CARPAL TUNNEL SYNDROME

INTRODUCTION

Background

Carpal tunnel syndrome (CTS) is often a debilitating disorder that is commonly

encountered in primary care. It is the most common entrapment neuropathy of the upper
extremity.1 Carpal tunnel syndrome is by far the most common and most important
peripheral nerve compression syndrome. It can generally be diagnosed from the history
and physical examination alone on the basis of its typical symptoms and signs.2 In
United States, the incidence of carpal tunnel syndrome is 1-3 cases per 1000 subjects
per year; prevalence is approximately 50 cases per 1000 subjects in the general
population. Incidence may rise as high as 150 cases per 1000 subjects per year, with
prevalence rates greater than 500 cases per 1000 subjects in certain high-risk groups,
the incidence and prevalence in developed countries seems similar to the United
States.3 CTS affects about 1% of working-aged people and is the most common cause
of hand pain in manual workers. It is also a costly musculoskeletal disorder with
450,000 carpal tunnel releases out annually in USA, at a total cost of 2 billion dollars.4
An increase in pressure within the carpal tunnel is the major factor known in the
etiology. The increased pressure impairs the blood supply of the median nerve and
causes nerve damage.5
Conservative treatment is the first therapeutic alternative, especially in patients without
significant sensory or motor deficits. However, despite its prevalence and the impact
of CTS on health systems, there is still much controversy regarding optimal therapy.6

ANATOMY REVIEW

Anatomy of The Hand

Muscles of Hand
The intrinsic muscles of the hand are located in five compartments:
1. Thenar muscles in thenar compartment: abductor pollicis brevis, flexor pollicis
brevis and opponens pollicis
2. Adductor pollicis in the adductor compartment
3. Hypothenar muscles in the hypothenar compartment: abductor digiti minimi,
flexor digiti minimi brevis, and opponens digiti minimi

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 4. Short muscles of the hand, the lumbricals, in the central compartment with the
long flexor tendons.
5. The interossei in separate interosseus compartments between the metacarpals.12

Thenar Muscles
The thenar muscle form the thenar eminence on the lateral surface of the palm. They
are chiefly responsible for opposition of the thumb. Movements of the thumb is
important for the precise activities of the hand. The high degree of freedom of the
movements results from the 1st metacarpal being independent with mobile joints at both
ends. Several muscles are required to control the freedom of the thumb movements.
 Extension: extensor pollicis longus, extensor pollicis brevis, and abductor
pollicis longus
 Flexion: flexor pollicis longus and flexor pollicis brevis
 Abduction: abductor pollicis longus and abductor pollicis brevis
 Adduction: adductor pollicis and 1st dorsal interosseus
 Opposition: opponens pollicis

Adductor Pollicis
The adductor pollicis is located in adductor compartment of the hand. The fan shaped
muscle has two heads of origin, which are separated by the radial artery as it enters the
palm to form the deep palmar arch. Its tendon usually caontain a sessomoid bone. The
adductor pollicis adducts the thumb, moving the thumb to the palm of the hand, thereby
giving power to the grip.

Hypothenar Muscles
The hypothenar muscles produce the hypothenar eminence in the medial side of the
palm and move the little finger. These muscles are in the hypothenar compartment with
the 5th metacarpal.
 Abductor Digiti Minimi. The abductor digiti minimi is the most superficial of
the three muscles forming the hypothenar eminence. The abductor digiti minimi
abducts the 5th finger and helps flex its proximal phalanx
 Flexor Digiti Minimi Brevis. The flexor digiti minimi brevis is variable in size;
it lies lateral to the abductor digiti minimi. The flexor digiti minimi brevis flexes
the proximal phalanx of the 5th finger at the metacarpophalangeal joint.
 Opponens Digiti Minimi. The opponens digiti minimi is a quadrangular
muscle that lies deep to the abductor and flexor muscles of the 5th finger. The
opponens digiti minimi draws the 5th metacarpal anteriorly and rotates it

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 laterally, thereby deepening the hollow of the palm and bringing the 5th finger
into opposition of the thumb
 Palmaris Brevis. Small muscle in in the subcutaneous tissue of the hypothenar
eminence. The palmaris brevis wrinkles the skin of hypothenar eminence and
deepens the hollow of the palm, thereby aiding the palmar grip12

