Entrapment neuropathies of the upper extremity: Current practice





Introduction


Dysfunction of a nerve due to external physical compression is commonly called entrapment neuropathy . Broadly, compression neuropathies can occur for the following reasons. First, a nerve trunk can be compressed externally by any dense anatomical structure in its route in the upper extremity and hand. Such compression mostly results from changes in the structures external to the nerve when these structures have lost their normal elasticity due to degeneration, trauma, arthritic changes of an underlying joint, or compression from scar, fibrosis, or tumors. This is entrapment neuropathy, which is linked to external compression. Second, the compression can result from pathological changes inside the nerve. The intrinsic changes can originate from axons, Schwann cells, or connective tissue cells within the nerve. The possible pathogenetic mechanisms of nerve disturbance include (1) myelin distortion due to direct compression, which leads to disturbed nerve conduction; (2) increased intraneural pressure causing impaired intraneural vascularity and local nerve ischemia; and (3) intra- and perineural fibrosis, which impairs nerve gliding and stretching capacities of the myelin or intraneural vessels. Third, double- or multilevel compression may occur. Some degree of compression at a proximal level may increase the likelihood of loss of function in another more distal segment, even if the distal segment may be normal. This is considered as the third category of etiology because the etiology of clinical problems in one site is the increased tension in the nerve, which is caused by external compression in a distant site. The reason for this increased susceptibility to otherwise subclinical or minor compression lies in the impaired plasmic flow due to the more proximal or distal compression. This phenomenon is called “double crush” (or double compression). Therefore, this category of neuropathy is slightly different from entrapment neuropathy due to external causes ( Box 18.1 ). However, because the cause of “double crush” is physical, having clinical presentation after external compression, it is discussed together with the first category, entrapment neuropathy.



BOX 18.1

Broad Causes of Compression Neuropathies




  • 1.

    Entrapment neuropathy : caused by external compression.


  • 2.

    Neurological disorders : changes in structures inside the nerve, such as diseases or tumors, compressing neural structures.


  • 3.

    Double or multiple compression : Entrapment at one site of a nerve increases the susceptibility of the entire nerve; subclinical or minor external compression at other sites leads to clinical problems. This is called “double crush,” but this can occur at multiple (i.e., more than two) sites.



Systemic diseases may reveal nerves to be more susceptible to develop neuropathies, which is considered the fourth cause by some surgeons.



In addition, systemic diseases may reveal nerves to be more susceptible to develop neuropathies (e.g., diabetic neuropathy) with relatively less severe local structural abnormalities. Some pharmaceutical agents, such as vinca alkaloids, are also known to decrease the biological resistance of peripheral nerves, facilitating the way for the development of a compression neuropathy. This may be regarded as the fourth category as a composite form of peripheral neuropathy ( Box 18.1 ) ( Fig. 18.1 ). A combination of more than one cause often can be seen.




Fig. 18.1


Median nerve compression caused by systemic diseases. (A) Synovitis of the wrist after rheumatoid arthritis causing median nerve compression. (B) Carpal tunnel syndrome in a patient with gout.

(Courtesy Shu Guo Xing).


Nerve entrapment is common, and hand surgeons deal with this pathology quite regularly, although incidence of individual pathologies may differ greatly in different regions. In this chapter, the three authors present and analyze their clinical approaches and current practices. All of us feel it is key to note that entrapment sites often cited in past textbooks were based on anatomical dissections and are often not equal to the clinical sites of compression. In addition, precise diagnoses and limited surgical approaches are used by us all. A correct diagnosis and determining the indications and timing for intervention are keys to successful treatment.


The understanding of entrapment neuropathies has undergone great changes over the past decades. We expect further evolution of clinical nomenclature and development of more precise and less invasive treatment approaches.


Entrapment neuropathies in the wrist, forearm, and elbow


Carpal tunnel syndrome


Incidence and etiology.


Carpal tunnel syndrome (CTS) is the most commonly diagnosed nerve entrapment in the upper extremity. In eastern Asian countries, although CTS is commonly seen, it is not as often operated as in Western countries. In some countries, the annual number of surgical patients of CTS is only a little higher than for cubital tunnel syndrome. There is a dramatic difference in its ratio in daily practice between surgeons in the East and West. This difference may be related to differences in anatomy, such as geometry of the carpal tunnel among different populations or races, differences in surgical indications, or for social reasons, because patients may not go to see doctors for minor sensory disturbances.


The incidence in women is reported to be slightly higher than in men, perhaps three times higher, but CTS disorder is common in both genders. A study of MRI scans of 50 men and 50 women showed that the carpal tunnel cross-sectional area relative to the size of the hand is smaller in women than in men. This may be a predisposing factor in women. Most cases are idiopathic. In some patients, a pathology inside or near the carpal tunnel may be identified, such as ganglion cysts, tumors, idiopathic calcinosis, a lumbrical muscle originating in the region, or the presence of an abnormal muscle belly. After trauma, fibrotic tissue developing around the median nerve may cause recurrent symptoms. Systemic diseases increase the incidence, including renal insufficiency and dialysis (prevalence 32%), rheumatic arthritis, diabetes (prevalence up to 20%), and during the third trimester of pregnancy (prevalence 17%). ,


Many patients do not have a history of work-related injury. However, the incidence is 3 to 7 times higher in blue-collar workers than in white-collar workers due to repeating movements and intense vibration. , In some countries—for example, Germany since 2009—CTS is even recognized as an official occupational disease, if the work profile consists of such movements, and patients therefore receive a financial compensation.


Anatomical points.


The carpal tunnel is the space with the boundaries of the volar carpal ligament dorsally, the transverse carpal ligament palmarly, the scaphoid laterally, and hamate and triquetrum medially. Within the carpal canal, the median nerve runs together with nine tendons—four flexor digitorum superficialis (FDS), four flexor digitorum profundus (FDP), and one flexor pollicis longus (FPL). The relationship of these tendons with the median nerve within the carpal tunnel is rather constant. The median nerve is superficial right beneath the transverse carpal ligament, which is 14 to 16 mm long from proximal to distal and 0.8 to 2.5 mm thick. ,


Condensation of this ligament is the most common cause for compression of the median nerve. The compressed median nerve often has a decreased diameter. After months or years of compression, the median nerve segment can develop fibrosis in the epineurium or adhesions to the surrounding tendons or to the transverse carpal ligament.


