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Carpal tunnel syndrome ( CTS) is a nerve compression syndrome caused when the median nerve, in the carpal tunnel of the wrist, becomes compressed. CTS can affect both wrists when it is known as bilateral CTS. After a wrist fracture, inflammation and bone displacement can compress the median nerve. With rheumatoid arthritis, the enlarged synovial lining of the tendons causes compression.
The main symptoms are numbness and Paresthesia of the thumb, index finger, middle finger, and the thumb side of the ring finger, as well as pain in the hand and fingers. Symptoms are typically most troublesome at night. Many people sleep with their wrists bent, and the ensuing symptoms may lead to awakening. People wake less often at night if they wear a wrist splint. Untreated, and over years to decades, CTS causes loss of sensitivity, weakness, and shrinkage (muscle atrophy) of the thenar muscles at the base of the thumb.
Work-related factors such as vibration, wrist extension or flexion, hand force, and repetitive strain are risk factors for CTS. Other risk factors include being female, obesity, diabetes, rheumatoid arthritis, thyroid disease, and genetics.
Diagnosis can be made with a high probability based on characteristic symptoms and signs. It can also be measured with electrodiagnostic tests.
Injection of may or may not alleviate symptoms better than simulated (placebo) injections. There is no evidence that corticosteroid injection sustainably alters the natural history of the disease, which seems to be a gradual progression of neuropathy. Surgery to cut the transverse carpal ligament is the only known disease modifying treatment.
Prolonged pressure can lead to a cascade of physiological changes in neural tissue. First, the blood-nerve barrier breaks down (increased permeability of Perineurium and endothelial cells of Endoneurium blood vessels). If the pressure continues, the nerves will start the process of demyelination under the area of compression. This will result in abnormal Action potential even when the pressure is relieved leading to persistent sensory symptoms until remyelination can occur. If the compression continues and is severe enough, may be injured and Wallerian degeneration will occur. At this point there may be weakness and muscle atrophy, depending on the extent of axon damage.
The critical pressure above which the microcirculatory environment of a nerve becomes compromised depends on diastolic/systolic blood pressure. Higher blood pressure will require higher external pressure on the nerve to disrupt its microvascular environment. The critical pressure necessary to disrupt the blood supply of a nerve is approximately 30mm Hg below diastolic blood pressure or 45mm Hg below mean arterial pressure. For normohypertensive (normal blood pressure) adults, the average values for systolic blood pressure is 116mm Hg diastolic blood pressure is 69mm Hg. Using this data, the average person would become symptomatic with approximately 39mm Hg of pressure in the wrist (69 - 30 = 39 and 69 + (116 - 69)/3 - 45 ~ 40). Carpal tunnel syndrome patients tend to have elevated carpal tunnel pressures (12-31mm Hg) compared to controls (2.5 - 13mm Hg). Applying pressure to the carpal tunnel of normal subjects in a lab can produce mild neurophysiological changes at 30mm Hg with a rapid, complete sensory block at 60mm Hg. Carpal tunnel pressure may be affected by wrist movement/position, with flexion and extension capable of raising the tunnel pressure as high as 111mm Hg. Many of the activities associated with carpal tunnel symptoms such as driving, holding a phone, etc. involve flexing the wrist and it is likely due to an increase in carpal tunnel pressure during these activities.
Nerve compression can result in various stages of nerve injury. The majority of carpal tunnel syndrome patients have a degree I nerve injury (Sunderland classification), also called Neurapraxia. This is characterized by a conduction block, segmental demyelination, and intact axons. With no further compression, the nerves will remyelinate and fully recover. Severe carpal tunnel syndrome patients may have degree II/III injuries (Sunderland classification), or axonotmesis, where the axon is injured partially or fully. With axon injury, there would be muscle weakness or atrophy, and with no further compression, the nerves may only partially recover.
While there is evidence that chronic compression is a major cause of carpal tunnel syndrome, it may not be the only cause. Several alternative, potentially speculative, theories exist that describe alternative forms of nerve entrapment. One is the theory of nerve scarring (specifically adherence between the mesoneurium and Epineurium), preventing the nerve from gliding during wrist/finger movements, causing repetitive traction injuries. Another is the double crush syndrome, where compression may interfere with axonal transport, and two separate points of compression (e.g. neck and wrist), neither enough to cause local demyelination, may together impair normal nerve function.
