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Oral steroid in the treatment of carpal tunnel syndrome
  1. A C F HUI,
  2. S M WONG,
  3. K S WONG,
  4. E LI,
  5. R KAY
  1. Department of Medicine
  2. Department of Orthopaedics
  3. Prince of Wales Hospital
  4. The Chinese University of Hong Kong
  5. Centre for Clinical Trials and Epidemiological Research
  6. The Chinese University of Hong Kong
  1. Dr S M Wong, Department of Medicine, Prince of Wales Hospital, 30–32 Ngan Shing Street, Shatin, New Territories, Hong Kong, Special Administrative Region China
  1. P YUNG,
  2. L K HUNG
  1. Department of Medicine
  2. Department of Orthopaedics
  3. Prince of Wales Hospital
  4. The Chinese University of Hong Kong
  5. Centre for Clinical Trials and Epidemiological Research
  6. The Chinese University of Hong Kong
  1. Dr S M Wong, Department of Medicine, Prince of Wales Hospital, 30–32 Ngan Shing Street, Shatin, New Territories, Hong Kong, Special Administrative Region China
  1. L M YU
  1. Department of Medicine
  2. Department of Orthopaedics
  3. Prince of Wales Hospital
  4. The Chinese University of Hong Kong
  5. Centre for Clinical Trials and Epidemiological Research
  6. The Chinese University of Hong Kong
  1. Dr S M Wong, Department of Medicine, Prince of Wales Hospital, 30–32 Ngan Shing Street, Shatin, New Territories, Hong Kong, Special Administrative Region China

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A range of options are available for the conservative treatment of carpal tunnel syndrome (CTS).1-4 Non-operative methods include immobilisation of the affected hand with wrist splint; local injection of steroids and drugs such as diuretics and non-steroidal anti-inflammatory drugs.6-11 These oral drugs are thought to decrease the volume of swollen tissue within the CTS and are widely used, but there is limited clinical evidence for their role.

This prospective randomised, double blind, placebo controlled study aimed at evaluating the effect of oral steroids in the symptomatic treatment of CTS. We recruited patients with newly diagnosed CTS of more than three months' duration with confirmatory electrophysiological results (prolonged median nerve distal motor latencies >4 ms or median ulnar palmar sensory latency difference >0.5 ms) including electromyographic recordings of the abductor pollicis brevis (APB)5; co-interventions such as drug or injection treatment were withheld during the study. Exclusion criteria included (a) patients with evidence of severe CTS: fibrillation potentials or reinnervation on needle examination of the APB; (b) coexisting disorders or conditions which may mimic CTS, such as cervical radiculopathy or peripheral neuropathy; (c) contraindication to steroid use; and (d) history of underlying disorders associated with CTS, such as diabetes mellites or rheumatoid arthritis.

Patients who fulfilled the criteria were treated conservatively for two months with splinting. If symptomatic after this period, patients were allocated, using a random computer generated code, to a 10 day course of prednisolone 25 mg/day or a 10 day course of placebo. Both were given as single tablets which were identical in appearance. A physician (SMW) unaware of the treatment allocation assessed the mean global symptom score (GSS) of all patients at two and eight weeks. This is a scoring system first devised by Herskovitz which rates symptoms on a scale of 0 (no symptoms) to 10 (severe) in five categories: pain, numbness, paraesthesia, weakness/clumsiness, and nocturnal awakening. The sum of the scores in each category was the GSS.10Median (interquartile range (IR)) changes in GSS at two and eight weeks from baseline were analysed using the Mann-Whitney test. The null hypothesis was that there was no difference in symptom score between the treatment and placebo groups. Results were considered significant at p<0.05 (two sided). The sample population of 36 was planned to enable achievement of 80% power with an α=0.05 for detecting a 50% difference in GSS between the treatment groups, assuming the response rate in the oral steroid group to be 80% and that of the placebo group 30%.

Thirty six patients were recruited, of whom half were randomly allocated to receive oral steroids and half to placebo. There was no significant difference in demographics such as age and in the severity of electrophysiological parameters as shown in table 1. As compared with baseline, patients receiving steroid had a median (IR) change of −12.5 (−15 to −7) at two weeks, whereas the placebo group was −4.5 (−14 to 0), p=0.027 as shown in fig 1A . After eight weeks, the median (IR) reduction of GSS in the steroid group was −9 (−14 to −6) and in the placebo group −2 (−10 to 0), p=0.034 as shown in fig 1B. The median differences between the two groups at two and eight weeks were −6 (−11 to −1) and –6 (−11 to 0) respectively. All patients completed the short course of treatment.

Table 1

Patient characteristics

Figure 1

Box plots of changes in global symptom score (GSS) at (A) two weeks and (B) eight weeks.

This study shows a small but statistically significant reduction in GSS in the group prescribed a short course of prednisolone as compared with placebo. Steroid may have a role in the treatment of mild to moderate CTS in patients who decline or who are awaiting surgical decompression. Further trials with larger sample size and longer follow up, using low dose oral steroid in direct comparison with injected steroid, would further clarify the effect of this treatment.

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