10
Ulnar Nerve
ANATOMY
The ulnar nerve is derived from spinal nerves C8 and T1, with a frequent but inconsistent contribution from C7. These fibers pass through the lower trunk and the medial cord of the brachial plexus. The ulnar nerve itself arises from the plexus in the
proximal axilla, then lies on the lateral wall of the axilla and the medial aspect of the
upper arm (Fig. 10.1). In the proximal half of the upper arm the ulnar nerve is closely
related to the brachial artery and the median and radial nerves.
At about the midpoint in the upper arm, the ulnar nerve pierces the medial intermuscular septum that separates the flexor and extensor muscle groups, entering the
posterior compartment of the arm. Attached to this septum is a thin and filmy tissue that
has been called the “arcade of Struthers” (this is quite different from the ligament of
Struthers [see Chapter 9]; and apparently this eponym is wrong since Struthers did not
describe the arcade).1 This arcade is occasionally a thick structure that can compress the
ulnar nerve, although some have questioned that.2-5 The nerve then inclines somewhat
posteriorly to lie close to the humerus and to the medial head of the triceps muscle. Afterward it passes into the ulnar (condylar or retrocondylar) groove behind the medial
epicondyle. As it emerges from this groove, it passes under the aponeurotic arch of the
flexor carpi ulnaris muscle (Fig. 10.2). This important anatomical structure, also known
as the humeroulnar arcade,6 and sometimes Osborne’s ligament or band, is formed
from the attachments of the muscle to the medial epicondyle and to the olecranon. Its
edge usually lies about 1 cm distal to a line joining those points, but sometimes is more
proximal or distal than this.6 The thickness of this arcade also varies considerably. After
passing beneath this arch/arcade, the ulnar nerve traverses the substance of the flexor
carpi ulnaris muscle, lying in the cubital tunnel (cubit is the Latin for elbow and forearm, and the French name for the ulnar nerve is le nerf cubital). The roof of this tunnel consists of the aponeurotic arch and then muscle fibers of the flexor carpi ulnaris
(Figs. 10.2, 10.3). The floor is formed by the medial ligaments of the elbow and other
muscle fibers of the flexor carpi ulnaris. The nerve passes out of the tunnel through the
aponeurosis lining the deep surface of the flexor carpi ulnaris then courses between
muscle layers to the wrist.
It is important to consider the dynamic anatomy of the ulnar nerve at the elbow, particularly the changes that occur on flexion. When the elbow is extended, the cubital
tunnel has a somewhat circular shape and is at its roomiest. With elbow flexion, the distance between the medial epicondyle and the olecranon increases by about 1 cm,
causing the flexor carpi ulnaris aponeurosis to tighten over the nerve, and the tunnel to
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Figure 10.1. Anterior aspect of the right arm, showing the course and important branches of the ulnar nerve.
Figure 10.2. Inner surface of the right elbow showing the course of the ulnar nerve in the ulnar groove behind the
medial epicondyle and in the cubital tunnel. (Modified from Kincaid,157 with permission.)
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Figure 10.3. A: Left elbow in coronal section, showing the distal humerus and the olecranon. The medial ligament lies
deep to the ulnar nerve, and the aponeurotic arch of the flexor carpi ulnaris muscle overlies the nerve. B: On flexion of
the elbow, the distance between the attachments of the aponeurosis to the medial epicondyle and the olecranon increases (arrows), compressing the nerve.
become wider and flatter (Fig. 10.3).7-10 Also, the medial elbow ligaments bulge and
flatten the concave condylar groove.9 In addition, the medial head of the triceps muscle pushes against the nerve posteriorly.9 With extreme elbow flexion the tunnel narrows
by about 55%. In addition, in that position the nerve is stretched tightly around the
bony medial epicondyle. These dynamic changes have been studied in cadavers using
MR imaging and intra- and extraneural pressure recordings.7,11 When the elbow was
flexed to 90° and beyond, the cross-sectional areas of three levels within the cubital tunnel decreased substantially, and the pressures rose. Such increases of pressure within
the cubital tunnel adjacent to the nerve on flexion of the elbow have been recorded in
patients undergoing surgery for ulnar neuropathy, but understandably there were no
comparative values from control subjects. These dynamic changes are relevant in understanding some of the causes of ulnar neuropathies at the elbow.
At the wrist the ulnar nerve passes between the pisiform bone and the hook of the
hamate, through Guyon’s canal (Fig. 10.4; see also Figs. 9.2, 12.1). This is a tunnel
rather than a canal, and the alternative name is the ulnar tunnel. The floor of the tunnel/canal is formed by a fusion of the transverse carpal ligament and the pisohamate ligament. The roof consists of the palmar fascia (the volar carpal ligament) and the
palmaris brevis muscle. The nerve shares the canal with the ulnar artery and some fat,
but unlike the carpal tunnel, no tendons. The ulnar nerve divides into the superficial and
deep terminal branches within Guyon’s canal.
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Figure 10.4. Palmar aspect of the right hand, showing the course and branching of the distal ulnar nerve.
The asterisk denotes the branches to the hypothenar muscles (abductor, opponens, and flexor digiti minimi muscles).
The numbers refer to the four main sites of ulnar nerve lesions in the wrist and hand (see Table 10.5).
Branches
The ulnar nerve usually gives off no branches in the upper arm. Below the elbow, the
first branches are those to the flexor carpi ulnaris muscle; these usually arise within
the first 10 cm below the epicondyle (Fig. 10.1). Occasionally a branch to this muscle
arises proximal to the medial epicondyle.12,13 The flexor digitorum profundus is usually
supplied by a single branch that arises distal to those to the flexor carpi ulnaris.
The palmar cutaneous branch arises in the mid-forearm, and runs distally over the
volar aspect of the forearm and wrist without passing through Guyon’s canal; it supplies
the proximal part of the ulnar border of the palm (Figs. 10.1, 10.5; see also Fig. 12.1).
The dorsal cutaneous branch arises slightly more distally, about 5 cm above the wrist,
and winds around the ulna to innervate the ulnar side of the dorsum of the hand and the
dorsal surfaces of the fifth and half of the fourth digit (Figs. 10.1, 10.5; see also Fig.
12.2). This nerve may anomalously arise from the superficial radial nerve, which can
be a source of confusion when doing nerve conduction studies.14
At the wrist the ulnar nerve divides into the superficial and deep terminal branches
within Guyon’s canal. After giving off a small motor branch to the palmaris brevis, the
superficial terminal branch first supplies the skin of the distal ulnar border of the palm
and then divides into two palmar digital nerves that innervate the skin of the palmar surfaces of the fifth and half of the fourth digit (Figs. 10.4, 10.5). The deep terminal branch
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Figure 10.5. Cutaneous distribution of the three sensory branches of the ulnar nerve. (From Stewart,136 with permission.)
pierces the opponens digiti muscle which it innervates, then curves through the palm
deep to the flexor tendons of the fingers (Fig. 10.4; see also Fig. 12.1). The first
branches arising from it, shortly after it emerges from Guyon’s canal, are to the hypothenar muscles. Then in the palm it gives off branches to all the interossei and the
third and fourth lumbrical muscles. It terminates in the thenar eminence by supplying
the adductor pollicis and usually the flexor pollicis brevis. Thus, the deep terminal
branch is entirely motor, supplying nearly all of the ulnar-innervated hand muscles,
whereas the superficial terminal branch is mainly sensory.
Anatomic Variants and Anomalies
Anomalies that occur at the elbow are important in causing some ulnar neuropathies.
The anconeus epitrochlearis muscle is an anomalous slip of muscle that arises from the
triceps muscle and medial aspect of the olecranon and is attached to the medial epicondyle, crossing the ulnar nerve in the condylar groove. This muscle is present in 10%
of cadaver elbows and is frequently bilateral.6,15-17 Fibrous bands bridging the medial
epicondyle and the olecranon occur less often, in 5% of cadavers.6 Supracondylar spurs
are discussed in Chapter 9. Ulnar to median nerve communications in the forearm, patterns of anomalous innervations of the intrinsic hand muscles, and variations in the cutaneous innervation of the fingers are discussed in Chapters 9 and 12.
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ULNAR NEUROPATHIES IN THE AXILLA AND UPPER ARM
Damage to the ulnar nerve in the axilla and upper arm is uncommon (Table 10.1),
and when it occurs the other two major nerves of the arm, the median and the radial,
are often also involved because of their proximity; this has been termed triad neuropathy.18 The ulnar nerve can be compressed, on its own or with the other two major
nerves of the arm, during deep or drunken sleep, or during coma, when the arm hangs
over a sharp edge (see Fig. 11.5).18 Misuse of crutches can compress the nerve in the
axilla and the head of a sleeping partner may compress the nerve against the upper
humerus.12,19 In anterior shoulder dislocations nerve injury occurs in 48% of patients.20
The ulnar nerve is only affected in 8% of patients with such nerve injuries, either on
its own or in association with other nerve injuries.20 Similar patterns of damage to the
ulnar and other nerves occur in patients with proximal humeral fractures, which are
sometimes associated with shoulder dislocation.21 Tourniquets applied to the upper arm
can damage the ulnar nerve, as well as the radial and median nerves (see Chapter 11).22
Aneurysms, hematomas, and false aneurysms resulting from trauma to the subclavian
or axillary arteries can cause acute or chronic compression of the brachial plexus or one
or more of the three major nerves to the arm (see Chapter 7). A compartment syndrome
of the upper arm can occur following coma.23 Ischemic neuropathies of the ulnar and
other nerves can result from upper arm fistulas created for hemodialysis.24 Misplaced
injections, aimed for the posterior deltoid muscle, can damage the ulnar nerve.25
At about the midpoint of the upper arm, or slightly distal to that point, the ulnar
nerve pierces the medial intermuscular septum and in some persons there is an associated band of tissue called the arcade of Struthers (see above). Entrapment of the nerve
here is rare.26,27
Table 10.1. Causes of ulnar neuropathies in the axilla and upper arm.
External compression
Crutches
Tourniquet
During sleep, coma
Aneurysm, false aneurysm, hematoma
Compartment syndrome
Trauma
Anterior shoulder dislocation
Proximal humerus fracture
Injection injury
Nerve tumor
Others
Ischemia from dialysis fistula
Multifocal motor conduction block neuropathy
Acute brachial plexus neuropathy variant
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Nerve tumors, including nerve sheath tumors and perineuriomas, may occasionally
involve the proximal ulnar nerve.28 Multifocal motor neuropathy (see below) can present with severe proximal ulnar nerve lesions involving only motor fibers, but other
limb nerves are also usually involved.29 Proximal ulnar neuropathies, with marked
weakness and electrophysiologic evidence of demyelinative conduction blocks and
eventual full recovery, have been described.30,31 These cases may represent an unusual
variant of acute brachial plexus neuropathy (see Chapter 7).
ULNAR NEUROPATHIES AT THE ELBOW
In its course across the elbow, the ulnar nerve can be damaged at different sites and by
several types of injurious forces. Ulnar neuropathies at the elbow (UNE) is an appropriate, all-inclusive, and general term for these heterogeneous focal neuropathies; when
there is no evident cause the prefix idiopathic can be added. The terms tardy ulnar palsy
and cubital tunnel syndrome have been inappropriately used by many authors either to
refer to all ulnar neuropathies at the elbow or to those in which there is no evident cause.
These terms should be reserved for two very specific conditions described below.
Very little data exist regarding the epidemiology of UNE. The only study is from the
Italian province of Sienna, where UNE was found to have a standardized yearly incidence of 21 per 100,000, about one-thirteenth the incidence of carpal tunnel syndrome.32,33 The incidence in men was found to be about twice that in women, in
concordance with most, but not all other studies.32,34,35 Two studies have evaluated the
incidence of UNE in the workplace. In one, the symptoms and clinical criteria used for
the diagnosis, and the lack of electrophysiologic studies, preclude meaningful conclusions.36 The other was a study of female floor cleaners evaluated using well-defined
clinical and electrophysiologic measures.37 In the cohort of 179 women, mild carpal
tunnel syndromes were found in 48.3%, and mild UNEs in 6.8%. There is need for
more studies to determine if manual work, and of what type, is a risk factor (and to
what degree) for UNE.
A rational approach to the management of UNEs requires, as far as possible, the precise identification of both the location and the cause of the nerve damage. The two
major sites for UNEs are the condylar groove and the cubital tunnel. There are two additional sites: the most proximal is the medial intramuscular septum, which is just proximal to the condylar groove, and the most distal site is the point of exit of the nerve from
the flexor carpi ulnaris muscle. The causes of UNEs may be broadly categorized into:
(a) those with an identifiable structural and/or mechanical cause (Table 10.2); and (b)
those in which no such cause is apparent (idiopathic).
Ulnar Neuropathies with Structural or Mechanical Causes
Elbow Trauma
Trauma to the elbow may involve the ulnar nerve in three ways: acute injury to the
nerve; iatrogenic damage during surgery for the elbow injury; and delayed damage to
the nerve as a result of elbow deformity or scar tissue.38
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Table 10.2. Causes of ulnar neuropathies at the elbow.
Bony deformity at the elbow
Old fracture
Rheumatoid arthritis
Osteoarthritis
Congenital valgus deformity with shallow ulnar groove
Paget’s disease
Trauma
Fracture, dislocation, or both
Soft tissue injury
External pressure
Single episode
Multiple episodes
Delayed neuropathy following trauma without fracture
Prolonged or repetitive elbow flexion
Compression in the cubital tunnel (cubital tunnel syndrome)
Tumor arising from bone, nerve, other structure
Others
Prolapsing nerve
Abnormal muscle, fibrous band
Supracondylar spur
Diabetes mellitus
Leprosy
Idiopathic
Elbow dislocations may produce an acute ulnar neuropathy. Fractures of the distal
humerus involve widely varied patterns of bone damage. In a review of 320 successive
such fractures in adults, ulnar nerve injury due to the trauma was present in 2.5% of patients.39 It was most frequent in medial epicondyle avulsion fractures in young adults.
The nerve injury recovered spontaneously in all but one patient within 3 months; that
single patient underwent nerve transposition. Ulnar nerve damage may occur occasionally as a complication of reducing the fracture or fixation with pins or wires. Percutaneous cross-pinning of the fracture is particularly likely to damage the ulnar
nerve.40-42 Arthroscopic surgery at the elbow is a rare cause of ulnar neuropathy.43
Cubitus deformity following poorly reduced supracondylar fractures is a cause of delayed (or tardy) ulnar neuropathies. This was first clearly described by Panas in 1878:
“The following observation . . . establishes definitely the relationship that exists
between a fracture of the elbow and a tardy paralysis of the cubital (ulnar) nerve, of
indirect cause.”44 The bony injuries that lead to the later development of ulnar neuropathies include supracondylar fractures and fractures of either medial or lateral epicondyles. After these have healed the ulnar nerve is less well protected in the condylar
groove so is more exposed to external pressure. The nerve is also pushed anteriorly by
the displaced triceps muscle,45 and is often also stretched over the bony callus or by the
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abnormal angle of the elbow joint. There is a contemporary article46 redescribing this
condition that was delineated over a century ago.44,47 The term tardy ulnar neuropathy/palsy should be restricted to this group of delayed ulnar neuropathies at the elbow.
Blows or lacerations with or without dislocations and fractures can injure the
nerve.48,49 Sometimes such blows to the elbow lead to a delayed neuropathy, presumably due to fibrosis and scarring. Multiple episodes of quite minor trauma, often poorly
recalled by the patient, may also lead to fibrosis that constricts the nerve.50
Other Elbow Joint Deformities
Severe rheumatoid arthritis, osteoarthritis, and Paget’s disease can all produce major
disorganization of the elbow joint, making the ulnar nerve vulnerable to damage.8,50-52
Congenital abnormalities such as combinations of cubitus valgus, shallow condylar
grooves, and anterior dislocation of the head of the radius can also cause ulnar neuropathy.53 Simple shallowness of the condylar groove, in the absence of any other abnormality, may predispose the nerve to external trauma and pressure.54
External Pressure
Because of the ulnar nerve’s superficial and unprotected course through the condylar groove it is particularly susceptible to external pressure. Elbow flexion adds to the
likelihood of nerve damage because of the narrowing of the cubital tunnel. Multiple
episodes of minor pressure often associated with elbow flexion are probably the leading cause of UNE. Familiar examples are habitually leaning the elbow on hard chair
arms; prolonged or frequent use of the telephone that often combines leaning the inner
aspect of the elbow on a hard desk with prolonged elbow flexion; resting the flexed
elbow on car window frames by taxi drivers or persons on long journeys; watching television or reading while lying on the side with an elbow tightly flexed and supporting
the head (Fig. 10.6). Wheelchair-bound patients are particularly at risk for ulnar neuropathies both at the elbow and at the wrist.55-57 The former are probably the result of
prolonged leaning of the flexed elbow on inadequately padded arm rests. Bed-bound
or comatose patients are also at risk of developing UNEs because of prolonged or repeated external pressure on the nerve at the elbow with the arm often flexed at the
elbow.
Prolonged or Repetitive Elbow Flexion
Sometimes UNEs develop in situations in which the arm is kept flexed for long periods, but without any external pressure, such as when the arm is immobilized in tight
elbow flexion following a fracture or dislocation of the upper arm or shoulder.54 Habitually sleeping with the arm tightly flexed is probably an underrecognized cause of
ulnar neuropathy at the elbow (Fig 10.7). Some of these patients will wake recurrently
at night or in the morning with ulnar distribution sensory symptoms. Jobs involving
repetitive elbow flexion may put the nerve at risk for a similar reason: recurrent compression occurs as the aponeurosis tightens across the nerve each time the elbow is
ULNAR NERVE
A
B
C
D
267
E
Figure 10.6. Elbow leaning and flexion causing ulnar neuropathies at the elbow (UNE). A: A businessman with a
moderate right UNE spent many hours daily talking on the phone in this position. B: This man with a moderate left UNE
habitually spent hours every day at his computer in this position. C: Habitual leaning on the elbow while driving may cause
UNE. D, E: This man with a moderate left UNE habitually watched television for hours in this position, and would often
fall asleep while doing so.
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Figure 10.7. Positions during sleep that involve
prolonged flexion (sometimes combined with
external compression) of one or both elbows, that can
cause damage to the ulnar nerve.
flexed. However as with many suspected job-related neuropathies, establishing such a
cause-and-effect relationship is difficult.