Anatomical variations in the site of branching of the recurrent motor branch to the thenar muscles are not rare. The most common site of the branching is distal to the transverse carpal ligament ( Fig. 18.2 ). Early reports indicate that in 46% to 90% of hands, this branch has an extraligamentous recurrent course distal to the transverse carpal ligament and radial to the median nerve. The pattern of branching is based mainly on the report of Lanz in 1977 ( Fig. 18.2 ). A meta-analysis of 31 studies (3,918 hands) in 2015 indicates the pooled prevalence rates of the extraligamentous, subligamentous, and transligamentous courses of the recurrent motor branch were 75% (95% confidential interval: 55%–84%), 14% (4%–26%), and 11% (2%–23%), respectively. The prevalence of hypertrophic thenar muscles over the transverse carpal ligament was 18% (7%–33%). A transligamentous course of the motor branch was more commonly found in hands with hypertrophic thenar muscles (23%, 5%–43%) compared to those without hypertrophic musculature (1.7%, 0%–100%).




Fig. 18.2


(A) The length of the transverse carpal ligament and the most common pattern (75%) of branching of the median nerve near the transverse carpal ligament. The surgeon does not encounter the recurrent branch with a small incision over the transverse carpal ligament. (B and C) The second most commonly seen branching pattern (about 15%) is under the transverse carpal ligament, which can be in the distal (B) or proximal part (C) of the carpal tunnel. Transligamentous course is less common, reported to be around 10% or less, which needs careful visualization before cutting the ligament.


There are also rare incidences of branching from the ulnar aspect of the median nerve proximal or immediately distal to the transverse carpal ligament that may course over the proximal part of ligament, which make these branches susceptible to injury during carpal tunnel release. Ulnar side of branching was found in 2% (1%–4%) of hands.


However, the current popular use of a mini-incision to access the carpal tunnel may not reveal such branching variations as seen in anatomical dissections. We do not often encounter branching at or proximal to the ligament, which may relate to the use of a small incision. Nevertheless, such relatively small incidence of variable branching patterns does occur (15%–20% in our experience). The palmar cutaneous branch of the median nerve branches from the main trunk proximal to the wrist crease with a variety of patterns and courses, , This branch is also rarely encountered if a commonly used 2 to 3 cm longitudinal mini-incision is used, but it is best to be aware of this sensory nerve and to protect it in case a large incision is needed.


Clinical presentation.


Clinically, CTS is characterized by pain, with or without a decrease in sensation in the median nerve territory of the digits, i.e., the palmar aspect of the thumb, index, middle, and radial half of the ring finger, while sparing the palm and dorsum of the hand ( Fig. 18.3 ). The sensory disturbance in the pulp distal to the distal interphalangeal (DIP) joints of radial fingers or interphalangeal (IP) joint of the thumb is one of the most common and reliable signs, because the skin proximal to the DIP or IP joints is less sensitive to clinical examination and may have cross-innervation. Therefore, the clinical examination for light touch and 2-point discrimination (2PD) should be carried out volarly and distal to the DIP or IP joints.




Fig. 18.3


(A) Palmar aspect. Sensory disturbance (marked with light red) after median nerve compression at the wrist is in the radial three digits and radial half of the ring finger. The area in the palm (deep red) usually has normal sensation as the palmar cutaneous nerve branches from the median nerve proximal to the wrist. (B) Dorsal aspect. The dorsal parts of the distal index or middle fingers are not affected or have very mild tingling or numbness.


In the early stage, mild symptoms are usually absent during the day. The patient may complain waking up from sleep with hand numbness and tingling, or wake up in the morning with the symptoms, and the symptoms may become less severe with the use of the hand. In daytime, the patient may have intermittent symptoms with clumsiness of the hand and dropping held objects. Shaking the hand often improves symptoms. Decreased sleep quality can lead to absent-mindedness and accident-proneness during the day. As the disease progresses, the above typical disturbance area will appear constantly. In severe cases ( Fig. 18.3 ), which we do not see often now because patients are treated before such late development, motor weakness exists along with flatting of the thenar eminence, resulting in weakness in thumb motion and grip strength. Very severe constriction may lead to remarkable muscle atrophy, which is seen in patients with years of compression ( Fig. 18.4 ).




Fig. 18.4


(A) In severe carpal tunnel syndrome, motor weakness and atrophy of the thenar muscles (left hand) appears with flatting of the thenar eminence. (B) Severe constriction occurs if these patients are compressed for a long time, which leads to severe muscle atrophy.


On clinical examination, Tinel sign (taping over the nerve produces tingling and numbness) at the carpal tunnel is positive in most patients. The sensitivity and specificity are 60% to 70%, , especially with duration beyond the very early stage, but the absence of a Tinel sign does not rule out this diagnosis. The Phalen test (maximal wrist flexion for 60 seconds produces or exaggerates tingling and numbness of affected digits) is also useful, but less helpful than Tinel sign. However, others (including MB among us) find a positive Phalen test more frequently than Tinel sign. Reverse Phalen test (wrist in extension for 60 seconds) may also be positive. Durkan’s median nerve compression test may be of value. The test is positive when direct compression applied to the median nerve at the carpal tunnel for 30 seconds produces numbness or tingling in at least one of the radial digits. This test has a varying sensitivity depending on the pressure added. Strength of the thenar muscles should be examined and documented. In a more advanced stage, muscle weakness is present even without noticeable atrophy. In the early stage, clinical symptoms and a positive Tinel sign (or Phalen test) are the main indicators of the diagnosis, although as the disorder progresses, all the above signs become more evident.


Additional diagnostic tools.


CTS is a clinical diagnosis based on clinical findings and exclusion of other disorders. The nerve conduction test does not need to be obtained routinely. This is performed when there is any doubt of this diagnosis or when it is difficult to confirm the sites of compression at the elbow, forearm, or wrist. Ultrasound examination more often is replacing other clinical tools to detect narrowing of the carpal tunnel or median nerve, or sources of compression externally such as ganglion ( Fig. 18.5 ). We consider ultrasound routinely if there is any doubt about the site and etiology of the compression. In addition, ultrasound examination should also be routine for any revision carpal tunnel release in order to find and assess the causes and severity of recurrent compression. CT and MRI are unnecessary as a routine, and plain radiographs are used first when there is a previous distal radial fracture and a suspicion of bony protrusion to the carpal tunnel. Then a CT scan is used if necessary. If a tumor in the area or in the nerve is suspected, MRI is used. Nerve conduction tests are useful in predicting severity of functional impairment and recovery potential after treatment, but these tests are not fully accurate and are not necessary in establishing the diagnosis.




Fig. 18.5


Ultrasound is a common examination to detect the narrowing of the carpal tunnel or the median nerve under the carpal tunnel (indicated with arrows) and sources of compression.


Differential diagnosis.


It is not rare to make a misdiagnosis of CTS. Median nerve compression in the forearm is easily missed because many hand surgeons do not consider the uncommon disorders. Consequently, they label all these patients with numbness of the radial-side digits as having CTS. The key point of differential diagnosis is the patient with compression of the median nerve in the forearm has sensory disturbance in the palm because the lateral cutaneous nerve or the palmar cutaneous branch of the median nerve is affected. However, the patient may not be able to clearly state so, which creates difficulties in establishing that the compression is in the forearm. Therefore, surgeons should ask patients whether they have numbness in the palm and take care to examine whether there are tenderness points in the route of the median nerve in the proximal or midforearm. If there is such a tender point, median nerve compression in the forearm should be highly suspected. It is a common mistake either not consider compression of the median nerve in the forearm or to fail to examine there.


