|
Back to Physician Literature
CUBITAL TUNNEL SYNDROME AND THE PAINFUL UPPER EXTREMITY
A. Marc Tetro, MD, FRCSC, and David R. Pichora, MD, FRCSC What is cubital tunnel
syndrome? What is its relation to the painful upper extremity? What is its impact on the patient with a chronic pain syndrome? Cubital tunnel syndrome is the most common form of entrapment of the uInar nerve and the
second most common nerve compression syndrome of the upper extremity. It classically presents with arm and hand pain and associated sensory and motor dysfunction, making it a common cause of upper-extremity pain.
Prior to 1957, uInar neuropathy was felt to be a "stretch neuritis" caused by cubitus valgus. In fact, the predominant cause of ulnar neuropathy was secondary to elbow injuries. Osborne 57
proposed the concept of compression of the uInar nerve in 1957, with Feindel and Stratford 22
defining the "cubital tunnel" the following year. Since the advent of more successful orthopedic management of complex elbow injuries, the more frequent cause of ulnar nerve entrapment has become idiopathic or related to a "susceptible" patient .
41 Nonetheless, it appears that uInar nerve entrapment is increasing in prevalence (although no data are available), with pain often being a predominant morbidity.41
It is hoped that the
reader may develop an increased awareness of cubital tunnel syndrome and its place in the differential diagnosis of the painful upper extremity. An overview of the diagnostic and treatment options are presented, along
with complications that may occur.
SURGICAL ANATOMY OF THE
ULNAR NERVE
The ulnar nerve is formed from the medial cord of the brachial plexus, which originates from the C8 and T1 cervical roots
along the lateral wall of the axilla. As it passes through the proximal arm, it maintains a posteromedial relationship to the brachial artery, initially lying between the coracobrachialis and triceps muscles. In the
middle one third of the arm, the ulnar nerve accompanies the superior uInar collateral artery posteriorly through the intermuscular septum to lie on the anterior aspect of the medial head of the triceps muscle. The
nerve travels on the posterior surface of the intermuscular septum medial to the humerus, to reach the elbow. It traverses the elbow region bounded medially and anteriorly (superiorly) by the medial humeral epicondyle,
laterally by the olecranon and by a connective tissue roof spanning the two bony prominences-the "epicondylar groove." The nerve then enters the "cubital tunnel" by passing deep to the arcuate ligament
(Osborne's ligament), which connects the uInar and humeral heads of the flexor carpi uInaris (FCU) muscle. The nerve then passes between the two heads of the FCU and passes deep to the deep flexor pronator aponeurosis.
It then travels through the forearm between the FCU and flexor digitorum profundus (FDP), giving off motor branches to the FDP of the small and ring fingers. The nerve enters the wrist through Guyon's canal; a
fibro-osseous canal, extending 4 cm from the palmar carpal ligament to the fibrous edge of the hypothenar muscles. This is also a common site of uInar nerve entrapment.
The uInar nerve is primarily a motor and
sensory nerve for the hand. As such, it does not give off any branches in the arm (except small sensory articular branches to the elbow). It supplies the FCU muscle and the ring and small FDP muscles in the elbow/
proximal forearm region. Proximal to the wrist, it gives off the dorsal sensory branch to the dorsal/ulnar aspect of the hand. In the hand, it is the primary innervation to the intrinsic muscles (except for some of the
thenar muscles; superficial head of the flexor pollicis brevis, opponens pollicis, and abductor pollicis brevis), the index and long finger lumbricals, and the sensation to the uInar 1.5 digits.
The ulnar is also
well known to have anomalous connections (Martin-Gruber anastomosis) to the median nerve, primarily occurring in the forearm, which alter the motor contribution of the two nerves (primarily the intrinsic motor supply).
This is important when assessing for distal weakness caused by proximal median or ulnar nerve lesions.36,76
PATHOPHYSIOLOGY OF ULNAR
NERVE COMPRESSION AT THE
ELBOW
Cubital tunnel
syndrome is the common term used for uInar compressive neuropathies at the elbow (from the midarm to the midforearm). UInar entrapment neuropathy develops because of the predisposing anatomy of the elbow region and the
biomechanics of the ulnar nerve at the elbow; it is based on compressive, traction, and frictional forces, with the possible association of a nerve at risk. Systemic diseases such as diabetes, chronic alcoholism, renal
failure, and malnutrition may predispose the patient to compressive neuropathy (i.e., a nerve at risk).' Ultimately, the cumulative effect on the nerve is to cause a region of ischemia and inflammation resulting in
ulnar nerve dysfunction or cubital tunnel syndrome.
Compression of the ulnar nerve at the elbow may be idiopathic, but often there is a component of extrinsic compression aiding in the entrapment. Moreover, the
compression of the nerve may be dynamic or static. The dynamic anatomy and biomechanics of the cubital tunnel dramatically affect the uInar nerve, resulting in relative regional ischernia to the nerve .2, 60, 79
Dynamic impingement tends to occur early in the clinical course of the disease (i.e., position-dependent, intermittent). Although initially reversible, fixed structural changes occur over time, leading to static compression. Static compression also can develop from structural abnormalities of osseous architecture or space occupying lesions (Table 1).
78
With flexion of the elbow, the aponeurosis covering the cubital tunnel stretches, changing the cross-sectional geometry of the cubital tunnel from smooth and round to flattened and triangular. This
both decreases the volume of the tunnel by 55%,2
and significantly increases the intraneural pressure, therefore putting the nerve at risk of ischernia. Intraneural pressure can be increased up to 600% with shoulder abduction, elbow flexion, and wrist extension.
60 Moreover, contraction of the FCU muscle may increase the pressure on the ulnar nerve.62
Normally, the uInar nerve at the cubital tunnel is known to elongate 4.7 mm during elbow flexion. Should the nerve be tethered by perineural fibrosis (e.g., postoperative, posttrauma), it can no longer elongate and may experience up to doubled intraneural pressures.
60
The ulnar nerve has five common sites of compression in the elbow region 1, 25
(Fig. 1). The most common sites are at the level of the elbow. As the nerve passes by the medial epicondyle (or epicondylar groove) and into the cubital tunnel (passing deep to the aponeurosis linking the two heads of the FCU), it is at its greatest risk of compression. These are the primary sites of idiopathic disease.
