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Chapter 14 Electrodiagnostic Examination 253
muscles in each myotome, and only some of them can be
sampled. With suspected thoracic radiculopathies, only the
paraspinal and abdominal muscles are sampled routinely; the
intercostal muscles are typically not studied for fear of entering the pleural space. Generally, if NEE abnormalities are seen,
no attempt is made to identify a specic root lesion. Instead,
the localization is limited to upper thoracic, midthoracic,
or lower thoracic root involvement. Most patients found to
have thoracic radiculopathies have diabetes mellitus, and the
pathology is probably root infarction or ischemia rather than
compression. In any case, these radiculopathies oen produce
very severe axon loss and frequently apparently involve two
or more adjacent roots.
9,20,21
T1 radiculopathies are quite
rare and typically produce changes only in the lateral thenar
muscles.
22
Dierential Diagnoses
Although neurogenic thoracic outlet syndrome may technically be considered an extraspinal radiculopathy aecting the
T1 nerve root and to a lesser extent C8, it has classically
been categorized as a lower trunk brachial plexopathy (see
Table 14.5). e preferential involvement of the T1 nerve
root leads to prominent abnormalities of the abductor pollicis brevis muscle and the medial antebrachial cutaneous
sensory response, both of which are heavily innervated by
T1. In contrast, the ulnar-innervated segments, which are
predominantly innervated by C8, are sometimes spared or
only mildly aected. Abnormalities in the abductor pollicis
brevis are evident on motor NCS (manifested as decreased
CMAP amplitude) and NEE (brillation potentials or neuro-
genic recruitment pattern), whereas the medial antebrachial
cutaneous SNAP is reduced or absent. e latter abnormality
is helpful in distinguishing this syndrome from a typical T1
radiculopathy.
Lumbosacral Radiculopathy
Nerve root lesions are most commonly seen in the lumbosacral
spine—more than two-thirds of all radiculopathies occur in
this region.7 In contrast to lesions involving the cervical roots,
it is dicult sometimes to localize lumbosacral radiculopathies accurately to a vertebral level with the electrodiagnostic
examination. is diculty is primarily due to anatomic
reasons. Given their long intraspinal course, lumbosacral
nerve roots may be injured anywhere along their tract from
the T12–L1 vertebral level where they are formed, down
through the canal into the cauda equina, and the site where
they exit from their respective foramina. e L5 nerve root
can be compressed by a central disc herniation at the L3–L4
level, a posterolateral disc herniation at the L4–L5 level, or
foraminal stenosis at the L5–S1 level. Additionally, when
nerves are aected at the level of the cauda equina where the
bers are compact, a single lesion in this location can result
in injury to multiple roots bilaterally. It is important to perform
comparison NEE of the contralateral limb when any abnormalities are seen to exclude the possibility of subclinical nerve
root involvement.
L2, L3, and L4 radiculopathies are generally considered
together because of the myotome overlap of the thigh muscles
and the paucity of muscles that are innervated solely by one
individual nerve root. Localization of an L2 root lesion is
dicult because only the iliacus muscle may show abnormalities on NEE. Lesions at these levels typically produce denervation changes in the quadriceps, thigh adductors, and iliacus.
With L4 lesions, abnormalities may also be seen in the tibialis
anterior occasionally.
e most common lumbosacral radiculopathies involve
the L5 and S1 roots. Lesions of these two roots are most
amenable to recognition on electrodiagnostic examination. In
addition, the L5 nerve root is the most common single radiculopathy seen.3 L5 radiculopathies produce abnormalities in
the tibialis anterior, exor digitorum longus, and posterior
tibialis in greater than 75% of surgically proven cases.23 In a
more recent study, 100% of patients with L5 radiculopathies,
which were also surgically proven, showed abnormalities in
the peroneus longus and tensor fascia lata.24 Changes may
also be seen in the extensor digitorum brevis, gluteus medius,
and semitendinosus.
An exception to the rule that SNAPs are not aected in
radiculopathies has been found to occur with some L5 root
lesions. As stated before, SNAPs are typically spared in radiculopathies because the lesion is situated proximal to sensory
cell bodies (DRG), which lie in the intervertebral foramina
outside of the intraspinal canal. However, at the level of the
lumbosacral spine, the DRG is sometimes found proximal to
the intervertebral foramina within the intraspinal canal,
leaving them vulnerable to injury from a herniated disc or
other degenerative spine condition. Based on cadaveric,
radiographic, and MRI studies, 3% of L3 and L4 DRG are
intraspinal, 11% to 38% of L5 DRG are intraspinal, and up to
71% of S1 DRG are intraspinal.
24–26
us, in some cases, the
L5 nerve root may be aected distal to the DRG, resulting in
an abnormal supercial peroneal SNAP. In one retrospective
study, six patients with clinical and radiographic evidence of
an L5 radiculopathy were found to have reduced amplitude of
the ipsilateral supercial peroneal SNAP along with denervation changes in the L5 myotome.27 is condition has not been
found with S1 nerve root lesions, in which the sural SNAP
remains normal despite the higher percentage of DRG located
within the intraspinal canal.
S1 radiculopathies are the second most common root
lesion encountered. Needle EMG may show abnormalities in
the gastrocnemii, abductor hallucis, abductor digit quinti
pedis, glutei, and biceps femoris short head. In addition, the
H response is either absent or reduced in amplitude.
Dierential Diagnoses
As seen in the cervical spine, it is oen dicult to clinically
distinguish lesions of the lumbosacral nerve roots from lesions
of the lumbar and sacral plexuses (see Table 14.5). L2–L4
radiculopathies can look identical to lumbar plexopathies,
whereas L5–S1 nerve root lesions closely resemble lesions of
the sacral plexus. In both cases, the combination of brillation
potentials in the lumbosacral paraspinals and preserved
SECTION
II
254 DIAGNOSIS
sensory nerve conduction responses (lateral femoral cutaneous and saphenous SNAPs for L2–L4 lesions and sural and
supercial peroneal SNAPs for L5–S1 lesions) points to the
diagnosis of radiculopathy.
