CTSMonograph

Medical Communicators

Clinical Monographs

     Carpal tunnel syndrome (CTS) is a large and growing problem in the United States. Data from the National Center for Health Statistics indicates that 849,000 new problem visits were made to physicians in office-based practice in 1994 because of carpal tunnel syndrome. Approximately 260,000 carpal tunnel release operations are being performed each year.(1)
     It is a leading cause of on-the-job injuries. The Bureau of Labor Statistics indicates that in 1994, carpal tunnel syndrome accounted for 1.7 percent of workplace-related conditions in private industry that resulted in lost work. Although a relatively small component, carpal tunnel syndrome results in the highest median number of days of work lost (30 days) among all major work-related injury or illness categories.
     The carpal tunnel is a space in the proximal palm. A concave arch of carpal bones that are covered by the extrinsic palmar wrist ligaments forms the floor. The roof is made up of the transverse carpal ligament, which attaches radially to the scaphoid tuberosity and the crest of the trapezium and ulnarly to the pisiform and the hook of the hamate. It is a conduit for the median nerve and nine digital flexor tendons from the forearm into the palm.
     Although not a closed compartment, the carpal tunnel has been called a closed space (2). Because of the anatomy, any pathological process that reduces capacity or increases the volume tends to increase interstitial pressure within the carpal canal. This, in turn, can lead to compression of the median nerve.(3) In addition, the anterior position of the median nerve that runs directly under the rigid transverse carpal ligament is vulnerable to direct pressure from the flexor tendons.(4)

Symptoms

Compression of the median nerve at the wrist results in irritation that is known as the clinical disorder Carpal Tunnel Syndrome.(5) Major symptoms include pain in the wrist and hand that radiates to the forearm and parethesis in the thumb, index, middle and radial half of the ring finger. Advanced stages of medial nerve compression can result in thenar muscle weakness. (6,7)