1, 25,78
The other three tend to be sites of secondary or iatrogenic compression (often because of inadequate release). The most proximal site is the arcade of Struthers, a fascial band 8 cm proximal to the medial epicondyle, extending from the medial head of the triceps to the medial intermuscular septum.
(Note: This is different from the ligament of Struthers, which extends from a supracondylar process to the medial humeral epicondyle and is involved primarily with proximal median nerve compression.)
Table 1. CAUSES OF CUBITAL TUNNEL SYNDROME
Idiopathic
Trauma
Acute compression or direct injury
Entrapment in distal humeral fracture or elbow dislocation
Compression secondary to deformity--cubitus vaIgus, cubitus varus, malunion, nonunion
Heterotopic ossification-posttraurnatic, secondary to burns,80 secondary to head injury8l
Aberrant or abnormal musculature
anconeus epitrochlearis3O.45 reverse flexor carpi uInaris,69 triceps brachii (snapping)
Cumulative trauma disorders-keyboard operator, baseball pitcher
Arthritides
Osteoarthritis-secondary to osteophytes, loose bodies, synovial cysts37
Inflammatory arthritis-synovitis
Synovial chondromatosis
Vascular bands--often branches of uInar artery
latrogenic-postanesthetic palsy 61
Space-occupying lesions of the cubital tunnel and epicondyle region--e.g., lipomata
Although Struthers described the deep fascia of the arm, Spinner 72
coined the term arcade when he noted that it appeared as a distinct entity in revision ulnar nerve decompression (following anterior transposition). This structure is often indistinguishable from the
deep fascia at the primary surgery,41 however. The strong, taut intermuscular septum, normally not a structure to entrap the nerve, runs anterior to the nerve, inserting throughout the length of the
medial epicondyle. Following anterior transposition, the intermuscular septum acts secondarily as a point of local entrapment if its distal 3 cm is not excised. Finally, the last site is
at the deep flexorpronator aponeurosis. Although uncommon as a primary cause, it is often a secondary compression site following transposition.1, 25
There is increasing evidence that cumulative or repetitive trauma work disorders are a cause of cubital tunnel syndrome. Keyboard operators, for instance, appear to be at increased risk. It is
postulated that poor seating is a significant ergonomic factor; the keyboard placed too high and too close to the operator causes shoulder flexion, elbow flexion, wrist extension, and, therefore,
traction on the uInar nerve .42,62
 |
Figure 1. Five potential levels (boldface type) of compression of the uInar nerve in
the region of the elbow. (From Amadic, PC: Anatomical basis for a technique of uInar nerve transposition. Surg Radiol Anat 8:158, 1986; by permission of the Mayo Foundation.)
When considering the painful upper extremity, reflex sympathetic dystrophy (RSD) often comes to mind. Although often reported as a
posttraumatic or postoperative condition, it can occur without insult. In a series of 35 patients with RSD, 30 were noted to have peripheral nerve entrapment (single or multiple).48 Grundberg and Reagan27
also noted that, in their study of 93 cases of RSD, 29 patients did not respond to standard treatment. Further investigation of those 29 demonstrated carpal tunnel syndrome in 22 and cubital
tunnel syndrome in 5. Surgical decompression in those 27 patients led to complete resolution of their symptoms. RSD therefore may be a pertinent painful manifestation of upper-limb peripheral nerve
compression syndromes such as cubital tunnel syndrome.
There are many other causes of uInar nerve compression in the region of the forearm, as listed in Table 1.
CLINICAL PRESENTATION OF
CUBITAL TUNNEL SYNDROME
Patients with cubital tunnel syndrome tend to present with a pain, often aching or lancinating, primarily in the region of the elbow. It
may radiate proximally or distally. The most frequent complaint, however, is of paresthesias in the ring and small fingers, initially intermittent and position-related, often waking them at night.23
Objective sensory loss usually occurs later, with progression of the disease (Table 2). A clue to the location of proximal uInar nerve entrapment is the presence of dorsal sensory loss. There is usually
no sensory loss along the medial forearm because it is supplied by the medial antebrachial cutaneous nerve, a branch of the medial cord of the brachial plexus. Most importantly, examining for Tinel's
sign helps localize the entrapment.
Patients often note they have "weak or clumsy hands," often dropping objects or being unable to open jars. Muscle weakness or
atrophy often occurs and, in many patients, in the absence of any objective sensory change. The fascicles to the intrinsic ulnarly supplied hand muscles are more susceptible because of their
superficial topographic location within the ulnar nerve at the cubital tunnel (FCU and FDP often are spared). Muscle weakness may be demonstrated by clawing of the hand, Wartenberg's sign or
Froment's sign although these indications are not helpful in localizing the lesion. 23,41 Because of the common anomalous connections between the median and uInar nerves (17% incidence
of Martin-Gruber anastomosis) that primarily affect the intrinsic innervation, however, weakness from significant cubital tunnel syndrome may be absent.
DIAGNOSIS
The elbow flexion test, a provocative test, is analogous to Phalen's test for carpal tunnel syndrome. Patients are positioned with their arms at their side, and elbows flexed approximately 120 degrees.
The patient maintains that position for 3 minutes in an attempt to reproduce their symptoms (by compression or tension on the nerve).6 Rayan63 found this test positive in 10% of the control group
and therefore questioned its usefulness. Novak and Mackinnon50 recently demonstrated that elbow flexion combined with pressure over the uInar nerve for 30 seconds was the most sensitive and
specific provocative test for cubital tunnel syndrome.
Routine radiographs are often desirable to establish the presence of abnormal skeletal anatomy, malalignment, or compressive osseous
structures. On specialized plain radiographs of the elbow, approximately 20% to 29% of patients with cubital tunnel syndrome had abnormalities, compared with 6% of controls .67
Table 2.
