COMPRESSION NEUROPATHIES OF THE UPPER EXTREMITY

At the level of the wrist, the median nerve lies within
the confined space of the carpal tunnel along with the long flexor
tendons to the fingers and thumb. The tunnel is bounded on three sides
by the bones of the carpus, which make up the floor of the canal, and
on the fourth by the transverse carpal ligament (TCL), which forms the
roof (Fig. 52.7). Compressive neuropathy of the
median nerve within the carpal tunnel may result from any
space-occupying lesion under the TCL (19,67,145).
A frequent cause is flexor tenosynovitis; other causes are fractures
and dislocations of the floor of the canal and distal radius, and other
space-occupying lesions such as tumors and ganglia. These
space-occupying lesions increase the volume of the contents of the
noncompliant carpal tunnel, raising the pressure on its contents, which
include the median nerve. In many cases, there are no particular
identifiable causes even though the nerve is clearly compressed.
Although many of these cases are attributed to “nonspecific synovitis,”
pathologic examination of the synovium obtained from the carpal canal
in these cases usually fails to reveal signs of inflammation. Rather,
fibrosis and/or edema changes are seen, which may themselves be
secondary to compression rather than the primary cause of the
entrapment neuropathy (62,82).

The diagnosis of CTS is strongly suggested by the
patient’s history. Typically, he complains of aching or burning pain
along the median nerve distribution and of numbness and tingling in the
median-nerve-innervated digits (Fig. 52.8A)
during the night and early morning as well as during activities.
Numbness may extend into the ulnar digits in some patients. These
symptoms are aggravated by elevation, repetitive activities, and
prolonged flexion positioning of the wrist (130).
Radiation of symptoms proximal to the wrist is not unusual. Complaints
of the hand feeling fat, clumsiness in manipulation, and dropping items
are also frequent. The incidence is greater in women than in men,
although the difference is decreasing. In the past, postmenopausal
women were the most common patients; commonly associated diagnoses were
rheumatoid arthritis and distal radius malunion. Recently, a large,
younger group of patients with essentially equal distribution of women
and men has emerged. In this group the carpal tunnel disease has been
labeled idiopathic (62).

Examination includes sensory, provocative, sudomotor,
and strength testing. Sensibility may be reduced throughout the area
normally supplied by the median nerve except for the thenar eminence,
the distribution of the palmar cutaneous branch (Fig. 52.8A), which does not

enter the carpal canal (135).
As noted previously, the most consistent and reliable way to evaluate
sensibility in nerve compression is to use threshold testing
(Semmes–Weinstein monofilaments, vibrometry, and 256 cps vibration
testing) (126,127,132,133,134).
Provocative tests compress or percuss the median nerve to elicit
numbness and paresthesias in the distribution of the median nerve in
patients with CTS. Phalen’s wrist flexion test, in which the wrist is
maximally flexed with the fingers slightly curled, is sensitive (Fig. 52.9) (43).
A positive test for CTS is reproduction of symptoms within 60 sec.
Tinel’s nerve percussion test, in which the median nerve is percussed
as it enters the carpal canal to elicit symptoms (Fig. 52.10), is specific and indicates CTS in cases in which Phalen’s test is also positive (65). Another useful test is the direct compression test, which is sensitive and specific. The examiner’s thumbs apply direct pressure to the median nerve as it enters the carpal tunnel (Fig. 52.11) (29).
A positive test is reproduction of symptoms, which appear within 30 sec
and disappear with release of compression. Together, these tests
provide added clinical evidence of median nerve compression at the
wrist (Table 52.2).

Sudomotor activity (sweating) may be diminished. This is easy to detect clinically by sliding a metal object (e.g.,

a pen) between the patient’s fingers, which are held together. The
object slides much more easily on dry skin than on skin with normal
perspiration. Strength testing is difficult and somewhat subjective.
The most easily evaluated muscle of the thenar eminence is the abductor
pollicis brevis (APB) muscle. Most often, this muscle is innervated
solely by the median nerve, but it can also have a contribution from
the radial nerve. It is the most superficial of the thenar muscles and
can be palpated during active opposition or resisted palmar abduction
of the thumb. Relative weakness of palmar abduction of the thumb
against resistance or muscle atrophy occurs in more advanced cases.

Flattening or concavity of the normally bulging thenar eminence indicates atrophy of the APB (Fig. 52.12A). A weak, soft, or small APB is seen in severe cases of CTS and indicates denervation of the muscle.

Radiographic examination is not indicated in all cases because there is a low yield of findings (9);
it should be restricted to patients with a history of trauma or
arthritis and those with decreased wrist range of motion on
examination. One of us (JT) obtains radiographs to rule out Kienböck’s
disease in younger patients and peritrapezial arthritis in older ones.
Additional diagnoses uncovered by preoperative radiographs include
scapholunate advanced collapse (SLAC) wrists, ununited fractures of the
scaphoid, and radiopaque masses within the carpal tunnel (136). The views recommended include posteroanterior (PA), lateral, and carpal tunnel views.

Additional examinations include electrodiagnostic
studies and laboratory tests. Positive nerve conduction velocities show
increased latencies. In severe cases, EMG exams may show abnormalities
and may give information regarding treatment prognosis. In mild or
exertion-related cases, electrodiagnostic studies may be negative. This
negative finding does not rule out CTS in the presence of typical signs
and symptoms. Provocative nerve conduction evaluation may help to
uncover these dynamic forms of CTS (14). EMG
examination may be helpful when a cervical radiculopathy is suspected.
Order laboratory testing to screen for metabolic disorders that may
contribute to or cause CTS, (a) when there is suspicion of these
disorders, (b) when there is bilateral presentation, and (c) in
children who may have rare mucopolysaccharidosis or mucopolylipidosis (139).
Tests include erythrocyte sedimentation rate, rheumatoid factor, serum
glucose level, uric acid, thyroid panel, and renal indices. Liver
function tests may be indicated if alcohol-related peripheral
neuropathy is suspected. If doubt persists about the correct diagnosis,
an injection of a small amount of a steroid preparation mixed with
local anesthetic into the carpal

tunnel (not into the nerve) can be a therapeutic and diagnostic aid (Fig. 52.13) (Table 52.3) (45).
The entry site for the needle is slightly proximal to the distal wrist
crease, ulnar to the palmaris longus (PL) to avoid impaling the median
nerve, and approximately 1 cm radial to the flexor carpi ulnaris (FCU)
to avoid entrance into the canal of Guyon. Insert the needle at a 45°
angle, beneath the proximal margin of the TCL and directed in line with
the ring finger ray. Palpation in the midpalm just distal to the TCL
while injecting can help confirm proper needle placement by enabling
you to feel the flush of fluid into the canal.

Patients with CTS may be classified into three
categories. The mild group consists of patients with intermittent
symptoms that have been present less than 1 year, who have normal
two-point discrimination, no thenar weakness or atrophy, no denervation
potentials on EMG, and mildly elevated NCV. With conservative treatment
and steroid injection, 40% will be free of symptoms at 12 months. The
severe group consists of those with profound, persistent symptoms that
have been present longer than 1 year, thenar weakness or atrophy, and
marked abnormalities on electrodiagnostic studies (40).
Patients in the severe group fail to respond adequately to conservative
therapy and should receive operative treatment, which may include
tendon transfers concurrent with carpal tunnel release. In the moderate
group, conservative treatment shows findings and gives results
intermediate between those of the mild and severe groups. The presence
of underlying disorders or advanced age in any of these patients
diminishes the response to conservative (and possibly operative) care.

Initially, institute nonoperative treatment in all
patients except those with severe disease. Splint the wrist in neutral
to slight extension at night and during activities that exacerbate
symptoms. In exertional or dynamic cases, modification of activities
that exacerbate symptoms may be helpful. Vitamin B₆ has no effect on the natural history of CTS (3,4).
Steroid injection offers transitory relief in 80% of patients, with
only 22% being free of symptoms at 12 months. The patients in the mild
group fare better than others with steroid injection (40). Treat or correct underlying disorders if possible.

Indications for surgery include failure of nonoperative
treatment, persistent or progressive symptoms, acute onset with
profound sensory loss associated with trauma, and weakness or atrophy
of thenar muscles. Results of surgery vary according to severity of
disease, choice of surgical treatment, and individual patient
physiology and social issues. As a general rule, we believe that with
adequate release of the carpal tunnel, major or complete relief of
discomfort associated with CTS is likely, as is relief of transient
numbness. Persistent or profound numbness may not disappear with
release if it has been present for a prolonged period (over 12 months).
Weak or atrophied

muscle
is not expected to recover with release, but if it is not complicated
by underlying disease, its progression will likely be halted. Nolan et
al. (87)
showed that patients with severe disease, followed for more than 2
years after carpal tunnel release, show improvement. Therefore, surgery
is indicated in these patients, especially if symptoms of discomfort
are present.

Make the decision to perform surgical release in a
patient with CTS in the context of the patient’s general condition. You
must be certain of the diagnosis of CTS and that its cause is
compression of the median nerve at the wrist. Within reason, exclude
other potential sources of the symptoms and maximally correct any
contributing conditions. With these issues resolved, you must include
the particular considerations of the patient in the surgical care. If
malunions and carpal instabilities are severe enough to compromise
results, treat them prior to or concurrently with release. In patients
with severe atrophy of the thenar musculature, perform opponensplasty
at the time of release. A particularly suitable procedure for
restoration of thumb palmar abduction in the patient with severe CTS is
the Camitz opponensplasty, in which the PL is harvested and extended
with a strip of palmar fascia, then routed subcutaneously and sutured
into the thumb at the level of the metacarpophalangeal (MP) joint along
the APB tendon (Fig. 52.14).