A major limitation is encountered when SNAPs are absent
bilaterally. In the workup of a lesion in the lumbar plexus
versus an L2–L4 nerve root lesion, the sensory nerve conduction responses are not consistently obtainable from a technical standpoint, even in normal individuals. Likewise, in the
evaluation of a sacral plexus versus an L5–S1 lesion, SNAPs
may be absent in elderly patients or patients with a history of
a polyneuropathy. In both instances, the diagnosis rests on a
single crucial nding: the absence or presence of denervation
in the paraspinals. is nding in itself is unreliable, as noted
earlier, in that paraspinal brillation potentials may be present
rarely in normal individuals older than 60 years, in patients
with a history of prior spine surgery, and in patients with
diabetes. Denervation changes may be absent because of early
reinnervation or sampling error. As a result, in patients with
bilaterally absent SNAPs (owing to technical or other reasons),
the nal electrodiagnostic impression may be inconclusive.
For similar reasons, bilateral S1 radiculopathies, particularly when chronic, may be confused with distal axon-loss
polyneuropathies. In younger patients (<60 years old), an
absent sural response combined with abnormalities seen in
the intrinsic foot muscles on NEE typically indicates the presence of a polyneuropathy rather than S1 radiculopathy.
Electrodiagnostic Findings of Other Spine-Related Disorders
Spinal
cord
Preganglionic
sensory fibers
Cauda
equina
Sacrum
FIG. 14.10 Coronal view of inferior spinal cord, cauda equina, and
surrounding structures. Dorsal root ganglia are located in the intervertebral
foramina so that all the sensory bers composing the cauda equina are
“preganglionic.” Axon-loss lesion of cauda equina generally has no eect on
lower limb sensory nerve conduction studies, regardless of its severity.
Dorsal root
ganglion
Filum terminale
Lumbar Canal Stenosis
Cauda Equina Syndrome
Multiple lumbosacral radiculopathies are encountered with
some frequency. Typically, the involvement is bilateral and
oen asymmetric.
midline lumbar disc protrusions or lumbar canal stenosis.
Characteristically, S1 and S2 roots, being the most medial of
the roots supplying the lower limbs, are aected. In many
patients, more extensive lumbosacral root involvement occurs;
a common combination is bilateral S1 and S2 root compromise
accompanied by unilateral or bilateral L5 root involvement.
e electrodiagnostic ndings most commonly seen consist
of a mixture of low-amplitude CMAPs and normal SNAPs on
NCS, along with brillation potentials and MUP dropout on
needle EMG (Fig. 14.10). On NEE, the abnormalities oen are
more severe in muscles located distal to the knees. With some
substantial lesions of recent onset, they are just as prominent
in the more proximal muscles. Whenever the disorder is
subacute or chronic, brillation potentials usually are accom-
panied by chronic neurogenic MUP changes. Low lumbar or
high sacral paraspinal brillation potentials oen are found
bilaterally with more acute lesions, but are undetectable with
many chronic ones. Typically, the H responses cannot be
elicited, and even the M components of the H responses,
recorded from the gastrocnemius/soleus muscles, are quite
low in amplitude.
10,20
Most of these lesions are attributable to
Lumbar canal stenosis has no single characteristic electrodiagnostic presentation. Rather, the ndings are extremely
variable, depending on the degree of axon loss aecting the
lumbosacral motor roots. At one extreme are patients who
experience only intermittent, short-lived symptoms that oen
can be relieved completely by various maneuvers (e.g., sitting,
exing at the waist). In these patients, the electrodiagnostic
examination oen is completely normal. At the opposite end
of the spectrum are patients who have substantial cauda
equina lesions with severe, bilateral, xed motor and sensory
decits. ese lesions produce the electrodiagnostic presentation described previously.
Between these two extremes are numerous dierent elec-
trodiagnostic patterns: (1) two or more radiculopathies, far
more oen bilateral than strictly unilateral; (2) a single radiculopathy, typically S1, that is sometimes detected in the less
symptomatic or asymptomatic limb; (3) unilateral or bilateral
absent H responses alone; (4) NEE changes restricted to just
one or two limb muscles, most commonly those innervated
by the S1 roots; or (5) brillation potentials limited to the
paraspinal muscles.
9,19
Myelopathy
e eect that a focal myelopathy has on the electrodiagnostic examination depends principally on whether the
Chapter 14 Electrodiagnostic Examination 255
anterior horn cells or their existing bers are compromised
at the level of the lesion. If only the descending corticospinal
tracts of the spinal cord are aected (upper motor neuron
lesion), the only abnormality found on the electrodiagnostic
examination concerns the MUP ring pattern of muscles
receiving innervation from spinal cord segments caudal to
the lesion. In these muscles, the MUPs show no or incomplete
activation (i.e., they re in decreased numbers at a slow to
moderate rate).
In contrast, if the anterior horn cells or the intramedullary
bers derived from them are involved, the electrodiagnostic
ndings are those of a focal intraspinal canal lesion that is
characteristically bilateral, but oen asymmetric. How promi-
nent the electrodiagnostic changes are with such focal disorders depends mainly on where the lesions are located along
the spinal cord. Lesions situated in C5–T1 segments and L4–S2
segments produce substantial abnormalities on motor NCSs
and NEE, and generally are readily recognized as intraspinal
canal lesions. All such disorders result in low-amplitude
CMAPs or CMAPs that cannot be elicited and normal SNAPs
on NCS, accompanied by brillation potentials, MUP dropout,
and, depending on lesion duration, chronic neurogenic MUP
changes on needle EMG. Conversely, lesions involving T2
through L3 segments result only in NEE changes (i.e., motor
NCSs using various limb muscles as recording sites are
normal). Finally, lesions involving the upper cervical cord
segments (C1–C4) have essentially no electrodiagnostic manifestations because that region of the spinal cord cannot be
assessed.