STAGING OF ULNAR NERVE COMPRESSION AT THE ELBOW
Mild
Sensory,
Intermittent paresthesias; vibratory perception increased
Motor, Subjective weakness, clumsiness, or loss of coordination
Tests, Elbow flexion test or Tinel's sign may be positive
Moderate
Sensory, Intermittent paresthesias; vibratory perception normal or decreased
Motor, Measurable weakness in pinch or grip strength
Tests,
Elbow flexion test or Tinel's sign is positive; finger crossing may be abnormal
Severe
Sensory, Persistent paresthesias; vibratory perception decreased; abnormal two-point discrimination
(static >6 mm, moving >4 mm)
Motor, Measurable weakness in pinch and grip plus muscle atrophy
Tests, Positive elbow flexion test or positive Tinel's sign may be
present; finger crossing usually abnormal
Electrophysiologic Studies in Cubital
Tunnel Syndrome
Electrophysiologic investigations are very helpful in the diagnosis of cubital tunnel syndrome, particularly in a difficult diagnostic problem, such as the patient with multiple complaints or diffuse
upper-extremity pain.41 In some circumstances, however, the studies may prove to be normal in a clinically diagnostic case of cubital tunnel syndrome (often mild and intermittent). One review
noted nerve conduction study abnormalities ranged from 23% to 93% in classic cases of cubital tunnel syndrome.11 Moreover, the severity of the clinical manifestations does not always correlate with
the objective electrodiagnostic changes .35 Determination of exact location of entrapment may be difficult and, more importantly, -the accuracy of these studies is user-dependent. The most commonly
described abnormality is a decrease of 10 meters/second in conduction velocity over the region of the elbow. Raynor et aI64 recently found that surface-recorded sensory and mixed nerve
studies are more sensitive than motor studies in the diagnosis of cubital tunnel syndrome, particularly in cases with subtle clinical involvement.
Many do not believe that nerve conduction studies are necessary if the diagnosis of cubital tunnel syndrome is obvious.41, 43 In fact, Mackinnon and Dellon41
stated: "It is clear that there is no reason to deny surgery to a patient with a normal preoperative electrical study, or to require all patients to have such a study if the history
and physical examination of the patient are themselves consistent with uInar nerve compression at the elbow." Ideally, however, most upper-extremity surgeons believe that an electrodiagnostic
abnormality should be present to establish a diagnosis of cubital tunnel syndrome.56 Moreover, some have stated that a normal electrophysiologic study is a contraindication to surgery.9, 78
Electrodiagnostic studies postoperatively do not have a strong correlation with the recovery the patient experiences. There is a high rate of velocity and latency recovery following surgery, but the
nerve conduction recovery does not always correlate with the functional recovery, particularly the distal motor recovery.
Differential Diagnosis of Cubital
Tunnel Syndrome
The diagnosis of cubital tunnel syndrome is based on the clinical symptoms and signs, along with the objective electrophysiologic findings. Reaching the correct diagnosis in a timely fashion is
difficult but plays an important role in outcomes. Chan 3,7 noted that, if treated within 1 year of onset of symptoms, 88% of patients with cubital tunnel had a good result, compared with only 67%
showing improvement in those treated longer than 1 year after onset. A delay in diagnosis therefore puts the patient at increased risk of chronic neuritis and pain caused by the prolonged and increasing injury.
Awareness of the differential diagnosis is important to be aware of to arrive at the correct diagnosis in a timely manner. Compression of the u1nar nerve at the cubital tunnel is most often confused with
other sites of uInar nerve (or its fibers) compression, proximal or distal to the elbow.
1. Cervical disc disease-in particular, that of the C8 root (C7-TI
level)-often causes paresthesias in the small and ring fingers, sometimes with associated weakness of the intrinsic muscles of the hand. It often has associated painful, limited cervical motion, however.
2. Thoracic outlet syndrome is a compression of the medial structures of the brachial plexus, primarily the medial cord, as they exit the thoracic outlet. It often mimics cubital tunnel syndrome
(pain, paresthesias, and weakness). The clinical diagnosis can be made or at least suspected with provocative testing ("hands up" test-90-degree shoulder abduction, external rotation while making a
fist, often replicates the symptoms). Electrodiagnostic studies are often not reliable.23
3. Compression of the uInar nerve at Guyon's canal, at the level of
the wrist, is often very similar in presentation. The uInar nerve may have sensory, motor, or combined dysfunction, depending on the level of compression in the canal.
The discriminating clinical findings are a lack of sensory changes on the dorsum of the hand and more distal pain (variable).
Uncommon sites of compression may occur proximally, such as by
a Pancoast tumor. So called double crush syndromes may also occur, whereby the nerve is compressed or irritated at two sites, with the effect being additive. Examples include thoracic outlet
syndrome plus uInar nerve compression at the elbow and compression of the cubital tunnel along with Guyon's canal. Indeed, we have observed a number of cases in which clinical or
electrodiagnostic examination suggested pathology at both the cubital tunnel and Guyon's canal. Our practice has been to decompress both sites (with good results) when we were unable to
identify a single predominant site preoperatively.
Errors or delay in the diagnosis of cubital tunnel syndrome may have a profound impact on the outcome. With continued neural
dysfunction caused by any unusual repetitive stress, load, or anatomical abnormality in the region, chronic compression may lead to irreversible neural inflammation and fibrosis.35 The longer the
injury to the nerve continues without treatment, the higher the likelihood the nerve will not recovery completely.7 In fact, Gabel and Amadio25 noted the time from onset of symptoms to index
treatment in their group of failed decompressions averaged 35 months (range 8-180 months). A delay in diagnosis therefore puts the patient at increased risk of chronic neuritis and pain because of
the accumulating injury.
TREATMENT OF CUBITAL TUNNEL
SYNDROME
Progress in the management of ulnar nerve syndromes has been affected by: (1) delayed diagnosis and (2) treatment that is often
based on personal bias rather than scientific results.13 The principles of treatment of uInar nerve compression and chronic arm pain are:
1.identification of the presenting signs and symptoms
2.reaching the correct diagnosis and ruling out other common differential diagnoses
3.treating the patient appropriately to optimize recovery of neural
function and lower the risk of postoperative complications (neuroma, neuritis, inadequate release)
Nonoperative Treatment
As discussed, idiopathic uInar neuropathy often initially manifests
as intermittent or mild symptoms. At the early, mild stage, the process may be reversible if treated prior to the onset of chronic neural changes.78 The goals of conservative treatment are to reduce
the inflammatory state of the perineural tissues, to enhance vascular perfusion of the nerve, and, indirectly, to restore normal axonal transport. The results are quite encouraging for those with
mild symptoms. Dimond and Lister 18 reported on 73 patients with cubital tunnel syndrome, treated with long arm splints. Dellon et al16 noted that, with more progressive clinical and
electrophysiologic findings, it is more likely that the patient will require surgery. Specifically, 89% of those with only mild, intermittent disease were successfully treated nonoperatively,
whereas only 38% of those with moderate disease (persistent paresthesias, muscle weakness, abnormal two-point discrimination [< 10 mm]) were successfully managed conservatively. Moreover, if
the neuropathy was posttraumatic in nature, there was an increased chance of failure with conservative treatment.
