Putting It All Together

Now that we have an understanding of the muscle physiology in myopathy and its electrical correlates, it is time to make the final diagnosis. Again, as we mentioned in Section 1., EMG is

Table 4

Electrodiagnostic Clues to the Diagnosis of Specific Myopathies

Myopathies that may present with normal EMG Metabolic myopathies Endocrine myopathies

Hypokalemic periodic paralysis (in between attacks) Myopathy with fiber type disproportion Myopathies that may present with fibrillation potentials only Inflammatory myopathies Chloroquine myopathy Acute rhabdomyolysis Myopathies that may present with myotonia

Myotonic dystrophy Myotonia congenita (MUAPs normal) Proximal myotonic myopathy Paramyotonia congenita Colchicine myopathy Acid maltase Deficiency

Hyperkalemic periodic paralysis (in between attacks) Centronuclear myopathy Myopathies with denervating features (fibrillation potentials and positive sharp waves) Inflammatory myopathies Muscular dystrophies Congenital myopathies Metabolic myopathies Toxic myopathies Infectious myopathy only one part of the puzzle. We have to blend the clinical history and physical examination findings with the EMG results to arrive at a final diagnosis.

Although the examiner is generally expected to wear the "electromyographer hat" during the study, taking care not to be biased with the available clinical information, the final report should be formulated after considering all of the technical factors and the inherent subjective nature of analyzing the MUAPs on the EMG monitor. Some caveats are worth remembering when interpreting abnormal EMG findings in a patient with suspected myopathy.

• Small MUAPs in the early stages of reinnervation after severe denervation may be misinterpreted as caused by myopathy.

• Individual MUAPs may have a normal or even high amplitude in patients with mild myopathies or in clinically unaffected muscles from patients with myopathy; for instance, if the needle electrode is close to normal or hypertrophic muscle fibers (as a compensatory reaction in early stages).

• EMG mainly reflects activity of type I fibers (diseases of the adrenal or pituitary glands as well as steroid-related myopathy show type 2 atrophy without degenerative change).

• The spike duration may sometimes seem extremely prolonged because of late satellite potentials. (In Duchenne's dystrophy, polyphasic MUAPs with prolonged spike duration are rather typical (Fig. 6).

It is also important to remember that although EMG is useful in the diagnosis of myopathies, there are a number of diseases of muscle that may present as challenges to the electromyographer (Table 4). Metabolic and endocrine myopathies may not have abnormal EMG findings.

Myopathic Units Emg
Fig. 21. The cycle of needle electrode examination changes that can be observed during the various stages of a reversible necrotizing myopathy, such as polymyositis. Fibs, fibrillation potentials; MUPs, motor unit potential. From Wilbourn, 1993 with permission.

Fibrillation potentials may be the only abnormal findings in the early stages of necrotizing myopathies, such as inflammatory myopathies. Likewise, myotonic discharges may be the only abnormal EMG finding in a number of myotonic myopathies.

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