Prolapse of the Ulnar Nerve
Prolapse of the ulnar nerve out of the condylar groove over and sometimes anterior to
the medial epicondyle on flexion of the elbow has been a topic of interest since the mid1800s.58,59 Although such prolapse often occurs in traumatic deformities of the elbow
joint,48,58-60 it also occurs in the absence of any structural abnormality. Surveys have shown
that prolapsing ulnar nerves are present in up to 16% of healthy individuals, the degree
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269
of prolapse being variable.61,62 A prolapsing nerve may be another reason for repeated
elbow flexion to cause UNE. Recurrent prolapsing may continually traumatize the
nerve, but in addition, a prolapsed nerve that lies on the medal epicondyle in elbow
flexion is more at risk of external compression than a nerve lying safely in the condylar groove.
Soft Tissue Masses, Tumors
Ganglia, lipomas, fibrolipomas, and epidermoid cysts can all compress the ulnar
nerve in the condylar groove or within the cubital tunnel.8,63-65 Masses arising from the
elbow joint such as thickened synovium in patients with rheumatoid arthritis, giant cell
tumors, and synovial cysts can do likewise.66,67 A case of fat necrosis with cystic myxoid degeneration causing subacute painful compression of the ulnar nerve within the cubital tunnel has been described.68 Such masses can sometimes be palpated. Primary
nerve tumors such as nerve sheath tumors, perineuriomas,69 and intraneural ganglia can
arise from the ulnar nerve here or elsewhere along its course.
Anconeus Epitrochlearis Muscle and Fibrous Bands
Although the anconeus muscle is present in 10% of cadavers it is a rare cause of
ulnar nerve compression.8,16,70-72 In one brief report of 215 cases of UNE, this muscle
was found in 21, but was the cause of nerve compression in only 4.73 Because the anconeus epitrochlearis muscle cannot be palpated or seen on imaging studies, the diagnosis can only be made during surgical exploration. It is an uncommon but important
cause of UNE because these patients will not improve with conservative measures,
whereas surgical treatment is simple and effective. Fibrous bands that stretch, from the
tip of the medial epicondyle to the olecranon (like the anconeus muscle), cause ulnar
nerve compression even less frequently than that muscle.74
Supracondylar Spurs
Supracondylar spurs are usually situated on the medial side of the humerus, several
centimeters above the medial epicondyle (see Chapter 9 and Fig. 9.4). Although present in about 1% of persons, these spurs seldom cause neuropathies; median nerve damage is more common than ulnar nerve damage.75-78
Compression in the Cubital Tunnel
Compression of the ulnar nerve within the cubital tunnel, particularly under the edge
of the flexor carpi ulnaris aponeurosis, is a frequent cause of UNE.54,79,80 The aponeurosis can be thick and fibrotic. Flexion of the elbow is an important aggravating factor
in these patients, because it tightens the aponeurosis further.81,82 Feindel and Stratford80
proposed the admirable term cubital tunnel syndrome for this type of ulnar neuropathy.
Unfortunately this term is widely misused to refer to all UNEs.
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Diabetes Mellitus
Ulnar neuropathies are probably more frequent in diabetics than non-diabetics, although the data to support this are flawed. In a clinical and electrophysiologic study of
103 unselected diabetic patients, 5 were found to have UNEs (double this number had
carpal tunnel syndrome).83 In another study of patients attending a diabetic clinic, 51 had
mononeuropathies, 15 of whom had UNEs (an equal number to those with carpal tunnel
syndrome).84 Looking at the issue the other way round, some reports of series of patients
operated on for ulnar neuropathies include more diabetics than the prevalence of this disorder would lead one to predict;85 another study did not identify diabetes mellitus as a risk
factor.35 I agree with others that ulnar neuropathies in diabetics are often severe, are predominantly motor, and are usually found in longstanding diabetics with systemic complications.86 Perhaps the presence of a sensory polyneuropathy obscures the usual warning
paresthesias of a developing ulnar neuropathy. Some ulnar neuropathies in diabetics have
a sudden onset, suggesting nerve infarction.
Leprosy
This infection has a particular predilection for the ulnar nerve. The patient may have
an isolated ulnar neuropathy or there may also be involvement of other peripheral
nerves (see Chapter 23).
Perioperative Ulnar Neuropathies
General anesthesia was introduced in the mid-1800s. The first reports of nerve injuries arising after an operation involving a general anesthetic were in 1894 and
1897,87,88 and the first description of a perioperative UNE in 1901.89-91 Ulnar neuropathy is now the most frequent nerve injury cited in litigation claims involving anesthesiologists in the United States of America.92 The traditional explanation for these
neuropathies is that because of poor positioning or inadequate padding, or both, of the
arm during anesthesia, the nerve is compressed against hard objects.93,94 Prolonged
elbow flexion could be an additional damaging factor. Anesthetized patients are not
able to perceive the warning paresthesias that lead the awake and alert person to move
the arm and relieve the pressure on the nerve.
It is now apparent that there are four time periods during which a patient may develop such a neuropathy: in the preoperative period, during the operation, in the postoperative period in hospital, and when convalescing at home or elsewhere after
discharge from hospital (see Chapter 2 and Fig. 2.8).95 It is therefore highly recommended that the term perioperative neuropathy be used in the context of these patients
and their nerve lesions.
Perioperative UNEs were studied in detail by Wadsworth93 particularly in the light
of new anatomical descriptions of the passage of the ulnar nerve through the cubital tunnel.80 He reasoned that when a patient was lying on their back on the operating table,
and the arm prone (palm downward) on a flat supporting surface, the nerve would be
at risk of external compression in the condylar groove. If the arm were supine (palm
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upward), such compression would be avoided. He noted the potential danger of elbow
flexion, and recommended several arm positions that should help avoid ulnar nerve
damage. At about the same time others were advocating the use of protective elbow
padding.96 Padding and positioning of the elbows to protect the ulnar nerve are now routine practices in operating rooms. However, it has never been established just how much
padding and of what type, and what positions are safe or dangerous. In 1993 Stoelting97
reviewed the literature92,98-102 and concluded that despite positioning the arms as recommended, and using padding at the elbow, there was no evidence that these practices
decreased the occurrence of perioperative UNEs. Others have supported this view.103
These conclusions are further underscored by the fact that the frequency and severity
of perioperative UNEs have not changed significantly in two decades despite widespread use of intraoperative ulnar nerve protection.104
In the analysis of the American Society of Anesthesiologists Closed Claims Study
(a database of malpractice claims related to anesthesia care that have been legally settled) an important fact regarding perioperative UNEs came to light.92 Of 77 patients
with UNEs, 22 noted the time of onset of their symptoms: 5 were on waking from the
anesthesia, 3 during the first postoperative day, 10 during the first postoperative week,
and 4 at some time in the 2–4 weeks following surgery. This clearly indicates that a substantial number of patients develop UNE in the postoperative period.
There have been four landmark studies on perioperative neuropathies done by
Warner and colleagues at the Mayo Clinic, Rochester MN.104-107 The first was a large
retrospective analysis of over 1 million consecutive patients who had undergone diagnostic and noncardiac surgical procedures with concurrent anesthetic management from
1957–1991.104 The authors’ findings were: UNE was identified in 414 patients (0.04%);
a very small number of UNEs were bilateral; the initial symptoms for most patients
were noted more than 24 hours after the procedure; factors associated with persistent
UNE included male gender (70% of patients), duration of hospitalization more than 14
days, and body habitus (neuropathy more frequent in very thin or obese patients), increasing age, and pre-existing diabetes. The duration of the surgery or anesthesia, the
type of anesthetic technique, and the patient position were all not associated with the
development of neuropathy. UNEs developed in some patients who had not undergone
a general anesthetic. Warner et al.105 then performed a prospective study on 1502 adult
patients undergoing noncardiac surgical procedures (cardiac surgery was excluded because of the well-known complication of brachial plexus injury associated with those
procedures).108-110 UNE developed in 7 patients (0.5%), 6 of whom were men (this
marked male predominance has been consistently reported in all studies on perioperative UNEs). Symptoms began 2–7 days after surgery. The manifestations were mild
and confined to sensory deficits in 6 patients. Apart from the association with male
gender, no other patient or procedural characteristic was found to be associated with
UNE, but the small sample size precluded definitive statements regarding risk factors.
The authors emphasized that in all patients the symptoms developed 2 or more days
following the surgery. They speculated that perioperative UNE may be caused by
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postoperative rather than intraoperative factors. It is noteworthy that these 7 patients developed UNE in spite of intraoperative padding of the elbow.
The Warner study published in 1999 was followed by another in 2000 in which UNE
was evaluated prospectively in medical patients.106 The reasoning was that because the
previous study had shown delayed onset of UNEs in patients following anesthesia and surgical procedures, perhaps factors associated with hospitalization, rather than intraoperative events, were the cause of such neuropathies. They asked the fundamental question:
do medical patients who are not undergoing surgery also develop UNE during hospitalization? They studied 990 patients admitted with medical conditions who had very similar hospital care characteristics (mainly bed rest and intravenous treatments) to
postoperative patients. Two patients (0.2%), both men, developed UNE. Because of the
small patient numbers they could not identify any specific patient or other characteristics
associated with the development of UNE. They concluded that prolonged periods of bed
rest in the supine position may be an important risk factor for UNE. They pointed out that
a common position for hospitalized patients is lying on their back with elbows flexed
and their hands resting on their upper abdomen or chest (Fig. 10.7). In this position elbow
flexion predisposes the ulnar nerve to compression within the cubital tunnel, and also the
nerve may be subjected to prolonged external compression between a firm hospital mattress and the condylar groove. Convalescing patients often spend long periods of time sitting in chairs, with the risk of compressing the ulnar nerve while leaning their elbows
against the arm of the chair. These were the same points made earlier by Williams111 when
he suggested that perioperative UNEs begin “not on the operating table, but in bed with
the patient sitting up, resting on his elbows . . . often sit[ting] in an easy chair, resting his
elbows as he reads a book or watches television.”
A subgroup of patients with perioperative UNEs is that of patients undergoing coronary artery bypass graft surgery who seem to be particularly prone to developing this
complication.112 Brachial plexus damage is also particularly frequent following median
sternotomy with the usual picture being that of unilateral lower trunk/medial cord damage, so patients are often thought to have an ulnar neuropathy (see Chapter 8). Prospective studies have shown UNEs to occur in 1–2% of patients undergoing
sternotomy.109,113 Another prospective study included pre- and postoperative clinical
and electrophysiologic evaluations showed that 3 of 33 ulnar nerves developed
conduction slowing postoperatively.114 No patient had symptoms and these electrophysiologic abnormalities resolved in time.
In their last prospective study Warner et al.107 evaluated the issue of neuropathies
developing in the lower limbs following surgical procedures in the lithotomy position.
They identified lower extremity neuropathies in 15 of 991 (1.5%) patients, and various
nerves were involved. The crucial finding was that symptoms were reported within
4 hours of completion of the anesthetic in all patients. Symptoms were thus readily
noted by patients despite persisting sedation or concomitant narcotic administration.
This refutes the frequently stated belief that patients may not report symptoms of UNE
early after an operation because of such medications. In the authors’ views, this very
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early onset of symptoms strongly suggests intraoperative nerve damage, contrasting
strikingly with the delayed onset of symptoms in most perioperative UNEs.107 They
reasoned that this was further evidence that perioperative UNEs most likely occur in
the postoperative rather than intraoperative period.
An important issue both in understanding the causes of perioperative UNEs and
medicolegally is establishing the time of onset of the symptoms. Patients and their families may be motivated to claim that symptoms occurred immediately on wakening
from anesthesia, but careful medical record entries may clearly indicate the onset to be
much later.95,105 It is not known whether an intraoperative insult to the nerve could produce delayed symptoms, but this is very unlikely.
An anatomic study of the elbow to explore the marked male predominance of perioperative UNEs has reported two findings.115 The proximal end of the ulna, the coracoid process, forms part of the floor of the cubital tunnel. The tubercle of this process
is consistently larger in male skeletons so may predispose the overlying nerve in males
to external pressure. The subcutaneous fat that overlies the nerve at the elbow, as judged
by ultrasound studies, is substantially greater in women, and this may provide protection against external compression.115
The role of position of the arm during surgery and the pressure exerted over the ulnar
nerve at the elbow has been re-evaluated by Prielipp et al.116 Greater pressure is exerted when the arm is lying on a firm surface in the pronated position, confirming
Wadsworth’s conclusions of almost four decades previously. In another study these investigators evaluated the onset and severity of paresthesias and somatosensory evoked
potential (SEP) changes during intentional ulnar nerve compression.117 Half of their 16
(male) volunteers reported paresthesias within 60 minutes of nerve compression, and
they had accompanying SEP changes. The others, who did not have paresthesias, had
similar SEP changes. This led to the interesting conclusion that significant ulnar nerve
compression and dysfunction can occur in unsedated males in the absence of symptoms. Thus a conscious male patient recovering from an operation may not be aware
of warning ulnar nerve paresthesias during certain arm positions and hence could develop a UNE. Another study involved SEP recording following stimulation of the ulnar,
median, and radial nerves during general anesthesia when the brachial artery was temporarily occluded proximal to the elbow.118 The SEP changes were most marked in the
ulnar nerve, suggesting that it is more sensitive than the other nerves to ischemia, and
that limb ischemia plays a role in perioperative ulnar neuropathies.
A further study on a larger cohort of volunteers evaluated the changes in current perception thresholds (a type of quantitative sensory testing—see Chapter 4) in the fifth
digit accompanying flexion of the elbow, direct pressure on the ulnar nerve, and local
ischemia to the arm.119 Changes in current perception thresholds indicative of early
nerve dysfunction were induced by the latter two maneuvers.
There appear to be no studies assessing the types and quantity of elbow padding. An
interesting report is that of a patient in whom it was felt that an upper limb neuropathy
was caused by too much padding.103 Another concern is that the padding could be too
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tight.120 Nonetheless, careful positioning of the arm with padding and protection of the
ulnar nerve remains advisable even though patients in whom these measures have been
taken may still develop perioperative ulnar neuropathies. Guidelines have been
published by the American Society of Anesthesiologists Task Force on Prevention of
Perioperative Peripheral Neuropathies.103 A study in which male patients in the postoperative period would be educated to avoid leaning on their elbows and to wear elbow
pads would be of great interest.
The prognosis of perioperative UNEs is uncertain. No studies have addressed this
issue systematically and with adequate numbers of patients to allow meaningful
conclusions, and there was often a referral bias with the more severely affected
patients brought to medical attention. An article that describes 8 patients with severe and
persistent perioperative UNEs concludes that this condition carries a poor prognosis,94
but such a statement is suspect because of likely referral bias. A retrospective study
reported that on follow-up 3 months or more postoperatively, roughly one-third of the
patients were recovered or improved, one-third unchanged, and one-third worse.90 In a
prospective study in which 17 patients were followed at times of 2–7 months after
surgery, 9 (53%) were recovered or improved, 5 (29%) were unchanged, and 3 (18%)
were worse.100 In their first (retrospective) study, Warner et al.104 reported that of the
patients with UNE who survived the first postoperative year, 53% were asymptomatic
and regained complete motor function and sensation; those with symptoms persisting
more than a year had moderate or greater disability from pain or weakness. Assessments were based on self-reported symptoms, so were probably biased toward more
severe ulnar neuropathies, and may not be representative of all such neuropathies. A
further prospective study by these authors105 included only 7 patients: 4 recovered in
6 weeks, and the other 3 had residual symptoms 2 years later. Another study of patients
with UNEs following total hip arthroplasty reported that 8 of the 10 patients recovered
completely.121 My pragmatic conclusion from these studies is that somewhat more than
half of the patients are likely to recover or improve to a satisfactory state, while the
others may have symptoms which may be severe and persisting, or even worsen to
become severe and permanent. Medicolegal aspects of perioperative UNEs are
discussed in references 91, 95, and 116.
In summary, most perioperative UNEs occur in the postoperative period and are
likely to result from leaning on and flexing the elbow. When symptoms develop within
a few hours of waking from anesthesia it is likely that the nerve damage occurred
intraoperatively, however there is no evidence that any amount or any particular type
of padding will prevent such UNEs. Efforts to reduce the occurrence of this neuropathy should be focused on protecting the nerve in the postoperative period.
Ulnar Neuropathies of Uncertain Cause
In many patients, a structural abnormality or specific episode(s) of trauma cannot be
identified with certainty. A variety of causes are possible in such patients, for example,
unnoticed injury or external compression of the nerve in the condylar groove,
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prolonged elbow flexion during sleep, the presence of an anconeus trochlearis muscle
or fibrous bands, or a true cubital tunnel syndrome (entrapment within the flexor carpi
ulnaris muscle/aponeurosis). Some of these—for example, external compression and
prolonged flexion—can be identified by taking a careful history. Others, such as the last
two causes mentioned, can only be diagnosed with certainty by surgical exploration.
The location of these UNEs of uncertain cause can be the condylar groove, or the
cubital tunnel, or (rarely) more proximally or distally. Making this distinction is
important when deciding on surgical treatment. Surgical observations, cadaver
dissections, and histological and electrophysiologic studies have all contributed to the
understanding of these neuropathies. Constriction of the nerve by the flexor carpi ulnaris aponeurosis, with proximal swelling of the nerve, has been observed during surgical exploration in many patients.8,52,79-82 However, fusiform swelling of the ulnar nerve
behind the medial epicondyle was found in half of 400 cadaver arms,122 so this finding
is probably not a reliable indicator of the presence or site of nerve compression. Furthermore, Dr. W. W. Campbell, who has observed and electrophysiologicly studied
many ulnar nerves during surgical explorations, states that the appearance of the nerve
does not reliably identify the site of damage (oral communication, 2009). Probably a
better way of establishing during surgery what the role of the flexor carpi ulnaris
aponeurosis is playing is to test whether it becomes abnormally tight when the elbow
is flexed (see below). The definitive test at present is a careful intraoperative nerve
conduction study (see below).
Microscopic studies have been performed on ulnar nerves taken at autopsy from patients not known during life to have had UNEs, as well from a patient who probably did
have a UNE.123 Teased fiber preparations showed that in several nerves, abnormalities
were present at the edge of the aponeurosis of the flexor carpi ulnaris. However, this
finding does not prove that all or even the majority of UNEs of uncertain cause occur
at the aponeurosis of the flexor carpi ulnaris.
