Hand and Wrist Surgery - part 3 pdf

18
Cervical Root Compression
Bradley M. Thomas, John M. Olsewski, and Jerry G. Kaplan
His tory and Clinical Presentation
A 49-year-old right hand dominant electrician presented with complaints of pro-
gressive weakness in his right arm. He also described having pain in his neck ex-
tending down the front of his arm to his hand. He was having difficulty lifting
objects with his right hand and performing repetitive-type motions, with weakness
of his right shoulder and biceps. He reported occasional numbness in his thumb
and index finger while at work.
He did not recall any trauma to his neck or arm. He denied bowel or bladder
dysfunction, and was not experiencing disturbances in his gait. On further ques-
tioning he denied any history of smoking, diabetes, or hypertension. He also de-
nied night pain.
Phy sic al Ex ami nat ion
Examination revealed a patient in no acute distress, with a full range of motion
of the cervical spine. Reproduction of his right arm pain was elicited with ex-
tension of the neck and rotation of his head to the right (Spurling’s maneuver).
He appeared to have mild deltoid wasting on his right with prominence of his
acromion. Motor testing was symmetric with 5/5 strength in bilateral deltoids,
biceps, triceps, wrist flexors, wrist extensors, finger flexors, finger extensors, and
hand intrinsics. His deep tendon reflexes were 2+ and symmetric, with the ex-
ception of the biceps reflex, which was depressed on the right side compared
with the left. He had a negative Hoffman’s sign and his gait was within normal
limits. Tinel’s and Phalen’s testing of the median nerve at the wrist were not
provocative.
Dia gno stic Studies
Radiographs taken included an anteroposterior, lateral, obliques, and flexion/exten-
sion laterals of the cervical spine. There is evidence of multilevel degenerative
changes, with principal changes at the C5-C6 level. These changes include loss of

C5–6 disk height on the lateral and narrowing of the C6 neural foramen with en-
croachment on the foramina by osteophyte on the oblique views (Fig. 18–1). Mag-
netic resonance imaging (MRI) of the cervical spine showed evidence of multilevel
mild cord impingement with disk herniation at C3–4, C4–5, C5–6, and C6–7,
along with focal increased signal intensity within the cord at the C5–6 level on the
T2-weighted images consistent with cord edema (Fig. 18–2). There is also bilateral
foraminal narrowing on the axial images at the C5–6 level (not shown). A needle
electromyogram (EMG) was performed, which showed membrane instability of the
C6 innervated muscles on the right side. C5, C7, and C8 muscles were normal. The
nerve conduction studies did not exhibit peripheral nerve slowing as evidence for
peripheral nerve compression.
C O M P R E S S I O N N E U R O P A T H Y
102
PEARLS
• Spurling’s maneuver repro-
duces a patient’s arm pain
and paresthesias by turning
the patient’s head toward
the symptomatic side and ex-
tending the neck. This position
decreases the size of the neu-
roforamina.
• Use an EMG to differentiate
first-degree shoulder problems
from a C5 root problem.
• Biceps weakness may be the
first sign of rotator cuff disease,
although a herniated C6 root
can give similar findings.
PITFALLS

• Patients with sensory changes
in the thumb and index fin-
ger may have carpal tunnel
syndrome and not a C6
radiculopathy.
• Check for a local Tinel’s and
Phalen’s sign.
• An incomplete cervical spine
exam in a patient with upper
extremity problems often leads
to an incorrect diagnosis.
• A full cervical spine x-ray series
should be used to see on
oblique films encroachment on
the foramina by osteophytes.
103
A B
Figure 18–1. (A) Lateral radiograph of the cervical spine showing multilevel degenerative changes with narrowing at the C5–6 disk space.
(B) Oblique radiograph showing narrowing and osteophyte (4) formation within the C5–6 neuroforamen.
Figure 18–2. T2-weighted sagittal
magnetic resonance imaging (MRI)
of the cervical spine shows disk
herniations at C3 lumen 4, C4–5,
C5–6, and C6–7, along with focal
increased signal intensity within
the cord at the C5–6 level on the
images consistent with cord edema.
Dif feren tia l Diagnosis
Carpal tunnel syndrome
Rotator cuff tear

C5 radiculopathy
C6 radiculopathy
Brachial neuritis
Thoracic outlet syndrome
Dia gno sis
C6 Ra diculopathy
Cervical radiculopathy represents impingement of an exiting cervical nerve root
generally caused by herniated disk material or from degenerative cervical spon-
dylosis, or commonly a combination of the two. In cases where the etiology is
a herniated disk, the symptoms are more acute in onset and may be exacer-
bated by coughing or other Valsalva-type maneuvers. Cervical spondylosis as a
cause for radiculopathy has an insidious onset, with degenerative changes oc-
curring at the disk and the zygapophyseal and neurocentral joints (Fig. 18–3).
Other causes of cervical root irritation or compression include intraspinal tu-
mors, infection, inflammatory arthritic changes, and chemical irritation from
neurohumeral factors.
The presentation of cervical radiculopathy begins with varying degrees of pain,
paresthesias, and motor weakness in the neck and upper extremity. Significant neck
pain is often associated with the radicular pain and sensory changes, which generally
follow a dermatomal distribution. Breast pain and angina-like symptoms should also
be considered as potential radicular complaints. Weakness and reflex changes are also
root specific, but significant overlap exists in the muscular innervation of the upper
extremity and may occasionally be confusing. Table 18–1 outlines the clinical symp-
toms and findings seen with individual root involvement, and other potential causes
for similar findings.
C O M P R E S S I O N N E U R O P A T H Y
104
Cervical nerve
root
Cord