Severe CTS is associated with measurable loss of sensibility. As the median neuropathy progresses, there is loss of sensibility in the thumb, index, middle, and the thumb side of the ring finger. As the neuropathy progresses, there may be first weakness, then atrophy of the muscles of thenar eminence (the flexor pollicis brevis, opponens pollicis, and abductor pollicis brevis). The sensibility of the palm remains normal because the superficial sensory branch of the median nerve branches proximal to the transverse carpal ligament (TCL) and travels superficial to it.
Median nerve symptoms may arise from nerve compression at the level of the thoracic outlet or the area where the median nerve passes between the two heads of the pronator teres in the forearm, (2026). 9780808924234, Saunders Elsevier. ISBN 9780808924234 although this is debated.
Severe CTS is also associated with weakness and atrophy of the muscles at the base of the thumb. The ability to abduct the thumb may be lost.
A person with idiopathic carpal tunnel syndrome will not have any sensory loss over the thenar eminence (bulge of muscles in the palm of the hand and at the base of the thumb). This is because the palmar branch of the median nerve, which innervates that area of the palm, separates from the median nerve and passes over the carpal tunnel. (2026). 9780808924234, Saunders Elsevier. ISBN 9780808924234
The association of other factors with CTS is a source of notable debate. It is important to distinguish factors that provoke symptoms and factors that are associated with seeking care from factors that make the neuropathy worse.
Genetic factors are believed to be the most important determinants of who develops carpal tunnel syndrome. In other words, one's wrist structure seems programmed at birth to develop CTS later in life. A genome-wide association study (GWAS) of carpal tunnel syndrome identified 50 genomic loci significantly associated with the disease, including several loci previously known to be associated with human height.
Some other factors that contribute to carpal tunnel syndrome are conditions such as diabetes, alcoholism, vitamin deficiency or toxicity as well as exposure to toxins. Conditions such as these don't necessarily increase the interstitial pressure of the carpal tunnel. One case-control study noted that individuals classified as obese (BMI >29) are 2.5 times more likely than slender individuals (BMI <20) to be diagnosed with CTS. It is not clear whether this association is due to an alteration of pathophysiology, a variation in symptoms, or a variation in care-seeking.
Association between common benign tumors such as lipomas, ganglion, and vascular malformation should be handled with care. Such tumors are very common and are more likely to compress the median nerve. Similarly, the association between transthyretin amyloidosis-associated polyneuropathy and carpal tunnel syndrome is under investigation. Prior carpal tunnel release is often noted in individuals who later present with transthyretin amyloid-associated cardiomyopathy. There is consideration that bilateral carpal tunnel syndrome could be a reason to consider amyloidosis, timely diagnosis of which could improve heart health. Amyloidosis is rare, even among people with carpal tunnel syndrome (0.55% incidence within 10 years of carpal tunnel release). In the absence of other factors associated with a notable probability of amyloidosis, it is not clear that biopsy at the time of carpal tunnel release has a suitable balance between potential harms and potential benefits.
Other specific pathophysiologies that can cause CTS via pressure include:
The international debate regarding the relationship between CTS and repetitive hand use (at work in particular) is ongoing. The Occupational Safety and Health Administration (OSHA) has adopted rules and regulations regarding so-called "cumulative trauma disorders" based concerns regarding potential harm from exposure to Ergonomic hazard.
A review of available scientific data by the National Institute for Occupational Safety and Health (NIOSH) indicated that job tasks that involve highly repetitive manual acts or specific wrist postures were associated with symptoms of CTS. There was no clear distinction between paresthesia (appropriate) from pain (inappropriate), and causation was not established. The distinction from work-related arm pains that are not carpal tunnel syndrome was unclear. It is proposed that repetitive use of the arm can affect the biomechanics of the upper limb or cause damage to tissues. It is proposed that postural and spinal assessment, along with ergonomic assessments, should be considered, based on the observation that addressing these factors has been found to improve comfort in some studies, although experimental data are lacking, and the perceived benefits may not be specific to those interventions. A 2010 survey by NIOSH showed that two-thirds of the 5million carpal tunnel diagnoses in the US that year were related to work. Women are more likely to be diagnosed with work-related carpal tunnel syndrome than men. Many if not most patients described in published series of carpal tunnel release are older and often not working.