27
Postlaminectomy Electrodiagnostic Findings
Electrodiagnostic examinations are obtained frequently on
patients who have undergone neck or back surgery. e spe-
cic diagnostic benet derived from such assessments varies
considerably, depending on the reason for referral and the
time that has elapsed since operation. Overall, such postoperative studies are of limited value, however, unless they are
obtained aer very remote surgery to diagnose a recent-onset
lesion. In the immediate postoperative period (rst 10–14
days aer surgery), the electrodiagnostic examination can
reveal preexisting abnormalities because any NEE changes
observed during that period, with the exception of a reduced
MUP recruitment, are caused by a lesion that predated the
operation.
During the early postoperative period (3 weeks to 3–4
months aer surgery), the electrodiagnostic examination is of
considerable benet in assessing patients with postoperative
weakness, principally because a normal CMAP amplitude
recorded from a weak muscle (e.g., the tibialis anterior, resulting in footdrop) 7 or more days aer onset of symptoms virtu-
ally excludes motor axon loss as the cause. e remaining
possibilities include a proximal conduction block (neurapraxia), an upper motor neuron lesion, or hysteria or malingering. In the rare patient who develops nonorganic weakness
postoperatively, the electrodiagnostic examination can prove
that the symptoms are not the result of signicant nerve ber
damage.
e electrodiagnostic examination usually cannot answer
reliably the early postoperative question: “Was the root
adequately decompressed?” Axon loss features of radiculopathy persist for weeks to months or indenitely. Even
an electrodiagnostic examination performed 2 to 3 months
postoperatively is not likely to show signicant improvement compared with a preoperative study. An exception is
radiculopathy resulting from conduction block at the root
level, which may resolve rapidly aer the pressure is relieved.
With an S1 radiculopathy, an H response that could not be
elicited preoperatively may reappear in the early postoperative
period. Similarly, on NEE, reduced MUP recruitment (and
clinical weakness) could resolve rapidly in the aected muscles
postoperatively.
An electrodiagnostic examination can be valuable in identifying root damage as the cause of new or worsening weakness
in the postoperative period. e extent, amount, and distribution of brillation potentials provide information when
compared with the preoperative study.
Cervical Root Avulsion
Root avulsions, which are usually restricted to the cervical
region, dier from the typical single compressive radiculopa-
thy principally in the degree of axon loss that results. Because
the entire motor supply from one or both roots innervating
the particular muscle has been disrupted, that muscle is
severely or totally denervated. If it is used as a recorded muscle
during motor NCS, the CMAP obtained is of very low amplitude, if it can be elicited. Similarly, during needle EMG of that
muscle, brillation potentials are abundant, and MUPs are
either absent or, if present, quite sparse and show reduced
recruitment. Sensory NCS responses derived from the same
roots are normal because the sensory roots are interrupted
proximal to their DRG. Fibrillation potentials are oen not
found in the appropriate paraspinal muscles in patients with
cervical avulsion injuries; thus, their absence does not exclude
this diagnosis.
9
Acknowledgments
I acknowledge the late Dr. Asa J. Wilbourn for his contributions to the original version of this chapter.
KEY POINTS
1. The electrodiagnostic examination is an essential tool in the
evaluation of radiculopathy. When performed by an experienced
electrodiagnostic consultant, the electrodiagnostic examination
can conrm the diagnosis and determine the localization, lesion
duration, and severity.
2.
The electrodiagnostic examination assesses the integrity of large
sensory and motor nerve bers, but not small bers, such as
small C-type bers that mediate pain. Therefore, pain alone
cannot be assessed by electrodiagnostic testing.
Electrodiagnostic testing is more valuable when pain is
associated with large nerve ber dysfunction, such as weakness.
3.
For a comprehensive study, the electrodiagnostic examination
should be performed at least 3 weeks after the onset of
symptoms.
SECTION
II
256 DIAGNOSIS
4. The most widely used criterion for diagnosing radiculopathies
by NEE is that abnormalities (e.g., brillation potentials or
neurogenic MUP changes) should be found in at least two limb
muscles within the same myotome that is innervated by
dierent peripheral nerves.
5.
Sensory nerve conduction responses are typically normal in
radiculopathy owing to the location of the DRG outside of the
intraspinal canal, distal to the site of the nerve lesion. In
contrast, amplitudes of the motor NCS may be decreased when
root damage is severe, extensive, or both.
KEY REFERENCES
1. Wilbourn AJ, Amino MJ. AAEM Minimonograph #32: the
electrodiagnostic examination in patients with radiculopathies.
Muscle Nerve. 1998;21:1612-1631.
This review article describes and critically analyzes the various
neurophysiologic techniques used in assessment of radiculopathy
and details the ndings with root lesions at various levels.
2.
Wilbourn AJ. Nerve conduction studies: types, components,
abnormalities, and value in localization. Neurol Clin.
2002;20:305-338.
This article reviews the types of pathophysiology manifested by focal
nerve ber lesions and what eect each has on NCS; it also describes
the types of localization possible with the electrodiagnostic
examination and the major sources of error.
3.
Shea PA, Woods WW, Werden DH. Electromyography in
diagnosis of nerve root compression syndrome. Arch Neurol
Psychiatry. 1950;64:93-104.
4.
Woods WW, Shea PA. The value of electromyography in
neurology and neurosurgery. J Neurosurg. 1951;8:595-607.
Key References 3 and 4 were the rst to discuss the methodology
used for diagnosing radiculopathies in the clinical EMG laboratory
(which is still used currently).