Causes

     At its most basic level, any process that reduces the capacity or increases the contents of the carpal canal can lead to higher interstitial pressure and compression of the median nerve.(2) Since the anterior portion of the median nerve lies directly under the transverse carpal ligament, there is also an increased vulnerability to direct pressure from the flexor tendons. (3)
     Although the mechanism for developing CTS is relatively straightforward, there are many causes that could lead down this final pathway. Kerwin and colleagues suggested classifying the causes of CTS as idiopathic, intrinsic or extrinsic.(8)
    Idiopathic CTS (ICTS) has a different clinical presentation from other forms. As noted by Phalen, it occurs in healthy adults, more frequently in women, has an older onset (40-60 years of age) and may be bilateral.(9)
    Early studies indicated that chronic tenosynovitis might be responsible for increased volume in the carpal tunnel. Newer research, however has called that into question.
    Fuchs took tenosynovial biopsy specimens from 177 wrists undergoing carpal tunnel release procedures and a control group of 19. They found that inflammation was present in only 10% of the patient specimens. Thus, tenosynovitis is “uncommon” in those with idiopathic CTS undergoing carpal release surgery. (10)
     Nakamichi and Tachibana found similar results. Histology of the transverse carpal ligament and flexor tenosynovium was investigated in 166 wrists from 130 patients with idiopathic CTS. Nine control wrists were used for comparison. Consistent with Fuchs, tenosynovium showed inflammation in 10.2% of the cases with 65% showing no histological changes. They also noted that 73.5% of the ligaments showed normal pathology upon examination. They concluded that ICTS often shows normal histology in both the ligament and tenosynovium and that there were no typical changes that could be associated with the syndrome.(11)
     It has also been noted that variations in the tunnel’s diameter occur in the normal population. Studies by Dekel and Papaioannou have shown that patients with CTS have smaller carpal canals than the normal population. Computed tomography (CT) studies suggest that this may account for increased prevalence of CTS in women. Although the role, if any, of this phenomena in CTS is still not clear.(12)
    Intrinsic CTS (InCTS) was defined by Kerwin as being from “[f]actors that increase the volume of the contents of the carpal tunnel…” and lead to increases in interstitial pressure and a typical series of events that ends with the clinical symptoms of CTS.
      For example, increased edema has been implicated in the development of the syndrome during pregnancy as the fluid compresses the median nerve. The majority of patients become symptomatic during the third trimester and resolve following delivery. (3,13)
    Chronic hemodialysis patients also have a high incidence of median nerve related neuropathy. Hirasawa and Ogura examined 110 patients with CTS and chronic renal failure requiring dialysis. They found a significant relationship between the incidence of CTS and duration of dialysis treatment.(14)
    The suggested mechanisms vary from elevations in canal pressure secondary to increases in body water to distal stenosis or a vascular steal phenomenon related to the required vascular shunt. (15) Longer-term, the higher incidence of CTS has been attributed to compression of the nerve by Beta-2 Microglobulin amyloid deposition that increases as renal function is lost.(16)
    CTS is also seen in patients with hypothyroidism. The etiology in this case is thought to be the accumulation of myxedemateous tissue under the transverse carpal ligament.(17)
    Inflammatory conditions such as rheumatoid arthritis (RA) and gout have also been tied to increased incidence of CTS. Solomon and colleagues published a case-controlled study of New Jersey Medicare or Medicaid enrollees looking at risk factors for carpal tunnel release procedures. Inflammatory arthritis was strongly associated with release surgery with an odds ratio of 2.9. (18)
Hypertrophic flexor tenosynovitis distending the parathenon-covered flexor tendons may be responsible for compression of the median nerve. Radiocarpal subluxation and joint deformity may also play a part in the development of CTS. (3,19)
    One of the extrinsic factors (ECTS), according to Kerwin, is change in the dimensions of the carpal arch or canal that may result in increased interstitial pressure since the volume of the contents are unchanged. For example, CTS has been described in association with scaphoid non-union and rotary subluxation of the scaphoid.(20)
    Diabetes, hemophilia and myeloma have also been linked to CTS. Solomon found a weak but significant association between diabetes and carpal tunnel release in his study of New Jersey Medicare and Medicaid patients (OR 1.7).(17) Dell and colleagues found about 17% of patients with CTS also had a history of diabetes. (18) As of now, the underlying pathology is not well understood.
     The causes for increased CTS found among those with hemophilia is similarly unsettled. Nerve compression from a surrounding hematoma, intramuscular hemorrhage or ischemia from hemorrhage within the nerve itself, have all been suggested.(21)
     To say that occupational causes of CTS are controversial is almost an understatement. Some studies show that workers engaged in repetitive flexion and extension of the wrist, strong grip or exposure to vibration are at greatest risk.
     Tanaka, et al., estimated the prevalence of self-reported CTS among workers using the Occupational Health Supplement of the 1988 National Health Interview Survey (NHIS). Among the 127 million people who had worked during the 12 months prior to the survey, 1.87 million self-reported CTS and an additional 675,000 stated prolonged hand discomfort had been called CTS by a medical person. The risk factor in this group most strongly associated with medically confirmed CTS was exposure to repetitive bending/twisting of hands or wrists at work (OR=5.2).(22)
     Others have argued that the condition would be seen more frequently if it were a truly occupational disease. Nathan and colleagues looked at 471 employees from 27 occupations in four industries. They evaluated the role of occupational hand activity as a risk factor for CTS using a slowing of sensory conduction of the median nerve at the carpal tunnel. The found no consistent association between the type and level of hand activity and the prevalence or severity of the slowing. (23) Their follow-up study over the years from 1985 to 1989 noted that slowing was still highly correlated to increasing age and that slowing was no longer correlated to occupational hand use in any fashion.(24)