Short Muscle of Hand

The short muscle of the hand are the lumbricals and interossei.
 Lumbricals. The lumbrical flex the fingers at the metacarpophalangeal joints
and extend the interphalangeal joints.
 Interossei. The four dorsal interossei abduct the fingers, and the three palmar
interossei adduct them. The dorsal and palmar interossei12

Carpal Tunnel
The carpal tunnel is a flat tubular tunnel located at the base of the hand. It is bordered
by the carpal bones dorsally and covered by the flexor retinaculum on the palmar side.
It is roughly 1–1.5 cm wide and encompasses the median nerve, eight digital flexor
tendons (superficial and deep flexor tendons for digit II-V) and the flexor pollicis
longus. Two bursae limit friction between the osseous structures and the tendons during
movement. The digital flexor tendons are enveloped by the ulnar bursa and the thumb
flexor is bordered by the radial bursa with communication between the two being quite
common. The carpal tunnel shows a unique arrangement where not only both bursae
provide friction prevention but also the tissue between the structures and the visceral
layer of the bursa. This specific connective tissue is described as subsynovial
connective tissue and in a non-pathological state will loosely connect the tendons and
nerve to each other. Guimberteau described that a single gliding unit is formed by the
flexor tendon, the carpal bones, the visceral synovium that moves against the parietal
synovium (which on the palmar side is fixed to the flexor retinaculum), and the
underlying SSCT. The SSCT consists of multiple layers of collagenous fibers in which
the blood and lymphatic vessels are richly represented. The fibers within the SSCT
have been visualized by electron microscopy and show multiple sheets of fibrous tissue
running parallel to the tendon, connected to each other by loose fibers, consisting of
collagen types I, III, IV, V and VI bundles. During flexor tendon movement, the
vertical fibers of the layer closest to the tendon will stretch out first. When the tendon
movement is continued, the next horizontal sheet is enlisted and subsequently the next
layer of vertical fibers will be stretched out etc., resulting in progressive recruitment of

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the layers. During movement, the SSCT provides an adaptive scaffold for the vascular
and lymphatic vessels and similar structural organizations and can be found throughout
the body.
It has been shown that as the tendons move, the SSCT layers pose a limit to the
differential movement of the adjacent tendons, inhibiting them more than what would
be theoretically possible given normal tendon and joint excursions.
Interestingly, it has been suggested that there is a difference between the vertical
orientations of individual SSCT fibers, which would result in only a certain amount of
fibers processing the tension of tendon movement at any given time. If, due to for
example excessive force, these vertical fibers tear, the next set of vertical fibers will
carry the next tension load.8

Fig 1. Cross section of the wrist with carpal tunnel structures

Nerves of Hand
The median, ulnar, and radial nerve supply the hand. In addition, branches or
communications from the lateral and posterior cutaneous nerves may contribute some
fibers that supply the skin of the dorsum of the hand. In the hand, these nerves convey
sensory fibers from the spinal nerves C6-C8 to the skin, so that C6-C8 dermatomes
include the hand.12

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Median Nerve in Hand
The median nerve enters the hand through the carpal tunnel, deep to the flexor
retinaculum, along with the nine tendons of the FDS, FDP, and FPL. The carpal tunnel
is the passageway deep to the flexor retinaculum between the tubercles of the scaphoid
and trapezoid bones on the lateral side and the pisiform and hook of the hamate on the
medial site. Distal to the carpal tunnel, the median nerve supplies two and a half thear
muscle and the 1st and 2nd lumbricals. It also sends sensory fibers to the skin of the
entire palmar surface, the side of the first three digits, the lateral half of the 4th digit and
the dorsum of the distal halves of the digits.12

DEFINITION
Carpal tunnel syndrome is a disorder caused by disturbances in nerve
function(neuropathy), leading to pain and numbness or tingling (paresthesia) primarily
in thewrist and hand.7 Carpal tunnel syndrome is the most prevalent surgically treated
problem in the hand said to affect 1–3% of the population. It is commonly described as
a compression neuropathy, affecting the median nerve at the level of the transverse
carpal ligament. CTS has been linked to vibrations, highly repetitive and forceful
finger-, hand- and wrist motions and an increase in carpal tunnel (CT) pressure, but the
exact cause remains unknown in most cases. Carpal Tunnel Syndrome (CTS) is the
most common surgically treated problem in the hand. Aside from the neuropathy itself,
the most common findings are fibrosis of the subsynovial connective tissue (SSCT)
and increased intra carpal tunnel pressure.8