Another approach to localize these neuropathies is to perform intraoperative motor
nerve conduction studies in which the nerve is stimulated at regular intervals across
the elbow looking for a precise site at which conduction abnormalities occur. In a very
large series of operations for UNE during which intraoperative nerve conduction studies were performed, the usual finding was that the conduction abnormalities were in the
condylar groove, and only rarely in the cubital tunnel.123 Smaller but perhaps more
precise studies have been published by clinical neurophysiologists. In one, 7 patients
with UNE were studied intraoperatively and all had conduction abnormalities localized to the cubital tunnel entrance.81 These patients had a thickened aponeurosis with
tightening of the cubital tunnel on elbow flexion. Another study showed the abnormalities to be mainly in the condylar groove rather than at the entrance to the cubital
tunnel. In most cases, the nerve was bound down by fibrous tissue in the groove, and
only a few nerves were compressed by the aponeurosis of the flexor carpi ulnaris.124 A
further study found that of 19 UNEs, the site was the condylar groove in 9, the cubital
tunnel in 4, both locations in 3, and a more distal site in 1.125
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MR imaging studies have also addressed the issue of localization of UNEs (see
below).
In summary, for UNEs of uncertain cause, the nerve damage is usually either in the
condylar groove, in the cubital tunnel, or in both places (a third and fourth site also
exist—see below). UNEs in these two adjacent sites are clinically identical. It has been
thought important to precisely localize the focal damage in order to develop a rational
approach to the treatment, but the value of such information in terms of selecting conservative treatment or particular types of surgery is still somewhat uncertain.
Clinical Features
Sensory symptoms in the ulnar-innervated parts of the hand and fingers are often the
patient’s major complaint. Pain may be present in the same distribution, but is frequently more widespread in the arm and is of less diagnostic value than the distribution of the paresthesias. Some patients identify the inner elbow as being the most painful
area, and may even report that their “funny bone” is unusually sensitive. Motor symptoms vary from none at all to marked weakness of the hand. Patients sometimes present with progressive wasting of the hand muscles but no sensory symptoms; this is
particularly seen in diabetics.
The sensory examination should include a careful evaluation with light touch of the
cutaneous territories of each of the three sensory branches: the superficial terminal, the
dorsal ulnar cutaneous, and the palmar cutaneous nerves (Fig. 10.5). Involvement of the
dorsal and palmar cutaneous branches, which arise above the wrist and do not pass
through Guyon’s canal, clearly shows the site of an ulnar nerve lesion to be proximal
to the wrist. Frequently, in spite of a history of paresthesias in both the fingers and the
hand, sensory loss cannot be detected on light touch examination and testing with pin
prick may be more revealing. In some patients, the sensory abnormalities are present
only on the palmar surface of the tips of the fifth and the ulnar half of the fourth digit.
Sensory abnormalities that extend more than about 2 cm above the wrist crease indicate involvement of the medial cutaneous nerve of the forearm, the brachial plexus, or
the T1 root; such a finding is an important clinical sign in differentiating these lesions
from an ulnar neuropathy.
Patients with severe ulnar neuropathies have wasting of the ulnar-innervated muscles of the hand and sometimes of the forearm flexor muscles (Fig.10.8). An ulnar claw
hand deformity may be present; various types exist, depending on the relative
involvement of the individual ulnar-innervated muscles. Early textbooks emphasized
the diagnostic importance of recognizing these different deformities, but it is easier to
make a correct diagnosis by the systematic examination of individual muscles. In a
suspected ulnar neuropathy these include the flexor carpi ulnaris, the flexor digitorum
profundus of the fourth and fifth digits, and the ulnar-innervated intrinsic hand muscles
(the examination of which can usually be restricted to the first dorsal interosseous and
abductor digiti minimi). It is also important to test muscles innervated by the median
and radial nerves with nerve fibers derived from C8 and T1 nerve roots that pass
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Figure 10.8. Dorsal and palmar views of a patient with a severe left ulnar neuropathy at the elbow due to osteoarthritis. On the dorsal view, note the marked wasting, particularly of the first dorsal interosseous muscle (white arrow) and
mild clawing of the fifth digit. On the palmar view, wasting of the ulnar-innervated muscles of the thenar eminence and
first web space are seen (black arrow). (From Asbury and Gilliatt,306 with permission.)
through the lower trunk and medial cord of the plexus (Table 10.3). The most important of these are the median-innervated intrinsic hand muscles. A host of signs and tests,
some dating back to the late 1800s and often with obscure eponyms attached, have
been described as being useful in demonstrating weakness in ulnar nerve-innervated
forearm and intrinsic hand muscles. These have been diligently catalogued.126 Such
signs and tests, like the interpretation of claw hand deformities, have much less value
than the meticulous examination of selected individual muscles (Table 10.3), and the
findings interpreted with a knowledge of the neural anatomy of the upper limb and of
the selective fascicular involvement that frequently occurs in UNEs (see below).
Provocative tests have been advocated as useful adjunctive clinical tests for
diagnosing UNEs. There are many similarities and drawbacks to those tests used in
diagnosing carpal tunnel syndrome (e.g., Tinel’s and Phalen’s signs) (see Chapter 9).
Tinel’s sign (test) for the diagnosis of UNE consists of tapping the nerve at the elbow
and asking the patient if this produces paresthesias in the distribution of the ulnar nerve.
As with doing this test for carpal tunnel syndrome, there is no accepted standard as to
how hard to hit the nerve and with what (e.g., finger or tendon hammer), the length
over which the nerve is percussed, or the role of simply palpating the nerve rather than
percussing it. Nor is it clear how prominent the paresthesias should be to constitute a
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Table 10.3. Muscles particularly useful when testing for lesions of C8 and T1 roots and the lower trunk
and medial cord of the brachial plexus.*
Muscle tested
Muscles receiving some C8 and/or T1 innervation
Triceps
Extensor digitorum communis
Extensor carpi ulnaris
Extensor pollicis longus, brevis
Suspected nerve involved
Radial nerve**
Flexor carpi ulnaris
Flexor digitorum profundus (digits 4, 5)
Ulnar nerve
Flexor digitorum profundus (digits 2, 3)
Flexor pollicis longus
Median nerve
Intrinsic hand muscles
Ulnar and median nerves
Lower trunk-innervated muscles
Triceps
Extensor digitorum communis
Extensor carpi ulnaris
Radial nerve**
Flexor carpi ulnaris
Flexor digitorum profundus (digits 4, 5)
Ulnar nerve
Flexor digitorum profundus (digits 2, 3)
Flexor pollicis longus
Median nerve
Intrinsic hand muscles
Ulnar and median nerves
Medial cord-innervated muscles
Flexor carpi ulnaris
Flexor digitorum profundus (digits 4, 5)
Ulnar nerve
Flexor digitorum profundus (digits 2, 3)
Flexor pollicis longus
Median nerve
Intrinsic hand muscles
Ulnar and median nerves
* Refer to Fig. 7.1 and Appendix Table A.2 when using this table.
** These radial-innervated muscles are largely supplied by C6 and C7 but often have a significant C8 (though not T1)
contribution.
“positive” response. One study reported that 24% of 102 normal persons had a positive
response at one or both elbows when tested by the gentle tapping of the ulnar nerve with
two fingers “in the cubital tunnel.”127 Another study evaluated Tinel’s sign in both arms
of 100 healthy college students. The nerve was tapped twice with the examiner’s finger “at the cubital tunnel” and a positive response was found in 34% of arms.128 A difficulty in interpreting both of these studies is knowing where the nerve was being
percussed since the cubital tunnel lies just below the medial epicondyle and it would
be better to tap the nerve above, at, and below the epicondyle, encompassing the range
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279
of most common sites of damage. In the figure shown in one article the site of percussion appears to be immediately behind the epicondyle, or very slightly proximal to it.128
In a study of 32 patients with 44 UNEs diagnosed on the basis of sensory symptoms and
confirmed by motor nerve conduction abnormalities in the ulnar nerve at the elbow
(and 66 control arms), Tinel’s sign was evaluated by tapping the ulnar nerve 4–6 times
“just proximal to the cubital tunnel.”129 A positive response was found in 70% of the elbows with UNEs and only 2% of the control elbows. A further study describes lightly
tapping the nerve “around the medial condylar groove,” which presumably covers the
segment of nerve from just above to just below the epicondyle.130 These authors found
a positive response in 62% of patients with UNE diagnosed on criteria including symptoms and signs, abnormal electrophysiologic tests or abnormal sonography, or both of
these tests; 47% of a control group (patients referred with various arm symptoms that
were not due to UNE) had a positive result. They conclude that Tinel’s sign has poor
sensitivity, specificity, and diagnostic accuracy.
There are further nuances regarding this sign. First, if the response to light tapping
of the nerve is extreme sensitivity (marked paresthesias and discomfort or pain where
the nerve is being tapped), and if this is absent on the contralateral clinically unaffected
side, then this probably indicates focal ulnar nerve damage. Second, if there is a Tinel’s
sign on the normal side and none on the affected side, this may indicate damage on the
latter side; Tinel’s sign is usually absent in severe UNEs. Thus the presence or absence
of Tinel's sign probably relates to the severity of the UNE. This variable has not been
factored into any of the studies of provocative tests. Third, if this test is being done the
nerve should be percussed from about 5 cm above to 5 cm below the elbow to encompass the segments of the nerve that can be involved in UNEs, although it is not at all
clear if the location of Tinel’s sign reliably indicates the exact site of the UNE.
A motor Tinel’s sign indicates abnormal mechanosensitivity of the motor nerve fibers
at the elbow. On light tapping of the nerve, the ulnar-innervated intrinsic hand muscles
contract briefly.131 This sign is rarely found and is of curiosity value only.
The elbow flexion test consists of fully flexing the elbow for 1–5 minutes and is regarded as positive if this initiates or aggravates sensory symptoms and signs in the
ulnar nerve distribution.129,132,133 One study reports a positive test in all of 13 patients
with UNE, but there were no controls.133 Another study found that 10% of normal persons had symptoms at 1 minute of elbow flexion.127 This test was further evaluated in
both arms of 100 healthy college students, recording the presence of paresthesias at 1,
2, and 3 minutes.128 Positive responses were obtained in 2%, 10%, and 21% of arms at
these times. A further study reported that this test was positive at 1 minute in 75% of
44 arms with UNEs and none of 66 control arms.129
The pressure provocation test has been described in which the examiner presses on the
ulnar nerve with their fingers just proximal to the cubital tunnel for 60 seconds. A positive
result is when the “subject reported symptomatology in the distribution of the ulnar
nerve.”129 This was found in 89% of 44 arms with UNE and 2% of 66 control arms.129
A combination of elbow flexion and pressure provocation (flexion compression test)
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Figure 10.9. Clinical findings in 25 cases of ulnar neuropathy at the elbow. Four muscles were examined, two in the
forearm (flexor carpi ulnaris [FCU] and flexor digitorum profundus of the fourth and fifth digits [FDPu]) and two in the hand
(abductor digiti minimi [ADM] and first dorsal interosseous [FDI]). The three sensory branches examined were the
palmar cutaneous (PC), dorsal ulnar cutaneous (DC), and terminal digital (TD) branches. “Only” refers to the number of
patients in whom a single sensory area was involved or to patients with weakness of only one of the four muscles. (From
Stewart,136 with permission.)
has been evaluated as a provocative test for UNE. One study showed a positive response in 98% of patients with UNEs and only 2% of controls.129 These authors conclude that this “is a quick, cost-effective, and reliable clinical test.” By contrast, in
another study also consisting of patients with UNE and a control group, 60% in each
cohort had positive responses after 1 minute of elbow flexion and ulnar nerve compression.130 These authors concluded that, as for Tinel’s sign, the elbow flexion test has
poor sensitivity, specificity, and diagnostic accuracy.
A scratch collapse test has been described as an adjunct for the diagnosis of carpal
tunnel syndrome and UNE.134 This is based on dubious physiology and requires further
studies to establish its validity and utility.
In summary, these tests require more rigorous study and validation for their diagnostic roles to be fully established. An underlying problem is the lack of a gold standard diagnostic test for UNE with which to evaluate the true sensitivity and specificity,
positive and negative predictive values of these provocative tests (indeed if there was
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such a definitive diagnostic test there would be little interest in finding adjunctive clinical tests). In the two studies with patients considered to have UNE by reasonable criteria and a control group, the findings are strikingly different. Novak et al.129 found
very high numbers of positive tests in patients but in very low numbers of control subjects. These findings are out of keeping with common clinical experience, and with the
results from studies of normal persons. Beekman et al.130 found markedly less differences in provocative tests between patients and controls. Logistic regression analysis
showed that only minimal added value was accrued by adding these maneuvers to routine clinical examination. The study design, diagnostic, and statistical methods used in
the Beekman et al.130 study were more rigorous than those of Novak et al., 129 so I endorse the former authors’ conclusion that “the diagnostic value of provocative tests in
UNE is poor and should not be recommended for clinical decision making.” The most
reliable way of diagnosing a UNE is a careful motor and sensory examination as outlined above. It follows that performing surgery for patients alleged to have UNE based
entirely on abnormal provocative tests, in the absence of a standard motor and sensory
examination of the affected limb and in the absence of electrophysiologic studies, is to
be strongly discouraged.135
Of more importance than these signs is the examination of the ulnar nerve from axilla to wrist in a search for soft tissue masses, bony abnormalities, and sites of unusual
tenderness. Prolapse of the nerve should be examined by palpating the nerve in the
condylar groove with the elbow straight, then flexing the elbow while continuing to
feel for the position of the nerve. Focal thickening of the ulnar nerve at the elbow has
been shown to be of no value in the diagnosis of UNEs in routine Western practice,130
but may well be of value in countries where leprosy is common. Likewise, palpating
for local tenderness of the ulnar nerve at the elbow has shown to be of little value in
diagnosing UNEs,130 but it may be the clue to a diagnosis of a schwannoma or other
uncommon ulnar nerve lesion, particularly when present somewhere other than the
elbow.
Theoretically, ulnar neuropathies at the elbow should be easily to localize by the
motor and sensory examinations, but in practice this is sometimes difficult. The propensity for partial focal nerve lesions to involve fascicles differentially within a nerve is
discussed in Chapter 4. These fascicular phenomena are particularly common in ulnar
neuropathies at the elbow and can give rise to considerable difficulties in clinical localization. The ulnar intrinsic hand muscles have long been noted to be more frequently
affected than those in the forearm. The results of a systematic study of the variable involvement of four ulnar-innervated muscles and the three sensory branches are summarized in Figure 10.9.136 The two forearm muscles (flexor carpi ulnaris and flexor
digitorum profundus of the fourth and fifth digits) are frequently normal even when
the ulnar nerve lesion is clearly proximal to the branches that innervate them. The cutaneous areas innervated by the three sensory branches are also variably involved. These
clinical findings were mirrored by electrophysiologic evaluations of ulnar muscles and
sensory branches.136
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Two patients illustrate these difficulties in distinguishing clinically between a lesion
at the elbow or the wrist/hand. A 50-year-old woman presented with numbness in the
distribution of the terminal digital branch in one hand. There was a history of habitual
leaning on that elbow and of sleeping with the elbow tightly flexed. Examination confirmed the restricted sensory loss. All muscles were normal except for mild weakness
of the first dorsal interosseous. The ulnar nerve was tender in the condylar groove. The
distribution of the sensory and motor signs suggested that this ulnar nerve lesion was
in the hand or wrist (Fig. 10.4, Table 10.5 below). However, motor conduction studies
to the first dorsal interosseous muscle showed a conduction block at the elbow. In addition, electromyographic (EMG) studies of the flexor digitorum profundus showed
the presence of fibrillations and positive sharp waves. These two findings, plus the
focal tenderness of the nerve, localized the lesion to the elbow.
A 62-year-old man presented with terminal digital distribution sensory loss and no
symptoms to indicate a cause for ulnar nerve damage at the elbow or hand. All of the
ulnar-innervated intrinsic hand muscles were weak, whereas those in the forearm were
normal. These findings suggested a lesion of the distal ulnar nerve, proximal to the motor
branches to the hypothenar muscles, that is, in Guyon’s canal (Fig. 10.4). However, motor
nerve conduction studies to the first dorsal interosseous muscle showed a conduction
block across the elbow, confirming that to be the site of the ulnar neuropathy.
In summary, an ulnar neuropathy is usually localized to the elbow by a careful clinical examination of the motor and sensory deficits. However, because of the apparent
differential involvement of the nerve fascicles in some patients, the clinical signs can
misleadingly suggest a more distal lesion. Electrodiagnostic studies are a valuable aid
for localizing the site of the damage.
The severity of the UNE can be graded on the basis of the symptoms and clinical examination. The McGowan classification is often used, particularly by surgeons, but as
originally defined, this is extremely imprecise, essentially grading neuropathies as mild,
moderate, or severe (grades 1, 2, 3) using scanty criteria.53 The following is a useful and
pragmatic classification, based on that by Bartels.137 (Other grading systems
exist.123,138,139 A more detailed classification that lends itself to clinical trials has been
developed.140 A severity scale based on electrophysiologic abnormalities has also been
described.141)
Grade 1 (mild): Sensory symptoms with or without motor symptoms; may or may
not have sensory loss; no muscle atrophy or weakness.
Grade 2 (moderate): Sensory symptoms; detectable sensory loss; mild atrophy; grade
4 or 4+ muscle weakness.
Grade 3 (severe): Usually constant sensory symptoms; detectable sensory loss; moderate to marked atrophy; grade 4- or less muscle weakness.
Some patients differ from the above, for example, those with severe ulnar nerve pain
and tenderness at the elbow but are otherwise in the mild group, and those who have
predominantly or only sensory or motor abnormalities.
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Differential Diagnosis
Ulnar neuropathies at the elbow must be distinguished from disorders of the spinal
cord, nerve roots, brachial plexus, and small cerebral infarcts. Amyotrophic lateral sclerosis (ALS) often causes wasting of the hand muscles, and this may occur early in the
disease. However, a careful examination usually reveals more widespread muscle involvement, upper motor neuron signs, and no sensory loss. Benign monomelic atrophy
(also called monomelic amyotrophy, monomelic neurogenic syndrome, monomelic
motor neuron disease) is a syndrome thought to be due to anterior horn cell degeneration, but without the relentless and fatal progression that characterizes ALS.142-149 It is
considerably more frequent in India and in the Far East than in Europe and North America. Most patients are otherwise healthy young males. In the initial phase, the wasting
and weakness is confined to an arm or a leg, is alarmingly progressive over 2–3 years,
but then the progression slows or stops. In the distal arm type there can be marked
wasting of the ulnar-innervated muscles. Careful examination and electrophysiologic
studies will show involvement of muscles supplied by other nerves.