Pathophysiology

    The pathophysiological mechanism of CTS is the same irrespective of the duration or severity of the symptoms. In normal hands, the average interstitial pressure within the tunnel is 2.5 mm Hg with maximum pressure elevations in wrist extension or flexion well below 32 mm Hg, the average capillary refill pressures.(25)
    Any increase in pressure within the tunnel results in distortion or ischemia of the median nerve. Obstruction of venous return in the epineural or perineural vascular plexuses causes anoxia and endoneural edema of the nerve.(26) The magnitude of edema formation and subsequent nerve conduction blockage is related to the magnitude and duration of the compression.(27) It can also lead to venous congestion, hyperemia and circulatory slowing.(28)
    As the pressure become higher and/or more sustained, swelling of the nerve bundle can occur within the endoneurium related to the accumulation of exudates and edema. In addition, the endoneural edema alone interferes with nerve function due to alterations in the local ionic environment of the axons.(29)
    There are also data indicating that increased canal interstitial pressure has a direct mechanical effect on axonal transport. Experimental outcomes suggest that persistent compression at 20 mm Hg results in a reduction of orthograde fast axonal transport with reductions in orthograde slow transport at 30 mm Hg.(30)
    The longer the pressure increases are allowed to continue, disturbances in blood flow and axonal transport worsen and can lead to permanent changes. Destruction of the epineurium and endoneurium with a dense, fibrous scar tissue is the final result.(31)