Normal pressure of the carpal tunnel has been defined as a range of . Wrist flexion increases the pressure eight-fold and extension increases it ten-fold. There is speculation that repetitive flexion and extension in the wrist can cause thickening of the synovial tissue that lines the tendons within the carpal tunnel.
CTS can be detected on examination using one of several maneuvers to provoke paresthesia (a sensation of tingling or "pins and needles" in the median nerve distribution). These so-called provocative signs include:
Diminished threshold sensibility (the ability to distinguish different amounts of pressure) can be measured using Semmes-Weinstein monofilament testing. This test establishes impaired or loss of sensation.
Electrodiagnostic testing including electromyography, and nerve conduction studies can objectively measure and verify median neuropathy.
Ultrasound can image and measure the cross-sectional diameter of the median nerve, which has some correlation with CTS. The role of ultrasound in diagnosis—just as with electrodiagnostic testing—is a matter of debate. Data suggests that electrodiagnostic testing cannot detect the presence of CTS in 16% to 34% of people who have the condition.
The role of confirmatory electrodiagnostic testing is controversial. The goal of electrodiagnostic testing is to compare the speed of conduction in the median nerve with conduction in other nerves supplying the hand. When the median nerve is compressed, it will conduct more slowly than normal and more slowly than other nerves. Nerve compression results in damage to the myelin sheath and manifests as delayed latencies and slowed conduction velocities. Electrodiagnosis rests upon demonstrating impaired median nerve conduction across the carpal tunnel in the context of normal conduction elsewhere.
It is often stated that normal electrodiagnostic studies do not preclude the diagnosis of carpal tunnel syndrome. The rationale for this is that a threshold of neuropathy must be reached before study results become abnormal, and also that threshold values for abnormality vary. Others contend that idiopathic median neuropathy at the carpal tunnel with normal electrodiagnostic tests would represent very, very mild neuropathy that would be best managed as a normal median nerve. Even more important, notable symptoms with mild disease are strongly associated with unhelpful thoughts and symptoms of worry and despair. Notable CTS should remind clinicians to always consider the whole person, including their mindset and circumstances, in strategies to help people get and stay healthy.
A report published by the American Association of Neuromuscular & Electrodiagnostic Medicine (AANEM), the American Academy of Physical Medicine and Rehabilitation (AAPM&R), and the American Academy of Neurology defines practice parameters, standards, and guidelines for electrodiagnostic testing studies of CTS based on an extensive critical literature review. This joint review concluded that median and sensory nerve conduction studies are valid and reproducible in a clinical laboratory setting, and a clinical diagnosis of CTS can be made with a sensitivity greater than 85% and specificity greater than 95%. The AANEM has issued evidence-based practice guidelines for the diagnosis of carpal tunnel syndrome, both by electrodiagnostic studies and by neuromuscular ultrasound.
When the symptoms and signs point to atrophy and muscle weakness more than numbness, consider neurodegenerative disorders such as Amyotrophic Lateral Sclerosis or Charcot-Marie Tooth.
Given that biological factors, such as genetic predisposition and anthropometric features, are more strongly associated with carpal tunnel syndrome than occupational/environmental factors such as hand use, CTS may not be prevented by activity modifications.
Some claim that worksite modifications such as switching from a QWERTY computer keyboard layout to Dvorak are helpful, but Meta-analysis of the available studies note limited supported evidence.
The American Academy of Orthopedic Surgeons recommends proceeding conservatively with a course of nonsurgical therapies tried before release surgery is considered. A different treatment should be tried if the current treatment fails to resolve the symptoms within 2 to 7 weeks. Early surgery with carpal tunnel release is indicated where there is evidence of median nerve denervation or a person elects to proceed directly to surgical treatment. Recommendations may differ when carpal tunnel syndrome is found in association with the following conditions: diabetes mellitus, coexistent cervical radiculopathy, hypothyroidism, polyneuropathy, pregnancy, rheumatoid arthritis, and carpal tunnel syndrome in the workplace. CTS related to another pathophysiology is addressed by treating that pathology. For instance, disease-modifying medications for rheumatoid arthritis or surgery for traumatic acute carpal tunnel syndrome.
