Non-surgical Decompression Treatment for Carpal Tunnel Syndrome
Carpal tunnel syndrome CTS is often referred to as a repetitive strain disorder (RSD) or cumulative trauma disorder (CTD) because of the repetitive forces that act as a catalyst for this condition. It has been variously classified as a disease, an illness, a disorder, a syndrome, and/or an injury. There continues to be uncertainty regarding its true origin or genesis with research findings yielding conflicting conclusions. Many people tend to associate CTS primarily with occupational settings but, surprisingly, it has an equal presence as a non-occupational or an incidental CTS. CTS is a problem that is enormous in terms of direct and indirect costs, with the incidence of the condition appearing to be on the rise, especially as an occupational health problem. Carpal tunnel syndrome has been around for a long time with early reports of hand/wrist pain/paresthesia and resultant loss of function dating back as far as the 1860s in the meatpacking industry. More recently, in the 1980s and 1990s we saw a rise in CTS with data entry personnel, carpenters, assembly line operators,and generally with the increased use of computers (keyboarding).1 Classic carpal tunnel syndrome develops when the median nerve is compressed or entrapped as it passes through the carpal tunnel at the level of the wrist joint (see Figure 1).
There appears to be a general consensus that any condition that applies pressure or a compression force on the median nerve as it passes through the carpal tunnel region of the wrist has the potential to create a median nerve neuropathy/entrapment and, ultimately, CTS (see Figure 2). The most common mechanical reason for carpal tunnel syndrome might be overuse-induced swelling of the flexor tendons which are adjacent to, and share space with, the median nerve in the carpal tunnel region. Tendon swelling enlarges the tendons as synovial and inflammatory fluid accumulates between the tendon and its sheath (tenosynovitis) sometimes choking off vital tendon nutrition pathways via the circulation. As tendons enlarge or hypertrophy, they act as space-occupying lesions would in any other part of the body and begin to encroach and/or compress, in this case, on the median nerve that runs parallel to and alongside these wrist flexor tendons. Median nerve pressure will cause obstruction to venous outflow, back pressure, edema formation and, ultimately, ischemia in the nerve. This persistent median nerve pressure will ultimately lead to symptoms of pain and paresthesia and eventually alter hand function since the median nerve is a mixed nerve containing sensory, motor, and autonomic fibers. Chronic median nerve neuropathy can lead to thenar atrophy (see Figure 3). Other medical conditions such as pregnancy, hypothyroidism, alcoholism, and diabetes can also lead to CTS. There is also evidence to suggest that persons might have a higher susceptibility to developing CTS than others, including median nerve and bony anomalies associated with hand/wrist anatomy. In most cases, however, classic CTS develops as intra-carpal tunnel pressure increases, so that the more successful interventions have focused on methods of decompression.
Carpal tunnel syndrome has been identified as a major cost generator for workman’s compensation carriers across North America. CTS is one of the leading workplace or occupational injuries of all time. There is no reliable estimate of CTS prevalence in occupational settings but population-based estimates for idiopathic CTS varies between 1 and 4%. Some estimates have the incidence of CTS in the United States at 1-3 cases per 1000 subjects per year and prevalence at approximately 50 cases per 1000 subjects in the general population. In certain high risk groups, the incidence may rise as high as 150 cases per 1000 subjects per year, with prevalence rates greater than 500 cases per 1000 subjects. When prevalence studies have been undertaken in occupational settings, the condition appears almost epidemic in nature, but caution needs to be taken in interpretation of these data since there is a wide variation in how studies have defined diagnostic criteria used to characterize CTS.
Statistically, whites appear to be at higher risk than blacks. Females appear to be at higher risk than males with the female/male ratio estimates varying from 3-10:1. The peak age for developing CTS is between 45-60 years of age. It is estimated that over 8 million Americans are affected by CTS and that the costs shared among private business, government agencies, and insurance companies total more than 20 billion dollars annually in workers compensation alone. The cumulative costs for evaluating and treating repetitive strain disorders in general are estimated to be between 60 and 90 billion dollars annually when considering costs of surgery/medications, ergonomic interventions, physician/hospital visits, rehabilitation, lost time from work, temporary help, and job retraining.2
The various treatment options available for CTS are as diverse and varied as the persons who are diagnosed with the condition. Unfortunately, due to poor understanding of the condition itself (clinical presentation) along with similar pathologies that mimic CTS, the diagnostic label of CTS has become somewhat of a “wastebasket diagnosis” with various medical problems that affect the hand being inappropriately lumped into a CTS diagnosis. This has lead to ineffectual treatment and driven up the cost of disability. Carpal tunnel syndrome is characterized by paresthesia/pain in the palm of the hand and fingers (digits 1-3) consistent with the sensory/motor distribution of the median nerve. Part of the problem is that we have no gold standard test that has a universally-accepted reliability, validity, and precision throughout the entire course of CTS—from initial symptoms to resolution.
Some may argue that the EMG is the gold standard test to identify CTS and that electro diagnostic testing should be at the forefront of differential diagnosis. Others may argue that problems associated with using EMG as a diagnostic tool for CTS include, but are not limited to, error in signal (technological) and or data acquisition, error in interpretation, and the limited ability of EMG exam to detect the presence or absence of related pathology in the absence of signal distortion. We do know that patients can be experiencing symptoms in the hand/wrist yet not manifest with signal distortion upon EMG testing thus yielding a false negative test for exam purposes. We are not yet certain whether anatomical distortions (median nerve flattening or hypertrophy) occur prior to actual electric signal distortions, and whether anatomical irregularities correlate with electromyographic findings. In other words, does more nerve flattening or compression lead to increased electric signal variation on EMG exam?