5.
Yoss RE, Corbin KB, MacCarty CS, et al. Signicance of symptoms
and signs in localization of involved root in cervical disc
protrusion. Neurology. 1957;7:673-683.
This unique article remains the best source regarding the specic
symptoms and clinical ndings with lesions of each of the cervical
roots (C5 through C8).
REFERENCES
1. Wilbourn AJ. Nerve conduction studies: types, components,
abnormalities, and value in localization. Neurol Clin.
2002;20:305-338.
2. Preston DC, Shapiro BE. Electromyography and Neuromuscular
Disorders. Boston: Butterworth-Heinemann; 1998.
3. Wilbourn AJ, Ferrante MA. Clinical electromyography.
In: Joynt RJ, Greggs RC, eds. Baker’s Clinical Neurology on
CD-ROM. Philadelphia: Lippincott Williams & Wilkins;
2000.
4. Dimitru D, Amato AA, Awarts MJ. Electrodiagnostic Medicine.
2nd ed. Philadelphia: Hanley & Belfus; 2002.
5. Shea PA, Woods WW, Werden DH. Electromyography in
diagnosis of nerve root compression syndrome. Arch Neurol
Psychiatry. 1950;64:93-104.
6. Woods WW, Shea PA. e value of electromyography in
neurology and neurosurgery. J Neurosurg. 1951;8:595-607.
7. Wilbourn AJ, Amino MJ. Radiculopathies. In: Brown WF,
Bolton CF, eds. Clinical Electromyography. 2nd ed. Boston:
Butterworth-Heinemann; 1993:177-209.
8. Wilbourn AJ. e value and limitations of the
electromyographic examination in the diagnosis of lumbosacral
radiculopathy. In: Hardy RW, ed. Lumbar Disc Disease. New
York: Raven Press; 1982:65-109.
9. Wilbourn AJ, Amino MJ. AAEM Minimonograph #32: the
electrodiagnostic examination in patients with radiculopathies.
Muscle Nerve. 1998;21:1612-1631.
10. Raynor EM, Kleiner-Fisman G, Nardin RA. Lumbosacral and
thoracic radiculopathies. In: Kitirji B, Kaminski HJ, Preston
DC, et al., eds. Neuromuscular Disorders in Clinical Practice.
Boston: Butterworth-Heinemann; 2002:859-883.
11. Levin KH. Radiculopathy. In: Levin KH, Luders HO, eds.
Comprehensive Clinical Neurophysiology. Philadelphia: WB
Saunders; 2000:189-200.
12. Johnson EW. Electrodiagnosis of radiculopathy. In: Johnson
EW, ed. Practical Electromyography. 2nd ed. Baltimore:
Williams & Wilkins; 1988:229-245.
13. Braddom RI, Johnson EW. Standardization of “H” reex and
diagnostic use in S1 radiculopathies. Arch Phys Med Rehabil.
1974;55:161-164.
14. Schuchmann J. H-reex latency in radiculopathy. Arch Phys
Med Rehabil. 1978;59:185-187.
15. Eisen A, Schomer D, Melmad C. An electrophysiological
method for examining lumbosacral root compression. Can J
Neurol Sci. 1977;4:117-123.
16. Fisher MN, Shidve AJ, Terxera C, et al. e F response—a
clinically useful physiological parameter for the evaluation
of radicular injury. Electromyogr Clin Neurophysiol. 1979;19:
65-75.
17. Yoss RE, Corbin KB, MacCarty CS, et al. Signicance of
symptoms and signs in localization of involved root in cervical
disc protrusion. Neurology. 1957;7:673-683.
18. Marinacci AA. A correlation between operative ndings
in cervical herniated disc with the EMGs and opaque
myelograms. EMG. 1966;6:5-20.
19. Levin KH, Maggiano HJ, Wilbourn AJ. Cervical
radiculopathies: comparison of surgical and EMG localization
of single-root lesions. Neurology. 1996;46:1022-1025.
20. Wilbourn AJ. e electrodiagnostic examination. In: Herkowitz
HN, Garn SR, Barlderston RA, et al., eds. e Spine. 4th ed.
Philadelphia: WB Saunders; 1999:135-150.
21. Wilbourn AJ. Diabetic neuropathies. In: Brown WF,
Bolton CF, eds. Clinical Electromyography. 2nd ed. Boston:
Butterworth-Heinemann; 1993:447-515.
22. Levin KH. Neurological manifestations of compressive
radiculopathy of the rst thoracic root. Neurology.
1999;53:1149-1151.
23. Bodner RA, Levin KH, Wilbourn AJ. Lumbosacral
radiculopathies: comparison of surgical and EMG localization.
Muscle Nerve. 1995;18:1071.
24. Tsao BE, Levin KH, Bodner RA. Comparison of surgical
and electrodiagnostic ndings in single root lumbosacral
radiculopathies. Muscle Nerve. 2003;27:60-64.
25. Hamanishi C, Tanaka S. Dorsal root ganglia in the lumbosacral
region observed from the axial view of MIR. Spine.
1993;18:1753-1756.
26. Sato K, Kikuchi S. An anatomic study of foraminal nerve root
lesions in the lumbar spine. Spine. 1993;18:2246-2251.
27. Levin KH. L5 radiculopathy with reduced supercial peroneal
sensory responses: intraspinal and extraspinal causes. Muscle
Nerve. 1998;21:3-7.
Intraoperative Neurophysiologic Monitoring
SECTION
15
CHAPTER
e primary objective in intraoperative neurophysiologic
monitoring is to identify and prevent the development of a
new neurologic decit or worsening of a preexisting neuro-
logic injury to a patient who is undergoing surgery. e aim
of most spinal cord monitoring is to prevent intraoperative
injury that results in irreversible paraplegia or quadriplegia.
