Entrapment Neuropathies

John D. England, MD
Chairman of Neurology and Director of Neurosciences
Department of Neurosciences
Deaconess Billings Clinic
2825 8 th Avenue North
Billings, Montana 59107 USA
Telephone: 406.238.2280
Fax: 406.238.2805
Email: jengland@billingsclinic.org

Summary
Entrapment neuropathies occur when nerves are chronically compressed or mechanically injured at
specific locations. Some of these focal neuropathies such as carpal tunnel syndrome are common
and others such as neurogenic thoracic outlet syndrome are rare. This article highlights recent
advances and interesting observations that cover a wide spectrum of such focal neuropathies.
Selected disorders which can affect individual peripheral nerves and masquerade as "entrapment
neuropathies" are also emphasized.
Introduction
The term entrapment neuropathies refers to isolated peripheral nerve injuries occurring at specific
locations where a nerve is mechanically constricted in a fibrous or fibro-osseous tunnel or
deformed by a fibrous band.
In some instances the nerve is injured by chronic direct
compression, and in other instances angulation or stretching forces cause mechanical damage to
the nerve. Common examples of nerve compression in a fibro-osseous tunnel are the carpal
tunnel syndrome and ulnar neuropathy at the cubital tunnel. Angulation and stretch injury are
important mechanisms of nerve injury for ulnar neuropathies associated with gross deformity of
the elbow joint (tardy ulnar palsy) and neurogenic thoracic outlet syndrome.
Recurrent
compression of nerves by external forces may also cause focal nerve injuries such as ulnar
neuropathy at the elbow and deep branch lesions of the ulnar nerve in the hand. Although these
latter neuropathies do not satisfy the strict definition of entrapment neuropathies, they are often
considered in a discussion of the topic. The pathological features of all of these isolated
neuropathies include a varying combination of focal demyelination and wallerian axonal
degeneration (1, 2).
There are several well-written monographs on this topic, and readers are referred to these for a
comprehensive review of the subject (3, 4).

Carpal tunnel syndrome

Carpal tunnel syndrome (CTS) due to entrapment of the median nerve within the carpal tunnel is
the most common entrapment neuropathy. The clinical diagnosis of CTS is generally straight
forward, but should be confirmed with electrodiagnostic studies.
The combination of
electrodiagnostic study findings and symptom characteristics provides the most accurate diagnosis

of carpal tunnel syndrome (5 - 7). There is abundant scientific evidence that nerve conduction
studies (NCSs) add a high degree of sensitivity (>85%) and specificity (>95%) to the diagnosis
of carpal tunnel syndrome (5, 6).
Most studies suggest that median sensory and mixed nerve
conduction studies are more sensitive than motor studies (6, 8). The most sensitive NCSs for the
diagnosis of carpal tunnel syndrome are the median sensory conduction measured over a short
distance (8 cm) across the wrist and techniques comparing the median sensory with ulnar sensory
or radial sensory conduction in the same hand (6).
Repetitive motion disorders defined as stresses and strains resulting from free bodily motions
with no impact involved have become commonly diagnosed work - related ailments (9). In a
1994 Bureau of Labor Statistics survey of injuries and illnesses, work - related CTS was the
most commonly reported disabling condition and accounted for more than 41% of all repetitive
motion disorders (10). Although these figures are commonly quoted as evidence supporting a
cause - and - effect relationship between work and the development of CTS, careful scrutiny of
previous studies raises questions concerning the validity of these conclusions (11). In particular,
most studies have not adequately excluded concurrent medical diseases such as diabetes mellitus,
hypothyroidism, or arthropathies that are capable of causing CTS. Atcheson and colleagues
evaluated 297 patients who had been medically certified with a work - related upper extremity
industrial illness (12). All of the patients underwent a systemic search for concurrent medical
diseases. Previously, 198 of these patients had been diagnosed as having CTS a total of 420
times in more than 1000 physician visits, yet laboratory studies to check for concomitant medical
diseases had been ordered only 25 times. Careful evaluation of these patients revealed that
medical diseases were significantly more common in those with CTS, and approximately two
thirds of these patients had either a medical illness or were obese. Diabetes mellitus and
hypothyroidism, both of which are known to be associated with CTS, were the most prevalent
concurrent medical diseases. Thus, unrecognized medical diseases capable of causing CTS were
common in this population of patients. Studies claiming an association between work and CTS
are flawed unless they account for potentially confounding medical illnesses. In view of the
significant medical and legal ramifications of work - related carpal tunnel syndrome, other
prospective controlled studies are warranted (13).
The treatment options for CTS are well known, but until recently controlled trials have not been
done. Most physicians have utilized several options for the treatment of CTS, but there is no
consensus regarding the most effective treatment. In general, conservative therapies such as wrist
splinting and steroid injection of the carpal tunnel are tried in mildly to moderately severe cases,
and surgery is utililized when conservative measures fail or when CTS is severe.
Oral
medications , especially diuretics, nonsteroidal anti - inflammatory drugs (NSAIDs), and oral
steroids are also used by many physicians. However, the effectiveness of such commonly used
oral medications is poorly known. This question was addressed in a prospective, randomized,
double - blind, placebo - controlled study of 73 patients with mild to moderate CTS confirmed
by electrodiagnostic testing (14). Patients were randomized to one of 4 treatment arms: 1) 4
weeks of placebo; 2) 4 weeks of the diuretic trichlormethiazide, 2 mg daily; 3) 4 weeks of the
NSAID tenoxicam-SR, 20 mg daily; or 4) 2 weeks of prednisolone, 20 mg daily, followed by
another 2 weeks of prednisolone, 10 mg daily. Symptoms were rated by the patients and
followed prospectively. The only clear and statistically significant improvement in symptoms
occurred in the steroid group. Thus, for patients with mild to moderate CTS, a short course of
low dose oral steroids may provide at least short - term improvement in symptoms. Whether
oral steroid treatment can provide long - term symptom relief or change the natural history of
CTS are unknown.