EPIDEMIOLOGY

In United States, the incidence of carpal tunnel syndrome is 1-3 cases per 1000 subjects
per year; prevalence is approximately 50 cases per 1000 subjects in the general
population. Incidence may rise as high as 150 cases per 1000 subjects per year, with
prevalence rates greater than 500 cases per 1000 subjects in certain high-risk groups,
the incidence and prevalence in developed countries seems similar to the United
States.3 Demographic and occupational risk factors for CTS during 2007–2014 using
California’s workers’ compensation claims, the overall incidence of CTS was 6.3 per
10,000 FTE, and the rate was approximately three times higher in women than in
men.10

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RISK FACTORS ASSOCIATED WITH CTS
CTS remains an idiopathic syndrome, but there are certain risk factors that have been
associated with this condition. The most significant of these are environmentaLrisk
factors. Prolonged postures in extremes of wrist flexion or extension, repetitive use of
the flexor muscles, and exposure to vibration are the primary exposures that have been
reported. Medical risk factors can be divided into four categories: (1) extrinsic factors
that increase the volume within the tunnel (outside or inside the nerve); (2) intrinsic
factors within the nerve that increase the volume within the tunnel; (3) extrinsic factors
that alter the contour of the tunnel; and (4) neuropathic factors. Extrinsic factors that
can increase the volume within the tunnel include conditions that alter the fluid balance
in the body. These include pregnancy, menopause, obesity, renal failure,
hypothyroidism, the use of oral contraceptives and congestive heart failure. Intrinsic
factors within the nerve that increase the occupied volume inside the tunnel include
tumours and tumour-like lesions. Extrinsic factors that can alter the contour of the
tunnel could be the aftermath of fractures of the distal radius, directly or via
posttraumatic arthritis. Neuropathic factors, such as diabetes, alcoholism, vitamin
toxicity or deficiency, and exposure to toxins, can play a role in eliciting CTS
symptoms. This is because they affect the median nerve without necessarily increasing
the interstitial pressure within the carpal tunnel. In fact, diabetic patients have higher
tendency to develop CTS due to lower threshold for nerve damage.

ETIOLOGY AND PATOPHYSIOLOGY

Research has shown that highly repetitive and forceful motions are related to an
increased risk of CTS development and therefore focus has been directed towards digit
tendon motion and how it affects the surrounding tissue. Since the SSCT is the
connecting layer between the nerve and the digital tendons, with the superficial flexor
tendon of the third finger (FDS III) usually lying closest to the nerve, much of the
research has been focused on assessing the consequences of FDS III tendon excursions
on the SSCT structure, its force bearing potential and gliding resistance (GR). Flexion
and extension are often mimicked by having an actuator pull and release load bearing
tendons to a pre-programmed extent. A load cell is usually attached to measure force.
The term gliding resistance is used to describe the amount of force necessary to displace
a structure from point A to point B, like a tendon moving through the carpal tunnel. If
the resistance to the displacement increases, this will be reflected in the increased
necessary force and energy, meaning that high GR implicates that a relatively high
amount of force (in this context usually measured with a load cell) needed to be applied.

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Another possible term to describe relative motion is shear index. This has been defined
as the ratio of the difference in motion between structure A and B divided by the motion
of structure A.8

Fig 2. Mechanism of subsynovial connective tissue as gliding unit

Chronic pressure elevation within the carpal tunnel is associated with nerve ischemia,
but the cause of the elevation has been a topic of investigation. The fact that increased
CT pressure and SSCT fibrosis are common findings in the SSCT of patients with CTS
indicates that finding the cause(s) of the pressure difference and fibrosis might help
illuminate some of the pathology behind CTS. Increased SSCT thickness and increased
shear strain between the SSCT and FDS III tendon has been found in symptomatic CTS
patients compared to healthy controls, indicating that altered SSCT might be involved
in symptomology.8

