Figure 1.1. Chapter 1 atlas overview: NCS workstation, signal pathway, electrode placement, waveform measurements, conduction velocity, motor and sensory studies, F-waves, H-reflexes, workflow and technical factors.
By the end of this chapter, the learner should be able to:
1. Define nerve conduction studies (NCS).
2. Explain the purpose of NCS in clinical neurophysiology.
3. Describe the fundamental principles of nerve stimulation and electrical recording.
4. Identify the major components of an NCS system.
5. Differentiate NCS from needle electromyography (EMG).
6. Explain the major measurements obtained during NCS.
7. Describe the major clinical applications of NCS.
8. Recognize physiological and technical factors that influence NCS results.
9. Explain why knowledge of physics and instrumentation is essential for accurate NCS.
10. Describe the workflow of a standardized NCS examination.
Nerve conduction studies (NCS) are electrodiagnostic investigations used to assess the functional properties of peripheral nerves. The technique involves applying a controlled electrical stimulus to a peripheral nerve and recording the resulting electrical response from a muscle or sensory nerve.
NCS provides objective physiological measurements that complement the patient's history and neurological examination. It is an important component of electrodiagnostic medicine and clinical neurophysiology.
NCS is commonly used in the assessment of entrapment neuropathies, focal peripheral nerve lesions, generalized polyneuropathies, traumatic nerve injuries, selected plexopathies, demyelinating neuropathies and axonal neuropathies.
The principal measurements obtained during NCS include onset latency, peak latency, amplitude, duration, area, conduction velocity, F-wave parameters, H-reflex parameters, conduction block and temporal dispersion.
Correct interpretation requires integration of clinical information, anatomy, neurophysiology, stimulation technique, recording technique and electrical instrumentation.
The fundamental NCS process is:
ELECTRICAL STIMULUS → NERVE DEPOLARIZATION → ACTION-POTENTIAL PROPAGATION → ELECTRICAL RECORDING → AMPLIFICATION → SIGNAL PROCESSING → MEASUREMENT → INTERPRETATION
During an examination, the stimulator delivers a brief electrical pulse through stimulating electrodes positioned over or near the nerve. If the stimulus produces sufficient depolarization of excitable nerve fibres, action potentials are generated and propagate along the nerve.
The resulting electrical activity may be recorded from a muscle, producing a compound muscle action potential (CMAP), or from a sensory nerve, producing a sensory nerve action potential (SNAP). The recorded waveform is amplified, filtered, digitized, displayed and measured by the NCS system.
Conduction timing: the interval between stimulation and a defined point on the recorded response, usually expressed as latency in milliseconds.
Conduction velocity: an estimate of how rapidly an impulse travels along a defined nerve segment.
Response amplitude: the magnitude of the recorded response, commonly expressed in mV for motor responses and µV for sensory responses.
Waveform duration and morphology: the temporal width and shape of the compound response, providing information about synchrony of conduction.
Late responses: F-waves and H-reflexes provide additional information about selected portions of motor and reflex pathways.
Latency is the interval between delivery of the electrical stimulus and a defined point on the recorded response. It is usually expressed in milliseconds (ms).
Amplitude represents the magnitude of the recorded electrical response. Motor response amplitudes are usually expressed in millivolts (mV), while sensory responses are commonly expressed in microvolts (µV).
Conduction velocity is estimated from distance and the corresponding latency difference. For motor studies, the usual calculation uses the distance between proximal and distal stimulation sites divided by their onset-latency difference.
DURATION describes the temporal width of a response. AREA represents the integrated electrical content of a waveform over a defined interval.
Motor NCS evaluates conduction in motor nerve fibres by stimulating a motor nerve and recording the resulting response from an appropriate muscle. The response is the compound muscle action potential (CMAP).
Typical measurements include distal motor latency, CMAP amplitude and duration, motor conduction velocity and F-wave parameters.
Sensory NCS evaluates conduction through sensory nerve fibres. The recorded response is the sensory nerve action potential (SNAP). Because SNAPs are generally small, they are particularly susceptible to technical problems and electrical interference.
Orthodromic conduction refers to propagation in the physiological direction of sensory conduction toward the central nervous system. Antidromic conduction refers to propagation in the opposite direction. Both approaches can be useful, but waveform characteristics and normative values may differ; reference values must therefore correspond to the technique used.
The F-wave is a late motor response following supramaximal stimulation of a motor nerve. Some of the stimulus travels proximally toward the spinal motor neuron, and a proportion of motor neurons may generate a backfiring response that travels distally to the muscle.
Important parameters include minimum F-wave latency, persistence and chronodispersion.
The H-reflex is an electrically evoked reflex involving a sensory afferent pathway, spinal synapse and motor efferent pathway. It is commonly assessed by stimulating the tibial nerve and recording from the soleus or gastrocnemius-soleus region.
NCS evaluates peripheral nerve conduction using electrical stimulation and surface recording. Needle EMG evaluates muscle and motor units using a needle electrode. The two techniques are complementary and are often combined in electrodiagnostic assessment.
Entrapment neuropathies; generalized polyneuropathies; focal nerve lesions; selected demyelinating patterns; and axonal patterns characterized by reduced CMAP or SNAP amplitudes.
NCS is fundamentally a measurement of bioelectrical signals. The practitioner must understand voltage, current, resistance, impedance, the electrode-skin interface, amplification, differential recording, common-mode rejection, filtering, sampling, digitization and signal-to-noise ratio.
A waveform may appear abnormal because of a technical problem rather than genuine nerve pathology. Good neurophysiology therefore begins with good signal acquisition.
Stimulator; recording electrodes; ground electrode; amplifier; filters; analogue-to-digital converter; computer and software; and measurement tools.
1. Clinical assessment
2. Select nerves
3. Prepare patient
4. Control technical conditions
5. Place electrodes
6. Stimulate
7. Record
8. Verify waveform quality
9. Measure
10. Repeat where necessary
11. Interpret
12. Report
Patient factors include age, height, limb length, body habitus, edema and skin condition.
Physiological factors include limb temperature, peripheral circulation, nerve pathology and tissue characteristics.
Technical factors include electrode position, stimulation distance, stimulus intensity, pulse duration, filter settings, grounding, skin impedance and measurement technique.
Equipment factors include calibration, amplifier characteristics, sampling rate, filter configuration, electrical interference and electrode/cable integrity.
Temperature is one of the most important controllable physiological variables in NCS. Cooling can prolong distal latencies, slow conduction velocities and alter waveform characteristics. Limb temperature should therefore be assessed and controlled according to the laboratory's protocol.
Incorrect electrode placement; inadequate stimulation; incorrect distance measurement; poor grounding; high skin impedance; incorrect filter settings; stimulus artefact; failure to control temperature; and incorrect anatomical localization.
1. PRE-ACQUISITION → confirm patient, clinical question, equipment, temperature and electrodes.
2. ACQUISITION → confirm stimulation, recording, electrode placement, settings and waveform quality.
3. POST-ACQUISITION → confirm measurements, reference values, internal consistency, clinical correlation and reporting.
Before accepting an abnormal NCS result, ask:
1. Is the recording technically valid?
2. Does the abnormality fit known nerve physiology?
3. Does the finding fit the patient's clinical presentation?
Technical quality precedes physiological interpretation.
NCS evaluates peripheral nerve function using controlled electrical stimulation and recording.
Motor studies produce CMAPs; sensory studies produce SNAPs.
Major measurements include latency, amplitude, duration, area and conduction velocity.
F-waves and H-reflexes provide additional information about selected motor and reflex pathways.
Temperature, electrode placement, stimulation and signal-processing settings can substantially influence results.
NCS and needle EMG are complementary.
Technical quality must be established before physiological interpretation.
1. Define a nerve conduction study.
2. What is the fundamental principle of NCS?
3. Differentiate a CMAP from a SNAP.
4. Define latency and conduction velocity.
5. Why is limb temperature important during NCS?
6. What is an F-wave?
7. What is an H-reflex?
8. List the major components of an NCS system.
9. List five technical factors that can alter NCS results.
10. Why can a technically poor recording mimic peripheral neuropathy?
Nerve conduction studies are quantitative electrophysiological investigations used to assess the functional properties of peripheral nerves. The examination combines controlled stimulation, action-potential propagation, electrical recording and quantitative analysis. Reliable interpretation depends on both physiological knowledge and technically sound signal acquisition.
NERVE CONDUCTION STUDIES
Technical Physics, Instrumentation, Physiology and Clinical Protocols
CHAPTER 1
INTRODUCTION TO NERVE CONDUCTION STUDIES
1.1 Learning Objectives
By the end of this chapter, the learner should be able to:
1. Define nerve conduction studies (NCS).
2. Explain the basic purpose of NCS in clinical neurophysiology.
3. Describe the fundamental principle underlying nerve stimulation and recording.
4. Identify the major components of an NCS system.
5. Differentiate NCS from needle electromyography (EMG).
6. Explain the major measurements obtained during NCS.
7. Describe the major clinical applications of NCS.
8. Recognize factors that can produce technically inaccurate results.
9. Explain why understanding physics and instrumentation is essential for accurate NCS.
10. Describe the basic workflow of a complete NCS examination.
1.2 Introduction
Nerve Conduction Studies (NCS) are electrodiagnostic investigations used to evaluate the functional integrity of peripheral nerves.
The technique involves applying a controlled electrical stimulus to a peripheral nerve and recording the resulting electrical response. The recorded response provides information about the ability of the nerve to conduct an electrical impulse along its course.
NCS is one of the fundamental components of electrodiagnostic medicine and clinical neurophysiology. It is widely used in the assessment of peripheral neuropathies, entrapment neuropathies, focal nerve lesions, polyneuropathies, plexopathies and selected neuromuscular disorders.
The investigation provides objective physiological measurements rather than relying solely on symptoms or physical examination findings.
The major parameters obtained include:
Correct interpretation requires understanding both neurophysiology and electrical instrumentation.
1.3 The Basic Principle of NCS
The fundamental NCS process can be represented as:
Electrical stimulus → Nerve depolarization → Action potential propagation → Electrical recording → Amplification → Signal processing → Measurement → Interpretation
SHAPE \* MERGEFORMAT SHAPE \* MERGEFORMAT
SHAPE \* MERGEFORMAT
A stimulator delivers a brief electrical pulse through electrodes positioned over or near a peripheral nerve.
If the stimulus is sufficient to activate the nerve, an action potential is generated and propagates along the nerve.
Depending on the study being performed, the resulting electrical activity is recorded:
The waveform is displayed on the NCS machine and analysed quantitatively.
1.4 What Does NCS Actually Measure?
NCS does not directly "see" the nerve.
Instead, it measures the electrical consequences of nerve activation.
The measurements provide indirect information about:
A. Conduction speed
How rapidly an impulse travels between two stimulation sites.
B. Conduction timing
How long it takes from stimulation to the beginning or peak of the recorded response.
C. Response size
The amplitude of the recorded electrical response.
D. Waveform characteristics
The morphology, duration and area of the response.
These measurements allow the examiner to identify abnormalities affecting peripheral nerve function.
1.5 Major Measurements in NCS
1.5.1 Latency
Latency is the time between delivery of the stimulus and a defined point on the recorded response.
It is usually expressed in:
milliseconds (ms)
Latency can be measured to:
depending on the protocol and laboratory convention.
Prolonged latency may occur with:
Therefore, prolonged latency should not automatically be interpreted as pathological.
1.5.2 Amplitude
Amplitude represents the magnitude of the recorded electrical response.
For motor studies, it is usually expressed in:
millivolts (mV)
For sensory studies, it is commonly expressed in:
microvolts (µV)
Reduced amplitude may indicate loss or dysfunction of functioning axons, although amplitude is also influenced by technical factors such as electrode placement, stimulus intensity and recording conditions.
1.5.3 Conduction Velocity
Conduction velocity estimates how rapidly an impulse travels along the nerve.
It is generally calculated using the difference in stimulation distance divided by the difference in stimulation latencies.
The basic relationship is:
Conduction velocity = Distance / Time
For motor studies, the difference between proximal and distal onset latencies is particularly important because it helps reduce the contribution of neuromuscular junction and muscle depolarization time.
1.5.4 Duration
Duration describes the temporal width of a recorded response.
Increased duration may be associated with dispersion of conduction across nerve fibres.
1.5.5 Area
The area under the waveform can provide additional information about the total electrical response.
Area can sometimes be useful when amplitude alone does not adequately characterize a response.
1.6 Motor Nerve Conduction Studies
Motor NCS evaluates the ability of a motor nerve to activate its target muscle.
A recording electrode is placed over an appropriate muscle.
The nerve is stimulated at one or more locations.
The resulting electrical response is called the:
Compound Muscle Action Potential (CMAP)
The CMAP represents the summated electrical activity of many muscle fibres activated through the stimulated motor nerve.
Typical motor NCS measurements include:
Commonly studied motor nerves include:
1.7 Sensory Nerve Conduction Studies
Sensory NCS evaluates conduction through sensory nerve fibres.
The resulting waveform is called the:
Sensory Nerve Action Potential (SNAP)
SNAPs are generally much smaller than CMAPs and therefore require careful attention to:
Common sensory studies include:
1.8 Orthodromic and Antidromic Studies
Sensory nerve studies can be performed using different stimulation and recording directions.
Orthodromic conduction
The electrical impulse travels in the physiological direction of sensory conduction toward the central nervous system.
Antidromic conduction
The impulse travels in the opposite direction.
Both techniques can provide useful information, although waveform characteristics and normative values may differ.
The laboratory must therefore use appropriate reference values for the specific technique employed.
1.9 F-Waves
The F-wave is a late motor response produced following supramaximal stimulation of a motor nerve.
The stimulus travels:
Distally → toward the motor neuron → back down the motor axon → muscle
F-waves are useful for evaluating conduction along more proximal portions of motor nerves that may not be adequately assessed by routine distal stimulation alone.
Important parameters include:
1.10 H-Reflex
The H-reflex is an electrically evoked reflex response involving a sensory afferent pathway, spinal synapse and motor efferent pathway.
It is particularly useful in selected assessments of:
The H-reflex is commonly assessed through stimulation of the tibial nerve and recording from the soleus/gastrocnemius region.
1.11 NCS Versus Needle EMG
NCS and needle EMG are complementary but distinct techniques.
|
Feature |
NCS |
Needle EMG |
|
Primary target |
Peripheral nerve |
Muscle/motor unit |
|
Stimulation |
Electrical nerve stimulation |
Usually voluntary activation/insertion |
|
Recording |
Surface electrodes commonly used |
Needle electrode |
|
Major response |
CMAP/SNAP |
Motor unit action potentials |
|
Measures |
Latency, amplitude, velocity |
Spontaneous activity, MUAP morphology, recruitment |
|
Particularly useful |
Peripheral neuropathy/entrapment |
Radiculopathy, myopathy, denervation |
|
Invasive? |
Generally non-invasive |
Minimally invasive |
A complete electrodiagnostic evaluation frequently combines both methods.
1.12 Major Clinical Applications
NCS can assist in evaluating:
Entrapment neuropathies
Polyneuropathies
Focal nerve lesions
Demyelinating disorders
NCS may demonstrate:
Axonal disorders
NCS may demonstrate:
These patterns must always be interpreted in the context of the clinical examination and the technical quality of the study.
1.13 Why Physics Matters in NCS
NCS is fundamentally an electrical measurement.
The examiner must understand:
A waveform can appear abnormal because of a technical problem rather than nerve pathology.
For example:
Poor electrode contact → increased impedance → increased noise → distorted waveform → potentially incorrect interpretation
Therefore:
Good neurophysiology begins with good signal acquisition.
1.14 Basic NCS Equipment
A modern NCS system generally contains:
1. Stimulator
Produces controlled electrical stimuli.
2. Recording electrodes
Detect the biological electrical response.
3. Ground electrode
Helps reduce interference and improve recording quality.
4. Amplifier
Increases the size of the recorded signal.
5. Filters
Restrict unwanted frequencies.
6. Analogue-to-digital converter
Converts the electrical signal into digital information.
7. Computer/software
Displays, stores and analyses the waveform.
8. Measurement tools
Allow the operator to measure:
1.15 The NCS Examination Workflow
A standardized NCS examination can be conceptualized as:
Step 1 — Clinical assessment
Determine the clinical question.
Step 2 — Select nerves
Choose appropriate motor and sensory nerves.
Step 3 — Prepare the patient
Explain the procedure and position the limb.
Step 4 — Control technical conditions
Check:
Step 5 — Place electrodes
Position recording, reference and ground electrodes correctly.
Step 6 — Stimulate
Deliver an appropriate electrical stimulus.
Step 7 — Record
Acquire the CMAP or SNAP.
Step 8 — Verify waveform quality
Check baseline, artefact, stimulus adequacy and waveform morphology.
Step 9 — Measure
Determine latency, amplitude, duration and conduction velocity.
Step 10 — Repeat where necessary
Confirm unexpected findings.
Step 11 — Interpret
Integrate findings with the clinical question.
Step 12 — Report
Produce a clear, structured electrodiagnostic report.
1.16 Factors That Affect NCS Results
NCS results are influenced by both physiological and technical factors.
Important variables include:
Patient factors
Physiological factors
Technical factors
Equipment factors
1.17 Temperature: A Critical Consideration
Temperature is one of the most important controllable variables in NCS.
Cold limbs can produce:
Therefore, limb temperature should be assessed and controlled according to the laboratory's protocol before interpreting potentially abnormal results.
A technically excellent recording from a significantly cold limb can still produce misleading physiological measurements.
1.18 Common Technical Errors
Common errors include:
Incorrect electrode placement
Can alter amplitude and waveform morphology.
Inadequate stimulation
May result in an apparently low response.
Incorrect distance measurement
Produces incorrect conduction velocity.
Poor grounding
Increases electrical interference.
High skin impedance
Produces unstable or noisy recordings.
Incorrect filter settings
May remove important components of the waveform.
Stimulus artefact
May obscure the onset of a response.
Failure to control temperature
Can create false slowing.
Incorrect anatomical localization
May result in stimulation of the wrong nerve or recording from the wrong muscle.
1.19 Quality Assurance Principle
The quality of an NCS examination should be considered in three stages:
Pre-acquisition → Acquisition → Post-acquisition
Pre-acquisition
Acquisition
Post-acquisition
1.20 Key Points
1. NCS evaluates peripheral nerve function using controlled electrical stimulation and recording.
2. Motor studies produce CMAPs.
3. Sensory studies produce SNAPs.
4. Major measurements include latency, amplitude, duration and conduction velocity.
5. F-waves and H-reflexes provide information about specific parts of the peripheral/reflex pathways.
6. Temperature can substantially affect nerve conduction measurements.
7. Electrode placement and stimulation technique are critical.
8. Poor signal acquisition can mimic disease.
9. NCS and needle EMG provide complementary information.
10. Technical quality must be established before physiological interpretation.
1.21 Review Questions
Short-answer questions
1. Define a nerve conduction study.
2. What is the basic principle of NCS?
3. Differentiate CMAP from SNAP.
4. What is latency?
5. What is conduction velocity?
6. Why is limb temperature important?
7. What is an F-wave?
8. What is an H-reflex?
9. List five major components of an NCS system.
10. Give five technical factors that can alter NCS results.
Discussion question
Explain how a technically poor NCS recording can produce a false impression of peripheral neuropathy.
Practical question
A patient has a prolonged median sensory latency. List the technical factors that should be checked before concluding that the patient has median neuropathy at the wrist.
1.22 Chapter Summary
Nerve Conduction Studies are quantitative electrophysiological investigations that assess the ability of peripheral nerves to conduct electrical impulses. Their accuracy depends on the interaction between nerve physiology, electrical stimulation, electrode technology, amplification, filtering, digital signal processing and measurement technique.
For this reason, an NCS practitioner must not only understand anatomy and neurophysiology but also possess a sound understanding of the physics and instrumentation of bioelectrical signal acquisition.
The following chapters will progressively develop these principles, beginning with the physics of bioelectric signals, followed by electrical properties of nerves, instrumentation, stimulation, recording electrodes, amplification, filtering and finally practical NCS protocols.
CHAPTER 2
BASIC PHYSICS OF BIOELECTRIC SIGNALS
2.1 Learning Objectives
By the end of this chapter, the learner should be able to:
1. Explain the electrical basis of biological tissues.
2. Define voltage, current, resistance, impedance and conductance.
3. Apply Ohm's law to basic NCS instrumentation.
4. Explain the difference between voltage and current stimulation.
5. Describe how electrical current spreads through biological tissues.
6. Explain the electrode–skin interface.
7. Describe capacitance and its importance in biological recording.
8. Explain the concept of signal-to-noise ratio.
9. Identify common sources of electrical interference in NCS.
10. Relate basic electrical principles to practical NCS recording.
2.2 Introduction
Nerve Conduction Studies are fundamentally electrical measurements of biological activity.
