EMG & Nerve Conduction Studies

Electrodiagnostic testing is the physiologic extension of the neurologic examination — a way to interrogate the peripheral nervous system one nerve, one junction, and one muscle at a time. A complete study has two halves that are almost always performed together: nerve conduction studies (NCS), in which we stimulate a nerve and record the response, and needle electromyography (EMG), in which a recording electrode samples the electrical behavior of muscle at rest and during voluntary activation. Read together, the two halves answer the questions the clinician actually cares about: Where is the lesion? What is the pathophysiology — axonal or demyelinating? And how severe and how chronic is it?

Nerve Conduction Studies: Stimulate and Record

In NCS, a brief electrical pulse depolarizes a nerve and we record the resulting potential. There are two flavors:

• Motor studies record the compound muscle action potential (CMAP) — the summated electrical response of all the muscle fibers activated by stimulating their motor nerve. The recording electrode sits over the muscle belly.
• Sensory studies record the sensory nerve action potential (SNAP) — the response recorded directly from a sensory (or mixed) nerve. SNAPs are an order of magnitude smaller (microvolts vs. millivolts) and are exquisitely sensitive to pathology distal to the dorsal root ganglion.

For each response we measure three core parameters:

• Amplitude — a surrogate for the number of functioning axons (and muscle fibers, for the CMAP). The single most important indicator of axon loss.
• Distal latency — the time from stimulus to response onset across the most distal segment; reflects conduction (and, for motor studies, neuromuscular transmission and the terminal nerve segment).
• Conduction velocity — computed by stimulating at two points and dividing the inter-stimulus distance by the difference in latencies. A measure of how fast the fastest myelinated fibers conduct.

Late responses extend the reach of NCS to the proximal nerve segments that a distal stimulus cannot otherwise sample:

• F-waves — a small, late motor response produced when the stimulus travels antidromically up to the anterior horn cell and a fraction of those cells "backfire" orthodromically to the muscle. F-waves test the entire proximal motor pathway, including the root and plexus, and are often the earliest abnormality in acquired demyelinating polyradiculoneuropathy (e.g., Guillain-Barré syndrome).
• H-reflex — the electrophysiologic analog of the ankle reflex: an afferent (Ia) → efferent (motor) monosynaptic arc, classically recorded from soleus/gastrocnemius after tibial stimulation. A delayed or absent H-reflex is a useful marker of S1 radiculopathy.

Demyelinating vs. Axonal: The Central Dichotomy

Almost every NCS interpretation begins by sorting the pathology into one of two physiologic patterns. The distinction is the heart of electrodiagnosis.

• Demyelinating injury attacks the myelin sheath that makes saltatory conduction possible. The hallmarks are markedly slowed conduction velocities, prolonged distal latencies, and — when demyelination is focal or non-uniform — conduction block (a drop in CMAP amplitude/area across a segment) and temporal dispersion (a spread-out, longer-duration response as fibers desynchronize). Crucially, because the axons themselves survive, amplitude is relatively preserved until the process is severe.
• Axonal injury destroys the conducting fibers themselves. The hallmark is reduced amplitudes (fewer axons firing) with relatively preserved conduction velocity — the surviving, fastest fibers still conduct at near-normal speed. Velocity may dip only mildly if the largest, fastest axons are lost.

Pearl: When velocity collapses but amplitude is intact, think demyelinating. When amplitude collapses but velocity holds, think axonal. This single rule of thumb resolves the majority of polyneuropathy referrals at the bench.

Repetitive Nerve Stimulation: Probing the Junction

The neuromuscular junction (NMJ) is tested with repetitive nerve stimulation (RNS), where a train of stimuli is delivered and we watch how CMAP amplitude changes from the first to subsequent responses.

• A decrement in CMAP amplitude with low-frequency (2–3 Hz) stimulation reflects a postsynaptic defect. Because loss or blockade of acetylcholine receptors lowers the postsynaptic safety factor, the normal physiologic rundown of quantal release across a low-frequency train drops some endplates below the threshold for generating a muscle fiber action potential — and the lost fibers register as a falling CMAP. This is the signature of myasthenia gravis. (Presynaptic depletion of transmitter is the Lambert-Eaton mechanism, not myasthenia gravis.)
• An increment (facilitation) — a dramatic rise in CMAP after brief maximal exercise or with high-frequency (rapid) stimulation, typically on a backdrop of a low baseline CMAP — reflects a presynaptic defect. Calcium accumulates in the terminal and boosts quantal release. This is the signature of Lambert-Eaton myasthenic syndrome (LEMS).
• Single-fiber EMG (jitter), which measures the variability in transmission time between two muscle fibers of the same motor unit, is the most sensitive test of neuromuscular transmission and can be abnormal when RNS is normal.

Needle EMG at Rest: Listening for Spontaneous Activity

The needle electrode is the second half of the study. Normal muscle, with the needle still, is electrically silent (apart from physiologic endplate noise where the needle sits over the motor point). Abnormal spontaneous activity at rest is therefore always pathologic:

• Fibrillation potentials and positive sharp waves — the discharges of individual denervated muscle fibers; markers of active denervation / ongoing axon loss (and also seen in some active myopathies).
• Fasciculation potentials — spontaneous discharge of an entire motor unit; characteristic of anterior horn cell disease (e.g., ALS), though benign fasciculations exist.
• Myotonic discharges — waxing-and-waning runs producing the classic "dive-bomber" sound; seen in myotonic dystrophy, myotonia congenita, and some other disorders.
• Complex repetitive discharges (CRDs) — abrupt, machine-like runs with a fixed frequency; a nonspecific marker of chronic denervating or myopathic processes.

Needle EMG on Activation: Reading the Motor Unit

When the patient gently contracts the muscle, we analyze the motor unit action potentials (MUAPs) — their size, shape, and how they are recruited as effort increases. Two opposite patterns emerge:

• Neurogenic / chronic reinnervation — after axon loss, surviving axons sprout to adopt orphaned muscle fibers, building large-amplitude, long-duration, polyphasic motor units. Because fewer units remain, recruitment is reduced (the few surviving units fire faster to generate force).
• Myopathic — when the disease lies in the muscle fibers themselves, each unit loses fibers and produces small-amplitude, short-duration, polyphasic potentials. To generate force the patient must recruit many weak units up front, yielding early (full) recruitment at low force.

Pearl: The recruitment pattern alone is often diagnostic — reduced recruitment of large units = neurogenic; early/full recruitment of small units = myopathic.

How the Study Localizes Disease

Synthesizing NCS and needle EMG lets the electromyographer localize the lesion and assign a mechanism. The study reliably distinguishes:

• Peripheral neuropathy — and its subtype (axonal vs. demyelinating), distribution (length-dependent vs. multifocal), and fiber type (sensory, motor, or both).
• Radiculopathy — needle EMG abnormalities in a myotomal distribution with normal sensory studies (the lesion is proximal to the dorsal root ganglion).
• Anterior horn cell disease (ALS) — widespread denervation and chronic reinnervation across multiple spinal segments and regions, with normal sensory studies.
• NMJ disorders — myasthenia gravis vs. LEMS, separated by the RNS pattern.
• Myopathy — small, short, early-recruiting units, often with normal NCS.