To date, no guidelines have been widely agreed upon as to whom
should be treated conservatively. Urbaniak78 believes patients with the following traits should undergo a trial of conservative treatment:
1.early symptoms, intermittent episodes
2.mild paresthesias without significant
pain
3. minimal physical findings (slight numbness), with normal motor examination
It is well recognized that those with severe findings of weakness,
decreased two-point discrimination, and electromyographic evidence of denervation potentials should undergo operative exploration without a trial conservative treatment.3, 16, 23, 41, 78
The principles of conservative treatment are: (1) avoiding aggravating factors (i.e., pressure on the elbow, repetitive flexion/extension), (2) avoiding full flexion (particularly at night), and (3) optimizing the
environment (nutrition, decrease inflammation).23, 78 Effective measures include the avoidance of pressure with elbow pads,16, 18, 23 splints (particularly at night) to prevent elbow flexion,
16, 18 avoidance of repetitive movements, and ergonomic workplace modification.42,12 The use of nonsteroidal anti-inflammatory drugs,18, 23, 35, 62 local corticosteroids, and vitamin B6
25 may be beneficial. Patients should be followed at 1 to 3 month intervals until improvement is noted and maintained. If no improvement occurs or if
the symptoms progress, repeat electrodiagnostic studies are warranted, particularly in noncompliant patients.3, 16,43
Operative Treatment
If the symptoms are moderate or severe, or if the patient has failed nonoperative treatment, surgical decompression is the next treatment option. Most authors agree that the patient should have
an electrodiagnostic abnormality to be considered an operative candidate.9, 56
Local procedures to decompress the u1nar nerve aim to restore a
favorable environment for the nerve but maintain its normal anatomic position, whereas transposition procedures reposition the uInar nerve into an uninvolved environment.78 Understanding the effects of
surgery on the nerve is critical to deciding which procedure to undertake. Ogata et al53 have shown that the segmental blood supply of the ulnar nerve is significantly reduced for 72 hours
following transposition, whereas neither of the local procedures alter its vascularity. Conversely, if there is a disease process in the region of the cubital tunnel, a transposition procedure removes the
nerve from the pathology. Urbaniak and GabeI78 make the following recommendations about primary procedures:
1.If decompressed in situ or by medial epicondylectomy, there
should be no evidence of abnormalities within the cubital tunnel (i.e., no structural changes, inflammatory arthritis, or prior fractures)
2.If the nerve is transposed, the surgeon should take care to ensure
no new foci of compression are created.25
Local Procedures
Local decompression of the ulnar nerve can be achieved in situ by
either simple decompression or by medial epicondylectomy. In situ decompression involves the release of the deep fascia overlying the nerve in the epicondylar groove and of the FCU aponeurosis. In one
review, 90% of those with mild symptoms had relief with any surgical procedure, but local decompression was rarely successful for moderate disease.13 Bednar3 recommends that this procedure
be limited to those with compression isolated to the FCU aponeurosis. Ferlic24 recommends decompression alone only when (1) symptoms are mild or intermittent, (2) there is no subluxation or
instability of the uInar nerve (anterior to the epicondyle), (3) there is absence of pain, (4) osseous architecture of the elbow is normal, and (5) the findings at surgery are consistent with compression in
the cubital tunnel. In situ decompression is therefore recommended for those with a short history, normal architecture of the cubital tunnel and osseous structures, and in whom the ulnar nerve is
compressed by the FCU arcade (Osborne's ligament).78
The most common complication of in situ decompression is a failure to relieve symptoms. Anterior subluxation is a problem that
tends to become a complication only if it is not detected at surgery (and treated with anterior transposition) .3
Medial epicondylectomy has been advocated by many for treatment
of all stages (mild to severe) of ulnar nerve compression at the elbow.28, 29 Dellon's review,13 however, noted good results in 90% of those with mild disease but in only 50% of those with moderate
disease. Moreover, the procedure had the highest rate of recurrence of all procedures reviewed. Heithoff et al28 found that extensive or complete epicondylectomy was associated with improved results
but controversy surrounds the possibility of medial collateral ligament (MCL) instability by excessive resection of the epicondyle (and MCL origin).52 With only a single report of instability following
epicondylectomy, this concern is reasonable but remains theoretical.8 O'Driscoll et al52 reported the precise anatomy of the origin of the MCL and described an oblique osteotomy of the
epicondyle to preserve its origin 52 (Fig. 2A, B). We believe this technique provides excellent decompression of the nerve, at the same time preserving stability. Other possible complications
include failure to fully decompress the nerve and inadequate resection, with persistent Symptoms. 3, 8
We believe that local decompression with or without
epicondylectomy should include neurolysis proximal (to include the arcade of Struthers) and distal into the FCU (aponeurosis and flexor pronator aponeurosis). We have had good success employing an
extensive local decompression combined with medial epicondylectomy. Care must be taken to preserve the origin of the MCL with an oblique osteotomy of the epicondyle, to repair the
flexor-pronator origin, and to cover the exposed bone with fascia and muscle to prevent nerve adherence to bone.
 |
Figure 2. A, Medial part of the distal humerus removed by orthogonal osteotomies.
On right 2 mm thick coronal slice through the widest part of the AMCL origin and the tip of the epicondyle. (Mean values are shown.) B, As the AMCL origin is
anterior and inferior on the medial epicondyle, an osteotomy in a plane between the sagittal and coronal planes would permit removal of more bone while
minimizing violation of the AMCL origin. (From O'Driscoll, et al: Origin of the medial ulnar collateral ligament. J Hand Surg 17(A): 165-166, 1992; with permission.)