The nerve ischaemia causes reperfusion nerve injury. Reperfusion nerve injury
included as the etiology of peripheral nerve demyelination.10 Individual myelin sheaths
in a seemingly random pattern, resulting in discontinuous damage of myelin segments.
In response to this damage the schwann cells or the schwann precursors proliferate and
initiate repair through the formation of new myelin, but these again tend to be shorter
and thinner than the original ones. The electrophysiologic hallmark of these disorder is
slowed nerve conduction velocity, reflective of the loss of myelin.11

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Fig. 3 Damaged subsynovial connective tissue

Fig. 4 Left: normal movement of median nerves in a dorsoulnar direction. Right: In

CTS patients, SSCT ingibits the excursion and translate the nerve path to palmar
direction

SIGNS AND SYMPTOMS

The hallmarks of CTS are pain and paresthesias in the distribution of the median nerve,
which includes the palmar aspect of the thumb, index and middle fingers, and radial
half of the ring finger. Symptoms can vary widely and occasionally localize to the wrist
or the entire hand or radiate to the forearm or rarely the shoulder. Patients often awaken
with symptoms and shake out their hand to provide relief. This is known as the flick
sign and is 93% sensitive and 96% specific for CTS.6 Other provoking factors include

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tasks that require repetitive wrist flexion or hand elevation, such as driving or holding
a telephone for extended periods. Because sensory fibers are more susceptible to
compression than motor fibers, paresthesias and pain usually predominate early in the
course of CTS. In more severe cases, motor fibers are affected, leading to weakness of
thumb abduction and opposition. Patients may describe difficulty holding objects,
opening jars, or buttoning a shirt. Disappearance of pain is a late finding that implies
permanent sensory loss.

Fig. 5 Patophysiology
of Carpal Tunnel
Syndrome

A complete examination of the entire upper extremity, including neck, shoulder, elbow,
and wrist, should be conducted to exclude other causes. Most patients with early, mild
to moderate CTS will not have physical examination findings. However, initial
inspection of the hand and wrist can provide clues to precipitating factors, such as signs

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of injury or arthritic changes. A square-shaped wrist (increased depth-to-width ratio)
has an odds ratio of 4.56 (95% confidence interval, 2.97 to 6.99) for CTS, likely related
to obesity.
In more severe disease, permanent sensory and motor deficits occur. Patients may have
decreased sensation to pain (hypalgesia) on the palmar aspect of the index finger com-
pared with the ipsilateral little finger on the affected hand. Lack of two-point
discrimination manifests as the inability to distinguish between points less than 6 mm
apart. Sensation over the thenar eminence should be normal in patients with CTS
because it is supplied by the palmar cutaneous branch of the median nerve, which
branches off proximal to the carpal tunnel. Therefore, decreased sensation over the
thenar eminence indicates a median nerve lesion proximal to the carpal tunnel.
Weakness of thumb abduction and opposition and atrophy of the thenar eminence may
occur in advanced CTS.
The diagnostic accuracy of provocative maneuvers for CTS varies widely. However,
these tests are simple to perform, and a combination of positive findings increases the
likelihood of CTS. The hand elevation test has similar sensitivity and specificity as the
Phalen maneuver and the Tinel sign. To perform the hand elevation test, the patient
raises his or her hands above the head for one minute; the onset of symptoms is a
positive result. One systematic review found that a classic or probable pattern on a hand
symptom diagram has a higher diagnostic accuracy than any single maneuver.1

Table 1. Diagnostic value in history and physical findings

Finding Sensitivity (%) Specificity (%)
Flick Sign 93 96
Tinel and Phalen (+) 80 92
Classic or probable pattern 64-75 73
Nighttime or morning symptoms 70 43
Phalen (+) 57-68 59-73
Thumb abduction weakness 29-65 65-80
Median nerve compression test 64 83
Square shaped wrist 53 80
Tinel sign 36-50 77
Hypalgesia 39 88
Thenar athropy 12-16 90-94

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DIAGNOSIS

A clear history and targeted examination, which identifies standard features and
provocative factors, increases the likelihood of a diagnosis. Diagnosis can be achieved
by use of criteria agreed by. The criteria comprise eight questions followed by a
decision tree.
1. Do you have any numbness or tingling in your wrist, hand, or fingers?
2. Do your symptoms spare your little finger?
3. Are the symptoms worse at night?
4. Do the symptoms wake you up at night?
5. Have you noticed your hand is weak; for example, have you found yourself
dropping things?
6. Do you find shaking your hand, holding your hand or running it under warm
water improves your symptoms?
7. Are the symptoms made worse by activities such as driving, holding a
telephone, using a vibration tools, or typing?
8. Have splints or injections helped with your pain if you have had in the past?

