CHAPTER 23

Peripheral Nerve Injury

Barton A. Brown

Principles oj'Neurosurgery,
edited by Robert G. Grossman. Rosenberg © 1991.
Published by Raven Press, Ltd., New York.

Incidence, 467
Etiology, 467
Pathology, 467
Symptoms, 468
Signs, 469
Natural History, 469
Diagnostic Tests, 469

Indications for Surgery, 470
Preoperative Management, 470
Operative Management, 471

Neurolysis, 471
Nerve Suture, 471
Outcome, 472

References, 472

INCIDENCE

Peripheral nerve injuries continue to be challenging
problems despite recent technical advances. Peaks of in-

terest in peripheral nerve problems occur with wars, be-
cause large numbers of cases are then concentrated for

study. However, civilian injuries in home, industry, and
recreational accidents provide another large group for
study and treatment.

Accurate figures of the incidence of peripheral nerve

injuries in civilian practice are difficult to establish be-
cause such lesions are treated by a number of specialists.
Treatment may be provided by a general, orthopedic,
plastic, hand, or neurologic surgeon. The particular spe-
cialty of the treating surgeon is unimportant as long as he
or she is well versed in the neuroanatomic and neuro-
physiologic principles and surgical techniques pertaining
to peripheral nerve injuries.

Of 1,123 admissions to an urban neurosurgical service

in a 12-month period, 45 were peripheral nerve injuries,
constituting 4 percent of admissions. In a given neurosur-
gical practice, the number might be considerably greater,
depending upon the physician's interest in such lesions.

The incidence of involvement of a specific nerve, as

recorded in a general neurosurgical practice, is illus-
trated in Table 1.

B. A. Brown: San Francisco, California 94118.

ETIOLOGY

Causes of nerve injury can be conveniently divided

into penetrating and nonpenetrating types. Penetrating
injuries usually result in partial or complete discontinu-
ity of the nerve. Examples include gunshot wounds, frac-
tures, and lacerations by glass or metal. Exceptions
would be injection palsies (1) and blast injuries from
gunshot wounds in which continuity is preserved despite
penetration.

Nonpenetrating injuries may be contusions, as from a

direct blow over the nerve; compressions, as seen with
sleep palsies, entrapments (2), compartment syndromes,
hematomas, tourniquet palsies, casts, and obstetric pal-
sies; friction injury, as in tardy ulnar palsy and certain
occupational palsies; or stretch injuries.

PATHOLOGY

On a cross section, a peripheral nerve is composed of a

multiplicity of axons surrounded by an endoneurial col-
lagenous tube. Varying numbers of axons and their in-
vesting sheaths are grouped together in fascicles by a

loose connective tissue called the perineurium. Groups
of such fascicles are bound into the entity of the mixed
peripheral nerve by the epineurium, the thickened exter-

nal layer of which constitutes the external nerve sheath.

The blood supply to a peripheral nerve has a linear

467

CHAPTER 23

TABLE 1. Frequency of injury

Nerve

Axillary

Brachial plexus
Dorsal scapular
Femoral
Gluteal
Greater auricular
Greater occipital
Hypoglossal
Ilioinguinal
Lateral femoral cutaneous

Long thoracic

Lumbosacral plexus
Median (carpal tunnel 111)

M usculocutaneous

Peroneal
Polyneuropathy

Radial
Saphenous
Sciatic
Suprascapular
Sural
Spinal accessory

Tibial

Ulnar

Total

Number

16
86

2

18

1
1
1

2

1

8

11

8

222

8

73

10

106

9

67

10

2

13
13

317

1,005

Percentage

1.6%
8.5%

1 .8%

1.1%

22.0%

7.3%

1.0%

10.5%

6.6%

1 .0%

1 .3%
1 .3%

31 .5%

distribution, with major feeding vessels entering the
nerve at different levels and distributing branches longi-
tudinally up and down the course of the nerve. Smaller
branches penetrate to the innermost portions of the

nerve.

The mixed peripheral nerve is made up of both motor

and sensory fibers, the latter subserving various types of
function. Within the nerve, the axons are generally
grouped according to anatomic distribution rather than
function. The intraneural plexuses change continually
through the course of the nerve, and cross sections of a

peripheral nerve one or more centimeters apart will

show a different pattern of fascicular arrangement (3).
Branches usually leave the main nerve trunk at an acute
angle, a factor of some importance in surgical treatment.

Sunderland has pointed out that the axonal content,

as opposed to the connective tissue content, of a periph-
eral nerve at any point in its course is variable but that it

is usually 50 percent or less and may be as low as 12
percent, as in the sciatic nerve at the sciatic notch (3).