Although the clinician is interested in nerve function, the NCS instrument does not directly measure "nerve health." Instead, it detects very small changes in electrical potential generated by excitable tissues.
To understand why an NCS waveform looks the way it does—and why it sometimes becomes distorted—the practitioner must understand the underlying physics.
The essential chain is:
Electrical stimulus → Biological tissue → Ionic movement → Electrical potential → Electrodes → Amplifier → Filter → Digital conversion → Waveform
Every component of this chain can influence the final recording.
A technically excellent NCS therefore requires knowledge of both:
2.3 Electricity in Biological Systems
Electricity involves the movement or separation of electrical charge.
In conventional electrical circuits, charge is primarily carried by electrons.
In biological systems, however, electrical activity is largely produced by the movement of ions.
Important ions include:
These ions are distributed unevenly across cell membranes.
This unequal distribution creates an electrical potential difference.
The neuronal membrane therefore behaves somewhat like an electrical system containing resistive and capacitive properties.
2.4 Electrical Charge
Electrical charge is a fundamental property of matter.
It can be:
The SI unit of charge is the coulomb (C).
In biological systems, charged particles such as Na⁺ and K⁺ are responsible for much of the electrical behaviour of nerve and muscle cells.
The movement of these ions across the cell membrane changes the membrane voltage.
2.5 Voltage
Definition
Voltage is the electrical potential difference between two points.
It represents the potential energy available to drive electrical charge through a circuit.
Voltage is measured in:
Volts (V)
In NCS, recorded biological signals are usually much smaller than one volt.
Common units include:
Thus:
1 mV = 1,000 µV
This distinction is particularly important because CMAPs are commonly measured in millivolts, whereas SNAPs are often measured in microvolts.
2.6 Current
Definition
Electric current is the rate at which electrical charge moves through a conductor.
Current is measured in:
Amperes (A)
For clinical nerve stimulation, the current delivered is typically in the milliampere range.
The instrument controls the stimulus according to parameters such as:
Current intensity is one of the major determinants of whether a sufficient number of nerve fibres are activated.
2.7 Resistance
Resistance is the opposition to the flow of electrical current.
It is measured in:
Ohms (Ω)
A material with high resistance restricts current flow.
A material with low resistance allows current to flow more easily.
Biological tissues do not all have the same electrical properties.
For example, tissues containing more fluid and electrolytes generally conduct electricity better than relatively dry or poorly hydrated materials.
2.8 Ohm's Law
The fundamental relationship between voltage, current and resistance is:
V = I × R
Where:
Therefore:
I = V/R
and:
R = V/I
This relationship is important for understanding electrical circuits used in NCS.
For example, if resistance increases while the applied voltage remains constant, the current decreases.
This helps explain why poor electrical contact can interfere with stimulation and recording.
2.9 Conductance
Conductance is the ability of a material to conduct electrical current.
It is the reciprocal of resistance.
The unit of conductance is:
Siemens (S)
High conductance means current flows relatively easily.
Low conductance means current flow is more restricted.
Biological tissues have different conductivities, meaning that electrical stimulation does not spread uniformly through the body.
2.10 Impedance
In NCS, impedance is more useful than resistance alone.
Impedance represents the opposition to alternating or time-varying electrical current.
It includes both:
and is measured in:
Ohms (Ω)
The electrode–skin interface has impedance that changes with:
High impedance at the recording electrode can increase susceptibility to electrical noise.
2.11 Resistance Versus Impedance
|
Resistance |
Impedance |
|
Opposition to current flow |
Total opposition to time-varying current |
|
Primarily resistive |
Includes resistance and reactance |
|
Important in simple DC circuits |
Particularly important in biological signal recording |
|
Measured in Ω |
Measured in Ω |
For NCS instrumentation, understanding impedance is essential because biological signals are not perfectly steady DC signals.
2.12 Capacitance
Capacitance is the ability of a system to store electrical charge.
It is measured in:
Farads (F)
Cell membranes have important capacitive properties because the membrane separates conductive intracellular and extracellular fluids.
The membrane can therefore behave approximately like a capacitor.
This is important because biological membranes do not respond to electrical changes instantaneously.
The electrical behaviour of a membrane depends on both:
Together these properties influence how rapidly the membrane responds to electrical stimulation.
2.13 The Cell Membrane as an Electrical System
A useful conceptual model of the nerve membrane is:
Membrane resistance + membrane capacitance
The lipid bilayer provides insulating properties, while ion channels provide pathways through which ionic current can flow.
The membrane therefore behaves approximately like an RC electrical circuit.
This model helps explain:
A detailed understanding of membrane electrophysiology will be developed in later chapters.
2.14 Electrical Stimulation of a Nerve
During NCS, an electrical stimulator applies a brief pulse through surface electrodes.
The goal is to generate an electrical field strong enough to depolarize excitable nerve fibres.
The stimulus is characterized by parameters such as:
Current intensity
How much electrical current is delivered.
Pulse duration
How long the stimulus lasts.
Polarity
The orientation of the stimulating electrodes.
Frequency
Relevant when repeated stimuli are delivered.
The relationship between stimulus intensity and duration is important because a weaker stimulus may require a longer duration to achieve equivalent activation.
This principle is related to concepts such as:
These will be discussed in detail in the stimulation chapter.
2.15 Electrical Fields in Biological Tissue
When current is applied to the body, it does not travel as a narrow straight line between the electrodes.
Instead, current spreads through the tissues according to their electrical properties.
The resulting electrical field is influenced by:
Therefore, precise electrode positioning is essential.
A small change in electrode position can alter the effective stimulation field.
2.16 The Electrode–Skin Interface
The electrode is the physical connection between the electrical instrument and the patient's body.
This interface is extremely important.
The system can be conceptualized as:
Machine → electrode → conductive medium → skin → biological tissue
The skin itself provides electrical resistance and impedance.
Poor contact can therefore produce:
2.17 Skin Preparation
Good skin preparation can significantly improve signal acquisition.
Depending on the electrode system and local protocol, preparation may include:
1. Cleaning the skin.
2. Removing excessive oils.
3. Removing excessive sweat.
4. Reducing excessive hair when necessary.
5. Ensuring good electrode contact.
Aggressive preparation should be avoided because damaged or irritated skin may cause discomfort and may compromise the examination.
2.18 Grounding
The ground electrode is an important component of the recording system.
It helps reduce environmental electrical interference and can improve the quality of the differential recording.
The ground is usually positioned between the stimulating and recording electrodes or according to the manufacturer's recommended protocol.
Poor grounding may result in:
2.19 Differential Recording
NCS systems generally use differential amplification.
The amplifier compares the voltage detected at two input electrodes.
Conceptually:
Output = Input 1 − Input 2
This allows the system to amplify the difference between the active and reference electrodes while rejecting electrical signals that are common to both inputs.
This property is called:
Common-mode rejection
It is particularly valuable for reducing environmental electrical interference.
2.20 Common-Mode Interference
Electrical interference can affect both recording electrodes simultaneously.
If the interference is essentially identical at both inputs, a good differential amplifier can substantially reject it.
This is one reason electrode placement, cable arrangement and grounding are important.
However, common-mode rejection is not perfect.
Differences in:
can reduce the effectiveness of common-mode rejection.
2.21 Signal-to-Noise Ratio
One of the most important concepts in electrophysiology is the:
Signal-to-Noise Ratio (SNR)
It describes the strength of the desired biological signal relative to unwanted electrical noise.
A high SNR means:
Strong signal + low noise
A poor SNR means:
Weak signal + substantial noise
This is particularly important in sensory NCS because SNAPs may have very small amplitudes.
2.22 Sources of Noise
Common sources include:
Environmental electrical interference
Often associated with mains electricity.
Patient movement
Movement can produce large low-frequency artefacts.
Muscle activity
Unwanted muscle contraction can contaminate recordings.
Poor electrode contact
Creates unstable electrical connections.
Equipment interference
May originate from nearby electrical devices.
Cable movement
Can introduce motion artefact.
Electrode polarization
Can contribute to baseline instability.
2.23 The 50/60-Hz Problem
Electrical mains systems commonly operate at approximately:
depending on the country.
Mains interference can appear as repetitive electrical contamination on the recording.
In a clinical NCS laboratory, minimizing this interference requires attention to:
Filtering may help, but good signal acquisition should come before relying on filters.
2.24 Filters
Filters selectively attenuate certain frequency components of a signal.
Two fundamental filter types are:
High-pass filter
Reduces frequencies below a selected cutoff.
Low-pass filter
Reduces frequencies above a selected cutoff.
Together they define a frequency band through which the desired signal is recorded.
Improper filter settings can distort the waveform.
Therefore:
Filters should reduce unwanted noise without removing clinically important signal information.
Detailed filter characteristics will be addressed in a dedicated instrumentation chapter.
2.25 Amplification
Biological signals are often very small.
The amplifier increases their measurable voltage so that they can be processed and displayed.
The amount of amplification is determined by:
Gain
For example, a system may amplify a small signal several hundred or thousand times.
However, excessive gain does not create additional physiological information. It simply enlarges the signal—and the noise along with it.
Therefore, appropriate gain and sensitivity are essential.
2.26 Analogue and Digital Signals
The biological signal initially exists as an analogue electrical signal.
Modern NCS systems convert this signal into digital information.
The process is:
Biological signal → amplification → filtering → sampling → analogue-to-digital conversion → digital waveform
Digital processing allows:
2.27 Sampling
Sampling is the process of measuring an analogue signal at regular intervals.
The sampling frequency determines how accurately the digital system represents the original signal.
If the sampling rate is too low, important waveform information may be lost.
This phenomenon is related to the Nyquist sampling principle.
In practical NCS systems, the sampling frequency must be sufficiently high to capture the frequency components relevant to the response being measured.
2.28 Quantization
During analogue-to-digital conversion, continuous voltage values are represented by discrete digital values.
This process is called:
Quantization
Higher digital resolution allows the system to represent smaller voltage differences more accurately.
This becomes particularly important when recording low-amplitude sensory responses.
2.29 Why SNAP Recording Is Technically Challenging
SNAPs may have amplitudes in the microvolt range.
This means the desired biological signal may be relatively small compared with environmental electrical interference.
Therefore, sensory NCS requires careful attention to:
The smaller the signal, the more important the signal-to-noise ratio becomes.
2.30 Electrical Safety
NCS involves applying electrical stimulation to a patient.
Therefore, equipment must be designed and operated according to appropriate electrical safety standards.
The practitioner should:
Electrical safety is not simply an equipment issue; it is part of professional clinical practice.
2.31 Practical Example
Consider a patient undergoing median sensory NCS.
The expected SNAP is small.
Suppose the recording shows a noisy baseline.
Before interpreting the waveform as abnormal, the operator should consider:
Is the patient moving?
Is the skin adequately prepared?
Are the electrodes firmly attached?
Is the ground electrode functioning properly?
Are there nearby sources of electrical interference?
Are the cables positioned appropriately?
Are the filter settings appropriate?
Is the stimulus adequate?
Only after technical factors have been addressed should the waveform be interpreted physiologically.
2.32 Important Physical Relationships
Several relationships introduced in this chapter will recur throughout the textbook.
Ohm's Law
V = IR
Conductance
G = 1/R
Power
P = VI
Frequency and Period
f = 1/T
These relationships provide the foundation for understanding electrical stimulation, recording and signal processing.
2.33 Clinical Interpretation Principle
An abnormal waveform should always be evaluated through three questions:
Question 1
Is the waveform technically valid?
Question 2
Does the abnormality fit the physiology?
Question 3
Does it fit the patient's clinical presentation?
This prevents the common error of interpreting every abnormal-looking waveform as evidence of neuropathy.
2.34 Common Technical Errors
|
Error |
Possible consequence |
|
High electrode impedance |
Increased noise |
|
Poor grounding |
Mains interference |
|
Incorrect electrode placement |
Abnormal amplitude/morphology |
|
Excessive stimulus artefact |
Difficulty identifying onset |
|
Inadequate stimulation |
Low or absent response |
|
Excessive filtering |
Waveform distortion |
|
Inadequate sampling |
Loss of waveform information |
|
Patient movement |
Baseline artefact |
|
Cold limb |
Slowed conduction |
|
Incorrect distance |
Incorrect conduction velocity |
2.35 Key Points
1. NCS is fundamentally an electrical measurement.
2. Biological electrical activity is largely generated by ionic movement.
3. Voltage represents electrical potential difference.
4. Current represents movement of electrical charge.
5. Resistance opposes current flow.
6. Impedance is particularly important in biological signal acquisition.
7. Cell membranes have both resistive and capacitive properties.
8. Electrical stimulation creates an electrical field within biological tissues.
9. Electrode–skin impedance strongly influences recording quality.
10. Differential amplification helps reject common-mode interference.
11. Signal-to-noise ratio is critical, especially for SNAPs.
12. Filtering must be used carefully to avoid waveform distortion.
13. Digital NCS systems require adequate sampling and analogue-to-digital conversion.
14. Technical quality must be established before clinical interpretation.
2.36 Review Questions
Short-answer
1. Define voltage.
2. Define electrical current.
3. What is resistance?
4. State Ohm's law.
5. What is impedance?
6. Why is impedance important in NCS?
7. What is capacitance?
8. What is differential amplification?
9. What is common-mode rejection?
10. Define signal-to-noise ratio.
Applied questions
1. A sensory nerve response is very small and contaminated by 50-Hz interference. List five technical factors you would check.
2. Explain why poor electrode contact can produce a noisy NCS recording.
3. Explain why excessive filtering can be dangerous when interpreting an NCS waveform.
4. Why is signal-to-noise ratio particularly important when recording SNAPs?
2.37 Chapter Summary
The physics of NCS begins with the fundamental properties of electrical charge, voltage, current, resistance, impedance and capacitance. These principles determine how electrical stimuli interact with nerves and how biological electrical signals are detected by electrodes.
The signal then passes through a complex measurement pathway involving electrodes, differential amplifiers, filters, sampling and digital processing.
Understanding this pathway is essential because every stage can influence the waveform ultimately interpreted by the neurophysiology practitioner.
CHAPTER 3
ELECTRICAL PROPERTIES OF PERIPHERAL NERVE FIBRES
3.1 Learning Objectives
By the end of this chapter, the learner should be able to:
1. Describe the basic structure of a peripheral nerve fibre.
2. Explain the electrical properties of the neuronal membrane.
3. Define resting membrane potential.
4. Explain the role of sodium and potassium ions.
5. Describe depolarization and repolarization.
6. Explain the action potential.
7. Describe refractory periods.
8. Explain saltatory conduction.
9. Relate axon diameter and myelination to conduction velocity.
10. Explain how pathological changes in nerve fibres affect NCS findings.
3.2 Introduction
A nerve conduction study ultimately depends on one fundamental biological event:
The ability of an excitable nerve fibre to generate and propagate an electrical signal.
The electrical stimulus delivered during NCS does not simply "send electricity down the nerve." Instead, the stimulus changes the electrical state of the nerve membrane sufficiently to activate voltage-dependent ion channels.
This produces an action potential, which propagates along the axon.
The recorded NCS waveform is therefore the result of the synchronized activity of many individual nerve fibres.
Understanding the electrical properties of the nerve fibre is essential for understanding:
3.3 Basic Structure of a Peripheral Nerve
A peripheral nerve is not a single axon.
It contains many nerve fibres organized into bundles.
The major structural components include:
Axon → Endoneurium → Fascicle → Perineurium → Epineurium
Axon
The axon is the conducting portion of the neuron.
It transmits electrical impulses away from the neuronal cell body.
Myelin
Many peripheral axons are surrounded by myelin produced by Schwann cells.
Fascicle
A fascicle is a bundle of nerve fibres.
Perineurium
The perineurium surrounds individual fascicles.
Epineurium
The epineurium surrounds the entire peripheral nerve.
These anatomical structures also influence the spread and recording of electrical activity.
3.4 The Axonal Membrane
The axonal membrane separates:
These compartments contain different concentrations of ions.
The unequal distribution of ions produces an electrical gradient across the membrane.
The membrane is selectively permeable, meaning that different ions cross it through different channels and transport mechanisms.
This selective permeability is fundamental to nerve excitability.
3.5 Major Ions
The most important ions for nerve electrophysiology include:
|
Ion |
Major location |
Charge |
|
Sodium (Na⁺) |
Mainly extracellular |
Positive |
|
Potassium (K⁺) |
Mainly intracellular |
Positive |
|
Chloride (Cl⁻) |
Mainly extracellular |
Negative |
|
Calcium (Ca²⁺) |
Mainly extracellular |
Positive |
The concentration gradients of these ions create electrochemical forces that influence membrane voltage.
3.6 Resting Membrane Potential
When a nerve fibre is not generating an action potential, the inside of the membrane is electrically negative relative to the outside.
This is called the:
Resting membrane potential
In a typical neuron, the resting membrane potential is approximately −70 mV, although the precise value varies with cell type and physiological conditions.
The negative intracellular potential results from several factors, including:
The resting membrane potential places the nerve in a state capable of responding to stimulation.
3.7 Sodium-Potassium Pump
The Na⁺/K⁺ ATPase is an important membrane transport mechanism.
It uses cellular energy in the form of ATP to transport:
3 Na⁺ out of the cell
and
2 K⁺ into the cell
for each cycle.
This contributes to maintaining the ionic gradients required for normal neuronal function.
The pump is therefore essential for maintaining the conditions required for repeated action-potential generation.
3.8 Ion Channels
Ion channels are specialized membrane proteins that allow specific ions to cross the membrane.
They may be:
For NCS, voltage-gated ion channels are particularly important.
When the membrane voltage reaches a sufficient threshold, voltage-gated sodium channels open rapidly.
This initiates the rising phase of the action potential.
3.9 Threshold
A nerve does not necessarily generate an action potential in response to every electrical stimulus.
The membrane must be depolarized to a critical level known as the:
Threshold potential
Once threshold is reached, a rapid regenerative process occurs.
This is the basis of the:
All-or-none principle
An individual nerve fibre either generates an action potential or does not.
The amplitude of the action potential of an individual axon is not progressively increased simply by increasing stimulus strength.
However, increasing stimulus strength in an NCS examination recruits more nerve fibres, causing the recorded compound response to increase.
This distinction is extremely important.
3.10 Depolarization
When sufficient stimulation occurs, voltage-gated sodium channels open.
Sodium ions move rapidly into the axon.
The membrane potential becomes less negative and may become positive.
This process is called:
Depolarization
The rapid depolarization phase corresponds to the rising portion of the action potential.
3.11 Repolarization
After sodium channels become inactivated, potassium channels open more prominently.
Potassium moves out of the cell.
The membrane potential becomes negative again.
This process is called:
Repolarization
The membrane therefore returns toward its resting electrical state.
3.12 Hyperpolarization
Following repolarization, the membrane potential may temporarily become more negative than its resting level.
This is called:
After-hyperpolarization
It occurs partly because potassium conductance remains elevated for a period after the main action potential.
The membrane then gradually returns to its resting state.
3.13 The Action Potential
The action potential can therefore be simplified into several phases:
Resting state → Threshold → Depolarization → Repolarization → Hyperpolarization → Resting state
The sequence is driven primarily by changes in membrane permeability to sodium and potassium ions.
The action potential is the fundamental electrical event responsible for nerve impulse transmission.
3.14 Refractory Periods
Following an action potential, the nerve fibre temporarily becomes less responsive to another stimulus.
There are two important refractory periods.
Absolute refractory period
During this period, another action potential cannot normally be generated regardless of stimulus strength.
Relative refractory period
During this period, another action potential can occur, but a stronger-than-normal stimulus may be required.
Refractory periods are important for understanding:
3.15 Propagation of the Action Potential
An action potential generated at one point of the axon causes local electrical changes that influence adjacent membrane regions.
The adjacent region reaches threshold and generates another action potential.
The process continues along the axon.
Thus:
Local depolarization → adjacent membrane activation → continued propagation
The action potential therefore travels along the nerve without progressively disappearing.
3.16 Why the Action Potential Does Not Simply Stop
Each region of membrane regenerates the electrical signal.
This means the action potential is not a single electrical charge physically travelling down the axon like water moving through a pipe.
Instead, it is a self-regenerating wave of membrane depolarization.