There is insufficient evidence to recommend gabapentin, non-steroidal anti-inflammatories (NSAIDs), yoga, acupuncture, low level laser therapy, magnet therapy, vitamin B6 or other supplements.
Many health professionals suggest that for the best results, one should wear braces at night. When possible, braces can be worn during the activity, primarily causing stress on the wrists. The brace should not generally be used during the day as wrist activity is needed to keep the wrist from becoming stiff and to prevent muscles from weakening.
In cases of epineural tethering in the upper extremity, manual therapy can reduce this dysfunction. It can have a positive impact on the gliding of the nerves through the carpal tunnel while moving the elbow, fingers, or wrist. Manual therapy included the incorporation of specified neurodynamic techniques, functional massage, and carpal bone mobilizations. People who receive physical therapy report less pain and an increased functional ability of their wrists and hands.
Self-myofascial ligament stretching has been suggested as an effective technique, although a meta-analysis claimed this form of therapy does not show significant improvement in symptoms or function. However, stretching with a physical therapist can be more beneficial than if the patient stretches alone. Tendon and nerve gliding exercises appear to be useful in carpal tunnel syndrome.
Atrophy of the thenar muscles, weakness of palmar abduction, and loss of sensibility (constant numbness as opposed to intermittent paresthesia) are signs of advanced neuropathy. Advanced neuropathy is often permanent. The nerve will try to recover after surgery for more than 2 years, but the recovery may be incomplete.
Paresthesia may increase after the release of advanced carpal tunnel syndrome, and people may feel worse than they did before surgery for many months.
Troublesome recovery seems related to symptoms of anxiety or depression, and unhelpful thoughts about symptoms (such as worst-case or catastrophic thinking), as well as advanced neuropathy with potentially permanent neuropathy.
Recurrence of carpal tunnel syndrome after successful surgery is rare. Caution is warranted in considering additional surgery for people dissatisfied with the result of carpal tunnel release as perceived recurrence may more often be due to renewed awareness of persistent symptoms rather than worsening pathology.
Sir James Paget described median nerve compression at the carpal tunnel in two patients after trauma in 1854.Paget J (1854) Lectures on surgical pathology. Lindsay & Blakinston, Philadelphia The first was due to an injury where a cord had been wrapped around a man's wrist. The second was related to a distal radial fracture. For the first case, Paget performed an amputation of the hand. For the second case, Paget recommended a wrist splint.
The first to notice the association between the carpal ligament pathology and median nerve compression appears to have been Pierre Marie and Charles Foix in 1913. They described the results of a postmortem of an 80-year-old man with bilateral carpal tunnel syndrome. They suggested that division of the carpal ligament would be curative in such cases. Putman had previously described a series of 37 patients and suggested a vasomotor origin. The association between the thenar muscle atrophy and compression was noted in 1914. The name "carpal tunnel syndrome" appears to have been coined by Moersch in 1938.
Physician George S. Phalen of the Cleveland Clinic drew attention to the pathology of compression as the reason for CTS after working with a group of patients in the 1950s and 1960s.
This procedure may have been pioneered in Canada by orthopedic surgeon Herbert Galloway in 1924.
Endoscopic release was described in 1988.
Alternative medicine
A 2018 Cochrane review on acupuncture and related interventions for the treatment of carpal tunnel syndrome concluded that "Acupuncture and laser acupuncture may have little or no effect in the short term on symptoms of carpal tunnel syndrome (CTS) in comparison with placebo or sham acupuncture." It was also noted that all studies had an unclear or high overall risk of bias and that all evidence was of low or very low quality.
Prognosis
The natural history of untreated CTS seems to be gradual worsening of the neuropathy. It is difficult to prove that this is always the case, but the supportive evidence is compelling.
History
CTS was first described around 1850 but was infrequently diagnosed until findings were publicized by neurologist W. Russell Brain in 1947. People were often diagnosed with acroparesthesia. Clinicians would often ascribe it to "poor circulation" and not pursue it further.
Treatment
In 1933, Sir James Learmonth outlined a method of nerve decompression of the nerve at the wrist.
See also
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