Due to the inability of performing a neurologic examination
in an anesthetized patient, intraoperative neurophysiologic
monitoring is used to determine the patient’s neurologic status
during surgery. By evaluating the responses produced by the
patient’s nervous system to a variety of stimulation, the integrity of that neural pathway can be monitored. ese recordings
are started prior to surgery, referred to as baseline recordings,
then continued throughout the surgery. Any signicant
changes or uctuations from these baseline values are then
used to determine whether any signicant neurologic injury
has occurred. With this strategy, the patient’s own responses
serve as the control for the detection of any abnormalities that
may occur during the surgery. e term signicant change is
used in reference to the degree of changes seen in the neurophysiologic recordings. Changes termed signicant have been
shown to correlate well with intraoperative injury to the
nervous system. However, it is also possible that some of these
signicant changes may also arise from other changes in
physiologic parameters, anesthetic parameters, or possibly
technical issues. It is then up to the intraoperative neurophysiologic monitoring team to determine whether the signicant
changes noted in the neurophysiologic responses are truly
related to the surgical procedure at hand. e challenge to the
intraoperative neurophysiologist and the monitoring team is
to alert the surgeon of these changes as early as possible and
to evaluate and rule out various technical and nonsurgical
causes that may also aect the responses being recorded.
Key to the success of intraoperative neurophysiologic
monitoring is a good understanding of the capabilities and
limitations of the neurophysiologic tests being monitored.
ese limitations should be understood not only by the
intraoperative neurophysiologist but also by the anesthesiologist and surgeon. For seamless integration of intraoperative
neurophysiologic monitoring into the intraoperative team,
a good working relationship among the intraoperative
of the Spine
Dileep R. Nair
Ajay Gupta
neurophysiology team, anesthesiologist, and surgeon is
imperative. is allows for rapid communication between
teams and a quick resolution of issues, thus optimizing the
benets of intraoperative neurophysiologic monitoring for the
patient.
One of the rst issues to address when planning for intraoperative neurophysiologic monitoring is to determine the
types of neurophysiologic tests to perform on a particular
patient undergoing surgery. is is accomplished by understanding the type of surgery the patient will undergo, the types
of intraoperative injuries that may occur, and the mechanisms
of how these injuries occur in surgery. By planning ahead with
these issues in mind, the team can also attempt to anticipate
the type of changes that could occur as well the risky periods
during surgery when these changes would be likely. Ideally,
they would prospectively plan for interventions to reduce
intraoperative neurologic injury.
Intraoperative Monitoring of the Spinal Cord
Somatosensory-evoked potential (SEP) monitoring has been
used for many years to monitor spinal function intraoperatively during a variety of surgeries involving the spine (e.g.,
corrective surgery for scoliosis or other congenital deformities, removal of intraspinal tumors or arteriovenous malformations). is monitoring modality has been shown to reduce
the incidence of neurologic damage in large-scale studies of
experienced monitoring teams.1 SEPs only monitor sensory
transmission through the dorsal column pathways. In other
words, this modality does not provide a direct measure of
motor function. In addition, it is important to be aware that
the dorsal columns receive their blood supply from the posterior spinal arteries, whereas the anterior spinal arteries supply
the motor pathways. erefore ischemic damage to the spinal
cord from an anterior spinal artery may go undetectable with
SEP monitoring.
monitoring might mandate further assessment of the patient’s
motor function by waking the patient up during surgery to
evaluate leg and arm motor function (the “wake-up test”). e
disadvantages of this strategy include the lack of online
2,3
erefore a signicant change in SEP
II
257
258 DIAGNOSIS
intraoperative motor function assessment as well as the anesthesia risks associated with performing the wake-up test. An
alternative is monitoring the motor pathway through the
recording of motor-evoked potentials (MEPs).
MEP monitoring has been performed in the past by
directly relying on stimulation of the spinal cord.4 Spinal cord
stimulation can be done with the use of epidural electrodes
inserted aer a laminectomy or by percutaneous intraspinous
needle electrodes. e epidural electrodes are invasive and
oen require placment by a skilled anesthesiologist. Percutaneous intraspinous needles are dicult to place accurately
and thus may not achieve adequate or consistent stimulation
of the spinal cord. In addition, there is the question of whether
MEPs generated through spinal cord stimulation arise solely
from propagation through the motor pathway or if multiple
pathways are involved in their generation.
5,6
ere are reports
of MEP monitoring in which spinal cord stimulation resulted
in no signicant intraoperative changes but yet a postoperative
neurologic motor decits occurred (so-called false-negative
result).7 It has been suggested that motor cortex stimulation
with transcranial electrical stimulation would provide a more
reliable methodology for monitoring the motor pathways.
is technique has become a routine modality in spinal cord
monitoring along with SEPs.
FIG. 15.1 Signicant amplitude change in cortical response due to
ischemic etiology. The stack on the left shows the leg cortical response; the
stack on the right shows the popliteal fossa response. Both were obtained
after left posterior tibial stimulation. The baseline responses are shown at
the top of the stack and the end of monitoring is shown at the bottom of
the stack. A drop in the leg cortical amplitude can be appreciated at the
point depicted by the arrow. Note the popliteal fossa responses are intact
during this time. There is a return of the response by the end of surgery
seen at the bottom of the stack. This change was attributed to an ischemic
change to the cord with the retractor placed over the left iliac artery. The
responses returned when the retractor was adjusted away from the artery.
