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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.
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