It sure in hell is...Not once did I claim this to be mine, however I did state that this is what I found. Maybe I should have put it in quotation marks so that people would not be confused by it. LOL
lol I dont care. Here's a better source if you're interested. MM might be.
Etiology of carpal tunnel syndrome
Author
Robert P Sheon, MD
Section Editor
Jeremy M Shefner, MD, PhD
Deputy Editor
John F Dashe, MD, PhD
Last literature review version 17.1: January 2009 | This topic last updated: May 31, 2008 (More)
INTRODUCTION — Carpal tunnel syndrome (CTS) is the most common nerve entrapment disorder. It is caused by increased pressure and consequent compression of the median nerve within the anatomic area referred to as the carpal tunnel. This area is an elliptically shaped canal enclosed by the inelastic flexor retinaculum ventrally, and the carpal bones dorsally. The major features of the cross-sectional anatomy of the wrist are illustrated in the figure (show figure). In addition to the median nerve, eight deep and superficial flexor tendons and their sheaths, the flexor pollicis longus tendon and sheath, and occasionally the radial and ulnar palmar bursae or the median artery pass through the carpal tunnel [1].
Median nerve impingement may result from diseases that invade the carpal tunnel, swelling of tendon sheaths within the tunnel, stenosis of the tunnel by bone enlargement, or thickening and degeneration of the volar carpal ligament. Pain, paresthesias, and ultimately muscle wasting of the hand may result.
The pathophysiology and etiology of CTS will be reviewed here. The clinical manifestations, diagnosis, and treatment of this disorder are discussed separately. (See "Clinical manifestations and diagnosis of carpal tunnel syndrome", and see "Treatment of carpal tunnel syndrome").
PREVALENCE — The prevalence of CTS in the general population was assessed in a study of 2466 individuals randomly selected from the general population in one area of Sweden; 354 reported symptoms suggestive of CTS (14 percent) [2]. Further clinical and/or electrophysiologic assessment of symptomatic patients confirmed the diagnosis in approximately 20 percent, resulting in a prevalence of 2.7 percent. Among 262 symptomatic persons who were clinically evaluated, there were nearly twice as many women as men (65 and 35 percent, respectively).
The reported prevalence depends upon the diagnostic criteria used to define the presence or absence of CTS. This issue is particularly important in work related CTS (see "Role of the workplace" below). Attempts to find an optimal combination of symptoms, physical findings, and electrodiagnostic test results have not yielded a generally agreed upon case definition of work related CTS. As an example, symptom surveys, physical examinations, and bilateral nerve conduction testing were used to evaluate 824 workers [3]. The agreement between the outcomes of various combinations of these procedures was assessed by determining the kappa coefficient. Overall, among 449 with at least one symptom or finding suggestive of CTS only 23 (5 percent) had abnormalities in all three domains (symptoms, physical findings, and electrophysiological results) for the dominant hand. The different screening procedures showed poor or no agreement (kappa values ranging between 0 and 0.18).
The poor overlap among the various screening procedures suggested to the authors that the use of electrodiagnostic findings in the absence of symptoms or physical findings to define CTS is unfounded. The results of this study also point to a need for the further development and evaluation of methods for detecting carpal tunnel syndrome.
PATHOPHYSIOLOGY — Histologic examination of the median nerve in patients with CTS leads to variable results and provides few clues to the mechanism responsible for impaired nerve conduction. One report, for example, noted an increase in perineurial and endoneurial connective tissue and a marked reduction in the caliber of the nerve fibers [4].
One mechanism of injury may relate to the complex pressure system that operates within the canal [4]. As an example, a study of patients with CTS found that pressure within the carpal canal rose three-fold during passive flexion or extension of the wrist [5]. Edema within the nerve tissue may follow the increase in pressure, resulting in venous congestion, stasis, ischemia, and compression of the nerve [6].
ETIOLOGY — A variety of host factors including heredity, size of the carpal tunnel, associated local and systemic diseases, and habits may contribute to the genesis of CTS.