There have been significant differences of opinion about
whether internal neurolysis improves the results of carpal tunnel
release in patients with severe CTS manifested by thenar atrophy or
fixed sensory deficit (33,34,42,71,73).
In a combined series of patients (69 hands) from San Diego and
Sacramento, added benefit from internal neurolysis in the treatment of
severe CTS could not be demonstrated (42). Lowry and Follender (71)
confirmed this finding with a prospective, randomized, double-blind,
controlled study. We therefore no longer perform or recommend internal
neurolysis in the treatment of CTS. Concomitant release of the canal of
Guyon in patients with evidence of compression of the ulnar nerve at
the level of the wrist in conjunction with CTS is not recommended (117).
Transection of the TCL during carpal tunnel release alone results in an
increase in the volume of the carpal tunnel of approximately 24% and a
change in the orientation and shape of the canal of Guyon (102). Clinically, this results in resolution of the symptoms referable to ulnar nerve compression at the wrist in these patients.

Open carpal tunnel release is considered the preferred
surgical technique, especially for surgeons not doing a large volume of
these surgeries, because it offers good visualization of the TCL, the
superficial arch, and the carpal canal contents. It is a proven,
reliable method. Nonetheless, some herald endoscopic carpal tunnel
release as a step forward in the treatment of CTS (15,21,94).
Proponents of the latter technique claim decreased morbidity as a
result of the smaller scar, which occurs away from the base of the
palm, and more rapid rehabilitation (35,142).
Several systems exist for the purpose of endoscopic release; they have
in common visualization of the undersurface of the TCL with an
arthroscope as the ligament is divided from within the canal using
special knives or a blade mechanism. Agee et al. (2) and Chow (21) developed independent systems that are available commercially.

In a multicenter prospective randomized study, Agee et al. (2)
demonstrated a decrease in early postoperative pain and morbidity using
his device, but by 6 weeks, results were comparable to those of
standard carpal tunnel release.

Additional studies have evaluated endoscopic release (15,35).
Although scar pain has been reduced and time to recovery of
preoperative grip and pinch strength minimally shortened, pillar pain
and palmar tenderness have not been eliminated. In cadaver studies,
incomplete release of the TCL has been demonstrated to occur in up to
50% of the specimens (111). Clinically,
however, patients do obtain symptomatic relief from the endoscopic
technique. As endoscopic release systems have been refined and
experience with the technique gained, results have improved. The
procedure remains hazardous in inexperienced hands and requires
specialized training. A risk of cutting neurovascular structures or
tendons exists because of limited visualization and deviations from
proper technique (81,110).
Recurrent or incomplete relief of symptoms from endoscopic release has
been shown to be related to incomplete release of the TCL. This
improves after subsequent open carpal tunnel release (36,53).

Endoscopic carpal tunnel release remains a controversial
method for treatment of CTS. However, with a thorough knowledge of the
pertinent anatomy and with experience, it can be a safe and effective
treatment in appropriate patients if the surgeon adheres to several
tenets. The surgical consent form must specify both an endoscopic and
an open carpal tunnel release, because several conditions may
necessitate aborting the former and proceeding with the latter. These
include (a) difficulty in visualization that results from equipment
problems, fogging, or the inability to clear synovium from the
undersurface of the ligament, (b) presentation of atypical anatomy, and
(c) difficulty in manipulating the endoscope. The surgeon must place
the endoscope in the ulnar aspect of the carpal tunnel and keep it
aligned with the ring finger ray to prevent injury to the median nerve
and the superficial vascular arch (108).
(Specific techniques are not discussed here; refer to the
manufacturer’s technique manual for each system.) The surgeon must
verify absolutely that the endoscope is within the carpal tunnel and
not in the canal of Guyon before making any cuts. Endoscopic carpal
tunnel release is inappropriate in patients with bony deformity caused
by fracture or dislocation and in those with inflammatory synovitis who
require synovectomy or whose synovitis may make visualization
difficult. If endoscopic tunnel release is considered, preoperative
radiographs are necessary to evaluate these issues.

Multiple limited- and minimal-incision methods and
systems have been developed for carpal tunnel release and are
commercially available (13,68,86).
These differ from endoscopic techniques in that the TCL is divided by a
relatively blind method rather than being visualized with an
arthroscope. The benefits of this technique over open carpal tunnel
release are similar to those of the endoscopic methods, as are the
risks.

Immediately postoperatively, encourage active, gentle finger range-of-motion exercises. Patients should also maintain

mobility of the elbow and shoulder. Elevation is crucial, especially
during sleep, to reduce edema. Remove bulky dressings and splints 5
days postoperatively. The patient then wears a removable prefabricated
wrist splint for comfort only. [One of us (MNH) instructs the patient
to wear the splint full time.] The wrist is put through gentle
range-of-motion excercises several times a day, independently of finger
motion. Continue the splint for 2–3 weeks for patient comfort only,
during which time encourage progressive use of the hand. Then
discontinue daytime splinting. Continue nighttime wear for an
additional 3–4 weeks if desired (96).
Use physiotherapy selectively for patients who are progressing poorly.
Recovery takes months, so patients who are told that the carpal tunnel
release is a minor operation and full recovery can be anticipated in 2
weeks are grossly misled and usually unhappy.

The patient’s return to work depends largely on the demands of his occupation. Gellman et al. (44)
have shown that grip strength returns to preoperative levels 3 months
after surgery, and pinch strength returns at 6 weeks. Their work
provides us with an indication of when patients ought to be able to
return to their previous levels of occupational activity. Many studies
employ “return to work” as a measure of outcome without clearly
delineating what criteria are to be met to determine when a patient
should return to work. Many factors influence the actual return-to-work
time. Palmar tenderness, a particularly important consideration in
manual laborers, may persist for longer than 6 months. Full recovery of
nerve function may not occur, depending on the severity of nerve
damage. Persistent palmar pain and early recurrent symptoms in workers’
compensation cases are increasing, unsolved problems for patients,
physicians, and industry. Without job modification for these patients,
carpal tunnel release alone may lead to failure in returning the
patient to gainful employment.

Complications are caused by misdiagnosis or technical
factors. Conditions associated with peripheral neuropathies must be
suspected, recognized, and treated before surgery, or concurrently with
the surgical release. Upton and McComas (137)
proposed a “double crush” syndrome as a hypothesis to explain the
failure of distal decompressions in nerves subject to compression in
multiple sites. Many patients with CTS have a cervical radiculopathy.
Others may have concomitant compression at the carpal tunnel as well as
under the PT. Release of the carpal tunnel in these cases may not
relieve symptoms because the more proximal compression remains.
Hypertrophic synovium, if not removed at the time of surgery, may cause
persistent compression despite ligament release.

Complicating technical factors include improper
placement of the incision (i.e., usually too far radially), which
jeopardizes the median nerve and its motor branch, as well as leading
to injury or entrapment of the palmar cutaneous nerve or its branches (Fig. 52.17).
Poor exposure may result in incomplete division of the TCL or in injury
to the superficial palmar arch. Do not use transverse incisions at the
wrist crease for blind decompression of the carpal tunnel.

A rare complication is a tendency of the flexor tendons
to the little finger to sublux during strong gripping. This is often
only a transitory problem. Bowstringing of the flexor tendons with
flexion of the wrist has been noted. This complication is easily
prevented by postoperatively immobilizing the wrist in slight
dorsiflexion for 2–3 days (138), which additionally may prevent adherence of the nerve and tendons to palmar structures and improve grip strength (88).
Reserve reconstruction of the TCL for instances where immobilization of
the wrist in flexion is necessary after carpal tunnel release.
Complications from deficient postoperative management usually result
from swelling and edema or poor control of pain, leading to loss of
finger or wrist motion (particularly if a synovectomy was performed)
and to reflex sympathetic dystrophy. The benefits of a good
postoperative dressing, an aggressive exercise program, and elevation
cannot be emphasized enough.

Pillar pain—pain at the base of the thenar and hypothenar eminences after carpal tunnel release—is a common

finding in patients. It varies greatly from case to case in both
severity and duration of its symptoms. Its etiology is poorly
understood, although many theories have been proposed. It generally
subsides and resolves over time. Seradge and Seradge (113)
noted ulnar-sided wrist pain in 1% of their patients after carpal
tunnel release. They attributed this pain to the pisotriquetral joint,
whose mechanics are altered by division of the TCL. Treatment consisted
of excision of the pisiform in cases with transient response to steroid
injection of the joint. We have no evidence to substantiate this theory
or to recommend this approach.

The median nerve lies anterior to the brachial artery
and medial to the biceps muscle in the midarm. In the distal arm, it
crosses the brachial artery to lie medial to it, coursing on the
brachialis muscle. The supracondylar process is an anomalous spur
arising on the anteromedial aspect of the distal humerus, 5 cm proximal
to the medial epicondyle, in as many as 3% of individuals. The ligament
of Struthers is a fibrous band that may arise from the supracondylar
process (spur) of the humerus (7) and attaches
to the medial epicondyle, forming a fibro-osseous tunnel through which
the median nerve and, at times, the brachial artery pass (Fig. 52.18) (66).
The median nerve enters the antecubital fossa coursing beneath the
lacertus fibrosus (bicipital aponeurosis), then travels between the
superficial (humeral) and deep (ulnar) heads of the PT muscle. It
continues distally beneath the arch of origin of the flexor digitorum
superficialis (FDS), coming to lie between it and the flexor digitorum
profundus (FDP). The median nerve maintains this relationship
throughout its course to the wrist. Potential sites of compression
include the supracondylar process and the ligament of Struthers, the
lacertus fibrosus, the arch of the origin of the PT, and the arch of
the origin of the FDS (Fig. 52.26, Table 52.4).