One even more often missed is compression at the cervical spine. In middle-aged or elderly persons, CTS may coexist with cervical root compression, but surgeons may fail to consider and diagnose cervical spine degeneration, i.e., cervical radiculopathy of C6 and C7 roots . In patients with cervical radiculopathy, release of the carpal tunnel would only partly relieve symptoms. Another frequent casualty to be considered is polyneuropathia. All of the above should be considered as an essential part of the differential diagnosis. General practitioners often label all or most hand-related pain as CTS, and hand surgeons may also not consider other possible diagnoses. Therefore, make sure there is no median nerve compression in the forearm and take care to judge whether cervical radiculopathy is more likely or present together with CTS, and then inform patients that carpal tunnel release may not fully solve the clinical problems.


The use of electrophysiological testing in the above situations differs among surgeons. Electrophysiological testing helps reliably to differentiate these reasons for compression. In the case of atypical complaints, often caused by the overlapping of several clinical pictures, differential diagnostic discussions and extended electrodiagnostics are necessary by some surgeons, but they are not considered necessary or better than clinical examination by others, as the disease is often at an early stage without positive electrophysiologic findings.


Steroid injection into the proximal part of the carpal tunnel or just proximal to the carpal tunnel is both a diagnostic and therapeutic tool. If clinical findings can lead to diagnosis, such an injection is unnecessary for diagnostic purposes, but if there is any doubt, such an injection provides additional information. If the symptoms disappear or are largely relieved for several weeks after the injection, CTS is confirmed. Some surgeons weight diagnostic steroid injection heavily, but most others, including us, consider it to be a treatment rather than an aid for diagnosis.


Conservative treatment.


Indications for conservative treatment are not consistent and may differ among groups of surgeons or patients in different countries. However, in some countries the nationwide guidelines for conservative treatment are implemented and followed. In general, suspected CTS at its very early stage with atypical clinical presentation does not need surgery. Resting, changing the working habits of the affected hand, avoiding repetitive labor, and going through therapy or steroid injection are among often used treatments. There is no solid evidence to support whether these treatments benefit recovery, as in its early stage CTS may be self-resolving, but these are among conservative treatments to alleviate pain or discomfort of the hand. The benefits of the injection of steroids are uncertain, but such injections may temporarily relieve pain for a few weeks, , which is worthwhile. Ultrasound can guide injection for accuracy, but peritendinous and perineural injection have equal effectiveness. Splinting the hand may reduce pain and discomfort, especially at night.


Not rushing to surgery for the patient with atypical symptoms and signs allows time to make more confirmative diagnosis before proceeding to surgery, and many patients do respond well to conservative measures. If the symptoms are severe and quite typical at the initial visit, the surgeon can proceed to surgical release without or with only a short course of conservative treatment.


Indications for surgery


Surgery is indicated in the patient with severe problems at initial clinical visits or failure of conservative treatment ( Box 18.2 ): (1) weakness of intrinsic muscles or visible thenar atrophy, (2) severe sensory disturbance, or (3) persistent symptoms or progression after several months of conservative treatment.



BOX 18.2

Tips for Treating Carpal Tunnel Syndrome




  • 1.

    Proceed to surgery if there is muscle atrophy or persistent symptoms. However, if the symptoms are mild, only presenting sensory disturbance or clamminess, try conservative treatment for 3 months.


  • 2.

    For uncomplicated patients with compression to the median nerve by the transverse carpal ligament as the definitive etiology and no muscle atrophy present, release through a mini-incision of about 2–3 cm or endoscopic release. Wide-awake local anesthesia is the best surgical setting.


  • 3.

    For complicated patients with severe systemic diseases or definite etiologies such as a cyst, gout, local inflammation, or foreign bodies, use an incision of 3–5 cm or longer if necessary. A mini-incision does not sufficiently work to explore the area.


  • 4.

    Patients with severe muscle atrophy as marked with flatting of the thenar muscles usually require a larger incision, because the involved nerve segment is lengthy and compression is severe.


  • 5.

    A larger incision for revision surgery or recalcitrant carpal tunnel syndrome.


  • 6.

    In all of the severe or recurrent patients, scar or fibrotic tissues around the median nerve should be removed, which usually includes removal of epineurium if it is fibrotic, but intraneural dissection is prohibited unless there is very remarkable scarring in some area inside the nerve. Always take care not to injure the recurrent branch of the median nerve to the thenar muscle, and direct visualization before cutting the ligament or dissection is always advised.


  • 7.

    These patients in 4 or 5 are best operated in main operating theaters with Bier block or brachial plexus block, as the exposure is much wider than uncomplicated patients.




Surgical methods.


It is a standard approach now to use local anesthetics (10–15 mL, 1% lidocaine with 1:100,000 epinephrine) and field sterility to do a carpal tunnel release through a longitudinal skin incision of about 2 cm over the transverse carpal ligament. The site of incision is just distal to the palmar wrist crease between thenar and hypothenar eminences. The setting can be simple, and minor procedure room is sufficient for such surgery. For local anesthesia, one of us (JBT) only injects at two sites (each site 4–5 mL of local anesthetics), with 2 cm apart, over the carpal tunnel ( Fig. 18.6 ). The skin incision is made between the two sites of injection. To reach the transverse carpal ligament, the subcutaneous tissue and dense fibrous tissues (the palmar aponeurosis) over the ligament should be cut through with a scalpel or scissors directly deep to the skin incision. Do not use scissors to transversely spread the subcutaneous tissues (which we see some surgeons commonly do), because the direct vertical dissection creates the minimal traumatic surfaces (hence minimal postoperative bleeding and risk of hematoma or edema) and minimal disturbance to any nerve branches passing from the forearm to the palm or any branches from the median nerve emerging from or adjacent to the transverse carpal ligament. The surgeon does need to look carefully in order not to injure any nerve branches over the ligament. With this narrow and direct dissection, surgeons seldom encounter a large nerve branch.




Fig. 18.6


(A and B) Injection at two sites (each site receiving 5 cc of local anesthetic), 2 cm apart over the carpal tunnel.