Alternative diagnoses that should be considered including cervical radiculopathy,

peripheral neuropathy, wrist/trapeziometacarpal, arthrosis, wrist tendonitis/
tenosynovitis and ulnar neuropathy. Contributing factors such as diabetes,
hypothyroidism, and inflammatory conditions should be considered and managed
appropriately, although there is no evidence that routine screening should be
undertaken. Electromyography and nerve conduction studies may be considered if the
diagnosis is uncertain, if surgery is being considered, or in the case of litigation
although care pathways and local availability may vary.1

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 Fig.6 CTS diagnose decision tree

Nerve Conduction Studies

All the electrophysiological examinations were performed according to the American

Association of Electrodiagnostic Medicine (AAEM) guidelines for CTS. The skin
temperature was maintained at >33 _C. The filter setting was set to between 20 Hz
and 10 kHz, the stimulation frequency to 1 Hz and the stimulation time to 0.2 ms. for
motor conduction studies. The filter setting was set to between 20 Hz and 2 kHz, the
stimulation frequency was set to 1 Hz, and the stimulation time was set to 0.2 ms. for
the sensory conduction studies. The median nerve and ulnar nerve sensory and motor
conduction studies were performed on both arms of patients, and median and
ulnar nerve F responses were observed. The sensory and motor NCSs proceeded as
follows:
1. The median sensory nerve conduction study was performed by placing an active
ring electrode on the metacarpophalangeal joint of the second finger. The
reference electrode was placed 3–4 cm distal to the active electrode. The
stimulus was performed 14 cm proximal to the active electrode between the
flexor carpi radialis and the palmaris longus tendons at the proximal of the wrist
fold. If the finger-wrist segment was normal, the second finger-palm segment
was used.
2. The ulnar sensory nerve conduction study was conducted by placing an active
electrode on metacarpophalangeal joint on fifth finger, and the reference

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 electrode was performed 14 cm proximal to the active electrode and on the
slightly medial to the flexor carpi ulnaris tendon.
3. In the median nerve conduction study, an active electrode was placed on the
center of abductor pollicis brevis muscle and the reference electrode was placed
between the first metacarpophalangeal and distal interphalangeal joint in the 4
cm distal of active electrode. Distal stimulation was performed on the medial
biceps tendon in the antebrachial fossa.
4. In the ulnar nerve motor conduction study, an active electrode was placed on
the midpoint of abductor digiti mini muscle, and the reference electrode was
placed on the bone ridge at the fifth metacarpophalangeal joint. Stimulation was
performed at three points: on the wrist (close to the flexor carpi ulnaris tendon,
7 cm proximal to the active electrode), under the elbow (3 – 4 cm distal to the
medial epicondyle) and over the elbow (on medial humerus, between the triceps
and biceps muscles, 10 – 12 cm proximal to the stimulation point under ekbow)
5. If the measurements obtained by these methods were within the normal range,
comparative tests were performed for possible minimal CTS. If
a. The median and ulnar nerve sensory peak latency difference of the
fourth finger was > 0.4,
b. The median and radial nerve sensory peak latency difference of the first
finger was > 0.5
c. The median and ulnar nerve mix peak latency difference of palm was
>0.4, minimal CTS diagnosis was accepted
According to the results of NCSs, the CTS patient were divided into six groups on the
basis of impairment severity.13

Table 2. Nerve Conduction Analysis

Negative CTS Normal finding on all tests
Minimal CTS Abnormal findings only on comparative tests
Mild CTS Sensory conduction velocity (SCV) slowed in the finger – wrist
tract with normal distal motor latency (DML)
Moderate CTS SCV slowed in the finger-wrist tract with increased DML
Severe CTS Absence of sensory response in the finger-wrist tract with
increased DML
Extreme CTS Absence of thenar motor response