In multifocal motor neuropathy (see Chapter 23) the ulnar-innervated muscles can
be strikingly affected. The characteristic pattern is that of weakness with little wasting,
the involvement of other nerves, and the lack of sensory loss. Electrophysiologic studies often show conduction blocks at different sites than the usual ones for compressive
ulnar neuropathies. Conduction blocking is often detected in other nerves, and sensory
conduction studies are normal.
In syringomyelia, wasting of the intrinsic hand muscles is frequent, but it is usually
more extensive than that of an ulnar neuropathy, and the sensory abnormalities are quite
different. Occasionally, there may be wasting of the hand muscles in cervical spondylotic radiculopathy/myelopathy, but other motor, reflex, and sensory signs help to differentiate this condition from an ulnar neuropathy (see Chapter 6). A C8 radiculopathy
is uncommon but it is usually recognizable by muscle weakness that extends beyond
ulnar-innervated muscles (Table 10.3, see also Chapter 6).150,151 However, the sensory
disturbance of a C8 radiculopathy may closely mimic that of an ulnar neuropathy. A T1
radiculopathy is very uncommon. A Horner’s syndrome (from the involvement of sympathetic fibers in this spinal nerve), involvement of median-innervated muscles, and
more extensive sensory loss are distinctive signs in a T1 root lesion (see Chapter 6).
Radicular pain, neck stiffness, and associated signs of myelopathy, when present, are
also helpful in distinguishing spinal nerve root compressions from ulnar neuropathies.
Brachial plexus lesions involving the lower trunk or medial cord of the plexus also
mimic ulnar neuropathies and are important differential diagnoses. These include the
true neurologic thoracic outlet syndrome, neoplastic infiltration, radiation-induced plexopathy, and acute brachial plexus neuropathy (see Chapter 7). In general, these are
distinguished from ulnar neuropathies by involvement of radial- and median-innervated muscles (Table 10.3), and sensory impairment that extends beyond the distribution of the ulnar nerve. A Horner’s syndrome is an important sign associated with lower
trunk neoplastic infiltration—the Pancoast syndrome. Lacunar cerebral infarcts in the
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thalamus or corona radiata may produce sensory symptoms and signs that mimic those
of ulnar neuropathy.152
Investigations
Electrophysiologic Studies
The goals of electrophysiologic studies are to confirm that the nerve damage is confined to the ulnar nerve, to localize the ulnar nerve lesion (particularly to distinguish between elbow and wrist/hand lesions), and to assess severity. Motor nerve conduction
studies are performed by recording from an ulnar-innervated intrinsic hand muscle,
and stimulating the nerve at the wrist and above and below the elbow. Amplitude
changes, slowing of conduction velocity, and dispersion of the compound motor action potentials confirm an ulnar neuropathy at the elbow.153-159 Because of different involvement of the abductor digiti minimi and first dorsal interosseous muscles both in
elbow and in wrist/hand ulnar neuropathies, it is best to perform motor conduction
studies while recording from both,136,160,161 although one study found that recording
from the first dorsal interosseous muscle did not add to the sensitivity of the motor
conduction studies in patients with UNEs.162 The presence of certain types of MartinGruber anastamoses may produce a reduction in amplitudes of the proximally evoked
compound motor action potentials (see Chapter 9 and Fig. 9.3). Stimulating the median
nerve at the elbow should help to differentiate between such an anastomosis and a UNE.
The inching technique (short segment nerve conduction studies) involves recording
from a hand muscle while stimulating the ulnar nerve above and below the elbow at a
series of sites anywhere from 1 inch (2.5 cm) to 1 cm apart.81,162-167 This is done in an
attempt to (a) improve on the sensitivity of the standard motor conduction studies, and
(b) to attempt to localize the lesion more accurately to the condylar groove, the cubital
tunnel, or more distally at the exit point from the cubital tunnel, and thus to guide surgical management. There is general agreement that short segment nerve conduction
studies are substantially more sensitive than routine studies, so should be done when
the latter are normal. In terms of localizing the UNE, most studies report that the majority of conduction abnormalities are found in the condylar groove or at the level of
the condyle, with fewer localized distal to this, that is, in the cubital tunnel. However,
there is not always satisfactory concordance between these percutaneous studies and
those performed intraoperatively.81,163,164 One careful study has shown that this technique distinguishes ulnar compression in the condylar groove from that in the cubital
tunnel 80% of the time (the definitive diagnosis in these cases was made by intraoperative conduction studies).163
Sensory conduction studies performed by stimulating the fifth digit while recording
from the ulnar nerve at the wrist are abnormal in ulnar neuropathies at the elbow if
there has been axonal degeneration. Similar abnormalities also occur in lesions of the
lower trunk or medial cord of the brachial plexus. Sensory studies with recording above
the elbow are potentially more precise in localizing the lesion to the elbow but are more
demanding technically and the nerve action potentials may be small or absent even in
apparently normal persons.153,155,157
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The dorsal ulnar cutaneous sensory conduction study is a valuable aid in distinguishing lesions at the elbow from those at the wrist or hand, for the same reasons that
the clinical examination of this nerve is so useful.168,169 This sensory potential can be absent if there is anomalous innervation from the superficial radial nerve, although a technique has been described for electrophysiologicly identifying this anomaly.14
Electromyographic (EMG) studies of the two ulnar-innervated forearm muscles are
also helpful in distinguishing between elbow and wrist ulnar nerve lesions. When they
are abnormal, the lesion is clearly not at the wrist; but they may be normal on both
clinical and EMG examinations in UNEs at the elbow, presumably due to sparing of
those fascicles.136 EMG is also useful in evaluating the paraspinal muscles, and other
non-ulnar muscles innervated by the C8 and T1 roots and the brachial plexus (Table
10.3).
In spite of performing these well established electrophysiologic techniques the results may be inconclusive. The American Academy of Neurology, the American Association of Electrodiagnostic Medicine, and the American Academy of Physical
Medicine and Rehabilitation have produced a practice parameter paper on electrodiagnostic testing for UNE.158 A review of a number of studies shows sensitivities of
37–86% and specificities of 95% or greater. Many expert electrophysiologists have expressed frustration at this low sensitivity rate and sometimes being unable to confirm
a UNE in a patient in whom the diagnosis is very clear clinically. However, a thorough
electrophysiologic test, even if negative for UNE, goes a long way to exclude other
neurological diagnoses. Such a patient should be managed as for a UNE and the tests
repeated if there is no improvement or worsening.
Imaging Studies
Until recently the role of imaging studies in patients with UNE was to search for clinically undetectable elbow joint damage, osteophytes, or soft tissue masses such as ganglia and lipomas; such abnormalities are present in only a few patients. Most mass lesions
are easily seen on CT and MR imaging. Now under consideration is the role of MRI and
ultrasonography (US) in diagnosing the majority of UNEs, that is, those caused not by
mass lesions but by compression in the condylar groove or in the cubital tunnel. One
study of patients with 31 UNEs diagnosed using solid clinical criteria reported MR imaging that showed increased signal (in 97% of nerves), enlargement of ulnar nerves
(74%), or both.170 No such abnormalities were seen in control subjects. Electrophysiologic
testing demonstrated UNE in 77% of patients. Eleven patients underwent surgery and
were found to have nerve compression within the cubital tunnel. Another study had a cohort of patients with 59 UNEs selected using strict clinical criteria and studied with MRI
and electrophysiologicly.171 MRI abnormalities, mainly those of nerve hyperintensity and
enlargement, were found in 90% of neuropathies while the electrodiagnostic studies were
confirmatory for UNE in 63%. These authors report that the MRI abnormalities localize
the UNE to specific sites: retroepicondyler groove, cubital tunnel, a combination of these,
the cubital tunnel and distal forearm, distal forearm only, or diffuse involvement of the
nerve. Unfortunately there was no correlation with surgical findings. Two other brief
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reports probably include overlapping groups of patients. One is of 21 patients with UNEs
who were studied by MRI and electrodiagnostic testing.172 All showed MR abnormalities;
71% had abnormal electrodiagnostic studies preoperatively and 90% intraoperatively.
The surgical findings are not described. The other similar report is of 48 patients: MRI
showed increased nerve signal intensity in 98% (focal in 90%) and focal nerve enlargement in 79%.173 Preoperative electrodiagnostic studies were diagnostic for UNE in 63%;
intraoperative studies were abnormal in 81%. Unfortunately, the surgical correlates of
these imaging and nerve conduction findings were not discussed.
Studies of ultrasonography (US) in UNEs have evaluated swelling of the ulnar
nerve, the ratio of the swollen section of the nerve to the normal section, and the crosssectional area of the cubital tunnel.174-177 A prospective study that included patients with
82 UNEs and 9 probable UNEs were studied electrophysiologicly and with US nerve
diameter measurements above, at, and below the medial epicondyle.174 The main finding was that patients with UNE had a significantly larger diameter nerve than controls.
The sensitivity of US was 80% and specificity 86%. In another study of patients with
UNEs diagnosed on a combination of clinical and electrophysiologic criteria, swelling
of the ulnar nerve was found in just under 50% of patients.177 A further study evaluated
the maximum cross-sectional areas of the ulnar nerve in 38 patients (50 elbows) with
UNEs, comparing these with a control group and correlating the findings with severity of UNE on electrodiagnostic studies.178 There was a strong correlation between the
maximal cross-sectional area and the severity score derived from the electrodiagnostic testing. An interesting brief report is of 4 patients with clinically likely UNE, but
with normal electrodiagnostic studies; US showed abnormal swelling of the ulnar nerve
in each patient.179
In summary, it is clear that specialized MR imaging done by experts in the field is
now capable of showing abnormalities diagnostic of UNE in over 90% of patients. This
sensitivity considerably exceeds that of electrodiagnostic studies. From a practical point
of view, the main role for MRI in patients with UNEs remains the detection of mass lesions or nerve tumors. Perhaps in the near future it will be used in patients with negative or ambiguous electrodiagnostic test results and in whom surgery is being
considered (so confirmation of the diagnosis and information regarding the precise site
of nerve damage is particularly desirable). At present access to such highly specialized
MR imaging is extremely limited. Further studies are required to establish the role of
US in the evaluation of UNEs, but it is likely that this will become a useful adjunctive
and cost-effective diagnostic test, particularly in patients in whom the electrophysiologic studies are negative or inconclusive.180
Management
Natural History and Management Decisions
As in the case of carpal tunnel syndrome (CTS), it would be very useful to know the
natural history of UNEs. Do any spontaneously improve, and if so how many? Do some
inexorably worsen, and are those recognizable? Which ones should be treated and with
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287
what methods? A fundamental difficulty in addressing these questions is that UNEs are
of diverse causes so the natural history and responses to treatment will vary, particularly when there is a structural abnormality. There have been several studies allegedly
focusing on the natural history of idiopathic UNEs. An early study of 30 patients with
mild UNEs followed for a mean period of 22 months showed that 67% of the patients
became asymptomatic, 23% improved, and 10% worsened.181 It is unclear whether
these patients were treated conservatively or not. Another early study of only 13 patients
with UNEs of varying severity reported that after several months 62% had an “excellent recovery,” a further 23% were improved, while 15% worsened.182 These numbers
are very small and details of what conservative measures were used, if any, are not provided. A more recent study has also addressed the natural history.183 In a group of 30
patients with electrophysiologicly confirmed UNEs, 24 were “untreated” and 6 underwent surgery. A follow-up evaluation was performed 9–19 months later. Of the 24 untreated UNEs, symptoms improved in 12 (50%), were unchanged in 7 (29%), and
worsened in 5 (21%). Eleven patients were re-evaluated electrophysiologicly: 7 showed
some improvement and the others were the same; none had worsened. A difficulty with
this study is that the “untreated” patients were thoroughly educated regarding the dangers of elbow leaning and prolonged flexion, and most patients changed their habits regarding these, so this study really evaluated conservative management. Other
drawbacks include a heavy reliance on symptoms but a lack of clinical examinations,
and small numbers of patients. In summary, there is no clear natural history data regarding UNEs and the questions posed above remain unanswered.
The major management decision regarding treatment for UNEs lies in choosing between conservative measures aimed at preventing further damage to the nerve mainly
from external compression and elbow flexion, thereby allowing the nerve to recover,
and surgery. The results of surgery have sometimes been disappointing (particularly
by contrast with the generally successful results of CTS decompression), and there has
been a relatively high complication rate of one of the surgical procedures, anterior subcutaneous transposition of the nerve. These factors have led to a growing interest in conservative measures, and there is no doubt that these are effective in probably a large
proportion of patients with UNEs.
There are three surgical procedures for ulnar neuropathies at the elbow. The simplest is cubital tunnel decompression. This involves slitting the flexor carpi ulnaris
aponeurosis in order to decompress the nerve.52,79,80 The traditional approach is transposition of the nerve from the condylar groove to the anterior surface of the elbow “out
of harm’s way.”48,82,184-189 This involves slitting the aponeurosis, mobilizing the nerve
and moving it anteriorly, then either embedding it subcutaneously, intramuscularly, or
submuscularly. The other approach is medial epicondylectomy, which involves removal
of the bony prominence against which the nerve is stretched during tight flexion of the
elbow, as well as to slackening of the entrance and roof of the cubital tunnel.190-194
Because UNEs are a heterogeneous group of disorders, management begins by categorizing the patients into one of four major groups: (a) bony abnormality of the elbow
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joint; (b) suspected or confirmed soft tissue mass; (c) grossly prolapsing nerve; and (d)
no detectable structural abnormality (Fig.10.10). The management of these disorders
differs.
Bony Abnormality of the Elbow Joint
Temporary measures include instructing the patient to avoid leaning on or bumping
the nerve and to desist from prolonged or repeated flexion of the elbow. An elbow pad
(see below) helps to protect the nerve against external compression, and also restricts
flexion. However, surgery is indicated in most of these patients. If there is marked valgus deformity, orthopedic correction should be considered, with or without transposition of the nerve. If no orthopedic measures are required, transposition of the nerve
anterior to the elbow joint is indicated. This shortens the course of the nerve, eliminates stretching over the callus or the valgus deformity, and helps to protect the nerve
from external pressure and trauma.
Soft Tissue Masses
The treatment is surgical excision of the mass. This often involves opening the roof
of the cubital tunnel, which aids in decompressing the nerve. Transposing the nerve is
not usually necessary.
Grossly Prolapsing Ulnar Nerve
Two surgical procedures have been advocated for this relatively rare condition: anterior transposition or subperiosteal medial epicondylectomy (see below).66,191-193
No Detectable Structural Abnormality
Most patients fall into this group and are sometimes labeled “idiopathic UNE.” This
is often incorrect since with diligent enquiry a cause or causes are often identifiable; such
recognition aids in the rational choices of treatment. Unfortunately, no good
controlled or comparative studies have been done on conservative versus surgical treatments of UNEs. In addition to controlled trials, another potentially helpful approach—
not yet done for UNEs except regarding the different surgical approaches (see below)—is
a decision analysis. This is a technique for attempting to consider all possible outcomes
of treatment strategies for a condition, taking into account factors that might affect those
outcomes, and selecting the best of these strategies.
Conservative Measures
In spite of the paucity of data, it is possible to follow a rational plan in managing
these patients. For those with mild or moderate (grade 1 and 2) neuropathies, the first
step is to interrogate the patient regarding habitual elbow leaning and bending, and
about possible elbow flexion during sleep (Figs. 10.6, 10.7). They should be taught the
location of the nerve and how to avoid putting pressure on it. These approaches are
often sufficient to eliminate compressive damage and bring about improvement.
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Figure 10.10. Management of ulnar neuropathies at the elbow.
Categorize into 1 of 4 types
Bony abnormality of
elbow joint
Suspected soft
tissue mass
Grossly prolapsing
nerve
No detectable structural
abnormality
Temporary measures to
protect nerve
Imaging studies
Surgery: transposition or
medial epicondylectomy
Identify possible causes
Surgery: correction of
deformity, transposition of
nerve, or both
Excision of mass
Eliminate possible
causes; consider
using elbow pad
Better or same
Worse
Continue conservative
measures
Imaging studies
Surgery
Padding can be used to protect the nerve against external pressure. One option is for the
patient to wear an elbow pad during the day. This should have generous padding and
most of the commercially available ones are too flimsy. Sports elbow pads are readily
available and are better (Fig. 10.11.A). Wrestlers’ elbow pads are recommended by one
expert,195 and another recommends a junior size volleyball knee pad. Pads can also be
custom made by an occupational therapist. Another option is to pad the arm of the chair
(Fig. 10.11.B). If elbow flexion during sleep is a likely cause the elbow pad should be
worn at night.196 Many of the sports elbow pads have a thickly and a thinly padded
side. During the day, the thick side should be on the extensor aspect of the elbow to
cushion and protect the nerve; at night it should be reversed so the thicker side prevents tight elbow flexion (Fig. 10.12.A) . Some commercially available elbow braces
lend themselves to use at night but they are quite rigid, cumbersome, need to be sized
properly, and are not widely available.197,198 A useful home-made approach is to wrap
the elbow in a medium-size towel and fasten it with large safety pins, adhesive tape, or
Velcro straps (Fig 10.12.B). Many patients can train themselves to sleep with their elbows straight. Patients in whom the neuropathy is attributable to a single episode such
as compression during sleep on an airplane journey, or who have a perioperative UNE
should also be advised how to protect the nerve against further external pressure. The
role of steroid injections for the treatment of UNE is unclear.199
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Many patients with mild or moderate (grades 1 and 2) UNEs will recover with these
conservative measures, and studies have reported improvement or complete recovery
in 30–90% of these patients.181-183,200-202 These patients must be followed closely in order
to detect any deterioration before it becomes marked. My practice is to see such patients
every 2 months. If worsening occurs in spite of these measures, imaging of the elbow
with CT or MR is indicated, although the likelihood of finding a structural abnormality is low, and surgical exploration is indicated regardless of the imaging results. This
approach is similar to that of Harding and Morris,202 who found that 20% of such patients required surgery. The timing of surgery is important; conservative measures
should be abandoned before the neuropathy becomes severe because surgery at that
time may be less likely to produce much improvement.