Making such a direct cut for a depth of 1 to 1.5 cm will expose a rigid fibrous band, the transverse carpal ligament ( Fig. 18.7 ). A careful visualization of this ligament is indispensable to avoid injury even with a mini-incision. A scalpel is used to cut this ligament directly. Sometimes, scissors can be used to cut the deepest layers or the proximal or distal edges of the ligaments. This ligament is about 5 mm thick, and it is safer to use scissors to cut the ligament entirely or its deepest layer after a cut with a scalpel in its superficial layers, although a scalpel can be used to make the cut through its entire thickness. Make sure the distal and proximal edges of the ligament are reached so the ligament is released entirely ( Fig. 18.7 ). Usually, the release requires a subcutaneous dissection proximally to the wrist flexion crease because an insufficient proximal release is a common cause of recurrence ( Fig. 18.8 ). At this point, the median nerve can be directly seen, and it can be gently released from tendons or just checked to ensure that the nerve is normal. Often, some narrowing of the nerve is present, which is not an indication to release the nerve internally, but if fibrous bands, fibrotic epineurium, or adhesions around the nerve are found, these external bands or adhesions should be removed. Such resection may include condensed epineurium, but intrafascicular neurolysis is unnecessary when epineurium is fibrotic and has been resected.




Fig. 18.7


Making such a direct incision first encounters superficial fascia (A), and then further incising to a depth of 1 to 1.5 cm reaches a rigid fibrous band (B), which is the transverse carpal ligament of about 2 cm wide and 5 to 6 mm thick.



Fig. 18.8


After incising the transverse carpal ligament, the skin incision is retracted proximally, using scissors the release can extend slightly proximally over 0.5 to 1 cm proximal to the proximal edge of the transverse carpal ligament. This relieves any mild compression caused by the fascia of the distal forearm.


A distal forearm fascial release 0.5 to 1.0 cm proximal to the transverse carpal ligament is not necessary in all patients, but after cutting the entire transverse carpal ligament, the median nerve is still restrained, which can be sensed with the tip of scissors between the median nerve and fascia, such an extended proximal release is justified. Such release of the very distal forearm fascia is usually possible within the confines of the skin mini-incision. The median nerve glides under this tense fascia with wrist flexion, so check the nerve gliding once release is complete. Skin is then closed with an absorbable suture.


The above-described direct release through a 2-cm incision is very straightforward and usually takes only 5 to 10 minutes. There is no need to do it in a major surgical room. Another technique is the biportal carpal tunnel release reported by Biyani and Downes in 1993, which has wide acceptance by some surgeons. The protection of the central, mechanically highly stressed skin bridge between thenar and hypothenar muscles is preserved and so also are the subcutaneous nerve branches, possibly avoiding pillar pain. Endoscopic carpal tunnel release is another valid option, and it can also be performed in the office or minor operating room. We all see it as a technical advancement and agree the techniques are well established. A number of studies have shown the outcomes and complications of endoscopic approach are similar to the mini-incision open approach. We believe the selection is subject to the surgeon’s preference. It is a common view and experience that the ultimate outcomes of the two approaches are similar, but some (including MB among us) often use the endoscopic approach and have found that recovery is faster, which is consistent with published reports. , In term of surgical trauma, a 2-cm mini-incision is perhaps equal to 1 or 2 incisions made with an endoscopic release. Direct visualization is technically easy, so many (including JBT and GL) prefer an open release.


Postoperative care.


No splinting is needed. When a small incision is used, the hand can be in any position that is comfortable. Often a sling to hold the forearm to the chest is sufficient. If the incision is large, hand elevation onto the opposite shoulder when sitting or standing and propped up on pillows at night is preferred for the first a few days should the patient find that position comfortable. There is no prohibition of finger motion. The patient can go back to normal hand use or job in about 2 weeks or, at most, 4 to 5 weeks without the need for therapy.


Outcomes and revision surgery.


Carpal tunnel release is a very rewarding surgery if the diagnosis is correct. The numbness disappears almost immediately. In severe cases with muscle atrophy, which is rather frequent in patients over 80 years old who seem to tolerate paresthesia and pain better than younger patients, the recovery of muscle atrophy may take a few years or may not fully recover. We do see the need of revision release in <5% our patients, which is caused by scar formation or compression by fibrous connection of an uncut portion of the transverse carpal ligament. This incidence of reoperation is in line with those in previous reports (1.7%–7%). Endoscopic release has a higher reoperation rate (7% of 88 releases) compared with open release (0% out of 103 releases). For inexperienced surgeons, an incomplete section of the transverse carpal ligament is often the cause for revision. Ultrasound or sometimes MRI examination is particularly useful in detecting or assessing local compression before proceeding to revision surgery.


Incomplete relief of symptoms in most cases may not lead to revision surgery, because incomplete relief of symptoms may relate to a wrong or incomplete diagnosis (such as in patients who have CTS with cervical spine degeneration). Compression in the forearm would also lead to incomplete or no relief of symptoms. To proceed to revision carpal tunnel release, one should find physical evidence of local compression at the carpal tunnel, i.e., very typical median nerve compression at this site with positive Tinel sign, and/or ultrasound findings of compression at this site. This would avoid failure of revision surgery. The surgical incision and exposure should be larger (4–6 cm) for revision surgery for complete release of the median nerve ( Fig. 18.9 ). Tenolysis may be necessary at the same time, sometimes together with epineural neurolysis ( without intraneural dissection except that partial laceration of the nerve is found), conduit wrapping, fat padding, or local flap transfers. These measures provide a better environment for the median nerve.




Fig. 18.9


The incision for recurrent carpal tunnel syndrome or the surgery for median nerve compression with systemic disease or severe compression to the median nerve.


Recalcitrant carpal tunnel syndrome.


This is a term used by some colleagues to group those patients who are difficult to treat, , some of whom may need revision surgery as noted above. The problems of pain and lasting symptoms of these patients may be caused by incorrect diagnosis or lengthy compression to the nerve, which results in little recovery of nerve function, or by operative trauma to the tendons and nerves through a large surgical incision. Sometimes, there are no apparent causes. The patients end up with a need for lengthy therapy, repeated surgeries, or lasting pain and disability without the expected recovery or relief. To prevent this from happening, a careful diagnosis, surgery with a confined incision, and causing no or minimal trauma to the exposed structures are key.


In proceeding to surgery for these patients, careful physical examination and use of ultrasound, MRI, or nerve conduction studies is necessary, as the causes of the problems can be complex, and surgery should deal with all existing problems. That will help find scarring, constriction, or any abnormal muscles/tendons. This is a point very different from treating most cases of CTS in its mild form.


The time interval between each of the repeated surgeries should be no less than 3 months, as the surgical areas should settle down and functional recovery should re-evaluated after each one. Repeated surgery or rush to surgery are often causes of worsening problems in these patients. In conjunction with the above treatments, because these patients often have a motor deficit, a tendon transfer to restore thumb opposition is often necessary.


Ulnar nerve compression at the wrist (guyon canal syndrome or ulnar tunnel syndrome)


Incidence.


This syndrome is much less common than CTS, and the exact incidence is unclear. In our experience, we each see perhaps 2 or 3 such patients per year. Nobody has the experience to be an expert on this syndrome. However, the diagnosis is quite straightforward. There is little information about the incidences of this disorder around the world, but we, from different regions of the world, can attest that this is much less common than cubital tunnel syndrome.