Somatosensory-Evoked Potential Monitoring
e use of SEPs in intraoperative monitoring of complex spine
surgeries began in the early 1970s.8 Although SEP monitoring
primarily evaluates the integrity of the posterior columns, it is
oen used to give an overall assessment of the spinal cord
based on the assumption that many intraoperative mechanisms of injury aect the spinal cord diusely. An example of
such an injury is spine distraction during scoliosis surgery. In
addition, ischemic injury may initially result in a more diuse
dysfunction of the spinal cord that could be detected by SEPs
(Fig. 15.1). SEP responses are thought to pass through both
large ber somatosensory pathways of the dorsal column as
well as possibly the anterior spinothalamic tract. is may be
another reason why anterior spinal artery ischemia could be
detected by this technique.
Generators of the Somatosensory-Evoked Potential Responses
e cortical response for the lower extremity is called the P37
potential. e generator of this response arises from the
primary somatosensory cortex of the leg, which is located in
the mesial parietal cortex. e cortical response for the upper
extremity, which is generated from the primary somatosensory
cortex of the hand, is called the N20 potential (Fig. 15.2). Two
important characteristics of these waveforms include (1)
amplitude, which is recorded in microvolts and determined by
either a baseline to peak or peak to trough measure of the
waveform, and (2) latency, which is recorded in milliseconds
and is the time interval from the stimulus to the occurrence
of the potential. An amplitude change from the initial baseline
measure to a decrease of more than 50% is oen termed a
TABLE 15.1 Signicant Changes in Dierent Monitoring Modalities
Highly Signicant
Type of Study Signicant Changes
Somatosensory-
evoked potentials
Motor-evoked
potentials
Pedicle screw
stimulation
Amplitude <50%;
latency >10%
Increase threshold
voltage >
Current intensity
<
50–100 V
7–10 mA
Changes
Complete loss of
amplitude
Complete loss of
amplitude
signicant change in SEP amplitude.9 Signicant latency
changes in SEP monitoring consist of a 10% prolongation
beyond the baseline latency value (Table 15.1).10 Although
these deviations from the baseline measures are thought to be
signicant, they should be interpreted with caution, taking
into account various factors that include the evolution of the
changes (e.g., a trend toward worsening is an ominous sign)
and various other intraoperative factors that include length of
the surgery, type of anesthetic agent, and temperature eects.
It is also important to remember that signicant latency and
amplitude changes can occur in isolation. It is quite common
to see a signicant amplitude change without any associated
latency changes. e most signicant change is a complete loss
of the cortical potential.
Another measurement made in posterior tibial or peroneal
nerve SEP monitoring is the popliteal fossa (PF) potential.
is is a nerve action potential that is recorded as the impulses
pass under the popliteal fossa in the peripheral nervous
system. is measurement ensures that an adequate stimulus
has been applied. If the PF response is absent in addition to
an absent leg cortical (P37) response, the changes seen may
Chapter 15 Intraoperative Neurophysiologic Monitoring of the Spine 259
FIG. 15.2 Typical morphology of the cortical generators of median nerve and posterior tibial nerve
somatosensory-evoked potential (SEP) waveforms are shown. Note that the display time is dierent between
the two modalities. Median nerve SEP is shown in a 5 ms per division display and posterior tibial nerve SEP is
shown in a 10 ms per division display.
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II
not be a result of a lesion at the level of the spinal cord. In this
case, the change may be either technical (e.g., the stimulating
needles may have dislodged) or the leg may be ischemic (e.g.,
in the case of femoral artery catheterization during thoracoabdominal aneurysm surgery or direct compression of the
peripheral nerve) (Fig. 15.3).
Another posterior tibial stimulation SEP response that
can be monitored is the P31/N34 complex, oen termed the
subcortical response, because the generator for these responses
is at the level of medulla and midbrain. ese responses are
relatively more resistant to the eects of anesthesia compared
with the cortical P37 response (see Fig. 15.2). e same is true
for the subcortical potentials from median nerve stimulation
(P14/N18) potential. In pediatric cases, the subcortical potentials may also be better formed and more easily monitored
than cortical responses. Some of this eect may be the result
of the variation of myelination in the younger age groups
and more signicant eects of anesthetics on these patients.
Moreover, these dierences from the adult morphology can
persist into the early teenage years. Other factors aecting the
responses include core body temperature changes. It is not
uncommon for the core body temperature to change more
than 1°C. e cooling aects the limbs disproportionately to
the core body temperature, which can result in slowing of
conduction.
Motor-Evoked Potential Monitoring
A variety of methods have been used to monitor spinal motor
pathways during surgery, as mentioned earlier. Most of these
methods involve recording of electromyographic (EMG) readings from appropriate muscles in response to stimulation of a
motor pathway rostral to the operative site. e dierence
among the various methods is the nature of the stimulation.
ere are three basic categories of stimulation: rostral spinal
stimulation, transcranial magnetic stimulation, and transcranial electrical stimulation (TCES). Magnetic stimulation is
eective in nonanesthetized patients for motor pathways
evaluation, but the suppression of cortical responsiveness
under anesthesia (mainly inhalational anesthetics) renders
this method less eective for surgical use. In addition, the
equipment used for magnetic stimulation is expensive, bulky,
and has a tendency to overheat.
Noninvasive stimulation of the brain using TCES was rst
reported in 1980.11 Soon aer, single-pulse TCES was used in
monitoring motor pathways.
12-17
Because of the eects of
general anesthesia, single-pulse stimulation was found to be
less reliable in recording MEPs.
18-22
With the introduction of
the multipulse technique for motor pathway monitoring, reliable and robust MEP recording can now be obtained in most
patients using specic general anesthesia protocols.
