Carpal Tunnel Syndrome--Revisited

                   Carpal Tunnel Syndrome--Revisited

                       

                                                    DR KS Dhillon

Chronic carpal tunnel syndrome was first described by James Jackson Putnam in 1880. Other medical luminaries have shed more light on the subject in the subsequent years including Paget, Marie, Ramsay Hunt, Phalen and Osler [1]. Carpal tunnel syndrome is probably the most common peripheral compression neuropathy and is defined by compression of the median nerve at wrist level.

Anatomy of the carpal tunnel

The carpal tunnel is a rigid non expendable osteofibrous tunnel situated on the front of the wrist. Anteriorly it is bound by the flexor retinaculum and posteriorly lies the carpal sulcus. Medially lies the hamate hook,triquetral bone and pisiform bone, and laterally lies the scaphoid bone, trapezoid bone and tendon of the flexor carpi radialis (FCR) muscle. The sulus is formed by the capsule, and the anterior radiocarpal ligaments which cover the proximal row of carpal bones.

Besides the median nerve there are four superficial and four deep flexor tendons of the fingers in the tunnel. On the radial side there is the long flexor of the thumb.
The location of the median nerve in relation to other structures changes as it traverses the tunnel. At the entrance the nerve lies deep to the palmaris or between the palmaris and the flexor carpi radialis.
In neutral wrist position, it usually lies anterior to the superficial flexor of the index or the middle finger with the long thumb flexor on the radial side.

More distally in the palm the nerve divides into six branches: the thenar motor branch; three specific palmar digital nerves to the radial and ulnar side of the thumb and radial side of the index finger and two common palmar digital nerves of the second and third web spaces.

Anatomical variations of the carpal tunnel structures

There are several anatomical variations in and around the carpal tunnel which affect the nerves, tendons and arteries. These variation are responsible for variation in the clinical presentation and may lead to intraoperative complication during surgery.

Some of the variations include the following [2]:

A. Nerve anomalies

• High bifurcation of median nerve (1% to 3.3% of patients undergoing surgery). The radial median branch may have its own tunnel.
• Aberrant origin of motor branch of median nerve. There can be 5 variation. Most often the branch arises distal to the carpal tunnel which is the norm. In about a third of the cases it arises within the canal and in about a quarter of the cases the branch pierces the transverse carpal ligament and courses to the thenar muscles. Rarely the branch arises on the ulna and anterior side of the median nerve and crosses anterior to the median nerve on its way to the thenar area. In some patients it enters the palm superficial to the transverse carpal ligament.
• Variations in path of palmar cutaneous branch of median nerve. Normally the palmar cutaneous branch arises proximal to the carpal tunnel and enters the palm superficial to the carpal ligament. There are two other variations, one where it pierces the carpal ligament on its way to the palm and second where it courses on the ulna side of the median nerve.
• Anomalous course of ulnar nerve. The ulnar nerve usually enters the palm through the Guyon’s canal, a depression between the pisiform bone and the hook of the hamate. Occasionally the ulnar nerve has been found to traverse the carpal tunnel and the patients can present with carpal tunnel syndrome associated with symptoms of ulnar nerve compression.
• Median nerve (MN) and ulnar nerve (UN) anomalous anastomoses. There are four commonly described anomalous connections between the MN and UN. The most common anomalous anastomosis is between the connection from MN to UN in the forearm which is known as the Martin Gruber anastomosis (MGA). The interneural connections from UN to the MN is known as the Marinacci anastomosis. When there is an interneural connection between common digital nerves of UN and MN nerves in the palm of the hand it is called the Barrettini anastomosis.  An anomalous connection from the UN to the MN in the hand is known as the Riche–Cannieu anastomosis where there is a crossover in the palm, between the deep branch of the UN and the recurrent branch of the MN. 

 B.Tendon anomalies

• Conjoint FPL and FDP II (Linburg-Comstock syndrome). In some individuals there is an anomalous tendinous connection between the FPL and the FDP tendons to the index and sometimes the middle finger. In such circumstance the individual is unable to flex the DIP joint of the thumb without concomitant flexion of the dip joint of the the finger. This can lead to tendonitis which can mimic symptoms of carpal tunnel syndrome.

C. Vascular anomalies

• Persistent median artery. A persistent median artery is sometimes seen traversing the carpal tunnel. It can significantly contribute to vascularity of the hand. Sometimes it is present with bifurcated median nerve. The presence of this artery does not produce any symptoms but may get severed during a carpal tunnel release.
• Superficial ulnar artery.The ulnar artery sometimes takes a superficial course within the forearm and travels superficial to the muscles but deep to the antebrachial fascia where it risks being severed during an extended carpal tunnel release.