Of course, for persistent, progressive, or severe CTS, carpal tunnel release surgery is the
treatment of choice, and it is usually highly successful in relieving symptoms. A recent
randomized controlled trial comparing splinting vs.surgery (open release) for carpal tunnel
syndrome clearly demonstrated that surgery is more effective than splinting in the long - term
(7).
Splinting is an excellent adjunctive treatment in early cases and provides improvement in
symptoms in the short term (one month), but is less effective on a long term basis. In this
study, more patients in the surgery group improved after 3, 6, 12, and 18 months. At 18
months, the success rate was 90% in the surgery group compared to 75% for the splinting group.
Additionally, by 18 months, 41% of the patients in the splint group had required surgery for
relief of their symptoms. Thus, in the long term, treatment of CTS by open carpal tunnel
release surgery provides better outcomes than treatment with wrist splinting alone (7).
The traditional surgical approach has been to transect the transverse carpal ligament using an
open carpal tunnel release procedure. As one can see from the above noted study and other
studies, the success rate of this procedure is greater than 90 - 95% with a complication rate of
less than 3% (7, 15]. Interest in less invasive surgery led to the development of several
endoscopic procedures for carpal tunnel release. Questions have arisen as to whether the
endoscopic carpal tunnel release procedures are as good as the traditional open procedures.
Jimenez and others have now provided an extensive review of published articles on the subject of
endoscopic carpal tunnel release surgery (15). Since the procedure was first reported in 1987,
7091 patients have undergone 8068 operations (16, 17). The overall success rate has been
96.52%, with a complication rate of 2.67% and a failure rate of 2.61%. These rates are very
comparable to those of the open carpal tunnel release procedures. Additionally, in most studies
in which the open and endoscopic techniques were compared, patients who underwent the
endoscopic procedures experienced significantly less pain and returned to work and activities of
daily living earlier. The decision to perform an open or endoscopic carpal tunnel release
ultimately lies with the surgeons and depends upon their experience. When performed by
experienced surgeons on adequately selected patients, both techniques produce excellent results.
Ulnar neuropathy at the wrist
Entrapment neuropathies of the ulnar nerve are relatively common with ulnar neuropathy at the
elbow more prevalent than ulnar neuropathy at the wrist. The diagnosis of ulnar neuropathy at
the elbow is usually confirmed in a relatively straight forward manner by nerve conduction
studies; however, ulnar neuropathy at the wrist can be difficult to localize by nerve conduction
studies. The usual protocol for diagnosis of ulnar neuropathy at the wrist is the finding of
prolonged distal motor latency to the first dorsal interosseous muscle combined with a normal
dorsal ulnar sensory response and denervation on needle EMG exam restricted to ulnar
innervated hand muscles (18). A more refined technique appears to provide a more accurate
diagnosis of ulnar neuroapthy at the wrist (18). The more sensitive and specific technique is an
ulnar motor study to the first dorsal interosseous (FDI) muscle stimulating the ulnar nerve at the
wrist and palm. The finding of conduction block or slow wrist palm FDI CV (<37m/s) was
present in 19/20 (ie, 95%) of patients with clinically defined ulnar neuropathy at the wrist. The
performance of this relatively simple technique significantly improves the electrodiagnostic
accuracy for the diagnosis of ulnar neuropathy at the wrist.
Thoracic outlet syndrome
The spectrum of thoracic outlet syndrome remains a controversial topic. Some authors believe
that this entity accounts for a relatively large group of patients who experience pain, paresthesias,
and dysfunction of the arm and hand (19). Others acknowledge that thoracic outlet syndrome
exists but suggest that it accounts mainly for the small group of patients who have objective