The symptoms arising from compression of the median
nerve at this level, including numbness in the radial three and
one-half digits and thenar weakness, may be attributed to CTS. In
pronator syndrome, unlike in CTS, paresthesias are typically absent at
night. Important additional symptoms that may help differentiate this
condition from CTS are pain in the anterior aspect of the proximal
forearm and numbness in the thenar region—the territory of the palmar
branch of the median nerve that does not travel through the carpal
tunnel, having branched from the median nerve several centimeters
proximal to the wrist. Sensory threshold testing detects decreased
sensation in the radial three and one-half digits, as in CTS, with the
addition of numbness in the thenar eminence, the area innervated by the
palmar cutaneous branch (Fig. 52.8A). The findings of weakness and atrophy in the thenar musculature

may be indistinguishable from those seen in CTS, although they are less severe and are most often absent.

The portion of the physical examination that will
further differentiate pronator syndrome from CTS is provocative
testing. Phalen’s test should be negative, but it may be positive (47,95).
Tinel’s percussion test, in which the median nerve is percussed at the
level of the pronator muscle, elicits paresthesias in the distribution
of the median nerve in the proximal forearm rather than at the carpal
tunnel (Fig. 52.19). To perform the pronator
compression test, place direct thumb pressure just proximal and lateral
to the proximal edge of the PT muscle belly (Fig. 52.20).
(The brachial pulse will be palpable lateral to the nerve.) A positive
test is reproduction of paresthesias in the median-nerve-innervated
digits within 30 seconds, and it supports the diagnosis of pronator
syndrome (38). According to Olehnik et al. (95),
the pronator compression test is the most accurate diagnostic test.
Several tests have been designed to give clues to the specific site of
compression of the median nerve in pronator syndrome. The production of
pain or aggravation of paresthesias with simultaneous resisted forearm
supination and resisted elbow flexion beyond 120° indicates probable
entrapment of the median nerve at the lacertus fibrosus (Fig. 52.21) (7,33,58,115,122).
Entrapment of the nerve between the two heads of the PT muscle is
indicated by elicitation of paresthesias in the median nerve sensory
distribution with resisted forearm pronation while the elbow is slowly
extended from full flexion (Fig. 52.22) (33,58,121,122).
Paresthesias elicited in the radial three and one-half digits with
resisted independent flexion of the proximal interphalangeal (PIP)
joint of the long finger suggest entrapment beneath the superficialis
arch of origin (Fig. 52.23, Table 52.5) (33,122).

Special diagnostic procedures include electrodiagnostic
studies and radiographs of the elbow. Median nerve conduction
velocities from the elbow to the wrist are decreased in less than one
third of cases (16,47,95).
The value of obtaining these studies is to evaluate for the presence of
CTS. A normal conduction velocity at the level of the wrist supports
proximal compression of the median nerve in the presence of symptoms
and signs of pronator syndrome. A study consistent with CTS indicates
the necessity

of
treatment directed at the wrist but does not rule out a double crush
phenomenon, with compression both at the carpal tunnel and in the
proximal forearm. Failed carpal tunnel releases that respond to
subsequent operative release in the proximal forearm support the
occurrence of simultaneous compression of the nerve at these two sites (95).
Four views of the elbow—anteroposterior (AP), lateral, and two
obliques—are obtained to evaluate the presence of a supracondylar
process. Although its presence is suggestive of compression of the
median nerve beneath the ligament of Struthers, it is not
pathognomonic; this is a very rare site of entrapment. The absence of a
supracondylar process does not rule out the presence of a ligament of
Struthers and entrapment at this site (Table 52.6).

Nonoperative treatment consists of anti-inflammatory
medications, splinting, and rest for 4–6 weeks. Modification of
activities is particularly important because symptoms are often related
to repetitive elbow flexion and extension and to forearm pronation and
supination. Physiotherapy in the form of massage, stretching, and
iontophoresis to mobilize and relax potentially tight structures may be
helpful. Carefully placed steroid injections in the site of maximal
tenderness and pain (but not into the nerve) may be useful for
diagnostic and therapeutic purposes.

Surgery generally is not necessary because most patients
respond to nonoperative care. Surgery is indicated in those cases where
symptoms persist longer than 6 weeks to 3 months following adequate
conservative management.

Improvement after surgical release is reported in approximately

80% to 90% of cases (38,47,59,95).
Complete relief of symptoms occurs in only about one third of those who
improve. There appears to be no preoperative indicator of which
patients will have the better results (95). As
in CTS, return to work will depend in part on the demands of the
patient’s particular vocation. Of the 36 patients in the series
reported by Olehnik et al. (95), 25 returned to
their preoperative or similar occupations and eight returned to work
but had to change jobs. The final work status of the remaining three
patients was unknown.

To plan the surgical incision, you must determine
whether the site of compression is above or below the elbow. If there
is evidence of compression under an arcade of Struthers, center the
surgical exposure at the radiographic projection of the supracondylar
process. If the compression is below the elbow, extend the incision
distal to the elbow flexion crease onto the forearm to expose the
pronator and the arch of the FDS.

Alternative incisions that are oriented fairly transversely, with a goal of minimizing unsightly scarring, have been described (38). These have been criticized for not providing adequate exposure of the nerve and the sites of compression (58). Olehnik et al. (95) described an oblique incision centered over the point of maximal tenderness in the proximal forearm (Fig. 52.27).
The fascia was then split longitudinally to allow adequate access to
the soft-tissue structures in the antecubital fossa to the midforearm.
Deep digital palpation and dissection were used to evaluate for
compression of the nerve proximally by a ligament of Struthers. They
additionally released intramuscular fascial bands of the PT and FDS
that crossed the nerve. The authors of this study point out the
importance of tracing the nerve along its course, releasing all fibrous
bands and vascular structures that are potential sites of compression.

After skin closure, apply a well-padded compression
dressing and a posterior plaster splint with the elbow flexed at right
angles and the forearm in semipronation. Encourage shoulder and finger
motion immediately after the operation. After 5 days, discontinue
immobilization; allow the patient to resume elbow flexion and extension
and forearm rotation and to gradually return to full activities as
tolerated.

As for CTS, misdiagnosis and technical factors are
responsible for most complications. The most important is failure to
release constriction at one of the four sites of possible entrapment.
You must also address all other potential sources of compression by
visualizing the nerve along its course. Avoid accidental damage to
branches of the median nerve by initially exposing and dissecting the
nerve along its lateral aspect, which is free of branches.

The anterior interosseous nerve (AIN) is a branch of the
median nerve that is essentially entirely motor except for a few
terminal branches that are sensory to a portion of the carpus. The most
common pattern of muscles innervated by the AIN includes the FDP to the
index finger, the flexor pollicis longus (FPL), and the pronator
quadratus (PQ). This innervation pattern varies significantly, which
can cause confusion during clinical examination. The nerve arises from
the dorsal aspect of the median nerve as it passes between the two
heads of the PT. In some cases, it passes deep to the deep head of the
PT. It passes beneath the arcade of the FDS and courses distally along
the anterior surface of the interosseous membrane between the FDP and
the FPL, accompanied by the anterior interosseous artery. The AIN gives
branches to the FPL and the radial aspect of the FDP muscles
approximately 4 cm distal to its origin from the median nerve (Fig. 52.28).
Compression may be caused by one of many structures, including the deep
head of the PT, the FDS, accessory muscles (e.g., Gantzer’s muscle, and
an accessory FPL) (28,74), aberrant vessels (e.g., anomalous radial artery), and tendinous bands along the course of the nerve.

Patients initially complain of vague, aching pain in the
proximal forearm and sometimes in the wrist. This occurs at rest and is
exacerbated by activities. There is no sensory deficit with AIN
syndrome, which is different from carpal tunnel and pronator syndromes.
Patients may note difficulty with activities such as writing, or
weakness in tip pinch. Frequently, there is a history of a single
episode of strong contraction of elbow, wrist, and finger flexors
accompanied by pain and followed shortly thereafter by motor loss.

Findings on clinical examination include weakness or paralysis of the muscles innervated by the AIN (18).
Weakness of the FPL and of the radial half of the FDP makes it
difficult or impossible for the patient to tip pinch with the index
finger and thumb (i.e., to make the so-called OK sign). The lack of
long flexors results in a hyperextension attitude of the distal joints
of these two digits (Fig. 52.29) (119).
You can test the weakness of the PQ by asking the patient to pronate
against resistance, with the elbow flexed to neutralize the stronger
PT. However, isolated paralysis of any one or a combination of these
muscles has been reported (50).

It is important to differentiate between an FDP or FPL
rupture and AIN syndrome in the patient with acute presentation. This
is done best by looking for the tenodesis effect of the FPL and index
FDP (79). Innervation anomalies add variability
to the classic examination findings. Martin-Gruber connection (median
to ulnar motor nerve connection in the forearm) occurs in 15% of
individuals; 50% of these arise from the AIN. The presence of this
anomaly may cause weakness of additional intrinsic muscles

of
the hand in patients with AIN syndrome. Additionally, in 50% of
individuals, the FDP to the index is innervated by branches from the
median nerve, not the AIN (50).
The diagnosis is usually confirmed by EMG studies. Nerve conduction
studies are usually not affected, although side-to-side differences may
be noted (Table 52.7).

In a patient who presents acutely, obtain
neurodiagnostic studies 2–3 weeks after injury, and again at 6 and 12
weeks if no clinical improvement is noted. Chronic cases, presenting
after 6 weeks, should have neurodiagnostic examination performed
initially and the patient should be followed clinically; if no
improvement is noted, perform another study at 12 weeks after the
injury. Although no specific protocols have been evaluated,
nonoperative treatment may consist of avoidance of exacerbating
activities, immobilization of the elbow in flexion and the forearm in
pronation, and the use of NSAIDs.