Intervertebral
foramina
(neuroforamen)
Uncinate process
(joint of Luschka)
Disk
Vertebral body
Articular process
(facet joint)
Figure 18–3. Axial anatomy
of the cervical spine at the
level of the disk and exiting
nerve root at the interverte-
bral foramina. Note the disk
herniation on the left side
impinging the nerve root.
The physical exam should be focused on identifying a dermatomal distribution
of radicular complaints and sensory changes. Specific muscle group weakness and
reflex changes as compared with the opposite side should also be recorded. Special
tests like the previously mentioned Spurling’s sign and the Valsalva maneuver can
reproduce a patient’s radicular complaints by decreasing the size of the neuroforam-
ina. Davidson’s shoulder abduction relief sign functions to relieve a patient’s radicu-
lar complaints with abduction of the shoulder and presumably decreased tension on
the cervical root.
In this patient’s presentation a typical C6 radiculopathy is present with neck pain
radiating down the biceps region of the arm to the lateral aspect of the forearm into
the thumb and index fingers. Although he did not exhibit weakness on testing, he did
report difficulty maintaining biceps strength with repetitive motion, and he had a de-
pressed biceps reflex. Spurling’s maneuver was provocative for reproducing his radic-
ular pain. The radiographs and MRI are significant for loss of C5–6 disk space, C6

neural foramen narrowing, encroachment on the foramina by osteophyte, and focal
cord edema at the C5–6 level. The EMG confirmed denervation at the C6 level.
Dif feren tia l Diagnosis
Other conditions that may mimic C6 radiculopathy include other level radiculopa-
thies, carpal tunnel syndrome, rotator cuff tendinopathies, brachial neuritis, and
thoracic outlet syndrome.
C E R V I C A L R O O T C O M P R E S S I O N
105
Table 18–1 Clinical Symptoms and Physical Findings Seen in Individuals with
Cervical Root Involvement and Other Potential Causes for Similar Findings
Pain or
Root Level Sensory changes Motor Reflex Diagnosis with Similar Findings
C3 C2–3 Back of the neck XX“Tension headache”
Mastoid region
Ear
C4 C3–4 Back of the neck XXMyofascial pain
Along the trapezius
Anterior neck
C5 C4–5 Side of the neck to Deltoid X Primary shoulder problem
top of the shoulder Rotator cuff
Over the deltoid
C6 C5–6 Lateral side of the Biceps Biceps Carpal tunnel syndrome (CTS)
arm and forearm Wrist extensors Brachioradialis Upper trunk BPN
Thumb and index
fingers
C7 C6–7 Back of the forearm Triceps Triceps CTS
to the middle finger Wrist flexors Pronator syndrome
Finger extensors Radial tunnel synd.
Posterior cord BPN
C8 C7–T1 Ulnar side of the Finger flexors X Ulnar nerve entrapment at Guyon’s

forearm to the Intrinsics canal or the cubital tunnel
ring and small AIN palsy
fingers Lower trunk BPN
AIN, anterior interosseous nerve; BPN, brachial plexus neuropathy.
Clinical neurophysiologic testing is very important for differentiating radiculopa-
thy from peripheral neuropathies. Needle EMG has traditionally been the most use-
ful electrophysiologic tool for diagnosing cervical radiculopathy. If compression
produces axonal interruption in some fibers, the EMG reveals changes in muscles
from decreases in motor unit action potentials to fibrillation potentials of muscles.
In radiculopathy the nerve compression is proximal to the dorsal primary ramus,
which should produce changes in the paraspinal muscles, differentiating this lesion
from a brachial plexus injury or more distal nerve compression.
The sensory changes involving the thumb and index finger seen in C6 radicu-
lopathy are also present in carpal tunnel syndrome. The differences can be seen in
the dorsal and volar distribution of sensory changes in the hand and the proximal
findings associated with radiculopathy.
Coexisting distal nerve entrapment and cervical radiculopathy can occur, known
as the double crush phenomenon. EMG is useful for differentiation of proximal
versus distal nerve entrapment, with nerve conduction velocities identifying periph-
eral neuropathy.
Pain that originates in the neck and extends to the shoulder and arm is very typical
for radiculopathy, but patients with rotator cuff disease often have associated neck pain
due to shoulder weakness and trapezium muscle spasm. In addition, biceps weakness
may be a subjective complaint with rotator cuff disease due to an associated biceps
tendinopathy causing pain and restricted motion. Specific testing of the rotator muscu-
lature and an MRI of the shoulder are helpful in diagnosing a rotator cuff tear.
Proximal arm pain and weakness may be present in brachial neuritis. In this con-
dition of unknown etiology a patient might awaken with shoulder pain and arm
weakness without an inciting event. The symptoms are usually self-limited and
treated symptomatically. Again, electrodiagnostic testing along with a thorough his-

tory and physical examination should differentiate this entity from radiculopathy.
Thoracic outlet syndrome may involve nerves of the brachial plexus and may present
with weakness and numbness of the hand. Physical findings of asymmetric pulses, vas-
cular bruits, and a positive Adson’s test are tips to suspect thoracic outlet syndrome.
Nonsurgical Ma nagement
The majority of patients with first-time symptoms of radiculopathy may be man-
aged nonoperatively. Initial management should include immobilization in a soft
collar with the neck slightly flexed, antiinflammatory medications, and physical
therapy. Narcotic medications may be used in conjunction with nonsteroidal anti-
inflammatory drugs (NSAIDs) in the acute period in cases of severe pain. Physical
therapy consists of heat and ultrasound modalities to make the patient more com-
fortable, cervical traction, and stretching exercises when tolerated. Epidural or se-
lective nerve root corticosteroid injections are also an option, but require accurate
needle placement around an irritated nerve root. Improvement in symptoms should
be seen within 2 weeks; if symptoms worsen or marked neurologic deficits are pres-
ent, more aggressive management should be considered.
Surgical Management
Cases of cervical radiculopathy that require surgical intervention are those with
unrelenting pain despite conservative management, progressive neurologic deficit,
C O M P R E S S I O N N E U R O P A T H Y
106
upper extremity weakness, and nerve root compression that is proven diagnostically
and correlates clinically.
Surgical choices include anterior cervical diskectomy and fusion as described by
Robinson, or posterior diskectomy involving a hemilaminectomy or foraminotomy.
The anterior approach is considered the best option for the acute disk herniation
to decompress the nerve root from impinging disk fragments in the intervertebral
foramen, and for cases where the nerve root is compressed by osteophytes from
the joints of Luschka (Fig. 18–3). This anterolateral approach in the neck takes ad-
vantage of the fascial plane between the carotid sheath laterally and the trachea

