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Nerve
conduction studies/findings in certain disease entities
Anterior
Horn Cell Disease
Patients with this disease show normal sensory potentials, both in amplitude
and latency unless the extremity is cold (from lack of adequate musculature).
Changes in motor nerve conductions begin with a decrease in the amplitude
of the motor response, due to the loss of axons, then prolongation of latency,
and a tendency to slowed motor conduction velocities as a result of the
loss of the fastest conducting fibers. At times the response is of very
low amplitude, making it difficult to evaluate conduction velocities.
Root
Lesion
When a spinal nerve root is compressed, nerve conduction studies are
sometimes helpful, depending somewhat on whether the sensory or motor root
is involved.
If the compression involves the sensory root, it usually does so proximal
to the dorsal root ganglion. Such compression has no effect peripherally
and sensory nerve conductions will be normal. In appropriate locations
(C7 and S1), the presence of sensory nerve compression can be investigated
by use of the H-reflex which would be either delayed or absent.
In motor radiculopathies, nerve conduction studies may reveal low motor
amplitudes, in the appropriate areas, and slowed conduction velocity if
the axonal loss is severe. The H-reflex and F-wave may be delayed or absent
in the areas of involvement.
In routine nerve conduction testing, we only test the median and ulnar
motor response in the arm; therefore only C8 and T1 radiculopathies would
be picked up unless special studies to the radial nerve or the brachial
plexus are performed. In the leg, we routinely test the peroneal and posterior
tibial nerves so that only the L5 and S1 roots are tested.
Plexus
Lesions
Nerve conduction studies may be most helpful in evaluating plexus injuries.
Because the lesion is distal to the dorsal root ganglion, the sensory nerve
action potentials will be diminished or absent in the appropriate distribution
(see Table XIX). Their conduction velocities would remain normal or tend
toward slowing if the axonal loss is pronounced.
Motor responses are also of low voltage, and their conduction velocities
normal or slightly slowed.
The brachial plexus can be stimulated at Erb's point. The point of stimulation
is in the distal trunk area, over the divisions of the brachial plexus
so that lesions in the trunk or roots will be as easily delineated as a
lesion in the cord or below. The C8 root can be tested (for thoracic outlet
compressions) by stimulating with a needle electrode at the C7 transverse
process and recording from the APB.
Brachial plexus lesions can result from trauma (motorcycle accidents,
a very common cause), local tumor infiltration and idiopathic plexitis.
Conduction times along the lumbar and sacral plexi can be computed by
stimulating the plexus from the roots proximal to it, and a peripheral
nerve off of that plexus distal to it. The difference between these two
latencies represents the plexus conduction time.
For the lumbar plexus, the L2 to L4 nerve roots can be stimulated by
using a needle electrode inserted 2-3 cm laterally to the L4 spinous process
and the response recorded from the quadriceps. The distal stimulation site
is the femoral nerve at the groin also with quadriceps recording. The difference
between these two latencies would give an idea of plexus conduction time.
For the sacral plexus, the roots are stimulated with a needle electrode
inserted medially and just caudally to the posterior superior iliac spine
and the response recorded from the abductor hallucis. The distal stimulation
is done by stimulating the sciatic nerve at the sciatic notch and also
recording the abductor hallucis. The difference between these two latencies
represents plexus conduction time.
H-reflex and F-wave studies can be helpful in plexus dysfunction in
that responses may be delayed, diminished, or absent.
Lumbosacral plexus lesions may be caused by trauma, local tumor and
idiopathic plexitis (much less common than is the brachial plexus), but
can also result from local hemorrhage to the psoas muscle and diabetic
plexopathy.
Compression/Entrapment
Neuropathies
Nerve conduction studies are the definitive test in compression/entrapment
neuropathies. In myelin lesions, when the nerve is stimulated below the
point of entrapment, the latencies and conduction velocities should be
normal. When the nerve is stimulated above the point of entrapment, there
is slowing of conduction velocities or prolongation of the distal latency
across the entrapment. The amplitude varies with the process. If there
is a complete or partial conduction block, then stimulation above the lesion
will either yield no response or one with a low amplitude. In either case
stimulation below the lesion, when feasible, will give a normal amplitude.
If only focal slowing is present, the amplitude from stimulation above
the lesion will be slightly decreased as the duration of the response is
prolonged. Below the lesion the amplitude becomes normal. In axonal lesions
the amplitude is decreased diffusely regardless of the point of stimulation
above or below the lesion. Conduction velocities and distal latencies are
unaffected until late in the process.
In lesions of both the myelin sheath and the axons, the above changes
are seen in combination.
Myopathy
Normal motor amplitudes are the rule with normal sensory potentials
and motor-nerve conduction velocities, as the process usually involves
the proximal musculature. In the distal myopathies, however, motor amplitudes
may be decreased.
Neuromuscular
Transmission Defect
In diseases of the postsynaptic neuromuscular junction, such as myasthenia
gravis, motor amplitudes can be normal to decreased in the early stages
of the illness. Later, however, they are decreased and resemble a myopathy.
The sensory potentials are normal and the motor latencies and conduction
velocities are as a rule preserved until very late in illness. Slow repetitive
stimulation of an involved muscle will produce a decrement (see nerve conduction
work-ups).
In diseases of the presynaptic junction, such as the Lambert-Eaton syndrome
and botulism, motor amplitudes are diffusely decreased though their distal
latencies and conduction velocities are usually preserved. The sensory
potentials are normal. Postexercise studies reveal a significant improvement
of the motor amplitudes (see nerve conduction work-ups).
Polyneuropathies
Whatever the nature of the lesion, sensory fibers, with few exceptions,
are always affected first. With myelin lesions, the duration of their action
potential is increased, resulting in a lower amplitude and prolonged distal
latency.
In axonal lesions, their amplitudes are decreased with little or no
prolongation of the distal latencies.
At a later stage, the motor fibers are affected much in the same fashion,
with the conduction velocity slowed in myelin lesions and relatively unaffected
with axonal loss.
F-wave and H-reflex studies may become abnormal long before routine
sensory and motor studies in proximal neuropathies. As most lesions consist
of a mixture of myelin involvement and axonal loss, the above changes are
usually seen in combination at one time or another.
Trauma
Multiple levels of nerve stimulation may be done, depending on where
the injury is. It is desirable to stimulate the nerve both below and above
the suspected site of injury. At the appropriate study time, a normal response
from stimulation below the injury site suggests a conduction block lesion,
partial or complete. A low amplitude response suggests that axonal damage
has occurred.
 Table
of Contents Chapter Index 
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