Essentially all reported cases have gone on to
spontaneous recovery, although in some instances this has taken up to 2
years. Most authors agree that recovery can be enhanced by surgical
exploration when spontaneous recovery is not apparent or is slow (50).
Recovery is generally complete within 6 months after surgery.
Persistence of the motor symptoms without signs of significant
improvement for 8–12 weeks is an indication for surgical exploration
and decompression (122). Evidence of clinical motor recovery or signs of reinnervation on EMG would call for further observation.

The surgical technique and postoperative management are very similar to those used in the pronator syndrome.

As in pronator syndrome, it is important to visualize
the entire nerve and divide all suspected offending structures. The
postoperative management is essentially identical to that after
treatment of the pronator syndrome.

Possible complications are similar to those described
for the carpal tunnel and PT syndromes. The main problem is an error in
diagnosis, particularly for the patient with an incomplete syndrome
involving either the thumb or the index long flexors, but not both (Fig. 52.29) (50). Such a

presentation may lead to the erroneous diagnosis of tendon rupture and
to a negative tendon exploration. Perform the tenodesis test with the
wrist in maximal extension along with MP joint and PIP joint extension.
This should produce slight flexion at the distal interphalangeal (DIP)
joint of the index and the IP joint of the thumb with AIN syndrome but
not with tendon rupture (79).

Suspect Parsonage–Turner syndrome (brachial neuritis) in
cases with an acute onset of pain in the forearm followed by weakness
in the muscles normally affected in AIN syndrome a few days to weeks
later (at times associated with a febrile illness, vaccination, or
unrelated surgery), especially in bilateral cases (149).
In Parsonage–Turner syndrome, there will also be shoulder pain and
involvement of the shoulder muscles at times. AIN compression syndrome
generally presents after an acute injury or in conjunction with
repetitive activity, whereas brachial neuritis is insidious in nature.
In Parsonage–Turner syndrome there is pain not associated with an
injury, which may involve more proximal areas of the upper extremity
than that seen in AIN syndrome. Parsonage–Turner syndrome often
produces EMG results similar to those of AIN syndrome in the FPL, FDP,
and PQ. Sampling of more proximal muscles innervated by the brachial
plexus, such as the deltoid, may also demonstrate EMG abnormalities,
which is different from AIN entrapment (Table 52.8).

Complete recovery is seen in 90% of cases treated
surgically or nonoperatively. Surgical exploration and decompression
are reserved for cases associated with trauma.

The most common location for entrapment of the ulnar
nerve is about the elbow; this condition is known as cubital tunnel
syndrome. There are five potential compression sites of the nerve that
occur along its course. At the midarm level, the ulnar nerve pierces
the medial intermuscular

septum
and runs distally posterior to it. Approximately 8 cm proximal to the
medial epicondyle, the nerve may pass through an inconstant fibrous
tunnel, the arcade of Struthers, formed by a band connecting the medial
intermuscular septum to the tendon of the medial head of the triceps.
This is the first potential site of compression (Fig. 52.30).
The nerve continues posterior to the intermuscular septum. The edge of
the septum becomes a second potential site of compression, usually
after failed anterior transposition. The nerve then comes to lie in the
retrocondylar groove of the medial epicondyle, the third potential site
of compression, where it gives off a few articular sensory branches to
the elbow joint; it then enters the cubital tunnel, the fourth
potential site of compression. The cubital tunnel is a fibro-osseous
canal formed by the medial epicondyle anteriorly, the ulnohumeral
ligament posterolaterally, and a structure termed the cubital tunnel
retinaculum (92), which is superficial and
forms the roof of the tunnel. The fifth potential site of compression
occurs as the nerve passes under Osborne’s fascia, a thick fascial
layer that connects the heads of the FCU to the medial epicondyle and
olecranon in nearly 80% of individuals and is often confluent with the
cubital tunnel retinaculum (24). The nerve then
courses to enter the forearm between the two heads of the FCU. At this
level, it gives off several motor branches to the FCU. It comes to lie
medial to the FDP, piercing the deep flexor pronator aponeurosis—a
fascial structure serving as a common origin and aponeurosis of the
humeral head of the FDS and the FCU—as it exits the cubital tunnel (61).
This aponeurosis is the sixth and most distal potential compression
site, and it, like the medial intermuscular septum, is usually a site
of secondary compression after anterior transposition (Fig. 52.31, Table 52.9).

Compression of the nerve is often of a dynamic nature.
Both constriction of the nerve and traction are implicated in its
dysfunction. Flexion of the elbow has been shown to cause increased
intraneural pressure in the ulnar nerve at the cubital tunnel and
decreased volume in the cubital tunnel itself (92). The ulnar nerve at the elbow normally

glides to accommodate elbow flexion (6). When tethered by scar or fibrosis, the ulnar nerve experiences traction forces, which affect nerve function.

Additional causes of compression include trauma,
deformity (e.g., cubitus valgus), malunion or nonunion of the medial
epicondyle, elbow instability, spurs or bone fragments within the floor
of the cubital tunnel (Fig. 52.32), tumors,
abnormal muscles (e.g., anconeus epitrochlearis), and a nerve that
subluxates or dislocates repeatedly over the medial epicondyle.

The presenting complaint is usually numbness and
paresthesias along the ulnar nerve distribution, the small finger, the
ulnar half of the ring finger, and the ulnar aspect of the hand (Fig. 52.8).
This is exacerbated by leaning on the elbow or positioning it in
flexion. Aching pain may be referred to the medial aspect of the elbow.
Numbness on the medial half of the forearm is not usually present.

Weakness of grip or loss of dexterity in the fingers may accompany these symptoms.

Physical examination includes sensory evaluation,
provocative testing, and motor examination. Threshold sensory
evaluation, including Semmes–Weinstein monofilaments and vibratory
testing, is most sensitive and is recommended. Two-point discrimination
yields abnormal results in more advanced cases. Sensation is decreased
in the ring and small fingers as well as in the ulnar half of the
dorsum of the hand, which indicates compression proximal to the origin
of the dorsal cutaneous branch of the ulnar nerve and therefore
proximal to the wrist.

Employ provocative testing to help localize the site of
compression, as well as uncover dynamic forms of the disorder. Tinel’s
test is positive if paresthesias are elicited in the distribution of
the nerve when it is gently percussed. The location of percussion with
maximal elicitation of symptoms may indicate the site of compression.
Tinel’s test is sensitive but not specific, giving a high rate of false
positive results at the cubital tunnel (23). The elbow flexion test described by Buehler and Thayer (17) and others (101),
which is flexion of the elbow beyond 90° with the forearm in supination
and the wrist in extension, is positive when symptoms are produced
within 1 minute, and it may localize compression to the level of the
elbow. Novak et al. (90) modified this test to
include direct compression of the ulnar nerve with the examiner’s
finger just proximal to the cubital tunnel while the elbow is flexed
maximally (Fig. 52.33). The test is considered
positive when paresthesia symptoms are produced in the ulnar nerve
distribution within 30 seconds. This test is reported to have 0.91
sensitivity and 0.97 specificity. Evaluate potential subluxation of the
ulnar nerve over the medial epicondyle by direct palpation while the
elbow is brought from full extension to full flexion. Ulnar nerve
subluxation is seen in 16% of normal individuals (20)
and therefore is not considered pathologic per se. If associated with
neuritic symptoms, it may be the cause of injury to the nerve.
Palpation may also elicit tenderness and disclose an enlarged,
sensitive nerve.

Motor examination is helpful in patients with more
advanced disease. Atrophy may be seen most commonly in the hypothenar
musculature and in the first dorsal interosseous muscle. When weakness
is present, it involves not only the ulnar innervated intrinsic muscles
but typically the FDP to the ring and small fingers. When both ulnar
innervated intrinsic and extrinsic muscles are involved, the ulnar claw
hand, a sign of intrinsic–extrinsic imbalance, does not appear as
severe. Grip strength testing is often normal unless there is
significant loss of power to the long flexors of the ring and small
finger. Pinch strength, especially key position, is decreased as a
result of loss of strength to the flexor pollicis brevis (FPB), the
adductor pollicis, and the first dorsal interosseous muscle. Froment’s
sign (hyperflexion of the IP joint) and Jeanne’s sign (hyperextension
of the MP joint of the thumb) are elicited during key pinch (Fig. 52.34).
Weakness or paralysis of the FPB concentrates the flexion force of the
FPL at the IP joint, causing hyperflexion of this joint (11). The EPL compensates for the adductor pollicis and enhances hyperextension

of the MP joint of the thumb because it is unopposed by the intrinsic flexor of the thumb (the EPB).

For subjective evaluation, directly test the strength of
the first dorsal interosseous muscle against resistance, and measure it
by side-to-side comparison in unilateral cases. In some individuals,
contribution of innervation to this muscle from the median nerve can
occur (109), and therefore this test is not
specific. Evaluation of the abductor digiti quinti is also subjective.
Side-to-side comparison is facilitated by a confrontation test. Ask the
patient to maximally abduct her fingers while holding her hands out in
front, palms facing her. She brings the tips of her small fingers
together and, while she resists collapse of the abducted small fingers,
she brings her hands together. In unilateral cases with abductor
weakness, the weak hand’s small finger collapses to the side of the
ring finger (Fig. 52.35).

Wartenberg’s sign is abduction of the small finger with
extension of the fingers at the MP joint level. It indicates
interosseous dysfunction. The cross finger test (30)
is very useful and also evaluates function of the interossei. Ask the
patient to cross his index and long fingers. Patients with ulnar nerve
dysfunction often have trouble performing this task. Atrophy and
weakness of intrinsic muscles innervated by the ulnar nerve indicate a
moderate to severe lesion of the nerve (Table 52.10).

Radiographs are indicated in cases of previous trauma,
deformity, and suspected arthritis, and where there is incomplete range
of motion. AP, lateral, and oblique views are obtained, as well as
axial views of the distal humerus and olecranon for evaluation of the
ulnar groove.

