Open Access Review

Article DOI: 10.7759/cureus.27053

Carpal Tunnel Syndrome: Pathophysiology and

Comprehensive Guidelines for Clinical Evaluation
Received 06/06/2022
and Treatment
Review began 06/13/2022
Review ended 07/09/2022 Aditya Joshi 1, 2 , Karan Patel 1 , Aleem Mohamed 1 , Solomon Oak 1 , Michelle H. Zhang 3 , Hailey Hsiung 4 ,
Published 07/20/2022 Alex Zhang 1 , Urvish K. Patel 5
© Copyright 2022
Joshi et al. This is an open access article 1. Medical School, Cooper Medical School of Rowan University, Camden, USA 2. Orthopaedics, Cooper Medical School
distributed under the terms of the Creative of Rowan University, Camden, USA 3. Psychological & Brain Sciences and Biology, Johns Hopkins University,
Commons Attribution License CC-BY 4.0., Baltimore, USA 4. Healthcare (Social Sciences), Independent, Highland Park, USA 5. Public Health and Neurology,
which permits unrestricted use, distribution,
Icahn School of Medicine at Mount Sinai, New York, USA
and reproduction in any medium, provided
the original author and source are credited.
Corresponding author: Aditya Joshi, joshia47@rowan.edu

Abstract
In carpal tunnel syndrome (CTS), the median nerve is compressed at the level of the carpal tunnel in the
wrist. This entrapment manifests as unpleasant symptoms, such as burning, tingling, or numbness in the
palm that extends to the fingers. As the disease progresses, afflicted individuals also report decreased grip
strength accompanied by hand weakness and restricted movement. The first half of this review elaborates on
CTS pathology by providing readers with a comprehensive understanding of the etiology, relevant anatomy,
and disease mechanism.

CTS is considered the most common entrapment neuropathy, affecting around 3-6% of the adult population.
Further, CTS prevalence has seen a dramatic increase in the last few decades paralleling the growth of
everyday technology usage. Despite how common it is to have CTS, it can be quite challenging for physicians
to make a definite diagnosis due to differentials that present with overlapping symptoms. Even more difficult
can be deciding on a course of treatment that is the most effective and considerate of patient needs. Thus
arises the need for clear clinical direction, and hence we end with a discussion around such guidelines that
serve as a starting point toward effective diagnoses and patient treatment.

Categories: Orthopedics
Keywords: carpal tunnel syndrome, art of diagnosis, comprehensive physical exam, review article, treatment
guidelines

Introduction And Background

Carpal tunnel syndrome (CTS) is widely regarded as the most common compressive neuropathy. In the
United States, an incidence of 1-3 per 1,000 people and a prevalence of 50 per 1,000 individuals have been
reported [1]. The peak incidence years are between the ages of 45 and 54 [2], and women are three times
more likely to be afflicted by CTS than males [3]. CTS is often listed as an occupational hazard, with the US
Department of Labor and Statistics reporting the occupational incidence rate of CTS to be 0.5 per 10,000
workers [2], costing employers billions in workers’ compensation. A report by the Centers for Disease
Control and Prevention (CDC) identified the most at-risk occupations to be production workers, material
movers, and office administrative staff [4]. These occupations require repetitive motion with hands.
Occupational cases of CTS have an average duration of 27 days away from work, and nearly 23% of workers
may not return to their previous work even after undergoing surgical treatment [5].

Review
Relevant anatomy
To fully understand the carpal tunnel, one must first begin with learning the basic anatomy of the forearm
and the nerves that are associated with it. While complex, the relevant jargon serves as a prerequisite to
understanding this syndrome. In the following sections, we detail the relevant anatomy such that readers
can obtain a more complete appreciation for CTS starting from the fundamentals.