Heredity — It has been estimated that approximately 50 percent of the risk for developing CTS is genetically determined [7]. In one study of female twins there was a significantly higher concordance rate for CTS among monozygotic than dizygotic twin siblings (35 versus 24 percent, respectively).
A rare autosomal dominant disorder, hereditary neuropathy with liability to pressure palsies (HNPP), may cause CTS. Genetic analysis for an associated deletion on chromosome 17 is a rapid and reliable alternative to nerve biopsy for this disorder. (See "Hereditary sensory autonomic neuropathies" section on Hereditary neuropathy with pressure palsy).
Carpal tunnel size — There does not appear to be any association between hand size and the development of CTS [8]. However, the cross sectional area of the carpal tunnel may be smaller in patients with idiopathic CTS although this remains controversial.
* In some series, CT scanning in patients with symptoms of CTS has shown the canal to be significantly smaller than in controls [9,10]. One study found no correlation between age and the size of the canal, suggesting that the inherited size of the canal is important, and may lead to a propensity to develop carpal tunnel stenosis [10]. Female controls had significantly smaller carpal canals than male controls in this report, suggesting a possible explanation for the increased incidence of CTS in women.
* In contrast, another study of 19 patients with idiopathic CTS found no difference compared to controls in the cross sectional area of the carpal tunnel or the relative amount of synovium within the carpal tunnel [11].
* Large breast size is another possible contributing factor. In a study of 151 patients who underwent reduction mammoplasty, carpal tunnel syndrome was found in 30 patients (19.9 percent) (95 percent confidence interval, 13.8 to 27.1) and in none of the control women (with smaller breast size: brassiere cup size B or smaller). Breast size and, to a lesser degree, body mass index were found to be highly significant predictors of carpal tunnel syndrome in this series. Breast size displayed an independent risk ratio of 6.67 when comparing the upper quartile of size to the lower quartiles [12].
Associated conditions — Multiple local and systemic conditions have been associated with the development of CTS. These disorders may cause nerve compression due to externally applied trauma, factors within the canal such as tenosynovitis secondary to systemic rheumatic disorders, thickening of the retinaculum, hypertrophy of muscles, or infiltrative diseases of the canal (eg, amyloid, myeloma, myxedema, or bone involvement by disease or tumor). Nerve compression may also result from synovitis of the long flexor tendons due to overuse, fluid retention states, and systemic inflammation.
One study identified the comorbid conditions associated with 1000 patients with CTS [13]. No associated conditions were found in 43 percent (idiopathic). Findings in the remaining patients included the following:
* Colles' fracture or other wrist trauma — 13.4 percent
* Rheumatoid arthritis and other inflammatory rheumatic disease — 6.5 percent
* Menopause — 6.4 percent
* Diabetes — 6.1 percent
* Osteoarthritis of the wrist — 5.3 percent
* Pregnancy — 4.6 percent (and 7.0 percent in women between the ages of 15 and 44)
* Myxedema — 1.4 percent
* Other medical disorders (eg, acromegaly, amyloidosis, hepatic disease, fibromyalgia, benign local tumors) — 7.3 percent
A year 2003 systematic review of CTS and concurrent diseases concluded that there was evidence supporting an etiologic association for three disorders: diabetes (odds ratios [OR] 2,2 95 percent confidence intervals [CI] of 1.5 to 3.1), hypothyroidism (OR 1.4, CI 1.0 to 2.0), and rheumatoid arthritis (OR 2.2, CI 1.4 to 3.4) [14].
Other neurologic disorders that can present as carpal tunnel syndrome with atypical electrodiagnostic features include polyneuropathy, radiculopathy, motor neuron disease, spondylotic myelopathy, syringomyelia, and multiple sclerosis. Care must be taken to avoid an inappropriate carpal tunnel operation when clinical or electrodiagnostic features are atypical [15].