Neurodiagnostic studies include NCV and EMG evaluation.
These are helpful in confirming the diagnosis and in classifying the
case for treatment and prognostic purposes. NCV evaluations of the
segment of the ulnar nerve across the elbow are considered significant
if conduction values are reduced by 33% (33).
Segmental “inching” studies may be helpful in localizing the site of
compression, especially in previously operated cases with recurrence of
symptoms. EMG evaluation of the ulnar innervated muscles can provide
information on chronicity and progression as well as severity, and it
may indicate the approximate site of compression. More importantly, EMG
needle examination coupled with somatosensory evoked potential (SSEP)
evaluates for radiculopathies and more proximal lesions, including
thoracic outlet syndrome (TOS), which is suspected especially in cases
of bilateral ulnar nerve symptoms (Table 52.11).

Dellon (26) developed a useful classification system for cubital tunnel syndrome (Table 52.12).
He classified patients into mild, moderate, and severe categories
depending on physical and electrodiagnostic findings. Surgical
treatment options and the relative results with respect to the patient
classification will be discussed.

Neither vitamin B₆ nor NSAIDs have been shown
to have an effect on cubital tunnel syndrome. Injections are advocated
by some. Two of us (MNH and JT) occasionally use them. Water-soluble
steroid is injected at the proximal aspect of the cubital tunnel, not
into the tunnel. Take great care to avoid injury to the ulnar nerve,
which is at risk. Most agree, though, that injection is to be avoided
because of the great risk of injury to the nerve, especially if
injection is made into the cubital tunnel where the nerve is tightly
confined.

The most effective nonsurgical management of cubital
tunnel syndrome includes patient education and splinting. The
occupational or physical therapist instructs the patient in nerve
protection. This includes avoidance of repetitive flexion and extension
of the elbow, of prolonged positioning of the elbow in the flexed
position, and of leaning on the medial aspect of the elbow. Adjustments
are made in the height of work stations and seats when indicated, so
that the elbow is flexed no more than 30° during work. Elbow pads may
be worn to prevent direct pressure on

the nerve in its subcutaneous position (Fig. 52.36).
Hand therapists can provide Thermoplast or pillow extension splints
that hold the elbow in 30° to 45° of flexion during sleep to prevent
hyperflexion (Fig. 52.37). Recheck the patient
after 3 months of treatment. In mild cases and some moderate ones,
patients who comply with these instructions may have a good response
and be able to avoid surgery.

Progression or inadequate amelioration of symptoms with
nonoperative care is an indication for surgery. Inability of the
patient to comply with nonsurgical care in mild or moderate cases is a
relative indication. Severe involvement, including motor dysfunction,
requires surgical intervention. Ulnar neuropathies associated with
deformity, bony lesions, tumors, and elbow instabilities, among others,
require attention to the pathology contributing to the nerve
compression as well as the nerve itself.

The severity of disease, its chronicity, and the general
condition of the patient all influence the outcome of treatment.
Patients with intermittent symptoms, no atrophy, and mild
electrodiagnostic findings respond well to nonoperative treatment (32).
The choice of surgical procedure in some instances may also have an
effect. In most uncomplicated cases, return of sensation and motor
function occurs within 6 months. Nouhan and Kleinert (89)
evaluated 33 limbs that had been followed for an average of 49 months.
Preoperative nerve compression was classified as mild in 6, moderate in
7, and severe in 20. Surgical treatment consisted of submuscular
transposition with Z-lengthening of the flexor pronator mass. There were 97%

good to excellent results overall; the preoperative classification did not influence the final result.

Seradge and Willis (114)
evaluated the results of 160 cases undergoing cubital tunnel release
and medial epicondylectomy. Preoperative severity of compression was
mild in 7%, moderate in 86%, and severe in 7%. There were 87% good, 12%
fair, and 1% poor results (failure of treatment). Factors that
increased the rates of symptom recurrence in their patients included
female sex, the presence of concomitant CTS or TOS in the same
extremity, age in the third or fourth decade, and patients who did not
return to work within 3 months after surgery. Limb dominance, length of
preoperative conservative care, and EMG results did not have a
relationship to recurrence rate.

In a literature review by Dellon (26),
patients in the mild group had excellent results from surgery no matter
what technique was used. Patients in the moderate group did not improve
without surgery, and decompression in situ
was not effective. Medial epicondylectomy produced 50% excellent
results with a high recurrence rate, whereas submuscular transposition
gave 80% excellent results with the lowest recurrence rate. In severe
patients, surgery resulted in less than 50% excellent results for
sensory recovery and up to 25% for motor recovery. Recurrence developed
in 30% of these patients. In this group, the poorest results were in
those undergoing intramuscular transposition, and the best were in
those receiving submuscular transposition and internal neurolysis.

When a particular condition contributes to compression
of the ulnar nerve, consider additional diagnostic studies to further
delineate the pathology. Computed tomography (CT) scans can further
characterize suspected bony abnormalities, including space-occupying
spicules or fragments, fracture callus, and malunions or nonunions.
Suspected tumors are best visualized by magnetic resonance imaging
(MRI) evaluation. Progressive deformities (e.g., cubitus valgus due to
nonunion of the lateral condyle) must be stabilized at the time of
decompression and transposition of the nerve, or in a staged fashion.
Patients with previously failed decompressions should undergo inching
nerve conduction velocities to better localize the site of compression,
most often in the most proximal or distal portion of the previous
surgical exposure.

Better than 80% to 90% good results are obtainable with
any of the commonly employed operative methods. The choice of operative
technique is greatly influenced by the cause of the compression, the
patient’s age, and systemic conditions such as diabetes or alcoholism.
Operative techniques include simple decompression, medial
epicondylectomy, subcutaneous transposition, intramuscular
transposition, and submuscular transposition. The nerve may be
decompressed by simple division of the arch of origin of the FCU (or
the cubital tunnel) in the following cases: (a) if clinical findings
(e.g., a localized nerve percussion sign) suggest isolated entrapment
of the nerve beneath the arch (or cubital tunnel retinaculum), (b) if
the nerve presents a constricting groove caused by this arch (or
retinaculum), as visualized during operation (Fig. 52.38),
or (c) if the nerve is vulnerable to manipulation (e.g., in older
patients or patients with diabetic or alcoholic neuropathy) (148).

Anterior submuscular transposition is best suited for
neuropathies associated with elbow deformity, abnormalities of the
cubital canal, and the subluxing or dislocating ulnar nerve,
particularly in the younger population and in the more severe cases
with evidence of motor involvement (66,69).
A particular indication for medial epicondylectomy is the ulnar
neuropathy associated with nonunion of a fracture of the medial
epicondyle. Routine use of this technique has been shown to be
effective (48,60). Some prefer anterior subcutaneous transposition over submuscular transposition (1,31,99,104).
Subcutaneous transposition is commonly employed as part of other
operative procedures about the elbow, including fracture reduction,
elbow arthroplasty, and neurorrhaphy of the ulnar nerve in cases where
there is loss of nerve length.

Dissection of the ulnar nerve is delicate and requires
patience and diligence to prevent damage to the nerve, its branches,
and its accompanying blood supply. This is aided by use of
magnification, fine instruments, and bipolar cautery. A trained
surgical assistant is invaluable in facilitating these procedures and
in adding a level of safety to prevent potential complications related
to nerve injury.

In Situ Decompression

Support the arm in a sling for a few days. Encourage
immediate active flexion and extension of the elbow. Subluxation of the
nerve after decompression is rare. On the contrary, nerves that are as
tense as bow strings proximal to the constricting tendinous arch,
snapping over the medial epicondyle during elbow flexion and extension,
recover a normal excursion after decompression.

Postoperatively, leave the splint in place for 3–5 days.
Then remove it and begin active range-of-motion exercises. Use a sling
to protect the arm when it is not engaged in therapy. Full range of the
elbow should be achieved by 3–4 weeks. At that time, begin progressive,
gentle strengthening. Theoretically, the nerve will slowly transpose
itself anteriorly and come to rest in a position without tension,
anterior to or on the flexion–extension axis of the elbow. Seradge (112)
demonstrated a decreased incidence of elbow contracture and a decrease
in return-to-work time of 50% in patients who had mobilization of their
elbows within 3 days of surgery following medial epicondylectomy versus
those who were immobilized for 14 days postoperatively.

The three methods of anterior
transposition—subcutaneous, intramuscular, and submuscular—are
essentially similar in their means of initial decompression and
mobilization of the nerve, and this is described here. Both the way the
transposition is maintained and the rehabilitation vary with the
method, however, so they will be described under separate headings.

Eaton et al. (31) described a
technique (described next) that employs a fasciodermal sling fashioned
from the fascia of the medial epicondyle and sutured into the dermis of
the anterior skin flap (Fig. 52.43). The nerve
comes to lie in the plane between the dermis and fat of the anterior
flap, and the fascia of the flexor–pronator muscles, and it is
maintained there by the sling. An alternative method for creation of a
sling to maintain the anterior position of the nerve employs the medial
intermuscular septum as described by Pribyl and Robinson (99).
One of us (RMS) avoids the use of fascial slings and prefers to suture
the fat of the lateral skin flap to the medial fascia to create a
broad-based tunnel.

Postoperative care consists of a splint and sling for approximately 5 days, followed by early active range-of-motion

exercises. Weirich et al. (144)
demonstrated average return to work and activities of daily living by 1
month in patients immediately mobilized after subcutaneous
transposition, versus 2.75 months in those mobilized later than 7 days.
By 2–3 weeks, the patient should regain nearly full range of motion of
the elbow. Progress with strengthening thereafter, with a return to
most activities by 6 weeks postoperatively.

This technique was described by Adson at the turn of the
century, and it was evaluated in a series published by Kleinman and
Bishop in 1989 (63), from which the following
description is derived. We do not use this technique as part of routine
treatment for cubital tunnel syndrome.

