5.1 Nerve Conduction Studies Principles & Physics

5.1 Nerve Conduction Studies Principles & Physics

Biophysical Principles & Action Potential Physiology

Electrodiagnostic medicine quantifies bioelectrical potentials generated by peripheral nerves and muscles. Nerve conduction studies (NCS) evaluate large myelinated nerve fibers (A-alpha motor and A-beta sensory fibers). Unmyelinated C fibers and thinly myelinated A-delta fibers do not contribute to standard NCS waveforms due to low voltage and slow conduction velocities.

Electrical stimulation depolarizes the axonal membrane to threshold, opening voltage-gated sodium channels and initiating an action potential that propagates saltatorily along myelinated nodes of Ranvier. This is recorded peripherally as a Compound Muscle Action Potential (CMAP) for motor studies or a Sensory Nerve Action Potential (SNAP) for sensory studies.

Temperature Control & Technical Artifacts

Maintaining standardized limb skin temperature is mandatory for accurate diagnostic interpretation:

• Upper extremity skin temperature: Must be >32°C (target 33–34°C).
• Lower extremity skin temperature: Must be >30°C (target 32–33°C).

Biophysical Effects of Hypothermia

Limb cooling delays sodium channel inactivation, prolonging total action potential duration:

1. Conduction Velocity (CV): Decreases by 1.5 to 2.4 m/s per 1°C drop.
2. Distal Latency: Prolongs as temperature drops.
3. Amplitude (CMAP/SNAP): Paradoxically increases due to prolonged channel opening and enhanced spatial summation.
4. Duration: Widens due to slowed channel kinetics.

Failing to warm a cold limb can mimic a false demyelinating neuropathy. Radiant heat lamps or hydrocollators must be used prior to recording.

       +-------------------------------------------------------------+
       |                  EFFECTS OF LIMB COOLING                    |
       +-------------------------------------------------------------+
       |  Conduction Velocity (CV)   -->   Decreases (1.5–2.4 m/s/°C)|
       |  Distal & Peak Latencies   -->   Prolonged / Increased       |
       |  Waveform Amplitude        -->   Paradoxically Increased     |
       |  Waveform Duration         -->   Widened / Prolonged         |
       +-------------------------------------------------------------+

Electrode Configuration & Stimulation Setup

NCS waveforms use a differential amplifier setup with three surface electrodes:

• Active Electrode (E1/G1): Placed over the generator site (motor point / muscle belly for motor; nerve trunk for sensory).
• Reference Electrode (E2/G2): Placed over inactive tissue (tendon/bone for motor; 3–4 cm distal/proximal for sensory).
• Ground Electrode: Placed on neutral tissue between cathode and E1 to reduce stimulus artifact and common-mode electrical noise.

Supramaximal Stimulation

Stimulation requires a cathode (negative pole) and anode (positive pole). The cathode must face the recording electrode to prevent anodal block. Supramaximal stimulation increases current until maximal amplitude is reached, plus an additional 20% to 30% (typically 20–50 mA motor, 10–30 mA sensory) to recruit all axons.

Waveform Parameters & Pathophysiologic Interpretation

CMAP & SNAP Parameters

• Onset Latency (ms): Time to initial negative baseline deflection. Reflects fastest motor fiber conduction, NMJ transmission delay, and muscle depolarization time.
• CMAP Amplitude (mV): Measured baseline-to-peak. Correlates with the total number of conducting motor axons. Reduction indicates axonal loss or focal conduction block.
• SNAP Amplitude (µV): Measured baseline-to-peak or peak-to-peak. Reflects sensory axonal integrity.

Primary Demyelinating Criteria vs. Axonal Loss

According to AANEM criteria:

1. Axonal Loss: Reduced CMAP/SNAP amplitudes with preserved conduction velocities (CV >75% of Lower Limit of Normal [LLN]).
2. Primary Demyelination: Slowed velocity (CV <75% of LLN), prolonged distal latencies (>130% Upper Limit of Normal [ULN]), and prolonged late responses.
3. Conduction Block: >50% drop in CMAP area or amplitude between distal and proximal sites, with <15–30% duration widening. Indicates focal demyelination (e.g., MMN, GBS/AIDP).
4. Temporal Dispersion: Abnormal CMAP duration widening (>30% increase) between distal and proximal sites due to differential fiber slowing.

Late Responses: F-Waves & H-Reflexes

F-Wave Physiology & Clinical Utility

The F-wave is a late motor response produced by antidromic propagation of an electrical impulse along motor axons to the anterior horn cell soma. A small percentage (1–5%) of motor neurons undergo recurrent discharge, sending an orthodromic wave back down the motor axon. It has variable amplitude and latency, requiring 10 to 20 supramaximal stimuli to measure minimal latency. It evaluates proximal nerve segments, polyneuropathies (early AIDP), and radiculopathies.

H-Reflex Physiology & Clinical Utility

The H-reflex is the electrical analogue of the monosynaptic stretch reflex. Electrical stimulation of large Ia sensory afferent fibers in the tibial nerve travels centripetally to the S1 spinal cord segment, synapses monosynaptically with alpha motor neurons, and travels centrifugally via motor axons to record from the soleus/gastrocnemius. It is evoked using submaximal, long-duration stimuli and is a sensitive marker for S1 radiculopathy and generalized polyneuropathy.