Nerve tissues are subject to the same types of pathol-

ogy as other body tissues. They are affected by infectious,

metabolic, vascular, and traumatic lesions. In the last

category, three general types of nerve injury are recog-
nized:

1. Axonapraxia, in which the nerve loses its conductiv-

ity without any actual disruption of the axons or
nerve sheath and which may result from contusion,

entrapment, hcmatoma, or other pressure-related
phenomena in which there is no laceration of the
nerve substance;

Axonotmesis, in which the insult is severe enough to
cause Wallerian degeneration but insufficient to

disrupt the connective tissue framework of the nerve;

and

3. Neurotmesis, in which both axonal and connective

tissue elements of the nerve are disrupted.

Chronic compression, contusion, stretching, injec-

tion, or laceration of a nerve may cause vascular and
connective tissue damage and may cause edema and

hemorrhage in and about the nerve as well as axonal
damage. The result is external and internal fibrosis of the
nerve.

An injury of sufficient severity, whether caused by

contusion, compression, laceration, or injection, will
cause degeneration of the axons and their myelin sheath
distal to the site of trauma. There is also retrograde de-
generation, probably not exceeding one or two nodes of
Ranvier. The distal degeneration, fragmentation, and
phagocytosis of the axon and myelin sheath are termed

Wallerian degeneration. This degeneration occurs over a

period of approximately two to three weeks following
injury; at the end of that time, only the empty connective
tissue framework of the distal portion of the peripheral

nerve remains.

During this time an intracellular reaction is occurring

in the anterior horn cells of the spinal cord that corre-
spond to the injured axons. These cell bodies undergo a
reaction of varying severity, depending upon the extent
of injury to the peripheral nerve and the proximity of the
injury to the anterior horn cell. If an affected anterior
horn cell survives, it begins to produce axoplasm; thus,
growth of the axon from the proximal site of discontinu-
ity occurs. The regenerative process of the anterior horn

cell takes approximately three weeks before axoplasmic

flow will proceed from the site of injury. At the proximal
end of the divided nerve, axonal regrowth in combina-
tion with fibrosis will create a so-called "neuroma." The
distal end of the divided nerve will develop a bulbous

enlargement of fibrous tissue, the "glioma." A partially
divided nerve or one with chronic fibrosis will develop a

"neuroma in continuity."

The external nerve sheath has limited elasticity, and

increase in tissue elements within the nerve, either from

hemorrhage or fibrosis, can result in compression of ax-
ons. Thus, internal as well as external fibrosis may con-
tribute to nerve dysfunction.

Severe stretch injuries cause diffuse axonal and con-

nective tissue disruption along the trunks or plexuses

and seldom lend themselves to specific surgical treat-
ment.

SYMPTOMS

Peripheral nerve injury results in motor loss, sensory

loss, or both, in a distribution appropriate to the in-

PERIPHERAL NERVE INJURY / 469

volved nerve. Symptoms are paresthesias, weakness, and
pain, either intermittent or constant.

Patients will describe sensory loss in a general area and

motor loss in terms of the activities that cause them diffi-

culty. A patient with carpal tunnel syndrome, for exam-
ple, may say that "the entire hand gets numb," not just

the median nerve distribution. A patient with an ulnar
palsy will often complain of difficulty manipulating
coins and of catching the fifth finger on a pocket. A simi-
lar difficulty with manipulation of coins may be mani-
fest in a median neuropathy, but in this case the diffi-
culty will be secondary to the loss of sensation in thumb,
index, and long fingers rather than to specific loss of
dexterity, as in ulnar palsy.

Pain may be a significant symptom in certain nerve

injuries, particularly brachial plexus injuries, and in par-
tial median nerve lesions with resultant causalgia. Some-
limes pain is caused by muscular imbalance rather than
by direct insult to the nerve, as in spinal accessory nerve

palsy, with its loss of trapezius function and resultant
shoulder girdle imbalance.

SIGNS

Signs are elicited by a careful neurologic examination

with special study of the field of the injured peripheral

nerve. This examination involves testing motor power,
sensation, reflexes, and autonomic function and looking
for atrophy, fasciculations, and visible or palpable abnor-
malities on the nerve trunks. Any sign of motor deficit,

such as weakness of abduction and adduction of the

fingers in an ulnar lesion, or loss of dorsiflexion of the

foot in a peroneal palsy, should be carefully sought. Sen-
sory loss appropriate to the injured nerve is tested for
with pin, touch, and, especially in the hand, two-point

discrimination. It is helpful to have a reference text for
review of specific muscle innervation and sensory pat-

terns and to have motor and sensory examination charts

for recording the findings, as certain lesions are infre-
quently seen (4,5).

