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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.
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.
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.
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.
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.
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).
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.
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.