Anatomical points.


The ulnar nerve enters the Guyon canal at the level of the pisiform. This canal is formed by the volar carpal ligament and pisohamate ligament palmarly, the pisiform and the proximal belly of the abductor digiti minimi (ADM) ulnarly, and the transverse carpal ligament dorsally. The most proximal part (called zone 1) of the Guyon canal is at the level of the pisiform, where the ulnar nerve and ulnar artery pass through ( Fig. 18.10 ).




Fig. 18.10


Anatomical zones of the Guyon canal. The most proximal part (zone 1) is at the level of the pisiform. Here, the ulnar nerve and ulnar artery pass through. Zone 2 is the area distal to the pisiform up to the distal border of the pisohamate ligament. Zone 3 is distal to the pisohamate ligament.


The ulnar nerve bifurcates at the distal margin of zone 1. The motor branch, i.e., the deep branch, passes distally under the pisohamate ligament and then to the fibrous arch of the flexor and abductor digiti minimi muscles. The deep branch courses radially to innervate the interossei, lumbricals 4–5, adductor pollicis, and deep head of the flexor pollicis brevis. The superficial branch, i.e., sensory branch, courses superficially over the hypothenar muscles. The superficial branch may include some branches to innervate the palmaris brevis, but this can be overlooked, as the loss of this muscle is rarely noted. The area where the motor branch passes is called zone 2, and the sensory branch is in zone 3.


The point of bifurcating to the superficial and deep branches is at or just distal to the distal border of the pisiform ( Fig. 18.11 ). This is also the site where the hypothenar muscle starts to cover the ulnar nerve, so dissection during surgery becomes gradually deeper and more difficult. Going distally, the superficial branch sends branches over the palmar, ulnar, and dorsal aspect of the palm and to the little finger and ulnar half of the ring finger. The deep motor branch sends branches to the hypothenar muscles, while the main trunk of the motor branch makes a smooth turn around the hamate hook and travels transversely at the level of the metacarpal bases to innervate the palmar and dorsal interosseous, lumbricals to the ring and small fingers, and the first dorsal interosseous and likely the flexor pollicis brevis.




Fig. 18.11


A surgical picture showing that the superficial and deep branches of the ulnar nerve are exposed after cutting the pisohamate ligament. The superficial branch is seen in the upper part of the picture, and the deep branch in the lower part .

(Courtesy Gürsel Leblebicioğlu).


Etiologies.


There are four causes for Guyon canal syndrome: compression due to local soft-tissue trauma, a ganglion cyst, a fracture of the hamate hook, or damage to the ulnar artery (aneurysm or thrombosis).


Because the Guyon canal is narrow, trauma to the pisiform with edema of nearby structures can compress the ulnar nerve. Therefore, transit sensory disturbance to the ulnar nerve territory is not rare ( Fig. 18.12 ). However, in most cases such disturbance disappears within days to several weeks after trauma. For persistent symptoms, one should consider surgical release, shortening the time of recovery.




Fig. 18.12


Area of sensory disturbance in Guyon canal syndrome is the palmar aspects of the little and ring fingers. The areas (marked with deep red) in the palm and dorsal hand are innervated by palmar and dorsal cutaneous branches of the ulnar nerve bifurcating proximal to the Guyon canal, so these areas (marked with deep red) have intact sensation. Upper right drawing shows the dorsal aspect of the hand.


Repetitive motion of the wrist—sometimes job-related—may lead to degeneration of ligaments or muscles in the ulnar side of the wrist and compress the ulnar nerve. Disturbance to both sensory and motor function of the ulnar nerve would be present. Cycling by leaning forward and putting extensive weight on the hands can also cause ulnar nerve dysfunction in the Guyon canal.


Hypothenar hammer syndrome describes an uncommon vascular disorder caused by repeated trauma to the ulnar artery, usually as a result of occupational or sports activities that involve repetitively striking objects with the heel of the hand. The resultant thrombosis in the ulnar artery may compress the ulnar nerve. This condition is uncommon and likely does not warrant special attention. We suggest abandoning this terminology.


Ulnar nerve dysfunction associated with a distal radius fracture is rare. It mostly occurs due to laceration of the ulnar nerve in an open injury. However, in displaced hamate fractures, the reflection of the flexor carpi ulnaris tendon near its insertion on the pisiform may cause entrapment of the ulnar nerve by displaced hamate fractures or pisohamate ligament ( Fig. 18.13 ). Ulnar nerve motor branch irritation may be observed in basal fracture nonunions of the hamate hook. Thick fibrotic tissue around the nonunion can cause entrapment. Simple excision of the fracture fragment is a practical method used to relieve symptoms.




Fig. 18.13


A displaced hamate fracture can compress the ulnar nerve in the Guyon canal. Upper left : CT scan. Upper right and lower : surgical findings.

(Courtesy Gürsel Leblebicioğlu).


Space-occupying disorders in this area, such as ganglion or other tumors, foreign bodies, or vascular abnormalities, may cause symptoms ( Fig. 18.14 ). Depending on the exact location, clinical presentation may be purely motor, sensory, or both. Compression of the ulnar nerve due to trauma to the soft tissue often affects zone 1. Ganglions most commonly affect zones 1 and 2, hamate fractures zone 2, and vascular problems zone 3.




Fig. 18.14


(A) A patient with Guyon canal syndrome. (B) A ganglion was found to compress the ulnar nerve.

(Courtesy Gürsel Leblebicioğlu)


Clinical presentation.


Clinically, dull pain and clumsiness of the hand is a common finding. The initial presentation of sensory disturbance is numbness and decrease in touch sensibility (not total loss of sensation) and decrease in 2PD in the palmar aspects of the little finger and ulnar half of the ring finger ( Fig. 18.12 ) ( Box 18.3 ). Weakness in some hand functions, being unable to firmly hold an object, and dropping objects are common complaints. It is rare to see claw finger deformity initially. We do see mild claw finger deformity in patients with persistent compression of at least a few weeks duration. Therefore, it is not necessary to see any motor disturbance to establish diagnosis. In later stages, only when the compression is proximal to the bifurcation or at the motor branch do claw fingers become evident. Claw finger deformity is characterized with hyperextension of the MP joint with PIP and DIP flexion. It is also called claw hand deformity or intrinsic minus position. The deformity results from weak intrinsic muscles of the hand leading to loss of MP flexion and PIP extension. Perhaps intrinsic weakness is a better term than intrinsic minus. Because the deformity is prominent in the ring and little fingers after ulnar nerve damage, this deformity is also called ulnar claw.



BOX 18.3

Ulnar Nerve Entrapment: Guide to Diagnosis





  • Suspicion and clinical diagnosis



  • 1.