If the lesion is two or three weeks old, atrophy and

fasciculations of the muscles in the involved field may be
observed. In the limbs, the muscles should be accurately
measured as well, as described. There may be evidence of

autonomic dysfunction manifested by altered skin tem-

perature or color. Reflex changes will conform to the
appropriate nerve distribution.

Local signs should also be sought, such as tenderness

of a nerve trunk or Tinel's sign with percussion over the

nerve. Palpation of nerve trunks may reveal such lesions

as Struther's ligament, nerve tumor, or neuroma.

The examiner must be aware of trick movements and

secondary dysfunctions, as in radial nerve palsy in which
the wrist drop prevents satisfactory function of the ulnar-
innervated small hand muscles. Here the examiner must

hold the wrist in extension or place the hand on a flat
surface in order to get a more accurate evaluation of
ulnar function in the presence of radial nerve palsy.

NATURAL HISTORY

It is important that an accurate initial examination be

obtained so that recovery or lack thereof can be accu-
rately monitored. Mild compressive nerve lesions such
as sleep palsies will show a rapid recovery, with motor
and sensory function returning within a few minutes or a
few days. More severe lesions in which the continuity of

the nerve is intact may take several weeks to recover.
These lesions would fall into the category of axona-
praxia, however, and spontaneous resolution is likely.

If axonotmesis has occurred with Wallerian degenera-

tion but with preservation of the endoneurial tubes so
that each axon is directed back to the end-organ it origi-

nally subserved, function will usually be fully restored.

Clinically there will be complete loss of motor, sensory,
and sympathetic functions in the distribution of the
nerve. Axoplasmic regeneration will begin in approxi-
mately three weeks (6).

Reinnervation would be expected to proceed in an or-

derly fashion, with proximal muscles being reinnervated
prior to distal, and proximal sensory returning prior to
distal. The standard estimates for regrowth once axo-
plasmic flow has begun are approximately 1 inch/month
or 1 mm/day in an adult. One can calculate when return
of function can be expected by measuring from the site
of the lesion to the motor point of the first muscle or

sensory area supplied by the nerve.

In neurotmesis, or lesions in which the entire nerve

trunk is disrupted, no spontaneous return of function
would be anticipated. It is important to remember that
one cannot distinguish clinically between an axonotme-
sis and a neurotmesis on the basis of examination or
electrical studies. Both lesions show absence of function,
both clinically and electrically, and only direct explora-
tion of the nerve can differentiate them. How long to
wait before exploring a clinically complete lesion is a

question of surgical judgment.

DIAGNOSTIC TESTS

As in other medical fields, an accurate history and

careful examination are the most important elements of

diagnosis. A careful history will help differentiate trau-
matic neuropathies from those of infectious origin (diph-
theria, mumps, influenza, pneumonia, meningitis, ma-
laria, syphilis, typhoid, dysentery, tuberculosis, or

gonococcus) or metabolic causes (diabetes, rheumatoid

arthritis, gout, leukemia, vitamin deficiency, periarteritis
nodosa, sulfa, heavy metals, and carbon monoxide).

470 / CHAPTER 23

In the area of trauma, remote as well as recent injury

must be considered. Particular attention must be given

to the onset and course of the patient's symptoms. The

old neurologic adage holds that the history indicates the

pathology, and the examination gives the localization.

The examiner must also be aware of common anatomic
variations, such as overlap between the ulnar and me-
dian nerves in the hand, and must determine whether
the patient's course is progressive, static, or improving.

Electromyography and nerve conduction studies can

be helpful. Motor and sensory conduction studies are
done by using electric stimulation at one point on the

-nerve and recording at another. They reveal speed of

neural transmission, and an area of slowing may identify
the site of the lesion. Normal figures for conduction in

various nerve segments are available, and comparison

can also be made with the normal opposite side.

Nerve conduction varies with the size of the fiber and

the amount of myelin sheath: large, heavily myelinated
fibers are the most rapid conductors, and small, slightly
myelinated fibers are the slowest. Although a mixed
nerve consists of a combination of these two fibers as
well as their intermediate forms, the measured conduc-

tion velocity of a peripheral nerve will be that of the

fastest fiber.

Electromyography may reveal denervation potentials

in the affected muscles. The pattern of muscles involved
will help localize the lesion along the course of the nerve.
Subsequently, polyphasic potentials may indicate early

reinnervation prior to the presence of voluntary muscle
contractions. In addition, electrical studies may be help-

ful in differentiating organic pathology from a functional

state. If there is a question about the innervation of cer-
tain muscles or concern about aberrant innervation, lo-

cal anesthetic block of either the involved or the unin-
volved nerves will help delineate the situation.