This concept is fundamental to understanding nerve conduction.
3.17 Myelination
Many large peripheral axons are surrounded by a myelin sheath.
In the peripheral nervous system, myelin is produced by:
Schwann cells
The myelin sheath provides electrical insulation around the axon.
However, the myelin is not continuous.
There are small gaps called:
Nodes of Ranvier
The membrane at these nodes contains a high concentration of voltage-gated sodium channels.
3.18 Saltatory Conduction
In a myelinated nerve fibre, the action potential effectively propagates from one node of Ranvier to the next.
This process is called:
Saltatory conduction
The word "saltatory" means jumping.
The action potential does not literally jump as a physical object. Rather, depolarizing current spreads rapidly beneath the myelin to the next excitable node.
This greatly increases conduction velocity.
3.19 Why Myelin Increases Conduction Velocity
Myelin changes the electrical properties of the axon.
It:
Consequently, the next node can reach threshold rapidly.
This is one of the major reasons why large myelinated fibres conduct substantially faster than small unmyelinated fibres.
3.20 Axon Diameter and Conduction Velocity
Axon diameter also affects conduction velocity.
In general:
Larger axons conduct impulses faster than smaller axons.
Large axons have lower internal resistance to longitudinal current flow.
This allows depolarizing current to spread more efficiently along the axon.
Therefore, both:
Axon diameter + myelination
are major determinants of nerve conduction velocity.
3.21 Fibre Types
Peripheral nerve fibres can be broadly classified according to diameter, myelination and conduction characteristics.
Large myelinated fibres conduct rapidly and are particularly important for:
Smaller fibres conduct more slowly and are involved in functions such as:
Routine NCS primarily evaluates the larger, faster-conducting myelinated fibres.
This is an important limitation of NCS.
A patient may have clinically significant small-fibre dysfunction while routine NCS results remain relatively normal.
3.22 Stimulating a Nerve During NCS
When the NCS stimulator is activated, an electrical field is generated around the stimulating electrodes.
If the stimulus is sufficiently strong, excitable axons are depolarized.
The resulting action potentials propagate along the nerve.
The recording electrode detects the summed electrical activity associated with these activated fibres.
Thus:
Stimulus → Axonal depolarization → Propagation → Summation → Recorded waveform
3.23 Recruitment of Nerve Fibres
An individual axon produces an action potential of relatively fixed amplitude.
Increasing stimulus intensity does not simply make that individual action potential larger.
Instead, increasing stimulation recruits additional excitable axons.
Therefore:
More recruited axons → larger compound response
This is the physiological basis of the increasing CMAP amplitude seen as stimulus intensity is increased until a maximal response is obtained.
3.24 Supramaximal Stimulation
The goal of routine motor NCS is generally to achieve a stimulus strong enough to activate all readily excitable motor axons beneath the stimulating electrode.
This is called:
Supramaximal stimulation
The response is considered maximal when further increases in stimulus intensity do not produce a meaningful increase in CMAP amplitude.
This principle is essential because an inadequately stimulated nerve can produce an artificially low CMAP.
3.25 Conduction Velocity
Conduction velocity reflects the speed at which the electrical impulse propagates along the nerve.
It is influenced by:
A marked reduction in conduction velocity can suggest abnormal myelin function, although interpretation must consider technical and physiological factors.
3.26 Demyelination
Damage to the myelin sheath can impair saltatory conduction.
Potential NCS findings include:
The exact pattern depends on the disease and distribution of the pathology.
3.27 Axonal Injury
Axonal loss reduces the number of functioning axons available to contribute to the recorded response.
Therefore, an important NCS finding may be:
Reduced CMAP amplitude
or:
Reduced SNAP amplitude
Conduction velocity may be relatively preserved compared with the degree of amplitude reduction, although axonal disorders can also cause some slowing.
3.28 Demyelinating Versus Axonal Pattern
|
Feature |
Predominantly axonal |
Predominantly demyelinating |
|
CMAP/SNAP amplitude |
Often reduced |
May be preserved initially |
|
Conduction velocity |
Mild/moderate slowing possible |
Marked slowing |
|
Distal latency |
May be mildly prolonged |
Often substantially prolonged |
|
F-wave latency |
May be affected |
Often markedly prolonged |
|
Conduction block |
Not a typical primary feature |
May occur |
|
Temporal dispersion |
Usually limited |
May be prominent |
These are general patterns rather than absolute diagnostic rules.
3.29 Temperature and Nerve Physiology
Temperature affects ion-channel kinetics and membrane conduction.
Cooling a limb can produce:
Therefore, temperature must be considered whenever conduction measurements appear abnormal.
3.30 Relationship to NCS Waveforms
The waveform obtained during NCS represents the combined activity of many individual nerve fibres.
For motor studies:
Many motor axons → neuromuscular transmission → muscle fibre activation → CMAP
For sensory studies:
Many sensory axons → synchronized sensory response → SNAP
The recorded waveform therefore reflects the collective behaviour of a population of nerve fibres.
3.31 Why Synchronization Matters
If all activated nerve fibres conducted at exactly the same velocity, their electrical responses would arrive at the recording site simultaneously.
In reality, individual fibres have different conduction velocities.
This produces some degree of temporal dispersion.
The range of conduction velocities within the nerve therefore influences waveform duration and morphology.
3.32 Clinical Importance
Understanding nerve fibre physiology allows the practitioner to interpret NCS abnormalities more accurately.
For example:
Low CMAP amplitude
May indicate:
Slow conduction velocity
May indicate:
Prolonged distal latency
May indicate:
Therefore, the physiological interpretation must always be combined with technical assessment.
3.33 Common Misconceptions
Misconception 1
"More stimulus makes one axon produce a bigger action potential."
Correction: Increasing stimulus intensity primarily recruits more axons once individual fibres are activated.
Misconception 2
"The electrical impulse physically travels down the nerve."
Correction: The action potential is regenerated sequentially along the excitable membrane.
Misconception 3
"All nerve fibres conduct at the same speed."
Correction: Fibre diameter and myelination create a range of conduction velocities.
Misconception 4
"A normal NCS excludes all peripheral nerve disease."
Correction: Routine NCS primarily evaluates large myelinated fibres and may not detect isolated small-fibre dysfunction.
3.34 Practical Clinical Example
A patient with diabetes presents with numbness and burning in both feet.
NCS demonstrates:
The physiological interpretation is compatible with a predominantly axonal large-fibre peripheral neuropathy, assuming technical factors and appropriate reference values have been considered.
However, if the patient's symptoms are predominantly burning pain with completely normal routine NCS, small-fibre dysfunction may still be considered clinically.
3.35 Common Technical Errors Related to Nerve Physiology
|
Problem |
Potential effect |
|
Inadequate stimulation |
Failure to recruit all available fibres |
|
Cold limb |
Slower conduction |
|
Incorrect distance |
Incorrect velocity |
|
Incorrect nerve identification |
Misleading waveform |
|
Poor recording electrode position |
Reduced amplitude |
|
Excessive stimulus artefact |
Difficult latency measurement |
|
Patient movement |
Baseline instability |
|
Incorrect reference values |
Misclassification |
3.36 Key Points
1. A peripheral nerve contains many individual axons.
2. The axonal membrane has specialized electrical properties.
3. Ion gradients create the resting membrane potential.
4. Voltage-gated sodium and potassium channels are central to action-potential generation.
5. Depolarization is followed by repolarization and often transient hyperpolarization.
6. Myelin increases conduction efficiency.
7. Nodes of Ranvier enable saltatory conduction.
8. Larger and more heavily myelinated fibres generally conduct faster.
9. Routine NCS primarily evaluates large myelinated fibres.
10. Increasing stimulus intensity recruits more axons rather than simply enlarging the action potential of each axon.
11. Supramaximal stimulation is essential for reliable motor NCS.
12. Demyelination primarily affects conduction speed and synchronization.
13. Axonal loss commonly reduces CMAP and/or SNAP amplitude.
14. Temperature and technical factors can mimic pathological slowing.
3.37 Review Questions
Short-answer
1. What is the resting membrane potential?
2. Which two ions are particularly important in action-potential generation?
3. What is depolarization?
4. What is repolarization?
5. What is the refractory period?
6. What is a node of Ranvier?
7. Define saltatory conduction.
8. How does myelin increase conduction velocity?
9. Why do larger axons conduct faster?
10. Why is supramaximal stimulation used in NCS?
Applied questions
1. A patient's median CMAP amplitude increases progressively as stimulus intensity is increased and then reaches a plateau. Explain the physiological basis of this finding.
2. A patient has markedly slowed conduction velocities in several nerves. The limbs are cold. Explain why temperature must be corrected or considered before diagnosing demyelinating neuropathy.
3. Explain why a patient can have severe burning feet with a normal routine NCS.
4. Compare the expected NCS pattern of axonal loss with that of primary demyelination.
3.38 Chapter Summary
Peripheral nerve conduction depends on the electrical properties of the axonal membrane, ion gradients, voltage-gated channels, axon diameter and myelination.
The action potential is a regenerating electrical event produced by sequential changes in membrane permeability. In myelinated fibres, saltatory conduction between nodes of Ranvier allows rapid transmission.
During NCS, electrical stimulation activates a population of nerve fibres. The resulting synchronized electrical activity is recorded as a CMAP or SNAP.
CHAPTER 4
RESTING MEMBRANE POTENTIAL AND ACTION POTENTIAL GENERATION
4.1 Learning Objectives
By the end of this chapter, the learner should be able to:
1. Explain the origin of the resting membrane potential.
2. Describe the distribution of major ions across the nerve membrane.
3. Explain the role of membrane permeability.
4. Describe the Nernst equilibrium potential concept.
5. Explain the basis of the resting membrane potential.
6. Describe the sequence of an action potential.
7. Explain sodium and potassium channel behaviour.
8. Define threshold potential.
9. Explain absolute and relative refractory periods.
10. Explain the strength–duration relationship.
11. Relate these principles to electrical nerve stimulation during NCS.
4.2 Introduction
The nerve conduction study begins with a fundamental event:
An external electrical stimulus changes the electrical state of the nerve membrane sufficiently to generate an action potential.
To understand how this happens, we must understand what the nerve membrane is doing before stimulation.
At rest, the inside of a nerve fibre is electrically negative relative to the outside. This electrical difference is maintained by:
When an adequate stimulus is applied, these conditions change rapidly.
The membrane depolarizes, an action potential develops, and the electrical disturbance propagates along the axon.
This chapter explains the physiology underlying that process.
4.3 The Nerve Membrane
The nerve membrane is primarily composed of a lipid bilayer containing specialized proteins.
Important membrane proteins include:
The lipid bilayer acts as a relatively poor conductor of ions, while ion channels provide selective pathways through which ions can cross.
This arrangement gives the membrane both:
Electrical resistance
and
Electrical capacitance
The membrane can therefore be considered, conceptually, as an electrical RC system.
4.4 Ion Distribution Across the Membrane
The major ions are distributed unevenly.
|
Ion |
Predominantly higher concentration |
|
Na⁺ |
Outside |
|
K⁺ |
Inside |
|
Cl⁻ |
Outside |
|
Ca²⁺ |
Outside |
This concentration difference creates a chemical gradient.
Because the ions are electrically charged, there is also an electrical gradient.
The combination of these two forces is called the:
Electrochemical gradient
4.5 Chemical Gradient
A chemical gradient exists when the concentration of a substance differs between two locations.
For example:
K⁺ concentration is higher inside the axon than outside.
If potassium channels are open, potassium tends to move outward because of its concentration gradient.
Similarly:
Na⁺ concentration is higher outside than inside.
If sodium channels open, sodium tends to move inward.
These gradients are fundamental to action-potential generation.
4.6 Electrical Gradient
Charged particles are also influenced by electrical forces.
At rest, the intracellular environment is relatively negative.
Positive ions are therefore attracted toward the inside of the cell.
The direction of ion movement is determined by the combined effect of:
Chemical gradient + electrical gradient
This is why ion movement across the membrane cannot be understood from concentration alone.
4.7 Equilibrium Potential
For a particular ion, there is a membrane voltage at which the electrical force exactly balances the chemical force.
At this point there is no net movement of that ion through an open pathway.
This voltage is called the:
Equilibrium potential
The theoretical equilibrium potential for an ion can be estimated using the Nernst equation.
For a monovalent ion, the simplified relationship is:
where:
The Nernst equation is primarily a conceptual tool here: it demonstrates that equilibrium potential depends on the ion concentration gradient and temperature.
4.8 Potassium Equilibrium Potential
Potassium is particularly important in establishing the resting membrane potential.
Because intracellular K⁺ concentration is high, potassium tends to move outward through potassium leak channels.
As positive charge leaves the cell, the inside becomes increasingly negative.
Eventually, the electrical attraction pulling K⁺ inward balances the chemical force pushing K⁺ outward.
This produces a potassium equilibrium potential that is typically substantially more negative than the normal resting membrane potential.
4.9 Why the Resting Membrane Potential Is Not Exactly the Potassium Equilibrium Potential
The resting membrane is not exclusively permeable to potassium.
There is also some permeability to:
Therefore, the actual resting membrane potential reflects the combined influence of several ions and their relative membrane permeabilities.
A more complete mathematical treatment uses the:
Goldman-Hodgkin-Katz equation
This considers multiple ions simultaneously.
For clinical NCS, the important concept is:
The resting membrane potential is determined by ionic concentration gradients together with the relative permeability of the membrane to those ions.
4.10 The Sodium-Potassium ATPase
The sodium-potassium pump helps maintain the concentration gradients required for normal nerve function.
For each ATP-dependent cycle, it generally moves:
3 Na⁺ outward
and
2 K⁺ inward
This maintains:
The pump therefore supports the conditions necessary for repeated action potentials.
4.11 Resting Membrane Potential
At rest, the inside of a typical nerve fibre is approximately:
−70 mV
relative to the extracellular environment.
The exact value varies depending on:
The negative value means that the inside is electrically negative relative to the outside.
4.12 What Does −70 mV Mean?
If the extracellular reference is considered 0 mV, the inside of the nerve fibre is approximately 70 mV more negative.
It does not mean that the entire axon contains a large reservoir of negative electricity.
Rather, it represents a voltage difference across the membrane.
Only a very small redistribution of charge is required to establish this membrane potential.
4.13 Depolarization
Depolarization means that the membrane potential becomes less negative.
For example:
−70 mV → −50 mV → −30 mV → 0 mV
If the membrane reaches the appropriate threshold, voltage-gated sodium channels activate rapidly.
This produces further depolarization.
The process is therefore regenerative.
4.14 Threshold Potential
The membrane has a critical voltage at which an action potential is initiated.
This is called:
Threshold potential
The exact threshold varies with:
Once sufficient sodium-channel activation occurs, inward sodium current causes further depolarization.
This creates a positive feedback loop:
Depolarization → sodium channels open → Na⁺ enters → further depolarization → more sodium channels open
This rapidly drives the membrane toward the peak of the action potential.
4.15 The Rising Phase of the Action Potential
Once threshold is reached:
1. Voltage-gated sodium channels open rapidly.
2. Sodium conductance increases.
3. Sodium enters the axon.
4. The membrane becomes less negative.
5. More sodium channels activate.
6. The membrane rapidly depolarizes.
The membrane potential can briefly become positive.
This produces the rising phase of the action potential.
4.16 Sodium Channel Inactivation
Voltage-gated sodium channels do not remain open indefinitely.
After activation, they rapidly enter an:
Inactivated state
This stops sustained sodium entry through those channels.
The timing of sodium-channel inactivation is critical because it helps terminate the rapid depolarizing phase.
4.17 Potassium Channel Activation
Voltage-gated potassium channels generally activate more slowly than sodium channels.
As potassium channels open:
K⁺ leaves the axon.
Positive charge therefore moves outward.
The membrane potential becomes negative again.
This produces:
Repolarization
4.18 Hyperpolarization
Potassium conductance can remain elevated after the membrane has returned toward its resting level.
Continued potassium efflux may make the membrane temporarily more negative than its resting potential.
This is:
After-hyperpolarization
The membrane subsequently returns to its resting state.
4.19 Action Potential Sequence
The complete sequence can be summarized as:
Resting potential
↓
Threshold
↓
Rapid Na⁺ channel activation
↓
Depolarization
↓
Na⁺ channel inactivation
↓
K⁺ channel activation
↓
Repolarization
↓
After-hyperpolarization
↓
Return to resting potential
4.20 Absolute Refractory Period
Immediately following activation, sodium channels are either open or inactivated.
During this period, another normal action potential cannot be generated regardless of how strong the stimulus is.
This is the:
Absolute refractory period
It ensures that action potentials do not continuously overlap at the same membrane location.
4.21 Relative Refractory Period
Following the absolute refractory period, some sodium channels have recovered, but potassium conductance may remain elevated.
The membrane may therefore require a stronger stimulus than normal.
This is the:
Relative refractory period
The refractory periods are important for understanding the response of nerves to repeated stimulation.
4.22 Strength–Duration Relationship
An important concept in NCS is the relationship between:
Stimulus intensity
and
Stimulus duration
A brief stimulus may need to have relatively high intensity to activate the nerve.
A longer stimulus can often activate the nerve at a lower intensity.
This relationship is known as the:
Strength–duration relationship
It is fundamental to electrical nerve stimulation.
4.23 Rheobase
Rheobase
Rheobase is the minimum current intensity required to excite a nerve when a sufficiently long stimulus duration is used.
It provides a measure of excitability.
4.24 Chronaxie
Chronaxie
Chronaxie is the minimum stimulus duration required to excite a nerve using a current approximately twice the rheobase.
Chronaxie is useful for describing membrane excitability.
Although these measurements are not routinely calculated during standard clinical NCS, the underlying principle is highly relevant to stimulator design.
4.25 Why Pulse Duration Matters in NCS
The NCS operator selects both:
A stimulus that is too weak or too brief may fail to activate enough nerve fibres.
A stimulus that is appropriately selected can produce reliable activation.
This is why the NCS stimulator allows control over pulse duration and current intensity.
4.26 Threshold Is Not the Same as Supramaximal Stimulation
These concepts must be distinguished.
Threshold stimulation
The minimum stimulation sufficient to activate some excitable fibres.
Maximal stimulation
Increasing stimulation produces no further meaningful increase in the recorded response.
Supramaximal stimulation
The stimulus is increased beyond the level required for a maximal response to provide a safety margin.
In routine motor NCS, supramaximal stimulation is generally preferred.
4.27 How Increasing Stimulus Intensity Changes the CMAP
Suppose stimulation begins at a low intensity.
Only the most easily excitable fibres are activated.
The CMAP is small.
As stimulus intensity increases:
More axons are recruited → CMAP amplitude increases
Eventually:
All readily excitable motor axons are recruited → CMAP reaches a plateau
Further increases in stimulus intensity produce little or no additional response.
This plateau indicates that a maximal response has been reached.
4.28 Recruitment and Fibre Excitability
Different axons may have different thresholds.
This can depend on:
Therefore, increasing stimulus intensity progressively recruits additional axons.
4.29 Cathode and Anode
The stimulating circuit contains:
Cathode (−)
and
Anode (+)
The electrical field produced between these electrodes alters the membrane potential.
In conventional peripheral nerve stimulation, the cathode is generally the more effective site for local depolarization because it creates extracellular negativity that favours membrane depolarization beneath the electrode.
This principle is important when positioning the stimulator.
4.30 Cathodal Depolarization
The cathode creates a region of relative extracellular negativity.
This alters the transmembrane potential in the underlying nerve membrane.
If the resulting depolarization reaches threshold:
Voltage-gated sodium channels activate → action potential generated
This is one reason correct polarity is important during NCS.
4.31 Anodal Effects
The anode creates relative extracellular positivity.
This tends to produce hyperpolarizing effects beneath the electrode.
Under certain circumstances, stimulation can produce complex effects including anodal block or changes in excitability.
Therefore, electrode polarity and positioning must be controlled carefully.
4.32 Current Spread
Electrical current does not remain directly beneath the stimulating electrode.
It spreads through the surrounding tissues.
The amount and direction of current spread depend on:
This is one reason why anatomical knowledge is essential when performing NCS.
4.33 The Concept of Excitability
Nerve excitability refers to the ability of an axon to respond to an appropriate stimulus by generating an action potential.
Excitability is influenced by:
Changes in excitability can alter NCS responses.
4.34 Effects of Temperature
Cooling generally slows ion-channel kinetics.
As a result, a cold nerve may demonstrate:
Therefore, temperature is a physiological variable that must be controlled or documented.