Diagnosis

    Diagnosis of CTS is based on a combination of clinical signs, symptoms and abnormal nerve conduction studies.
    The classical symptoms of CTS are pain, numbness or parethesias in digits 1, 2 or 3. The proximoradial nerve is spared since it branches off prior to the tunnel. Wrist pain, digital weakness, inability to pinch and frequent dropping of articles are also common complaints. Typically the symptoms are worse at night and are aggravated by repetitive tasks, as well as wrist extension or flexion.
      Two studies that have been widely used and examined are Phalen’s test and Tinel’s sign.
      The simplest one is the test for Tinel's sign, which involves tapping lightly with a rubber mallet above the median nerve. A tingling sensation at the tips of the thumb and first three fingers indicates the possibility of a lesion or injury to the nerve.
    A Phalen's test can also be a part of making a diagnosis of CTS. For this test, the patient places the backs of their hands together, letting the fingers dangle downward from limp wrists. If a tingling sensation starts in less than a minute, it is a sign of CTS.
     Although widely used, the literature shows very wide reported differences in the specificity and sensitivity of these in the detection of CTS.
    Gerr and Letz, in their recent review article found that estimates of sensitivity for Phalen’s test range from 10% to 88% and of Tinel’s sign from 26% to 79%. Similar variations were found in the assessments of specificity for both tests.(32)
     Basing diagnostic decisions solely on signs and symptoms can lead to confusion with other common disorders that have similar presentations, such as tendonitis and cervical radiculopathy.(33) However, Herbert and his group note that clinical symptoms and these two tests may “have some limited utility for improvement of the positive predictive value of clinical evaluation when electrodiagnostic studies are not available”.(34)
    Although there remains some controversy over which electrodiagnostic studies are the “gold standard” of CTS diagnosis, they are still a major objective tool and are often useful in clinical staging. Simpson was the first to show that focal slowing of the median nerve in the wrist was tied to CTS in 1956.(35)
    Nerve conduction studies involve stimulating the peripheral nerves and recording the evoked response from the muscle (motor conduction) or nerve (sensory conduction). Measurements of conduction times in addition to amplitude, duration and configuration of the compound motor action potential (CMAP) or sensory nerve action potential (SNAP) are used in the assessment of the function of these nerves.(36)
    Mixed nerves are stimulated supramaximally, which causes the simultaneous depolarization of all axons. This, in turn, starts an action potential traveling down the nerve. The impulse is transmitted across the neuromuscular junction and results in the CMAP or M response. The time in milliseconds it takes the impulse to travel from stimulation point to the recording electrode is the distal motor latency (DML). Subtracting the DML from the proximal motor latency (PML) and dividing that result by the distance between the two stimulating points gives the motor conduction velocity in meters per second.
     While the conduction velocity measurements are important, the shape of the M wave can also provide meaningful information. The area and amplitude of the motor action potential measure the sum of all firing fibers and correlates with the number of fibers functioning. Atrophy of muscle fibers or degeneration of nerve fibers will result in a lower M wave. In addition, increased duration of the M wave indicates an increase in the range of conduction velocities.
    Sensory nerve conduction is measured by the SNAP. This is recorded by stimulating a mixed nerve proximally and recording at a distal site where only sensory axons are present (antidromic). It can also be measured by stimulating the distal site and recording the results proximal over either a mixed or sensory nerve (orthodromic).
   Like motor studies, SNAP is the record of only the largest 15% to 20% of the myelinated axons within the nerve. It is the sum of hundreds of action potentials. The results are proportional to the number of axons and the synchronization of their firing.
    F waves and H reflexes are high latency nerve responses. They give information about the proximal segments of the nerves. F waves are low amplitude and occur much later than M waves during motor conduction studies. The F wave latency’s chief utility is in testing for conditions that might be impacting on the proximal portions of the nerve.
    The H reflex is obtained by submaximal stimulation of a nerve distally that results in proximal propagation of a SNAP to the spinal cord and a monosynaptic return to the muscle. It is commonly useful in suspected S1 radiculopathies.
    There are many factors that need to be taken into consideration when prescribing these texts. Age, skin temperature and height have all been found to impact on normative values for each laboratory.
    In the early 1990s, a group of 105 healthy and asymptomatic adults without occupational exposures for increased risk of CTS were evaluated. Height was negatively associated with sensory amplitude in all digits tested and positively associated with median and ulnar distal latencies, and sural latency. Index finger circumference was negatively associated with median and ulnar sensory amplitudes. It was also noted that age was related to slowing.(37)