clinical and electrophysiological deficits compatible with a lower trunk brachial plexopathy (20).
This latter clinical picture is called true thoracic outlet syndrome or the classic or undisputed
form of neurogenic thoracic outlet syndrome. In most cases of neurogenic thoracic outlet
syndrome an anomalous congenital ligamentous band stretches between a long C7 transverse
process (sometimes long enough to be a rudimentary cervical rib) and the first thoracic rib. This
ligamentous band chronically injures the C8 and T1 root- derived motor and sensory fibers as
they pass over it before forming the lower trunk of the brachial plexus (21). The well known
electrophysiological findings of this disorder consist of chronic denervation in the C8 - T1
distributions with nerve conduction studies (NCSs) showing decreased ulnar sensory and median
motor amplitudes, a less affected ulnar motor amplitude, and normal median sensory amplitudes
(21, 22). Recent observations by Levin and colleagues have refined the electrophysiological
picture of neurogenic thoracic outlet syndrome and contrasted it with median sternotomy - related
brachial plexopathy (22). These authors studied 10 patients with neurogenic thoracic outlet
syndrome and 14 patients with sternotomy - related brachial plexopathy. They utilized standard
electrophysiological techniques, and also performed medial antebrachial cutaneous NCSs on all
patients. In the patients with neurogenic thoracic outlet syndrome, the medial antebrachial
cutaneous amplitude was the most affected, followed in decreasing order of involvement by the
median motor, ulnar sensory, and ulnar motor amplitudes.
Thus, the medial antebrachial
cutaneous amplitude was the most sensitive NCS in the electrodiagnosis of neurogenic thoracic
outlet syndrome, followed by the median motor amplitude. Although the ulnar sensory amplitude
was almost always decreased also, it was less affected than the medial antebrachial cutaneous
response. Conversely, the ulnar sensory and motor amplitudes were most affected in the patients
with sternotomy - related brachial plexopathy. Taken together, these data suggest that there is
predominant involvement of T1 fibers in the neurogenic thoracic outlet syndrome, whereas there
is predominant involvement of C8 fibers in sternotomy - related brachial plexopathy. As such,
the lesions of these disorders are likely at the level of the anterior primary rami of the distal C8
and T1 roots proximal to the formation of the lower trunk of the brachial plexus.
Unusual compressive and entrapment neuropathies
Occasionally nerve injuries are secondary to uncommon causes. Many of these are preventable
or treatable, and are worth knowing. Hypoglossal nerve palsies are occasionally due to mass
lesions such as a tumor, but other compressive processes are unusual. Stricker and colleagues
reported the case of a 7 - year old girl with a hypoglossal nerve palsy secondary to deep
cervical lymphadenitis (23). CT scan revealed a contrast - enhancing lymph node in the
retropharynx at the level of C2.
After a one week course of antibiotic treatment, the
lymphadenopathy regressed Over the next few months the hypoglossal neuropathy resolved
completely.
We all know that exercise is good for you, but some people take things to extremes. Such is
the case with four bodybuilders who developed rare upper extremity mononeuropathies (24). All
four athletes used anabolic steroids and were well - muscled. Each bodybuilder sustained an
isolated mononeuropathy affecting either the thoracodorsal, dorsal scapular, suprascapular, or
medial pectoral nerves. The nerves were likely stretched or compressed between osteofibrous
surfaces and hypertrophied muscles. At one year there was partial improvement in two cases and
complete recovery in the other two.
Although most "traumatc" brachial plexopathies have an immediate onset, some orthopedic
injuries of the shoulder or clavicle can cause delayed nerve injury secondary to progressive bony
deformities and nerve entrapment. England and Tiel reported a patient who sustained a midshaft
clavicular fracture and several months later developed a severe brachial plexopathy (25). An

