We report a controlled, prospective study to investigate the effect of treatment by low-energy extracorporeal shock waves on pain in tennis elbow. We assigned at random 100 patients who had had symptoms for more than 12 months to two groups to receive low-energy shock-wave therapy. Group I received a total of 3000 impulses of 0.08 mJ/mm 2 and group II, the control group, 30 impulses. The patients were reviewed after 3, 6 and 24 weeks. There was significant alleviation of pain and improvement of function after treatment in group I in which there was a good or excellent outcome in 48% and an acceptable result in 42% at the final review, compared with 6% and 24%, respectively, in group II.J Bone Joint Surg [Br] 1996;78-B:233-7. Received 30 November 1994; Accepted after revision 17 November 1995 Although tennis elbow was first described more than 100 years ago its aetiology and pathophysiology remain uncertain (Ernst 1992;Foley 1993). The best method of treatment has not been established (Labelle et al 1992) and both conservative (Mucha and Wannske 1989;Haker and Lundeberg 1991) and operative regimes (Wittenberg, Schaal and Muhr 1992;Verhaar et al 1993) have been advocated.Low-dose extracorporeal shock-wave therapy has been found to be effective in treating persistent elbow pain in isolated cases. In this form of hyperstimulation analgesia, pain is alleviated by a moderate-to-intense sensory input which is usually applied at the site of greatest discomfort for a period ranging from a few seconds to 20 or 30 minutes. This may relieve chronic pain for days, weeks and sometimes permanently (Melzack 1989).We have studied the use of this treatment in patients with tennis elbow. PATIENTS AND METHODSOver a three-year period we treated 115 patients with lateral elbow pain by low-dose extracorporeal shock-wave therapy. During the first six weeks 15 patients discontinued the treatment leaving 100 who completed the full course.Patients were included in the study if they had had pain in the lateral epicondyle for more than 12 months and had received unsuccessful conservative therapy in the previous six months. In addition, the pain had to be induced by two or more of the following tests: 1) Palpation of the lateral epicondyle. 2) Resisted wrist extension (Thomsen test). With the shoulder flexed to 60°, the elbow extended, the forearm pronated and the wrist extended about 30°, pressure is applied to the dorsum of the second and third metacarpal bones in the direction of flexion and ulnar deviation to stress the extensor carpi radialis brevis and longus. 3) Resisted finger extension. With the shoulder flexed to 60°, the elbow extended, the forearm pronated and the fingers extended the middle finger is actively extended against resistance. 4) Chair test. With the shoulder flexed to 60° and the elbow extended the patient attempts to lift a chair weighing 3.5 kg.Patients were excluded if they were under 18 years of age or had dysfunction of the shoulder, neck and/or thoracic region, local arthritis, generalised polyarthritis, ne...

We aimed to determine whether extracorporeal shock waves of varying intensity would damage the intact tendo Achillis and paratenon in a rabbit model. We used 42 female New Zealand white rabbits randomly divided into four groups as follows: group a received 1000 shock-wave impulses of an energy flux density of 0.08 mJ/mm2, group b 1000 impulses of 0.28 mJ/mm2, group c 1000 impulses of 0.60 mJ/mm2, and group d was a control group. Sonographic and histological evaluation showed no changes in group a, and transient swelling of the tendon with a minor inflammatory reaction in group b. Group c had formation of paratendinous fluid with a significant increase in the anteroposterior diameter of the tendon. In this group there were marked histological changes with increased eosin staining, fibrinoid necrosis, fibrosis in the paratenon and infiltration of inflammatory cells. We conclude that there are dose-dependent changes in the tendon and paratenon after extracorporeal shock-wave therapy and that energy flux densities of over 0.28 mJ/mm should not be used clinically in the treatment of tendon disorders.

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Fifty patients who suffered from persistent tennis elbow for more than 12 months, and were referred for surgical treatment, were assigned at random to 2 groups of low-energy extracorporal shock wave therapy. Group I received a total of 3000 impulses of 0.08 mJ/mm2; group II (controls) 30 impulses of 0.08 mJ/mm2. Follow up was after 3 and 12 weeks. We found no significant differences between the 2 groups before treatment, there was but significant relief of pain and improvement of function in group I with good or excellent outcome in 56% at the last evaluation.

This study compares sonographical, histopathological, magnetic resonance imaging (MRI), and electromyographical (EMG) findings following acute muscle denervation. We performed an experimental denervation of the supraspinatus and infraspinatus muscles on 35 New Zealand white rabbits by segment resection of the suprascapular nerve. The sonographical appearance of the supraspinatus muscle was followed and documented at short time intervals within a 2-month follow-up period. The sonographical, histopathological, and MRI changes due to denervation suggest a regular pattern. Apart from the reduction of the muscle diameter, there were considerable sonographical signs of denervation with an increase of echointensity and inhomogenicity of echotexture that appeared on day 14 after injury, and progressed continuously with time. MRI revealed a remarkable increase in signal intensity 3 weeks after denervation and reproducible T2 times. Pathological spontaneous activity on EMG could also be detected from day 14 after injury. Conventional histopathological staining methods (H&E, NADH, ATPase, basic and acid phosphatase) confirmed denervation and absence of reinnervation. The first nonspecific histopathological changes were seen 11 days after denervation in the form of moderately atrophic fibers. Typical histopathological signs of denervation appeared 3 weeks after nerve dissection. In summary, EMG, ultrasound, MRI, and histopathology each showed first abnormalities after about 2 weeks. In addition to EMG, sonography and MRI can document the course of muscle atrophy and mesenchymal abnormalities in neurogenic muscle lesions.