brevis (ECRB) when turning a key in the lock, lifting and tipping akettle and playing badminton. The patient reported painin the ECRB when writing with a duration of longer than ten minutes. In view of theabove, coupled with the subsequent failure of anti-inflammatory medication,leads to the diagnosis of lateral epicondyalagia (LE). LE comprises of 3 mutually related components;changes in the pain system, the local tendon pathology, and impairments in themotor system (Coombes, Bisset and Vicenzino, 2009).
Luk, Tsang and Leung (2014)reports that histological examination of LE shows: – angiofibroblastichyperplasia, – tenocytehyperplasia – increased groundsubstance ground substance. The absence of inflammatorycells indicates the process is non-inflammatoryin nature, although neurogenic inflammation may play a role (Coombes, Bisset andVicenzino, 2009). This is likely to be the cause of theshort-term symptom relief of NSAIDS. NSAIDS and corticosteroids arefound to have no medium or long-term role when treating LE. Lateralepicondyalagia is regarded as adegenerative process with dysfunctional and immaturehealing. Changes to the normal tendon architecture including neovessal ingrowthhas recently been linked with pain in LE. Thisemphasises the involvement between neural structures,microvascular and neurochemicals at the insertion of ECRB (Coombes, Bisset andVicenzino, 2009). Tendons adapt to mechanical forces by changing theirstructure.
Loading promotes both synthesis and degradation of collagen lead by theformer process, resulting in increased type 1 collagen (Luk, Tsang & Leung,2014). The patient reporteda 6-week history of pain, this suggests that the patient may be undergoing bothnociceptive and non-nociceptive processes in addition to neuronal andnon-neuronal tissues. Increased concentrationsof glutamate and substance P have been found in LE affected tendons inassociation with small blood vessels. This illustrates how the disordered pain systemof this condition correlates with its pathophysiology (Coombes, Bisset andVicenzino, 2009). Theseneurochemicals are potent modulators of pain and regulators of local tendoncirculation and neurogenic inflammation.
Thecardinal features of LE are angiofibroblastic hyperplasia in response to anoxious stimulus. Some patients with LE can develop different degrees ofcentral sensitisation resulting in mechanical pain hypersensitivity in thecontralateral elbow or other locations. These patients may require differentpain management strategies (Jespersen etal., 2013). Central sensitisation begins with activity in peripheralnociceptors and is sustained in the absence of peripheral nociceptor input. Furthersupporting the involvement of this process in LE, is the evidence ofmyelinated group A fibres mediating the reduced mechanical pain thresholdbeyond that of the original site of tissue injury (Coombes, Bisset andVicenzino, 2009).
Evidence has shown that patients most likely to experience LEare amongst the population of manual workers and athletes who repeatedly makerepetitive movements of the forearm muscles against resistance. Miss Lionelplays recreational badminton twice a week. Playing atan amateur level indicates that she may not employ correct technique and couldpotentially be over extending.
The grip strength balance activitybetween the wrist agonist and antagonist muscles togetherwith muscle strength of upper limb extremities are effective evaluationsused to determine LE (Lee et al., 2016). This theory isparticularly prominent in Miss Lionel’s case as her job as an accountantdemands extensive use of a computer. Typing involves prolonged wrist extension,whilst writing or over-gripping a mouse would generate continued contraction ofthe wrist extensors. This all indicates that the ergonomics of her desk set upmay need to be reviewed. A poor desk set-up maybe another possible contributingfactor to her neck pain. Miss Lionel didnot present with any contraindicationsfor physiotherapy treatment.
Precautions need to betaken in relation to the phase of LE. A known family history of rheumatoidarthritis predisposes a person to developing the condition (Toms, 2009). The patient has reported that hersister was diagnoses with rheumatoid arthritis 8 years ago, therefore close monitoring is required. Precaution is requiredsecondary to her high Visual analogue scale (VAS) scorewhen doing manual therapy.