    Needle electrode examination, also known as electromyography (EMG), is performed most often to identify muscle membrane instability, changes in amplitude, duration or shape of the motor unit action potential and changes in numbers of rates and voluntary recruitment of those motor units.(38) It is useful in defining the severity of a lesion, distinguishing CTS from proximal median nerve entrapment and cervical radiculopathies and peripheral neuropathy. When mild CTS is found, these tests may not be warranted because of they are painful and unlikely to show abnormalities.
    The American Association of Electrodiagnostic Medicine (AAEM) has produced suggested practice parameters for electrodiagnostic studies in CTS. They released two practice standards (what they viewed as generally accepted principles which reflect a high degree of clinical certainty), one guideline (recommendations with moderate certainty) and one option (strategy of patient management for which the clinical utility is uncertain.
    The practice standards call for sensory conduction studies across the wrist of the median nerve and, for those wrists with abnormal results, of one other sensory nerve in the symptomatic limb. If the initial median sensory nerve study has a conduction distance greater than 8 cm and normal results, then a repeat test over a shorter (7-8 cm) conduction distance or comparing the median sensory conduction across the wrist with radial or ulnar sensory conduction across the wrist in the same limb is called for.
    The guidelines suggest motor conduction studies of the median nerve recording from the thenar muscle and of one other nerve in the symptomatic limb, to include distal latency. Finally, they suggest EMG of a sample of muscles innervated by C-5 to T-1 spinal roots, including a thenar muscle innervated by the median nerve of the symptomatic limb as a diagnostic option.(39)
    Electrodiagnostic tests have many uses in CTS patients. They have been suggested for use in diagnosis, staging and, more recently, as a possible method of predicting surgical outcomes. There are also studies ongoing to address methods that are useful in screening populations with higher risks of CTS.
    Stevens, in his 1997 review of electrodiagnosis of CTS suggested median and ulnar distal latencies and forearm tests should be performed in all patients. The ulnar motor tests will help sort out those patients with neuropathies. He also advocates comparison of the median and ulnar orthodromic latencies. When these tests are abnormal in one limb or the symptoms are bilateral, median sensory test should be done on the opposite side, with median motor follow-up considered if CTS is found again.(40)
    Sanders and colleagues described two methods for medial-to-ulnar motor conduction comparison in the diagnosis of CTS. They looked at the median-thenar to ulnar latency difference (TTLD) and the median-thenar to ulnar-hypothenar latency difference (THLD). They based their abnormal cutoffs on the results of 34 controls.
      In patients with clinically defined CTS, the diagnostic sensitivities were 95-98% and 85-88%. These tests are sensitive, easily performed and can be added to current routines with few problems.(41)
    Others have proposed sensory nerve tests as being useful in early diagnosis. Sharma and group compared sensory nerve conduction velocity (SNCV) from digit one to the wrist with those of the distal/proximal (D/P) ratio of the median SNCV from palm to digit 3/ palm to wrist. They prospectively studied 370 patients referred for mild CTS from January of 1997 through October of 1998. After exclusions, 213 participants (302 hands) had nerve conduction studies completed.
    They found that the median SNCV digit 1 to wrist was more sensitive (89.5%) than the D/P ratio (67.2%). Specificity was similar. They also noted that median distal motor latency was significantly prolonged in patients as compared to controls.(42)
    You examined the severity of symptoms in relation to nerve conduction measures of the median nerve. They evaluated 64 hands in 45 patients with CTS. Using a symptom severity questionnaire, six typical symptoms (pain, weakness, clumsiness, numbness, tingling and nocturnal symptoms) were assessed for magnitude, frequency, or duration of the episode.
    Their analysis found that the symptoms could be classified as primary (numbness, tingling and nocturnal symptoms) and secondary (pain, weakness and clumsiness). Primary symptoms are considered to be more specific for nerve injury and secondary more commonly found in soft-tissue injuries.
     There were also significant relationships between the overall symptom scale and median sensory nerve conduction velocity. In addition, there were indications that the severity scale for primary symptoms was more closely related to the nerve conduction measures than were the secondary ones.(43)
    Multiple tests may be useful in the diagnosis of CTS. Lew, Wang and Robinson evaluated the reliability of single nerve conduction tests versus the Combined Sensory Index (CSI). CSI is the sum of median-ulnar ring finger antidromic latency at 14 cm (ring-diff), median-radial thumb antidromic latency difference at 10 cm (thumb-diff) and median-ulnar midpalm latency differences at 8 cm (palm-diff).