Management decisions for the patient who presents with a grade 3 (severe) UNE are
more difficult. The factors to be considered are: some patients may respond well to conservative measures; if there is delay and further worsening then the response to surgery
may be lessened; surgery results in improvement in 61–83% of patients regardless of the
severity of the UNE.139,140 An important consideration is whether there are identifiable
factors when the patients in this category of UNEs without detectable structural abnormalities first present for evaluation that could be used to help choose conservative or surgical treatment. Few such factors have been identified. The presence of motor conduction
blocking and slowing (electrophysiologic signs for demyelination) is associated with a
better prognosis whether the patient is treated conservatively or surgically.203,204 But others have stated that electrodiagnostic abnormalities do not predict surgical outcomes in
severe UNEs.139 An ultrasound finding of pronounced ulnar nerve swelling at the elbow
is associated with poor outcome, particularly in patients treated conservatively.203 My approach to such a patient is to institute conservative measures, arrange for imaging studies to be done expeditiously, and to see the patient within a month. If there is any hint
of worsening or if a structural abnormality is found, or both of these, then the patient
should have surgery as soon as can be arranged. If the patient is stable or improving and
imaging studies are normal, I continue to follow the patient at monthly intervals, abandoning the conservative measures for surgery if there is any worsening. Only one study
has addressed recurrence rates following conservative treatment for UNE.201 Unfortunately “recurrence” is defined as “no change and/or worse,” rather than the accepted
meaning in which the patient improves or recovers, followed by the return of UNE manifestations, so no conclusions can be drawn from this study.
Surgery
The best surgical procedure for these patients has been long and vigorously debated.205 Anterior transposition has been widely performed in the past. The nerve is
moved to the front of the elbow and placed subcutaneously, intramuscularly, or submuscularly. Subcutaneous placement has the highest incidence of failures and complications.137 Failure to improve has been attributed to poor technique and to damage of
the vasa nervorum during transposition. Other complications of transposition include
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291
A
B
Figure 10.11. Padding to protect the ulnar nerve at the elbow. A: Elbow pad to protect the ulnar nerve (this is a small
size volleyball knee pad). B: A thick sponge attached to the arm of a chair.
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A
B
Figure 10.12. Preventing elbow flexion during sleep. A: Sports elbow pad worn with the thick side on the flexor/volar
surface of the elbow. B: Towel wrapped around the elbow and held in place with Velcro straps. Both pictures show the
maximum amount of comfortable flexion when wearing these devices.
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293
scar formation leading to further nerve compression, and persistent, painful paresthesias.206 These paresthesias can be in the region of the incision, in the distribution of
branches of the medial cutaneous nerve of the forearm,207 or in the territory of the ulnar
nerve itself. The ulnar nerve at the elbow can become exquisitely sensitive to even trivial pressure. These pain syndromes can be very difficult to treat. Cubital tunnel decompression has the advantages of surgical simplicity with preservation of the normal
position of the nerve and its vascular supply, and early rehabilitation of the patient.
However, if the nerve damage is in the condylar groove, not in the cubital tunnel, this
is not the operation of choice. In a very large series of operations for UNE during which
intraoperative nerve conduction studies were performed, the usual finding was that the
conduction abnormalities were in the condylar groove, and only rarely in the cubital
tunnel.123 This argues in favor of transposition and against cubital tunnel decompression. Other intraoperative nerve conduction studies have shown that about one-third
of UNEs are in the cubital tunnel (see above). Because transposition involves slitting
the aponeurosis in order to free the nerve, some of the success of transposition may be
due to concomitant cubital tunnel decompression. Medial epicondylectomy, like
cubital tunnel decompression, involves limited dissection and mobilization of the nerve,
potentially reducing the risk of direct and vascular damage.
An analysis of the literature on surgery for UNE has provided useful guidelines.137
It was found that simple decompression and submuscular transposition had the best
outcomes. Medial epicondylectomy and subcutaneous or intramuscular transpositions
had the worst outcomes. Since then there have been four randomized controlled trials
comparing simple cubital tunnel decompression with transposition (two submuscular
and two subcutaneous).139,140,208,209 A meta-analysis has synthesized the data from these
studies.210 Excellent or good results are obtained in 61–83% of patients. Both operations
are equally effective regardless of the severity and durations of symptoms of the UNE.
Simple decompression is quicker and has fewer complications and so is the surgical
procedure of choice for idiopathic UNEs. A further meta-analysis found no statistically
significant difference between decompression and transposition but there was a trend
toward a better outcome with the latter.211 A decision analysis comparing decompression, epicondylectomy, and two types of transpositions concluded that simple decompression is the preferred strategy.212 A subsequent study showed that simple
decompression was associated with less health care and non-health care costs (e.g.,
time off work).213
Although these important studies answer some basic questions about the best choice
of operation for UNEs with no identifiable structural cause, there remain some unresolved issues. One is the conundrum that the majority of preoperative and intraoperative short segment nerve conduction studies show that only about one-third of UNEs
are in the cubital tunnel. Why then should cubital tunnel decompression be effective for
most patients with UNEs? The surgical failures may be for this very reason, but it is
surprising that the failure rates are not higher. Given that there are four sites where
nerve damage can occur in the elbow area (see above) it is predictable that surgical
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decompression of the cubital tunnel will not relieve compression at other sites. What
is needed, but is lacking except in a very few centers, is expert intraoperative electrophysiologic testing to aid the surgeon in localizing the lesion and then to choose between decompression or transposition.
The issue of how best to manage the patient whose neuropathy has not improved
postoperatively, or that deteriorates after some initial improvement, is unclear. This can
occur following all three of the surgical procedures. Possible reasons are discussed
above and outlined in several papers; the consensus is that reoperation with extensive
exploration of the nerve followed by transposition or retransposition may be the best
strategy.140,214-217 One study reported that 40% of these patients improved.217
A new development in surgery for UNE is that of endoscopy with extensive “decompression” of the ulnar nerve across the elbow.218-221 The results in two open studies
were comparable to other surgical approaches and the complication rates were low. A
further paper describes an endoscopic technique for ulnar nerve transposition.222
For the patient with a severe chronic ulnar neuropathy from any cause, physiotherapy is important to minimize contractures and claw deformities. Reconstructive techniques such as tendon transfers can considerably improve hand function.223
ULNAR NEUROPATHIES IN THE FOREARM
Ulnar neuropathies in the forearm are uncommon (Table 10.4). A lesion here can be
difficult to diagnose and this is one reason for failure of surgery at the elbow.
Causes
Compression occurring within the distal part of the flexor carpi ulnaris by hypertrophied muscle and by abnormal fibrous or fibrovascular bands and entrapment where
the nerve exits through the deep aponeurosis of the flexor carpi ulnaris have been found
at surgical exploration.224-228 Hemophiliacs may bleed into the forearm muscles with
the hematoma compressing the nerve.229 Severe damage to both the ulnar and the median nerves in the forearm have been reported following extravasation of an intravenous
streptokinase infusion.230 Ischemic neuropathies of all three major nerves and their
branches in the forearm may occur as a result of the creation of arteriovenous shunts
for dialysis (Chapter 9).231 Compartment syndromes involving the forearm following
coma can also cause ulnar nerve damage.232 Ulnar nerve damage occurs rarely in fractures of the forearm bones.233 Nerve sheath tumors and perineuriomas can occur in the
forearm.234 External compression of the ulnar nerve in the distal forearm can be caused
by handcuffs, although the superficial radial nerve is much more frequently damaged
in this situation.235
Diagnosis
It would be expected that these neuropathies should be distinguishable from those
at the elbow because they are distal enough that the branches to flexor carpi ulnaris
and flexor digitorum profundus muscles would be spared. However these muscles are
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295
Table 10.4. Ulnar neuropathies in the forearm.
Compression
In distal flexor carpi ulnaris muscle and aponeurosis
Hematoma
Compartment syndrome
Handcuff
Forearm fracture
Ischemia from dialysis fistula
often not involved even in neuropathies at the elbow. Some patients will have helpful
localizing signs such as a point of tenderness or swelling in the forearm. When nerve
conduction studies show no focal conduction abnormalities at the elbow or wrist, this
should raise the suspicion of a forearm lesion. Stimulating the ulnar nerve
percutaneously along its length may reveal a focal point of conduction block in the
forearm, but the nerve lies deeply and adequate stimulation is often difficult.226,227 Stimulation with a monopolar needle may be required.226,227 If the ulnar nerve is explored at
the elbow and no abnormalities (with or without intraoperative nerve conduction studies being done) are found, the surgeon should extend the incision more distally to look
for a lesion in the forearm.
ULNAR NEUROPATHIES AT THE WRIST AND HAND
Sites of Damage
The distal ulnar nerve and its two branches, the superficial and the deep terminal
branches, can be damaged at one of four sites in the wrist or hand (Fig. 10.4, Table
10.5).
1. The main trunk of the nerve at the entrance or within Guyon’s canal. A similar syndrome is produced by compression of the two main terminal branches immediately
after they have divided from the main nerve within the canal. These lesions produce
sensory loss in the distribution of the superficial terminal branch and weakness of
all the ulnar-innervated intrinsic muscles.
2. The deep terminal (motor) branch of the ulnar nerve distal to Guyon’s canal but
proximal to the branches that innervate the hypothenar muscles. This produces
weakness of all of the ulnar-innervated muscles of the hand and no sensory loss.
3. The deep terminal (motor) branch distal to the branches that innervate the hypothenar muscles. This also produces no sensory loss, but there is weakness of all
the ulnar-innervated intrinsic hand muscles except the hypothenar muscles.
4. The superficial terminal (sensory) branch. This produces sensory loss and no muscle
weakness.
Only type 1 involves a lesion of the nerve within Guyon’s canal and therefore
“Guyon’s canal syndrome” is an unsatisfactory term for the whole group of ulnar neuropathies in the wrist and hand. Of the four syndromes, type 3 is the most frequently
seen, followed by type 1 and then type 2; type 4, the pure sensory syndrome, is rare.
Compared with the carpal tunnel syndrome and ulnar neuropathies at the elbow, all of
these syndromes are uncommon.
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Causes
External compression from chronic, sustained, or repetitive occupational or recreational hand usage is the best-known cause. Since Ramsey Hunt’s236 original descriptions in the early 1900s of these ulnar neuropathies occurring in persons using tools that
pressed into the base of the hand, they have been attributed to a wide variety of occupations and pastimes. Another cause of external compression, bicycle riding, had been
described even earlier by Destot.237 This has continued to be an important cause and has
an interesting relationship to sociopolitical events. Guillain et al.238 noted large numbers of affected cyclists following the evacuation of French civilians during the Second
World War. Fuel oil shortages and the popularity of long-distance bicycle touring have
led to more recent increases in the number of patients with this focal neuropathy.239243
Studies done on cyclists before and after long-distance events have shown a high incidence of sensory (mainly ulnar distribution) and motor symptoms; examination
showed that in 25 cyclists, 14% had sensory abnormality in the fifth digit and 22% had
weakness of intrinsic hand muscles.244 An electrophysiologic study on a similar cohort
of cyclists showed significant prolongation of the distal motor latency to FDI but not
ADM, and no sensory nerve conduction changes.245 The use of padded gloves and
padded handlebars are probably helpful, but it is more important to make cyclists aware
of the condition and advise them to frequently change their hand position on the handlebars to prevent nerve damage. Further additions to the list of occupational or recreational causes of ulnar neuropathies at the hand and wrist include pizza cutting,
prolonged playing of video games, the intensive use of a computer mouse, and wheelchair racing and other sports in paraplegics.56,57,246-250 The use of walking frames and
crutches are surprisingly rare cause of ulnar neuropathies at the wrist/hand.251-254
Ganglia constitute the other important cause of wrist and hand ulnar neuropathies.8,63,255-263 These can be divided into two groups.8 In some patients, the ganglion arises in the wrist and produces a type 1 syndrome; these ganglia may be palpable.
In others, the ganglion in the hand compresses the deep motor branch distal to the origin of the branches to the hypothenar muscles, producing a type 3 syndrome; these
ganglia are not palpable.
Other mass lesions within the wrist and hand that produce ulnar neuropathies are
listed in Table 10.5. These include lipomas,258,264,265 rheumatoid synovial cysts and synovial proliferation,266-267 tumors (chondromas, schwannomas, giant cell tumors),262,268270
and villonodular tenosynovitis.271 Other compressive lesions include anomalous
intrinsic hand muscles,257,272,273 abnormal ligaments,261,263 abnormal vascular structures,274 ununited hook of the hamate,263 and calcinosis associated with scleroderma.275
The ulnar nerve can be damaged at the wrist by lacerations and acute blunt injuries.
Trauma to not only the median nerve but to the ulnar nerve has been reported following
injections of corticosteroids and of endoscopic surgery for carpal tunnel syndrome.276278
Damage from or associated with wrist dislocations and fractures is surprisingly uncommon.253,255,279-284 In some patients a cause for the neuropathy cannot be found.
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Table 10.5. Ulnar neuropathies in the wrist and hand.*
Part of the nerve compressed
1.Main trunk of nerve at
wrist just proximal to or
within Guyon’s canal
Clinical features
Superficial terminal branch
sensory loss; weakness of all
ulnar intrinsic hand muscles
Possible causes
Ganglion
Lipoma
External pressure
Rheumatoid synovial cyst
Chondroma
Schwannoma
Anomalous muscle
2.Deep terminal branch
(proximal to branches
to hypothenar muscles)
No sensory loss; weakness
of all ulnar intrinsic
hand muscles
External pressure
Ganglion
Ligamentous compression
Nerve and other tumors
Scleroderma/calcinosis
3.Deep terminal branch
(distal to branches to
hypothenar muscles)
No sensory loss; weakness
of all ulnar intrinsic hand
muscles except hypothenar
muscles
Ganglion
External pressure
Giant cell tumor
Ligamentous compression
Anomalous muscle
4.Superficial terminal
branch
Sensory loss only
Ununited fracture hook
of hamate
Ulnar artery aneurysm
*These sites of nerve damage are shown, using the same numbers, in Fig. 10.4.
Clinical Features
The patient with a suspected wrist/hand ulnar neuropathy must be asked about work
habits, hobbies, and injuries. The area should be examined for evidence of swellings,
deformities, localized skin callus from habitual tool use, and areas of localized tenderness on deep palpation. A cardinal symptom and sign is the sparing of the cutaneous
areas supplied by the dorsal ulnar and palmar cutaneous branches (Fig. 10.5). The muscles tested should include those in the hand innervated by the ulnar (first dorsal interosseous as well as the other interossei, and the abductor digiti minimi) and median
(abductor pollicis brevis) nerves, and forearm muscles supplied by the ulnar and by
the other nerves containing contributions from C8 and T1 roots and the lower trunk of
the brachial plexus (Fig. 10.13; Table 10.3).
Difficulties in diagnosis arise from the fairly frequent anomalous innervation of the
intrinsic hand muscles, and also from those ulnar neuropathies at the elbow with restricted motor and sensory involvement, as discussed above. The differential diagnosis includes ulnar neuropathy at the elbow or forearm, amyotrophic lateral sclerosis,
benign monomelic atrophy, and multifocal motor conduction block neuropathy.
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Investigations
Radiographs of the wrist and hand may show arthritis or previous fractures. CT scanning is very effective in delineating new and old fractures.285 Soft tissue masses such
as ganglia, giant cell tumors, and lipomas are well shown by CT and MR imaging (Fig.
10.14).258-260,269,285-287 Ultrasonography is also an effective method of detecting mass lesions here, particularly ganglia.288
Electrophysiologic studies are very useful in localizing an ulnar neuropathy to the
wrist or hand. Prolonged motor latencies from the wrist to the first dorsal interosseous
or abductor digiti minimi (or both) indicate focal involvement of the distal branches to
these muscles.160,161,251,261,289,290 Recording the motor latency to the ulnar-innervated palmar interosseous muscles and comparing this to the latency to the median-innervated
second lumbrical muscle may be a more sensitive test.291,292 “Inching” techniques (shortsegment incremental studies discussed above) are another way to show a focal block
at the wrist.293 Stimulating the ulnar nerve above and below Guyon’s canal can be effective in showing focal blocking.251,294 Motor studies of the proximal segment of the
nerve must be done to exclude conduction abnormalities across the elbow.
Sensory conduction studies from the fifth digit to the wrist are also useful. Slowing
and dispersion of the potential indicates a focal lesion in the wrist or hand; reduced
amplitude with no slowing does not localize the neuropathy. An abnormal dorsal ulnar
cutaneous sensory conduction study clearly places the lesion proximal to the wrist or
hand; a misleadingly absent potential can be the result of an anatomic anomaly as discussed above. Electromyography of the intrinsic hand muscles helps to detect or confirm abnormalities but will not distinguish between elbow and wrist ulnar neuropathies.
Of more importance is the EMG examination of the flexor carpi ulnaris and flexor digitorum profundus muscles; when they are abnormal the lesion lies proximal to the wrist.
Management
If an occupational or recreational cause for the neuropathy can be identified and subsequently avoided, many patients recover spontaneously.8,294-296 Surgical exploration is
indicated when: (a) no clear cause for the neuropathy can be identified and the lesion
is either severe or worsening; (b) an occupational or recreational cause has been found,
but in spite of avoiding further trauma to the nerve, the condition is worsening; or (c)
a swelling is palpable or has been detected on imaging studies. An interesting therapeutic approach to an expanding ganglion cyst (imaged by CT and ultrasound) causing
damage to the deep motor branch of the ulnar nerve was puncture of the cyst and injection with corticosteroid; the patient recovered promptly.297
DORSAL ULNAR CUTANEOUS NERVE
The dorsal ulnar cutaneous (DUC) nerve arises above the wrist and winds medially
around the ulna, deep to the tendon of the flexor carpi ulnaris muscle. It then supplies
the skin of some of dorsum of the hand and fifth digit (Figs. 10.1, 10.5; see also Fig.
12.2).
ULNAR NERVE
A
299
B
Figure 10.13. A: Dorsal view of the hand of a patient with a lesion of the deep terminal branch of the ulnar nerve due
to trauma (lesion type 3 in Fig. 10.4, Table 10.5). The patient is attempting to spread all fingers apart. The hypothenar
muscles are contracting normally, but the other ulnar-innervated muscles are paralyzed. There was no sensory loss.