Transposition Procedures
Anterior transposition procedures move the ulnar nerve anterior to the axis of elbow motion and thereby theoretically decrease the
traction and compressive forces upon the nerve. 62 There are three types of transposition-subcutaneous, submuscular, and intramuscular. Subcutaneous transposition moves the nerve into the
subcutaneous plane and holds it there with a fascial sling. 19, 20 Submuscular transposition moves the nerve deep to the flexor pronator mass .62 Intramuscular transposition places the nerve in a
channel within the flexor pronator mass without damaging the muscle origin.34, 35
Gabel and Amadio25 have observed that "anterior transposition can
remove the nerve from the environment of the cubital tunnel and medial epicondyle, but the surgeon may overlook or even create other levels of mechanical impingement." Does the decreased blood
flow caused by anterior transposition predispose the nerve to fibrosis?13 The results of anterior subcutaneous transposition were 90% good for mild disease, 70% good for moderate disease, and
50% good for severe disease.13 The results of submuscular and intramuscular transfer were equally good for mild and moderate disease, but the intramuscular transpositions had the worst results
of any treatment of severe disease.3 The risk of scar formation and perineural fibrosis appears to be equal with both intramuscular and submuscular transposition, according to an in vivo study by Dellon et al.
17
Internal Neurolysis
The question has arisen as to whether decompression should include internal neurolysis. The recommendation for internal
neurolysis is based on anecdotal results, with no studies demonstrating its efficacy in uInar neuropathy.13 Moreover, internal neurolysis may incite prolonged pain along the uInar nerve.1
External neurolysis tends to cause minimal trauma to the nerve whereas internal neurolysis has been shown to be detrimental in both clinical and experimental studies 1, 78 It disrupted the
segmental as well as the longitudinal blood supply over the neurolysed segment.52 Gabel and Amadic,25 reported that two of six patients who underwent internal neurolysis at the index
procedure experienced permanent loss of motor/sensory function upon repeat decompression. Very extensive external neurolysis may also be harmful and it should be limited to the extent needed to decompress the nerve.
COMPLICATIONS OF TREATMENT
OF CUBITAL TUNNEL SYNDROME
Complications of Nonoperative
Management
1.Poor outcome of treatment of moderate or severe compression
2.Poor outcome in the noncompliant patient
3. Failure to recognize progression of symptoms
Complications of Operative
Treatment
Complications of operative management are primarily:
1. Injury to the medial antebrachial cutaneous nerve
2. Failure to completely decompress the nerve
3. Formation of new points of constriction
Injury to the medial antebrachial cutaneous nerve (MACN) is the
most common complication of uInar nerve surgery. 15 In fact, in one study, 7 of 14 failed decompressions had painful neuromata of the MACN.65 Understanding the anatomy of the MACN is the key to
preventing this painful complication. Masear et al46 noted at least one branch of the MACN (from the posterior division) crossing the region of the classic cubital tunnel incision in 40% of cadavers.
Most have a branch at the level of the medial humeral epicondyle.46 These branches, one to three in number, can lie from 6 cm proximal to 6 cm distal to the humeral epicondyle .16
If transected, the manifestations of injury to the MACN are hypesthesia, painful scar "neuroma pain," or hyperalgesia. Hypesthesia is usually of little
concern. The painful "neuromatous" scar and hyperalgesic nerve are often extremely symptomatic complications. The pain, localized to the elbow and the scar, is often aggravated by movement or
touching the region. It may overshadow a successful restoration of u1nar nerve function. The diagnosis is usually by MACN block and treatment is initially nonoperative, with a 6-month course of
desensitization. Surgery is reserved for those who fail therapy and have a well-localized, tender scar.
Surgical treatment is varied. If injury to the MACN is noted at the
time of initial surgery, then the nerve may be either primarily repaired 46 or resected and buried in muscle.15, 36 Re-exploration for a neuroma usually involves resecting the neuroma and burying
the nerve end deep into muscle, away from the scar tissue. Awareness, recognition, and prevention are the keys to successful treatment.
Failed Treatment of Cubital Tunnel
Syndrome
"The patient's best opportunity for full, permanent relief of symptoms is at thefirst operation." 35 Undoubtedly, no matter how diligent the
surgeon, there will always be patients who fail their initial management procedure. Although Dellon 13 noted that approximately 20% of all patients treated had fair or poor results
(prior to 1987), very little is reported on the failure and management of failed uInar nerve decompression.
Typically, treatment failures are attributable to "Pain." 25, 65 Rogers et al 60
noted that the primary complaint leading to repeat surgery in all 14 of their patients was unremitting pain. Gabel and Amadio,25 found that of pain and sensory and motor dysfunction, on average,
pain was the most severe finding in their 30 patients failing initial treatment.
Unfortunately, very little is reported in the literature on why these
patients have painful outcomes following their initial surgery. Gabel and Amadio,25 reported in their series that, in the surgeon's opinion, on average, 2.2 levels were found to be compressed (from the
arcade of Struthers to the flexor pronator aponeurosis) at revision neurolysis, whereas, on average, only one level was involved at the initial surgery. The failure to adequately release the nerve or the
creation of new levels of entrapment by transposing over a short distance at the initial decompression certainly contribute to poor and typically painful outcomes. Although 20 of 30 patients for
revision neurolysis did not experience improvement following their index procedure, 10 patients initially had complete resolution of symptoms, only to relapse after approximately 5 months. This latter
group, hypothetically, may have developed fibrosis around and, possibly, within the nerve.25 At repeat decompression, they noted tremendous fibrosis at the level of the epicondyle (both medially and
anteriorly) in 80% of their patients.
Our experience is similar with respect to re-explorations of ulnar nerves. The primary surgeon may have never looked for a second
site of involvement (i.e., double crush syndrome with involvement usually at Guyon's canal) or did not release extensively enough, especially into the FCU. We have seen secondary compression by
the arcade of Struthers in a few instances. Although failures may have sensory or motor deficits, perhaps worse than preoperatively, it is usually pain that brings the patient back for further treatment.
When we find a clear site(s) of entrapment at the primary operation, the outcome is usually very good. Pain and sensory recovery are consistent and even motor deficits recover a significant percentage.