and esophagus medially, which affords visualization of the entire surgical spine. The
posterior approach is useful for cases of chronic compression due to degenerative
changes at the facet joints, and for cases where several levels need to be addressed.
Both approaches produce excellent results for relieving radiculopathy, but the an-
terior approach is more consistent for relieving axial neck pain. Postoperatively, the
patients are immobilized in a hard collar in cases of fusion and a soft collar if a sim-
ple diskectomy is performed.
Suggested Readings
An HS. Cervical root entrapment. Hand Clin 1996;12:719–730.
Bohlman HH, Emery SE, Goodfellow DB, et al. Robinson anterior cervical dis-
cectomy and arthrodesis for cervical radiculopathy. J Bone Joint Surg 1993;75A:
1298–1307.
Dumitru D. Electrodiagnostic Medicine. Philadelphia: Hanley & Belfus; 1995.
Levine MJ, Albert TJ, Smith MD. Cervical radiculopathy: diagnosis and nonopera-
tive management. J Am Acad Orthop Surg 1996;4:305–316.
Lomen-Hoerth C, Aminoff MJ. Clinical neurophysiologic studies: which test is
useful and when? Neurol Clin 1999;17:65–74.
Morgan G, Wilbourn AJ. Cervical radiculopathy and coexisting distal entrapment
neuropathies: double-crush syndromes? Neurology 1998;50:78–83.
Persson LC, Moritz U, Brandt L, Carlsson CA. Cervical radiculopathy: pain, muscle
weakness and sensory loss in patients with cervical radiculopathy treated with
surgery, physiotherapy, or cervical collar. A prospective, controlled study. Eur Spine J
1997;6:256–266.
Saal JS, Saal JA, Yurth EF. Nonoperative management of herniated cervical inter-
vertebral disc with radiculopathy. Spine 1996;21:1877–1883.
Stewart JD. Focal Peripheral Neuropathies. 2nd ed. New York: Raven Press; 1993.
C E R V I C A L R O O T C O M P R E S S I O N
107
19
Complex Regional

Pain Syndrome Type 1
(Reflex Sympathetic Dystrophy)
Carole W. Agin
History and Clinical Presentation
A 50-year-old woman was undergoing magnetic resonance imaging (MRI) with
contrast. Intravenous access was started in her right antecubital fossa. As the infu-
sion of gadolinium was started, the patient reported a burning pain in her arm from
the antecubital fossa to her fingers. Her forearm and hand swelled. As the swelling
increased, she reported numbness and cyanosis. Over the next few days the swelling
resolved. Slowly sensation returned to her arm; however, the patient reported a con-
stant burning pain. The patient also noted changes in the color of her hand and
pain with movement of her wrist, elbow and shoulder.
Diagnostic Studies
There are no radiologic findings that are pathognomonic for complex regional pain
syndrome (CRPS) type 1, reflex sympathetic dystrophy (RSD). Radiologic findings
are often nonspecific, and many findings are a result of prolonged disuse, which
is attributable to the pain associated with the syndrome. However, imaging studies
can support a diagnosis of CRPS (RSD).
Fine detail radiography may help to suggest the presence of CRPS. Early radiologic
changes seen with sympathetic hyperdysfunction include patchy demineralization of
the epiphyses and short bones of the hands and feet. Periarticular osteoporosis in long
bones and diffuse osteoporosis in small bones may be seen on plain radiographs. Sub-
periosteal resorption, striation, and tunneling of the cortex may occur. Comparison
with the unaffected limb is always required. Unfortunately, these findings may be seen
whenever there is disuse of a limb. As CRPS advances, patchy osteopenia may be seen.
Triple-phase scintigraphy has also been used to help diagnosis CRPS (RSD).
Three-phase bone scanning measures the uptake of a radionucleotide tracer at three
different times: arterial phase, measured seconds after the injection of tracer; soft
tissue phase, measured after several minutes have passed; and mineral phase, mea-
sured hours after the tracer is given. The triple-phase bone scan pattern most consis-

tently seen in a patient with CRPS (RSD) is that of increased flow to the involved
extremity and delayed static images that show diffusely increased uptake activity
throughout the involved extremity, usually in a periarticular distribution.
MRI studies may show skin thickening and tissue edema. Nuclear bone density
measurements have been used to follow the progression of the syndrome.
Differential Diagnosis
Peripheral neuropathy disease
Inflammatory disease
C O M P R E S S I O N N E U R O P A T H Y
108
PEARLS
• When presented with a ques-
tionable case of CRPS early
after symptom development,
a three-phase bone scan may
be helpful.
• CRPS (RSD) is often a diagnosis
of exclusion.
PITFALLS
• Radiologic studies performed
late in the disease process
may show changes secondary
to disuse atrophy, which may
be caused by other medical
conditions.
• If the sympathetically main-
tained pain is the result of a
persistent but treatable condi-
tion, the condition needs to
be treated. Treating only the