D.Muscle anomalies

• Palmaris longus. The palmaris longus muscle is one of the most variable muscles in the human body. Two variations of palmaris longus are related to the anatomy of the carpal tunnel. In some individuals the tendon of the palmaris longus traverses the carpal tunnel and inserts into the palmar fascia distally. In other individuals the muscle belly of the palmaris longus may be situated in the carpal tunnel.
• Index lumbrical. The lumbrical muscle to the index finger may arise  proximally on the FDS within the carpal tunnel and can cause carpal tunnel compression syndrome.
• Flexor digitorum superficialis indicis. In some individuals the FDS muscle may be present in the carpal tunnel along the index finger tendon and cause carpal tunnel syndrome.

Etiology of carpal tunnel syndrome(CTS)

In most of the patients there is no known cause for the CTS and it is than referred to as idiopathic CTS. In some case it is due to factors around the canal or within the canal and than it is referred to as secondary CTS.

Idiopathic carpal tunnel syndrome

Idiopathic CTS is usually seen in females (65–80%), between the ages of 40 and 60 years. In about 50–60% of the patients it is bilateral [3]. Anthropometric factors such as size of the canal, sex, age and genetic factors are the most important predisposing factors. Repetitive manual
activities, exposure to vibrations, cold temperatures, obesity and smoking have also been implicated as predisposing factors for carpal tunnel syndrome [4,5].

Secondary carpal tunnel syndrome [6]

A. Abnormalities of the wall of the carpal tunnel

Conditions that alter the condition of the walls of the canal can cause compression of the median nerve. These include:

• Carpal bone subluxation or dislocation
• Distal radius fractures and implants used for fixation of fractures can reduce the carpal tunnel space
• Wrist joint arthritis, degenerative and inflammatory
• Acromegaly.   

 B. Abnormalities of content of the tunnel [6]

• Tenosynovial hypertrophy 
• Inflammatory tenosynovitis due to rheumatism, lupus and infection
• Metabolic tenosynovitis due to diabetes mellitus, amyloidosis, gout and chondrocalcinosis
• Abnormalities of fluid distribution due to pregnancy, hypothyroidism and chronic kidney failure  
• Intratunnel tumors such as lipoma, synovial cyst, synovial sarcoma, schwannoma, neurofibroma or lipofibroma
• Hematoma due to hemophilia, anticoagulant accident or trauma
• Obesity

Repetitive flexion and extension of the wrist, flexion of the fingers and forearm supination has been implicated in an increase of pressure within the canal which can predispose an individual to CTS. An increase in prevalence of CTS has been seen in individuals who work more than 20 hours per week on the computer [7]. Exposure to vibration causes injury of the myelin and axons leading to ultrastructural microcirculatory compression problems and intraneural edema which can sometimes produce CTS [8] .

Diagnosis of carpal tunnel syndrome

The typical symptoms are nocturnal acroparesthesias comprising of tingling, numbness, swelling or hypoesthesia, with or without pain reaching at least two of the first three fingers and the palm. Night pain is the most  sensitive symptom predictor (96%) in patients with CTS [9].

The Durkan's compression test [10] which is performed by compression of the median nerve in the carpal tunnel for as long as thirty seconds has a 89% sensitivity [9].

Semmes-Weinstein Monofilament Testing and Phalen's maneuver has a 83% sensitivity and hand diagram scores have a 76% [9] to 80% sensitivity [11]. The Tinel's sign has a 71% sensitivity. Some have found that the Tinel’s sign has no diagnostic value in patients with CTS [12].

Electroneuromyography (ENMG) examination

An ENMG examination is used to study the sensory and motor nerve conduction of the median nerve through the wrist. Analysis of the amplitude and duration of the sensory and motor responses is done.
Bilateral ulna and median nerve studies are carried out.

In CTS focal demyelination occurs, hence nerve conduction study (NCS) is usually more valuable than needle electromyography (EMG) study. Meticulous attention has to be paid to ‘electrode placement, distance measurements, stimulation intensity, skin temperature, and many others factors are important to prevent misdiagnosis of CTS’ [13]. The skin temperature should be maintained at about 32C for NCS.

Sensory Conduction Studies

In patients with mild or early CTS there is a mild sensory nerve conduction slowing across the carpal tunnel. A delayed or prolonged peak latency of the median sensory nerve action potential (SNAP) is typically seen.

The peak latency is usually used, instead of onset latency, for detecting CTS because of difficulty in identifying the onset of the SNAP in the presence of a large stimulus artifact [13]. With progress of the CTS the  sensory peak latency gets further delayed with the amplitude becoming smaller. In severe CTS, there usually is no recordable SNAP despite signal averaging and enhancement.
The most commonly used protocol (antidromic technique), for median nerve sensory conduction study, is the one where stimulation is applied at the wrist and median SNAPs are recorded at the thumb, the index, the middle and ring fingers [13].