If, at the primary surgery, however, the nerve is not found to be particularly compressed, but rather is inflamed (indicative of intrinsic neuritis or neuropathy), the results are often poor or, at least,
recovery is slow to occur.
The indications for repeat ulnar nerve decompression at the elbow have not been well established. Broudy and colleagues4 believed
significant pain or progressive motor or sensory loss after surgery, unresponsive to conservative measures, warranted repeat decompression. One must be diligent, however, to ensure another
cause is not the source of complaints. In particular, the double crush syndrome, proximal or distal ulnar nerve entrapment, and MACN injury may have similar complaints. Repeat electromyography is warranted in all cases.
The best method of treating a failed ulnar nerve decompression remains a matter of discussion. Rogers et al65 used submuscular transposition in all cases, whereas Kleinmann36 advocates
intramuscular transposition as his procedure of choice. Dellon13 noted that most repeat decompressions are done using submuscular transposition to correct failures of other procedures. In
one of the few reports on the treatment of failed u1nar nerve decompression, Urbaniak and GabeI78 recommend that the key elements of revision surgery involve (1) re-exploration and
decompression of each level of the ulnar nerve from the midarm to the midforearm (to locate missed and second degree or iatrogenic entrapment). And (2) at reoperation, placing the nerve in a healthy
environment, preferably void of scar tissue (i.e., if initially decompressed in situ, then transpose anteriorly to healthy tissue. If subcutaneously transposed, then transpose intra- or submuscularly).
Repeat decompression of the ulnar nerve achieves its objective in many cases. Broudy et al4 reported all of their patients had a diminution of pain and all were improved clinically. Rogers and associates
65 noted that repeat procedures were highly successful for relief of pain (all 14) and paresthesias, but recovery of motor function and return of sensibility were variable and unpredictable. Gabel and Amadio
25, 65 state that revision ulnar nerve decompression gave the greatest benefit in relief of pain, moreso than sensory and motor improvement. In fact 25 of 30 were
improved, 3 were unchanged, and only 2 were worse following repeat surgery. But motor and sensory recovery were not improved as reliably. They identified the following factors associated with a poor outcome:
1.previous submuscular transposition
2.age greater than 50 years at index procedure
3.denervation on electromyography
Amadio and Gabel 1, 26 suggest that medial epicondylectomy is
ineffective as a revision procedure (because of fibrosis), but we have had success in a few cases. We agree, however, that the presence of significant inflammation or fibrosis of the nerve or its bed
mandates transposition to a healthy bed. In situations of multiple reoperations or posttrauma, the local tissue bed may be too compromised even for sub- or intramuscular transposition. In these
cases, there are few other good alternatives. We, as others (Masear VR, personal communication, 1987) have had some success in a small number of cases using autogenous saphenous vein wrapping.
Allograft and xenograft vein wrapping are also reported in small series or anecdotally but they may incite increased fibrosis (Masear VR, personal communication).66 Few local flaps are available to
cover a fibrotic or ischemic nerve bed. In some cases, an island fasciocutaneous forearm flap may be rotated on the ulnar artery pedicle. In the case of extensive or proximal damage posttrauma,
we have had success rotating or freely transferring a latissimus dorsi flap to provide healthy soft-tissue coverage. Recent reports note improvement of chronic neuritic pain with free or pedicle tissue
transfers to circurnferentially wrap the fibrotic or ischemic nerve.33
Authors' Preferred Surgical Approach. When planning a decompression of the u1nar nerve at the elbow, the method of
treatment is decided upon with consideration given to the patient, the degree of compression, the architecture of the elbow, the soft-tissue bed, and, often most importantly, the findings at the time
of surgery. With this in mind, our preferred surgical approach is:
1.external neurolysis alone for very localized compression and a stable nerve
2.external neurolysis with medial epicon
dylectomy for more extensive compression, subluxation of the nerve, or excessive nerve tension when the elbow is flexed
3.anterior transposition for an environment compromised by fibrosis
of the tissue bed, joint pathology, architectural abnormality of the elbow region, or extensive entrapment or fibrosis of the nerve. This is usually reserved for revision or posttraumatic procedures.
SUMMARY
Cubital tunnel syndrome is the secondmost-common compressive neuropathy. With the increasing prevalence of entrapment neuropathies, the presentation of uInar nerve compression with a
painful upper extremity appears to be more common. Although our knowledge and understanding of this disease are increasing, the principles of management remain constant. We are obliged to reach
a timely and appropriate diagnosis to minimize the extent of neurologic injury and institute an appropriate treatment regimen to preserve and restore normal neural function. Although there are
many ways to reach these goals, the avoidance of complications is paramount to achieve a reliable and pain-free outcome. Preventing injury to the medial antebrachial cutaneous nerve, complete release
of all sites of compression, and avoidance of creating new compressive sites are the keys to this end.
References
1.Amadio PC, Gabel GT: Treatment and complications of failed decompression of the uInar nerve at the elbow. In Gelberman RH (ed): Operative Nerve Repair and Reconstruction. Philadelphia, JB Lippincott, 1991, pp 1107-1120
2.Apfelberg DB, Larson SJ: Dynamic anatomy of the u1nar nerve at the elbow. Plast Reconstr Surg 51:7681, 1973
3.Bednar MS, Blair SJ, Light TR: Complications of treatment of cubital tunnel
syndrome. Hand Clin 10:8392,1994
4.Broudy AS, Leffert RD, Smdth RJ: Technical problems with uInar nerve transposition at the elbow: Findings and results of reoperation. J Hand Surg 3:85-89, 19
5.Brumback RA, Bobele GB, Rayan GM: Electrodiagnosis of compressive nerve lesions. Hand Clin 8:241-254, 1992
6.Buehler MJ, Thayer DT: The elbow flexion test: A clinical test for the cubital
tunnel syndrome. Clin Orthop 233:213-216, 1988
7. Chan RC, Paine KWE, Varughese G: Ulnar neuropathy at the elbow: Comparison of simple decompression and anterior transfer. Neurosurgery 7:545-550, 1980
8.Cole JR, Jernison DM, Hayes CW: Anterior elbow dislocation following medial epicondylectomy: A case report. J Hand Surg Am 19A:614-616, 1994
9.Craven PR, Green DP: Cubital tunnel syndrome: Treatment by medial
epicondylectomy. J Bone joint Surg Am 62A:986-989, 1980
10.Dahlin LB, Rydevik B: Pathophysiology of nerve compression. In Gelberman RH (ed): Operative Nerve Repair and Reconstruction. Philadelphia, JB Lippincott,
1991, pp 847-866
11.Dawson DM, Hallett M, Millender LH: Entrapment Neuropathies. Boston, Little, Brown, 1983, pp 99-116
12.Dellon AL: Musculotendinous variations about the medial humeral epicondyle.