    Sensory disturbance in the little finger and half of the ring finger is the early presentation of ulnar neuropathy. This should lead to high suspicion of compression neuropathy if the ulnar nerve has not received an open injury.


  • 2.

    Mild compression may not cause motor dysfunction, so motor-related signs may be absent. However, sensory disturbance in the ulnar nerve area with tenderness at any sites of the ulnar nerve should lead to the diagnosis.


  • 3.

    Ultrasound or MRI examination can identify space-occupying masses.


  • 4.

    If weakness of the abductor digiti minimi is found, the diagnosis is further confirmed.




  • Where the compression site is?



  • 5.

    Weakness of the flexion of the distal interphalangeal (DIP) joint of the little finger (often also the ring finger) indicates ulnar nerve involvement proximal to the wrist, so cubital tunnel syndrome is suspected. In Guyon canal syndrome, flexion strength of the DIP joints of the ulnar two fingers is not affected.


  • 6.

    Possible sites of compression of the ulnar nerve, from distal to proximal, are (1) the Guyon canal, (2) the cubital tunnel, and (3) extremely rarely, the area of Struthers ligament, if this ligament exists. The Struthers ligament is ruled out through a plain radiograph looking for a bony spur on the medial border of the distal portion of the humerus. When tumors, fractures, or osteoarthritis are present, local nerve compression can occur at the sites of these disorders.




  • What is the value of clinical signs and when?



  • 7.

    Three signs can often be positive in the early stage of the disease: Froment sign is a common and sensitive test for ulnar nerve dysfunction. Jeanne sign and Wartenberg sign are other signs. Claw finger deformity (atrophy) and intrinsic muscle spasm are seen in the late stage.


  • 8.

    Some of the above signs may be negative, but positive signs almost always confirm the diagnosis. Nonetheless, these signs are common to all patients with ulnar nerve dysfunction, so compression sites and etiologies are subjected to further exam, such as the site of Tinel sign, tenderness, etc.




A series of clinical tests or signs can be used ( Box 18.3 ). Froment sign (testing the ability to hold a flat object such as a piece of paper between the thumb and index finger, i.e., pinch grip, while the examiner attempts to pull the object out of the patient’s hand) is a common test for ulnar nerve dysfunction ( Fig. 18.15 ). Jeanne sign (hyperextension of the thumb MP joint during pinch with reciprocal IP flexion) and Wartenberg sign (slightly greater abduction of the little finger) are due to weakness or paralysis of the adducting palmar interosseous muscle and unopposed action of the radial nerve innervated extensor digiti minimi and extensor digitorum communis. Other signs indicating ulnar nerve palsy include the Bunnell sign (intrinsic spasm causing MP joint flexion), André Thomas sign (clawing made worse by an unconscious effort to extend the fingers by tenodesing the extensor tendons with flexion of the wrist), and Pitres-Testut sign (the inability to actively move the middle finger in a radial or ulnar direction when the palm is placed flat on a table).




Fig. 18.15


(A) Among the examinations for ulnar nerve compression, Froment sign is the most commonly used, which tests the capability of holding a piece of paper by the thumb. (B) Atrophy of the first interosseous muscle is evident (right hand), and the right thumb of patient has to flex the interphalangeal joint in pinch action after ulnar neuropathy. This is a mild form of Jeanne sign. The left hand is normal.


Regarding these signs, surgeons have different experiences, as exemplified by the authors. GL found that Froment, Jeanne, Wartenberg, Bunnell, Froment, André Thomas, and Pitres-Testut signs become positive in his patients, but JBT uses mainly sensory disturbance, Froment sign, and tenderness at the Guyon canal for clinical diagnosis and feels one does not need all these tests to be positive. Some may be positive only in instances of prolonged or severe compression.


In patients with a ganglion or vascular abnormality, mild clawing may not interfere with performance of most daily activities. In any case, sensory disturbance always presents if the compression is not confined to the deep motor branch and is usually noted earlier than motor disturbances.


A detailed examination of sensory and motor function helps roughly localize the site of entrapment. Many surgeons note that the decreased sensibility of the dorsoulnar hand indicates entrapment of the ulnar nerve proximal to the branching of the dorsal sensory branch, which occurs in the distal forearm. Weakness of the adductor minimi indicates entrapment of the motor branch. Normal strength of the adductor minimi but weakened first dorsal interosseous muscle indicates entrapment of the superficial branch. However, because cross-innervation of some intrinsic muscles, these clinical findings do not prove, but only suggest, the sites of entrapment.


Tinel sign is a mandatory examination, and local tenderness at the Guyon canal is almost always present in compression to the main trunk (zone 1) or superficial branch (zone 3), but less frequent in compression to the motor branch (zone 2). The sensitivity of the Tinel sign is higher in this syndrome than in CTS, as the Guyon canal is narrow and superficial with a much thinner ligament covering the nerve.


Allen’s test needs to be a part of an examination as thrombosis of the ulnar artery is possible, especially in patients with repetitive labor, and ultrasound examination can augment this test.


Other diagnosis tools.


Plain radiographs and ultrasound are two major tools to assist in diagnosis and confirming or ruling out other disorders. In trauma patients, plain radiographs are always necessary to find any fractures of carpal bones including the hamate and pisiform. If a fracture of the hamate hook is suspected, a CT scan is indicated. Radiographs are also useful for investigating the presence of radiopaque foreign bodies ( Fig. 18.16 ). Ultrasound is particularly needed when the symptoms are long-lasting, development is gradual, and the patient does not recall a specific injury to the wrist. In these patients, the presence of tumors or vascular abnormalities are likely, and there are other possible causes, so an outpatient ultrasound is helpful to quickly search for a cause. Angiography or MRI may be needed if vascular abnormities are found on ultrasound or an invasive tumor is suspected, but these two tools are not necessary for most patients.




Fig. 18.16


A patient with a foreign body (a thin metal rod) in the Guyon canal compresses the ulnar nerve. In the pictures, the site of entry of the needle has a bleeding site on the palm (left) , and radiographic findings are shown in the middle and the metal rod after being taken out (right) .

(Courtesy Gürsel Leblebicioğlu).


Treatment.


In patients with ulnar nerve dysfunction, a detailed clinical evaluation should be carried out before the diagnosis of idiopathic Guyon canal syndrome is made. Many of the patients do have a cause, such as rare lesions that irritate the ulnar nerve. In CTS, the opposite is the case. Therefore, we recommend that a thorough etiologic investigation be performed before attempting treatment.


Conservative treatment is appropriate for patients with mild symptoms that may occur after trauma. Such symptoms usually disappear in 1 to 2 weeks. It is hard to define the length of such conservative treatment, but it is wise to wait for 2 to 3 weeks for any surgical decompression. For the patients with a foreign body or space-occupying disorder, there is no need to wait, and surgery should be proceeded once the diagnosis is established.


Surgical methods.


