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Chapter 13 Spine Imaging 233
3. The most critical imaging information regarding spinal
neoplasms used in forming a dierential diagnosis involves
determining whether the lesion is intramedullary, intradural
extramedullary, or extradural.
4.
CT remains the method of choice for detecting retropulsed
bony fragments and for showing fractures of the posterior
elements.
5.
MRI is useful in the immediate postoperative period for
evaluating uid collections including hemorrhage and for
showing mass eect on the thecal sac, cord, and cauda equina
but not for dening residual disc material.
6.
Paravertebral enhancement on fat-suppressed axial T1-weighted
images is very helpful in dening early disc space infection.
7.
The apparent size of neural foramina on axial gradient MR
images is critically dependent on the sequence echo time;
longer echo times give susceptibility artifact, which may give
the false appearance of stenosis.
8.
Synovial cysts are very dicult to identify on T1-weighted
images and require T2-weighted images or intravenous
contrast medium enhancement, or both, for denition.
9.
Early disc space infection and degenerative disc disease with
type 1 endplate change can be indistinguishable by MRI alone.
10.
Acute spinal hemorrhage may show no characteristics of
“blood” on MRI owing to the lack of susceptibility eect of
oxyhemoglobin.
11.
OPLL may be missed on T1-weighted images by merging into
the low signal of CSF.
12.
Use of contrast medium may mask spinal bony metastatic
disease by causing the enhancing tumor signal to match that
of adjacent normal fatty marrow.
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SECTION
14
CHAPTER
e electrodiagnostic examination is comprised of two parts:
the nerve conduction studies (NCSs) and the needle electrode
examination (NEE). Together, they assess the peripheral
sensory and motor nervous system. Sensory NCSs assess the
integrity of dorsal root ganglion (DRG) cells (usually residing
within the intervertebral foramina), their axonal projections
within mixed sensory and motor nerve trunks, and arborizations into individual nerve bers innervating sensory organs
subserving primarily vibration and proprioception. Motor
NCSs assess the integrity of anterior horn cells (in the anterior
region of the spinal cord), their axonal projections within pure
motor or mixed nerve trunks, arborizations into individual
motor nerve bers, the neuromuscular junctions, and attached
muscle bers.
e electrodiagnostic examination is best conceptualized
as an extension of the neurologic examination of the peripheral nervous system. In the setting of abnormalities identied
in the neurologic history and examination, the electrodiagnostic examination can be valuable in (1) conrming the
clinical impression, (2) investigating the presence of other
conditions in the dierential diagnosis, and (3) localizing the
precise site of a focal nerve trunk lesion not clearly dened on
clinical examination.
e electrodiagnostic examination can discriminate
between the two main types of pathologic responses that
can aect nerve bers: axon loss (neurotmesis and axonot-
mesis) and demyelinating conduction block (neurapraxia).
In cases of axon loss, the electrodiagnostic examination has
the potential of discriminating acute, subacute, and chronic
nerve lesions. It can identify early evidence of reinnervation
and can quantitatively track the reinnervation process over
weeks to months. In the setting of diuse signs and symptoms,
the electrodiagnostic examination can discriminate among
generalized sensory and motor polyneuropathy, myopathy,
and diuse motor axon loss processes, such as motor neuron
disease.
A well-executed electrodiagnostic examination can conrm
or refute the presumptive diagnosis and can provide a screening assessment for other peripheral nerve and muscle conditions that could reasonably be the cause of the patient’s
symptoms. In that way, the electrodiagnostic examination
should be thought of as an electrodiagnostic consultation and
not solely a test to rule in a specic diagnosis. Qualied
Electrodiagnostic Examination
Jinny Tavee
electrodiagnostic consultants usually are board certied in
electrodiagnosis, clinical neurophysiology, or neuromuscular
medicine, having completed an approved training program
and having shown competence by examination. e electro-
diagnostic examination must be interpreted by the individual
performing the study, because there is no single machinegenerated tracing (as would be the case for an electrocardiogram or electroencephalogram) that can be interpreted simply
by reviewing data collected elsewhere.
Pathophysiology
e clinical practice of electrodiagnosis is based on numerous
precepts that are derived from the pathophysiology of nerve
and muscle function. ese provide the basic principles that
dene the clinical utility and limits of this procedure.
Regardless of etiology, most focal nerve lesions—including
lesions at the root level—result in either axon loss or demyelin-
ation. Axon loss produces nerve transmission failure along the
aected bers; focal demyelination causes either conduction
block or conduction slowing at the lesion site, depending on
its severity. One fundamental dierence between these two
types of lesions is that focal demyelination remains localized
and does not materially aect the segments of the axon proximal or distal to the lesion. In contrast, an axon-loss lesion
results in wallerian degeneration, which eventually involves
the entire course of the nerve aected.