4.35 Effects of Demyelination
Myelin normally:
When myelin is damaged:
Current leakage increases → conduction becomes slower and less synchronized
Potential NCS consequences include:
4.36 Effects of Axonal Loss
If axons are lost, fewer fibres remain available to contribute to the recorded response.
Therefore:
Fewer functioning axons → smaller CMAP/SNAP
This is why reduced response amplitude is an important indicator of axonal involvement.
4.37 Clinical Example: Carpal Tunnel Syndrome
Consider a patient with suspected median neuropathy at the wrist.
The median nerve is stimulated and the sensory response is recorded.
Suppose the median sensory latency is prolonged compared with an appropriate comparison nerve.
The abnormality may reflect focal slowing across the wrist.
However, before interpreting the finding as pathology, the examiner should confirm:
The physiology and the technical measurement must agree.
4.38 Clinical Example: Axonal Polyneuropathy
A patient with longstanding metabolic disease presents with distal numbness.
NCS demonstrates:
This pattern may support a predominantly axonal large-fibre polyneuropathy.
The interpretation should still incorporate:
4.39 Important Distinction: Action Potential vs Compound Response
An individual axon produces an:
Action potential
The NCS machine records the combined electrical activity of many activated fibres.
The resulting response is a:
Compound action potential
Examples:
CMAP — compound muscle action potential
SNAP — sensory nerve action potential
Thus, a CMAP is not the action potential of one axon.
It is the summed response of many activated motor axons and their target muscle fibres.
4.40 From Membrane Physiology to the NCS Machine
The complete sequence is:
Stimulator
↓
Electrical field
↓
Membrane depolarization
↓
Voltage-gated channel activation
↓
Action potential
↓
Propagation along axon
↓
Activation of many fibres
↓
CMAP/SNAP
↓
Electrode detection
↓
Amplification
↓
Filtering
↓
Digitization
↓
Waveform measurement
This sequence forms the physiological and technological foundation of NCS.
4.41 Common Errors in Understanding
Error 1
"An action potential is simply electricity flowing down the nerve."
Correction: It is a regenerative sequence of membrane depolarization.
Error 2
"More current makes each action potential larger."
Correction: More current generally recruits more excitable axons.
Error 3
"The sodium-potassium pump creates the action potential directly."
Correction: The pump maintains ionic gradients; voltage-gated channels produce the rapid action potential.
Error 4
"Myelin generates the action potential."
Correction: Myelin facilitates rapid propagation by insulating the axon; active regeneration occurs at excitable membrane regions, particularly nodes of Ranvier.
4.42 Key Points
1. The resting nerve membrane has a negative intracellular potential.
2. Ion concentration gradients are fundamental to membrane excitability.
3. Sodium and potassium are particularly important.
4. Membrane permeability determines how ions influence membrane voltage.
5. The resting membrane potential is not determined by one ion alone.
6. The Na⁺/K⁺ ATPase maintains important concentration gradients.
7. Threshold depolarization activates voltage-gated sodium channels.
8. Sodium entry produces rapid depolarization.
9. Potassium efflux contributes to repolarization.
10. Hyperpolarization may follow repolarization.
11. Absolute and relative refractory periods influence nerve excitability.
12. Stimulus intensity and duration interact according to the strength–duration relationship.
13. Supramaximal stimulation is used to obtain reliable maximal responses.
14. The cathode generally produces the strongest local depolarizing effect.
15. Demyelination primarily disrupts rapid and synchronized conduction.
16. Axonal loss reduces the number of fibres contributing to CMAP/SNAP amplitude.
4.43 Review Questions
Short-answer questions
1. What is the resting membrane potential?
2. Why is the inside of a resting axon negative?
3. What is the Nernst equilibrium potential?
4. What is depolarization?
5. What is repolarization?
6. What is hyperpolarization?
7. What is threshold potential?
8. What is the absolute refractory period?
9. What is the relative refractory period?
10. Define rheobase.
11. Define chronaxie.
12. What is supramaximal stimulation?
13. Why is the cathode important in nerve stimulation?
14. Why does demyelination slow nerve conduction?
15. Why does axonal loss reduce CMAP or SNAP amplitude?
Applied questions
1. A motor response increases in amplitude as stimulus intensity is increased and then reaches a plateau. Explain the physiology.
2. Explain why a cold limb can produce an apparently demyelinating pattern on NCS.
3. A patient has a markedly reduced SNAP but relatively preserved conduction velocity. Explain the likely physiological mechanism.
4. Explain the difference between an individual action potential and a CMAP.
4.44 Chapter Summary
The resting membrane potential provides the electrical starting point from which nerve excitation occurs. Unequal ion concentrations, selective membrane permeability and active ion transport establish the conditions required for nerve excitability.
An adequate electrical stimulus changes the membrane voltage, reaches threshold and activates voltage-gated sodium channels. Rapid sodium entry produces depolarization, followed by sodium-channel inactivation and potassium-mediated repolarization.
During NCS, the stimulator exploits these physiological principles to activate a population of nerve fibres. The resulting electrical activity is then recorded as a CMAP or SNAP.
CHAPTER 5
ACTION POTENTIAL PROPAGATION AND SALTATORY CONDUCTION
5.1 Learning Objectives
By the end of this chapter, the learner should be able to:
1. Explain how an action potential propagates along an axon.
2. Describe the role of local circuit currents in propagation.
3. Explain continuous and saltatory conduction.
4. Describe the structure and function of nodes of Ranvier.
5. Explain how myelin changes axonal electrical properties.
6. Explain the relationship between axon diameter and conduction velocity.
7. Describe the importance of internodal distance.
8. Explain why conduction is normally rapid and reliable in myelinated nerves.
9. Describe the effects of demyelination on impulse propagation.
10. Relate propagation physiology to NCS measurements.
5.2 Introduction
The generation of an action potential is only the beginning of nerve conduction.
For a nerve to perform its physiological function, the electrical signal must travel along the axon.
During NCS, the electrical stimulus activates peripheral nerve fibres at a selected site. The resulting action potentials then propagate along the nerve until they reach the recording region.
The speed and reliability of this propagation determine many of the measurements obtained during NCS.
The fundamental sequence is:
Stimulus → Action potential → Local current flow → Adjacent membrane depolarization → Regeneration of action potential → Continued propagation
In myelinated fibres, this process is greatly accelerated by saltatory conduction.
5.3 What Is Action Potential Propagation?
Action potential propagation is the process by which a change in membrane potential at one part of an axon causes successive depolarization of neighbouring regions.
The action potential does not simply travel as a fixed electrical object.
Instead, each adjacent segment of excitable membrane is brought to threshold and generates its own action potential.
Therefore, propagation is:
A continuously regenerated electrical process along the axon.
5.4 Local Circuit Currents
When one region of an axon becomes depolarized, positive charge enters that region.
This creates electrical currents that spread longitudinally through the axon and surrounding extracellular space.
These currents alter the voltage of neighbouring membrane regions.
If the neighbouring membrane reaches threshold:
Voltage-gated sodium channels open → new action potential generated
This process repeats along the axon.
5.5 The Propagation Sequence
Consider three adjacent regions of an axon:
Region A → Region B → Region C
If Region A generates an action potential:
1. Region A depolarizes.
2. Local current spreads toward Region B.
3. Region B becomes depolarized.
4. Region B reaches threshold.
5. Region B generates an action potential.
6. Current spreads toward Region C.
7. Region C reaches threshold.
8. The process continues.
Thus:
A → B → C → D → E
The action potential propagates along the axon.
5.6 Why Propagation Normally Moves Forward
The region immediately behind a newly generated action potential is temporarily refractory.
Because that membrane cannot immediately generate another normal action potential, propagation does not normally travel backward through the same region.
The refractory period therefore contributes to the directional nature of physiological propagation.
However, if an axon is artificially stimulated at an intermediate point, action potentials can propagate both proximally and distally from the stimulation site.
This is important in NCS.
5.7 Orthodromic and Antidromic Propagation
Orthodromic propagation
Propagation in the normal physiological direction.
For a motor axon stimulated distally, the impulse can travel:
Antidromic propagation
Propagation opposite to the usual physiological direction.
Electrical stimulation of a nerve can therefore produce both directions of propagation.
This is one reason electrical nerve stimulation differs from normal physiological activation.
5.8 Collision of Action Potentials
If an antidromic impulse generated by stimulation travels toward a motor neuron while an orthodromic impulse travels toward the muscle, they may encounter each other.
Because both are travelling through the same axonal pathway, they can collide and extinguish one another.
This phenomenon is known as:
Collision
It is an important physiological concept in nerve stimulation and late responses.
5.9 Continuous Conduction
In an unmyelinated axon, the action potential is regenerated sequentially along essentially continuous sections of excitable membrane.
This is:
Continuous conduction
It is relatively slow compared with saltatory conduction.
The entire membrane along the axon participates in the propagation process.
5.10 Myelinated Axons
Most large peripheral nerve fibres examined in routine NCS are myelinated.
The axon is surrounded by multiple layers of myelin produced by Schwann cells.
The myelin sheath:
The result is much faster conduction.
5.11 Nodes of Ranvier
The myelin sheath is interrupted at regular intervals by small exposed sections of axonal membrane.
These are:
Nodes of Ranvier
Nodes contain a high density of voltage-gated sodium channels.
They are therefore highly excitable regions.
The nodes are the principal sites where the action potential is actively regenerated.
5.12 Saltatory Conduction
In myelinated axons, depolarizing current spreads rapidly beneath the myelin from one node toward the next.
The next node reaches threshold and generates a new action potential.
This process is called:
Saltatory conduction
Conceptually:
Node 1 → Node 2 → Node 3 → Node 4
The term "saltatory" refers to the apparent jumping of the impulse from node to node.
The action potential does not physically jump through space. Instead, the electrical current travels rapidly beneath the insulating myelin, with active regeneration occurring at successive nodes.
5.13 Why Myelin Speeds Conduction
Myelin produces two important electrical effects.
1. Increased membrane resistance
Less current leaks through the membrane.
2. Reduced effective membrane capacitance
The membrane can change voltage more rapidly.
Together, these properties allow depolarizing current to spread farther and faster along the axon.
Therefore:
Better insulation → less current loss → faster arrival at next node
5.14 A Useful Electrical Analogy
Imagine trying to send water through a long pipe.
If the pipe leaks heavily:
More water is lost → less water reaches the end.
If the pipe is well insulated and has minimal leakage:
More of the flow reaches the next section efficiently.
Myelin provides a somewhat analogous electrical insulation function.
However, unlike water flow in a pipe, nerve conduction is an active biological process involving voltage-dependent ion channels.
5.15 Axon Diameter
Axon diameter is another major determinant of conduction velocity.
Larger axons have lower internal resistance to longitudinal current flow.
Therefore:
Larger axon → lower internal resistance → faster current spread → faster conduction
This explains why large myelinated fibres are among the fastest conducting fibres in the peripheral nervous system.
5.16 Conduction Velocity and Fibre Type
Peripheral nerves contain fibres with different:
Large myelinated fibres generally conduct rapidly.
Small myelinated fibres conduct more slowly.
Unmyelinated fibres conduct more slowly still.
Routine NCS predominantly assesses the larger, faster-conducting fibres.
5.17 Internodal Distance
The distance between adjacent nodes of Ranvier is called:
Internodal distance
Internodal distance is related to axon diameter and fibre organization.
The relationship must be optimized.
If nodes are excessively close:
If they are excessively far apart:
Normal myelinated fibres therefore have a highly organized relationship between:
Axon diameter + myelin thickness + internodal distance
5.18 Myelin Thickness
The thickness of the myelin sheath is related to axon diameter.
Efficiently myelinated fibres have a proportionate relationship between axon and myelin.
This arrangement permits efficient conduction while maintaining structural stability.
5.19 The Role of Schwann Cells
In peripheral nerves, Schwann cells produce myelin.
A single Schwann cell forms a segment of myelin around an axonal region.
The gaps between successive Schwann-cell myelin segments correspond to the nodes of Ranvier.
Therefore:
Schwann cells → myelin segments → internodes → nodes of Ranvier
Damage to Schwann cells or myelin can disrupt conduction.
5.20 Propagation and Conduction Velocity
Conduction velocity represents the rate at which the electrical impulse travels along a nerve.
It is influenced by:
In routine NCS, conduction velocity is estimated from measured distance and latency differences.
5.21 NCS Measurement of Conduction Velocity
For a motor nerve stimulated at two sites:
Distal stimulation → distal latency
Proximal stimulation → proximal latency
The difference between the two latencies estimates the time required for the impulse to travel between the stimulation sites.
Conceptually:
For example, if the stimulation sites are 240 mm apart and the latency difference is 6 ms:
The calculation is simple, but accurate measurement of distance and latency is critical.
5.22 Why Two Stimulation Sites Are Useful
Distal latency contains several components:
Nerve conduction + neuromuscular transmission + muscle depolarization
By comparing proximal and distal stimulation, the common distal components are largely cancelled.
The latency difference therefore provides a better estimate of conduction along the nerve segment between the two stimulation sites.
This is one of the fundamental principles of motor NCS.
5.23 What Happens in Demyelination?
When myelin is damaged, several things can happen.
Increased current leakage
The electrical signal becomes less efficiently insulated.
Reduced conduction speed
The next node takes longer to reach threshold.
Desynchronization
Different axons may conduct at increasingly different speeds.
Conduction failure
Some fibres may fail to propagate the impulse through the affected segment.
These changes produce characteristic NCS abnormalities.
5.24 Conduction Slowing
Demyelination can cause substantial reduction in conduction velocity.
This may be accompanied by:
The degree and distribution of slowing are clinically important.
5.25 Conduction Block
If an action potential fails to propagate through a diseased segment of nerve, fewer axons contribute to the proximal response.
This can produce:
Conduction block
Conceptually:
Distal stimulation → many axons activated → large CMAP
but:
Proximal stimulation → some impulses fail across lesion → smaller CMAP
Conduction block is particularly important in the evaluation of certain demyelinating neuropathies and focal nerve lesions.
However, technical factors such as inadequate stimulation can mimic conduction block.
5.26 Temporal Dispersion
In a normal nerve, individual fibres conduct at different speeds, but the differences remain within a physiological range.
When conduction velocities become more widely distributed, the components of the compound response arrive at different times.
The waveform becomes:
This is:
Temporal dispersion
Temporal dispersion is particularly relevant to demyelinating pathology.
5.27 Axonal Loss
Axonal loss is fundamentally different from demyelination.
In axonal loss:
Fewer functioning axons remain.
Therefore, fewer fibres contribute to the recorded CMAP or SNAP.
The major effect is often:
Reduced amplitude
Conduction velocity may be relatively preserved compared with the degree of amplitude reduction.
However, axonal neuropathies can also show secondary slowing, particularly when the fastest fibres are preferentially affected.
5.28 Demyelination Versus Axonal Loss
|
Feature |
Axonal loss |
Demyelination |
|
Primary problem |
Loss/dysfunction of axons |
Impaired myelin/conduction |
|
CMAP/SNAP amplitude |
Often reduced |
May be preserved |
|
Conduction velocity |
Relatively preserved or mildly reduced |
Often markedly reduced |
|
Distal latency |
May be mildly prolonged |
Often markedly prolonged |
|
F-wave |
May be reduced/absent |
Often prolonged |
|
Conduction block |
Not typical primary feature |
May occur |
|
Temporal dispersion |
Usually limited |
May be prominent |
These patterns must always be interpreted using clinical context and appropriate electrodiagnostic criteria.
5.29 Effects of Temperature on Propagation
Temperature affects the kinetics of voltage-gated channels.
Cooling slows the electrical processes involved in conduction.
Therefore, a cold limb may show:
This is why temperature control is essential for high-quality NCS.
5.30 Propagation in Peripheral Nerve Injury
After nerve injury, propagation may be affected depending on the type and severity of injury.
Potential consequences include:
The pattern evolves with time.
This becomes particularly important when performing serial NCS after traumatic nerve injury.
5.31 Wallerian Degeneration
When an axon is severely disrupted, the distal portion of the axon undergoes degeneration.
This process is called:
Wallerian degeneration
As distal axons degenerate, their contribution to the CMAP or SNAP decreases.
Therefore, the timing of an NCS examination after nerve injury matters.
A study performed immediately after injury may not show the same abnormalities as a study performed later.
5.32 Bidirectional Propagation During Electrical Stimulation
When a nerve is stimulated at a point along its course, the generated action potentials generally travel in both directions:
Proximally ← stimulation site → distally
This differs from normal physiological activation, where the direction is determined by the location of the neuronal cell body and peripheral receptor or muscle.
This bidirectional propagation is important when interpreting:
5.33 The F-Wave and Propagation
F-waves provide an excellent example of bidirectional propagation.
Following distal motor nerve stimulation:
1. The impulse travels distally toward the muscle.
2. Another component travels proximally toward the anterior horn cell.
3. Some motor neurons are activated antidromically.
4. A small proportion of these neurons then generate a recurrent orthodromic impulse.
5. The impulse travels back down the motor axon.
6. A late muscle response is recorded.
This illustrates the importance of understanding propagation direction and collision.
5.34 Why F-Waves Are Variable
F-waves are not generated by exactly the same motor neurons with every stimulus.
Consequently, F-wave responses can vary in:
This variability is physiologically normal.
Parameters such as minimum latency and persistence are therefore particularly useful.
5.35 Propagation and the NCS Waveform
The final waveform reflects the combined conduction characteristics of many nerve fibres.
If fibres conduct at relatively similar velocities:
Response = narrow, synchronized waveform
If conduction velocities vary substantially:
Response = prolonged, dispersed waveform
If many axons are lost:
Response = reduced amplitude
If conduction is markedly slowed:
Response = prolonged latency
Thus, waveform morphology contains physiological information.
5.36 Practical Example: Focal Demyelination
Suppose a patient has a focal demyelinating lesion affecting a nerve segment.
Distal stimulation may produce:
Normal or relatively preserved CMAP
while proximal stimulation produces:
Delayed and dispersed CMAP
If a substantial proportion of fibres fail to propagate through the affected segment, proximal stimulation may also produce a substantial amplitude reduction.
The comparison between stimulation sites therefore helps localize conduction abnormalities.
5.37 Practical Example: Axonal Polyneuropathy
A patient with length-dependent polyneuropathy may have:
The predominant physiological abnormality is reduced numbers of functioning axons rather than severe failure of saltatory conduction.
5.38 Practical Example: Cold Limb
A patient undergoes lower-limb NCS in a cold examination room.
The study demonstrates:
Before diagnosing demyelinating neuropathy, the examiner should first consider the limb temperature.
This illustrates a fundamental principle:
A physiological variable can produce an apparent pathological pattern.
5.39 Common Errors
Error 1
"Saltatory conduction means the action potential jumps through the air."
Correction: Depolarizing current spreads beneath myelin, while active regeneration occurs at successive nodes.
Error 2
"Myelin produces the action potential."
Correction: Myelin facilitates propagation; the excitable axonal membrane generates action potentials.
Error 3
"Slow conduction always means demyelination."
Correction: Temperature, age, nerve length, technical factors and axonal pathology can also influence conduction velocity.
Error 4
"Low amplitude always means axonal loss."
Correction: Inadequate stimulation, poor electrode placement and conduction block can also reduce amplitude.
5.40 Key Points
1. Action potential propagation is a regenerative process.
2. Local circuit currents depolarize adjacent membrane regions.
3. The refractory period contributes to directional propagation.
4. Electrical stimulation can produce propagation in both directions.
5. Myelinated axons conduct rapidly through saltatory conduction.
6. Nodes of Ranvier contain high concentrations of voltage-gated sodium channels.
7. Myelin increases membrane resistance and reduces effective capacitance.
8. Larger axons generally conduct faster.
9. Internodal organization is important for efficient conduction.
10. Demyelination slows and desynchronizes conduction.
11. Conduction block represents failure of some impulses to propagate across a nerve segment.
12. Temporal dispersion reflects increased differences in conduction times between fibres.
13. Axonal loss primarily reduces the number of functioning fibres contributing to CMAP/SNAP amplitude.
14. Temperature can significantly alter conduction.
15. Conduction velocity calculations depend critically on accurate distance and latency measurements.
5.41 Review Questions
Short-answer
1. Define action potential propagation.
2. What are local circuit currents?
3. What is continuous conduction?
4. What is saltatory conduction?
5. What is a node of Ranvier?
6. How does myelin increase conduction velocity?
7. How does axon diameter influence conduction?
8. What is internodal distance?
9. Define conduction block.
10. Define temporal dispersion.
11. What is Wallerian degeneration?
12. Why does axonal loss reduce CMAP amplitude?
Applied questions
1. Explain how an action potential propagates along a myelinated peripheral nerve.
2. A motor nerve is stimulated at two sites. The distance between sites is 240 mm and the latency difference is 6 ms. Calculate the conduction velocity.