signs/symptoms of CRPS with-
out addressing the underlying
condition may prove futile.
• If the patient has a diagnosed
psychiatric illness (i.e., post-
traumatic stress disorder, de-
pression), this must be treated
or it can adversely affect any
potential improvements ob-
tained from other treatment
modalities.
Infectious disease
Vascular disease
Connective tissue disorder
Reflex sympathetic dystrophy
CRPS (RSD) is often a diagnosis of exclusion. Other causes of similar pain com-
plaints include peripheral neuropathies, which may also present with neuropathic
pain. Traumatic injuries to nerves may present with dysesthesia and hyperpathia,
but without the sympathetic component. Inflammatory and infectious causes for
pain needed to be ruled out when autonomic dysfunction is the primary presenting
symptom. Examples of this would include tenosynovitis and bursitis. Vasculitis and
vascular disorders can also manifest with similar findings. In many instances vascu-
lar diseases present with bilateral symptoms. Raynaud’s disease produces vasospasm
that will lead to findings of pallor, cold skin, and potentially cyanosis. Connective
tissue disorders also have to be ruled out. Myofascial pain may also present with a
nondermatologic distribution of pain. These patients may report burning pain as a
symptom and have tender trigger points in the affected muscles. Malingering and
psychiatric disorders must also be ruled out as a cause of the patient’s unremitting
pain, which presents out of proportion to the inciting event.
Diagnosis

Complex Regional Pain Syndrome, Type 1 (Reflex Sympath etic Dyst roph y)
The Committee on Taxonomy of the International Association for the Study of
Pain (IASP) recently renamed reflex sympathetic dystrophy as complex regional
pain syndrome type 1. This new taxonomy was promulgated in an attempt to estab-
lish uniform diagnostic criteria. This will aid in the development of treatment pro-
tocols for the syndrome. Previously many symptom constellations were included
within the category of RSD, making treatment pathways and outcome studies dif-
ficult. A study done to evaluate the validity of the IASP’s CRPS diagnostic criteria
to distinguish between CRPS and other neuropathies showed that the new classifi-
cation did assist in improved accuracy of diagnosis.
To meet criteria for CRPS type 1 a patient must present with regional pain out-
side of the distribution of a single peripheral nerve and out of proportion to the in-
citing event. CRPS has been reported to develop after compression/crush injuries,
lacerations, fractures, sprains, burns, or surgery. Allodynia and hyperalgesia are typ-
ically present. Abnormalities in skin blood flow (causing changes in skin tempera-
ture and color), abnormal sudomotor activity, and edema are also present. Dystonia
and weakness, although not necessary for the diagnosis, may also be present.
Trophic changes and personality changes may develop as the disease progresses.
CRPS type 2 has all of the same signs and symptoms; however, it follows injury of
a major peripheral nerve.
Methods of Management
As the pathophysiology of CRPS type 1 (RSD) is not well understood, multiple
treatment protocols have been described. The consensus is that these patients do
best with a multidisciplinary treatment plan (Table 19–1). This includes regional
blockade (Fig. 19–1), physical therapy, pharmacologic therapy, and psychological
C O M P L E X R E G I O N A L P A I N S Y N D R O M E T Y P E 1 ( R E F L E X S Y M P A T H E T I C D Y S T R O P H Y )
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110
Table 19–1 Treatment Modalities
Pharmacologic Interventional Techniq ue Physical Modalities Psychological Interventions

Antidepressants, Sympathetic blockade Physical/occupational Psychiatric evaluation
TCAs, SSRIs Stellate ganglion therapy
Lumbar sympathetic
IV regional
Membrane stabilizers Spinal cord stimulator Contrast baths Cognitive behavior skills
Anticonvulsants
Local anesthesia
Antiarrhythmic
NSAIDs TENS Relaxation training
Topical medications Heat/cold Imagery
EMLA
Capsaicin
Opiates Massages Hypnosis
Clonidine
Calcitonin
NSAID, nonsteroidal antiinflammatory drug; TCA, tricyclic antidepressant; TENS, transcutaneous electrical nerve stimulation; SSRI, selective serotonin reuptake
inhibitor.
Figure 19–1. Anatomy of the neck and placement of the needle for a stellate ganglion block.
intervention. The earlier the syndrome is diagnosed and treatment is started, the
better the chances for complete recovery.
Pharmacologic Therapy
Kingery reviewed the literature with respect to controlled clinical trials for CRPS.
He found great disagreement as to the effectiveness of many of the medications cur-
rently being used in the treatment of CRPS. He concluded that further double-
blind controlled studies are needed.
Tricyclic antidepressants (TCAs) have been well studied in neuropathic pain.
TCAs (amitriptyline, nortriptyline, desipramine) inhibit monoaminergic transmit-
ters by blocking reuptake of serotonin and norepinephrine. The dose used for treat-
ment of neuropathic pain is typically much less than antidepressant doses. The
selective serotonin reuptake inhibitors (paroxetine, sertraline), although used anec-