exuberant callus associated with the clavicular fracture acted as a mass lesion to compress the
brachial plexus within the costoclavicular space (i.e., between the clavicle and the first rib).
Electrophysiological features were very helpful in suggesting the diagnosis, which was
subsequently confirmed by MRI studies and surgical exploration. Surgical excision of the callus
and freeing of the entrapped brachial plexus resulted in marked improvement of the patient's
condition. Physicians should be aware of the possibility of delayed brachial plexopathy after
fractures of the clavicle and, accordingly, should advise patients with fractured clavicles to report
promptly any neurological symptoms.
Neuropathies masquerading as entrapment neuropathies
Occasionally, other disorders of peripheral nerve can mimic entrapment neuropathies. Such
conditions are important to recognize since the pathophysiology of these neuropathies is intrinsic
to peripheral nerves, and they do not require surgical therapy. One such neuropathy is hereditary
neuropathy with liability to pressure palsies (HNPP).
This autosomal dominant inherited
neuropathy is most commonly due to a 1.5 megabase (Mb) deletion on chromosome 17p11.2
which encompasses the gene for the peripheral myelin protein PMP22 (26 28). A few cases
are due to a frame shift mutation in the PMP22 gene (26). This disease commonly presents with
recurrent transient sensorimotor neuropathies that are typically painless. Nerve conduction studies
often demonstrate focal conduction slowing, abnormal temporal dispersion, or conduction block
localized to common entrapment sites. A high index of suspicion is required for the diagnosis of
this disease, but a history of recurrent focal mononeuropathies, brachial plexopathy, and
electrophysiological abnormalities of multiple nerves as well as a family history are keys to the
diagnosis. These patients do not usually require surgical interventions, and the genetic test for
the PMP22 deletion is commercially available.
Two other peripheral nerve diseases that have been misdiagnosed as entrapment neuropathies are
multifocal motor neuropathy and neuralgic amyotrophy. Such misdiagnosis should rarely occur
since the nerve involvement in either of these disorders is rarely at sites of common nerve
entrapment. Multifocal motor neuropathy usually presents with slowly progressive focal weakness
and atrophy without pain or sensory complaints. Most commonly, there is focal or multifocal
involvement of the upper extremity motor nerves in the forearm or upper arm.
Electrophysiologically, there is focal slowing and conduction block of motor nerve fibers within
nerve segments, but they are not at common entrapment sites, and sensory nerve conduction
studies are normal (29, 30). The treatment of this disease is high - dose intravenous immune
globulin (31).
Neuralgic amyotrophy usually presents with pain in the shoulder girdle or arm, which is followed
by focal or multifocal neuropathic deficits (32). Although many individual nerves can be
affected, nerve lesions rarely occur at sites of common nerve entrapment.
Additionally,
electrophysiologically the nerve lesions are predominantly axonal -loss and multifocal in variety.
Because the disorder can occur after surgery or childbirth, the nerve lesions may be erroneously
ascribed to compression or stretch injuries. Some of the nerve lesions of neuralgic amyotrophy
such as anterior interosseous nerve palsy can be mistaken for "entrapment neuropathies". In such
cases making a diagnosis of neuralgic amyotrophy is important since this will likely save the
patient from an unnecessary surgical procedure. When evaluating a patient with focal or
multifocal nerve deficits in the upper extremity (particularly if preceded by "neuralgic" type pain),
one should at least consider neuralgic amyotrophy as a possible diagnosis. Once considered in
the differential diagnosis, thorough clinical and electrophysiological examinations will generally
provide the appropriate answer.