Postoperatively, hold the forearm in the semipronated
position and the elbow in flexion for 3 weeks, then institute
progressive range of motion exercises. Permit unrestricted use by 6
weeks.

Learmonth (66,69)
provided the classical description of the technique of submuscular
transposition of the ulnar nerve. He lengthened the flexor–pronator
muscle mass by a stepcut, or Z-lengthening,
of the common tendinous origin from the medial epicondyle to decrease
the tension on the nerve in its anterior position on the fascia of the
brachialis muscle and anterior capsule of the elbow (89).

Postoperatively, maintain the arm in plaster
immobilization for 7–12 days. Then remove the immobilization, place the
arm in a sling, and institute active range-of-motion exercises. The
wrist can be protected from extending with a removable Velcro splint.
Full elbow range is expected by 3 weeks, when the sling is removed.
Restrict the patient from forceful gripping with the hand for an
additional 1–3 weeks, but encourage light activities. Begin
strengthening 4–6 weeks postoperatively, and have the patient return to
nearly full activities at 6–9 weeks, with unrestricted use at 9–12
weeks depending on individual progress and demands.

The most common causes of recurrent cubital tunnel
syndrome are incomplete decompression and inadequate mobilization of
the nerve at the time of transposition. Failure to decompress the nerve
at the site of entrapment often results in failure to relieve symptoms,
and this can be avoided by carefully evaluating all potential sites of
compression. When initial relief of symptoms is followed by recurrence,
common causes are kinking of the nerve proximally at the arcade of
Struthers or on the margin of the intermuscular septum, and distally at
the deep pronator aponeurosis. You can avoid this by making the
incisions adequate for exposure and by examining the nerve at surgery,
before closing the wound, to ensure that it is not entrapped by the
procedure anywhere along its length.

Reoperation should be preceded by nonoperative care and
repeat neurodiagnostics, including the inching studies previously
mentioned, to evaluate for the potential site of secondary compression.
When revision surgery is appropriate, the procedure of choice is
submuscular transposition (26) unless this was
the initial procedure. In that case, the choice of revision surgical
technique is often determined at surgery, at which time the status of
the nerve and its bed can be evaluated. The results of repeat
decompression are poor in comparison to those of initial decompression (5,106).
The medial antebrachial cutaneous nerve (particularly the posterior
branch) is at risk for injury during the dissection. This injury
commonly results in pain and an unhappy patient.

Ulnar tunnel syndrome is caused by the compression of
the motor, sensory, or motor and sensory portions of the ulnar nerve in
the canal of Guyon. The canal of Guyon is a confined fibro-osseous
triangular space on the ulnar aspect of the volar wrist (Fig. 52.47).
The roof of this space is formed by the volar carpal ligament
proximally (the thickened distal extension of the antebrachial fascia,
which becomes confluent with the tendinous insertion of the FCU onto
the pisiform) and the pisohamate ligament distally (which is the
extension of the FCU from the pisiform onto the hook of the hamate).
The lateral wall is formed by the TCL proximally and the hook of the
hamate distally. The medial wall is formed by the pisiform and its
associated fibrous structures, and the abductor digiti minimi. The
ulnar artery and nerve enter the canal of

Guyon
at the wrist, deep and radial to the FCU tendon, the artery lying
radial to the nerve. In the proximal portion of the canal, the motor
and sensory bundles of the nerve lie side by side as one nerve. Just at
the distal margin of the pisiform, the nerve divides into deep and
superficial branches. The deep branch, which is the motor division,
dives through a fibrous arch formed by the origins of the abductor
digiti minimi and flexor digiti minimi at the base of the hypothenar
muscle group. It continues on to innervate the intrinsic muscles of the
hand. The superficial branch continues on through the canal, beneath
the pisohamate ligament, to course along the palmar surface of the
hypothenar musculature and become, in its terminal branches, the proper
digital nerves of the ulnar and radial small finger and the ulnar ring
finger.

Gross and Gelberman (46) described the ulnar tunnel and divided it into clinically relevant zones (Fig. 52.48).
Zone I is the area of the canal from the proximal margin of the volar
carpal ligament to the distal margin of the pisiform—more specifically,
where the nerve bifurcates. It is defined by the presence of both the
motor and the sensory divisions of the ulnar nerve. With division of
the nerve into motor and sensory branches, zones II and III are
defined; the former is associated with the motor and the latter with
the sensory division. These last two divisions run side by side in the
canal up to the level of the hypothenar fibrous arch.

Entrapment of the ulnar nerve in the ulnar tunnel may be
a result of space-occupying lesions. Ganglions arising from the
triquetrohamate joint are the most common cause. Others include
aneurysms (Fig. 52.49), lipomas, fractures of
the bony walls (particularly the hook of the hamate) of the canal of
Guyon, anatomic variations of the canal, and accessory or aberrant
muscles. Repeated blunt trauma to the hypothenar region is the second
most common cause (10,116). Compression in zones I and II is most

often caused by ganglions and fractures of the hook of the hamate. Zone
III is most often affected by a vascular lesion of the ulnar artery (116,128).

Entrapment at the wrist may produce pure motor, sensory, or mixed symptoms (10). Shea and McClain (116)
described three ulnar nerve compression syndromes at and distal to the
wrist. These correspond to the three anatomic areas of the canal. In
type I, the entrapment takes place in the proximal zone, resulting in
mixed motor and sensory deficit. Type II is purely motor, secondary to
compression in the canal of Guyon or at the hook of the hamate in
association with the origins of the abductor digiti minimi and the
flexor digiti minimi and within the substrate of the opponens digiti
quinti. Type III is caused by pressure on the superficial branch of the
ulnar nerve, producing a sensory deficit in the ring and small fingers
without associated muscle weakness or atrophy (Table 52.13).

Ulnar tunnel syndrome may be difficult to distinguish
from cubital tunnel syndrome. One difference is the sparing of
sensation of the dorsal ulnar half of the hand in ulnar tunnel
syndrome. This area is innervated by the dorsal branch of the ulnar
nerve, which arises variably from the ulnar nerve, but always proximal
to the wrist crease, and does not enter the canal. Another difference
is sparing of the long flexors of the ring and small fingers, leading
to a more pronounced ulnar claw deformity in patients with ulnar tunnel
versus cubital tunnel syndrome. Additionally, a history of repeated
trauma to the hypothenar region may direct special attention to
evaluation of this area in patients who present with
ulnar-nerve-related symptoms (Table 52.14).

A careful examination is extremely helpful in precisely
localizing the site of compression. Palpation of the deep structures
within the hypothenar region may suggest a mass, not infrequently a
ganglion within the canal. Allen’s test (an evaluation of the
contributions made by the radial and ulnar arteries to the blood supply
of the hand) is performed because thrombosis or aneurysm of the ulnar
artery may be the cause of the neuropathy. Tinel’s test over the ulnar
nerve at the level of the wrist and compression of the nerve over zone
I may be helpful in distinguishing ulnar tunnel from cubital tunnel
syndrome, although this has not been verified by studies. Phalen’s test
may also be positive in ulnar tunnel syndrome.

Because of the high incidence of space-occupying lesions
and fractures associated with compression of the ulnar nerve in the
canal of Guyon, obtain radiographs. Plain radiographs, including PA,
lateral, and carpal tunnel (ulnar tunnel) views, can be used to screen
for fractures,

dislocations,
and arthritis. If a hook-of-the-hamate fracture is suspected but not
proven in plain radiographs, a CT scan is the diagnostic study of
choice. Mass lesions include ganglia and aneurysms and are best
evaluated by MRI. In some cases of vascular lesions, arteriograms may
be of additional help. Electrodiagnostic studies show slowing of the
NCV across the wrist of the sensory and/or motor portions of the nerve.
In theory, isolated slowing in the sensory portion is not diagnostic of
isolated sensory division compression because the sensory fibers of the
nerve are more susceptible to compression than are the motor fibers. If
EMG evaluation shows abnormalities in the FCU and FDP muscles in
addition to the intrinsics, compression of the ulnar nerve is present
proximally (Table 52.15).

Except for cases resulting from repeated blunt trauma,
in which cessation of trauma may lead to complete resolution of
symptoms, and for the mild type II neuropathy, the ulnar tunnel
syndrome is best treated surgically. In the absence of identifiable
lesions causing compression of the nerve in the ulnar tunnel,
nonoperative treatment consists of splinting, NSAIDs, and avoidance of
activities that aggravate or precipitate symptoms. Failure to
adequately improve symptoms is an indication for surgery.

As noted in the preceding section, most cases of ulnar
tunnel syndrome are treated operatively because there is often a mass
lesion or a vascular injury or anomaly causing compression of the
nerve. In cases of acute onset of ulnar tunnel syndrome in association
with wrist trauma and swelling, Vance and Gelberman (140) recommend operative release and exploration if no improvement is noted within 48 hours. Alternatively, Howard (52)
suggests observation for 6–8 weeks after the injury before exploration.
It is reasonable to treat acute, traumatic ulnar tunnel syndrome
expectantly in cases of incomplete or mild neurologic deficit, and to
reserve urgent operative decompression for those cases with dense
sensory deficits and/or paralysis of intrinsic muscles. Results of
operative management are generally good, and recurrence is rare. Return
of muscle function is adequate to avoid the need for tendon transfer.
The rate and extent of recovery are likely related to the preoperative
duration and severity of symptoms.

Identification of the cause and site of compression is
essential to treat the offending lesion at surgery. Plan for and inform
the patient of excision of a fractured hook of the hamate or arthritic
pisiform. Vascular reconstruction may

be
necessary in ulnar artery aneurysms and thrombosis. Ganglia must be
identified and excised. If no particular lesion is identifiable,
suspicion of a particular zone of compression will help direct
particular attention to the segment of the nerve corresponding to that
zone.

