EMG, Nerve Conduction & Acute Muscle Disease
Key Takeaways
Demyelination generally affects conduction speed, latency, dispersion, or block; axonal loss often reduces response amplitudes.
Preserved sensory responses with myopathic motor units support a muscle process, whereas reduced sensory responses support a peripheral sensory-motor neuropathy in context.
Motor neuron disease can cause ventilatory and bulbar failure despite preserved sensation.
Rhabdomyolysis requires assessment of potassium, kidney function, volume status, and the precipitating cause.
What the Tests Measure
The outline requires basic electromyography (EMG) interpretation and recognition of motor neuron disease, acute myopathies, rhabdomyolysis, and critical illness neuromyopathy. Nerve conduction studies assess evoked responses; needle EMG assesses spontaneous activity and motor-unit behavior. They complement the examination rather than replacing localization or emergency airway assessment.
A compound muscle action potential (CMAP) is the recorded muscle response to motor-nerve stimulation. A sensory nerve action potential (SNAP) reflects a sensory-nerve response. Reduced amplitude can suggest axonal loss or reduced excitable tissue, but technical factors also matter. Latency, conduction velocity, temporal dispersion, conduction block, and late responses provide additional information about myelin and proximal conduction.
Axonal Versus Demyelinating Patterns
| Pattern | Typical electrodiagnostic features | Important caution |
|---|---|---|
| Axonal neuropathy | Reduced CMAP or SNAP amplitudes, with less prominent slowing | Early studies and technical limitations can obscure the pattern |
| Demyelinating neuropathy | Slowed conduction, prolonged distal or late latencies, dispersion or block | Formal criteria require multiple findings, not one slow segment |
| Myopathy | Often low CMAP with preserved SNAP; short-duration, low-amplitude recruited motor units when assessable | A sedated patient may not recruit voluntarily |
| Junctional disorder | Abnormal decrement or other transmission findings on specialized testing | Use a suitable protocol and clinical context |
In Guillain–Barré syndrome, early studies can be nondiagnostic; repeat testing may clarify an axonal or demyelinating pattern. Normal early CSF protein also does not exclude GBS. Treatment of a rapidly progressive high-risk syndrome should not be delayed solely to obtain an ideal electrophysiologic label. Assess respiratory reserve and autonomic instability in parallel.
Needle fibrillation potentials and positive sharp waves indicate muscle-fiber irritability and may occur with denervation or myopathy. They are not synonymous with motor neuron disease. Denervation-related changes take time to appear and depend on the lesion. Large, long-duration motor units can reflect chronic neurogenic reinnervation, while short-duration, low-amplitude units with early recruitment can support myopathy in a cooperative patient.
Critical Illness Weakness
Critical illness polyneuropathy (CIP) is typically an axonal sensory-motor process with reduced sensory and motor responses. Critical illness myopathy (CIM) often preserves sensory responses while impairing muscle responses and motor-unit characteristics. The disorders frequently overlap. Sepsis, organ failure, immobility, nutrition, medication exposure, and prolonged ICU care contribute to risk; one history of NMBA use does not prove the mechanism.
Direct muscle stimulation can help distinguish nerve from muscle inexcitability in expert hands. Do not memorize an isolated ratio without knowing how it was calculated and recorded. Edema, low limb temperature, electrode placement, electrical artifact, and inability to cooperate can make a simplistic pattern misleading. Review the full report and clinical context rather than declaring a permanent prognosis from one low amplitude.
Management focuses on the underlying illness, appropriate mobilization and rehabilitation, nutrition, and avoiding unnecessary prolonged sedation or paralysis. Recovery differs by mechanism and severity. A patient may require prolonged respiratory rehabilitation even after systemic sepsis resolves; failure to wean does not necessarily establish persistent brain injury.
Motor Neuron Disease and Ventilation
Motor neuron disease, including ALS, can produce progressive limb, bulbar, and respiratory weakness with relative sensory preservation. A respiratory infection, secretion burden, aspiration, or medication effect may precipitate acute decompensation. Assess cough effectiveness, swallowing, orthopnea, respiratory mechanics when feasible, and gas exchange. A normal saturation does not exclude inadequate ventilation.
Noninvasive ventilation and cough-assistance strategies can benefit selected patients, while severe bulbar dysfunction or acute airway compromise may require a different plan. Discuss invasive ventilation in the context of known patient preferences, communication needs, disease trajectory, and available support. Do not equate an acute respiratory setback with a new diagnosis based solely on EMG, and do not infer decision-making incapacity from dysarthria or inability to move.
Acute Myopathies and Rhabdomyolysis
Acute weakness can result from inflammatory or immune-mediated myopathy, toxic exposure, endocrine or electrolyte disorders, infection, or critical illness muscle disease. Immune checkpoint inhibitors can produce overlapping myositis, myocarditis, and neuromuscular junction dysfunction, requiring respiratory and cardiac assessment. Creatine kinase, examination, exposure history, selected antibodies, imaging, and sometimes biopsy complement EMG.
Rhabdomyolysis can follow prolonged seizures, crush injury, electrical injury, drugs, ischemia, or metabolic disease. Muscle injury releases potassium, phosphate, and myoglobin and can cause dangerous arrhythmia and AKI. Dark urine is not required. Evaluate potassium and ECG promptly, follow renal function and urine output, and treat the precipitant. Give fluids according to perfusion and tolerance, especially when brain edema, pulmonary edema, or cardiac dysfunction complicates the usual resuscitation. Routine alkalinization or mannitol is not a universally proven preventive strategy for every case.
The useful examination distinction is between diagnosing the cause and protecting the patient while uncertainty remains. In progressive weakness, secure ventilation or manage hyperkalemia when indicated before awaiting a complete electrodiagnostic or biopsy result.
Sources checked October 17, 2026: ABPN content outline and AANEM clinical resources.
Which pattern most supports a myopathic rather than sensory-motor axonal neuropathic process in the appropriate context?
Isolated absence of all sensory responses with normal muscle findings
A normal test necessarily excludes all acute disease
One slow segment proves every demyelinating criterion
Preserved SNAPs with myopathic motor units
A patient has rhabdomyolysis after prolonged seizures. Which complication requires prompt assessment?
Hyperkalemia and kidney injury
Only long-term cosmetic muscle change
Only an isolated low blood pressure reading from last month
Normal saturation excludes systemic danger
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