ABEM (EDX) key terms

The summed electrical response recorded from a muscle after electrical stimulation of its motor nerve. Its amplitude reflects the number of functioning motor axons and muscle fibers.

The summed electrical response of sensory axons recorded after stimulating a sensory nerve. Amplitude and latency help distinguish axonal loss from demyelination and localize lesions.

The electrical waveform produced by a single motor unit during voluntary contraction, recorded with a needle electrode. Its duration, amplitude, and shape help identify neuropathy, myopathy, or normal muscle.

A spontaneous, brief, biphasic spike from a single muscle fiber firing without neural input. It indicates active denervation or muscle membrane instability and is seen in neuropathies and some myopathies.

A spontaneous waveform with an initial positive deflection followed by a slow negative return, arising from an injured muscle fiber. It signals active denervation and often accompanies fibrillation potentials.

A spontaneous discharge of an entire motor unit, producing a larger, longer waveform than a fibrillation. It is common in anterior horn cell disease but can occur in healthy people.

The orderly activation of additional motor units as voluntary effort increases. Reduced recruitment with fast-firing units suggests loss of motor axons, while early recruitment suggests myopathy.

The overlapping electrical activity of many motor units during maximal voluntary contraction, which obscures individual MUAPs. Its density helps assess motor unit loss and central drive.

The speed at which an electrical impulse travels along a nerve, calculated from distance and latency. Slowing indicates demyelination, while normal velocity with low amplitude suggests axonal loss.

The time from nerve stimulation to the onset of the evoked response at a fixed distance. Prolongation suggests distal demyelination, such as in carpal tunnel syndrome.

A late motor response caused by antidromic activation of anterior horn cells and their return volley. It assesses proximal nerve segments and is prolonged in demyelinating neuropathies.

A monosynaptic reflex recorded from muscle after submaximal nerve stimulation, analogous to the ankle jerk. It evaluates proximal sensory and motor pathways, especially S1 radiculopathy.

Widening and amplitude reduction of an evoked response caused by different conduction speeds among axons. It is a hallmark of acquired demyelinating neuropathy and can mimic conduction block.

A significant drop in CMAP amplitude when a nerve is stimulated proximally versus distally, without temporal dispersion. It indicates focal demyelination and is a key finding in compressive neuropathies.

Degeneration of nerve axons after injury, producing reduced response amplitudes with relatively preserved conduction velocity. It can result from ischemia, toxins, metabolic disease, or severe compression.

Loss or damage of the myelin sheath around axons, slowing conduction or causing block. Electrodiagnostic findings include prolonged latency, slowed velocity, and conduction block.

A single anterior horn cell, its motor axon, and all the muscle fibers it innervates. It is the functional unit of motor control and the source of the MUAP.

The motor neuron in the spinal cord ventral horn whose axon innervates skeletal muscle. Its degeneration causes weakness and denervation, as in amyotrophic lateral sclerosis.

A cluster of sensory neuron cell bodies located beside the spinal cord. Lesions before the ganglion preserve the SNAP, while lesions after it may reduce the SNAP.

The synapse between a motor nerve terminal and a muscle fiber, where acetylcholine release triggers contraction. Disorders here cause fatigable weakness with normal sensory studies.

The rapid jumping of an action potential between nodes of Ranvier along a myelinated axon. It increases conduction speed and is lost when myelin is damaged.

Degeneration of the axon and its myelin sheath distal to a nerve injury. It begins within days and leads to denervation changes on needle EMG.

An autoimmune disorder causing fatigable weakness due to antibodies against acetylcholine receptors or related proteins at the neuromuscular junction. Electrodiagnosis includes repetitive nerve stimulation and single-fiber EMG.

A presynaptic neuromuscular junction disorder caused by antibodies to voltage-gated calcium channels, often paraneoplastic. It produces proximal weakness and increased CMAP amplitude after brief exercise.

A progressive neurodegenerative disease affecting upper and lower motor neurons. Needle EMG often shows widespread active denervation and enlarged, unstable MUAPs.

An acute immune-mediated polyneuropathy causing ascending weakness and areflexia. Early electrodiagnosis may show prolonged F-waves, conduction block, or reduced CMAP amplitudes.

Compression of the median nerve at the wrist, causing numbness and weakness in the median nerve distribution. Nerve conduction studies show prolonged distal sensory and motor latencies across the wrist.

Disease or compression of a spinal nerve root, causing pain, weakness, and reflex changes in a dermatomal or myotomal pattern. Needle EMG helps localize the affected level.

A group of inherited peripheral neuropathies causing slowly progressive distal weakness and sensory loss. Nerve conduction studies classify them as demyelinating or axonal types.

A distal symmetric sensory and motor neuropathy caused by chronic hyperglycemia. It typically produces reduced SNAP and CMAP amplitudes with mild conduction slowing.

A technique using a needle electrode inserted into muscle to record spontaneous and voluntary electrical activity. It helps assess denervation, myopathy, and motor unit remodeling.

The low- and high-frequency limits used to display or record electrical signals. Correct settings reduce noise and preserve the true waveform for nerve and muscle studies.

The display scale that determines how large a signal appears on the screen, measured in microvolts or millivolts per division. Appropriate sensitivity helps measure amplitude accurately.

The rate at which the display trace moves horizontally, usually expressed in milliseconds per division. It affects the visibility of waveform timing and duration.

Practices that prevent electric shock or injury during nerve stimulation and needle EMG. They include proper grounding, equipment inspection, and avoiding current paths through the heart.

A program of checks and standards that ensures electrodiagnostic studies are accurate, reproducible, and safe. It includes equipment calibration, reference values, and technologist competency.

Normal ranges for nerve conduction and needle EMG measurements derived from healthy subjects. They must match the laboratory's technique, temperature, and equipment for valid interpretation.

Cooling slows nerve conduction and alters waveform amplitudes, potentially causing misinterpretation. Limb temperature should be measured and maintained near 32°C for upper extremities.