Preoperative electrodiagnosis
NCSs and needle EMG are the primary studies used to gain information on the location, number, and pathophysiology of lesions affecting the brachial plexus and other peripheral nerves before surgical exploration. NCSs are often accurate enough to localize lesions within several centimeters along the course of a nerve segment. In motor NCSs, a mixed or pure motor nerve is stimulated at several places along the nerve. The
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summated electrical response of all muscle fibers innervated by the activated axons (typically recorded with surface electrodes) is called the compound muscle action potential (CMAP). The size of the CMAP recorded after supramaximal stimulation of the peripheral nerve is directly related to the number of functioning motor axons. The size of the CMAP quantifies the number of activated axons, whereas the conduction velocity and distal latency measure conduction along the course of the motor axons.
To properly localize a lesion with motor NCSs, the physician must stimulate the nerve or fascicles of interest in isolation from other nearby nerves, or isolate the recording to muscle fibers innervated exclusively by the nerve or fascicles of interest. Another important criterion for localizing lesions involves stimulation or recording "through" the lesion. Stimulating or recording above and below the involved segment should isolate the segment of nerve that contains the lesion.
Sensory conduction studies involve the stimulation and recording of mixed or cutaneous nerves at one or more locations, recording the triphasic sensory nerve action potential (SNAP) at another location along the nerve. The SNAP represents summated action potentials of sensory axons. Thus, the SNAP has a lower amplitude, shorter duration, and different configuration (triphasic versus biphasic) than the CMAP (Fig. 1). These characteristics make the SNAP more difficult to record under "noisy" conditions.
The sensory neuron is unique in that the cell body is located outside the spinal cord in the DRG, which creates a pre- and postganglionic portion of the peripheral sensory axon (Fig. 2). When the lesion affects the preganglionic portion
- Fig. 1. (A) CMAP recording. Note the biphasic appearance, large amplitude, and long duration of the potential. (B) SNAP recording. Note the triphasic appearance, small amplitude, and short duration of the potential.
(between the DRG and spinal cord), the postganglionic axon remains in continuity with the DRG cell body, thus retaining its electrical excitability. In contrast, when the lesion is distal to the DRG (postganglionic), Wallerian degeneration occurs and the distal segment becomes electrically inexcitable. This phenomenon can be used to help localize lesions within the PNS. In the setting of a clinical sensory loss, the preservation of the SNAP in the distribution of the sensory loss indicates pathology proximal to the DRG (Fig. 3), whereas pathology distal to the DRG will reduce the amplitude of the SNAP in proportion to the severity of sensory axon loss.
Needle EMG is used to examine the characteristics of individual or groups of motor units within individual muscles. A loss of functioning motor units is represented by reduced recruitment, where few motor unit potentials (MUPs) are present but discharge at faster frequencies in an attempt to maintain force production. Reduced recruitment is the hallmark of lower motor neuron or PNS weakness and is differentiated from poor activation, which occurs in weakness of central nervous system origin (or is from poor effort caused by pain, hysteria, or malingering). Reduced MUP recruitment is present as soon as weakness of lower motor neurons develops. There is no time delay. After 10 to 21 days, denervated muscle fibers begin to discharge under the influence of their intrinsic pacemaker (fibrillation potentials), and MUP begin to become polyphasic and enlarge (increase in duration and amplitude).
The exact findings on needle EMG depend on the severity and completeness of injury, the distance from the site of injury to the involved muscle, the time since the injury has occurred, and the progress and mechanism of regeneration. If a muscle has fibrillation potentials or MUP changes suggesting denervation and reinnervation, then there is a lesion at or proximal to the nerve branch to that muscle. Because of the fascicular anatomy of nerves, the converse cannot be stated as true. That is, if the muscle is normal, the lesion may still be proximal to the branch to that muscle. This occurrence is frequent in focal neuropathies and represents one of the main limitations of relying too heavily on localization based on needle EMG findings alone.
The application of NCSs and needle EMG to the study of complicated focal neuropathies, such as brachial plexus injuries, can provide useful information, but there are also limitations of these techniques performed in the preoperative setting. In severe plexopathies with a flail anesthetic arm, the presence of well-defined SNAPs in the
1 v1 neuron
Fig. 2. Sensory and motor pathways. IVF, intervertebral foramen.
1 v1 neuron
Fig. 2. Sensory and motor pathways. IVF, intervertebral foramen.
distribution of all spinal segments (C5-T1) indicates complete root avulsion at all levels. In less severe plexopathies, general segmental (C5-T1) and longitudinal (trunk, cord, nerve) localization is possible in most cases.
The presence of partial lesions with residual innervation or ongoing collateral reinnervation of muscles can be confirmed with either NCSs or needle EMG. The severity of axon loss in partial lesions can be defined in most cases on preoper-ative studies. Fibrillation potentials in paraspinal muscles indicate at least partial root injury in at least one cervical spinal segment.
Improvement associated with reinnervation can be documented and quantified on serial examinations.
In severe plexopathies with a flail anesthetic arm, the absence of SNAPs indicates damage to postganglionic elements but does not exclude a mixed lesion with associated root avulsion. Thus, one limitation of preoperative studies is the inability to detect root avulsion in the setting of a severe coexisting postganglionic injury. In addition, because of overlapping innervation, the presence of fibrillation potentials at multiple cervical paraspinal levels does not exclude the possibility that some cervical roots are intact.
The precise segmental and longitudinal location of partial and complete lesions of postgan-glionic elements is also limited in many patients with complex brachial plexus injuries because of difficulties in stimulating and recording affected fascicles in isolation and difficulties stimulating areas proximal and distal to the lesioned segments. Needle EMG is also limited by false localization because of selective fascicular involvement and because early regeneration cannot be detected
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