Anatomy of the carpal tunnel

Before the median nerve can make its way to the wrist, it passes through the carpal tunnel [6]. The carpal
tunnel is an anatomical landmark whose depression is made up of the proximal (scaphoid, trapezium,
lunate, pisiform) and the distal row (trapezium, trapezoid, capitate, and hamate) [7,8] of carpal bones. The
roof of the tunnel is called the flexor retinaculum, and it attaches to the scaphoid and trapezium on the
lateral side of the wrist and the hamate and pisiform on the medial side [9]. The carpal tunnel serves as a
passageway for the extrinsic tendons of the forearm and prevents them from bowing as the wrist is flexed.
The extrinsic tendons of the forearm that run through the carpal tunnel are the four flexor digitorum

How to cite this article

Joshi A, Patel K, Mohamed A, et al. (July 20, 2022) Carpal Tunnel Syndrome: Pathophysiology and Comprehensive Guidelines for Clinical
Evaluation and Treatment. Cureus 14(7): e27053. DOI 10.7759/cureus.27053
 superficialis tendons, the four flexor digitorum profundus tendons, and the flexor pollicis longus tendon
[10].

Pathophysiology of carpal tunnel syndrome

While most cases of CTS are idiopathic, the pathophysiology of CTS can be simplified to compression of the
median nerve at the carpal tunnel level, as illustrated in Figure 1 [11]. There are multiple mechanisms that
can lead to median nerve entrapment along this passageway. The two major sites of compression are at the
outlet of the tunnel under the flexor retinaculum roof and at the hamulus of the hamate. Compression can
arise from increased compartmental pressure in the carpal tunnel, and the most common mechanism of this
is hypertrophy of the synovial tissue that surrounds the extrinsic tendons of the forearm. This hypertrophy
is an inflammatory response to extensive use, trauma to the wrist, or an underlying inflammatory process
such as arthritis.

FIGURE 1: Pathophysiology of carpal tunnel syndrome illustrating the

compression of the median nerve within the carpal tunnel space.
This image is available under the Creative Commons CC-BY-NC license and permits non-commercial use,
distribution, and reproduction in any medium provided the original work is properly cited [11].

Activities that excessively engage wrist flexion or prolonged wrist movements have been noted to increase
the fluid pressure [12] and result in ischemic injury to the median nerve. There are several plausible
mechanisms that can similarly lead to ischemic injuries, such as the breakdown of the blood-nerve barrier
producing a microcompartment syndrome in the carpal tunnel, fibrotic thickening of the vasculature, or a
dysfunction of the microvasculature resulting in intraneural edema [13]. Compression can also result from
obstruction in the carpal tunnel following trauma to the wrist joint.

A high-energy trauma in young patients or low-energy trauma in elderly patients can result in volar
displacement of the lunate bone into the carpal tunnel, resulting in gross obstruction. Common causes of
injury include falling onto an outstretched hand or motor vehicle accidents. Although relatively uncommon,
this displacement can lead to entrapment of the median nerve [14].

2022 Joshi et al. Cureus 14(7): e27053. DOI 10.7759/cureus.27053 2 of 7

 While it is critical to explore the mechanisms behind the common, easily discernible CTS pathophysiology, it
is equally important to discuss the less-apparent exacerbated night pains associated with CTS. Many
individuals report an increase in CTS symptoms at night during periods of inactivity. This is due to a couple
of reasons; individuals resting in the supine position have redistribution of fluid into their distal limbs
which increases the pressure. There is also a lack of interstitial drainage in this position due to the lack of
muscle pump and movement, further contributing to the increased pressure due to lack of clearance.
Individuals often flex their wrists at night, and the prolonged flexion further compresses the roof of the
tunnel against the median nerve [15].

Understanding the common signs and risk factors

Understanding the mechanism behind carpal tunnel also allows us to understand why certain actions and
risk factors may lead to the development of, or even episodic worsening of, the syndrome. Common signs
associated with carpal tunnel include aggravation of symptoms at night, and while driving, on the phone, or
typing on a computer keyboard. As one may have guessed, most of these scenarios (and similar ones that are
CTS-associated) involve the individual flexing their wrists, which further compresses the carpal tunnel onto
itself leading to an increase in pressure to the area. Another common sign of CTS is paresthesias in the
thumb, index, middle, and medial half of the ring finger on the palmar surface of the hand. This finding can
also be explained by an understanding of the anatomy. After the median nerve crosses the carpal tunnel in
the hand, it supplies the sensory innervation to these digits. Naturally, compression of the nerve explains
the burning/tingling sensation in the sensory distribution of the nerve that many afflicted individuals
complain of [16].