dotally in chronic CRPS, have not been formally studied for this purpose.
The mechanism of action of nonsteroidal antiinflammatory drugs (NSAIDs) is
the inhibition of cyclooxygenase. This leads to a reduction in the production of pain
mediators and a reduction in inflammation. NSAIDs may be helpful in the early
stages of CRPS type 1; however, the potential for gastrointestinal complications and
renal failure must be considered if continued use is to be recommended.
Membrane stabilizing medications are also used. This category includes anti-
convulsants, local anesthetics, and antiarrhythmic agents. Gabapentin, a selective
voltage-gated Ca
2+
channel blocker, has shown some efficacy in managing pain in
CRPS. Gabapentin has reduced side effects and an improved efficacy-to-toxicity
ratio when compared with phenytoin and carbamazepine. Lidocaine, mexiletine,
and tocainide effect sodium channels. Lidocaine has been used intravenously in the
management of neuropathic pain. Intravenous lidocaine therapy is often followed
by oral treatment with mexiletine.
Topical medications have been tried for the hyperpathia and allodynia associated
with CRPS. Topical application of local anesthetics, lidocaine, and prilocaine (eutec-
tic mixture of local anesthetics, EMLA) has been tried recently in the treatment
of neuropathic pain in patients with CRPS type 1 (RSD). Topical capsaicin causes
a reversible depletion in substance P and calcitonin gene-related peptide from the
C-fiber nerve terminals. There are anecdotal reports of its use for localized hyper-
algesia; therefore, it can be tried for patients with CRPS with local areas of pain. Pa-
tients need to be informed that initially its application may cause increased pain.
This is secondary to the release of substance P that occurs.
The use of opioids in the treatment of neuropathic pain, and specifically in
CRPS, has not been studied. Opioids are useful in nociceptive pain, and their effect
is related to interaction at the level of the spinal cord with the opioid receptors. Al-
though their use may be considered controversial in chronic, nonmalignant pain, a
patient with unremitting pain should be tried on opioid therapy. This should occur

early on in the treatment. It is important to control the patient’s pain utilizing all
available means so that active physical therapy can be pursued and disuse atrophy
avoided. As is true whenever using opioids, constipation should be expected and
treated prophylactically.
There have been anecdotal reports of the use of other medications for CRPS.
Medications that inhibit ␥-aminobutyric acid (GABA), such as baclofen, have been
reported to be useful in neuropathic pain. Controlled studies of their use in CRPS
have not yet been done. Clonidine has been shown to be useful when topically applied
C O M P L E X R E G I O N A L P A I N S Y N D R O M E T Y P E 1 ( R E F L E X S Y M P A T H E T I C D Y S T R O P H Y )
111
to areas of hyperalgesia. It acts by blocking release of catecholamines presynaptically.
Clonidine has also been administered epidurally and intrathecally in patients with
CRPS. These patients are at a much greater risk for hemodynamic complications when
the drug is used transdermally. Subcutaneous calcitonin has been shown to be effective
in treatment of spontaneous pain. Its use in CRPS has not yet been documented. In the
early stages of CRPS a patient may benefit from a trial of corticosteroids. This is partic-
ularly true for patients who present with edema or other signs of inflammation.
Regional Blockade
Regional blockade, specifically sympathetic nerve blocks, are useful in both estab-
lishing the diagnosis as well as in the treatment of CRPS (RSD). Patients with
CRPS report relief of pain with sympathetic blocks, which is very useful in giving
patients the analgesia that they require to participate in a physical therapy regimen.
If a patient responds positively to a trial of sympathetic block, these blocks should
be repeated as long as the patient continues to be afforded increasing duration of
pain relief and symptom improvement with subsequent blocks.
In addition to assessing the level of pain relief reported by the patient, patients
should be assessed for signs of a sympathetic block. Blocks of the sympathetic nervous
system interrupt nociceptor visceral and somatic afferents and vasomotor, sudomotor,
and visceromotor fibers. One would therefore look for signs of increased blood flow
to the limb(s) involved. As cutaneous blood flow affects skin temperature and this is

controlled by the sympathetic nervous system, an increase in skin temperature should
occur. This can be measured using surface temperature monitors or plethysmography.
The limb should be examined for visual signs of increased vasculature. Blocking of
sudomotor functions can be measured using Ninhydrin, cobalt blue, or starch-iodide.
A quantitative sudomotor axon reflex test (QSART) can also be used.
For CRPS affecting the upper limb a stellate ganglion block is usually performed.
Many patients develop Horner’s syndrome (enophthalmos, miosis, anhidrosis, and
ptosis) after a stellate (cervicothoracic) ganglion block. Block of the thoracic sym-
pathetic chain is technically difficult, requiring radiologic guidance, and is not
commonly done. For CRPS affecting the lower extremities, sympathetic blockade is
done either by performing a lumbar sympathetic block or by an epidural injection.
If required, continuous blocks can be done.
Intravenous Regional Blocks (Bier Blocks)
Intravenous regional blocks allow for prolonged exposure of the affected limb to the
ganglionic blocking agent. In the United States this technique is typically per-
formed with bretylium. Bretylium accumulates in adrenergic nerves and blocks
norepinephrine release. These blocks have also been performed with guanethidine
and reserpine.
Spinal Cord Stimulation
Spinal cord stimulation is hypothesized to affect pain based on the gate control theory
whereby stimulation of large myelinated fibers blocks pain transmissions through
smaller pain fibers (Fig. 19–2).
C O M P R E S S I O N N E U R O P A T H Y
112
Figure 19–2. Patient with spinal
stimulation of large myelinated fibers
that in theory blocks pain transmis-
sions through smaller pain fibers.
Patients who either do not respond to regional blocks, medications, or physical
therapy, or are unable to pursue those treatment options secondary to unacceptable