23-27
Multipulse techniques require that neuromuscular blockade not be
used during this part of the monitoring. Occasionally the use
of partial neuromuscular blockade may still allow for TCES
moniotring.28 is method reportedly achieves more reliable
stimulation of the motor cortex intraoperatively and is more
resilient to the eects of general anesthesia.
e methodology of MEP monitoring has been revolutionized by the use of multipulse TCES. Previous methods for
MEP recording used a variety of stimulation and recording
techniques. Spinally elicited neurogenic responses were used
and were putatively stated to be a result of activation of the
motor pathways in the spinal cord. Recent evidence has suggested that these spinally elicited neurogenic responses are
260 DIAGNOSIS
FIG. 15.3 Signicant change in left N20 cortical amplitude due to arm positioning and nonsignicant latency
prolongation of all cortical responses due to anesthetic eect. The top row of stacks shows popliteal fossa (PF)
and leg cortical (P37) responses from the posterior tibial stimulation, rst from left-side stimulation and then
right-side stimulation. The bottom row of stacks shows Erb’s point (EP) and arm cortical (N20) response from
median nerve stimulation, with the left side shown rst followed by right-side stimulation. There is a drop in
the left N20 amplitude (the rectangular box). At this point there is also a loss of the left EP response. This change
was attributed to left arm malposition. When the left arm was repositioned, the response returned to baseline.
Also noticeable in all the leg and arm cortical responses from both left and right sides is mild prolongation of
latencies in the stacks, but these latencies all returned to baseline by the end of surgery. These changes are
likely from an anesthetic eect because they are bilateral, aecting both the arm and left responses in a spine
operation, which was performed at the L3–S1 level.
generated through activation of the sensory pathways and
retrograde activation of the alpha motor neurons. In a collision experiment using stimulation of the spinal cord followed
by stimulation of the posterior tibial nerve at various interstimulus intervals, the neurogenic responses were abolished,
suggesting that the potentials were colliding in the spinal cord.
6
At the beginning of TCES-MEP monitoring, threshold
voltages for each side of the body and amplitudes of MEPs are
calculated.23 e motor cortex on the side of the brain receiving the anodal stimulus is typically the rst region to activate
at the lowest stimulus threshold. e initial current used is
typically 100 V, with a train of stimuli delivered to the cortex.
Following stimulation, a MEP response is monitored in the
muscles contralateral to the side receiving the anodal stimulus.
If no response is seen, the voltage is typically increased by
50-V increments and the process is repeated until an MEP
response is seen in all the muscles contralateral to the anodal
stimulus. is voltage is called the threshold voltage for that
side. e highest amplitude of the myogenic response below
the level of surgery is also noted. Typically, amplitude measures for myogenic responses are best recorded as the areaunder-the-curve measurements or simply documented as
either presence or absence of the myogenic response. is
procedure is repeated aer reversing the anodal-cathodal
conguration using a switch box. e voltage used for TCES-
MEP recordings typically does not exceed 500 V. Note that the
anticipated latency of the EMG responses ranges from 20 to
40 ms or more depending on the patient’s height, owing to the
conduction time in the descending motor pathways. Latency
values have not always been found to be reliable indicators of
signicant change in TCES monitoring in clinical practice.
Another advantage of the multipulse technique is that it
requires no averaging. A train of pulses elicits a clear response
of sucient amplitude, which requires no averaging.
Two dierent methods of recordings can be used. In
myogenic MEPs, responses can be recorded directly from
the muscle (either a surface electrode or needle electrodes
placed within the muscle). In spinal cord MEPs, responses
may be recorded directly from the spinal cord with use of
an epidural catheter electrode that records a direct D wave
and a volley of indirect I waves. Using single-pulse TCES,
recording both D and I waves is frequently required, meaning
a D wave could be recorded when a myogenic MEP is not yet
seen. is is because a series of D and I waves is required for
Chapter 15 Intraoperative Neurophysiologic Monitoring of the Spine 261
FIG. 15.4 Signicant change in transcranial electrical motor-evoked potential (MEP) response during spinal
instrumentation. The gure shows transcranial MEP responses from the left and right muscle groups. The traces
in red represent the responses at baseline (at the beginning of surgery). The rst two muscle groups on each
side of the gure represent upper extremity MEP response from the brachioradialis (BrRad) and rst dorsal
interosseous (FDI). The lower three traces on each side represent the responses from the lower extremities on
each side of the body: adductors of the thigh (Add), tibialis anterior (Tib), and adductor hallucis (AH). The green
traces represent the most recent acquisition and show the change from baseline over the left lower extremity
muscle groups. Notice the MEP responses of the left tibialis anterior and adductor hallucis are absent, whereas
they are preserved in the left upper extremity and adductor of the thigh as well as both lower and upper
extremity of the right side of the body. This is consistent with injury to the left lower lumbar and sacral nerve
roots (L5, S1, S2).
SECTION
II
the alpha motor neurons to generate a myogenic response.
e spinal recorded responses can also be recorded with full
muscle relaxation, whereas myogenic responses require either
no or very little muscle relaxation, even with the multipulse
technique.
Determining signicant changes during the course of
surgery typically is most reliable if there is an absolute loss of
myogenic responses to stimulation (Fig. 15.4). Some authors
have also suggested that amplitude drops of MEP to 25% of
baseline amplitude values are predictive of motor pathway
impairments.29 Signicant changes can also be determined by
a change of voltage required to obtain MEPs of greater than
50 V beyond baseline thresholds used in obtaining MEPs at
the beginning of monitoring (see Table 15.1).
30
Clinical Use of Intraoperative Monitoring
SEPs have become a useful modality in monitoring scoliosis
surgery and have been shown to reduce the risk of neurologic
decits, especially when used by surgeons experienced in
neurophysiologic monitoring. e occurrence of denite
neurologic decits in the presence of unchanged SEP recordings has been estimated to be approximately 0.063%.31 Intraoperative neurophysiology can play both a neuroprotective
(through the detection of early changes) and an educational
role during surgery.32 Surgeons who use intraoperative neurophysiologic monitoring over time may begin to understand
which specic surgical techniques have a higher propensity
for damaging the neurologic system. In this way surgeons may
nd methods to avoid the use of high-risk techniques.