Motor Conduction Studies

Motor nerve conduction of the median nerve is usually measured by obtaining recordings over the abductor pollicis brevis (APB) muscle. A delay of the distal motor latency (DML) usually supports the diagnosis of CTS. A mild prolongation of the median DML, however does not suggest focal demyelination of the median nerve [13].

Sensitivity of electroneuromyography (ENMG) examination

ENMG examination may be positive in 0–46% of asymptomatic subjects and negative in 16–24% of patients with a clinical diagnosis of CTS [14,15,16,17].

The sensitivity of motor distal latency in the diagnosis of CTS is about 54% [18]. ENMG examination does not provide extra evidence in diagnosis of CTS when the clinical diagnosis is obvious [19]. Anatomical variations such as the Martin–Gruber and Riche–Cannieu types can affect the interpretation of the ENMG examination.

Treatment of carpal tunnel syndrome

Conservative Treatment

In patients with medical causes for CTS, the underlying medical condition is treated such as ‘diuretics for fluid retention, thyroid supplementation for hypothyroidism, insulin for diabetes, and immune modulating agents for rheumatoid arthritis’ [13].

Nighttime splinting of the wrist in neutral position has been found to be useful in reducing nocturnal symptoms. Oral anti-inflammatory drugs do reduce synovitis and provide relief in some patients. The use of pyridoxine (vitamin B6) for treatment of CTS has been abandoned since it has been found to be of no value in the treatment of patients with CTS.

Though prospective studies [20,21] have shown effectiveness of the use of local steroid injections in the treatment of CTS, a Cochrane database  systematic review by Marshall et al [22] showed that local corticosteroid injection for carpal tunnel syndrome provides greater clinical improvement in symptoms for only one month after injection compared to placebo. They found that there was no significant symptom relief beyond one month. The clinical outcome was no better with steroid injection as compared to NSAIDs and splinting after 8 weeks. Steroid injections should probably not be used as an option in the treatment of CTS.

Patient education is useful in patients with work related CTS where they are advised to avoid activities which aggravate the symptoms and to do simple hand and wrist exercises. Evaluation of the workstation and redesigning the workstation along with ergonomic tool modification is often useful in work related CTS [9].

Surgical treatment for carpal tunnel syndrome

In patients with acute CTS due to trauma from fractures and dislocations around the wrist and due to bleeding, immediate surgical intervention to relieve the pressure on the nerve is usually mandatory.
In patients with subacute and chronic CTS where conservative treatment has not helped and in patients with moderate to severe symptoms, surgical release of the carpal tunnel is known to be effective [23].

Carpal tunnel release or carpal tunnel decompression surgery involves the division of the flexor retinaculum/transverse carpal ligament by open or endoscopic surgery. The existing literature shows that the long term outcome of open carpal tunnel release (OCTR) is generally good. There are wide variations in success and failure rates reported in literature, partly due to variations in patient selection and variations in the definition of success and failure. Clinical success has been reported in 75–90 % of the patients and recurrence rates of between 4–57 % have been reported [24].
The long term outcome with endoscopic surgery is indistinguishable from that of open carpal release. There are a small number of studies which suggest that there is a higher incidence of recurrence with techniques other than OCTR [24].

There is only one study by Pensy et al [25] which asserts that the functional outcome of surgical treatment is not significantly different from that of conservative treatment on long-term follow-up, though the improvement in symptom scores was greater in surgical patients.
Literature review shows that ENMG examination, the only objective data available, tends to suggest that there are long-term, persistent ENMG abnormalities in a high percentage of patients who had treatment for CTS [24].

Scholten et al [26] carried out systematic review, for the Cochrane Database, to compare the efficacy of the various surgical techniques in relieving symptoms and promoting return to work or activities of daily living in patients with CTS. They found no strong evidence to support the need for replacement of the standard open carpal tunnel release by other existing alternative surgical procedures for the treatment of carpal tunnel syndrome. They found that none of the existing alternatives including endoscopic release offered significantly better relief from symptoms in the short- or long-term.

Neurolysis

In the past many surgeons used to do internal neurolysis as an adjunctive
procedure in operative treatment of carpal tunnel syndrome. It is now, however, no longer recommended, since several clinical studies have now failed to demonstrate any benefit from neurolysis [27,28].

Release of Guyon’s canal

Patients with carpal tunnel symptoms sometimes have paresthesias in the little finger. Some surgeons used to recommend simultaneous release of Guyon’s canal. This, however, is no longer recommended because there is evidence now which shows that the dimensions of Guyon’s canal enlarges with carpal tunnel release [29].

References

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