side effects, may be candidates for spinal cord stimulation. All patients must meet
strict selection criteria and have a successful trial with a temporary lead. A trial is
deemed successful if the patient reports a decrease in pain, a reduction in medica-
tion requirements, and an improvement in function.
Physical Therapy
Physical therapy should be done concurrently with medications and sympathetic
blocks in the treatment of severe CRPS. It can be the main treatment modality for
children with CRPS. Multiple physical therapy modalities have been used to treat
CRPS. These include range-of-motion exercises, muscle strengthening and condi-
tioning, massage, paraffin wax, contrast baths, ultrasound, and transcutaneous elec-
trical nerve stimulation (TENS).
Psychiatric/Psychological Intervention
Secondary to the potential chronic pain and disability associated with CRPS, pa-
tients should be sent for psychological evaluation early on in their treatment. Pa-
tients often benefit from cognitive-behavioral skills training. Some patients may
require ongoing psychiatric intervention.
C O M P L E X R E G I O N A L P A I N S Y N D R O M E T Y P E 1 ( R E F L E X S Y M P A T H E T I C D Y S T R O P H Y )
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Complications
Early diagnosis of CRPS is essential for pain relief and restoration of function. The
incidence of poor outcomes is significantly higher in patients who present with a
duration of CRPS greater than 12 months, in the second and third stages of disease,
and in cases with coexisting nerve injuries or compression as a consequence of ini-
tial trauma. Studies have shown a correlation between CRPS and psychosocial dis-
orders. This may complicate treatment.
Suggested Readings
Aprile AE. Complex regional pain syndrome. AANA J 1997;65:557–560.
Galer BS, Bruehl S, Harden RN. IASP diagnostic criteria for complex regional pain
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C O M P R E S S I O N N E U R O P A T H Y
114
Section IV

Nerve Injuries/
Pa lsies
Acute Nerve Laceration
Kevin D. Plancher
A. Nerve Palsies
Low Median Nerve Palsy
Kevin D. Plancher
Ulnar Nerve-Tendon Transfer
Mark S. Cohen
High Radial Nerve Palsy
Kevin D. Plancher
20
Acute Nerve Laceration
Kevin D. Plancher
His tory and Clinical Presentation
A 20-year-old right hand dominant male laborer caught his left hand in a circular
saw with the “guard” off. He has a laceration to his left index finger and can’t feel
the tip of his finger, and has an open bleeding wound.
Phy sic al Ex ami nat ion
On physical examination, the patient has an acute open laceration involving the ra-
dial side of the right index finger. A careful motor examination was performed. The
functioning level of specific muscles is determined to assist with identifying periph-
eral nerve injuries. A two-point sensory discrimination test (Fig. 20–1), as deter-
mined by the Weber two-point discrimination test, using a dull pointed eye caliper
applied in the longitudinal axis of the digit without blanching the skin, and a two-
point discrimination (2-PD) (both moving and static), Semmes-Weinstein monofil-
aments, and vibrometer tests were used to assess the status of the nerves. Denervated
skin responds differently to stimuli; when the injured hand is placed in water, inner-
vated skin wrinkles and denervated skin does not. This test can be helpful in deter-
mining the affected peripheral nerves in the hand in unconscious patients.

Dia gno stic Studies
Radiographs were performed to rule out associated fractures.
Dif feren tia l Diagnosis
Vascular injury
Muscle laceration
Neurologic disorder
Nerve laceration
A C U T E N E R V E L A C E R A T I O N
117
PEARLS
• Microscopic repair is always
more accurate.
• Occupational therapy post-
operatively will successfully
complete a desensitization
program.
• The area of injury must be de-
fined for successful functional
nerve repair.
PITFALLS
• Clean ends of nerve must be
sewn together to avoid a neu-
roma in continuity.
• Missed diagnosis with a devas-
cularized finger may lead to
amputation
• Range of motion must be con-
trolled with splinting.
Figure 20–1. Weber static
two-point sensory discrimina-

tion test.
Dia gno sis
Acute Laceration, Ra dial Nerve, of the Index Finger
Neurapraxia is the mildest form of nerve injury. This usually involves demyelination
without axon disruption and degeneration. This type of injury has a relatively short
recovery time, and full function is expected without intervention.
Axonotmesis occurs when axons, myelin, and associated internal nerve structures
are disrupted. These injuries often result from situations in which traction over-
comes the inelastic internal structures but leaves the elastic epineurium intact.
When axons are disrupted and the endoneurium and the rest of the nerve are intact,
degeneration and regeneration occur. This is the first stage of injury that shows an
advancing Tinel’s sign. Because the endoneurium is intact, regeneration should be
full with complete sensory and motor function regained.
Another type of injury occurs when the axons and the endoneurium are damaged
and the perineurium and epineurium are intact. This leaves the blood–nerve barrier
intact but provides a disorganized bed through which the axons can travel. Nerve
regeneration may be slowed due to infiltration of scar tissue or a smaller number of
axons capable of survival and regeneration. An advancing Tinel’s sign, though some-
what slowed, should be present.
The worst form of closed nerve damage is when all structures are damaged except
the epineurial covering. This disables the intact axons and no conduction down the
nerve is possible. Surgical intervention is required to restore function. A Tinel sign
is present at the level of injury and does not move distally because the regenerating
nerve is kept from advancing by large amounts of scar tissue or debris.
Neurotmesis is the most severe type of injury. This class of injury is easy to diag-
nose because it usually involves an open wound with nerve deficits. Surgical repair is
a requirement for any return in function to occur. Results following the surgical re-
pair of digital nerves are inconsistent. Among the factors that could impact on out-
comes are the amount of direct trauma to the nerve, the length of nerve that has
been traumatized, and the age of the patient. Increased tension on the repair has