Imaging the peripheral nervous system

Presently, determinating the presence, the location, and the type of nerve injury is based upon the
neurological exam and electrophysiological studies. In experienced hands these methods have
high reliability, and will not soon be replaced by any technological advancements. However,
imaging the peripheral nervous system using magnetic resonance (MR) imaging techniques will
likely play an increasing role in the evaluation of diseases of the peripheral nervous system.
Already, MR imaging is extraordinarily useful in evaluating brachial and lumbosacral
plexopathies, especially when looking for neoplastic or other mass lesions which injure neural
structures (25, 33). High - resolution MR imaging of nerves is improving rapidly secondary to
advances in phased - array radiofrequency (RF) coil technology and more rapid acquisition of
imaging data (33. 34). Currently, with fat suppressed T2 - weighted, spin - echo imaging at
1.5T, individual fascicles within normal large nerves can be seen (33). Tumors, ganglion cysts,
and other lesions affecting individual peripheral nerves can also be seen (33, 35, 36). In
entrapment and compressive neuropathies, localized abnormal increases of the T2 signal can be
seen within the injured segments of nerves (33, 35). With further refinements MR nerve imaging
should be very helpful in confirming the diagnosis of entrapment neuropathies, eliminating the
possibility of mass lesions, and planning surgical therapy.
MR imaging of skeletal muscle should also become increasingly useful. Denervation of muscle
results in early MR signal intensity changes (high T2 -weighted signal) within the muscle itself
(37). Short inversion time inversion - recovery (STIR) images are very sensitive in showing
increased signal intensity in denervated muscles (38). Interestingly, denervated muscles can show
these MR signal changes as early as 2 to 4 days after nerve injury (37). The basis for these
increased signal intensities is not known, but experimentally they correlate best with increases in
extracellular water content (37, 38).
Thus, high - resolution MR nerve imaging is likely to become an increasingly useful modality in
the evaluation of peripheral nerve injuries. With higher - field strength magnets and further
improvements in radiofrequency (RF) coil technology, MR imaging of nerve should become much
better. Improvements in pulse sequence design may also make possible the application of
physiological or functional imaging techniques.
The next century should see tremendous
developments in this next frontier in neuroimaging (34).
Conclusions
Entrapment neuropathies are one of the most prevalent disorders of the peripheral nervous system.
Recent studies have helped clarify the diagnosis and treatment for many of these neuropathies.
The ability to recognize nerve entrapment syndromes and to distinguish them from other diseases
of peripheral nerve are important clinical skills. Although clinical and electrophysiological
assessments remain important in the diagnosis of neuropathies, advances in neuroradiology are
likely to make imaging of peripheral nerves an increasingly valuable ancillary diagnostic tool.

References and recommended reading

1.

Gilliatt RW. Chronic nerve compression and entrapment. In: The Physiology of Peripheral
Nerve Disease. 1st Edition. Edited by Sumner AJ. Philadelphia: WB Saunders Company;
1980. pp. 316-339.

2.

Thomas PK, Holdorff B. Neuropathy due to physical agents. In: Peripheral Neuropathy.
3rd Edition. Edited by Dyck PJ, Thomas PK, Griffin JW, Low PA, Poduslo JF (editors).
Philadelphia: WB Saunders Company; 1993. pp. 990-1013.

3.

Stewart JD. Focal Peripheral Neuropathies. 3rd Edition. Philadelphia: Lippincott Williams
& Wilkins; 2000.

4.

Kline DG, Hudson AR. Nerve Injuries. Operative Results for Major Nerve Injuries,
Entrapments, and Tumors. 1st Edition. Philadelphia: WB Saunders Company; 1995.

5.

Rempel D., Evanoff B., Amadio P.C., de Krom M., Franklin G., et. al. Consensus criteria
for the classification of carpal tunnel syndrome in epidemiological studies. Am J Public
Health 1998; 88:1447-1451.

6.

Jablecki C.K., Andary M.T., Floeter MK, Miller R.G., Quartly C.A., Vennix M.J., Wilson
J.R. Practice parameter: Electrodiagnostic studies in carpal tunnel syndrome. Report of the
American Association of Electrodiagnostic Medicine, American Academy of Neurology, and
the American Academy of Physical Medicine and Rehabilitation. Neurology 2002; 58:15891592.

7.

Gerritsen A. A. M., de Vet H. C. W., Scholten R. J. P. M., Bertelsmann F. W., de Krom

M. C. T. F. M., Bouter L. M. Splinting vs surgery in the treatment of carpal tunnel
syndrome. JAMA 2002; 288:1245-1251.

8.

Scelsa, Herskovitz S, Bieri P, Berger, AR. Median mixed and sensory nerve conduction
studies in carpal tunnel syndrome. Electroenceph Clin Neurophysiol 1998; 109:268-273.

9.

Work Injuries and Illnesses by Selected Characteristics, 1992. Washington, DC.

Labor Statistics 1994; US Dept of Labor publication: 94-213.

10.

Characteristics of Injuries and Illnesses Resulting in Absences from Work, 1994.

Washington, DC. Bureau of Labor Statistics 1996; US Dept of Labor publication: 96-163.

11.

Nathan PA, Keniston RC, Myers LD, Meadows KD, Lockwood RS. Natural history of
median nerve sensory conduction in industry: Relationship to symptoms and carpal tunnel
syndrome in 558 hands over 11 years. Muscle Nerve 1998; 21:711-721

12.

Atcheson SG, Ward JR, Lowe W. Concurrent medical disease in work - related carpal
tunnel syndrome. Arch Intern Med 1998; 158:1506-1512.

13.

Yocum DE. The many faces of carpal tunnel syndrome. Arch Intern Med 1998; 158:1496.

14.

Chang MH, Chiang HT, Lee SSJ, Ger LP, Lo YK.

syndrome. Neurology 1998; 51:390-393.