3. A nerve has a preserved distal CMAP but a substantially smaller proximal CMAP. What physiological phenomenon should be considered?
4. Explain why demyelination can produce both conduction slowing and temporal dispersion.
5. Why should a low CMAP amplitude not automatically be interpreted as axonal loss?
5.42 Chapter Summary
Action potential propagation depends on the sequential regeneration of electrical activity along the axon. In myelinated peripheral nerves, myelin and the nodes of Ranvier allow rapid saltatory conduction.
The speed of propagation is influenced strongly by axon diameter, myelin integrity, internodal organization and temperature.
These physiological properties directly determine the measurements obtained during NCS. Demyelination tends to produce slowing, conduction block and temporal dispersion, whereas axonal loss more commonly produces reduced CMAP and SNAP amplitudes.
CHAPTER 6
MYELINATION, NODES OF RANVIER AND CONDUCTION VELOCITY
6.1 Learning Objectives
By the end of this chapter, the learner should be able to:
1. Describe the structure of peripheral nerve myelin.
2. Explain the role of Schwann cells.
3. Describe the anatomy of the node of Ranvier.
4. Explain the function of the paranode and juxtaparanode.
5. Explain how myelin alters axonal electrical properties.
6. Describe the relationship between axon diameter and myelin thickness.
7. Explain the major determinants of conduction velocity.
8. Relate myelin abnormalities to NCS findings.
9. Distinguish physiological conduction slowing from pathological slowing.
10. Explain how conduction velocity is measured clinically.
6.2 Introduction
The remarkable speed of peripheral nerve conduction depends largely on the specialized organization of the axon–myelin unit.
A large myelinated peripheral nerve fibre is not simply an axon covered by insulation.
It is a highly organized structure containing:
This organization allows the action potential to travel rapidly and reliably over long distances.
For NCS, understanding this structure is particularly important because many abnormalities detected by electrodiagnostic testing arise from disruption of:
Myelin → Nodes → Paranodes → Axonal membrane
6.3 The Axon–Myelin Unit
The functional unit responsible for rapid peripheral nerve conduction can be conceptualized as:
Axon + Schwann cell + Myelin + Node of Ranvier
Each component contributes to efficient electrical transmission.
The axon carries the signal.
The myelin provides electrical insulation.
The node provides a highly excitable site for action-potential regeneration.
The paranodal and juxtaparanodal regions maintain the electrical organization of the internode.
6.4 Schwann Cells
In the peripheral nervous system, myelin is produced by:
Schwann cells
A myelinating Schwann cell wraps its plasma membrane repeatedly around a segment of a single axon.
Multiple layers of membrane become compacted to form the myelin sheath.
This creates an electrically insulating structure surrounding the axon.
6.5 One Schwann Cell and One Internode
A useful simplified concept is:
One myelinating Schwann cell forms one internodal segment around one axon.
The next Schwann cell forms the next internode.
Between these internodes is a specialized gap:
Node of Ranvier
Therefore:
Internode → Node → Internode → Node → Internode
This repeating organization is fundamental to saltatory conduction.
6.6 Structure of Peripheral Myelin
Myelin consists primarily of multiple layers of Schwann-cell plasma membrane wrapped around the axon.
It contains:
The high lipid content contributes strongly to its insulating properties.
Compact myelin minimizes ionic current leakage across the internodal membrane.
6.7 Why Myelin Is an Electrical Insulator
From an electrical perspective, myelin:
Increases membrane resistance
Less ionic current escapes across the internodal membrane.
Decreases effective membrane capacitance
The membrane can be charged and discharged more efficiently.
Together these properties allow current to spread rapidly along the inside of the axon.
6.8 Electrical Model of a Myelinated Axon
A simplified electrical model contains:
Axial resistance
and
Membrane resistance + membrane capacitance
Myelin increases membrane resistance and reduces capacitance.
This allows the depolarizing current generated at one node to travel farther along the axon before the next node is reached.
The next node can therefore reach threshold rapidly.
6.9 Nodes of Ranvier
The node of Ranvier is a short, specialized region of exposed axonal membrane between two myelin segments.
It contains a very high density of:
Voltage-gated sodium channels
These channels are responsible for rapid regeneration of the action potential.
The node is therefore an electrically excitable region.
6.10 Nodal Sodium Channels
Voltage-gated sodium channels are concentrated at the node.
When the depolarizing current arriving from the previous node reaches threshold:
Na⁺ channels open → Na⁺ enters → membrane depolarizes
This regenerates the action potential.
The high concentration of sodium channels is therefore critical for reliable saltatory conduction.
6.11 The Paranode
Immediately adjacent to the node is a specialized region called the:
Paranode
The paranode forms the transition between the node and compact myelin.
It contains specialized molecular structures that help attach the myelin sheath to the axon.
The paranodal region therefore has both:
importance.
6.12 The Juxtaparanode
Beyond the paranode lies the:
Juxtaparanode
This region contains potassium channels that are normally electrically shielded by the surrounding myelin.
Under normal conditions, these channels have limited influence on rapid saltatory conduction.
If myelin is damaged, however, these normally hidden channels may become functionally exposed.
This can contribute to conduction abnormalities.
6.13 The Internode
The region between two nodes is called the:
Internode
It contains:
The internode is relatively electrically insulated.
Its main role is to allow rapid passive spread of depolarizing current toward the next node.
6.14 The Saltatory Conduction Unit
The functional arrangement can be represented as:
Node → Paranode → Internode → Paranode → Node
The action potential is actively regenerated at the nodes.
Current spreads rapidly through the internodal region.
This produces fast conduction with relatively little metabolic expenditure compared with continuous activation of the entire axonal membrane.
6.15 Why the Node Does Not Need to Be Covered by Myelin
The node is intentionally exposed.
It must contain excitable membrane capable of generating the next action potential.
Therefore:
Myelin = insulation
while:
Node = active regeneration
This division of function is central to saltatory conduction.
6.16 Conduction Velocity
Conduction velocity is the speed at which an electrical impulse travels along a nerve.
In large myelinated peripheral nerves, conduction velocities may reach several tens of metres per second and can exceed 50–60 m/s in healthy nerves depending on the nerve, age, temperature and laboratory reference range.
The precise normal value is not universal.
It must always be interpreted using appropriate:
reference data.
6.17 Major Determinants of Conduction Velocity
The major physiological determinants include:
1. Axon diameter
2. Myelin thickness
3. Internodal length
4. Nodal structure
5. Ion-channel distribution
6. Temperature
7. Membrane properties
These factors work together.
6.18 Axon Diameter
Larger axons generally conduct faster.
The reason is that larger axons have lower internal axial resistance.
Therefore:
Larger diameter → lower axial resistance → faster longitudinal current flow
This allows the next node to reach threshold more rapidly.
6.19 Myelin Thickness
Myelin thickness is strongly related to axon diameter.
A larger axon generally has a thicker myelin sheath.
This provides better electrical insulation.
The relationship between axonal diameter and myelin thickness can be described using the:
G-ratio
The g-ratio is approximately:
It provides a measure of the relative thickness of myelin.
An appropriately optimized g-ratio contributes to efficient conduction.
6.20 The G-Ratio
Consider two fibres:
Fibre A
Axon diameter = 8 µm
Total fibre diameter = 10 µm
Fibre B
Axon diameter = 5 µm
Total fibre diameter = 10 µm
The two fibres have very different axon-to-myelin relationships.
The g-ratio is mainly a neurobiological and research concept, but it helps explain why myelin thickness must be appropriately matched to axon diameter for efficient conduction.
6.21 Internodal Length
The distance between nodes also influences conduction.
Longer internodes can permit faster conduction because fewer nodes need to be activated over a given distance.
However, internodes cannot simply become infinitely long.
The electrical properties of the axon and myelin impose limits.
Normal nerve fibres therefore have an optimized relationship between:
Axon diameter + myelin thickness + internodal distance
6.22 Nodal Safety Factor
For reliable conduction, the depolarizing current arriving at the next node must be sufficient to reach threshold.
The amount by which the available depolarizing current exceeds the minimum required to activate the next node is conceptually described as the:
Safety factor for conduction
A healthy myelinated fibre has a sufficient safety margin.
Disease can reduce this safety factor.
When it becomes inadequate, conduction may fail.
6.23 Conduction Failure
If the next node does not reach threshold, the action potential may fail to propagate.
This can occur because of:
The result can be:
Conduction block or conduction failure
The clinical significance depends on the location and mechanism.
6.24 Focal Demyelination
A localized myelin lesion may produce a discrete region where conduction is markedly slowed or fails.
Potential mechanisms include:
The electrical impulse therefore takes longer to cross the affected segment.
6.25 Segmental Demyelination
Demyelination can affect selected internodes while leaving the axon relatively intact.
The result is:
Slower conduction → prolonged latency → possible dispersion
With repeated or severe demyelination, conduction block can occur.
6.26 Remyelination
Following demyelination, the nerve may attempt to repair the myelin.
Newly formed myelin is often:
Consequently, conduction may improve but remain slower than normal.
This helps explain why conduction velocity can change over time during recovery from nerve injury.
6.27 Axonal Degeneration
When the axon itself is severely damaged, the problem is fundamentally different.
The issue is not primarily slow propagation through intact axons.
Instead:
The number of functioning axons decreases.
The result is often:
Reduced CMAP/SNAP amplitude
rather than the dramatic slowing characteristic of primary demyelination.
6.28 Myelin and CMAP Amplitude
Myelin abnormalities primarily influence:
Axonal loss primarily influences:
However, amplitude and velocity must never be interpreted independently.
A severe demyelinating lesion can also produce low amplitude through conduction block.
6.29 Temporal Dispersion
Different nerve fibres may be affected to different degrees.
Some may conduct relatively normally.
Others may conduct much more slowly.
Consequently, the individual components of the compound response arrive at different times.
The waveform becomes wider.
This is:
Temporal dispersion
It is an important marker of desynchronized conduction.
6.30 Conduction Block
Suppose 100 motor axons are activated distally.
If all conduct:
CMAP = large
If only 60 effectively conduct across a proximal diseased segment:
Proximal CMAP = substantially smaller
This can produce a pattern compatible with conduction block.
However, conduction block must be distinguished from:
6.31 Phase Cancellation
Individual motor units produce electrical signals with different orientations and timing.
When these signals overlap, some components may partially cancel each other.
This is called:
Phase cancellation
Changes in conduction synchrony can therefore alter CMAP amplitude and duration.
This is one reason waveform morphology must be considered alongside amplitude.
6.32 Temperature and Myelinated Nerves
Temperature strongly influences conduction.
Cold temperature can cause:
Therefore, the examiner should ensure that the limb temperature is appropriate for the nerve being tested.
6.33 Age and Conduction Velocity
Conduction velocity is also influenced by age.
Children and older adults may have different normal values compared with young and middle-aged adults.
Therefore, a single universal cutoff should not be applied blindly.
Interpretation should use validated reference values appropriate to the patient population.
6.34 Height and Nerve Length
Longer limbs generally have longer conduction distances.
This can influence:
Height is therefore often considered when interpreting certain NCS parameters, particularly late responses.
6.35 Why Conduction Velocity Is Not a Pure Measurement of Myelin
It is tempting to say:
"Conduction velocity measures myelin."
This is incomplete.
Conduction velocity reflects the combined effect of:
Therefore:
Conduction velocity is a physiological measurement, not a direct measurement of myelin thickness.
6.36 Measuring Conduction Velocity
For motor NCS:
where:
For example:
Distance:
200 mm
Latency difference:
5 ms
6.37 Why Distance Measurement Matters
A small error in distance measurement produces an error in calculated conduction velocity.
For example, if the true distance is 200 mm but it is incorrectly measured as 220 mm:
The calculated value would therefore be falsely high.
Accurate measurement is essential.
6.38 Why Latency Measurement Matters
Latency measurements are equally important.
If onset latency is incorrectly identified because of:
the calculated conduction velocity may be inaccurate.
6.39 The Stimulus Artefact
The electrical stimulus itself creates an artefact on the recording.
This may appear before the physiological response.
The examiner must distinguish:
Stimulus artefact
from:
True nerve/muscle response
Failure to do so can produce incorrect latency measurements.
6.40 NCS and Structural Pathology
The relationship can be summarized as follows:
Node
Problems can alter excitability and conduction reliability.
Myelin
Problems primarily affect conduction speed and synchronization.
Axon
Loss primarily reduces response amplitude.
Muscle
Abnormal muscle activation affects the recorded CMAP.
This structural framework helps organize electrodiagnostic interpretation.
6.41 Clinical Example: Demyelinating Neuropathy
A patient presents with progressive weakness.
NCS shows:
This pattern raises concern for a predominantly demyelinating process.
The diagnosis, however, requires clinical correlation and formal electrodiagnostic criteria.
6.42 Clinical Example: Axonal Neuropathy
A patient with length-dependent sensory symptoms undergoes NCS.
Findings include:
This pattern is more consistent with predominantly axonal involvement.
6.43 Clinical Example: Focal Entrapment
A nerve compressed at a specific anatomical site may demonstrate focal slowing.
For example, a focal lesion may produce:
Normal conduction outside the lesion
but:
Slowed conduction across the lesion
This principle is central to the electrodiagnosis of entrapment neuropathies.
6.44 Common Errors
Error 1
"All slowing indicates demyelination."
Correction: Temperature, age, nerve length, technical factors and axonal pathology can also affect velocity.
Error 2
"Low CMAP automatically means axonal degeneration."
Correction: Conduction block, inadequate stimulation and technical factors can also reduce amplitude.
Error 3
"Myelin is simply insulation."
Correction: Myelin is a highly specialized biological structure that interacts with nodes, paranodes and ion channels to enable rapid conduction.
Error 4
"The node is just a gap in the myelin."
Correction: It is a highly specialized excitable membrane region containing dense voltage-gated sodium channels.
6.45 Key Points
1. Peripheral myelin is produced by Schwann cells.
2. Myelinating Schwann cells form internodal segments.
3. Nodes of Ranvier contain a high density of voltage-gated sodium channels.
4. Paranodes connect the node with compact myelin.
5. Juxtaparanodal potassium channels are normally electrically shielded.
6. Myelin increases membrane resistance and reduces effective capacitance.
7. Larger axons generally conduct faster.
8. Myelin thickness and internodal length influence conduction velocity.
9. The g-ratio describes the relationship between axon diameter and total fibre diameter.
10. A healthy myelinated nerve has a safety margin that permits reliable propagation.
11. Demyelination reduces conduction efficiency and may produce conduction block.
12. Temporal dispersion results from increased differences in conduction times between fibres.
13. Axonal loss primarily reduces response amplitude.
14. Temperature, age and technical factors influence conduction velocity.
15. Conduction velocity is calculated from distance and latency difference rather than measured directly.
6.46 Review Questions
Short-answer
1. Which cell produces myelin in the peripheral nervous system?
2. What is an internode?
3. What is a node of Ranvier?
4. Why are sodium channels concentrated at the node?
5. What is the function of the paranode?
6. What is the juxtaparanode?
7. How does myelin increase conduction velocity?
8. What is the g-ratio?
9. How does axon diameter influence conduction velocity?
10. What is conduction safety factor?
11. What is temporal dispersion?
12. What is conduction block?
13. Why does remyelination often produce slower-than-normal conduction?
14. Why does axonal loss reduce CMAP amplitude?
15. Why must temperature be considered during NCS?
6.47 Applied Questions
Question 1
A patient has a conduction velocity of 28 m/s in a nerve that normally conducts at approximately 50 m/s under appropriate laboratory conditions.
List at least five factors that should be considered before concluding that the patient has demyelination.
Question 2
A nerve is stimulated distally and produces a CMAP of 10 mV. Proximal stimulation produces a CMAP of 5 mV.
What physiological phenomenon could explain this finding?
What technical factors must be excluded?
Question 3
Explain why a lesion affecting the myelin sheath can slow conduction without immediately destroying the axon.
Question 4
Explain why an axonal neuropathy can produce a low CMAP even when conduction velocity is relatively preserved.
Question 5
Why are the nodes of Ranvier essential for saltatory conduction?
6.48 Chapter Summary
Rapid peripheral nerve conduction depends on the precise structural organization of the axon, Schwann-cell myelin, nodes of Ranvier, paranodes and internodes.
Myelin provides electrical insulation, while the nodes provide sites of active action-potential regeneration. Axon diameter, myelin thickness and internodal organization determine how efficiently depolarizing current reaches the next node.
When myelin is damaged, conduction becomes slower and less synchronized, potentially producing prolonged latencies, slowed conduction velocity, temporal dispersion and conduction block. When axons are lost, the principal effect is often a reduction in CMAP or SNAP amplitude.
These structural and physiological principles form the foundation for interpreting actual NCS recordings.
CHAPTER 7
ELECTRICAL STIMULATION OF PERIPHERAL NERVES
7.1 Learning Objectives
By the end of this chapter, the learner should be able to:
1. Explain the physical principles underlying electrical nerve stimulation.
2. Define voltage, current, resistance, charge, and power.
3. Apply Ohm's law to nerve stimulation.
4. Explain current density and electric-field distribution.
5. Describe the functions of the cathode and anode.
6. Explain how a surface stimulus produces nerve depolarization.
7. Describe pulse amplitude and pulse duration.
8. Explain the strength–duration relationship.
9. Distinguish monophasic and biphasic stimulation.
10. Explain stimulus artefact and its effect on NCS recordings.
11. Describe the major technical factors affecting stimulation efficiency.
12. Relate electrical stimulation physics to practical NCS.
7.2 Introduction
Nerve conduction studies do not stimulate nerves using physiological neurotransmission.
Instead, the nerve is activated by an externally generated electrical field.
The NCS stimulator delivers a controlled electrical pulse through surface electrodes positioned over the nerve.
The sequence is:
Electrical pulse
↓
Electric field in tissue
↓
Change in transmembrane potential
↓
Membrane depolarization
↓
Threshold reached
↓
Action potential
↓
Propagation along nerve
↓
CMAP/SNAP recording
Understanding this process requires knowledge of both neurophysiology and electrical physics.
7.3 The Basic Electrical Quantities
Five electrical quantities are particularly important:
|
Quantity |
Symbol |
Unit |
|
Voltage |
V |
Volt (V) |
|
Current |
I |
Ampere (A) |
|
Resistance |
R |
Ohm (Ω) |
|
Charge |
Q |
Coulomb (C) |
|
Power |
P |
Watt (W) |
These quantities describe what the stimulator is doing electrically.
7.4 Voltage
Voltage
Voltage represents an electrical potential difference.
It can be thought of as the electrical "driving force" that can move charge.
In NCS, the stimulator creates a voltage difference between the stimulating electrodes.
This establishes an electric field within the tissues.
7.5 Current
Current
Current is the rate of movement of electrical charge.
It is measured in:
Amperes (A)
Clinical NCS stimulators commonly operate in the milliampere (mA) range.
For example:
20 mA
means that electrical charge is being delivered at a current of 20 milliamperes.
7.6 Resistance
Resistance represents opposition to current flow.
It is measured in:
Ohms (Ω)
Biological tissues have different electrical resistivities.
The effective resistance encountered during stimulation depends on:
Skin can contribute substantially to impedance.
7.7 Ohm's Law
The fundamental relationship is:
Therefore:
and:
This means that for a fixed voltage:
Higher resistance → lower current
For a current-controlled stimulator, the device adjusts the voltage required to deliver the selected current through the patient's tissues.
7.8 Example of Ohm's Law
Suppose:
and:
Then:
Therefore, approximately 10 volts would be required to drive 20 mA through a 500-ohm load.
7.9 Why Skin Impedance Matters
The skin is not a perfect conductor.
Dry skin may have relatively high impedance.
This can reduce the efficiency of stimulation and require greater voltage to deliver the selected current.
Factors that affect skin impedance include:
Good skin preparation therefore improves stimulation reliability.
7.10 Impedance Versus Resistance
In simple circuits we often discuss:
Resistance
In biological stimulation systems, the more general term is:
Impedance
Impedance includes resistance as well as frequency-dependent effects associated with capacitance and other electrical properties.
For practical NCS, electrode–skin impedance is an important technical consideration.
7.11 Electric Field
When a voltage difference is applied between two electrodes, an:
Electric field
is established in the tissues.