also been shown to effect the final results.
Nerve repair never results in the return of full sensibility. However, reasonable
protective sensibility to light touch and pin pricks can be obtained. Two-point dis-
crimination can approach normal in as many as one patient in three (33%).
Surgical Management
After usual draping and prepping of the patient, the skin is marked. The patient is
supine and a regional anesthetic is administered. If multiple structures need to be
repaired, then general anesthesia is used and the arm is exsanguinated using a
tourniquet on the forearm or arm.
Incision use for this procedure is a midaxial incision because it offers the best
extensile exposure to the palm and finger. Some surgeons use a Bruner zigzag to ex-
pose the nerve, but we feel excessive scarring results with this type of incision. Gross
exploration is accomplished under loupe magnification using tenotomy or other
scissors.
After initial exploration, using a microscope for high-power magnification, iden-
tify the nerve and trim any necrotic or bruised tissue until normal fascicles are
N E R V E I N J U R I E S / P A L S I E S
118
found (Fig. 20–2A). Then transect the nerves perpendicular to the main axis and
carefully examine them to ensure that they are healthy and uninjured fascicles are
found (Figs. 20–2B,C). Several sequential transections may be indicated before
finding appropriate endings for repair.
Use a systematic approach consisting of a simple suture first being placed on
either side of the nerve anteriorly. and this is followed by another in the midline
posteriorly. The intervening epineurium is then sutured (Fig. 20–3).
Many surgeons suggest the use of 9-0 or 10-0 nylon or Prolene sutures. If the
nerve is under too much tension, the sutures will not hold. If there is any question
about increased tension on the digital nerve repair, grafting should be considered be-
cause holding a digit in flexion to oppose nerve endings often leads to contracture.
Closure of the wound is accomplished with simple sutures. A bulky bandage is

wound circumferentially around the digit to help diminish swelling. A dorsal and
palmar splint may be applied.
A C U T E N E R V E L A C E R A T I O N
119
A
D
Figure 20–3. Epineurial repair of a nerve. (A) Suture
outside-in from one end. (B) Suture from inside-out on the
matching other end. (C) Nerve laceration systematically
approximated with complete repair and epineurial vessels
correctly aligned. (D) Intraoperative photo showing nerve
repaired.
Figure 20–2. (A) Intraoperative exposed injured radial digital nerve to the index finger. (B) Epineurial repair of a nerve. (C) Fascicular
repair of nerve.
BC
B
A
C
Postoperative Man agement
Splinting is done for a period of 3 weeks (Fig. 20–4), but one sequela can be stiff-
ness in the interphalangeal joints. Absent undue tension on the repair and full ex-
tension, range-of-motion exercises can be started at the time of suture removal or
earlier depending on the quality of the repair.
Hand therapy following nerve repair is individualized, and many patients require
no specific therapy. If stiffness does develop, supervised hand therapy and dynamic
therapy are useful interventions.
Regeneration of the nerve is followed by measuring the paresthesia radiating dis-
tally from the level of nerve repair when the nerve is percussed (Tinel’s sign). As
regeneration continues, the focus of the paresthesia migrates distally. As migration
and healing continue, sensibility is noted proximal to Tinel’s sign.

Complications
Nerve surgery has complications similar to those found in other kinds of surgeries.
Among the more common of these are infection, hematoma, seroma, and injury
to surrounding structures, including vascular structures. Of unique concern dur-
ing nerve surgery is the possibility of downgrading function by further injuring the
nerve, particularly in mixed nerve injuries.
Suggested Readings
Allan CH. Functional results of primary nerve repair. Hand Clin 2000;16:67–72.
Birch R, Raji AR. Repair of median and ulnar nerves. Primary suture is best. J Bone
Joint Surg 1991;73B:154–157.
Cabaud HE, Rodkey WG, Nemeth TJ. Progressive ultrastructural changes after
peripheral nerve transection and repair. J Hand Surg 1982;7A:353–365.
Chow JA, Van Beek AL, Meyer DL, Johnson MC. Surgical significance of the motor
fascicular group of the ulnar nerve in the forearm. J Hand Surg 1985;10A:867–872.
de Medinaceli L, Prayon M, Merle M. Percentage of nerve injuries in which pri-
mary repair can be achieved by end-to-end approximation: review of 2,181 nerve
lesions. Microsurgery 1993;14:244–246.
N E R V E I N J U R I E S / P A L S I E S
120
Figure 20–4. Dorsal block
splint for protection of repair
in a multiple nerve lacerated
hand with digital flexion
begun and an early range-of-
motion program.
Diao E, Vannuyen T. Techniques for primary nerve repair. Hand Clin 2000;16:53–66.
Fu SY, Gordon T. Contributing factors to poor functional recovery after delayed
nerve repair: prolonged denervation. J Neurosci 1995;15:3886–3895.
Hobbs RA, Magnussen PA, Tonkin MA. Palmar cutaneous branch of the median
nerve. J Hand Surg 1990;15A:38–43.

Jabaley ME. Techniques in nerve repair. In: Hunter JM, Schneider LH, eds. Tendon
and Nerve Surgery in the Hand: A Third Decade. St. Louis: Mosby; 1994:89–94.
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Clin 2000;16:13–24.
Lundborg G, Dahlin LB, Danielsen N, et al. Nerve regeneration across an extended
gap: a neurobiological view of nerve repair and the possible involvement of neu-
ronotrophic factors. J Hand Surg 1982;7A:580–587.
Millesi H. Techniques for nerve grafting. Hand Clin 2000;16:73–91.
Smith KL. Anatomy of the peripheral nerve. In: Hunter JM, Schneider LH, eds.
Tendon and Nerve Surgery in the Hand: A Third Decade. St. Louis: Mosby; 1994:
11–18.
Vanderhooft E. Functional outcomes of nerve grafts for the upper and lower ex-
tremities. Hand Clin 2000;16:93–104.
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Hand Surgery. Vol. 2. New York: Churchill Livingstone; 1993:1315–1340.
A C U T E N E R V E L A C E R A T I O N
121
N E R V E I N J U R I E S / P A L S I E S
122
PEARLS
• The EIP muscle belly must be
freed from surrounding soft tis-
sue completely so that when
the tendon is transferred dor-
sally, the muscle fibers are not
angulated.
• The use of the EIP in lieu of
the FDS spares the tendon for
use in an intrinsic transfer if
necessary.