Bureau of

Oral drug of choice in carpal tunnel

15.

Jimenez DF, Gibbs SR, Clapper AT. Endoscopic treatment of carpal tunnel syndrome: a
critical review. J Neurosurg 1998; 88:817-826.

16.

Okutsu I, Ninomiya S, Natsuyama M, et al. Subcutaneous operation and examination under

universal endoscope. J Jpn Orthop Assoc 1987; 61:491-498.

17.

Okutsu I, Ninomiya S, Takatori Y. Results of endoscopic management of carpal tunnel

syndrome. Orthop Rev 1993; 22:81-87.

18.

Cowdery S. R., Preston D. C., Herrmann D. N., Logigian E. L. Electrodiagnosis of ulnar

neuropathy at the wrist. Neurology 2002; 59:420-427.

19.

Roos DR. Thoracic outlet syndrome is underdiagnosed. Muscle Nerve 1999; 22:126-129.

20.

Wilbourn AJ.
136.

21.

Gilliatt RW, LeQuesne PM, Logue V, Sumner AJ. Wasting of the hand associated with a
cervical rib or band. J Neurol Neurosurg Psychiatry 1970; 33:615-624.

22.

Levin KH, Wilbourn AJ, Maggiano HJ. Cervical rib and median sternotomy - related
brachial plexopathies. A reassessment. Neurology 1998; 50:1407-1413.

23.

Stricker T, Steinlin M, Willi UV, Nadal D. Hypoglossal nerve palsy associated with deep
cervical lymphadenopathy. Neurology 1998; 50:1926-1927.

24.

Mondelli M, Cioni R, Federico A.

Rare mononeuropathies of the upper limb in
bodybuilders. Muscle Nerve 1998; 21:809-812.

25.

England JD, Tiel RL. AAEM case report 33: Costoclavicular mass syndrome.
Nerve 1999; 22:412-418.

26.

Lenssen PPA, Gabreels-Festen AAWM, Valentijn LJ, Jongen PJH, van Beersum SEC, van
Engelen BGM, et al. Hereditary neuropathy with liability to pressure palsies. Phenotypic
differences between patients with the common deletion and a PMP22 frame shift mutation.
Brain 1998; 121:1451-1458.

27.

Pareyson D, Solari A, Taroni F, Botti S, Fallacia E, Scaioli V, et al. Detection of

hereditary neuropathy with liability to pressure palsies among patients with acute painless
mononeuropathy or plexopathy. Muscle Nerve 1998; 21:1686-1691.

28.

Stogbauer F, Young P, Kerschensteiner M, Ringelstein EB, Assmann G, Funke H.

Recurrent brachial plexus palsies as the only clinical expression of hereditary neuropathy
with liability to pressure palsies associated with a de novo deletion of the peripheral myelin
protein - 22 gene. Muscle Nerve 1998; 21:1199-1201..

29.

Parry GJ, Clarke S. Pure motor neuropathy with multifocal conduction block masquerading
as motor neuron disease. Muscle Nerve 1988; 11:103-109.

Thoracic outlet syndrome is overdiagnosed.

Muscle Nerve 1999; 22:130-

Muscle

30.

Beydoun SR. Multifocal motor neuropathy with conduction block misdiagnosed as multiple
entrapment neuropathies. Muscle Nerve 1998; 21:813-815.

31.

Chaudhry V, Corse A, Cornblath DR, Kuncl RW, Drachman DB, Freimer ML, et al.
Multifocal motor neuropathy: response to human immune globulin. Ann Neurol 1993;
33:237-242.

32.

England JD. The variations of neuralgic amyotrophy. Muscle Nerve 1999; 22:435-436.

33.

Maravilla KR, Bowen BC. Imaging of the peripheral nervous system: Evaluation of
peripheral neuropathy and plexopathy. Am J Neurorad 1998; 19:1011-1023.

34.

Quencer RM. The next frontier in neuroradiology: Imaging the peripheral nervous system.
Am J Neurorad 1998; 19:1001.

35.

Loredo R, Hodler J, Pedowitz R, Yeh L-R, Trudell D, Resnick D. MRI of the common
peroneal nerve: Normal anatomy and evaluation of masses associated with nerve entrapment.
J Comput Assist Tomogr 1998; 22:925-931.

36.

Uetani M, Hashmi R, Hayashi K, Nagatani Y, Narabayashi Y, Imamura K. Peripheral

nerve intraneural ganglion cyst: MR findings in three cases. J Comput Assist Tomogr
1998; 22:629-632.

37.