(From Dawson et al.,66 with permission.) B: This patient sustained a gunshot wound (note the scar). There was mild sensory loss of the third digit due to a lesion of sensory branches of the median nerve. There was profound wasting and
weakness of the first dorsal interosseous muscle, but all of the other intrinsic hand muscles were normal and there was
no ulnar nerve sensory loss. This is an unusual lesion of the very distal part of the deep motor branch of the ulnar nerve
in the hand, not one of the classic four lesions of the ulnar nerve in the wrist and hand (Fig. 10.4, Table 10.5).
A
B
Figure 10.14. T2-weighted magnetic resonance images of the right wrist. A: Coronal view showing the base of the
thumb on the right and the hypothenar muscles (hy) on the left. Guyon’s canal lies between the pisiform bone (large
arrow) and the hook of the hamate bone (small arrow). A ganglion (black asterisk) is present at the exit of the canal. The
carpal tunnel containing the long flexor tendons of the fingers is labeled ct. B: Axial view through the wrist to show the
ganglion (black asterisk) lying between the hypothenar muscles (hy) and the hamate bone and the hook of the hamate
(small white arrow). Note the carpal tunnel (ct). Compare these images with Figs. 9.2, 10.4. The patient was a 38-yearold man who had discomfort in his hand and wrist while exercising in the gymnasium. Within hours he noticed weakness in the hand. Examination showed weakness of all ulnar intrinsic hand muscles and some mild terminal digital
branch sensory loss. The ganglion was excised and the patient made a full recovery. (Courtesy of Dr. R. Singh, Guelph,
Ontario.)
300
ULNAR NERVE
Disorders
The DUC nerve may be damaged by blunt injuries, lacerations, during surgical procedures on the wrist, and by handcuffs.298-300 Injury from repetitive wrist movement required for using a code-sensing machine at a checkout counter has been alleged.301 The
nerve may be bound down in posttraumatic scar tissue. In some of these patients, the
nerve becomes adherent to the extensor tendon of the little finger, causing pain on
movement of this digit.70 In one patient with spontaneous onset of wrist pain and sensory loss in the distribution of this nerve, the local infiltration of steroids where the
DUC nerve passes under the flexor carpi ulnaris tendon was curative. It was suggested
that the patient had an entrapment of the nerve at that site.302
Evaluation
Signs of previous trauma may be present. The nerve may be locally tender, and
Tinel’s sign may be elicitable. Nerve conduction studies are useful in confirming the
diagnosis.14,168,169,300,303 The problems of anatomic anomalies are discussed above.
Anatomic anomalies may be the reasons for the cautionary note in one study that found
the DUC sensory action potentials to be substantially smaller or absent on one side.304
Management
If it is thought that the nerve is bound down in scar tissue, surgical neurolysis may
be performed.
PALMAR CUTANEOUS BRANCH
The palmar cutaneous branch is a small nerve that arises above the wrist and passes
into the hand by traveling subcutaneously, not passing through Guyon’s canal. It supplies the ulnar aspect of the palm (Figs.10.1, 10.5; see also Fig. 12.1). It can be damaged by lacerations and during surgical procedures at the wrist. A technique for doing
nerve conduction studies of this nerve has been described.305
1.
2.
3.
4.
5.
REFERENCES
De Jesus R, Dellon AL. Historic origin of the
“Arcade of Struthers”. J Hand Surg [Am]
2003;28:528-531.
Al-Qattan MM, Murray KA. The arcade of
Struthers: an anatomical study. J Hand Surg
[Br] 1991;16:311-314.
Von Schroeder HP, Scheker LR. Redefining
the “arcade of Struthers”. J Hand Surg [Am]
2003;28:1018-1021.
Bartels RH, Grotenhuis JA, Kauer JM. The
arcade of Struthers: an anatomical study. Acta
Neurochir (Wien) 2003;145:295-300.
Siqueira MG, Martins RS. The controversial arcade of Struthers. Surg Neurol 2005;64:s1: 17-20.
6.
7.
8.
Campbell WW, Pridgeon RM, Riaz G, et al.
Variations in anatomy of the ulnar nerve at the
cubital tunnel: pitfalls in the diagnosis of
ulnar neuropathy at the elbow. Muscle Nerve
1991;14:733-738.
Patel VV, Heidenreich FP, Bindra RR, et al.
Morphologic changes in the ulnar nerve at the
elbow with flexion and extension: a magnetic
resonance imaging study with 3-dimensional
reconstruction. J Shoulder Elbow Surg
1998;7:368-374.
Vanderpool DW, Chalmers J, Lamb DW. Peripheral compression lesions of the ulnar
nerve. J Bone Joint Surg Br 1968;50:792-802.
ULNAR NERVE
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
23.
Apfelberg DB, Larson SJ. Dynamic anatomy
of the ulnar nerve at the elbow. Plast Reconstr Surg 1973;51:76-81.
Pechan J, Julis I. The pressure measurement
in the ulnar nerve. A contribution to the pathophysiology of the cubital tunnel syndrome. J
Biomech 1975;8:75-79
Gelberman RH, Yamaguchi K, Hollstien SB,
et al. Changes in interstitial pressure and
cross-sectional area of the cubital tunnel and
of the ulnar nerve with flexion of the elbow.
An experimental study in human cadavers. J
Bone Joint Surg Am 1998;80:492-501.
Sunderland S. Nerves and Nerve Injuries, 2nd
ed. Edinburgh: Churchill Livingstone, 1978.
Campbell WW, Pridgeon RM, Riaz G, et al.
Sparing of the flexor carpi ulnaris in ulnar
neuropathy at the elbow. Muscle Nerve
1989;12:965-967.
Peterson AR, Giuliani MJ, McHugh M, et al.
Variations in dorsomedial hand innervation.
Electrodiagnostic implications. Arch Neurol
1992;49:870-873.
Chang KS. Enlargement of the ulnar nerve behind the medial epicondyle. Anat Rec 1963;
145:149-153.
Hirasawa Y, Sawamura H, Sakakida K. Entrapment neuropathy due to bilateral epitrochleoanconeus muscles: a case report. J Hand Surg [Am]
1979;4:181-184.
Dellon AL. Musculotendinous variations
about the medial humeral epicondyle. J Hand
Surg [Br] 1986;11:175-181.
Marinacci AA. The value of the electromyogram
in the diagnosis of pressure neuropathy from
“hanging arm”. Electromyography 1967;1:5-10.
Subramony SH. Electrophysiologic findings
in crutch palsy. Electromyogr Clin Neurophysiol 1989;29:281-285.
Visser CP, Coene LN, Brand R, et al. The incidence of nerve injury in anterior dislocation
of the shoulder and its influence on functional
recovery. A prospective clinical and EMG
study. J Bone Joint Surg Br 1999;81:679-685.
Visser CP, Coene LN, Brand R, et al. Nerve
lesions in proximal humeral fractures. J
Shoulder Elbow Surg 2001;10:421-427.
Bolton FB, McFarlane RM. Human pneumatic tourniquet paralysis. Neurology 1978;
28:787-793.
Shields RW, Root KE, Wilbourn AJ. Compartment syndromes and compression neu-
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
301
ropathies in coma. Neurology 1986;36:13701374.
Bolton CF, Driedger AA, Lindsay RM. Ischaemic neuropathy in uraemic patients
caused by bovine arteriovenous shunt. J Neurol Neurosurg Psychiatry 1979;42:810-814.
Geiringer SR, Leonard JA. Injection related
ulnar neuropathy. Arch Phys Med Rehabil
1989;70:705-706.
Ochiai N, Honmo J, Tsujino A, et al. Electrodiagnosis in entrapment neuropathy by the arcade of Struthers. Clin Orthop Relat Res
2000;378:129-135.
Nakajima M, Ono N, Kojima T, et al. Ulnar
entrapment along the medial intermuscular
septum in the midarm. Muscle Nerve
2009;39:707-710.
Boyanton BL, Jones JK, Shenaq SM, et al. Intraneural perineurioma: a systematic review
with illustrative cases. Arch Pathol Lab Med
2007;131:1382-1392.
Katz JS, Wolfe GI, Bryan WW, et al. Electrophysiologic findings in multifocal motor neuropathy. Neurology 1997;48:700-707.
Katirji MB, Katirji PM. Proximal ulnar
mononeuropathy caused by conduction block
at Erb’s point. Arch Neurol 1988;45:460-461.
Krarup C, Sethi RK. Idiopathic brachial
plexus lesion with conduction block of the
ulnar nerve. Electroencephalogr Clin Neurophysiol 1989;72:259-267.
Mondelli M, Giannini F, Ballerini M, et al. Incidence of ulnar neuropathy at the elbow in
the province of Siena (Italy). J Neurol Sci
2005;234:5-10.
Mondelli M, Giannini F, Giacchi M. Carpal
tunnel syndrome in a general population.
Neurology 2002;58:289-294.
Richardson JK, Green DF, Jamieson SC, et al.
Gender, body mass and age as risk factors for
ulnar mononeuropathy at the elbow. Muscle
Nerve 2001;24:551-554.
Bartels RH, Verbeek AL. Risk factors for
ulnar nerve compression at the elbow: a case
control study. Acta Neurochir (Wien) 2007;
149:669-674.
Descatha A, Leclerc A, Chastang JF, et al.
Study Group on Repetitive Work. Scand J
Work Environ Health 2004;30:234-240.
Mondelli M, Grippo A, Mariani M, et al.
Carpal tunnel syndrome and ulnar neuropathy
at the elbow in floor cleaners. Neurophysiol
302
38.
39.
40.
41.
42.
43.
44.
45.
46.
47.
48.
49.
50.
51.
52.
ULNAR NERVE
Clin 2006;36:245-253.
Shin R, Ring D. The ulnar nerve in elbow
trauma. J Bone Joint Surg Am 2007;89:11081116.
Robinson CM, Hill RM, Jacobs N, et al. Adult
distal humeral metaphyseal fractures: epidemiology and results of treatment. J Orthop
Trauma 2003;17:38-47.
Ikram MA. Ulnar nerve palsy: a complication
following percutaneous fixation of supracondylar fractures of the humerus in children.
Injury 1996;27:303-305.
Lyons JP, Ashley E, Hoffer MM. Ulnar palsies
after percutaneous cross-pinning of supracondylar fractures in children’s elbows. J Pediatr Orthop 1998;18:43-45.
Taniguchi Y, Matsuzaki K, Tamaki T. Iatrogenic ulnar nerve injury after percutaneous
cross-pinning of supracondylar fracture in a
child. J Shoulder Elbow Surg 2000;9:160-162.
Dumonski ML, Arciero RA, Mazzocca AD.
Ulnar nerve palsy after elbow arthroscopy.
Arthroscopy 2006;22:577.
Panas P. Sur une cause peu connue de
paralysie du nerf cubital. Arch Gen Med
1878;2:5-22.
Uchida Y, Sugioka Y. Ulnar nerve palsy after
supracondylar humerus fracture. Acta Orthop
Scand 1990;61:118-119.
Jeon IH, Oh CW, Kyung HS, et al. Tardy ulnar
nerve palsy in cubitus varus deformity associated with ulnar nerve dislocation in adults. J
Shoulder Elbow Surg 2006;15:474-478.
Mouchet A. Paralysies tardives du nerf cubital
a la suite des fractures du condyle externe de
l’humerus. Journal de Chirurgie: Revue Critique (Paris) 1914;12:437-456.
Platt H. The pathogenesis and treatment of traumatic neuritis of the ulnar nerve in the post
condylar groove. Br J Surg 1926;13:409-431.
Lipscomb PR, Burleson RJ. Vascular and neural complications in supracondylar fractures
of the humerus in children. J Bone Joint Surg
Am 1955;37:487-492.
Osborne G. Ulnar neuritis. Postgrad Med J
1959;35:392-396.
Paine KW. Tardy ulnar palsy. Can J Surg
1970;13:255-261.
Chan RC, Paine KW, Varughese G. Ulnar
neuropathy at the elbow: comparison of simple decompression and anterior transposition.
Neurosurgery 1980;7:545-550.
53.
54.
55.
56.
57.
58.
59.
60.
61.
62.
63.
64.
65.
66.
67.
68.
69.
McGowan AJ. The results of transposition of
the ulnar nerve for traumatic ulnar neuritis. J
Bone Joint Surg Br 1950;32:293-301.
Buzzard EF. Some varieties of traumatic and
toxic ulnar neuritis. Lancet 1922;1:317319,325-326.
Aljure J, Eltorai I, Bradley WE, et al. Carpal
tunnel syndrome in paraplegic patients. Paraplegia 1985;23:182-186.
Davidoff G, Werner R, Waring W. Compressive
mononeuropathies of the upper extremity in
chronic paraplegia. Paraplegia 1991;29:17-24.
Burnham RS, Steadward RD. Upper extremity peripheral nerve entrapments among
wheelchair athletes: prevalence, location, and
risk factors. Arch Phys Med Rehabil 1994;
75:519-524.
Collinet P. Luxation congénitale du nerf cubital. Bull Soc Anat de Paris 1896;71:358-367.
Jopson JH. Dislocation of the ulnar nerve.
Philadelphia Med J 1898;2:522-524.
Arkin AM. Habitual luxation of the ulnar
nerve. J Mt Sinai Hosp N Y 1940;7:208-221.
Childress HM. Recurrent ulnar nerve dislocation at the elbow. J Bone Joint Surg Am
1956;38:978-984.
Ashenhurst EM. Anatomical factors in etiology of ulnar neuropathy. Can Med Assoc J
1962;87:159-163.
Brooks DM. Nerve compression by simple
ganglia: a review of thirteen collected cases. J
Bone Joint Surg Br 1952;34:391-400.
Barber KW, Bianco AJ, Soule EH. Benign extraneural soft tissue tumors of the extremities
causing compression of nerves. J Bone Joint
Surg Am 1962;44:98-104.
White WL, Hanna DC. Troublesome lipomata
of the upper extremity. J Bone Joint Surg Am
1962;44:1353-1359.
Dawson DH, Hallett M, Wilbourn AJ. Entrapment Neuropathies, 3rd ed. Philadelphia:
Lippincott-Raven, 1999.
Laurencin CT, Schwartz JT, Koris MJ. Compression of the ulnar nerve at the elbow in association with synovial cysts. Orthop Rev
1994;23:62-65.
Segal R, Saito R, Sen C. Ulnar neuropathy
caused by fat necrosis with cystic myxoid degeneration at the upper forearm: case report.
Neurosurgery 1988;23:669-671.
Beekman R, Slooff W-M, Van Oosterhout MF
et al. Bilateral intraneural perineurioma pre-
ULNAR NERVE
70.
71.
72.
73.
74.
75.
76.
77.
78.
79.
80.
81.
82.
83.
84.
85.
senting as ulnar neuropathy at the elbow.
Muscle Nerve 2004;30:239-243.
Spinner M. Injuries to the Major Branches of
Peripheral Nerve of the Forearm, 2nd ed.
Philadelphia: WB Saunders, 1978.
Dahners LE, Wood FM.Anconeus epitrochlearis,
a rare cause of cubital tunnel syndrome: a case report. J Hand Surg [Am] 1984;9:579-580.
Masaer VR, Hill JJ, Cohen SM. Ulnar compression neuropathy secondary to the anconeus epitrochlearis muscle. J Hand Surg
[Am] 1988;13:720-724.
St. John JN. Ulnar entrapment neuropathy associated with the anconeus epitrochlearis
muscle. Can J Neurol Sci 1985;12:203.
Kojima T, Kurihara K, Nagano T. A study on
operative findings and pathogenic factors in
ulnar neuropathy at the elbow. Handchirurgie
1979;11:99-104.
Peyroux LM, Dunaud JL, Moughabghab M.
[Supraepitrochlear process and median nerve
compression.] Ann Chir main Memb Super
1991;10:68-70.
Barnard LB, McCoy SM. The supracondyloid
process of the humerus. J Bone Joint Surg
1946;28:845-850.
Goulon M, Lord G, Bedoiseau M. [Damage
of the median and ulnar nerves by the
supraepitrochlear apophysis. Apropos of 2
cases.] Presse Med 1963;71:2355-2357.
Fragiadakis EG, Lamb DW. An unusual cause of
ulnar nerve compression. Hand 1970;2:14-16.
Osborne GV. The surgical treatment of tardy
ulnar neuritis. J Bone Joint Surg Br 1957;39:
782.
Feindel W, Stratford J. The role of the cubital
tunnel in tardy ulnar palsy. Can J Surg
1958;1:287-300.
Miller RG. The cubital tunnel syndrome: diagnosis and precise localization. Ann Neurol
1979;6:56-59.
MacNicol MF. The results of operation for
ulnar neuritis. J Bone Joint Surg Br
1979;61:159-164.
Mulder DW, Lambert EH, Bastron JA. The
neuropathies associated with diabetes mellitus. Neurology 1961;11:275-284.
Fraser DM, Campbell IW, Ewing DJ.
Mononeuropathy in diabetes mellitus. Diabetes 1979;28:96-101.
Wilbourn AJ. Diabetic entrapment and compression neuropathies. In: Dyck PJ, Thomas
86.
87.
88.
89.
90.
91.
92.
93.
94.
95.
96.
97.
98.
99.
100.
101.
102.
303
PK, eds. Diabetic Neuropathy, 2nd ed.
Philadelphia: WB Saunders, 1999:481-508.
Schady W, Abuaisha B, Boulton AJ. Observations on severe ulnar neuropathy in diabetes. J Diabetes Complications 1998;12:
128-132.
Budinger K. Ueber Lähmungen nach Chloroformnarkosen. Arch Klin Chir 1894;47:121145.
Garriques HJ. Anesthesia-paralysis. Am J
Med Sci 1897;133:81-89.
De Leon. Paralysie du nerf cubital et contracture consecutive main et pince. Nouvelle
Iconographie de la Salpêtrière 1901;14:409.
Cameron MG, Stewart OJ. Ulnar nerve injury
associated with anaesthesia. Canad Anaesth
Soc J. 1975;22:253-264.
Winfree CJ, Kline DG. Intraoperative positioning nerve injuries. Surg Neurol 2005;
63:5-18.
Kroll DA, Caplan RA, Posner K, et al. Nerve
injury associated with anesthesia. Anesthesiology 1990;73:202-207.
Wadsworth TG, Williams JR. Cubital tunnel
external compression syndrome. Br Med J
1973;1:662-666.
Miller RG, Camp PE. Postoperative ulnar
neuropathy. JAMA 1979;242:1636-1639.
Stewart JD, Shantz SH. Perioperative ulnar
neuropathies: a medicolegal review. Can J
Neurol Sci 2003;30:15-19.