• No pulley is required for the
Burkhalter transfer.
PITFALLS
• The EIP may not be sectioned
distal to the sagittal band. Loss
of independence of index MP
joint extension may then occur
with a small extension lag at
the MP joint.
• If there is an injury to the ulna
distal forearm, scar may cause
adhesions as it is in the path of
the transfer.
• This EIP transfer just reaches
the site of insertion with little or
no leftover tendon. Beware,
and be prepared if the transfer
is short.
21
Low Median Nerve Palsy
Kevin D. Plancher
History and Clinical Presentation
A 17-year-old girl presents following operative repair of a tendon with ulnar
and median nerve injuries to the distal forearm. Her surgery was ~1 year ago. She
is now unable to achieve thumb abduction or metacarpal flexion, and she has
noticed severe clawing of her digits. She has been in occupational therapy for
1 year. She would like to be able to grip wide-mouthed objects, as she was once
able to do.
Physical Examination
The patient cannot oppose her thumb to the little finger. Her skin is supple and

there is no contracture in her first digital web space.
Diagnostic Studies
Plain radiographs were read as normal. Nerve conduction and electromyogram
(EMG) were performed and revealed a combined low median and ulnar nerve
palsy.
Diagnosis
The thumb is key in providing strength for prehensile pinch and grasp. Opposition
is a complex motion involving abduction, flexion, and rotation of the carpometa-
carpal (CMC) joint and flexion and rotations of the metacarpophalangeal (MP)
joint. Median nerve palsy deprives the thumb of its ability to oppose. Restoration of
opposition requires the presence of transferable functioning tendons and a thumb
that has adequate mobility without contractures.
At the level of the wrist, the median nerve lies between the flexor carpi radialis
(FCR) and the palmaris longus tendons. The nerve lies volar to the flexor pollicis
longus and the flexor digitorum profundus. The nerve then enters the carpal tunnel
beneath the transverse carpal ligament. In the carpal canal the nerve may begin to
branch to supply the median-innervated hand intrinsic muscles.
Surgical Management (Burkhalter EIP Transfer)
This transfer of the extensor indicis proprius (EIP) to the abductor pollicis brevis
(APB) was descried by Burkhalter in 1974 and is perfect for patients with an iso-
lated thenar paralysis due to low or high median nerve injury. The transfer achieves
excellent thumb abduction, pronation, and MP flexion.
L O W M E D I A N N E R V E P A L S Y
123
Figure 21–1. Relationship of exten-
sor indicis proprius (EIP) on the
ulnar side of the extensor digitorum
communis (EDC), seen over the
index metacarpal (right hand dorsal
approach).

With the patient under either general or regional anesthetic, a tourniquet is ap-
plied to exsanguinate the operative extremity. The planned incisions are outlined
and a longitudinal incision is made over the index MP joint. The EIP tendon is then
identified ulnar to the extensor communis tendon (Fig. 21–1).
An incision is then made on the ulnar side of the EIP, through the sagittal band,
and extended distally. A similar incision is made on the radial side, separating it
from the extensor digitorum communis, and then connecting it to the distal inci-
sion on the ulnar side (Fig. 21–2). The sagittal band is repaired at this point in the
operation to avoid an extensor lag.
Once the distal attachment of the EIP is released, a linear incision is made over
the dorsal, ulnar aspect of the distal forearm and the deep fascia is divided longitu-
dinally. The EIP tendon and muscle are identified and delivered to the proximal
wound. If delivery is hampered by adhesions or connection of the EIP tendon in the
dorsum of the hand, another incision may be required to free the tendon and mus-
cle belly fully.
Once the EIP and muscle belly are freed, a small longitudinal incision is made
just distal to the pisiform, and a subcutaneous tunnel is created across the forearm
from the dorso-ulnar distal forearm incision to this second incision distal to the
pisiform (Fig. 21–3A). Care should be taken to ensure that the tunnel is large
enough to accept the muscle belly of the EIP or it may prevent full excursion of the
donor tendon. The tendon can be passed through the tunnel using a tendon passer
or hemostat.
A
B
Figure 21–3. (A) Clinical photo of the EIP tendon being
pulled subcutaneously from dorsal to volar to be distal to the
pisiform. (B) The EIP is transferred from the distal ulna
volar forearm to the insertion of the abductor pollicis brevis
(APB) subcutaneously.
Figure 21–2. Distal EIP is sutured to the EDC tendon and trans-

ferred subcutaneously to the midforearm.
Figure 21–4. The EIP is sewn into place, weaved into the APB
tendon.
L O W M E D I A N N E R V E P A L S Y
125
A second subcutaneous tunnel is made across the palm to the thumb MP joint.
The line of pull is estimated by placing the donor tendon to the proposed insertion
site on the distal thumb metacarpal (Fig. 21–3B).
Regardless of the method of attachment used, the transferred tendon needs to be
securely fixed in place. This can be accomplished using a bone tunnel or weaving
the EIP through the abductor pollicis brevis (Fig. 21–4).
The thumb is placed in full opposition to the small finger. The EIP transfer is
tensioned and secured. The tourniquet is then released, hemostasis is obtained, and
the wounds are closed (Fig. 21–5). When the procedure is completed, a bulky hand
A
C
B
Figure 21–5. (A,B) Artwork of volar and
dorsal incisions of the hand and forearm
closed once the tension of the transfer is
secured and tested with the tenodesis effect.
(C) Clinical photo of EIP transfer complete
with all skin wounds closed.