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DIAGNOSIS: ULTRASOUND

The use of ultrasound (US) has been implicated in the diagnosis of CTS because
thickening of the median nerve, flattening of the nerve within the tunnel and bowing
of the flexor retinaculum are all features diagnostic of CTS. Several studies have
concluded that cross sectional area is the most predictive measurement, but there is
debate regarding the level within the tunnel that this measurement should be taken, and
what constitutes abnormal values. The cross-sectional area of the median nerve has
been used in US to classify the severity of CTS as normal, mild, moderate and severe.
A recent prospective study comparing the diagnostic utility of US versus EDS found
that the two techniques had almost equal sensitivities. Sensitivities for EDS and US
were 67.1% and 64.7%, respectively. Interestingly, when EDS and US were used
together the sensitivity increased to 76.5%, suggesting a role for US as a diagnostic
adjunct to EDS. However, a significant flaw is that 23.5% of patients with clinically
diagnosed CTS remained undetected.14

DIAGNOSIS: MAGNETIC RESONANCE IMAGING

Magnetic Resonance Imaging (MRI) is excellent for picking up rare pathological

causes of CTS such as ganglion, haemangioma or bony deformity - the presence of
which may alter surgical intervention [93]. Furthermore, sagittal images are useful in
showing the site accurately and allow the determination of the severity of nerve
compression; with a sensitivity of 96%. However, specificity is extremely low at 33-
38%. Swelling of the median nerve and increased signal intensity on T2-weighted
images indicating accumulation of the axonal transportation, myelin sheath
degeneration or oedema are the signs to look out for when diagnosing CTS. MRI is
able to predict those patients who would benefit from surgical intervention, because
the length of the abnormal nerve signal on T2-weighted MRI and the medianulnar
sensory latency difference are good predictors of surgical outcome [98]. However, the
results do not correlate well with patients’ perceived severity of symptoms [98], mainly
because MRI provides anatomical information as opposed to information on nerve
impairment and function.14

DIFFERENTIAL DIAGNOSIS

 Carpometacarpal arthritis of the thumb. Painful thumb motion, positive

grind test, radiographic findings

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  Cervical radiculopathy (C6). Neck Pain, numbness of the thumb and index
finger only, positive spurling test
 De Quervain tendnopathy. Tenderness of the distal radial styloid
 Peripheral neuripathy. History of diabetes mellitus; bilateral, lower extremity
involvement.
 Pronator syndrome. Forearm pain; sensory loss over the thenar eminence;
weakness with thumb flexion, wrist extension, and forearm pronation.
 Raynaud syndrome. Symptoms related to the cold exposure, typical colour
changes
 Wrist arthritis. Painful wrist motion, radiographic findings

TREATMENT
The treatment of CTS falls under two categories: conservative and surgical.
Conservative treatment is generally offered to patients suffering from mild to
moderate symptoms of CTS. Options of such treatment include oral and transvenous
steroids, corticosteroids, vitamins B6 and B12, nonsteroidal anti-inflammatory drug
(NSAIDs), ultrasound, yoga, carpal bone mobilisation and the use of hand splints.
O’Connor et al., reported that patients experienced significant short term benefits
with this method of treatment, but have concluded that their efficacy in the long term
remains unclear. Other conservative treatment options such as magnet therapy,
exercise or chiropractic treatment did not show any significant improvement in
symptoms when compared to a placebo or control.
The use of steroid injections has been under significant scrutiny in research focusing
on the conservative treatment of CTS. A systematic review by Marshall et al.,
reported that steroid injections given to patients with clinical CTS produced a greater
clinical improvement in symptoms one month after the injection compared to a
placebo. On the other hand, they were unable to show any significant symptom relief
beyond one month.
Corticosteroid treatment is effective in reducing inflammation and oedema, but there
are possible side effects that have to be considered when prescribing them to CTS
patients. The main side effect is that it limits reduces collagen and proetoglycan
synthesis, thus limiting tenocytes and hereby reducing the mechanical strength of the
tendon. This leads to further degeneration.
Surgical treatment of CTS is in the form of a carpal tunnel release (CTR); a

15
procedure in which the transverse carpal ligament (TCL) is cut to increase the space
in the carpal tunnel and hence reduce the interstitial pressure. Approximately 70-
90% of patients have good to excellent long-term outcomes following CTR.
CTR remains an interesting option for diabetic patients with CTS as well as
peripheral neuropathy. In these patients, symptoms would not be expected to be
totally relived by CTR since some of their symptoms reflect non-entrapment
mechanisms.14

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