Murphy JP, Devers JC. Prevention of postsurgical ulnar neuropathy. JAMA 1974;227:
1123-1124.
Stoelting RK. Postoperative ulnar nerve
palsy—is it a preventable complication?
Anesth Analg 1993;76:7-9.
Mawk JR, Thienprasit P. Postoperative ulnar
neuropathy. JAMA 1981;246:2806-2807.
Seyfer AE. Upper extremity neuropathies
after cardiac surgery. J Hand Surg [Am]
1985;10:16-19.
Alvine FG, Schurrer ME. Postoperative ulnarnerve palsy. Are there predisposing factors? J
Bone Joint Surg Am 1987;69:255-259.
Roy RC, Stafford MA, Charlton JE. Nerve injury and musculoskeletal complaints after cardiac surgery: influence of internal mammary
artery dissection and left arm position. Anesth
Analg 1988;67:277-279.
Dawson DM, Krarup C. Perioperative nerve
lesions. Arch Neurol 1989;46:1355-1360.
304
ULNAR NERVE
103. Caplan RA, Posner KL, Cheney FW. Perioperative ulnar neuropathy: are we ready for shortcuts? Anesthesiology 1994;81:1321-1323.
104. Warner MA, Warner ME, Martin JT. Ulnar
neuropathy. Incidence, outcome, and risk factors in sedated or anesthetized patients. Anesthesiology 1994;81:1332-1340.
105. Warner MA, Warner DO, Matsumoto JY, et
al. Ulnar neuropathy in surgical patients.
Anesthesiology 1999;90:54-59.
106. Warner MA, Warner DO, Harper CM, et al.
Ulnar neuropathy in medical patients. Anesthesiology 2000;92:613-615.
107. Warner MA, Warner DO, Harper CM, et al.
Lower extremity neuropathies associated with
lithotomy positions. Anesthesiology 2000;93:
938-942.
108. Graham JG, Pye IF, McQueen IN. Brachial
plexus injury after median sternotomy. J Neurol Neurosurg Psychiatry 1981;44:621-625.
109. Lederman RJ, Breuer AC, Hanson MR, et al.
Peripheral nervous system complications of
coronary artery bypass graft surgery. Ann
Neurol 1982;12:297-301.
110. Seyfer AE, Grammer NY, Bogumill GP.
Upper extremity neuropathies after cardiac
surgery. J Hand Surg [Am] 1985;10:16-19.
111. Williams JR. Postoperative ulnar neuropathy.
JAMA 1980;243:1525-1526.
112. Cheney FW. Standard of care and anesthesia
liability. JAMA 1989;261:1599-1603.
113. Shaw PJ, Bates D, Cartlidge NE, et al. Early
neurologic complications of coronary bypass
surgery. Br Med J 1985;291:1384-1387.
114. Watson BV, Merchant RN, Brown WF. Early
postoperative ulnar neuropathies following
coronary artery bypass surgery. Muscle Nerve
1992;15:701-705.
115. Contreras MG, Warner MA. Charboneau WJ,
et al. Anatomy of the ulnar nerve at the elbow:
potential relationship of acute ulnar neuropathy to gender differences. Clin Anat 1998;
11:372-378.
116. Prielipp RC, Morell RC, Butterworth J. Ulnar
nerve injury and perioperative arm positioning. Anesthesiol Clin North America 2002;20:
589-603.
117. Prielipp RC, Morrell RC, Walker FO, et al.
Ulnar nerve pressure: influence of arm position
and relationship to somatosensory evoked potentials. Anesthesiology 1999;91: 345-354.
118. Swensen JD, Hutchinson DT, Bromberg M, et
al. Rapid onset of ulnar nerve dysfunction
119.
120.
121.
122.
123.
124.
125.
126.
127.
128.
129.
130.
131.
132.
during transient occlusion of the brachial artery. Anesth Analg 1998;87:677-680.
Morell RC, Prielipp RC, Harwood TN, et al.
Men are more susceptible than women to direct pressure on unmyelinated ulnar nerve
fibers. Anesth Analg 2003;97:1183-1188.
Warner MA, Blitt CD, Butterworth JF. Practice advisory for the prevention of perioperative peripheral neuropathies. Anesthesiology
2000;92:1168-1182.
Posta AG, Answorth AA, Nercessian OA.
Neurological injury in the upper extremity
after total hip arthroplasty. Clin Orthop Relat
Res 1997;345:181-186.
Neary D, Eames RA. The pathology of ulnar
nerve compression in man. Neuropathol Appl
Neurobiol 1975;1:69-88.
Kim DH, Han K, Tiel RL, et al. Surgical outcomes of 654 ulnar nerve lesions. J Neurosurg
2003;98:993-1004.
Brown WF, Ferguson GG, Jones MW, et al.
The location of conduction abnormalities in
human entrapment neuropathies. Can J Neurol Sci 1976;3:111-122.
Campbell WW, Sahni SK, Pridgeon RM, et
al. Intraoperative electroneurography: management of ulnar neuropathy at the elbow.
Muscle Nerve 1988;11:75-81.
Goldman SB, Brininger TL, Schrader JW, et
al. A review of clinical tests and signs for the
assessment of ulnar neuropathy. J Hand Ther
2009;22:209-220.
Rayan GM, Jensen C, Duke J. Elbow flexion
test in the normal population. J Hand Surg
[Am] 1992;17:86-89.
Kuschner SH, Ebramzadeh E, Mitchell S.
Evaluation of elbow flexion and Tinel tests for
cubital tunnel syndrome in asymptomatic individuals. Orthopedics 2006;29:305-308.
Novak CB, Lee GW, Mackinnon SE, et al.
Provocative testing for cubital tunnel syndrome. J Hand Surg [Am] 1994;19:817-820.
Beekman R, Schreuder AH, Rozeman CA, et
al. The diagnostic value of provocative clinical
tests in ulnar neuropathy at the elbow is marginal. J Neurol Neurosurg Psychiatry (online)
Jun 2009; doi:10.1136/jnnp.2009.180844.
Kingery WS, Park KS, Wu PB, et al. Electromyographic motor Tinel’s sign in ulnar
mononeuropathies at the elbow. Am J Phys
Med Rehabil 1995;74:419-426.
Wadsworth TG. The external compression
syndrome of the ulnar nerve at the cubital tun-
ULNAR NERVE
nel. Clin Orthop Relat Res 1977;124:189-204.
133. Buehler MJ, Thayer DT. The elbow flexion test.
A clinical test for the cubital tunnel syndrome.
Clin Orthop Relat Res 1988;233:213-216.
134. Cheng CJ, Mackinnon-Patterson B, Beck JL,
et al. Scratch collapse test for evaluation of
carpal and cubital tunnel syndrome. J Hand
Surg [Am] 2008;33:1518-1524.
135. Greenwald D, Blum LC, Adams D, et al. Effective surgical treatment of cubital tunnel
syndrome based on provocative clinical testing without electrodiagnostics. Plast Reconstr Surg 2006;117:87e-91e.
136. Stewart JD. The variable clinical manifestations of ulnar neuropathies at the elbow. J
Neurol Neurosurg Psychiatry 1987;50:252258.
137. Bartels RH, Menovsky T, Van Overbeeke JJ,
et al. Surgical management of ulnar nerve
compression at the elbow: an analysis of the
literature. J Neurosurg 1998;89:722-727.
138. Dellon AL. Review of treatment results for
ulnar nerve entrapment at the elbow. J Hand
Surg [Am] 1989;14:688-700.
139. Gervasio O, Gambardella G, Zaccone C, et al.
Simple decompression versus anterior submuscular transposition of the ulnar nerve in
severe cubital tunnel syndrome: a prospective
randomized study. Neurosurgery 2005;56:
108-117.
140. Bartels RH, Verhagen WI, van der Wilt GJ, et
al. Prospective randomized controlled study
comparing simple decompression versus anterior subcutaneous transposition for idiopathic
neuropathy of the ulnar nerve at the elbow: Part
1. Neurosurgery 2005;56:522-530.
141. Padua L, Aprile I, Mazza O, et al. Neurophysiological classification of ulnar entrapment across the elbow. Neurol Sci 2001;22:
11-16.
142. De Visser M, Ongerboer de Visser BW, Verbeeten B. Electromyographic and computed
tomographic findings in five patients with
monomelic spinal muscular atrophy. Eur Neurol 1988;28:135-138.
143. Oryema J, Ashby P, Spiegel S. Monomelic atrophy. Can J Neurol Sci 1990;17:124-130.
144. Sobue I, Saito N, Iida M, et al. Juvenile type
of distal and segmental muscular atrophy of
upper extremities. Ann Neurol 1978;3:429432.
145. Metcalf JC, Wood JB, Bertorini TE. Benign
focal amyotrophy: metrizamide CT evidence
146.
147.
148.
149.
150.
151.
152.
153.
154.
155.
156.
157.
158.
159.
160.
305
of cord atrophy. Case report. Muscle Nerve
1987;10:338-345.
Hirayama K, Tomonaga M, Kitano K, et al.
Focal cervical poliopathy causing juvenile
muscular atrophy of distal upper extremity: a
pathological study. J Neurol Neurosurg Psychiatry 1987;50:285-290.
O’Sullivan DJ, McLeod JG. Distal chronic
spinal muscular atrophy involving the hands.
J Neurol Neurosurg Psychiatry 1978;41:653658.
Gourie-Devi M, Nalini A. Long-term followup of 44 patients with brachial monomelic
amyotrophy. Acta Neurol Scand 2003;107:
215-220.
De Carvalho M, Swash M. Monomelic neurogenic syndromes: a prospective study. J
Neurol Sci 2007;263:26-34.
Murphey F, Simmons JC, Brunson B. Surgical treatment of laterally ruptured cervical
disc. Review of 648 cases, 1939 to 1972. J
Neurosurg 1973;38:679-683.
Wallace D. Disc compression of the eighth
cervical nerve: pseudo ulnar palsy. Surg Neurol 1982;18:295-299.
Lampl Y, Gilad R, Eshel Y, et al. Strokes mimicking peripheral nerve lesions. Clin Neurol
Neurosurg 1995;97:203-207.
Payan J. Electrophysiologic localization of
ulnar nerve lesions. J Neurol Neurosurg Psychiatry 1969;32:208-220.
Eisen A. Early diagnosis of ulnar nerve palsy.
Neurology 1974;24:256-262.
Odusote K, Eisen A. An electrophysiologic
quantitation of the cubital tunnel syndrome.
Can J Neurol Sci 1979;6:403-410.
Pickett JB, Coleman LL. Localizing ulnar
nerve lesions to the elbow by motor conduction studies. Electromyogr Clin Neurophysiol
1984;24:343-360.
Kincaid JC. The electrodiagnosis of ulnar
neuropathy at the elbow. Muscle Nerve
1988;11:1005-1015.
Campbell WW, Carroll DJ, Greenberg MK, et
al. Practice parameter for electrodiagnostic
studies in ulnar neuropathy at the elbow: summary statement. Muscle Nerve 1999;22:408411.
Kern RZ. The electrodiagnosis of ulnar nerve
entrapment at the elbow. Can J Neurol Sci
2003;30:314-319.
Olney RK, Wilbourn AJ. Ulnar nerve conduction study of the first dorsal interosseous mus-
306
ULNAR NERVE
cle. Arch Phys Med Rehabil 1985;66:16-18.
161. Seror P. Comparison of the distal motor latency of the first dorsal interosseous with abductor pollicis brevis. Report of 200 cases.
Electromyogr Clin Neurophysiol 1988;28:
341-345.
162. Azrieli Y, Weimer L, Lovelace R et al. The
utility of segmental nerve conduction studies
in ulnar mononeuropathy at the elbow. Muscle Nerve 2003;27:46-50.
163. Campbell WW, Pridgeon RM, Sahni KS.
Short segment incremental studies in the evaluation of ulnar neuropathy at the elbow. Muscle Nerve 1992;15:1050-1054.
164. Brown WF, Yates SK. Percutaneous localization of conduction abnormalities in human entrapment neuropathies. Can J Neurol Sci
1982;9:391-400.
165. Campbell WW. The value of inching techniques in the diagnosis of focal nerve lesions.
Inching is a useful technique. Muscle Nerve
1998;21:1554-1556.
166. Visser LH, Beekman R, Franssen H. Shortsegment nerve conduction studies in ulnar
neuropathy at the elbow. Muscle Nerve
2005;31:331-338.
167. Herrmann DN, Preston DC, McIntosh KA, et
al. Localization of ulnar neuropathy with conduction block across the elbow. Muscle Nerve
2001;24:698-700.
168. Jabre JF. Ulnar nerve lesions at the wrist: new
technique for recording from the sensory dorsal branch of the ulnar nerve. Neurology
1980;30:873-876.
169. Hoffman MD, Mitz M, Luisi M, et al. Paired
study of the dorsal cutaneous ulnar and superficial radial sensory nerves. Arch Phys
Med Rehabil 1988;69:591-594.
170. Britz GW, Haynor DR, Kuntz C, et al. Ulnar
nerve entrapment at the elbow: correlation of
magnetic resonance imaging, clinical, electrodiagnostic, and intraoperative findings.
Neurosurgery 1996;38:458-465.
171. Vucic S, Cordato DJ, Yiannikas C, et al. Utility of magnetic resonance imaging in diagnosing ulnar neuropathy at the elbow. Clin
Neurophysiol 2006;17:590-595.
172. Grant GA, Britz GW, Goodkin R, et al. The
utility of magnetic resonance imaging in evaluating peripheral nerve disorders. Muscle
Nerve 2002;25:314-331.
173. Hof JJ, Kliot M, Slimp J, et al. What’s new in
174.
175.
176.
177.
178.
179.
180.
181.
182.
183.
184.
185.
186.
MRI of peripheral nerve entrapment? Neurosurg Clin N Am 2008;19:583-595.
Beekman R, Schoemaker MC, van der Plas
JP, et al. Diagnostic value of high-resolution
sonography in ulnar neuropathy at the elbow.
Neurology 2004;62:767-773.
Park GY, Kim JM, Lee SM. The ultrasonographic and electrodiagnostic findings of
ulnar neuropathy at the elbow. Arch Phys Med
Rehabil 2004;85:1000-1005.
Yoon JS, Hong SJ, Kim BJ, et al. Ulnar nerve
and cubital tunnel ultrasound in ulnar neuropathy at the elbow. Arch Phys Med Rehabil
2008;89:887-889.
Mondelli M, Filippou G, Frediani B, et al. Ultrasonography in ulnar neuropathy at the
elbow: relationship to clinical and electrophysiologic findings. Clin Neurophysiol
2008;38:217-226.
Volpe A, Rossato G, Bottanelli M, et al. Ultrasound evaluation of ulnar neuropathy at the
elbow: correlation with electrophysiologic
studies. Rheumatology (Oxford) 2009;48:
1098-1101.
Yoon J, Walker FO, Cartwright MS. Ultrasonography in four cases of ulnar neuropathy
with negative conduction studies. Clin Neurophysiol 2009;120:e101.
De Noordhout AM. Diagnosing entrapment
neuropathies: probes and magnets instead of
electrodes and needles? Clin Neurophysiol
2006;117:484-485.
Eisen A, Danon J. The mild cubital tunnel
syndrome: its natural history and indications
for surgical intervention. Neurology 1974;24:
608-613.
De Jesus PV, Steiner JC. Spontaneous recovery of ulnar neuropathy at the elbow. Electromyogr Clin Neurophysiol 1976;16:239248.
Padua L, Aprile I, Caliandro P, et al. Natural
history of ulnar entrapment at the elbow. Clin
Neurophysiol 2002;113:1980-1984.
Laha RK, Panchal PD. Surgical treatment of
ulnar neuropathy. Surg Neurol 1979;11:393398.
Harrison MJ, Nurick S. Results of anterior
transposition of the ulnar nerve for ulnar neuritis. Br Med J 1970;1:27-29.
Levy DM, Apfelberg DB. Results of anterior
transposition for ulnar neuropathy at the
elbow. Am J Surg 1972;123:304-308.
ULNAR NERVE
187. Lugnegard H, Walheim G, Wennberg A. Operative treatment of ulnar neuropathy in the
elbow region: a clinical and electrophysiologic study. Acta Orthop Scand 1977;48: 168176.
188. Leffert RD. Anterior submuscular transposition of the ulnar nerves by the Learmonth
technique. J Hand Surg [Am] 1982;7:147155.
189. Broudy AS, Leffert RD, Smith RJ. Technical
problems with ulnar nerve transposition at the
elbow: findings and results of reoperation. J
Hand Surg [Am] 1978;3:85-89.
190. Goldberg BJ, Light TR, Blair SJ. Ulnar neuropathy at the elbow: results of medial epicondylectomy. J Hand Surg [Am] 1989;14:
182-188.
191. Craven PR, Green DP. Cubital tunnel syndrome: treatment by medial epicondylectomy.
J Bone Joint Surg Am 1980;62:986-989.
192. King T, Morgan FP. Later results of removing
the medial humeral epicondyle for traumatic
ulnar neuritis. J Bone Joint Surg Br 1959;41:
51-55.
193. Neblett C, Ehni G. Medial epicondylectomy
for ulnar palsy. J Neurosurg 1970;32:55-62.
194. Geutjens GG, Langstaff RJ, Smith NJ, et al.
Medial epicondylectomy or ulnar-nerve transposition for ulnar neuropathy at the elbow? J
Bone Joint Surg Br 1996;78:777-779.
195. Campbell WW. Ulnar neuropathy at the
elbow. Muscle Nerve 2000;23:450-452.
196. Seror P. Treatment of ulnar nerve palsy at the
elbow with a night splint. J Bone Joint Surg
Br 1993;75:322-327.
197. Apfel E, Sigafoos GT. Comparison of rangeof-motion constraints provided by splints used
in the treatment of cubital tunnel syndrome-a pilot study. J Hand Ther 2006;19:384-391.
198. Szabo RM, Kwak C. Natural history and conservative management of cubital tunnel syndrome. Hand Clin 2007;23:311-318.
199. Hong CZ, Long HA, Kanakamedala RV, et al.
Splinting and local steroid injection for the
treatment of ulnar neuropathy at the elbow:
clinical and electrophysiologic evaluation.
Arch Phys Med Rehabil 1996;77:573-577.
