ABEM (EDX) cheat sheet

Amyotrophic lateral sclerosis requires progressive upper and lower motor neuron dysfunction in at least three body regions, without sensory loss or sphincter involvement.

Myasthenia gravis: repetitive nerve stimulation shows a decrement greater than 10% in compound muscle action potential amplitude, and sensory conduction studies are normal.

Lambert-Eaton myasthenic syndrome: low baseline CMAP amplitude with greater than 100% facilitation after 10 seconds of maximal voluntary contraction or high-frequency stimulation.

Guillain-Barré syndrome: cerebrospinal fluid albuminocytologic dissociation; nerve conduction studies may show prolonged distal latencies, conduction block, temporal dispersion, and absent F-waves.

Chronic inflammatory demyelinating polyradiculoneuropathy requires demyelinating nerve conduction features in at least two nerves and a progressive or relapsing course lasting more than 8 weeks.

Inflammatory myopathy: needle EMG shows short-duration, low-amplitude, polyphasic MUAPs with fibrillation potentials; CK is often elevated and sensory nerve conduction is normal.

Cervical radiculopathy: fibrillation potentials in paraspinal and myotomal muscles with normal sensory nerve action potentials because the lesion is proximal to the dorsal root ganglion.

Diabetic polyneuropathy: length-dependent, symmetric, sensory-predominant axonal loss with reduced sural and superficial peroneal SNAP amplitudes.

Carpal tunnel syndrome: prolonged median sensory distal latency to digit 2 or palmar segment with normal ulnar sensory latency localizes the lesion to the median nerve at the wrist.

Motor conduction velocity in m/s equals interstimulus distance in millimeters divided by the proximal-to-distal latency difference in milliseconds.

Supramaximal stimulation is 10-20% above the intensity that produces no further increase in CMAP amplitude.

Conduction block: proximal CMAP amplitude less than 50% of distal CMAP amplitude with minimal increase in response duration.

Axonal loss reduces CMAP or SNAP amplitude while conduction velocity remains greater than 70% of the lower limit of normal.

Demyelination: conduction velocity below 70% of the lower limit of normal, distal latency above 130% of the upper limit, conduction block, or temporal dispersion.

F-wave minimal latency assesses proximal motor conduction and increases with limb length and height; absent or prolonged F-waves suggest proximal demyelination or radiculopathy.

H-reflex: submaximal tibial nerve stimulation with recording over soleus; prolongation suggests S1 radiculopathy or tibial neuropathy.

SNAP amplitude is measured peak-to-peak in microvolts and is preserved in preganglionic lesions because the dorsal root ganglion remains intact.

Cooling slows conduction and prolongs distal latency; upper limb temperature is maintained at 32°C or higher and lower limb temperature at 30°C or higher.

Fibrillation potentials and positive sharp waves appear 2-3 weeks after acute nerve injury and indicate active denervation.

Neurogenic MUAPs are long in duration, high in amplitude, and often polyphasic due to reinnervation and fiber type grouping.

Myopathic MUAPs are short in duration, low in amplitude, and polyphasic; recruitment is early and rapid.

Reduced recruitment with rapid firing of a few motor units indicates neurogenic weakness.

Paraspinal muscle examination increases sensitivity for radiculopathy because these muscles are innervated by posterior primary rami.

Single-fiber EMG measures jitter; increased jitter or blocking indicates neuromuscular junction transmission failure.

Myotonic discharges wax and wane in amplitude and frequency, producing a dive-bomber sound, and occur in myotonic dystrophy and other channelopathies.

Needle EMG of the diaphragm or paraspinal muscles carries risk of pneumothorax; ultrasound guidance reduces this risk.

Cranial nerve needle EMG can assess bulbar involvement; the genioglossus and facial muscles are commonly examined.

Myelinated peripheral nerve conduction is saltatory, jumping between nodes of Ranvier; velocity increases with axon diameter and myelination.

Hursh equation: conduction velocity in m/s approximates 6 times the myelinated axon diameter in micrometers in mammalian nerve.

A-alpha fibers are large, myelinated, and carry motor and proprioceptive signals; C fibers are unmyelinated and conduct at 0.5-2 m/s.

Brachial plexus roots C5-T1 pass through divisions and cords; the median nerve derives from medial and lateral cords (C6-T1), and the ulnar nerve derives from the medial cord (C8-T1).

Lumbosacral plexus: femoral nerve L2-L4, sciatic nerve L4-S3, tibial nerve L4-S3, and common peroneal nerve L4-S1.

The dorsal root ganglion lies in the intervertebral foramen; lesions proximal to it preserve sensory nerve action potentials.

Neuromuscular junction: action potential depolarizes the presynaptic terminal, opens voltage-gated calcium channels, and triggers acetylcholine release.

Wallerian degeneration occurs distal to axonal injury; reinnervation begins with axonal sprouting at 1-3 mm per day.

Differential amplifier rejects common-mode signals; common-mode rejection ratio exceeds 80 dB for clinical EMG equipment.

Typical filter settings: motor NCS 2 Hz to 10 kHz; sensory NCS 20 Hz to 3 kHz; needle EMG 10 Hz to 10 kHz.

Sensitivity for motor NCS is 1-5 mV/division; for sensory NCS 10-20 µV/division; sweep speed is 2-5 ms/division.

Supramaximal stimulation requires constant-current stimulator output typically up to 50-100 mA; electrode impedance is checked before stimulation.

Ground electrode reduces 60-Hz interference; notch filter use distorts waveforms and is avoided when possible.

Averaging multiple sensory responses improves signal-to-noise ratio; 10-20 responses are often averaged.

Electrical safety: patient leakage current remains below 100 µA in normal conditions for applied parts.

Stimulus artifact is reduced by adjusting ground placement, rotating anode-cathode orientation, or altering stimulus duration; it must not obscure the response.

AANEM guidelines recommend EDX studies be performed by physicians with formal training and interpreted in clinical context.

NCS and EMG reports include indication, technical parameters, findings, interpretation, and a specific diagnosis or differential diagnosis.

Temperature, age, height, and limb length affect reference values; normative data are matched to the laboratory.

Pacemakers and implanted defibrillators require caution with electrical stimulation; direct current paths through the chest are avoided.

Needle EMG is relatively contraindicated with severe thrombocytopenia or coagulopathy; hematoma risk is weighed against diagnostic benefit.

CPT coding distinguishes motor and sensory NCS by nerve and number of studies; unbundling and upcoding are compliance violations.

Informed consent and patient confidentiality are required; financial conflicts of interest are disclosed.

Quality assurance includes equipment calibration, electrode maintenance, and periodic review of report accuracy.