An incision is made over the Guyon canal for about 3 cm, and the volar ligament over the ulnar nerve is incised completely. Because there is only a thin layer of subcutaneous tissue over the ligament, the ligament is easily reached, and since this ligament is relatively thin (2 to 3 mm), it is easy to cut. The ulnar nerve is readily visible after the release ( Fig. 18.17 ). In our experience, pathological changes in the ligament or any pathology in the nerve or compression to the ulnar nerve is not as obvious as we see in most carpal tunnel releases. Since the Guyon canal is narrow, mild compression can cause clinical symptoms. The most proximal part of the canal, zone 1, should always be released ( Fig. 18.17 ). It is often a question how far distal to zone 1 the release should extend. Most of us first release this area up to the site of bifurcation of the ulnar nerve, at which point we use a mosquito or tips of scissors to explore around the deep and superficial branches of the ulnar nerve. If they are loose, movable, and free of compression by surrounding tissues, exploration and release can stop here, because the branched nerves are covered by looser tissue as they course distally, so release is more risky and mostly not necessary. Some surgeons always release the pisohamate ligament.




Fig. 18.17


Release of zone 1 to decompress the ulnar nerve. (A) The site of tenderness is shown with an arrow . (B) Surgical incision and exposure of the ulnar nerve. (C) Releasing the ulnar nerve from adhesions to the flexor carpi ulnaris tendon and fibrotic tissues from the pisiform. (D) The skin was closed after the ulnar nerve was released slightly distal to the pisiform. Inset shows the ulnar nerve after complete release in zone 1.

(Courtesy Jin Bo Tang)


Certainly if there is a space-occupying lesion or a vascular abnormality, or in revision surgery, the release should be directly to the specific pathology, and the surgical incision is usually longer ( Fig. 18.18 ). If there is compression to one or both branches, the release should proceed more distally, with care taken to protect branches to the intrinsic muscles. The sensory branch is traced superficially to the fibrous hypothenar arch, where it can be compressed by an ulnar artery aneurysm or thrombosis or a ganglion cyst. Integrity and complete release of the ulnar nerve (or its main branches) is to be checked after removal of a tumor or foreign body or dealing with a vascular abnormality.




Fig. 18.18


A case of revision surgery 7 months after decompression of the Guyon canal because of persistent sensory and motor symptoms. (A) Planning an extended incision for revision surgery; (B) Beginning proximally to identify the ulnar artery, veins, and the ulnar nerve. (C) Palmaris brevis muscle was identified crossing these structures. (D) The flexor retinaculum was completely transected. (E) Identification of the piso-hamate ligament (forceps below the ligament) crossing and compressing the deep branch of the ulnar nerve. (F) Complete release of this ligament.

(Courtesy Leila Harhaus).


Postoperative care.


No splinting is needed. Hand and finger motion is not prohibited. Edema of the hand usually is limited. The patient can return to normal activities in 2 to 3 weeks.


Prognosis.


We rarely see Guyon canal syndrome causes a lasting clinical problem if it is dealt with early, although reports of large case series are few. If the patient presents late with established ulnar nerve-related motor deficiencies, the release should be carried out, and secondary tendon transfers should be planned if the patient fails to recover intrinsic muscle function.


Ulnar nerve-related symptoms with carpal tunnel syndrome.


This was recognized and reported decades ago. Twenty of 59 hands (34%) of patients with CTS had abnormalities in sensibility testing of both median and ulnar nerves by either 2PD, Semmes-Weinstein monofilament testing, or both. Before surgery, 53% of patients complained of paresthesia and/or numbness in the ulnar nerve distribution. After surgery, 89% of patients had reduced symptoms in the ulnar nerve distribution. Most of these patients improved with carpal tunnel release alone. We see such patients sometimes, and the decreased sensation in the ulnar nerve territory is mild compared with that in the median nerve distribution. The patient complains of numbness of the radial digits mainly. Anatomically, the roof of the carpal tunnel is at the same time the floor of the Guyon canal. This explains why carpal tunnel release is sufficient, except when there is a definite cause of ulnar nerve compression, , because cutting the transverse carpal ligament changes the geometry of the ulnar tunnel.


Median nerve compression in the forearm


Incidence.


Median nerve compression in the forearm occurs more frequently than many have recognized, but it is hard to give a definite incidence. Most hand surgeons diagnose at most only a few cases a year each. Some surgeons have found a much higher incidence in their patient population than many others. , We believe this difference may relate to patient population and criteria of diagnosis, and also whether the compression is primary or secondary. However, such compression does exist and should be considered in any patient with hand numbness or motor disturbance. Ignoring its existence would miss the diagnosis, leaving lasting symptoms often after mistakenly performing a carpal tunnel release.


Anatomical points.


The common points of compression to the median nerve are at the lacertus fibrosus, pronator teres, and the arcade of the origin of the FDS ( Fig. 18.19 ). The lacertus fibrosus is the broad aponeurosis extending from the tendon of the biceps brachii in the cubital fossa of the elbow. The fibrosus spreads from the biceps tendon medially to over the flexor muscle bellies to the ulnar volar aspect of the forearm proximally. The lacertus fibrosus is dense near its origin in the biceps tendon and becomes thinner medially ( Fig. 18.20 ). The compression occurs in the area close to its origin from the biceps tendon where the median nerve passes under its fibers. Moving slightly distally, still in the proximal forearm, the median nerve passes between the two heads of the pronator teres or their tendinous edges, which may constitute a cause of compression, as does the tendinous arch of the origin of the FDS muscles, which is located very close to but slightly distal and deeper to the pronator teres. These tendinous parts may compress the median nerve, but even without presence of any tendinous structures, these muscles may also compress the median nerve because of the close anatomical proximity of these muscles to the median nerve.




Fig. 18.19


The relation of the flexor digitorum superficialis origin with the median nerve and the anterior interosseous nerve.

(Courtesy Julia Ruston)



Fig. 18.20


The location of the lacertus fibrosus and its relation with the median nerve.

(Courtesy Julia Ruston)


The anterior interosseous nerve (AIN) branches from the median nerve distal to the pronator teres and the origin of the FDS muscles ( Fig. 18.21 ). There are no rigid or potentially constricting structures around the trunk of the AIN. This is a very small nerve, lying anterior to the interosseous membrane between the radius and ulna. The AIN innervates three muscles in the forearm, the FPL, the radial half of the FDP muscles, and the pronator quadratus, although there is a variety of branching patterns to these muscles. One of us (GL) considers it possible that the AIN is compressed at its origin because of the pyramidal structure of FDS origin. The pressure on the AIN close to the apex on the radial side may be greater than the pressure on the main trunk of the median nerve. He found a slight compression on the median nerve in a patient, and the main compression was at the branching point of the AIN, but the main trunk of the AIN was not involved ( Fig. 18.22 ).