200. Dellon AL, Hament W, Gittelshon A. Nonoperative management of cubital tunnel syndrome: an 8-year prospective study.
Neurology 1993;43:1673-1677.
201. Mowlavi A, Andrews K, Lille S, et al. The
202.
203.
204.
205.
206.
207.
208.
209.
210.
211.
212.
213.
307
management of cubital tunnel syndrome: a
meta-analysis of clinical studies. Plast Reconstr Surg 2000;106:327-334.
Harding IJ, Morris IM. The aetiology and outcome of 170 ulnar nerve lesions confirmed
with electrophysiologic testing. Acta Orthop
Belg 2003;69:405-411.
Beekman R, Wokke JH, Schoemaker MC, et
al. Ulnar neuropathy at the elbow: follow-up
and prognostic factors determining outcome.
Neurology 2004;63:1675-1680.
Dunselman HH, Visser LH. The clinical, electrophysiologic and prognostic heterogeneity
of ulnar neuropathy at the elbow. J Neurol
Neurosurg Psychiatry 2008;79:1364-1367.
Bartels RH. History of the surgical treatment
of ulnar nerve compression at the elbow. Neurosurgery 2001;49:391-400.
Payan J. Cubital tunnel syndrome. Br Med J
1979;2:868.
Dellon AL, Mackinnon SE. Injury to the medial antebrachial cutaneous nerve during cubital tunnel surgery. J Hand Surg [Br]
1985;10:33-36.
Nabhan A, Ahlhelm F, Kelm J, et al. Simple
decompression or subcutaneous anterior
transposition of the ulnar nerve for cubital
tunnel syndrome. J Hand Surg [Br]
2005;30:521-524.
Biggs M, Curtis JA. Randomized, prospective
study comparing ulnar neurolysis in situ with
submuscular transposition. Neurosurgery
2006;58:296-304.
Zlowodzki M, Chan S, Bhandari M, et al. Anterior transposition compared with simple decompression for treatment of cubital tunnel
syndrome. A meta-analysis of randomized,
controlled trials. J Bone Joint Surg Am
2007;89:2591-2598.
Macadam SA, Gandhi R, Bezuhly M, et al.
Simple decompression versus anterior subcutaneous and submuscular transposition of the
ulnar nerve for cubital tunnel syndrome: a
meta-analysis. J Hand Surg [Am] 2008;33:
1314.e1-12.
Brauer CA, Graham B. The surgical treatment
of cubital tunnel syndrome: a decision analysis. J Hand Surg Eur Vol 2007;32:654-662.
Bartels RH, Termeer EH, van der Wilt GJ, et
al. Simple decompression or anterior subcutaneous transposition for ulnar neuropathy at
the elbow: a cost-minimization analysis--Part
308
ULNAR NERVE
2. Neurosurgery 2005;56:531-536.
214. Gabel GT, Amadio PC. Reoperation for failed
decompression of the ulnar nerve in the region
of the elbow. J Bone Joint Surg Am 1990;72:
213-219.
215. Rogers MR, Bergfield TG, Aulicino PL. The
failed ulnar nerve transposition. Etiology and
treatment. Clin Orthop Relat Res 1991;269:
193-200.
216. Kleinman WB. Revision ulnar neuroplasty.
Hand Clin 1994;10:461-477.
217. Bartels RH, Grotenhuis JA. Anterior submuscular transposition of the ulnar nerve. For
post-operative focal neuropathy at the elbow.
J Bone Joint Surg Br 2004;86:998-1001.
218. Tsai TM, Chen IC, Majd ME, et al. Cubital
tunnel release with endoscopic assistance: results of a new technique. J Hand Surg [Am]
1999;24:21-29.
219. Ahcan U, Zorman P. Endoscopic decompression of the ulnar nerve at the elbow. J Hand
Surg [Am] 2007;32:1171-1176.
220. Hoffmann R, Siemionow M. The endoscopic
management of cubital tunnel syndrome. J
Hand Surg [Br] 2006;31:23-29.
221. Merolla G, Staffa G, Paladini P, et al. Endoscopic approach to cubital tunnel syndrome.
J Neurosurg Sci 2008;52:93-98.
222. Krishnan KG, Pinzer T, Schackert G. A novel
endoscopic technique in treating single nerve
entrapment syndromes with special attention
to ulnar nerve transposition and tarsal tunnel
release: clinical application. Neurosurgery
2006;59:ONS89-100.
223. Ozkan T, Ozer K, Gulgonen A. Three tendon
transfer methods in reconstruction of ulnar
nerve palsy. J Hand Surg [Am] 2003;28:3543.
224. Harrelson JM, Newman M. Hypertrophy of
the flexor carpi ulnaris as a cause of ulnar
nerve compression in the distal part of the
forearm: case report. J Bone Joint Surg Am
1975;57:554-555.
225. Holtzman RN, Mark MH, Patel MR. Ulnar
nerve entrapment neuropathy in the forearm.
J Hand Surg [Am] 1974;9:576-578.
226. Campbell WW, Pridgeon RM, Sahni KS. Entrapment neuropathy of the ulnar nerve at its
point of exit from the flexor carpi ulnaris muscle. Muscle Nerve 1986;11:467-470.
227. Campbell WW. Ulnar neuropathy in the distal
forearm. Muscle Nerve 1989;12:347-352.
228. Amadio PC, Beckenbaugh RD. Entrapment of
229.
230.
231.
232.
233.
234.
235.
236.
237.
238.
239.
240.
241.
242.
243.
244.
the ulnar nerve by the deep flexor pronator
aponeurosis. J Hand Surg [Am] 1986;11:83-87.
Silverstein A. Neuropathy in hemophilia.
JAMA 1964;190:554-555.
Blankenship JC. Median and ulnar neuropathy after streptokinase infusion. Heart Lung
1991;20:221-223.
Wilbourn AJ, Furlan AJ, Hulley W. Ischemic
monomelic neuropathy. Neurology 1983;33:
447-451.
Shields RW, Root KE, Wilbourn AJ. Compartment syndromes and compression neuropathies in coma. Neurology 1986;36:
1370-1374.
Torpey BM, Pess GM, Kircher MT, et al.
Ulnar nerve laceration in a closed both bone
forearm fracture. J Orthop Trauma 1996;10:
131-134.
Hamazaki S, Fujiwara K, Okada S. Intraneural perineurioma involving the ulnar
nerve. Pathol Int 2004;54:371-375.
Scott TF, Yager JG, Gross JA. Handcuff neuropathy revisited. Muscle Nerve 1989;12:219220.
Hunt JR. The thenar and hypothenar types of
neural atrophy of the hand. Am J Med Sci
1911;141:224-241.
Destot M. Paralysie cubitale par l’usage de la
bicyclette. Gazette Hôpitaux 1896;69:11761177.
Guillain G, Bourguignon G, Corre M. Les
paralysies du nerve cubital chez les cyclistes.
Bull Mem Soc Med Hop Paris 1940;56:489492.
Eckman PB, Perlstein G, Altrocchi PH. Ulnar
neuropathy in bicycle riders. Arch Neurol
1975;32:130-131.
Hoyt CS. Ulnar neuropathy in bicycle riders.
Arch Neurol 1976;33:372.
Hankey GJ, Gubbay SS. Compressive
mononeuropathy of the deep palmar branch
of the ulnar nerve in cyclists. J Neurol Neurosurg Psychiatry 1988;51:1588-1590.
Maimaris C, Zadeh HG. Ulnar nerve compression in the cyclist’s hand: two case reports
and review of the literature. Br J Sports Med
1990;24:245-246.
Kennedy J. Neurologic injuries in cycling and
bike riding. Phys Med Rehabil Clin N Am
2009;20:241-248.
Patterson JM, Jaggars MM, Boyer MI. Ulnar
and median nerve palsy in long-distance cyclists. A prospective study. Am J Sports Med
ULNAR NERVE
2003;31:585-589.
245. Akuthota V, Plastaras C, Lindberg K, et al.
The effect of long-distance bicycling on ulnar
and median nerves: an electrophysiologic
evaluation of cyclist palsy. Am J Sports Med
2005;33:1224-1230.
246. Jones HR. Pizza cutter’s palsy. N Engl J Med
1988;319:450.
247. Friedland RP, St.John JN. Video-game palsy:
distal ulnar neuropathy in a video-game enthusiast. N Engl J Med 1984;311:58-59.
248. Davie C, Katifi H, Ridley A, et al. “Mouse”trap or personal computer palsy. Lancet 1991;
338:832.
249. Boninger ML, Robertson RN, Wolff M, et al.
Upper limb nerve entrapments in elite wheelchair racers. Am J Phys Med Rehabil 1996;
75:170-176.
250. Toth C. Peripheral nerve injuries attributable
to sport and recreation. Neurol Clin 2008;26:
89-113.
251. Cowdery SR, Preston DC, Herrmann DN, et
al. Electrodiagnosis of ulnar neuropathy at the
wrist: conduction block versus traditional
tests. Neurology 2002;59:420-427.
252. Malkan DH. Bilateral ulnar neurapraxia: a
complication of the elbow crutches. Injury
1992;23:426.
253. Chiodo A, Chadd E. Ulnar neuropathy at or
distal to the wrist: traumatic versus cumulative stress cases. Arch Phys Med Rehabil
2007;88:504-512.
254. Ginanneschi F, Filippou G, Milani P, et al.
Ulnar nerve compression neuropathy at
Guyon’s canal caused by crutch walking: case
report with ultrasonographic nerve imaging.
Arch Phys Med Rehabil 2009;90:522-524.
255. Waugh RP, Pellegrini VD. Ulnar tunnel syndrome. Hand Clin 2007;23:301-310.
256. Seddon HJ. Carpal ganglion as a cause of
paralysis of the deep branch of the ulnar
nerve. J Bone Joint Surg Br 1952;34:386-390.
257. Uriburu IJ, Morchio FJ, Marin JC. Compression syndrome of the deep motor branch of
the ulnar nerve (piso hamate hiatus syndrome). J Bone Joint Surg Am 1976;58:145147.
258. Kuschner SH, Gelberman RH, Jennings C.
Ulnar nerve compression at the wrist. J Hand
Surg [Am] 1988;13:577-580.
259. Giuliani G, Poppi M, Pozzati E, et al. Ulnar
neuropathy due to a carpal ganglion: the di-
260.
261.
262.
263.
264.
265.
266.
267.
268.
269.
270.
271.
272.
309
agnostic contribution of CT. Neurology
1990;40:1001-1002.
Subin GD, Mallon WJ, Urbaniak JR. Diagnosis of ganglion in Guyon’s canal by magnetic
resonance imaging. J Hand Surg [Am] 1989;
14:4:640-643.
Ebeling P, Gilliatt RW, Thomas PK. A clinical and electrical study of ulnar nerve lesions
in the hand. J Neurol Neurosurg Psychiatry
1960;23:1-9.
Bouche P, Esnault S, Broglin D, et al. Isolated
compression of the deep motor branch of the
ulnar nerve. Electromyogr Clin Neurophysiol
1986;26:415-422.
Shea JD, McClain EJ. Ulnar nerve compression syndromes at and below the wrist. J Bone
Joint Surg Am 1969;51:1095-1103.
Zahrawi F. Acute compression ulnar neuropathy at Guyon’s canal resulting from lipoma. J
Hand Surg [Am] 1984;9:238-240.
Sakai K, Tsutsui T, Aoi M, et al. Ulnar neuropathy caused by a lipoma in Guyon’s canal-case report. Neurol Med Chir (Tokyo)
2000;40:335-338.
Dell PC. Compression of the ulnar nerve at
the wrist secondary to a rheumatoid synovial
cyst: case report and review of the literature.
J Hand Surg [Am] 1979;4:468-473.
Murata K, Shih JT, Tsai TM. Causes of ulnar
tunnel syndrome: a retrospective study of 31
subjects. J Hand Surg [Am] 2003;28:647-651.
Foucher G, Bernard V, Snider G, et al. Distal
ulnar nerve entrapment due to tumors of
Guyon’s canal. A series of ten cases. Handchir
Mikrochir Plast Chir 1993;25:61-65.
Rafecase JC, Daube JR, Ehman RL. Deep
branch ulnar neuropathy due to giant cell
tumor: report of a case. Neurology 1988;38:
327-329.
Rengachary SS, Arjunan K. Compression of
the ulnar nerve in Guyon’s canal by a soft tissue giant cell tumor. Neurosurgery 1981;8:
400-405.
Uysal M, Ozkoc G, Akpinar S, et al. Combined ulnar and carpal tunnel syndrome
caused by pigmented villo-nodular tenosynovitis: a rare case. Arch Orthop Trauma Surg
2007;127:563-565.
Regan PJ, Feldberg L, Bailey BN. Accessory
palmaris longus muscle causing ulnar nerve
compression at the wrist. J Hand Surg [Am]
1991;16:736-738.
310
ULNAR NERVE
273. Jeffery AK. Compression of the deep palmar
branch of the ulnar nerve by an anomalous
muscle: case report and review. J Bone Joint
Surg Br 1971;53:718-723.
274. Kalisman M, Laborde K, Wolff TW. Ulnar
nerve compression secondary to ulnar artery
false aneurysm at the Guyon’s canal. J Hand
Surg [Am]1982;7:137-139.
275. Thurman RT, Jindal P, Wolff TW. Ulnar nerve
compression in Guyon’s canal caused by calcinosis in scleroderma. J Hand Surg [Am]
199;16:739-741.
276. Frederick HA, Carter PR, Littler JW. Injection
injuries to the median and ulnar nerves at the
wrist. J Hand Surg [Am] 1992;17:645-647.
277. Tavares SP, Giddins GE. Nerve injury following steroid injection for carpal tunnel syndrome: a report of two cases. J Hand Surg
[Br] 1996;21:208-209.
278. Del Pinal F, Cruz-Camara A, Jado E. Total
ulnar nerve transection during endoscopic
carpal tunnel release. Arthroscopy 1997;13:
235-237.
279. Howard FM. Ulnar nerve palsy in wrist fractures. J Bone Joint Surg Am 1961;43:11971201.
280. Zoëga H. Fracture of the lower end of the radius with ulnar nerve palsy. J Bone Joint Surg
Br 1966;48:514-516.
281. Vance RM, Gelberman RH. Acute ulnar neuropathy with fractures at the wrist. J Bone
Joint Surg Am 1978;60:962-965.
282. Kornberg M, Aulicino PL, DuPuy TE. Laceration of the ulnar nerve with a closed fracture
of the distal radius and ulnar. Orthopedics
1983;6:729-731.
283. McCarroll HR. Nerve injuries associated with
wrist trauma. Orthop Clin North Am 1984;15:
279-287.
284. Soong M, Ring D. Ulnar nerve palsy associated with fracture of the distal radius. J Orthop Trauma 2007;21:113-116.
285. Blum AG, Zabel JP, Kohlmann R, et al.
Pathologic conditions of the hypothenar eminence: evaluation with multidetector CT and
MR imaging. Radiographics 2006;26:10211044.
286. Zeiss J, Jakab E, Khimji T, et al. The ulnar
tunnel at the wrist (Guyon’s canal): normal
MR anatomy and variants. AJR 1992;158:
1081-1085.
287. Bordalo-Rodrigues M, Amin P, Rosenberg
288.
289.
290.
291.
292.
293.
294.
295.
296.
297.
298.
299.
300.
301.
302.
ZS. MR imaging of common entrapment neuropathies at the wrist. Magn Reson Imaging
Clin N Am 2004;12:265-279.
Teefey SA, Dahiya N, Middleton WD, et al.
Ganglia of the hand and wrist: a sonographic
analysis. AJR 2008;191:716-720.
Bhala RP, Goodgold J. Motor conduction in
the deep palmar branch of the ulnar nerve.
Arch Phys Med Rehabil 1968;49:460-466.
Olney RK, Hanson M. Ulnar neuropathy at or
distal to the wrist. Muscle Nerve 1988;11:
828-832.
Kothari MJ, Preston DC, Logigian EL. Lumbrical-interossei motor studies localize ulnar
neuropathy at the wrist. Muscle Nerve 1996;
19:170-174.
Sheean GL, Kanabar G, Murray NM. Lumbrical-interosseous comparison in a distal
ulnar nerve lesion. Muscle Nerve 1996;19:
673-674.
McIntosh KA, Preston DC, Logigian EL.
Short-segment incremental studies to localize
ulnar nerve entrapment at the wrist. Neurology 1998;50:303-306.
Seror P. Ulnar conduction block at the wrist.
Arch Phys Med Rehabil 1999;80:1346-1348.
Russell WR, Whitty CW. Traumatic neuritis
of the deep palmar branch of the ulnar nerve.
Lancet 1947;1:828-829.
Wioschneck D, Hussein S, Hollerhage HG.
[Bicycle rider’s ulnar nerve paralysis.] Neurochirurgia (Stuttg)1993;36:11-13.
Seror P, Lestrade M, Vacher H. Ulnar nerve
compression at the wrist by a synovial cyst
successfully treated with percutaneous puncture and corticosteroid injection. Joint Bone
Spine 2000;67:127-128.
Henderson M, Robinson LR. Dorsal ulnar cutaneous handcuff neuropathy. Muscle Nerve
1991;14:905-906.
Sheean GL, Morris JG. Handcuff neuropathy
involving the dorsal ulnar cutaneous nerve.
Muscle Nerve 1993;16:325.
Nazliel B, Baysal I, Gomceli YB. Dorsal ulnar
cutaneous neuropathy. Acta Neurol Belg
2001;101:232-233.
Wertsch JJ. Pricer palsy. N Engl J Med
1985;312:1645.
Gessini L, Jandolo B, Pietrangeli A. Entrapment neuropathy of the dorsal cutaneous
nerve of the hand. J Neurosurg Sci
1982;26:185-186.
ULNAR NERVE
303. Young SH, Kalantri A. Dorsal ulnar cutaneous
nerve conduction studies in an asymptomatic
population. Arch Phys Med Rehabil 2000;81:
1171-1172.
304. Dutra de Oliveira AL, Barreira AA, Marques
W. Limitations on the clinical utility of the
ulnar dorsal cutaneous sensory nerve action
potential. Clin Neurophysiol 2000;111:12081210.
311
305. Stowell ED, Gnatz SM. Ulnar palmar cutaneous nerve and hypothenar sensory conduction studies. Arch Phys Med Rehabil 1992;
73:842-846.
306. Asbury AK, Gilliatt RW, eds. Peripheral
Nerve Disorders. London: Butterworths,
1984.