Common risk factors for CTS include, but are not limited to, gender, inflammatory conditions, pregnancy,
diabetes, and hypertension. In the following, we explain these risk factors based on the current
understanding of the pathophysiology associated with CTS.

● With respect to gender, the female predominance of the condition is hypothesized to stem from the fact
that females tend to have a smaller relative cross-sectional area of the carpal tunnel than males at 9.0 and
11.3, respectively [17]. Therefore, females may be more susceptible to compression of the median nerve
within this area. However, from an occupational viewpoint, this predominance may be in part due to females
being overrepresented in occupations or assigned to tasks with a higher risk of CTS [18].

● Inflammatory conditions, such as rheumatoid arthritis (RA), lead to synovial hyperplasia (lining of the
joints). The infiltrating pannus can narrow the space in the carpal tunnel and cause compression of the
median nerve [19].

● Pregnancy is very similar to edema, in that during pregnancy the body tends to retain more fluid which
may lead to an increase in pressure. Further, pregnancy has been shown to alter levels of hormones such as
insulin; moreover, glucose metabolism has been associated with CTS development [20].

● With diabetes, the hyperglycemic conditions associated with the disease cause glycosylation and
inflammation of the tendons which prevents them from gliding past one another as they normally do.
Instead, these conditions promote stretching in the tendons [21].

● Finally, hypertension has been found to have an initial protective effect against CTS that deteriorates to a
risk factor in the long term. Hypertension presents with an elevation in arterial pressure. Thus, the loss of
blood flow from compression can be temporarily countered by hypertensive effects. However, this relief is
short-lived because the long-term effects of hypertension can produce small-vessel disease. The vasculature
will ultimately become compromised and the initial compensatory effects of hypertension will not suffice
[22].

Ways to test for carpal tunnel syndrome

The approach to diagnosing carpal tunnel syndrome includes physical tests as well as diagnostic testing via
imaging and electrophysiological measures. Physical examination techniques for CTS include Phalen’s and
Durkan’s tests. Phalen’s test is a maneuver that requires a patient to push the dorsal surface of their hands
together for 30-60 seconds. This technique increases the pressure on the median nerve by further
compressing it between the flexor retinaculum and the distal end of the radius. The test is positive if the
patient reproduces the symptoms associated with CTS, in particular, paresthesia. The sensitivity of the test
is 0.5 and the specificity is 0.33. Durkan’s test is a more provocative procedure where a patient holds out
their hand in a supinated position while an examiner places one thumb directly over the carpal tunnel along
the course of the median nerve distal to the flexor retinaculum. The examiner then places their other thumb
over the first and applies sustained pressure for 15-30 seconds. Similar to Phalen’s test, the patient is
assessed for the reproduction of symptoms, namely, paresthesia. The sensitivity of the test is 0.77 and the
specificity is 0.22 [23]. Upon physical examination, CTS also presents with a positive Tinel sign. A physician
taps the median nerve proximal to the flexor retinaculum and observes if this elicits any numbness/tingling
in the digits innervated by the median nerve [24]. However, physical examinations are not sufficient for a
definitive diagnosis and are often used adjunctively with other diagnostic tests.