With the history, clinical examination, and electrical

studies, one can make proper pathologic and anatomic
diagnosis in a high percentage of cases. Nevertheless, it is
not always possible to differentiate total physiologic loss

from anatomic disruption of the nerve. A significant

diagnostic aid is repeated examinations to determine
whether the patient's status is improving or declining.
Valuable, but not infallible, is Tinel's sign: after a com-
plete nerve lesion axonal growth may be determined by

percussion over the nerve, with the paresthetic response

being evoked by tapping over the growth cone progres-
sively more distally over the nerve as regrowth occurs.

INDICATIONS FOR SURGERY

In lesions in continuity, such as contusions, compres-

sion, or injection palsy, when there is no reason to
suspect that the nerve has been divided, the pathologic

process is one of partial or complete physiologic in-

terruption, usually compounded by external and inter-
nal fibrosis. If such a lesion is progressive, with increas-
ing loss of motor and sensory function, surgical
exploration should be carried out as soon as the patient is
otherwise medically fit. If the lesion is profound at the
time of the first examination and no improvement is
evident within four to six weeks following onset, surgical
exploration is indicated (7). Surgery should be withheld
if improvement is apparent during the four to six weeks
of observation. Pain alone, without any sensory or mo-
tor symptomatology, is rarely an indication for periph-
eral nerve surgery.

Nerve lacerations may be treated by either primary or

secondary repair. Primary repair (8) should be reserved
for situations in which (1) the surgeon is experienced in

the repair of peripheral nerves; (2) the wound is a clean
laceration with no crushing of nerve or other tissues; (3)
the nerve ends are easily found without wound exten-

sion; (4) there is no wound contamination; and (5) sutur-

ing can be done without mobilization or tension. If these
conditions are not met, secondary repair is indicated.

The initial surgical treatment, pending secondary re-

pair, involves tagging the nerve ends with markers to try
to maintain axial orientation and suturing the ends in
approximation to prevent their retraction during wound

healing. Careful debridement of other tissues should be

carried out as indicated.

Definitive secondary repair (9,10) should be done four

to six weeks later, when conditions should be optimum.

The initial wound should have healed without incident.
This delay will allow for resolution of the usual exuda-
tive phase of injury and for maturation of fibrous tissue.
This will make subsequent resection of proximal and
distal nerve ends more accurate. The epineurium will be
firmer and easier to suture. In addition, axoplasmic flow

will just be beginning in three weeks, and Wallerian de-

generation should be complete. Thus, anatomic and
physiological conditions are at the optimum.

With regard to nerve tumors, surgery should be under-

taken in the case of progressive loss of nerve function,
disabling symptoms, or suspicion of malignancy. Many
tumors will remain static for long periods of time, so
repeated observation is indicated to determine any need

for surgery.

PREOPERATIVE MANAGEMENT

Aside from careful neurologic evaluation, the patient's

general medical fitness should be established. Appro-

priate physiotherapy should be employed to maintain
range of motion and functional position, prevent edema,

and avoid pressure sores. Repeated examinations will
determine the patient's course. Any splints or casts that
might be needed in the immediate postoperative phase

PERIPHERAL NERVE INJURY / 471

can be prefabricated. It helps to try preoperatively plac-
ing the patient's limbs in the position in which the opera-
tion is planned, to make certain that there is no limita-

tion of the range of joint motion that would prevent
surgery in that position and that no compromise of neu-
rovascular structures would occur if the patient were

placed in that position for a long period of time. Careful

planning of the operative incision and review of anat-

omy and possible variations are advisable. Discussion

with the patient should include the patient's active role
in recovery and the risks and potential benefits of the

procedure.

OPERATIVE MANAGEMENT

Neurolysis

Lesions in continuity caused by extrinsic and intrinsic

scar tissue should be treated with external and internal
neurolysis. The former involves freeing the nerve from
its surrounding bed and from any extrinsic adhesions,
whereas the latter involves opening the nerve sheath and
dividing any scar constricting the fascicles (11,12). The

incision must be adequate to allow visualization of nor-

mal nerve on either side of the lesion. Pathology can be
localized by inspection and by palpation of the nerve and
surrounding structures. Thickening or abnormal firm-

ness is usually noted. The external findings are verified

when the nerve is opened and observed through the
operating microscope. Intraoperative electrical stimula-
tion above and below the level of the lesion both before
and after neurolysis may provide prognostic informa-
tion. The operating microscope and microinstruments