The electric field determines how the electrical stimulus interacts with the nerve.
The field is influenced by:
7.12 Current Density
Current density describes how much current passes through a given area.
Conceptually:
where:
For the same current:
Smaller electrode → higher current density
Larger electrode → lower current density
This is one reason electrode size matters during nerve stimulation.
7.13 Why Electrode Size Matters
Imagine two stimulating electrodes delivering the same current.
Small electrode
Current is concentrated over a smaller area.
Therefore:
Higher local current density
Large electrode
Current is distributed over a larger area.
Therefore:
Lower local current density
The stimulating electrode is generally designed to provide sufficiently concentrated stimulation over the nerve.
7.14 Cathode and Anode
The two stimulation electrodes are:
Cathode (−)
and
Anode (+)
Their electrical effects are different.
The cathode generally produces the strongest local depolarizing effect beneath the electrode.
The anode tends to produce a relative hyperpolarizing effect.
Therefore, correct electrode polarity is important.
7.15 Why the Cathode Depolarizes
The cathode creates relative extracellular negativity.
This changes the electrical gradient across the nerve membrane.
The membrane becomes more likely to depolarize toward threshold.
Conceptually:
Cathode → extracellular negativity → membrane depolarization → threshold → action potential
This is called:
Cathodal stimulation
7.16 Anodal Hyperpolarization
The anode creates relative extracellular positivity.
This tends to make the membrane less excitable immediately beneath the electrode.
Therefore:
Anode → relative extracellular positivity → hyperpolarizing effect
Under particular circumstances, anodal stimulation can also influence conduction in more complex ways.
7.17 The Stimulating Circuit
A simplified stimulation circuit is:
Stimulator
↓
Cathode
↓
Patient tissue
↓
Anode
↓
Stimulator
The electrical pulse passes through the tissues between the electrodes.
The nerve is exposed to the resulting electric field.
7.18 How the Nerve Is Actually Activated
The stimulator does not directly inject current into the axon.
Instead, the current flows through the tissues surrounding the nerve.
The resulting electric field changes the potential across the nerve membrane.
If the membrane is depolarized sufficiently:
Threshold is reached
↓
Voltage-gated sodium channels open
↓
Action potential generated
This is an important distinction.
7.19 Nerve Activation Is a Field Effect
The nerve is activated because the external electric field changes the local transmembrane voltage.
The electrical stimulus therefore interacts with the nerve according to:
This is why precise electrode placement is essential.
7.20 Pulse Amplitude
The stimulus amplitude describes the magnitude of the electrical stimulus.
Depending on the stimulator, it may be expressed as:
Modern clinical NCS systems commonly allow the operator to specify stimulation intensity in current units.
Example:
5 mA → 10 mA → 20 mA → 30 mA
7.21 Pulse Duration
Pulse duration is the length of time that the electrical stimulus is delivered.
It is usually expressed in:
milliseconds (ms)
For example:
0.1 ms
or
0.2 ms
A longer pulse delivers charge over a longer period.
7.22 Charge
Electrical charge is related to current and time:
where:
For example:
If:
and:
then:
or:
4 µC
7.23 Why Charge Matters
Nerve excitation depends on the relationship between:
Stimulus intensity
and
Stimulus duration
A short pulse may require higher intensity.
A longer pulse may require less intensity.
Therefore, nerve activation cannot be understood from current amplitude alone.
7.24 Strength–Duration Curve
The relationship between stimulus strength and pulse duration is represented by the:
Strength–duration curve
Conceptually:
Shorter duration → greater stimulus intensity required
Longer duration → lower stimulus intensity required
This relationship is fundamental to electrical stimulation.
7.25 Rheobase and Chronaxie
Rheobase
The minimum stimulus intensity capable of exciting the nerve when a sufficiently long pulse is used.
Chronaxie
The minimum pulse duration required to excite the nerve at approximately twice rheobase.
These concepts describe tissue excitability.
They are particularly useful in understanding why pulse width influences NCS stimulation.
7.26 Monophasic Stimulation
A monophasic pulse has a primary current phase in one direction.
A simplified representation is:
Positive → negative → baseline
or the reverse depending on polarity.
Monophasic stimulation has been used extensively in electrophysiological stimulation.
7.27 Biphasic Stimulation
A biphasic pulse contains two phases with opposite polarity.
Conceptually:
Phase 1 → Phase 2
The second phase may partially balance the electrical charge delivered during the first phase.
Different stimulator designs use different pulse shapes.
7.28 Pulse Shape
Stimuli can have different waveforms, including:
Clinical NCS systems commonly use controlled rectangular pulses because their amplitude and duration can be precisely defined.
7.29 Why Rectangular Pulses Are Useful
A rectangular pulse provides relatively stable stimulus amplitude during the pulse.
This allows precise control of:
The operator can therefore reproduce stimulation conditions more reliably.
7.30 Stimulus Intensity During NCS
The operator usually begins with a relatively low stimulus intensity and gradually increases it.
For example:
5 mA
↓
10 mA
↓
15 mA
↓
20 mA
↓
25 mA
↓
30 mA
The response is monitored.
When further increases no longer produce a meaningful increase in response amplitude, the examiner approaches the maximal response.
A margin beyond this point is generally used for supramaximal stimulation.
7.31 Threshold Stimulation
At threshold:
Only some fibres may be activated.
The recorded response may therefore be small.
This is not normally sufficient for definitive motor NCS measurements.
The stimulus is increased progressively.
7.32 Maximal Stimulation
As current increases:
More axons are activated.
The CMAP increases in amplitude.
Eventually:
Further current produces little or no additional increase.
This represents the maximal response.
7.33 Supramaximal Stimulation
After reaching maximal response, the stimulus is increased further to provide a safety margin.
This is:
Supramaximal stimulation
It helps ensure that small changes in:
do not result in incomplete nerve activation.
7.34 Why Supramaximal Stimulation Is Important
Suppose the maximal CMAP occurs at:
22 mA
Using exactly 22 mA may leave little margin for variation.
Increasing to:
25–30 mA
may provide more reliable activation, provided this remains within appropriate safe and tolerable limits.
The exact intensity depends on:
7.35 Stimulus Artefact
The electrical stimulus itself can be detected by the recording electrodes.
This produces:
Stimulus artefact
It may appear as a sharp electrical deflection immediately after stimulation.
The recording system must distinguish:
Stimulus artefact
from:
Physiological response
7.36 Why Stimulus Artefact Matters
Stimulus artefact can obscure the early part of a waveform.
This is particularly important when measuring:
A large stimulus artefact may make accurate onset measurement difficult.
7.37 Sources of Stimulus Artefact
Stimulus artefact can be influenced by:
Good technical practice reduces artefact.
7.38 Stimulus Duration and Patient Comfort
Increasing pulse duration can increase the total charge delivered.
Although electrical stimulation is usually safe and well tolerated when properly applied, excessive stimulation can become uncomfortable.
The examiner should therefore balance:
Adequate nerve activation
against:
Patient tolerance
7.39 Nerve Depth
The deeper the nerve lies beneath the skin, the more tissue the stimulus must traverse.
A deeper nerve may require greater stimulation intensity.
For example:
Superficial nerve → lower stimulation requirement
Deep nerve → potentially higher stimulation requirement
This is one reason why different nerves have different typical stimulation requirements.
7.40 Subcutaneous Fat
Subcutaneous fat affects the electrical path between electrode and nerve.
A greater tissue depth can increase the distance between the electrode and nerve.
This may increase the stimulation intensity required for activation.
Therefore, body habitus can influence technical NCS measurements.
7.41 Electrode Placement
The stimulating cathode should be positioned appropriately over the nerve.
Small positional errors can affect:
Therefore, anatomical landmarks are essential.
7.42 Interelectrode Distance
The distance between cathode and anode affects the electric field.
If the electrodes are positioned too close:
If too far apart:
Standardized electrode spacing improves reproducibility.
7.43 The Ground Electrode
A ground electrode is commonly used between the stimulation and recording regions.
Its purpose is to reduce:
The ground therefore contributes to recording quality even though it does not directly generate the nerve action potential.
7.44 Electrical Safety
Clinical nerve stimulation equipment must control:
The equipment should comply with applicable medical electrical safety standards.
The operator should never improvise electrical stimulation using unvalidated equipment.
7.45 Repetitive Stimulation
Repeated stimuli can be delivered at controlled intervals.
The interval between stimuli is important because the nerve and neuromuscular system require time for recovery.
Very high repetition rates can interact with:
The appropriate frequency depends on the specific test.
7.46 Stimulus Frequency
Frequency is:
where T is the interval between stimuli.
For example:
A stimulus every 1 second corresponds to:
A stimulus every 0.1 seconds corresponds to:
Different NCS protocols use different stimulation frequencies.
7.47 Current Versus Voltage Stimulation
NCS stimulators may be designed as:
Constant-current stimulators
The device attempts to maintain a selected current despite changes in patient impedance.
Constant-voltage stimulators
The device maintains a selected voltage.
Constant-current stimulation is particularly useful clinically because tissue impedance varies between patients and over time.
7.48 Why Constant Current Is Useful
Suppose skin impedance increases.
With constant voltage:
Resistance ↑ → current ↓
This may reduce stimulation effectiveness.
With constant current:
Current remains approximately constant
The stimulator automatically adjusts the voltage required to maintain the selected current.
This improves reproducibility.
7.49 Example
Suppose the desired stimulus is:
20 mA
Patient A:
Required voltage:
Patient B:
Required voltage:
The constant-current stimulator can increase voltage to maintain approximately the same 20 mA current.
7.50 The Complete Stimulation Chain
The physical process can be summarized:
Stimulator electronics
↓
Controlled current pulse
↓
Stimulating electrode
↓
Skin
↓
Subcutaneous tissue
↓
Electrical field
↓
Peripheral nerve
↓
Membrane polarization change
↓
Threshold
↓
Action potential
↓
Propagation
↓
Recording electrode
↓
Amplifier
↓
Digital signal
This is the bridge between electrical engineering and neurophysiology.
7.51 Clinical Example: Median Nerve Stimulation
Suppose the median nerve is stimulated at the wrist.
The cathode is positioned over the nerve.
A brief current pulse is delivered.
The resulting electric field depolarizes the nerve.
Motor axons generate action potentials.
These travel distally to the thenar muscle.
The muscle fibres depolarize.
Surface recording electrodes detect the resulting electrical activity.
The instrument displays the:
CMAP
The waveform can then be analyzed for:
7.52 Clinical Example: Sensory Nerve Stimulation
In sensory NCS, the stimulated nerve produces action potentials in sensory fibres.
The propagated electrical activity reaches the recording electrodes.
The machine records a:
SNAP
Because SNAPs are usually much smaller than CMAPs, technical factors become especially important.
7.53 Why Sensory Studies Are Technically Demanding
SNAP amplitudes may be relatively small.
Therefore they are more vulnerable to:
High-quality technique is essential.
7.54 Technical Optimization
Before stimulation:
Check the skin
Clean and prepare if necessary.
Check electrode contact
Ensure good adhesion and low impedance.
Identify the nerve anatomically
Use reliable landmarks.
Position the cathode correctly
Optimize the electric field over the nerve.
Place the ground appropriately
Reduce interference.
Deliver gradually increasing stimulation
Identify the maximal response.
Apply supramaximal stimulation
Provide a safety margin.
7.55 Common Technical Errors
Error 1: Wrong polarity
Can increase stimulation threshold or alter response.
Error 2: Poor electrode contact
Can increase impedance and artefact.
Error 3: Incorrect nerve location
May require unnecessarily high stimulation intensity.
Error 4: Inadequate stimulation
Can produce falsely low CMAP amplitudes.
Error 5: Excessive stimulation
May increase discomfort without improving the response.
Error 6: Poor grounding
Can increase electrical noise and stimulus artefact.
Error 7: Incorrect distance measurement
Can produce incorrect conduction velocity.
7.56 Important Concept
The NCS stimulator does not measure conduction velocity directly.
It performs one fundamental task:
It creates a controlled electrical field capable of activating nerve fibres.
The recording system then measures the physiological response.
Thus:
Stimulator = activation
Recording electrodes = detection
Amplifier = signal enhancement
Processor = measurement
Clinician = interpretation
7.57 Key Points
1. NCS uses externally applied electrical stimulation to activate peripheral nerves.
2. Voltage is electrical potential difference.
3. Current represents movement of electrical charge.
4. Resistance opposes current flow.
5. Ohm's law relates voltage, current and resistance.
6. Biological tissues have electrical impedance.
7. The stimulating electrodes create an electric field in the tissues.
8. The cathode generally produces the strongest local depolarizing effect.
9. Current density depends on current and electrode area.
10. Pulse duration influences nerve excitability.
11. Charge is related to current and pulse duration.
12. The strength–duration relationship explains why pulse width matters.
13. Supramaximal stimulation provides a margin beyond the maximal response.
14. Stimulus artefact can interfere with latency measurements.
15. Constant-current stimulation helps compensate for changes in tissue impedance.
16. Correct electrode placement is essential for reliable stimulation.
17. Grounding helps reduce electrical interference.
18. Stimulation intensity must be sufficient but patient-tolerable.
19. The stimulator activates the nerve; the recording system measures the response.
20. Understanding stimulation physics is essential for understanding NCS quality.
7.58 Review Questions
Short-answer
1. Define voltage.
2. Define current.
3. Define resistance.
4. State Ohm's law.
5. What is current density?
6. What is an electric field?
7. What is the role of the cathode?
8. What is the role of the anode?
9. What is pulse duration?
10. What is electrical charge?
11. Define rheobase.
12. Define chronaxie.
13. What is supramaximal stimulation?
14. What is stimulus artefact?
15. Why is a ground electrode used?
16. What is the advantage of constant-current stimulation?
17. Why does electrode size matter?
18. Why does nerve depth affect stimulation?
19. Why is skin impedance important?
20. Why is correct cathode positioning important?
7.59 Applied Calculations
Question 1
A stimulator delivers:
20 mA
through a tissue impedance of:
750 Ω
Calculate the approximate voltage required.
Question 2
A stimulus has:
25 mA current
and:
0.2 ms duration
Calculate the approximate electrical charge delivered.
Question 3
A constant-current stimulator is delivering 15 mA.
The patient's impedance increases from 500 Ω to 1,000 Ω.
What happens to the voltage required to maintain the same current?
7.60 Chapter Summary
Electrical nerve stimulation is the interface between physics, electronics and neurophysiology in NCS.
The stimulator creates a controlled electric field through the skin and underlying tissues. This field alters the transmembrane potential of the nerve. When threshold is reached, voltage-gated sodium channels generate an action potential that propagates along the nerve.
The effectiveness of stimulation depends on current, voltage, resistance/impedance, electrode size and position, pulse duration, tissue depth, polarity and temperature.
Reliable NCS therefore requires more than simply pressing the stimulation button. The operator must understand how the electrical stimulus interacts with biological tissue
.
CHAPTER 13
NEEDLE ELECTROMYOGRAPHY (EMG): ELECTRODE PHYSICS, MOTOR UNIT POTENTIALS AND SIGNAL ACQUISITION
13.1 Learning Objectives
By the end of this chapter, the learner should be able to:
1. Explain the physical basis of needle EMG.
2. Describe the structure and function of EMG needle electrodes.
3. Distinguish concentric and monopolar electrodes.
4. Explain insertional activity.
5. Identify normal resting muscle activity.
6. Explain fibrillation potentials and positive sharp waves.
7. Explain fasciculation potentials.
8. Define a motor unit.
9. Explain the motor unit action potential (MUAP).
10. Describe amplitude, duration, phases and turns of MUAPs.
11. Explain recruitment.
12. Explain the interference pattern.
13. Describe the EMG signal pathway from muscle to computer.
14. Identify common technical artefacts.
15. Understand the relationship between EMG findings and neuromuscular disease.
13.2 Introduction
Needle electromyography records the electrical activity generated within skeletal muscle.
Unlike nerve conduction studies, where an external electrical stimulus is applied to a peripheral nerve, needle EMG primarily records:
The electrical activity produced naturally by muscle fibres and motor units.
The basic pathway is:
Muscle fibre electrical activity
↓
Needle electrode
↓
Electrode–tissue interface
↓
Differential amplifier
↓
Filters
↓
Analog-to-digital conversion
↓
Computer
↓
Waveform
↓
Measurement
↓
Interpretation
13.3 What Does Needle EMG Measure?
Needle EMG can evaluate electrical activity during:
1. Needle insertion
2. Muscle relaxation
3. Minimal voluntary contraction
4. Increasing voluntary contraction
This allows assessment of:
13.4 The Motor Unit
A motor unit consists of:
One alpha motor neuron
plus:
All muscle fibres innervated by that neuron.
Conceptually:
Motor neuron
↓
Axon
↓
Terminal branches
↓
Neuromuscular junctions
↓
Multiple muscle fibres
This is the fundamental physiological unit assessed during voluntary EMG.
13.5 Motor Unit Action Potential
When a motor neuron fires, all of its connected muscle fibres depolarize.
The extracellular electrical activity detected by the needle electrode is called:
Motor Unit Action Potential
MUAP
The MUAP is therefore a summed extracellular signal from muscle fibres belonging to one motor unit, as detected by the recording electrode.
13.6 Why MUAPs Are Not Identical
MUAP morphology depends on:
Therefore, even within the same muscle:
MUAPs vary in shape.
13.7 Needle Electrode
The needle electrode provides a conductive pathway between:
Muscle tissue
and:
EMG amplifier.
The electrode detects extracellular voltage changes generated by nearby muscle fibres.
13.8 Concentric Needle Electrode
A concentric needle contains:
Central recording wire
surrounded by:
Conductive outer cannula
The central wire is the recording electrode.
The outer cannula provides the reference.
This arrangement provides a relatively focused recording field.
13.9 Monopolar Needle Electrode
A monopolar needle has:
One exposed recording tip
and uses a separate surface reference electrode.
The recording area is broader than that of a typical concentric needle.
13.10 Concentric Versus Monopolar
|
Feature |
Concentric |
Monopolar |
|
Recording configuration |
Central wire + cannula |
Single recording tip + surface reference |
|
Recording field |
Relatively focused |
Broader |
|
Common use |
Routine clinical EMG |
Selected EMG applications |
|
Signal amplitude |
Generally lower |
Generally higher |
|
Reference |
Cannula |
Separate surface electrode |
13.11 Electrode–Tissue Interface
The electrode does not directly measure intracellular voltage.
It records extracellular electrical fields.
Therefore the electrode–tissue interface influences:
13.12 Electrode Impedance
Electrode impedance is the opposition to electrical current at the electrode–tissue interface.
High impedance can increase:
Good electrode construction and amplifier design are therefore essential.
13.13 Differential Amplification
The EMG amplifier compares:
Recording electrode
with:
Reference electrode.
The measured voltage can be represented as:
This is similar to the principle used in surface electrophysiological recordings.
13.14 Common-Mode Rejection
Electrical interference may appear similarly at both recording inputs.
A differential amplifier can suppress signals common to both.
This is:
Common-Mode Rejection
It is particularly useful for reducing:
13.15 The EMG Signal Chain
The complete system can be represented as:
Muscle fibres
↓
Extracellular electric field
↓
Needle electrode
↓
Differential amplifier
↓
High-pass filter
↓
Low-pass filter
↓
Gain
↓
ADC
↓
Digital signal
↓
Display / audio
↓
Measurement
13.16 Gain
Gain determines how much the electrical signal is amplified.
For example:
If the input is:
100 µV
and the gain is:
×100
the output becomes:
The amplifier allows small biological signals to become measurable and visible.
13.17 Filtering
EMG systems use filters to restrict the frequency range of the recorded signal.
Two important filters are:
High-pass filter
and:
Low-pass filter
Together they define the effective recording bandwidth.
13.18 High-Pass Filter
The high-pass filter reduces very low-frequency components.
This can help reduce:
13.19 Low-Pass Filter
The low-pass filter reduces very high-frequency components.
This can help reduce:
However, excessive filtering can distort the physiological signal.
13.20 Sampling
The analog EMG signal must be converted into digital data.
This is performed by:
Analog-to-Digital Conversion
ADC
The system measures the signal repeatedly at a defined sampling rate.
13.21 Nyquist Principle
To accurately represent a signal with maximum frequency fmax, the sampling frequency should be at least:
2f_{max}" data-client-katex-layout="">
This is the basic Nyquist requirement.
In practice, EMG systems commonly sample at rates substantially higher than the minimum theoretical requirement.