The choice of incision and extent of exposure vary
according to the particular pathology suspected as the cause of
compression. The technique of exploration and decompression of the
nerve through its course in the ulnar tunnel is described here.

Postoperative care is as for carpal tunnel release. If
you treated other pathology simultaneously, institute specific
rehabilitation and advise precautions as indicated.

Complications are similar to those associated with CTS.
Incomplete release is potentially a problem if the nerve is not traced
distally enough into zone III, between the pisohamate and
pisometacarpal ligaments. An additional pitfall is failure to recognize
the existence of a vascular component within this syndrome.

The radial nerve travels along the posterior aspect of
the middle third of the humerus in a diagonal course between the
lateral and medial heads of the triceps. At the distal third of the
humerus, the nerve pierces the lateral intermuscular septum and then
travels anteriorly and distally between the brachialis and
brachioradialis muscles. Just proximal to the elbow, the nerve
bifurcates into superficial and deep branches. The superficial branch,
the sensory division, continues distally, traveling between the
brachioradialis and supinator muscles. The posterior interosseous
(deep) branch, essentially a purely motor nerve, passes between the two
heads of the supinator muscle under an inverted fibrous arch, the
arcade of Frohse, which is formed by the thickened edge of origin of
the superficial head and is seen readily (Fig. 52.51) (55). It continues beneath the supinator muscle, exiting under its

distal edge. The PIN innervates the muscles of the posterior forearm (Fig. 52.52).

There are five classic potential compression sites of the PIN (Fig. 52.53).
Just proximal to the radiocapitellar joint, after branching from the
radial nerve, the PIN travels through fibrous tissue that is associated
with the anterior capsule of the radiocapitellar joint. This fibrous
tissue may form bands that can cause constriction of the nerve (37).
The nerve continues distally and is crossed by the leash of Henry,
small radial recurrent vessels that have been reported to be a source
of compression (70). The fibrous leading edge
of the extensor carpi radialis brevis (ECRB) muscle travels diagonally
across the proximal edge of the supinator muscle and can cause
compression of the PIN just prior to its entrance under the arcade of
Frohse (70,107,118).
The edge of the ECRB and the fibrous arcade of Frohse, the thickened
proximal edge of the supinator muscle, are the most common sites of
compression in PIN syndrome (Table 52.16). The
nerve wraps around the proximal radius between the two heads of the
supinator and may also be compressed as it exits from beneath the
superficial head on its distal margin of this muscle.

Other causes of PIN compression include space-occupying lesions such as lipomas (103) and ganglions (77,93), radiocapitellar synovitis in patients with rheumatoid arthritis (78,147), fractures of the radial neck, and dislocations of the radial head (80).
PIN compression may also be iatrogenic, as after internal fixation of
fractures of the proximal radius, in which the nerve is extremely
vulnerable because it may lie directly on the periosteum opposite the
tuberosity of the radius (Fig. 52.54) (120).

The PIN syndrome is purely motor. Onset is usually
insidious. There may be a history of trauma to the radial head or neck.
Symptoms include weakness of the PIN-innervated muscles, and pain but
not sensory dysfunction. The bra-chioradialis and the ECRL are not
involved because they are innervated by the radial nerve. The ECRB may
be spared because its innervation may originate more proximally, or it
may appear to arise from the superficial bifurcation

of the radial nerve (Fig. 52.51).
The complete syndrome involves loss of extension of all digits and of
the extensor carpi ulnaris. The patient can dorsiflex the wrist but
with radial deviation. Middle and distal digital joints may still be
extended through their intact intrinsics. Partial syndromes may involve
just the extensor digitorum communis (EDC), with extension of the thumb
and index finger preserved (Fig. 52.55). Early
in the compression syndrome, a less striking clinical picture may
exist, with paresis or paralysis of isolated digits. Patients with
rheumatoid

arthritis
may present the same attitude of the hand whether the cause is a PIN
compression or rupture or dislocation of the EDC tendons. A careful
examination assists the clinician in differentiating between these two
entities (76,78).

Diagnostic studies include routine radiographs of the
elbow, especially in cases of trauma or arthritis. Soft-tissue masses
may stretch or compress the PIN near the proximal radius. Functional
loss of finger extension may be present, even though the patient is
completely unaware of the presence of a mass. MRI examinations are
extremely helpful in these patients, for preoperative evaluation of the
size, shape, and location of the mass. Electrodiagnostic studies are
imperative. The EMG portion of the examination is usually diagnostic (Table 52.17).

Patients rarely present with acute PIN syndrome except
in cases of trauma. In cases of fracture or dislocation, follow
management algorithms for treatment of such injuries complicated by
nerve dysfunction. In the rare case of acute onset of PIN without
injury, rule out the presence of a mass. In the absence of fracture,
dislocation, or tumor, the patient can be evaluated with EMG studies
and observed for 6–8 weeks. During this time, we recommend NSAIDs,
maintaining joint mobility to prevent contracture, and avoidance of
activities requiring repetitive or forceful elbow or wrist flexion and
extension and forearm pronosupination. Splinting of the wrist in slight
extension alone will often improve function of the hand markedly.
Additional dynamic splinting for MP joint extension aids in opening the
hand for grasp, but the splint itself may be cumbersome and interfere
with activities. Failure to improve clinically or electromyographically
in 6–8 weeks is an indication for operative treatment.

Surgical decompression for the treatment of PIN syndrome produces good to excellent results in 85% of patients (54).
Patients generally recover motor function, although improvement may
take 18 months to complete. If the paralysis has been longstanding
(more than 12–18 months), so that end organ innervation of the muscle
has atrophied, there will be residual loss or inadequate recovery.
These patients can be treated with appropriate tendon transfers (see Chapter 55 on radial nerve palsy) (54).

Be prepared to address concomitant fractures and
dislocations. You must delineate the sizes and locations of masses to
optimize the choice of approach. This requires a preoperative MRI. In
cases of suspected malignancy, perform a metastatic workup and choose a
treatment appropriate for the neoplasm. In patients with rheumatoid
arthritis and radiocapitellar disease, radial head excision may be
indicated.

There are several approaches to the radial nerve in the
proximal forearm. Use the one that allows complete visualization of the
potential compression sites of the nerve and that allows treatment of
any associated conditions. Three popular approaches are the
anterolateral extensile, posterior, and brachioradialis
muscle–splitting approaches. Perform the surgery under tourniquet
control and regional or general anesthetic.

After decompression of the nerve, release the tourniquet
and obtain hemostasis. Do not close any deep structures except as noted
for the brachioradialis-splitting technique. Suture the skin in layers.
Apply a padded dressing and a long-arm splint with the forearm in
supination and with the elbow flexed 90°.

Immediately postoperatively, encourage shoulder and
finger range-of-motion exercises. Because these approaches are carried
out between anatomic planes, you may discontinue immobilization as
early as 3–5 days and no later than 7–10 days. Depending on individual
patient recovery, slings or wrist splints may be used for up to 3 weeks
for comfort. Formal therapy for strengthening and range of motion is
not routinely implemented but should be used when the patient is slow
to progress. Return-to-work time is influenced by the severity of the
syndrome and the particular job demands.

In addition to the pitfalls common to other entrapment
syndromes, differentiation of the PIN syndrome from extensor tendon
ruptures or dislocations in the patient with rheumatoid arthritis is
important. Make this distinction by performing a tenodesis test. When
the wrist is passively flexed, the fingers will not extend at the MP
joints if the tendons are ruptured. If the tendons are intact, as in
PIN syndrome, extension of the MP joints will occur as the wrist falls
into flexion.

Avoid forceful dissection between the supinator muscle
and the extensor digitorum, because this will jeopardize the
innervation of the EDC muscle. Identification and resection of a
portion of the fibrous leading edge of the ECRB where it crosses the
PIN, as well as separate division of the arcade of Frohse, are critical
because these are the common sites of compression of the nerve.
“Recurrence,” or rather failure of operative treatment, is caused by
incomplete decompression of the nerve at all the potential sites of
entrapment.

The radial tunnel is the region along the course of the
radial nerve and its posterior interosseous (deep) branch, beginning
proximally where the radial nerve lies deep between the brachioradialis
and the brachialis, and extending distally to the distal border of the
supinator muscle (107). The five sites of compression are the same as those for PIN syndrome (97,107), easily remembered by the mnemonic FREAS (Table 52.16).
Unlike in PIN syndrome, the compression of the PIN in RTS is not caused
by masses, fractures, and disturbances of the radiocapitellar joint. It
is associated with repetitive elbow flexion and extension and forearm
rotation. It is likely a dynamic form of compression of the PIN (57).

Radial tunnel syndrome is a painful condition, without
motor deficit and usually without sensory changes. Patients present
with a dull, aching or burning pain over the lateral aspect of the
elbow in the region of the proximal extensor–supinator muscle mass.
Symptoms may radiate distally along the course of the extensor muscles
to the radial aspect of the hand or proximally to the shoulder. In some
cases, there may be paresthesias in the radial nerve distribution.
Symptoms are worsened by activities, especially those requiring
forceful and repetitive elbow motion or wrist flexion and extension and
forearm pronosupination, and are relieved by rest. The association
between lateral epicondylitis, or “tennis elbow,” and RTS has been
noted (107,141).
Patients may present with tennis elbow symptoms and evidence of lateral
epicondylitis, which may respond to local steroid injections followed
by localization of discomfort several centimeters distal to the lateral
epicondyle over the radial tunnel. The resultant RTS can then exist
solely or concurrently with the tennis elbow; 5% of patients with
lateral epicondylitis also have RTS (128). The diagnosis of RTS is differentiated from tennis elbow by examination.