Helms CA, Martinez S, Speer KP. Acute brachial neuritis (Parsonage-Turner syndrome):
MR imaging appearance - report of three cases. Radiology 1998; 207:255-259..

38.

Grainger AJ, Campbell RSD, Stothard J. Anterior interosseous nerve syndrome: Appearance
at MR imaging in three cases. Radiology 1998; 208:381-384.

Entrapment Neuropathies
Nerve
Carpal tunnel syndrome
(Median nerve at wrist)

Proximal median nerve at

elbow

Pathology
Flexor tenosynovitis (most
common); ganglion;
hypothyroidism;
pregnancy; acromegaly;
tumors (rare)
Supracondylar
spurs/ligaments; fibrous
bicipital aponeurosis;
pronator teres syndrome

Anterior interosseous
nerve

Fibrous bands; anomalous

muscles; ganglion; tumor

Ulnar nerve at elbow

External compression in
condylar groove;
compression within cubital
tunnel by aponeurosis of
flexor carpi ulnaris
External compression;
ganglion; tumor

Ulnar nerve at wrist

Radial nerve in upper arm

External compression in
spiral groove; fractures of
humerus; compression by
triceps muscle

Posterior interosseous
nerve

Entrapment in the
supinator muscle (arcade
of Frohse);
fractures/dislocations of
radius; tumors; fibrous
bands

Sciatic nerve

Trauma/compression in
gluteal/sciatic notch
region; hip arthroplasty;
piriformis syndrome
(controversial)

Common peroneal nerve

at knee

Compression at knee;
traction injury from ankle
sprains

Diagnosis
EMG-focal slowing of
median n. across wrist

EMG-focal slowing of
median n. at elbow;
denervation of median
forearm and hand muscles
May need X-ray,CT scan,
or MRI
EMG-denervation of
flexor digitorum
profundus(I-II), flexor
pollicis longus, pronator
quadratus
May need X-ray, CT
scan, or MRI
Important to distinguish
from neuralgic amyotrophy
EMG-focal slowing of
ulnar n. across elbow;
denervation of ulnar
forearm and hand muscles
EMG-focal slowing of
ulnar nerve across wrist;
denervation of ulnar hand
muscles
May need X-ray, CT
scan, or MRI
EMG-focal slowing of
radial nerve in upper arm;
denervation of radial
muscles in forearm with
sparing of triceps muscle
May need X-ray. CT
scan, or MRI
EMG-denervation of radial
forearm muscles distal to
extensor carpi radialis; no
deficit of cutaneous
sensation
May need X-ray, CT
scan, or MRI
EMG-denevaton in both
peroneal and tibial nerve
divisions (peroneal often
more affected)
May need X-ray, CT
scan, or MRI
EMG-denervation in
peroneal muscles below
the knee

Therapy
*Conservative vs. surgery;
surgery highly effective
when needed. CT release
better outcome than wrist
splinting (JAMA, 2002)
*Conservative vs. surgery;
usually requires surgery if
progressive or severe

*Conservative vs. surgery;

usually requires surgery if
progressive or severe

*Conservative vs. surgery;

may require surgery if
progressive or severe

*Conservative vs. surgery;

may require surgery if
progressive or severe

*Conservative vs. surgery;

may require surgery if
progressive or severe

*Conservative vs. surgery;

may require surgery if
progressive or severe

*Conservative vs. surgery;

may require surgery if
progressive or severe

*Conservative vs. surgery;

may require surgery if
progressive or severe

Tibial nerve at knee

Lateral femoral cutaneous

nerve (meralgia
paresthetica)

Masses (Bakers cysts,

ganglia); trauma to knee;
traction injury from ankle
sprains
Entrapment at inguinal
ligament (most common);
rarely masses in psoas
muscle or pelvis

Spinal accessory nerve in

posterior cervical triangle
of neck

Iatrogenic from lymph

node biopsy or other
surgery (most common);
compession from tumors

Multiple or sequential
mononeuropathies

May be compressive but

exclude: ischemic
neuropathies (vasculitides,
diabetes), hereditary
neuropathy with liability
to pressure palsy (HNPP),
neuralgic amyotrophy, etc.

