Objectives

Local corticosteroid infiltration is a common practice of treatment for lateral epicondylitis. In recent studies no statistically significant or clinically relevant results in favour of corticosteroid injections were found. The injection of autologous blood has been reported to be effective for both intermediate and long-term outcomes. It is hypothesised that blood contains growth factors, which induce the healing cascade.

Impingement syndrome in the shoulder has generally been considered to be a clinical condition of mechanical origin. However, anomalies exist between the pathology in the subacromial space and the degree of pain experienced. These may be explained by variations in the processing of nociceptive inputs between different patients. We investigated the evidence for augmented pain transmission (central sensitisation) in patients with impingement, and the relationship between pre-operative central sensitisation and the outcomes following arthroscopic subacromial decompression.

We recruited 17 patients with unilateral impingement of the shoulder and 17 age- and gender-matched controls, all of whom underwent quantitative sensory testing to detect thresholds for mechanical stimuli, distinctions between sharp and blunt punctate stimuli, and heat pain. Additionally Oxford shoulder scores to assess pain and function, and PainDETECT questionnaires to identify ‘neuropathic’ and referred symptoms were completed. Patients completed these questionnaires pre-operatively and three months post-operatively.

A significant proportion of patients awaiting subacromial decompression had referred pain radiating down the arm and had significant hyperalgesia to punctate stimulus of the skin compared with controls (unpaired t-test, p < 0.0001). These are felt to represent peripheral manifestations of augmented central pain processing (central sensitisation).

The presence of either hyperalgesia or referred pain pre-operatively resulted in a significantly worse outcome from decompression three months after surgery (unpaired t-test, p = 0.04 and p = 0.005, respectively).

These observations confirm the presence of central sensitisation in a proportion of patients with shoulder pain associated with impingement. Also, if patients had relatively high levels of central sensitisation pre-operatively, as indicated by higher levels of punctate hyperalgesia and/or referred pain, the outcome three months after subacromial decompression was significantly worse.

In a prospective randomised study we compared the results of arthroscopic subacromial bursectomy alone with debridement of the subacromial bursa followed by acromioplasty. A total of 57 patients with a mean age of 47 years (31 to 60) suffering from primary subacromial impingement without a rupture of the rotator cuff who had failed previous conservative treatment were entered into the trial. The type of acromion was classified according to Bigliani. Patients were assessed at follow-up using the Constant score, the simple shoulder test and visual analogue scores for pain and functional impairment. One patient was lost to follow-up.

At a mean follow-up of 2.5 years (1 to 5) both bursectomy and acromioplasty gave good clinical results. No statistically significant differences were found between the two treatments. The type of acromion and severity of symptoms had a greater influence on the clinical outcome than the type of treatment. As a result, we believe that primary subacromial impingement syndrome is largely an intrinsic degenerative condition rather than an extrinsic mechanical disorder.

Ulnar nerve function, during and after open reduction and internal fixation of fractures of the distal humerus with subperiosteal elevation of the nerve, was assessed by intra-operative neurophysiological monitoring. Intermittent recording of the compound muscle action potentials was taken from the hypothenar muscles in 18 neurologically asymptomatic patients.

The mean amplitude of the compound muscle action potential after surgery was 98.1% (sd 17.6; −37% to +25%). The amplitude improved in six patients following surgery. Despite unremarkable recordings one patient had progressive paresis. Motor impairment is unlikely if the compound muscle action potential is continuously preserved and not reduced by more than 40% at the end of surgery. Temporary decreases in amplitude by up to 70% were tolerated without clinical consequences. However, repeated clinical examination is obligatory to recognise and treat early post-operative palsy.