Many surgeons have found that TCES-evoked MEP monitoring during spinal surgery is a safe and reliable method of
monitoring corticospinal tract activity and is indispensable for
these surgeries.33 ere has been no evidence that TCES has
resulted in the development of new-onset epilepsy or brain
damage. ere are some risks associated with TCES monitoring, including tongue or lip laceration and, rarely, mandibular
fractures. e use of a so bite block may prevent these
injuries. Relative contraindications include epilepsy, cortical
lesions, convexity skull decits, raised intracranial pressure,
cardiac disease, intracranial electrodes or shunts, cardiac
pacemakers, and other implantable biomedical devices.
34
A study that looked at the reproducibility of various
monitoring methods during scoliosis surgery found that
MEPs could be obtained in 80% of patients compared with
SEPs, which could be obtained in 93% of patients.35 In spinal
surgery, MEPs obtained from upper and lower extremities
were consistently recorded in 22 patients with multipulse
stimulation using trains of 3 to 6 pulses separated by 2 ms,
with responses measuring more than 100 µV in all but one
patient. ese responses persisted with nitrous oxide con-
centration of up to 74%. One patient had loss of responses
from one lower limb in which increased weakness was noted
for a few days aer surgery; in three patients there was an
262 DIAGNOSIS
increase in weakness or spasticity without any accompanying intraoperative MEP changes.36 In another study,37 MEPs
during TCES were reproducibly recorded during spinal
surgery in 40 patients with partial neuromuscular blockade.
In two patients there were some signicant changes in the
motor potentials that correlated with postoperative neurologic
decits. No postoperative neurologic decits were observed in
nine patients in whom MEP amplitudes decreased to less than
20% of baseline values.
37
TCES-induced MEPs have been used to monitor cases of
intramedullary spinal cord tumor resection. In 32 consecutive
patients, MEPs were elicited in 19 patients before myelotomy,
and three of these patients had MEP amplitude decrease below
50% from baseline, all of whom had postoperative neurologic
decits.
38
In a review of 160 patients undergoing scoliosis surgery,
a combination of SEP and transcranial MEP monitoring was
successfully recorded in 81% of the patients, with changes seen
in 5% of monitored cases that was reversible aer taking appropriate surgical corrective measures. None of these patients had
new postoperative decits or worsening of preexisting decits.
is combination of techniques was considered safe, reliable,
and accurate and made the wake-up test unnecessary.
39
Use of TCES-evoked MEPs has been relatively easily
accomplished with an anesthetic combination of narcotic drip
accompanied by nitrous oxide. e use of isourane in addition to this combination resulted in a tendency for deterioration of amplitude of the MEP responses.40 MEPs elicited by
TCES are more feasible with total intravenous anesthesia
compared with balanced anesthesia using nitrous oxide, isourane, and fentanyl. Some of the suppressant eects of balanced anesthesia can be overcome with higher stimulation
intensities and repetitive stimulation.
41
Pedicle Screw Stimulation
Intraoperative assessment during pedicle screw insertion can
be used to avoid nerve root trauma from a misdirected screw.
e integrity of the pedicle screw placement can be assessed
by its direct electrical stimulation with simultaneous myogenic
response recordings from the appropriate myotomes. Using
a direct monopolar nerve stimulator, with serial increments
of the level of current intensity from 1 to 20 mA, triggered
EMG recordings can be performed (Fig. 15.5). Absence of
a myogenic response up to 10 mA is thought to be indicative of an intact pedicle. e presence of a pedicle breach is
suspected by a stimulation-induced myogenic response below
7 to 10 mA (see Table 15.1).
7
Summary
Intraoperative neurophysiologic monitoring of the spinal cord
can be used to help detect the early occurrence of neurophysiologic changes, thereby allowing corrective action to reduce
the incidence of neurologic injury to patients undergoing
spine surgery. In our opinion, the most important aspects of
successful intraoperative monitoring include the following:
FIG. 15.5 Nonsignicant triggered electromyographic (EMG) response with
pedicle screw stimulation. Pedicle screw stimulation of the T12 screw shows
threshold of triggered EMG response at an intensity of 12 mA.
1. Availability of the right equipment to allow multimodality
recordings (e.g., combinations of EMG, SEP, and/or MEPs)
2. Presence of a highly skilled and experienced technical and
neurophysiologic team that will ensure for optimal technical recordings and accurate interpretation of any changes
that may occur
3. Rapid communication between the neurophysiologic team
and the surgical/anesthesia teams
4. A knowledge of both the functional anatomy of the structures to be monitored and the limitations of the techniques
to be used
e combination of dierent monitoring techniques, such
as SEP and transcranial MEP monitoring, has enabled better
interpretations of the neurologic status of the spinal cord. e
newer techniques of MEPs with TCES have gained widespread
acceptance as a standard clinical intraoperative neurophysiologic application. MEPs have allowed for a more accurate
assessment and interpretation of the functional status of the
motor pathways at various levels of the neuraxis.
PEARLS
One key to the success of intraoperative neurophysiologic
1.
monitoring is a good understanding of the capabilities and
limitations of the neurophysiologic tests being monitored.
2.
One of the rst issues to address when planning for
intraoperative neurophysiologic monitoring is to determine the
types of neurophysiologic tests to perform on a particular
patient undergoing surgery.
3.
SEPs only monitor sensory transmission through the dorsal
column pathways; they do not provide a direct measure of
motor function.
4.
In SEP monitoring an amplitude drop of greater than 50% and
latency prolongation of more than 10% are considered
signicant. The most signicant change is a complete loss of the
cortical potential.
5.
MEP monitoring is a more direct technique that evaluates the
motor pathway. Motor cortex stimulation with TCES provides a
more reliable methodology for monitoring the motor pathways.