EMG-denervation in tibial
muscles below the knee

*Conservative vs. surgery;

may require surgery if
progressive or severe

EMG-usually normal;
clinical sensory loss over
anterolateral thigh
CT scan or MRI if
suspect psoas or pelvic
mass
EMG-denervation in upper
trapezius
muscle;distinguish from
serratus anterior muscle
weakness due to long
thoracic neuropathy
EMG-denervation in
multiple nerve
distributions

*Conservative vs. surgery;

may require surgery if
progressive or severe

*Usually conservative
since deficit is minor;
may require surgery for
compressive mass

Medical treatment of
underlying disease

Each case must be analyzed individually. Conservative therapy is generally indicated at the
outset unless there is severe ongoing compression or severe acute entrapment in which case
surgery would be indicated. If compression/entrapment persists for several weeks with persistent
or worsening neuropathy, surgery is indicated

Therapy of Traumatic Neuropathies

Nerve lesion
Nerve transection

Nerve in
continuity
(relatively focal
lesion)

Nerve in
continuity (long
lesion)

Brachial plexus

EMG

Operative NAP

Laceration from knife,

glass, razor blade,
propeller, etc

Pathology

Not necessary
acutely

Not necessary acutely

Blunt trauma; stretch,

gunshot wounds, etc.

Serial EMG for 2

to 4 mos;
(A) axonal integrity
or regeneration =
conservative Rx;
(B) no axonal
integrity = surgery
with NAP
Serial EMG for 4
to 6 mos;
1.Axonal integrity
or regeneration =
conservative Rx;
2.No axonal
integrity = surgery
with NAP
Serial EMG for 4
to 6 mos;
3.Axonal integrity
or regeneration =
conservative Rx;
4.No axonal
integrity = surgery
with NAP

Blunt trauma; stretch,

gunshot wounds, etc.

Transection requires
early operation;
Blunt trauma treated as
nerve in continuity
(long lesion)

Therapy
Early operation (72
hrs):
(A) If sharp
laceration repair
by end to end suture
(B) If blunt
laceration
secondary repair 2
to 4 weeks later
(C) If nerve intact
conservative therapy
(as below)

At surgery:
NAP present
NAP absent

At surgery:
NAP present
NAP absent

Each part of plexus

requires NAP:
NAP present
NAP absent
Important to
determine the most
proximal lesion(s)
since root avulsion
not helped by surgery

Simple neurolysis or
split repair
Resection and repair
(often with graft)

Simple neurolysis or
split repair
Resection and repair
(often with graft)

Simple neurolysis or
split repair
Resection and repair
(often with graft)

Research Areas in Nerve Injury

Graft Conduits
Graft

Pros

Autologous nerve

Best current conduit;

Relatively easy to obtain;
No rejection

Autologous combined vein muscle

Possibly as good or superior to

nerve grafts;
Relatively easy to obtain;
No rejection
Good axonal regeneration over short
distances;

Synthetic tubular Silicone

Synthetic tubular Bioabsorbable

Unlimited supply
Potential is great;

Cons
Axonal regeneration is limited;
Fibrosis;
Availability limited to a few
nonessential sensory nerves (eg,
sural, superficial sensry radial,
lateral antebrachial cutaneous)
Experimental;
Axonal regeneration is limited;
Fibrosis;
Experimental;
Irritation with fibrosis may require
re-operation
None available currently

Probably would cause little

irritation

Research Areas in Nerve Injury

*Molecular Factors
Class
Neurotropjic Factors and
Chemoattractants

Chemorepellent Factors

Inhibitors of Connective Tissue

Formation

Agent(s)
Ciliary neurotrophic factor (CNTF)
Nerve growth factor (NGF)
Insulin-like growth factors (IGFs)
Brain-derived neurotrophic factor
(BDNF)
NT-3
NT-4
Semaphorins
Netrins
Others
Inhibitors of fibroblasts
Collagenases
Others

Action
Promote neuronal survival and
regrowth
Attract and guide axons

Selectively repel some types of

axons
Decrease fibrosis at the site of
nerve injury to promote axonal
regeneration

*Future advances in the treatment of nerve injury will rely increasingly on understanding the
molecular basis of nerve regeneration.

Research Areas in Nerve Injury

The Peripheral Nerve Basis of Pain
Class
Ion Channels

Subtype or Agent
Sodium channels

Action
Upregulation in injured axons and
neuromas may account for axonal
hyperexcitability and pain

Specific isoforms (PN1, PN3) may

be selectively upregulated in nerve
injury
Ion Channels

Chemoactive Agents (released after

nerve injury)

Sympathetic Nervous System

Receptors

Potassium channels

Bradykinin
Prostaglandins
Leukotrienes
Serotonin
Adenosine
Histamine
NGF
CGRP
Alpha adrenergic receptors

Others

Stabilize resting potential in normal

axon
Alteration in injured axons possible,
but not well studied
Some of these agents reduce
nociceptor and axonal firing
thresholds

Upregulation in injured nerve may

be linked to axonal hyperexcitability
and pain
Unknown status in nerve injury