Rheumatoid arthritis — Patients with rheumatoid arthritis may develop CTS that is often related to the significant involvement of the tenosynovium within the carpal tunnel. In many cases, the symptoms of median nerve compression resolve as the synovitis is effectively treated.
Menopause — In order to avoid confounding by age, women who underwent surgical bilateral oophorectomy before age 44 were compared to healthy menstruating women of similar age and were found to have an increased risk of developing CTS (32 and 10 percent, respectively, with symptomatic disease) [16]. Nerve conduction studies were performed on 16 of the 53 postmenopausal women and on 7 of 70 controls; abnormally slow median nerve conduction was found in 87 and 14 percent, respectively (p<0.002). The pathogenetic link between loss of ovarian function and CTS is unclear.
Pregnancy — Accumulation of fluid is the likely etiology of CTS in pregnant women [17]. Symptoms may first be noted during any of the three trimesters, but the diagnosis of CTS is most often made during the final trimester and resolves with delivery [18].
Hypothyroidism — CTS occurs in approximately 7 percent of patients with hypothyroidism [19]. This may be due to accumulation of matrix substances in the carpal tunnel. (See "Neurologic manifestations of hypothyroidism" section on Carpal tunnel syndrome).
Acromegaly — Up to one-third of patients with acromegaly have median nerve compression which is frequently bilateral [20]. These findings are due to soft tissue enlargement (synovial edema and tendon hyperplasia). Correction of the acromegaly usually leads to rapid resolution of symptoms. (See "Rheumatic and bone disorders associated with acromegaly").
Dialysis — CTS is commonly seen in patients with end-stage renal disease, occurring in as many as 30 percent of patients who have been dialyzed for greater than nine years [21]. Multiple factors appear to be important in these patients. As an example, direct compression and ischemia of the nerve secondary to vascular access for hemodialysis may occur; this would explain the observation that symptoms of CTS tend to worsen during hemodialysis. However, factors other than vascular access are also likely to be important (eg, infiltration by amyloid fibrils composed of beta 2-microglobulin) since patients on peritoneal dialysis have a similar incidence of CTS compared to those on hemodialysis. (See "Uremic mononeuropathy" and see "Dialysis-related amyloidosis").
Fibromyalgia — CTS can occur and is frequently unrecognized in patients with fibromyalgia, although the overall incidence of CTS in this disorder may not be different from the general population. One study of 206 patients with fibromyalgia, for example, found that 60 patients complained of dermatomal paresthesias in the fingers innervated by the median nerve [22]. The overall prevalence of CTS was higher in the women with fibromyalgia compared to those in the general population (16 versus 10 percent), although this difference was not statistically significant. There was a clear difference, however, in the rate of undetected CTS in women with fibromyalgia compared to the general population (14.1 versus 6.7 percent).
End-stage renal disease — CTS is commonly seen in patients with end-stage renal disease, occurring in as many as 30 percent of patients who have been dialyzed for greater than nine years [16]. Multiple factors appear to be important in these patients. As an example, direct compression and ischemia of the nerve secondary to vascular access for hemodialysis may occur; this would explain the observation that symptoms of CTS tend to worsen during hemodialysis. However, factors other than vascular access are also likely to be important (eg, infiltration by amyloid fibrils composed of beta 2-microglobulin) since patients on peritoneal dialysis have a similar incidence of CTS compared to those on hemodialysis. (See "Uremic mononeuropathy" and see "Dialysis-related amyloidosis").