Physical examination will reveal tenderness centered
over the radial head and neck along the course of the radial nerve.
Comparison of the opposite, unaffected side is recommended because many
normal individuals find this area exquisitely tender to deep palpation.
Distal radiation of symptoms can occur with manual compression of

the
nerve in this region. Limitation of elbow extension and weakness of
grip further suggest RTS. Sensory deficits in the distribution of the
superficial radial branch may be seen in RTS and suggest compression of
the nerve in the proximal aspect of the tunnel at a point where both
divisions of the main trunk are simultaneously vulnerable, such as
beneath the fibrous bands proximal to the arcade of Frohse. Because of
its dynamic or exertional nature, provocative testing is invaluable in
detecting RTS and may give clues to the site of compression of the
nerve within the radial tunnel. Described provocative tests for RTS
include the elbow flexion test, the middle finger extension test (107), passive pronation of the forearm (33), and the supination test (70) (Table 52.18). In the elbow flexion test (Fig. 52.61),
ask the patient to flex his elbow against resistance. Reproduction of
pain with this maneuver indicates compression of the nerve by fibrous
bands on the capsule of the radiocapitellar joint. In the middle finger
extension test (Fig. 52.62), ask the patient to
extend his middle finger against resistance applied by you over the
proximal phalanx. Hold his forearm in full pronation and his elbow
extended. Reproduction of pain in the radial tunnel region with this
maneuver indicates entrapment of the PIN at the ECRB tendon.

Electrodiagnostic studies are not generally helpful in
diagnosis of RTS. Conduction velocities are often normal, and EMG
changes are present in patients with clinically evident weakness or
atrophy and therefore carry the diagnosis of PIN syndrome. There may be
a place for dynamic electrodiagnostic studies to detect subtle changes
in nerve function (64,100).
We believe that a localized injection of anesthetic, with or without
steroid, into the radial tunnel, which produces a PIN palsy and
relieves symptoms, is diagnostic for RTS. Localized steroid injection
may also assist in differentiating RTS from tennis elbow (Table 52.19).

Nonoperative management of RTS includes initially reducing inflammation in the area of the radial tunnel with

wrist splinting, administration of NSAIDs, and avoidance of activities
that involve forearm pronosupination. Prescribe formal hand therapy.
Administer steroid iontophoresis over the radial tunnel three times per
week for 2–3 weeks. After significant reduction in inflammation, begin
soft-tissue mobilization, gentle progressive stretching, and nerve
gliding exercises. Institute strengthening later, tailoring it so that
it does not exacerbate symptoms.

Failure to improve after 2–4 months of adequate
treatment, progressive symptoms, and the impracticality of permanent
activity modification are all indications for surgical intervention.

The relief of aching pain in the proximal forearm often occurs within the first few weeks after surgery, although

complete resolution of pain may take several months to a year. Lister et al. (70)
noted approximately 92% good to excellent results in a review of the
combined cases of three series, including their own. Jebson and Engber (57) reported 71% good results and 29% fair/poor results in their 8-year follow-up of 33 extremities in 31 patients. Ritts et al. (105)
reviewed the results of 34 cases performed over the span of 10 years.
They noted only 51% good results with surgery, and workers’
compensation cases often had an unsatisfactory result. There is no
difference in the operative results of patients with normal
preoperative electrodiagnostic studies and those with abnormal ones.
Peimer and Wheeler (97) noted that the best results were in patients whose nerves appeared normal at surgery. Ritts et al. (105) noted that the best prognostic factor for operative treatment was a good response to a preoperative injection.

The technique for decompression of the PIN in RTS is the
same as that described for PIN syndrome. Because of its simplicity and
sufficient exposure, the brachioradialis–splitting technique (107)
is preferred. If the site of compression has been well localized by
clinical methods to the arcade of Frohse, a limited skin incision may
be employed.

Apply a well-padded compression dressing from above the elbow to beyond the wrist, with the forearm and wrist in neutral.

Encourage immediate postoperative finger and shoulder
range-of-motion exercises. Remove the postoperative dressing at 5 days.
Place the arm in a sling and the wrist in a cock-up splint. Encourage
active range-of-motion exercises of the elbow and wrist so that full
range is achieved by 3 weeks postoperative. Remove the wrist splint and
sling at 3 weeks and institute therapy for elbow and wrist range of
motion if the patient is progressing slowly. If the patient is
progressing well, encourage progressive use of the upper extremity in
daily activities, but caution against forceful activities until 6 weeks
after surgery. If job demands are fairly strenuous, a strengthening
program may be prescribed under a therapist’s supervision. Return to
work is allowed at 6–8 weeks but may not be realized until

up
to 3–4 months for patients who are manual laborers. Complete recovery
can take up to a year. Job modification in conjunction with surgery may
be indicated, especially in workers’ compensation cases.

Radial tunnel syndrome is identified solely by clinical
examination and must not be overdiagnosed. Overdiagnosis leading to
incorrect treatment or overtreatment is the main cause of failure.
Lateral epicondylitis is far more common. Injections of local
anesthetic over the lateral epicondyle and more distally over the
radial tunnel are helpful in differentiating between these two entities
and in establishing the diagnosis. When the two conditions coexist and
are unresponsive to nonoperative management, treatment of the lateral
epicondylitis at the time of radial tunnel release is requisite for
maximal postoperative relief of symptoms. Postoperatively, transitory
but distressing partial paresis of the finger extensors may occur, but
it resolves spontaneously in 6–12 weeks.

The radial nerve bifurcates just proximal to the elbow,
in the interval between the brachioradialis and brachialis muscles. The
superficial sensory branch continues toward the wrist under cover of
the brachioradialis and medial to the ECRL muscle. It courses
superficially to the supinator in the proximal forearm, and then to the
PT insertion in the midforearm. In the distal third of the forearm, the
nerve pierces the antebrachial fascia between the tendons of the
brachioradialis and ECRL muscles. The nerve passes superficially to the
extensor retinaculum and divides into terminal branches to provide
cutaneous innervation to the dorsoradial aspect of the hand (Fig. 52.8).

When the forearm is in supination, the sensory branch
lies deep to the fascia, without compression from the tendons of the
brachioradialis and ECRL muscles. As the forearm pronates, the ECRL
tendon crosses beneath the brachioradialis tendon in a scissors-like
fashion, pinching or compressing the nerve (Fig. 52.64A). Palmar–ulnar deviation of the wrist places traction on the nerve (Fig. 52.64B).
Repetitive traumatization of the nerve causes swelling, which inhibits
its normal gliding through the fascia, leading to a traction injury (27).

Usually, a history of repeated, job-related forearm
pronosupination is given. Affected patients complain of pain, numbness,
tingling, and dysesthesias over the dorsoradial aspect of the hand.
Symptoms are brought on by wrist movement and are intensified when the
patient makes a tight grip with the thumb and index finger. Nighttime
awakening caused by symptoms is not common. Sensory examination reveals
alterations in moving two-point and vibratory sensation. There is no
motor dysfunction of radially innervated muscles, although grip and
pinch strength may be decreased secondary to pain. Percussion along the
course of the nerve, particularly as it emerges between the
brachioradialis and ECRL tendons, produces paresthesias. Dellon and
MacKinnon (27) described a provocative test for
eliciting symptoms in which the patient is instructed to pronate the
forearm with the elbow in extension. If within 30–60 seconds the
symptoms of paresthesias or dysesthesias are evoked or exacerbated over
the dorsal radial aspect of the hand, entrapment is confirmed (Fig. 52.65).

The entity most commonly confused with superficial
radial nerve entrapment is de Quervain’s stenosing tendovaginitis of
the first dorsal wrist compartment. Finklestein’s test (i.e., pain on
quick ulnar deviation of the hand with the patient’s thumb grasped in
the palm) is positive in both entities. The presence or absence of
swelling over the first dorsal compartment, a nerve compression test
over the course of the superficial radial nerve, and careful sensory
testing are used to differentiate these two entities. Electrodiagnostic
testing is rarely useful, although it often shows abnormalities in
conduction velocity or amplitude (27). Injury
to the LABC nerve as a source of the patient’s symptoms must also be
excluded because there is overlap in the innervation of the LABC and
the SBR nerves in the mid and distal forearm in 75% of patients (27).
Exclude it by performing serial blocks with local anesthetic. First
block the LABC nerve at the lateral arm, then block the SBR at the site
of suspected entrapment. Improvement in symptoms subsequent to the
second injection but not the first implicates the SBR as the cause (Table 52.20).

Nonoperative treatment includes avoidance of
pronosupination and radioulnar deviation of the wrist, splinting of the
wrist with or without inclusion of the thumb and forearm, and NSAIDs.
Physiotherapy, including tissue mobilization and nerve gliding
exercises, steroid iontophoresis, and progressive gentle stretching,
may be helpful. Administer steroid injections subfascially, and use
them judiciously

because
of the potential for depigmentation of the skin and subcutaneous fat
atrophy. Patients with long-term symptoms or onset of symptoms
associated with a fracture or crush injury tend not to improve with
nonoperative treatment.

Failure to improve, or inadequate improvement, after prolonged nonoperative treatment is an indication for surgery.

In the series reported by Dellon and MacKinnon (27),
pain relief was good or excellent in 86% of patients undergoing
surgery. Of these patients, 43% returned to their regular jobs, 22%
returned to modified work, and 35% remained disabled because of
associated injuries. Objectively, marked improvement was noted in grip
and pinch strength.

Remove the postoperative dressing after 7–10 days. We
discourage splinting. Begin a home program of scar therapy and tissue
mobilization. Encourage the patient to use the hand progressively in
regular activities.

As with the majority of compression neuropathies,
accurate diagnosis and good surgical technique will prevent
complications. You must differentiate between SBR entrapment and de
Quervain’s tendovaginitis by physical examination. If concomitant de
Quervain’s exists, treat it appropriately. Exclusion of entrapment of
the LABC nerve by differential anesthetic blocks is also imperative.
Avoid excessive handling of the nerve at surgery to prevent neuroma
formation.