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Anterior horn cell involvement shows evidence of diffuse active/chronic neurogenic changes and fasciculations. Early in the course of the disease, active denervation is seen, but as the disease evolves, the chronic changes are more prominent. In evaluating a patient referred for possible anterior horn cell disease, you must sample a large number of muscles. Involvement of at least one upper and one lower extremity should be evident, and it is desirable to demonstrate abnormal findings in a third extremity. Both proximal and distal muscles should show the changes. The presence of neurogenic units, fasciculations, and a drop out of motor units are most revealing. Similar findings in one extremity or both extremities of the same spinal level without findings in other spinal levels should direct your attention to the spinal cord and a focal destructive process in that area, e.g. syringomyelia, cord tumors, polio. The non-involved extremities should be carefully checked before calling them normal.
The basic EMG evaluation of a root lesion will only give evidence of involvement of the motor root. The muscles to be sampled should always include the limb musculature and the paraspinal muscles. Though paraspinal muscle involvement is often lacking by the time the patient is seen in the EMG laboratory, compulsive sampling of their different levels is essential. In addition, the innervation in the paraspinal muscles has considerable overlap. The deeper ones have less of this overlap and should be sampled for a more accurate level. In the needle examination for a root lesion, muscles from roots from multiple levels should be sampled. This sampling must include levels above and below the involved root in both the axial and extremity muscles.
The needle examination of the patient with a brachial plexus lesion should be a compulsive evaluation of the various levels from which branches arise within the plexus. The distal branches are sampled followed by the more proximal muscles innervated by the early plexus branches. In all instances the paraspinal muscles should be sampled to rule out a possible root lesion. Our policy is to identify one or two branches above the level of the lesion as being normal, and other areas of the plexus as being normal. This procedure requires a rather intimate knowledge of the different muscle groups innervated by the plexus (see Table III). Many brachial plexus lesions, especially traumatic lesions, may involve several segments of the plexus, so widespread sampling of the muscles is imperative. The same may be said for lesions of the lumbar and sacral plexi, though they tend to be a little more simplified and clear-cut.
Usually when you do the needle examination in entrapment neuropathies, you will already have the findings from nerve conduction studies. These findings help in determining which muscles to sample. All muscles below the point of entrapment should be sampled. It is usually best also to do a modified root search in the extremity involved just to make sure that a second process is not also present.
The findings in entrapment syndromes may be minimal early in the course of the illness (when only demyelination is present). Only when axonal loss occurs will you begin to see findings on the needle examination.
In the purely demyelinating neuropathies, the findings on needle examination are minimal and consist predominantly of a drop-off of motor units if the lesion is severe and a prolongation in the duration of the recruited motor units due to the desynchronization in conduction caused by demyelination. In the neuropathies with axonal lesions, denervation is seen both in its acute and chronic forms. In mild cases, only a few fibrillations and positive waves are found distally. In the more advanced cases, denervation is seen more proximally (upper leg or forearm muscle) along with chronic neurogenic motor units distally. In either case, the upper extremity is as a rule usually less involved than the lower extremity.
The changes seen in the motor units of patients with muscle disease have been described previously. These changes are most pronounced in the inflammatory myopathies and are accompanied by an abundant amount of spontaneous activity consisting of fibrillations, positive waves and complex repetitive discharges. During the recovery stages, and when the patient is receiving steroids, these changes are less prominent and the spontaneous activity is reduced to a minimum. In muscular dystrophies, these changes are less pronounced and are associated with less spontaneous activity. During the active stages of Duchenne’s muscular dystrophy, however, fibrillation and positive waves as well as complex repetitive discharges may be prominent.