    The researchers conducted a prospective study during which the same investigator performed test and retest sessions on one hand of 32 subjects. The CSI was then compared with results of each of its components separately. Their results showed that CSI had highest test-retest reliability when compared to ring-diff, thumb-diff and palm-diff.
    Various nerve conduction studies have also been shown to have use in correlating pre-operative studies with surgical treatment and outcomes. Harris looked retrospectively at 124 hands (101 patients) with CTS confirmed by conduction studies who went on to carpal release and were then followed for a minimum of six months after surgery.(44)
    They found that those with the most prolongation of nerve-conductions time had better results than those with less severe changes. Among the wrists with post-operative nerve conduction results available, it was noted in every instance that there was rapid subjective improvement, but a lag in the resolving of abnormal conduction studies suggests that the actual repairing of nerve damage is much slower.(45)
    More recently, Higgs and colleagues enrolled 93 workers having undergone carpal tunnel surgery. They were followed between 16 and 100 months. Significant differences were found in pre-operative nerve conduction values between groups reporting poor results and those reporting good results. Their data indicated that those with terminal latencies of 1 ms greater than the norm for that testing facility or with sensory conduction velocities 10 ms less than the facility norm were more likely to benefit from surgery. They suggested caution in performing surgery on those with normal or near normal nerve-conduction studies.
     Research is beginning to gain steam on the use of various nerve studies in predicting the future development of CTS. Nathan and his group completed a follow-up of their initial study of 942 hands of 471 randomly selected workers that began in 1984. This cohort was visited again in 1989, and 1994-95. The last group included 578 hands, about 92% of the original. They excluded those who had undergone release surgery since the procedure disturbed the area and interfered with the natural history of the disease process.(46)
    They found that the overall trend was for the mean sensory latency and prevalence of slowing to increase, the prevalence of symptoms to decrease and the prevalence of CTS to remain unchanged over the period. There also was a strong, direct linear correlation between initial slowing and development of CTS. However, most of those workers who developed de novo slowing did not go on to develop CTS or show symptoms. They concluded that the changes in conduction in the median nerve were normal for increasing age and did not necessarily lead to symptoms or CTS.(47)
    Continuing results from a long-term study by Werner and others lend credence to the possibility of using latency studies as a screening predictor for the development of CTS. They prospectively involved 77 workers who were asymptomatic but had electrodiagnostic findings consistent with median mononeuropathy. They were compared to an age- and sex-matched control group. Follow-up was completed an average of 70 months later with a rate of 70%.
    Among subjects with abnormal median sensory latencies, 23% went on to develop CTS during the observation period, compared with only 6% in the control group. After about 6 years, there was an increased risk of CTS if the worker had an abnormal early finding.(48)
    Although these tests may some day prove their worth in detecting CTS, they are not yet practical as a point-of-care screening tool or for monitoring response to therapy. Costs and inconvenience being the main concerns.
    One of the new techniques that may address those issues is the automated electrodiagnostic device (AEND). This device is battery-operated and hand-held that uses a standardized geometry for the placement of the stimulus, recording and ground electrodes. Unlike conventional techniques, the CMAP is of the abductor pollicis brevis muscle is detected by electrodes placed proximal to the wrist and is roughly comparable to the RR interval of the electrocardiogram. The device automatically identifies the maximal stimulus intensity, delivers a series of stimuli and calculates the DML and median F-wave latency. Each test takes about 2 minutes.
    To assess the reliability of the AEND, Leffler studied two groups of 75 consecutive patients each (one validation group and the other an initial group) who were referred to an academic electrodiagnosis laboratory for upper extremity complaints. The research standard for diagnosis of median neuropathy at the wrist was the neurologist’s diagnosis after formal clinic and electrodiagnostic evaluation with the diagnostician being blinded to the results of the AEND studies.
     In the validation group, the AEND yielded a DML in 97% of the hands with a conventional motor response and the correlation of AEND DML with the conventional DML was 0.94, significant at p<0.001. Of the 248 symptomatic hands, the AEND had a specificity of 90% and a sensitivity of 86% for median neuropathy at the wrist. Compared with a model based solely on clinical variables, an algorithm including symptom plus the AEND DML had an odd ratio of correct diagnostic classification of 6.3. The sensitivity at 90% specificity improved from 40% using the clinical model to 86% for the model that also included the DML. They concluded that there was a significant improvement in diagnosis using the AEND.(49)