13.22 Aliasing
If sampling is insufficient:
High-frequency signals can be misrepresented as lower-frequency signals.
This is:
Aliasing
Appropriate analogue filtering before digitization helps prevent aliasing.
13.23 Normal Muscle at Rest
A normal relaxed skeletal muscle is electrically silent on needle EMG apart from:
Brief insertional activity
and:
Normal endplate activity in appropriate locations.
Persistent spontaneous activity at rest may indicate abnormal muscle membrane excitability.
13.24 Insertional Activity
Insertional activity occurs when the needle enters or moves within the muscle.
Mechanical disturbance of muscle fibres generates transient electrical activity.
Therefore:
Insertional activity is a mechanical response of muscle tissue to needle movement.
13.25 Normal Insertional Activity
Normal insertional activity is:
The duration depends on the muscle and recording conditions.
13.26 Increased Insertional Activity
Insertional activity may be increased when muscle membrane excitability is abnormal.
It can occur in:
Interpretation must be integrated with spontaneous activity and MUAP findings.
13.27 Fibrillation Potentials
Fibrillation potentials are spontaneous discharges from individual muscle fibres.
They are commonly associated with:
Muscle fibre denervation
They are not generated by the whole motor unit.
13.28 Why Fibrillation Potentials Occur
After denervation, muscle fibres can become electrically unstable.
Changes in:
can make individual muscle fibres spontaneously depolarize.
13.29 Positive Sharp Waves
Positive sharp waves are another form of abnormal spontaneous muscle fibre activity.
They have a characteristic waveform with:
Initial positive deflection
followed by:
Slower return component.
They may occur with denervation and other muscle membrane disorders.
13.30 Fibrillation Potentials and Positive Sharp Waves
Both indicate:
Abnormal spontaneous muscle fibre activity.
They are commonly associated with:
13.31 Fasciculation Potentials
A fasciculation potential represents spontaneous activation of:
An entire motor unit
rather than a single muscle fibre.
It produces a larger and more complex waveform than a fibrillation potential.
13.32 Fasciculation Versus Fibrillation
|
Feature |
Fibrillation |
Fasciculation |
|
Structure activated |
Single muscle fibre |
Motor unit |
|
Amplitude |
Small |
Larger |
|
Source |
Muscle fibre |
Motor neuron/motor unit |
|
Appearance |
Regular/semiregular |
Often irregular |
|
Clinical meaning |
Often denervation |
May occur in benign or motor neuron disorders |
13.33 Complex Repetitive Discharges
Complex repetitive discharges are repetitive, highly organized electrical discharges.
They may sound like:
A machine-like or motor-like sound
through the EMG speaker.
They may occur in:
13.34 Myotonic Discharges
Myotonic discharges are spontaneous repetitive discharges that characteristically wax and wane in frequency and amplitude.
The audio may resemble:
A dive-bomber sound.
They are associated with disorders of muscle membrane excitability.
13.35 Endplate Activity
Near the neuromuscular junction, spontaneous electrical activity may include:
These should not automatically be interpreted as pathological denervation.
Correct anatomical localization of the needle is important.
13.36 Voluntary Motor Unit Recruitment
When a person voluntarily contracts a muscle:
Small number of motor units activate first.
As force increases:
Additional motor units are recruited.
This is:
Recruitment
13.37 Recruitment Principle
Low force:
Few motor units
↓
Moderate force:
More motor units
↓
High force:
Many motor units
The nervous system increases muscle force through:
1. Recruitment of additional motor units.
2. Increasing firing rates of active motor units.
13.38 MUAP Recording
During slight voluntary contraction, the examiner asks the patient to activate the muscle gently.
Individual MUAPs become visible.
The examiner can analyze:
13.39 MUAP Amplitude
MUAP amplitude depends on:
Therefore amplitude is not purely a measure of motor unit size.
13.40 MUAP Duration
MUAP duration reflects the temporal spread of electrical activity arriving at the recording electrode.
It depends on:
13.41 MUAP Phases
A MUAP can have:
Positive and negative phases
A common definition counts the number of baseline crossings plus one.
A typical MUAP may be:
Triphasic
or:
Biphasic
More complex waveforms may have increased numbers of phases.
13.42 Polyphasic MUAP
A polyphasic MUAP contains an increased number of phases.
Polyphasia can occur in:
Therefore:
Polyphasia alone is not diagnostic.
13.43 Motor Unit Remodeling
After axonal injury, surviving motor axons may sprout collateral branches.
These branches reinnervate denervated muscle fibres.
The motor unit becomes:
Larger
and:
More complex.
13.44 Chronic Neurogenic MUAP
Chronic reinnervation often produces:
This is a classic neurogenic pattern.
13.45 Myopathic MUAP
In many myopathies, motor units contain fewer muscle fibres.
This may produce:
A typical conceptual pattern is:
Small, short-duration MUAPs with early recruitment.
13.46 Neurogenic Versus Myopathic Pattern
|
Feature |
Neurogenic |
Myopathic |
|
MUAP amplitude |
Often increased |
Often reduced |
|
MUAP duration |
Often prolonged |
Often shortened |
|
Recruitment |
Reduced |
Early/increased |
|
Motor unit size |
Often enlarged |
Often smaller |
|
Common mechanism |
Denervation/reinnervation |
Loss/dysfunction of muscle fibres |
These are patterns, not absolute rules.
13.47 Recruitment
Recruitment describes the number of motor units activated for a given level of voluntary effort.
A reduced recruitment pattern means:
Fewer motor units are available or activated.
This can occur with:
13.48 Early Recruitment
Early recruitment occurs when many motor units become active despite relatively low force.
It may occur when individual motor units produce less force, as in many myopathies.
13.49 Interference Pattern
At maximal or near-maximal voluntary contraction, many MUAPs overlap.
The individual waveforms become difficult to distinguish.
This produces:
Interference Pattern
The screen appears densely filled with electrical activity.
13.50 Full Interference Pattern
A healthy muscle capable of generating strong force can produce a dense interference pattern.
The precise appearance depends on:
13.51 Reduced Interference Pattern
A reduced interference pattern means fewer motor units are contributing.
It can occur with:
Therefore patient cooperation must be considered.
13.52 Recruitment Ratio
Quantitative approaches may estimate recruitment by relating:
Number of active motor units
to:
Firing frequency
Different EMG systems use different recruitment algorithms.
13.53 Needle Movement Artefact
Needle movement can produce large electrical signals unrelated to physiological activity.
This is why:
The needle should remain stable during signal acquisition.
Movement artefact may be mistaken for:
13.54 Electrical Noise
EMG can be affected by:
Noise reduction is essential because EMG signals can be very small.
13.55 50/60 Hz Interference
Depending on the electrical supply system, mains interference may appear at:
50 Hz
or:
60 Hz
Kenya uses a:
50-Hz electrical supply
Therefore 50-Hz interference can be particularly relevant in local EMG laboratories.
13.56 Common-Mode Rejection and Grounding
Good differential amplification plus proper grounding can substantially reduce electrical interference.
However:
Grounding does not eliminate all electrical noise.
Cable arrangement, shielding and equipment placement also matter.
13.57 Patient Relaxation
The patient should understand when to:
Relax
and when to:
Contract.
Involuntary muscle activity can contaminate resting recordings.
Pain can also cause unwanted activation of adjacent muscles.
13.58 Needle Position
Correct muscle identification is critical.
A needle inserted into the wrong muscle may produce an apparently abnormal result.
Anatomical knowledge is therefore as important as electronic instrumentation.
13.59 EMG Sampling and Audio
EMG systems often provide:
Visual waveform
and:
Audio output.
The audio signal is generated from the electrical activity detected by the system.
Experienced examiners can recognize characteristic sounds associated with:
13.60 Safety
Needle EMG is an invasive procedure.
Important precautions include:
13.61 EMG Examination Sequence
A typical needle examination follows:
Step 1
Select the muscle.
Step 2
Explain the procedure.
Step 3
Position the patient.
Step 4
Insert the needle.
Step 5
Observe insertional activity.
Step 6
Allow the muscle to relax.
Step 7
Assess spontaneous activity.
Step 8
Ask for minimal contraction.
Step 9
Analyze individual MUAPs.
Step 10
Increase contraction.
Step 11
Assess recruitment.
Step 12
Assess interference pattern.
Step 13
Repeat in additional muscles.
13.62 Sampling Multiple Muscles
A single muscle rarely provides enough information to localize a lesion.
Multiple muscles are selected based on:
This allows pattern recognition.
13.63 Root-Level Localization
Suppose abnormalities are found in several muscles supplied by:
The same spinal root
but:
Different peripheral nerves.
This pattern can support a radiculopathy.
For example, muscles from different nerves sharing a root may show neurogenic changes.
13.64 Peripheral Nerve Localization
If abnormalities occur in muscles supplied by:
The same peripheral nerve
the pattern may support a peripheral mononeuropathy.
Therefore:
Muscle selection is a diagnostic strategy, not merely a sampling exercise.
13.65 Plexus Localization
If abnormalities involve muscles supplied by:
and:
but share a plexus region,
a plexopathy may be considered.
13.66 Motor Neuron Disease
Needle EMG may demonstrate:
The abnormalities typically occur in multiple anatomical regions.
Clinical correlation is essential.
13.67 Peripheral Neuropathy
EMG may demonstrate:
NCS findings are usually integrated with needle EMG.
13.68 Myopathy
Needle EMG may show:
Again:
No single EMG feature establishes a diagnosis by itself.
13.69 Normal EMG
A normal muscle typically demonstrates:
At rest
Electrical silence apart from normal physiological activity.
Minimal contraction
Individual MUAPs.
Increasing contraction
Increasing recruitment.
Maximal contraction
Dense interference pattern.
13.70 The Complete EMG Signal Pathway
Muscle fibre membrane
↓
Ion movement
↓
Action potential
↓
Extracellular electric field
↓
Needle electrode
↓
Electrode–tissue interface
↓
Differential amplifier
↓
Gain
↓
Filtering
↓
ADC
↓
Digital signal
↓
Waveform + audio
↓
Measurement
↓
Clinical interpretation
13.71 Physics Meets Clinical Neurophysiology
The EMG examiner must integrate three levels:
Level 1 — Biology
What is happening to the motor unit?
Level 2 — Physics
What electrical field is being generated?
Level 3 — Instrumentation
How accurately is the system detecting and displaying that field?
This integration is fundamental to high-quality EMG.
13.72 Key Points
1. Needle EMG records extracellular muscle electrical activity.
2. A motor unit consists of one motor neuron and its muscle fibres.
3. A MUAP is the recorded electrical response of a motor unit.
4. Concentric needles provide focused recordings.
5. Monopolar needles use a separate reference electrode.
6. Differential amplification improves rejection of common electrical noise.
7. Insertional activity occurs when the needle mechanically disturbs muscle fibres.
8. Fibrillation potentials arise from individual unstable muscle fibres.
9. Fasciculation potentials represent spontaneous motor-unit activity.
10. MUAP amplitude and duration reflect motor-unit architecture and electrode position.
11. Neurogenic disease often produces large, long-duration MUAPs with reduced recruitment.
12. Myopathic disease often produces small, short-duration MUAPs with early recruitment.
13. Recruitment reflects the number of motor units activated.
14. The interference pattern represents overlapping activity from many motor units.
15. Needle position and patient effort can strongly influence the recording.
16. Filtering and sampling affect the displayed signal.
17. EMG findings must always be interpreted in anatomical and clinical context.
13.73 Review Questions
1. What is needle EMG?
2. What is a motor unit?
3. Define MUAP.
4. How does a concentric needle work?
5. How does a monopolar needle differ?
6. What is insertional activity?
7. What is a fibrillation potential?
8. What is a positive sharp wave?
9. What is a fasciculation potential?
10. What is a complex repetitive discharge?
11. What is a myotonic discharge?
12. Define recruitment.
13. What is an interference pattern?
14. What is common-mode rejection?
15. Why is electrode impedance important?
16. What is aliasing?
17. Why does needle position matter?
18. How can EMG help distinguish neurogenic from myopathic patterns?
13.74 Practical Exercise
Case 1
A patient has:
Question: What general interpretation does this support?
Case 2
A muscle demonstrates:
Question: What broad physiological process does this pattern suggest?
Case 3
A muscle demonstrates:
Question: What broad pattern does this suggest?
13.75 Chapter Summary
Needle EMG is fundamentally an electrical measurement of muscle physiology.
The examiner inserts a recording electrode into muscle and observes the electrical consequences of:
The recorded signal is not simply a waveform on a monitor. It is the final product of:
Muscle physiology → extracellular electrical field → electrode → amplifier → filters → digital processing → waveform.
Understanding this complete pathway allows the neurophysiology practitioner to distinguish a true biological abnormality from an instrumentation or technical artefact.
CHAPTER 15
NERVE CONDUCTION AND EMG INSTRUMENTATION: AMPLIFIERS, FILTERS, SAMPLING, NOISE, ARTEFACTS AND QUALITY CONTROL
15.1 Learning Objectives
By the end of this chapter, the learner should be able to:
1. Describe the architecture of an NCS/EMG system.
2. Explain differential amplification.
3. Define input impedance.
4. Explain common-mode rejection ratio.
5. Explain amplifier gain.
6. Describe high-pass, low-pass and notch filters.
7. Explain sampling and analog-to-digital conversion.
8. Describe quantization and aliasing.
9. Explain signal-to-noise ratio.
10. Identify common NCS/EMG artefacts.
11. Troubleshoot electrical interference.
12. Understand stimulus artefact and amplifier saturation.
13. Describe basic equipment quality-control procedures.
14. Recognize the relationship between instrumentation and diagnostic accuracy.
15.2 Introduction
An NCS/EMG machine is essentially a specialized biomedical measurement system.
It converts extremely small biological electrical signals into:
The signal pathway is:
Patient
↓
Biological electrical activity
↓
Electrodes
↓
Amplifier
↓
Filters
↓
Analog-to-digital converter
↓
Computer
↓
Waveform
↓
Measurement
↓
Interpretation
A technically poor recording can produce a clinically misleading result.
15.3 Magnitude of Electrophysiological Signals
The signals encountered in neurophysiology vary greatly in amplitude.
Approximate examples:
|
Signal |
Typical scale |
|
SNAP |
µV |
|
Needle EMG |
µV–mV |
|
CMAP |
mV |
|
Stimulus artefact |
Can be much larger |
This large range places significant demands on the amplifier.
15.4 The Electrode
The electrode is the first component interacting with the biological signal.
It converts:
Ionic electrical activity
within tissue into:
Electronic electrical signal
within the recording system.
This interface is fundamental to the entire measurement process.
15.5 Electrode–Skin Interface
Surface electrodes involve an interface between:
This interface has:
Resistance
and:
Capacitive properties.
Therefore the electrode does not behave as a perfect resistor.
15.6 Electrode Impedance
Electrode impedance is the opposition to electrical current at the electrode interface.
High impedance may increase:
Balanced electrode impedances improve differential recording.
15.7 Why Impedance Matching Matters
Suppose:
G1 impedance = 5 kΩ
G2 impedance = 5 kΩ
This is generally preferable to:
G1 = 5 kΩ
G2 = 100 kΩ
Large differences can reduce the effectiveness of common-mode rejection.
15.8 Differential Amplifier
Most biomedical electrophysiology systems use differential amplification.
The amplifier measures:
where:
15.9 Why Differential Amplification Is Used
The biological signal may be small.
Environmental electrical interference may be relatively large.
If interference appears similarly at both electrodes:
then:
The common interference is therefore substantially reduced.
15.10 Common-Mode Signal
A signal appearing similarly at both amplifier inputs is called:
Common-mode signal.
Examples include:
15.11 Differential Signal
The signal that differs between the two inputs is the:
Differential signal.
The desired biological signal should ideally appear primarily as a differential signal.
15.12 Common-Mode Rejection Ratio
The ability of an amplifier to reject common-mode signals is expressed as:
CMRR
Common-Mode Rejection Ratio
A simplified expression is:
where:
It is commonly expressed in decibels:
15.13 High CMRR
A high CMRR means the amplifier is very effective at rejecting signals that appear equally at both inputs.
This is particularly important in:
where biological signals may be much smaller than environmental interference.
15.14 Amplifier Gain
Gain determines how strongly the input signal is amplified.
If:
and:
then:
15.15 Too Little Gain
If gain is too low:
15.16 Too Much Gain
If gain is too high:
15.17 Amplifier Saturation
When an input exceeds the amplifier's usable range, the amplifier cannot reproduce the waveform accurately.
The output may become:
Flattened
or:
Clipped.
This is:
Saturation
15.18 Clipping
A clipped waveform loses information because the amplifier has reached its maximum output.
This can distort:
Therefore clipped responses should not be used for precise quantitative interpretation.
15.19 Dynamic Range
Dynamic range describes the range of signal amplitudes that the system can measure accurately.
An NCS/EMG system must accommodate:
15.20 Filters
Filters selectively allow some frequencies to pass while attenuating others.
The major filters are:
High-pass
Low-pass
Notch
15.21 High-Pass Filter
A high-pass filter allows higher frequencies to pass while reducing lower-frequency components.
It can reduce:
15.22 Low-Pass Filter
A low-pass filter allows lower frequencies to pass while reducing higher-frequency components.
It can reduce:
15.23 Band-Pass Filtering
Using both high-pass and low-pass filters creates a:
Band-pass
recording range.
Conceptually:
span data-start="6475" data-end="6518" data-math-source="f_{high-pass}f_{signal}
Signals outside this range are attenuated.
15.24 Why Filter Settings Matter
Changing filters can change:
Therefore:
Filter settings must be standardized when comparing measurements.
15.25 Notch Filter
A notch filter removes a narrow frequency band.
A common target is:
50 Hz
in countries using a 50-Hz electrical supply.
Kenya uses:
50 Hz
mains frequency.
15.26 Why Notch Filters Should Be Used Carefully
A notch filter can reduce mains interference.
However, excessive filtering can also alter physiological signals.
Therefore the preferred approach is:
Fix the source of interference first.
Then use filtering as appropriate.
15.27 Mains Interference
A common source of noise is electrical mains interference.
On the screen it may appear as:
Regular oscillation
or:
Dense high-frequency activity.
Potential causes include:
15.28 Grounding
The ground electrode helps stabilize the recording and reduce electrical interference.
It is usually placed between:
Stimulator
and:
Recording electrodes
during NCS.
15.29 Ground Loops
A ground loop can occur when equipment is connected through multiple electrical grounding pathways.
This may create unwanted circulating currents.
The result can be:
Persistent electrical interference.
15.30 Shielding
Shielding reduces electromagnetic coupling between:
External electrical sources
and:
Recording cables.
Good cable management can substantially improve signal quality.
15.31 Cable Position
Recording cables should be:
Parallel placement beside power cables should be minimized.
15.32 Electromagnetic Interference
Electromagnetic fields can be produced by:
These fields can couple into recording cables.
15.33 Signal-to-Noise Ratio
Signal-to-noise ratio is:
A higher SNR means the biological signal is easier to identify.
15.34 Improving SNR
SNR can be improved by:
Increasing signal
and reducing noise:
15.35 Averaging
Averaging repeated responses can improve SNR.
If the physiological response is time-locked:
Signal reinforces.
Random noise:
Partially cancels.
This is particularly useful for:
15.36 Sampling
The analog signal must be sampled repeatedly.
For example:
10,000 samples/second
means:
10kHz
sampling frequency.
15.37 Sampling Frequency
The sampling frequency determines how accurately the digital system represents the original signal.
If the signal contains frequencies up to:
fmax
then the sampling frequency should satisfy:
2f_{max}" data-client-katex-layout="">
according to the Nyquist principle.
15.38 Aliasing
If the sampling frequency is insufficient:
High-frequency information is misrepresented.
This is called:
Aliasing
Anti-aliasing filters are therefore important before digitization.
15.39 Analog-to-Digital Conversion
The ADC converts:
Continuous voltage
into:
Digital numerical values.
The computer can then:
the signal.
15.40 Quantization
Digital systems represent voltage using discrete numerical levels.
This process is:
Quantization.
The number of available levels depends on:
ADC resolution.
15.41 ADC Resolution
An ADC with more bits can represent more voltage levels.
For an ideal n-bit ADC:
For example:
12-bit
levels.
A:
16-bit
system provides:
levels.
15.42 Quantization Error
Because digital voltage levels are discrete, the digitized value may differ slightly from the original analog value.
This difference is:
Quantization error.
Higher-resolution ADCs reduce this error.
15.43 Time Base
The time base controls how much time is displayed across the screen.