Fig. 18.21


The relation of anterior interosseous nerve (AIN) and neuritis or neuropathy.



Fig. 18.22


(A) Showing a patient with a tendinous band compressing the median nerve at the area of bifurcation to the anterior interosseous nerve (AIN), but the main part of the AIN was not involved. (B) Compression by a fibrous band over the median nerve in another patient.

(Courtesy Gürsel Leblebicioğlu)


Clinical presentation.


The difference of the compression of the median nerve in the proximal forearm from CTS is the presence of weakness of thumb and index finger flexion, especially at the interphalangeal joints, and sensory disturbance in the palm or sometimes distal forearm. A common mistake is neglecting these findings and misdiagnosing these patients with CTS.


Numbness of some area of the palm or fingers and thumb, or volar distal forearm, with weakness in pinch is a common symptom. The area of numbness may vary, but weak pinch is found in almost all patients and is a characteristic finding. With weakness of only the thumb IP joint and flexion of the DIP joint of the index finger, the pinch strength and clumsiness of the hand accompanied by mild pain and numbness in the palm, fingers, thumb, or distal forearm should lead to a high suspicion of median nerve compression in the proximal forearm.


With these symptoms present, the surgeon should proceed to examine the flexion power of the IP joint of the thumb and flexion of the index finger ( Fig. 18.23 ). Typically, the patient is unable to make an O sign when thumb and index finger come together for tip pinch, but lack of this sign does not rule out the diagnosis, because in its early stage this may not be obvious. In the later period, such an O sign would lead to the diagnosis. Examination of the strength of the FPL and index FDP muscles are more reliable ( Box 18.4 ). The strength may decrease at different degrees and be more pronounced in thumb IP joint flexion.




Fig. 18.23


Clinical examination: weakness of thumb flexor pollicis longus and index finger flexor digitorum profundus strength decreases the key pinch power. Severe compression results in failure to make an O sign as shown in the picture.


BOX 18.4

How to Recognize and Treat Lacertus Syndrome




  • 1.

    If there is numbness or decreased sensation in the palm along with hand clumsiness and sensory disturbance in some areas of the thumb, index, and middle fingers, always suspect median nerve compression in the forearm rather than at the carpal tunnel.


  • 2.

    If there is sensory disturbance in the distal forearm, such suspicion is strengthened.


  • 3.

    Then, press on the lacertus fibrosus and check the flexion strength of the thumb interphalangeal and index finger distal interphalangeal joints. If there is tenderness at the lacertus fibrosus and weakness in digital flexion, the diagnosis is almost certain.


  • 4.

    Be careful to check the condition of the cervical spine, because degeneration there may render the lacertus fibrosus site more susceptible, so surgical release will not entirely solve the problem. Explain to the patient such a possibility of double crush. Proceed to a minimally invasive release if the patient agrees.


  • 5.

    A 2 cm incision directly over the tender site can allow for exposure and release of the lacertus fibrosus for about 3 cm by providing traction on skin incision. We do not have to see the median nerve, as releasing the forearm compartmental fascia and the lacertus fibrosus decompresses this area sufficiently. Exploring the median nerve adds trauma.




Violinists perform by holding the bow mainly between their thumb and index finger. Meanwhile, they have to make controlled and strong pronation movements during performance ( Fig. 18.24 ). The pronator teres, FPL, and deep flexor of the index actively contract and can result in median neuropathy in the forearm. Therefore, if violinists or those who perform similar movements come to clinic, median nerve compression in the forearm should be considered.




Fig. 18.24


Violinists may be more susceptible to the compression of the median nerve by the flexor digitorum superficialis (FDS), as the FDS is tensioned during forearm pronation more often.

(Courtesy Gürsel Leblebicioğlu).


A Tinel’s sign in the proximal forearm is usually present, but local tenderness over the site of compression is even more common ( Box 18.4 ). Therefore, examination of local tenderness is as important and informative as weakness of thumb flexion strength. Tenderness should be compared with the contralateral side. The scratch-collapse test is often positive, but this test is not used by all surgeons because of their uncertainty of its value. This test adds confirmation to the site of compression if it is positive.


Although lacertus syndrome is a separate entity from pronator teres-FDS syndrome , symptoms are similar to those presented above, but the two have different findings on examination. With lacertus syndrome, local tenderness with compression at the lacertus fibrosus area (a few centimeters distal to the elbow joint) is a frequent sign. These findings clearly indicate compression of the median nerve in the forearm and lead to the diagnosis. On examination, it is suggested that one should press on the median nerve with the thumb tip under the leading (proximal) firm edge of lacertus fibrosus, not over it. It is a more sensitive sign that way. It is important to compare the findings with the contralateral extremity because this site can be naturally rather tender.


With pronator-FDS syndrome , because of the close proximity of the pronator teres and the FDS origin, it is almost impossible to know whether the pronator or FDS alone compress the nerve before surgery. Local tenderness is not always present because the compression is deep ( Box 18.5 ). However, if the site of the lacertus fibrosus is not tender, compression to the median nerve more distally should be suspected, and the pronator-FDS edge is the most likely cause. Compression at this site leads to forearm pain and weakness of thumb and index flexion indistinguishable from lacertus syndrome ( Box 18.5 ). In our patients, the only difference is often whether or not there is local tenderness at the site of the lacertus fibrosus.



BOX 18.5

How to Diagnose and Treat Pronator-FDS Syndrome




  • 1.

    We suggest the use of the expression “pronator-FDS syndrome” to recognize the fact that both structures can compress the median nerve in the forearm.


  • 2.

    The clinical symptoms are the same as with lacertus syndrome, but the site of tenderness is slightly distal and more midline, about 3 to 4 cm distal to the lacertus fibrosus. Tenderness may not be as remarkable as in lacertus syndrome, but weakness of thumb and index finger flexion is critical to make the diagnosis.


  • 3.

    The tenderness is deeper in the midline area of the proximal forearm, and when the examiner pushes harder, more tenderness is noted.


  • 4.

    Ultrasound examination will reveal possible sites of compression and whether there is any space-occupying lesion.


  • 5.

    However, even with negative ultrasound findings, surgery is indicated if clinical presentations lead to the diagnosis and have been present for at least three months. Symptoms of shorter duration may recover spontaneously.


  • 6.

    If surgery is performed, a small incision is sufficient to release any dense bands over the median nerve directly under the site of tenderness. Wider exposure is unnecessary as the preoperative ultrasound examination should check other areas.


  • 7.

    With slight traction on the skin incision proximally, the lacertus fibrosus can be exposed through this incision if the surgeon wishes to add this supplementary release.


  • 8.

    The release can be also done arthroscopically.


Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Mar 9, 2025 | Posted by in ORTHOPEDIC | Comments Off on Entrapment neuropathies of the upper extremity: Current practice

Full access? Get Clinical Tree

Get Clinical Tree app for offline access