One study reported results of electrodiagnostic features in 110 patients who had been having haemodialysis for chronic renal failure and who had CTS. There was a significant correlation between the incidence of CTS and the duration of haemodialysis. Compared with idiopathic CTS, CTS caused by long-term haemodialysis had relatively limited postoperative improvement. Electrophysiological measurements of sensory nerve conduction velocity showed that it was slower in distal segments of the median nerve in patients on haemodialysis compared with normal volunteers. Nerve conduction velocity in the carpal tunnel was significantly delayed (p<0.05) in the patients with CTS on long-term haemodialysis. N9-13 interpeak latencies were significantly longer (p<0.05) in subjects who had had haemodialysis for at least 10 years. These results suggest that CTS in patients on long-term haemodialysis has its basis in neuropathy. The clinical course of CTS in these patients is different from that of patients with idiopathic CTS, because the neuropathy involves not only the carpal tunnel region, but also the proximal part of the median nerve both diffusely and progressively. The electromyographer should be cautious in diagnosis if results are not specific; this study also noted symptoms recurred in 19 percent following surgery for CTS [23]. These results suggest that CTS in patients on long-term haemodialysis has its basis in neuropathy.
Obesity — Case control studies suggest an increased risk of CTS in obese persons. This was illustrated in a study of 1264 British women among whom obesity was associated with an adjusted odds ratio of 1.68 (95 percent confidence range 1.29 to 2.18) [24]. A similar association was found in earlier studies of 512 and 261 patients that included both men and women, with cases being approximately twice as likely as controls to be overweight (body mass index >25) [25] and obese people (body mass index >29) being 2.5-fold more likely to have electrodiagnostic evidence of CTS [26].
Other — Other causes of CTS include infections, particularly chronic granulomatous infections that may involve carpal bones, both primary and secondary amyloidosis, sarcoidosis, and gout.
Habits — Acute wrist flexion during resting positions when sleeping, reading, or driving may contribute to the development of CTS; this factor was present in 6 percent of patients in one study [13]. Poor alignment of the neck and upper body structures or poor head-neck-upper body posture with forward head and shoulders may accentuate symptoms. Exacerbation of symptoms due to clenching of the steering wheel while driving may be noted.
Role of the workplace — Cumulative trauma related to certain jobs may be related to the development of CTS. However, attributing the problem to the workplace can be difficult. As examples:
* One study compared median nerve sensory and motor latencies in poultry workers with significant repetitive hand usage to younger persons seeking employment at the company [27]. No significant differences were detected between the two groups.
* Many patients with possible work-related CTS have an underlying condition that may be responsible for this disorder. In one series of 198 such patients, up to two-thirds were either obese or had an underlying medical disease that could account for CTS (eg, hypothyroidism, diabetes, and inflammatory arthropathies) [28].
* In other reports, obesity, age, or oophorectomy (surgical menopause) were personal factors confounding the data; when these factors were eliminated, the corrected data showed no correlation of work type to median nerve compression [9,29].
Despite these limitations, there is increasing evidence, none definitive, that certain occupations can predispose to CTS [8,25,30-35]. Among those that have been associated with an increased prevalence of self-reported symptoms of CTS are manual labor, mail service, assembly, and fabrication as well as work in the food products, repair services, health care, construction, and transportation industries. Among workers with symptomatic CTS, an association has been noted between symptomatic CTS and the frequency of repetitive hand movements, increased required gripping force, abnormal finger and wrist postures, pinch-graspine, use of vibrating tools (see next section), or manipulating a computer pointing device (mouse) for more than 20 hours per week.
Hand-arm vibration syndrome — Hand-arm vibration syndrome (HAVS) is a condition associated with the use of vibrating tools. It consists primarily of "occupational" Raynaud phenomenon and digital polyneuropathy. (See "Clinical manifestations and diagnosis of the Raynaud phenomenon").
The CTS is associated with hand transmitted vibration exposure and can coexist with HAVS. Nonwork risk factors that are predisposing for HAVS include smoking, and exposure to vibration outside work. Cessation of exposure to vibrating tools (and cigarette smoking) is a critical part of treatment due to the dose response relationship of HAVS. In severe cases, calcium antagonists are also used, but treatment is often ineffective [36].
The patient with suspected job related CTS may benefit from consultation with a specialist in occupational health, an occupational therapist, or with an orthopedic or hand surgeon to better assess the contribution of work related activities to CTS.
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