are employed, and the nerve sheath is opened with sharp

dissection. The fascicles are identified in the normal area
of nerve and then followed into and through the area of

scar, superficial to the fascicles. This will prevent injury
to any interfascicular plexuses. The nerve is rotated, and

multiple superficial incisions are used rather than nerve

penetration. Retraction is done only on the connective

tissue elements. Use of a number 12 blade will allow the

surgeon to be always cutting away from the nerve tissue

[Fig. 1(A)]. Meticulous hemostasis, effected with the mi-

crobipolar coagulator, and delicate tissue handling are
important. Following decompression, the epineurial
flaps are generally resected [Fig. 1(B)]. Wound closure is

carried out with loose closure of deep fascia, subcutane-
ous sutures, and Steri-Tapes on the skin. No cast or im-

mobilization is required.

General anesthesia is usually used because the opera-

tion may last several hours and because any movement
of the patient could be disastrous. Surgery can usually be
done on an outpatient basis.

Nerve Suture

For similar reasons, general anesthesia is employed for

nerve suture, and a general preparation of the extremity
is done because extension of the incisions and mobiliza-
tion of the nerve may be required. After the nerve is
exposed, it must be mobilized sufficiently so that an ap-
proximation without tension can be accomplished (13).
Under the microscope, the end of the nerve must be

resected until relatively normal-appearing tissue is seen.
End-to-end anastomosis, utilizing an epineurial or fascic-
ular technique (14-16), is preferable (Figs. 2 and 3). This
may require extensive mobilization of the nerve to pro-
vide length, and it is accomplished primarily at the prox-

imal end because the acute angle of separation of distal

branches makes it more difficult to gain slack from the

distal segment.

B

FIG. 1. (A) The external nerve sheath is

opened with sharp dissection using the
operating microscope. The number 12

blade, with the blade directed away

from the fascicles, allows division of the
fibrous bands. (B) The completed dis-
section shows the various fascicles de-
compressed. The flaps of epineurium
can then be resected.

472 / CHAPTER 23

FIG. 2. End-to-end anastomosis. The suture is placed just
through the epineural tissue after axial orientation has been

established.

In addition, transposing a nerve, such as moving the

ulnar nerve anterior to the epicondyle at the elbow, may
help to add further length. Flexion of the limb is also
helpful, but it should not be employed beyond 90 de-
grees. A nerve reapproximated under such conditions

would probably be unable to withstand the tension on

the nerve when the limb is later extended. Use of the

microscope and microinstrumentation, delicate nerve

handling, careful hemostasis, accurate axial orientation
and coaptation of the nerve ends, lack of tension on the
suture line, and the use of a relatively inert suture mate-
rial (17) are the keys to success in nerve suture.

Should suturing prove impossible, autografting is the

best substitute currently available. A segment of the sural

or other sensory nerve may be employed with a fascicu-
lar suture technique, in which the ends of the injured
nerve are divided into groups of fascicles appropriate to
the number in the graft. End-to-end anastomosis of the
graft is carried out proximally and distally.

After nerve suturing, immobilization is indicated to

prevent disruption of the suture line, especially if flexion

of the limb was required to perform the anastomosis.

Nerve tumors can often be resected using the neuroly-

sis technique. The fascicles can be separated longitudi-

nally, and the tumor can be shelled out of the nerve. If a

malignant tumor is encountered, resection with gener-
ous margins is appropriate, with subsequent suturing or

grafting as the situation dictates.

FIG. 3. Fascicular anastomosis. The individual fascicles are
directly sutured after the adjacent epineurium has been re-
sected.

Outcome

No simple statement can be made about the results of

either neurolysis or nerve suture, but several factors can

be enumerated that are important in the quality of recov-

ery (18):

1. Type of nerve. A pure sensory or pure motor nerve

will do better than a mixed nerve in which motor and
sensory axons may enter opposite endoneurial tubes,
which will guide them to inappropriate targets.

2. Age of the patient. The younger the patient, the better

the prospects.

3. Level of injury. The more distal the lesion (i.e., the

closer the lesion is to the structures to be innervated

with respect to the total length of the nerve), the better
the prognosis.

4. Degree of deficit. In lesions in continuity, the more

profound the deficit, the worse the prognosis.

5. Extent of the defect. Prospects are better with direct

nerve suture than with grafting.

6. Time from injury. The longer repair is delayed

beyond the first few weeks or months, the poorer the
prognosis.

7. Surgical technique. The skill and experience of the

surgeon have a significant bearing on the outcome.

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