J Hand Surg Br 1113:175
181_1986
13.Dellon AL: Review of treatment results for ulnar nerve entrapment at the elbow. J Hand Surg Am
14A:688-700, 1989
14.Dellon AL: Patient evaluation and management considerations in nerve compression. Hand Clin 8:229 239,1992
15.Dellon AL, MacKinnon SE: Injury to the medial ante brachial cutaneous nerve
during cubital tunnel surgery. J Hand Surg Br 1013:33-36
16.Dellon AL, Hament W, Gittelshon A: Nonoperative management of cubital tunnel syndrome: An 8-year prospective study. Neurology 43:1673-1677, 1993
17.Dellon AL, MacKinnon SE, Hudson AR, et al: Effect of submuscular versus intramuscular placement of uInar nerve: Experimental model in the primate. J Hand Surg Br 11B:117-119,1986
18.Dimond ML, Lister GD: Cubital tunnel syndrome treated by long-arm splintage. J Hand Surg Am 10:430, 1985
19.Eaton RG: Anterior subcutaneous transposition. In Gelberman RH (ed):
Operative Nerve Repair and Reconstruction. Philadelphia, JB Lippincott, 1991, pp 1077-1086
20.Eaton RG, Crowe JF, Parkes JC: Anterior transposition of the u1nar nerve using a
noncompressing fasciodermal sling. J Bone Joint Surg 62A:820-825, 1980
21.Eversmann WW: Entrapment and compression neuropathies. In Green DP,
Hotchkiss RN (eds): Opera five Hand Surgery, ed 3. New York, Churchill Living stone, 1993, pp 1341-1386
22.Feindel W, Stratford J: Cubital tunnel compression in tardy uInar nerve palsy. Can Med Assoc J 78:351, 1958
23. Ferlic DC: Clinical assessment and conservative treatment of cubital tunnel syndrome. In Gelberman RH (ed): Operative Nerve Repair and Reconstruction. Philadelphia, JB Lippincott, 1991, pp 1055-1062
24.Ferlic DC: In situ decompression of the uInar nerve at the elbow. In Gelberman RH (ed): Operative Nerve Repair and Reconstruction. Philadelphia, JB Lippin cott, 1991, pp 1063-1068
25.Gabel GT, Amadio PC: Reoperation for failed decompression of the u1nar nerve in the region of the elbow. J Bone Joint Surg Am 72A:213-219
26.Goldberg BJ, Light TR, Blair SJ: Ulnar neuropathy at the elbow: Results of medial epicondylectomy. J Hand Surg Am 14A:182-188,1989
27.Grundberg AB, Reagan DS: Compression syndromes in reflex sympathetic
dystrophy. J Hand Surg Am 16A:731-736, 1991
28.Heithoff SJ, Millender LH: Medial epicondylectomy. In Gelberman RH (ed): Operative Nerve Repair and Reconstruction. Philadelphia, JB Lippincott, 1991, pp 1087-1096
29.Heithoff SJ, Millender LH, Nalebuff EA, et al: Medial epicondylectomy for the treatment of uInar nerve compression at the elbow. J Hand Surg Am 15A:2229,1990
30.Hodgkinson PD, McLean NR: Ulnar nerve entrapment due to the epitrochleo-anconeus muscle. J Hand Surg Br 19B:706-708, 1994
31.Hollinshead WH: In Anatomy for Surgeons, the Back and Limbs, ed 3.
Philadelphia, Harper & Row, 1982
32.Holtzman RN, Mark MH, Patel MR, et al: Ulnar nerve neuropathy in the forearm. J Hand Surg Am 9A:576-578, 1984
33. Jones NF, Shaw W, Katz RG: Circumferential wrapping of a flap around a scarred peripheral nerve for salvage of end-stage traction neuritis [abstract].
Presented at the 50th Annual Meeting of the American Society for Surgery of the Hand. San Francisco, CA, 1995
Kleinman WB: Anterior intramuscular transposition. In Gelberman RH (ed):
Operative Nerve Repair and Reconstruction. Philadelphia, JB Lippincott, 1991, pp 1069-1076
35.Kleinman WB: Revision u1nar neuroplasty. Hand Clin 10:461-477, 1994
36.Kleinman WB, Bishop AT: Anterior intramuscular transposition of the u1nar nerve. J Hand Surg Am 14A:972-979, 1989
37.Laurencin CT, Schwartz JT Jr, Koris MJ: Compression of the u1nar nerve at the
elbow in association with synovial cysts. Orthop Rev 23:62-65, 1994
38.Leibovic SJ, Hastings H 11: Martin-Gruber revisited. J Hand Surg Am 17A:47-53, 1992
39.Lister G: The Hand: Diagnosis and Indications, ed 3. New York, Churchill Livingstone 1993, pp 297-305
40.Lundborg G, Dahlin LB: The pathophysiology of nerve compression. Hand Clin 8:215-227, 1992
41.Mackinnon SE, Dellon AL: Surgery of the Peripheral Nerve. New York, Thierne, 1988
42.Mackinnon SE, Novak CB: Clinical commentary: Pathogenesis of cumulative trauma disorder. J Hand Surg Am 19A:873-883,1994
43.MacPherson SA, Meals RA: Cubital tunnel syndrome.