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 Electrophysiological studies can clarify any uncertainty regarding a CTS diagnosis. A nerve conduction study
(NCS) tests the integrity of the median nerve by measuring the conduction velocity of the nerve across the
carpal tunnel. The presence of slower conduction times or a delayed distal response by the median nerve
innervations in digits two or three indicates a positive electrodiagnosis [25]. Electromyography (EMG) is an
electrodiagnostic test for the integrity of the muscles innervated by the median nerve, namely, the abductor
pollicis brevis. If there are any changes in the motor unit action potentials or a notable increase in
spontaneous activity in the muscle, the EMG confirms a positive diagnosis [26]. In regards to diagnosis via
imaging, the most common modality is ultrasound. The presentation of CTS on ultrasound is demonstrated
by an increased cross-sectional area in the median nerve and outward flaring of the flexor retinaculum due
to an enlarged median nerve [27]. Review of Class I and Class II evidence-based studies suggest ultrasound
is accurate at diagnosing CTS and is recommended as a supplement to electrodiagnostic studies [28].

Treatment options
Treatment of CTS ranges from conservative techniques such as nightly bracing to more aggressive
management such as surgical removal of the flexor retinaculum. The American Academy of Orthopedic
Surgeons (AAOS) guidelines strongly recommend immobilizing the wrist to improve patient outcomes [29].
A wrist brace offers a simple solution to the compression along the median nerve by stabilizing the wrist
joint in a position that is often neutral, but occasionally slightly extended, to mitigate the pressure exerted
on the median nerve. Typically, the brace is worn at night but can also be recommended for activities that
can exacerbate the symptoms of CTS, such as when typing on a computer/keyboard. However, because the
splint somewhat immobilizes the joint, there is the possibility of muscle weakness in the wrist with
prolonged bracing [30].

Other non-operative procedures also include non-steroidal anti-inflammatory drug (NSAID) use or
corticosteroid injections at the carpal tunnel to reduce inflammation of the synovial tissue. AAOS guidelines
highly recommend steroid injections and moderately recommend oral treatments such as NSAIDs [29].
NSAIDs inhibit prostaglandin synthesis which are the primary mediators of inflammation associated with
CTS. The analgesic and anti-inflammatory properties of NSAIDs can provide short-term relief but are not
curative. Corticosteroids exert anti-inflammatory effects by altering the genetic transcription of
inflammatory genes. After translocating to a cell’s nucleus, the steroid binds to glucocorticoid responsive
elements and forms a complex that can inhibit histone acetyltransferases or recruit histone deacetylases to
reduce transcription of inflammatory genes or promoters of these genes. Corticosteroids can also
conversely, instead of suppressing inflammatory genes, promote anti-inflammatory ones. Similar to NSAIDs,
steroid injections can reduce the discomfort with CTS but symptoms can reappear in the long term [31].

Additional conservative approaches include hand therapy which aims to improve the gliding among the
carpal tunnel ligaments and nerves. This therapy introduces more space in the carpal tunnel through gentle
stretching. The increased mobilization improves nerve functionality while the additional space from
stretching exercises reduces compartmental pressure [32]. Ultrasound has been found to have a diagnostic
use as well as a therapeutic use for CTS. While the mechanism is not entirely elucidated, the delivery of
high-frequency waves can produce anti-inflammatory effects and improve nerve conduction [33].

Ultimately, though, if a patient’s prognosis is severe, operative intervention may be necessary to treat their
CTS. AAOS guidelines recommend surgery for individuals who have the risk of long-term complications,
including, but not limited to, hand muscle atrophy, irreversible median nerve damage, and/or inability to
continue their occupation. Prior to surgery, guidelines recommend electrodiagnostic studies to confirm the
diagnosis [29]. For the surgical procedure, the flexor retinaculum is removed to relieve the pressure on the
median nerve [34].