Treatment

    Although rarely mentioned in the literature, rest may be enough for a select group of patients with a recent onset of symptoms or in those whose symptoms tend to be transitory. As was noted by Futami and colleagues, approximately one of every three patients has resolution of their symptoms within five months, even without treatment.(50)
    Splinting remains the first line conservative treatment in CTS. It is most effective if applied quickly, usually within three months of symptom onset. Splinting the wrist in a neutral position serves to maximize space in the tunnel and minimize compression on the median nerve.(51)
    Kuo used ultrasound to determine the wrist angle that produces the least compression to the median nerve. They studied 17 wrists of 17 healthy volunteers who received dynamic, high-frequency (8 MHz), high-resolution sonography with the wrist splinted at 15 degrees of flexion, neutral position, and 15 degrees and 30 degrees of extension. The neutral position caused significantly lower compression of the median nerve.(52)
    Walker and colleagues recruited 21 outpatients (30 hands) with untreated CTS from a Veterans’ Administration Medical Center electrodiagnostic laboratory. They were given custom-molded neutral wrist splints and randomized to wearing them either full time or only at night. Despite compliance issues in both groups leading to a tendency for treatment crossovers, those assigned to the full time group still showed superior distal latency improvement in both motor and sensory areas. These outcomes lead the researchers to conclude that there was support for both neutral wrist splints and their use full-time in treating CTS.(53)
    Steroid injection has also been found to have some efficacy in the non-surgical treatment of CTS. Recently Dammers, et al., conducted a randomized, double blind, placebo controlled trial to assess the effect of 40 mg of methylprednisone injected proximal to the carpal tunnel. Participants were given either 10 mg of lidocaine or the same dose of lidocaine combined with 40 mg of methylprednisone. Non-responders to lidocaine only received the combined treatment in an open-study that followed.
     At one-month, 20% of 30 patients in the control group had improved compared with 77% of 30 in the intervention group. At one year, 2 of 6 improved patients in the control group did not require additional treatment, compared with 15 of 23 in the intervention group. Of the 28 who initially did not respond, 24 (86%) improved after methylprednisone treatment. The authors concluded that a single injection of steroids close to the carpal tunnel may result in long term improvement and should be considered prior to surgery.(54)
    Chang and others undertook a study to evaluate the effectiveness of diuretics, non-steroidal anti-inflammatory drugs (NSAIDs) or steroids in the treatment of mild to moderate CTS. Using used a prospective, randomized, double-blind and placebo-controlled method, they looked at patients with clinical signs and symptoms of CTS, confirmed with electrodiagnosis.
     Using the Global Symptom Scale (GSS), they found no significant reduction from baseline at either 2 or four weeks post therapy in the placebo, NSAID and diuretic groups. The mean GSS at four weeks in the steroid group decreased significantly indicating that corticosteroids are of greater benefit in this group.(55)
    Vitamin B6 (pyridoxine) deficiency is seen in some patients with CTS. However the link between the deficiency and the disorder is controversial, as is the impact of pyridoxine on treatment. The review by Jacobson and co-workers concluded “[t]he literature at this time does not give convincing evidence for use of pyridoxine as the sole treatment when confronted with a patient with idiopathic CTS.”(56)
     Yoga has also been considered as a possible conservative treatment for CTS. A randomized, single-blind controlled trial of 42 individuals with CTS had subjects assigned to either receiving an intervention of 11 yoga postures or a wrist splint in addition to previous treatment. The results were spotty with those in the yoga group showing significant improvements in grip strength, pain reduction and Phalen’s sign. However, there were no significant improvements in sleep disturbances, Tinel's sign and median nerve conduction times.(57)
    Tendon and nerve gliding exercises are another non-surgical modality that has been considered. Rozmaryn and others studied 197 patients (240 hands). They were divided into two groups. Both received standard conservative methods with the experimental group also treated with a program of nerve and tendon gliding exercises. Seventy-one percent of those in the control group underwent surgery compared with 43% of those who were prescribed the exercise regimen. Of those in the experimental group who did not undergo surgery, 70.2% reported good results at an average follow-up time of 23 months. A significant number of patients who would have otherwise undergone release surgery were spared the surgical morbidity.(58)
    Generally speaking, surgical management of CTS is suggested when the symptoms are not responsive to more conservative treatments after two or three months. Surgical options include either open or endoscopic carpal tunnel release.
     There have been many different methods of open release of the transverse carpal ligament (OCTR). Most involve a longitudinal incision ulnar to the third metacarpal and division of the flexor retinaculum. Local, regional or general anesthetic may be used.
     Endoscopic Carpal Tunnel Release (ECTR) has also been shown to be effective in reducing pressure within the carpal tunnel. The instruments used are inserted through one or two small holes in the wrist to the synovial sheath of the tunnel and directed along the axis of the ring finger. The ligament is seen using a small telescope that provides a magnified image on a television screen that the surgeon watches while performing the surgery.
     Jimenez, Gibbs and Clapper undertook a ten-year (1987-1997) review on endoscopic release of TCL in the management of patients with CTS. A total of 52 studies on six endoscopic techniques comprising 8068 cases were found and analyzed for this review. The overall success rate in those articles reviewed was 96.52% with a complication rate of 2.67 and a failure rate of 2.61%.
     The authors concluded “[t]his review indicates that the success, complication and failure rates of ECTR are comparable to those of OCTR procedures. However, as with OCTR techniques, there is significant variability in ECTR procedures.”(59)
     Among the positives touted for open release are that the larger incisions may make a complete release easier for the surgeon. ECTR, on the other hand, is said to lessen the problems with a high rate of scar tenderness and a delay in returning to normal activities of daily living that are seen with open surgery.(60) In addition, complication rates of between 10% and 20% have been seen in the past with open surgery.(61,62) However, some newer reports show similar frequency and severity in complications with both open and ECTR.(63)

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