Orthop Clin North Am 23:111-123, 1992
44. Manske PR, Johnston R, Pruitt DL, et al: Ulnar nerve decompression at the cubital tunnel. Clin Orthop 274:231-237, 1992
45.Masear VR, Hill JJ Jr, Cohen SM: Ulnar nerve compression secondary to the anconeus epitrochlearis muscle. J Hand Surg Am 13:720-724,1988
46. Masear VR, Meyer RD, Pichora DR: Surgical anatomy of the medial
antebrachial cutaneous nerve. J Hand Surg Am 14A:267-271,1989
47.Matsuura S, Kojima T, Kinoshita Y: Cubital tunnel syndrome caused by abnormal insertion of triceps muscle. J Hand Surg Br 1913:38-39, 1994
48.Monsivais JJ, Baker J, Monsivais D: The association of peripheral nerve compression and reflex sympathetic dystrophy. J Hand Surg Br 18B:337-338, 1993
49.Nathan PA, Keniston RC, Meadows KD: Outcome study of uInar nerve compression at the elbow treated with simple decompression and an early programme of physical therapy. J Hand Surg Br 2013:628637,1995
50.Novak CB, Lee GW, Mackinnon SE, et al: Provocative testing for cubital tunnel syndrome. J Hand Surg Am 19A:817-820, 1994
51.O'Driscoll SW, Horii E, Carmichael SW, et al: The cubital tunnel and u1nar
neuropathy. J Bone joint Surg Br 73B:613-617, 1991 O'Driscoll SW, Jaloszynski R, Morrey BF, et al: Origin of the medial u1nar collateral ligament. J Hand Surg Am 17A:164-168,1992
53.Ogata K, Naito M: Blood flow of peripheral nerves:Effects of dissection, stretching and compression. J Hand Surg 1111:10-14,1986
54.Ogata K, Manske PR, Lesker PA: The effect of surgical dissection on regional
blood flow to the ulnar nerve in the cubital tunnel. Clin Orthop 193:195, 198,1985
55. Omer GE Jr: Injuries to nerves of the upper extremity. J Bone Joint Surg Am 56A:1615-1624,1974
56. Omer GE Jr, Spinner M: Management of Peripheral Nerve Problems. Philadelphia, WB Saunders, 1980
57.Osbome GV: The surgical treatment of tardy ulnar neuritis. J Bone Joint Surg Br 39B:782, 1957
58.Osterman AL: Double crush and multiple compression neuropathy. In Gelberman RH (ed): Operative Nerve Repair and Reconstruction. Philadelphia, JB Lippincott, 1991, pp 1215-1221
59.Pasque CB, Rayan GM: Anterior submuscular transposition of the u1nar nerve for cubital tunnel syndrome. J Hand Surg Br 20B:447-453, 1995
60.Pechan J, Julius 1: The pressure measurement in the ulnar nerve: A contribution to the pathophysiology of the cubital tunnel syndrome. J Biomech 8:75-79, 1975
61.Perrault L, Drolet P, Famy J: UInar nerve palsy after general anaesthetic. Can J Anaesth 39:499-503, 1992
62.Rayan GM: Proximal u1nar nerve compression. Hand Clin 8:325-336, 1992
63.Rayan GM, Jensen C, Duke J: Elbow flexion test in the normal population. J Hand Surg Am 17A:86-89, 1992
64.Raynor EM, Sheffier JM, Preston DC, et al: Sensory and mixed nerve conduction
studies in the evaluation of u1nar neuropathy at the elbow. Muscle Nerve 17:785-792, 1994
65.Rogers MR, Bergfield TG, Aulicino PL: The failed ulnar nerve transposition. Clin Orthop 269:193-200, 1991
66.Ruch DS, Koman LA, Spinner RJ, et al: The effect of barrier vein wraps on peripheral nerve histology [abstract]. Presented at the 50th Annual Meeting of the
American Society for Surgery of the Hand. San Francisco, CA, 1995
67.St John JN, Palmaz JC: The cubital tunnel in ulnar entrapment neuropathy. Radiology 158:119-123, 1986
68.Schuind FA, Goldschmidt D, Bastin C, et al: A biomechanical study of the u1nar nerve at the elbow. J Hand Surg Br 20B:623-627, 1995
69.Seradge H: The reverse flexor carpi ulnaris; and ulnar neuropathy. J Hand Surg
Am 18A:352-354,1993
70.Seror P: Treatment of ulnar nerve palsy at the elbow with a night splint. J Bone Joint Surg Br 75B:322327,1993
71.Siegel DB, Gelberman RH: Ulnar nerve: Applied anatomy and operative
exposure. In Gelberman RH (ed): Operative Nerve Repair and Reconstruction. Philadelphia, JB Lippincott, 1991, pp 413-424
72.Spinner M, Kaplan EB: The relationship of the u1nar nerve to the medial
intermuscular septum in the arm and its clinical significance. Hand 8:239-242, 1976
73.Spinner M, Spencer PS: Nerve compression lesions of the upper extremity: A
clinical and experimental review. Clin Orthop 104:46-65, 1974
74.Stewart JD: Focal Peripheral Neuropathies, ed 2. New York, Raven Press, 1993, pp 157-195
75.Sunderland SS: Nerves and Nerve Injuries, ed 2. New York, Churchill Livingstone, 1978
76.Uchida Y, Sugioka Y: Electrodiagnosis of MartinGruber connection and its
clinical importance in peripheral nerve surgery. J Hand Surg Am 17A:54--59, 1992
77.Upton ARM, McComas AJ: The double crush in
nerve-entrapment syndrome. Lancet 2:359-361, 1973
78.Urbaniak JR, Gabel GT: Perspectives on the operative treatment of cubital tunnel syndrome. In Gelberman RH (ed): Operative Nerve Repair and Reconstruction. Philadelphia, JB Lippincott, 1991, pp 1121-1130
79. Vanderpool DW, Chalmers J, Lamb DW, et al: Peripheral compression lesions of the u1nar nerve. J Bone Joint Surg Br 5013:792-802, 1968
80. Vorenkamp SE, Nelson TL: Ulnar nerve entrapment due to heterotopic bone
formation after a severe bum. J Hand Surg Am 12A:378-380, 1987
81.Wainapel SF, Rao PU, Schepsis AA: Ulnar nerve compression by heterotopic ossification in a headinjured patient. Arch Phys Med Rehabil 66:512-514, 1985
Address reprint requests to
David R. Pichora, MD, FRCSC
Queen's University
Kingston General Hospital
76 Stuart Street
Kingston, Ontario, Canada
K7L 2V7
|