Importance of proper physician examination/physician-associated

challenges
Because of the prevalence of CTS in the population, physicians need to be informed on the best clinical
practice guidelines for its diagnosis and treatment. A comprehensive review of the literature recommends
the following evidence-based guidelines: a detailed patient history with pertinent questions regarding CTS, a
proper diagnostic physical examination, electrodiagnostic tests if necessary to confirm the differential, and,
lastly, the optimal treatment given the severity of the condition [35]. It is important for such guidelines to be
in place so that physicians can recognize symptoms and respond in a timely manner to prevent permanent
median nerve damage. In the United States, the medical costs related to the diagnosis and treatment of CTS
can be as high as 13,000 dollars per surgical case, upwards of 40,000 annually for nonoperative cases, [36]
and as noted earlier have resulted in billions of dollars of expenditure for workers’ compensation. Thus,
appropriate identification and management of CTS have fiscal merits. However, this examination hinges on
physician capacity and does not come without challenges. If not presented with a proper set of guidelines or
lacking technology such as electrodiagnostic tests to confirm the diagnosis, the condition can be difficult for
physicians to navigate. With guidelines in place, physicians can reproduce diagnoses with high accuracy and
have transparency with patients [37].

In addition to physician-associated challenges that can arise from logistical limitations, navigating CTS can

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 be difficult because of a broad differential that can present with similar symptoms [38].

Several types of arthritis present with the same pain, numbness/tingling, and decrease in range of motion
associated with CTS [39]. In contrast, arthritis presentation can include nodular growths or osteophytes in
the affected joint that are not present in CTS, and while arthritis affects all digits, CTS does not affect the
fifth digit [40].

A nerve root compression due to spinal disc herniation could also reproduce the paresthesias and decreased
functionality found in CTS. As noted above, the brachial plexus provides innervation to the nerves running
the length of the arm, including the median nerve. Radiculopathy of these nerve roots by a slipped disc,
particularly C6-C7/C7-C8, will produce the symptoms found in the hand with CTS. However, because CTS is
a distal neuropathy, its symptoms are limited to the distal limb whereas a disc herniation would follow the
length of a dermatome from the trunk. Therefore, careful mapping of sensory deficits is imperative to rule
out disc herniation.

Thoracic outlet syndrome is a neurovascular compression disorder that can increase pressure on the nerves
and vessels found in the thoracic outlet [41]. This compression can be a result of the presence of a cervical
rib, hypertrophy of the anterior scalene muscle, prominent C7 transverse processes infringing on the region,
or a Pancoast tumor [42]. The compression of the brachial plexus can present with symptoms such as
tingling/discomfort in the hand [43]. Rare instances of thoracic outlet syndrome can present with atrophy of
the intrinsic muscles of the hand [44]. Similar to a spinal disc herniation, thoracic outlet syndrome is a
proximal nerve impingement and presents with upper limb deficits in addition to the distal ones [45]. The
possibility of thoracic outlet syndrome can be excluded without these symptoms as well as with a negative
result on a maneuver known as the Adson’s test [46].

A common differential that also presents similarly to CTS is repetitive overuse resulting in a strain in the
intrinsic muscles of the hand or tendonitis [47]. These conditions primarily affect the muscles rather than
nerves. Patients present with myalgias and numbness/tingling in various regions of the hand that may
overlap with the area affected by CTS [48].

Conclusions
From this broad overview emerges the importance of comprehensive care in addition to ongoing research in
regards to optimizing patient diagnosis and treatment. In the long run, efficient diagnosis and effective
treatment result in improved quality of medical care and quality of life, as well as fiscal merits for both
patients and healthcare/occupational systems. This is only possible with an extensive understanding of the
pathophysiological causes behind median nerve compression and subsequent disease. For proper diagnosis,
a thorough patient assessment is critical, and physicians should use a combination of patient history and
physical examinations in conjunction with electrophysiological diagnostic tests, being careful to balance
being meticulous without being excessive. Treatment plans should largely be personalized based on the
underlying mechanism and severity of each case. In other words, while largely prevalent in the adult
population, CTS care is not one-size-fits-all and often requires careful planning and critical thinking.

Additional Information
Disclosures
Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the
following: Payment/services info: All authors have declared that no financial support was received from
any organization for the submitted work. Financial relationships: All authors have declared that they have
no financial relationships at present or within the previous three years with any organizations that might
have an interest in the submitted work. Other relationships: All authors have declared that there are no
other relationships or activities that could appear to have influenced the submitted work.

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