Abstract
Carpal tunnel syndrome (CTS) and trigger finger are known to occur together in association with conditions such as diabetes mellitus, rheumatoid arthritis and hypothyroidism. Although most cases that present to a hand clinic have no obvious predisposing cause, the two conditions often appear together in the same patient. We performed a prospective study of the prevalence of CTS in hospital outpatients presenting with trigger finger. Six hundred and eighty-one patients with CTS, trigger finger or both conditions were recruited prospectively. Diagnosis of both disorders was made on clinical grounds. The study group comprised 551 patients with no obvious predisposing cause. Of 211 patients with trigger finger, 91 (43%) also had CTS. This prevalence is substantially higher than the population prevalence of CTS of approximately 4%. Our data support an association between idiopathic CTS and idiopathic trigger finger and lend support to common pathophysiological factors.
An association between carpal tunnel syndrome (CTS) and trigger finger is well-established in patients with diabetes mellitus and rheumatoid arthritis. Clinical and neurophysiological evidence of a higher-than-expected prevalence of CTS in hypothyroidism has also been reported (Cakir et al., 2003).
A retrospective review of our patients suggested an association between the two conditions in patients with no obvious predisposing cause. Therefore, we performed a prospective study to examine the association between idiopathic CTS and idiopathic trigger finger.
PATIENTS AND METHODS
Data were collected prospectively from new patients (prior to any intervention) referred to the senior author’s out-patient clinic, between September 2001 and September 2004, with either CTS, trigger finger or both. Those presenting with one condition were questioned and examined in regard to the other. Six hundred and eighty-one patients presented with CTS and/or trigger finger during the study period and, after excluding 130 who had diabetes mellitus, rheumatoid arthritis or thyroid disease (disorders which are known to be associated with these conditions), 551 were included in the study. The mean age was 55 (range 23–90) years. Three hundred and forty-nine (63%) of the patients were women. Age, sex, hand dominance and the affected digit (when trigger finger was present) were recorded.
The diagnosis of CTS was made clinically based on a history of tingling/numbness in the radial side of the hand with a positive Phalen’s and/or Tinel’s test. Nerve conduction studies were used only in equivocal cases or if work-related compensation was involved. The diagnosis of trigger finger was made from a history of snapping or locking, together with a palpable nodule at the A1 pulley and triggering that was demonstrable on examination.
RESULTS
Two hundred and eleven of the 551 study patients suffered from triggering of at least one digit. In 150 (71%) of the cases only one digit was involved and in 61 (29%) multiple digits were involved. The right thumb was the most commonly affected digit, followed by the right ring finger and left thumb (Fig 1).
Four hundred and thirty-one of the study patients had CTS, which was bilateral in 238 (55%) cases. In 383 patients (89%), CTS was present in the dominant hand. Three hundred and seventy-two (86%) were diagnosed on clinical grounds with 59 (14%) requiring nerve conduction studies to confirm the diagnosis.
The number of patients with one or both conditions, and the relevant subgroups, are shown in Fig 2.
Of the 211 patients with trigger finger, 91 (43%) also suffered from CTS. These same 91 patients with trigger finger comprised 21% of the 431 with CTS. The age distribution and sex ratio (mean age 59; 66% female) were similar to the study group as a whole.
DISCUSSION
A study of 2466 randomly selected people found a prevalence of CTS of 3.8% using the same diagnostic criteria that we chose for our study (Atroshi et al., 1999). We can find no estimate of the population prevalence of trigger finger in the literature. The prevalence of CTS in our patients with trigger finger was 43%, which is much higher than one would expect in the general population.
Hayashi et al. (2005) found an 11.5% prevalence of trigger finger in patients who had undergone carpal tunnel decompression and concluded that the surgery itself was a significant risk factor in the development of trigger finger when CTS was mild or moderate. Our study found a prevalence of 21%, but as we did not distinguish between those having surgery and those who were treated conservatively or record the severity of CTS, we can draw no conclusions about an association with surgical intervention.
Clinical experience indicates that trigger finger is rather less prevalent than CTS and therefore the 21% prevalence of trigger finger in patients with CTS is probably greater than the population prevalence.
We considered whether the association between CTS and trigger finger could be due to selection bias in our study. Our study population comprised individuals referred by general practitioners. If people who suffer from both conditions were more likely to consult the general practitioner, and/or more likely to be referred to hospital, than individuals suffering from only one of the disorders, then the proportion of our study population suffering from both disorders would be greater than the proportion in the general population. Our study does not allow the magnitude of any such effect to be estimated, but we feel it is unlikely to explain the size of the association that we found.
The characteristic pathological finding in CTS is non-inflammatory fibrosis of the subsynovial connective tissue, but its role in compression of the median nerve is unclear (Ettema et al., 2006). These tissues also show vascular proliferation, vascular hypertrophy and vascular obstruction with wall thickening (Jinrok et al., 2004). In contrast, the chief histopathological finding in the A1 pulley in trigger finger is irregular connective tissue with small collagen fibres and abundant extracellular matrix containing chondroid metaplasia in the deep surface of the pulley (Sampson et al., 1991; Sbernardori and Bandiera 2007). Further work is needed to determine if the association between carpal tunnel compression and trigger finger suggested by our study reflects common pathogenetic mechanisms.