Because axon loss and demyelinating conduction block
stop nerve impulse transmission across the lesion site rather
than merely slowing it, both can result in clinical weakness
and sensory abnormalities whenever they aect a sucient
number of motor and sensory axons. However, demyelinating
conduction slowing does not aect muscle strength. is is
because all of the nerve impulses ultimately reach their destination, although slightly later in time than they normally
1
would.
e electrodiagnostic examination assesses the integrity of
large sensory and motor nerve bers, but not small bers, as
the electrical elds that they generate are too small to reach
the recording electrodes in routine studies. For this reason,
pain alone cannot be assessed because that sensory modality
is mediated through small C-type nerve bers. When pain is
II
241
242 DIAGNOSIS
TYPES OF NCS
mV
associated with large nerve ber dysfunction, such as weakness, electrodiagnostic testing is more valuable.
General Concepts of Electrodiagnostic Examination
Nerve Conduction Studies
NCSs are the rst component of the electrodiagnostic examination. During the NCS, a peripheral nerve is stimulated,
resulting in an electrical response generated directly by the
nerve itself (as with a sensory response) or the muscle that it
innervates (as with a motor response). e duration and
intensity of the stimulus are gradually increased until a
maximal response is generated. ese responses are recorded
using surface electrodes placed over the skin and then analyzed. During each study, valuable information is produced
regarding the number of functioning nerve bers, the speed
of conduction along those bers, and their relative rates of
conduction.
ree basic types of NCS are available: motor, sensory, and
mixed (Fig. 14.1). Motor and sensory NCSs are generally
performed on every patient. Mixed NCSs are typically used in
the evaluation of specic disorders, such as carpal tunnel
syndrome, and are of limited value in the evaluation of spinerelated nerve pathology. NCS protocols vary depending on the
diagnosis in question, and can be tailored to help exclude
other diagnoses in the dierential. Most electrodiagnostic
laboratories have a routine protocol for a general study of the
upper extremity (Table 14.1) and lower extremity (Table 14.2).
R
S
X
R
S
X
S
X
Motor
1
X
Sensory
1
mV
Mixed
mV
S
2
R
Motor Nerve Conduction Studies
For motor NCSs, the recording electrode is placed over the
muscle belly, and the reference electrode is axed over
the tendon. e nerve supplying that muscle is stimulated;
the resulting motor nerve response is a compound muscle
action potential (CMAP), a biphasic waveform that represents
summated muscle ber action potentials (Fig. 14.2). In routine
TABLE 14.1 Nerve Conduction Studies in the Upper Limb
Motor Sensory
Standard
Median: thenar (C8, T1) Median: index (C6, C7)
Ulnar: hypothenar (C8, T1) Ulnar: fth (C8)
Nonstandard
Ulnar: rst dorsal interosseous (C8, T1) Median: thumb (C6)
Radial: extensor indicis proprius (C8) Median: middle (C7)
Radial: brachioradialis (C5, C6) Ulnar: hand dorsum (C8)
Musculocutaneous: biceps (C5, C6) Radial: thumb base (C6, C7)
Axillary: deltoid (C5, C6) Lateral antebrachial cutaneous:
forearm (C6)
Medial antebrachial cutaneous:
forearm (T1)
The nerve being studied is listed rst, followed by the recording site, then the root
innervation (motor) or derivation (sensory). Bolded root provides major innervation.
FIG. 14.1 Three basic types of nerve conduction studies: motor, sensory,
and mixed (S1 and S2 are stimulation sites, R is the recording site, and X
overlies the shock artifact.) (Modied from Isle M, Krauss G, Levin K, et al.
Electromyography/Electroencephalography. Redford, WA: Spacelabs Medical;
1993:4.)
TABLE 14.2 Nerve Conduction Studies in the Lower Limb
Motor Sensory
Standard
Peroneal: extensor digitorum brevis
(L5–S1)
Tibial: abductor hallucis (S1)
Nonstandard
Peroneal: tibialis anterior (L5) Supercial peroneal sensory:
Tibial: abductor digiti quinti pedis (S1) Saphenous: medial ankle (L4)
Tibial: gastrocnemii (S1)
Femoral: quadriceps (L3, L4)
The nerve being studied is listed rst, followed by the recording site, then the root
innervation (motor) or derivation (sensory).
a
M component of H response.
b
Studies are technically dicult to perform.
a
Sural: lateral ankle (S1)
dorsum ankle (L5)
Lateral femoral cutaneous:
lateral thigh (L3, L4)
b
b