It is important for measuring:
15.44 Amplitude Scale
The amplitude scale controls vertical display sensitivity.
For example:
5 mV/division
or:
100 µV/division
The selected scale should allow the waveform to be measured without excessive compression or clipping.
15.45 Stimulus Artefact
The electrical stimulus can generate a very large recording artefact.
It may:
Appropriate electrode positioning and system design help minimize this problem.
15.46 Stimulus Artefact Versus Biological Response
A stimulus artefact:
A biological response:
15.47 Amplifier Recovery
After a large stimulus artefact, the amplifier may require time to return to normal operating range.
This is:
Recovery time.
If recovery is prolonged, early physiological responses may be obscured.
15.48 Baseline Drift
Baseline drift may result from:
High-pass filtering can reduce some baseline drift.
However, identifying and correcting the source is preferable.
15.49 Movement Artefact
Movement produces electrical changes through:
The waveform may be large and irregular.
15.50 Muscle Artefact
In NCS, patient muscle activity can contaminate the recording.
The patient should therefore be:
Comfortable
and:
Relaxed.
This is particularly important for sensory studies and small responses.
15.51 Equipment Placement
An NCS/EMG laboratory should ideally minimize:
A stable electrical environment improves recording quality.
15.52 Troubleshooting a Noisy Recording
When the waveform is noisy, use a systematic sequence.
Step 1
Ask:
Is the patient relaxed?
Step 2
Check:
Electrode contact
Step 3
Check:
Electrode impedance
Step 4
Check:
Ground electrode
Step 5
Check:
Cable placement
Step 6
Move away from:
Electrical equipment
Step 7
Check:
Mains interference
Step 8
Review:
Filter settings
Step 9
Check:
Amplifier saturation
Step 10
Repeat the recording.
15.53 Troubleshooting Decision Tree
Noisy waveform
↓
Patient relaxed?
→ No → Relax patient
→ Yes
↓
Electrodes secure?
→ No → Reposition
→ Yes
↓
Impedance acceptable?
→ No → Improve contact
→ Yes
↓
Ground adequate?
→ No → Correct ground
→ Yes
↓
Electrical interference?
→ Yes → Remove source/shield
→ No
↓
Filters appropriate?
→ No → Correct settings
→ Yes
↓
Repeat recording
15.54 Quality Control
Quality control should cover:
Electrical safety
Calibration
Electrode integrity
Stimulator performance
Amplifier performance
Software
Reference measurements
Documentation
15.55 Calibration
The system should be checked to ensure that:
Displayed amplitude
corresponds appropriately to:
Actual input amplitude.
Time measurements should similarly be accurate.
Calibration should follow:
15.56 Stimulator Quality Control
The stimulator should deliver:
A malfunctioning stimulator can produce systematically incorrect NCS results.
15.57 Amplifier Quality Control
The amplifier should demonstrate:
15.58 Electrode Quality Control
Electrodes should be:
Disposable electrodes should be within their recommended use period.
15.59 Reference Standards
Normal values should be derived from:
A value is meaningful only when compared with an appropriate reference.
15.60 Reproducibility
A good neurophysiology measurement should be:
Repeatable.
If a waveform changes dramatically with repeated testing without physiological explanation, investigate:
15.61 Quality Assurance Principle
The goal is not merely:
to obtain a waveform.
The goal is:
to obtain a physiologically valid and reproducible waveform.
15.62 Instrumentation Failure Can Mimic Disease
Examples:
Cold limb
→ apparent slowing
Poor stimulation
→ reduced amplitude
Poor electrode contact
→ low/noisy response
Wrong distance
→ incorrect conduction velocity
Excessive filtering
→ altered waveform
Stimulus artefact
→ obscured latency
Therefore:
Technical quality is part of diagnosis.
15.63 Example: False Low SNAP
A patient appears to have a very small sural SNAP.
Before diagnosing neuropathy:
1. Warm the limb.
2. Check electrode position.
3. Check stimulation.
4. Check ground.
5. Check impedance.
6. Repeat the study.
7. Compare with the opposite limb when appropriate.
Only then interpret the amplitude.
15.64 Example: False Prolonged Latency
A latency appears prolonged.
Possible causes:
Therefore the examiner should verify all technical parameters.
15.65 Instrumentation and Patient Safety
Electrical stimulation must be delivered within the safe operating parameters of the equipment and clinical protocol.
Special caution is required in patients with relevant implanted electrical devices or other contraindications according to current manufacturer and clinical guidance.
The equipment should be maintained and electrically safe.
15.66 Complete NCS/EMG Instrument Architecture
A modern system can be represented as:
Stimulator
↓
Patient / nerve / muscle
↓
Electrodes
↓
Input protection
↓
Differential amplifier
↓
Gain
↓
Analogue filters
↓
Anti-aliasing filter
↓
ADC
↓
Digital signal processing
↓
Computer
↓
Display
↓
Measurement software
↓
Report
15.67 The Three Main Sources of Error
Every NCS/EMG measurement can be affected by:
Biological variation
Example:
Technical variation
Example:
Instrumentation variation
Example:
A skilled examiner must control all three.
15.68 Quality-Control Checklist
Before starting a study:
Patient
☐ Correct patient
☐ Correct limb
☐ Clinical question identified
☐ Limb temperature assessed
Electrodes
☐ Correct electrodes
☐ Good contact
☐ Appropriate placement
☐ Impedance acceptable
Stimulator
☐ Correct location
☐ Correct polarity
☐ Appropriate duration
☐ Adequate intensity
Recording
☐ Ground correctly positioned
☐ Patient relaxed
☐ Low noise
☐ No saturation
☐ Appropriate filters
Measurement
☐ Distance accurate
☐ Cursor placement correct
☐ Waveform reproducible
☐ Appropriate reference values
15.69 Key Points
1. NCS/EMG systems measure very small biological electrical signals.
2. Differential amplification is central to electrophysiological recording.
3. CMRR determines how effectively common electrical interference is rejected.
4. Electrode impedance affects recording quality.
5. Gain controls signal amplification.
6. Excessive gain can cause saturation and clipping.
7. Filters alter the frequency content of the signal.
8. A notch filter may reduce 50-Hz interference in Kenya.
9. Sampling converts continuous signals into digital data.
10. Insufficient sampling can cause aliasing.
11. ADC resolution determines the number of quantization levels.
12. Stimulus artefact can obscure early responses.
13. Grounding and shielding reduce electrical interference.
14. Averaging improves the visibility of small time-locked signals.
15. Calibration is essential for accurate measurement.
16. Technical artefacts can mimic pathological findings.
17. Quality control must be continuous.
18. A waveform should never be interpreted without assessing recording quality.
15.70 Review Questions
1. What is a differential amplifier?
2. Define CMRR.
3. Why is high CMRR desirable?
4. What is amplifier gain?
5. What is saturation?
6. What is clipping?
7. What is a high-pass filter?
8. What is a low-pass filter?
9. What is a notch filter?
10. Why is 50-Hz interference relevant in Kenya?
11. What is sampling?
12. State the Nyquist principle.
13. What is aliasing?
14. What is quantization?
15. What does ADC resolution mean?
16. What causes stimulus artefact?
17. What causes baseline drift?
18. How would you troubleshoot a noisy EMG?
19. Why is calibration important?
20. How can instrumentation errors mimic neuropathy?
15.71 Practical Exercise
Case 1 — Noisy SNAP
A patient's SNAP recording contains continuous 50-Hz interference.
List five things you would check before changing the notch filter.
Case 2 — Low CMAP
A CMAP is unexpectedly small.
List the technical factors that should be checked before diagnosing severe axonal loss.
Case 3 — Prolonged Latency
A nerve conduction latency is unexpectedly prolonged.
List six possible technical or physiological explanations.
15.72 Chapter Summary
NCS and EMG are fundamentally measurement technologies.
The biological signal begins with:
Ion movement
and ends as:
Digital numerical data.
Between these two points are multiple opportunities for error:
Electrode → amplifier → filters → sampling → digitization → processing → measurement.
Understanding this chain allows the neurophysiology practitioner to recognize when an abnormal waveform represents:
True physiology
versus:
Technical artefact.
The most important practical principle is:
Never interpret an abnormal electrophysiological measurement before confirming that the recording itself is technically valid.
NEXT CHAPTER
CHAPTER 16 — MOTOR NERVE CONDUCTION STUDIES: CMAP PHYSICS, DISTAL MOTOR LATENCY, CONDUCTION VELOCITY, TEMPORAL DISPERSION AND CONDUCTION BLOCK
This chapter will integrate the physics and clinical technique of motor NCS, including:
CHAPTER 17
SENSORY NERVE CONDUCTION STUDIES: SNAP PHYSICS, ORTHODROMIC AND ANTIDROMIC RECORDING, LATENCY, AMPLITUDE AND CONDUCTION VELOCITY
17.1 Learning Objectives
By the end of this chapter, the learner should be able to:
1. Explain the physiological basis of sensory nerve conduction studies.
2. Define a sensory nerve action potential (SNAP).
3. Explain orthodromic and antidromic stimulation.
4. Describe sensory recording electrodes.
5. Measure sensory onset and peak latency.
6. Measure SNAP amplitude.
7. Calculate sensory conduction velocity.
8. Explain the effect of temperature on sensory conduction.
9. Identify factors that influence SNAP amplitude.
10. Recognize common technical errors in sensory NCS.
11. Explain the diagnostic importance of sensory responses.
12. Perform a systematic sensory nerve conduction protocol.
17.2 Introduction
Sensory nerve conduction studies evaluate the electrical conduction of peripheral sensory axons.
Unlike motor NCS, the response is recorded directly from a:
Sensory nerve
rather than from a muscle.
The recorded response is called:
Sensory Nerve Action Potential
SNAP
The basic sequence is:
Electrical stimulus
↓
Sensory axon depolarization
↓
Action potential propagation
↓
Recording electrode
↓
Differential amplifier
↓
Filtering
↓
ADC
↓
Digital waveform
↓
Measurement
17.3 What Is a SNAP?
A SNAP is the summed extracellular electrical response produced by a population of sensory axons.
It is usually much smaller than a CMAP.
Typical amplitudes are commonly in:
Microvolts (µV)
rather than:
Millivolts (mV).
17.4 Why SNAPs Are Small
Several factors contribute to the small amplitude:
Therefore high-quality instrumentation is particularly important.
17.5 Sensory Nerve Recording
A sensory NCS usually uses surface electrodes.
The recording electrodes are positioned over:
A sensory nerve
or:
A digital sensory nerve territory.
The exact placement depends on the nerve and protocol.
17.6 Orthodromic Conduction
Orthodromic stimulation means the impulse travels in the:
Physiological direction of sensory conduction.
For a sensory nerve:
Peripheral receptor → spinal cord
is the physiological direction.
Therefore stimulation and recording are arranged so the action potential travels in that direction.
17.7 Antidromic Conduction
Antidromic stimulation sends the sensory action potential:
Opposite to its usual physiological direction.
For sensory nerves:
Spinal direction → peripheral direction
is antidromic.
17.8 Why Use Antidromic Studies?
Antidromic sensory studies often produce:
Larger SNAP amplitudes
because the recording configuration may provide a stronger signal.
However, the technique may be more susceptible to:
Motor contamination
in some nerve studies.
17.9 Orthodromic Versus Antidromic
|
Feature |
Orthodromic |
Antidromic |
|
Direction |
Physiological sensory direction |
Opposite direction |
|
Typical SNAP |
Often smaller |
Often larger |
|
Motor contamination |
Generally less |
Can be greater |
|
Common application |
Selected sensory studies |
Widely used routine sensory studies |
17.10 Sensory Stimulation
A brief electrical stimulus is applied to the sensory nerve.
The stimulus parameters include:
The intensity is increased until an adequate and reproducible SNAP is obtained.
17.11 Sensory Recording Electrodes
The active electrode should be positioned over the expected nerve pathway.
The reference electrode is placed nearby according to the laboratory's validated protocol.
Small changes in electrode location can significantly affect SNAP amplitude.
17.12 Ground Electrode
The ground electrode is placed between:
Stimulator
and:
Recording electrodes.
It helps reduce:
17.13 Sensory Onset Latency
Onset latency is the time from:
Stimulus
to:
Initial departure of the SNAP from baseline.
It is commonly measured in:
milliseconds.
17.14 Sensory Peak Latency
Peak latency is measured from the stimulus to:
The peak of the sensory response.
Both onset and peak latency can be useful.
The laboratory must use a consistent convention.
17.15 Why Peak Latency Can Be Useful
SNAPs may have relatively small initial deflections.
The peak can sometimes be easier to identify reproducibly than onset.
However, peak latency is influenced by:
17.16 SNAP Amplitude
SNAP amplitude is usually measured in:
µV.
Common measurement approaches include:
Baseline-to-negative peak
or:
Peak-to-peak
depending on laboratory protocol.
17.17 SNAP Amplitude Is Highly Variable
SNAP amplitude depends on:
Therefore reference values are essential.
17.18 Sensory Conduction Velocity
Sensory conduction velocity can be estimated using:
when the recording configuration allows the latency to represent conduction over the measured segment.
For example:
Distance = 120 mm
Onset latency = 3.0 ms
Then:
17.19 Distance Measurement
The distance should be measured along the anatomical pathway between:
Stimulating electrode
and:
Recording electrode.
Errors in distance directly affect calculated conduction velocity.
17.20 Example of Distance Error
Suppose the true distance is:
140 mm
but the examiner records:
120 mm.
The calculated conduction velocity will be falsely low.
Therefore:
Accurate distance measurement is essential.
17.21 Temperature and Sensory NCS
Temperature strongly influences sensory nerve conduction.
Cold limbs can produce:
A cold hand or foot can therefore create a false impression of neuropathy.
17.22 Limb Warming
When the limb is cold, the examiner should follow the laboratory's validated warming protocol.
Possible methods include:
The limb should be rewarmed safely without causing burns.
17.23 Sensory Nerve Conduction in Entrapment Neuropathy
Sensory studies are particularly useful for focal entrapment neuropathies.
Examples include:
Median neuropathy at the wrist
Ulnar neuropathy
Radial sensory neuropathy
Sural neuropathy
17.24 Median Sensory Study
A common median sensory study evaluates conduction from:
Finger
to:
Wrist/forearm recording or stimulation configuration
depending on the protocol.
Median sensory responses are particularly important in assessment of:
Carpal tunnel syndrome.
17.25 Comparative Sensory Studies
When focal neuropathy is suspected, comparison with another sensory nerve can be useful.
For example:
Median versus ulnar sensory latency
may help detect subtle focal median nerve slowing at the wrist.
Comparative studies reduce the influence of:
because the nerves are tested under similar conditions.
17.26 Ulnar Sensory Study
The ulnar sensory response can be recorded from an appropriate digit or sensory distribution.
It is useful in evaluating:
17.27 Radial Sensory Study
The superficial radial sensory nerve can be tested using appropriate surface stimulation and recording locations.
It can help assess:
17.28 Sural Sensory Study
The sural nerve is a major lower-limb sensory nerve.
The sural SNAP is particularly useful in evaluation of:
Length-dependent peripheral neuropathy.
It is often compared between:
when appropriate.
17.29 Sensory Responses in Polyneuropathy
A generalized peripheral neuropathy may cause:
The pattern depends on:
17.30 Axonal Sensory Neuropathy
A predominantly axonal sensory neuropathy often produces:
Reduced SNAP amplitude
because fewer functioning sensory axons contribute to the response.
Conduction velocity may be relatively preserved compared with the marked amplitude loss.
17.31 Demyelinating Sensory Neuropathy
A predominantly demyelinating sensory neuropathy may produce:
The exact criteria depend on the diagnostic context.
17.32 Absent SNAP
An absent SNAP may result from:
Therefore:
An absent response must first be confirmed technically.
17.33 Technical Verification of an Absent SNAP
Before concluding that a SNAP is absent:
Check 1
Limb temperature.
Check 2
Stimulus intensity.
Check 3
Stimulator position.
Check 4
Recording electrodes.
Check 5
Ground electrode.
Check 6
Distance measurement.
Check 7
Filters.
Check 8
Electrical noise.
Check 9
Repeat the response.
Check 10
Compare with another nerve or the opposite side when clinically appropriate.
17.34 Stimulus Artefact
Stimulus artefact can obscure small sensory responses.
This is especially important because:
SNAPs are small.
The examiner must distinguish:
Stimulus artefact
from:
True sensory response.
17.35 Stimulus–Recording Distance
If the stimulus is too close to the recording electrode:
Stimulus artefact may obscure the response.
Appropriate anatomical positioning and electrode orientation reduce this problem.
17.36 Volume Conduction
Electrical activity from nearby nerves or muscles can contribute to the recorded waveform.
This can produce:
Contamination
or:
Unexpected waveform morphology.
17.37 Motor Contamination
In antidromic studies, the stimulus may activate nearby motor fibres.
The resulting CMAP can contaminate the sensory recording.
This is one reason why some sensory studies use:
Orthodromic techniques
or carefully selected stimulation sites.
17.38 Averaging
Because SNAPs can be small, repeated recordings may improve signal quality.
The principle is:
Reproducible signal → reinforces
Random noise → partially cancels.
This improves:
Signal-to-noise ratio.
17.39 SNAP Waveform
A typical SNAP may contain:
The exact morphology depends on:
17.40 SNAP Duration
Sensory response duration represents the temporal spread of the individual sensory axon action potentials.
Increased duration may reflect:
Greater dispersion of conduction velocities.
17.41 Temporal Dispersion in Sensory NCS
Different sensory axons may conduct at different velocities.
Their responses arrive at slightly different times.
The result is:
Broader SNAP.
17.42 Sensory Conduction and Myelin
Myelin increases the speed of action-potential propagation.
Therefore disorders affecting myelin may produce:
Slower conduction.
17.43 Saltatory Conduction
In myelinated axons, the action potential effectively propagates between:
Nodes of Ranvier.
This is:
Saltatory conduction
It increases conduction velocity and improves efficiency.
17.44 Node of Ranvier
The node is a short unmyelinated region containing a high density of voltage-gated sodium channels.
Depolarization is regenerated at successive nodes.
Conceptually:
Node
→
Internode
→
Node
→
Internode
→
Node
17.45 Sensory Axon Diameter
Larger myelinated axons generally conduct faster than smaller axons.
Therefore nerve conduction is influenced by:
17.46 Sensory NCS and Anatomy
A sensory nerve study is not simply an electronic measurement.
The examiner must understand:
Which nerve is being stimulated?
Which nerve is being recorded?
Which anatomical segment is being tested?
Which nearby structures can contaminate the recording?
17.47 Example: Median Versus Ulnar Comparison
Suppose:
Median sensory peak latency = 3.8 ms
Ulnar sensory peak latency = 3.1 ms
The difference is:
The significance depends on:
A difference should not be interpreted using an arbitrary universal cutoff.
17.48 Sensory NCS in Carpal Tunnel Syndrome
In median neuropathy at the wrist, the median sensory response may demonstrate:
Relative slowing across the wrist.
Comparative studies can improve sensitivity.
The key physiological concept is:
Focal slowing
rather than generalized slowing of the entire nerve.
17.49 Sensory NCS in Length-Dependent Neuropathy
A patient with distal symmetric polyneuropathy may demonstrate:
Reduced or absent distal sensory responses.
Lower-limb sensory nerves may be affected before upper-limb sensory nerves because of:
Length dependence.
17.50 Sensory NCS in Radiculopathy
A key principle is that many sensory nerve action potentials may remain:
Relatively preserved
in radiculopathy because the lesion is often proximal to the dorsal root ganglion.
This distinction makes sensory NCS particularly useful when combined with needle EMG.
17.51 Sensory NCS and Dorsal Root Ganglion
The location of the dorsal root ganglion is important.
A lesion:
Proximal to the DRG
may preserve the distal sensory axon.
A lesion:
Distal to the DRG
is more likely to reduce the distal SNAP.
This is a major anatomical principle in electrodiagnostic localization.
17.52 Sensory NCS and Plexopathy
Plexus lesions may affect sensory responses depending on:
Therefore sensory abnormalities can help distinguish some plexopathies from radiculopathies.
17.53 Sensory NCS and Temperature
Temperature should be treated as a:
Controlled experimental variable.
If two studies are performed at very different temperatures, their results may not be directly comparable.
17.54 Common Technical Errors
Error 1 — Incorrect distance
Produces incorrect conduction velocity.
Error 2 — Cold limb
Produces slowing.
Error 3 — Poor electrode placement
Reduces amplitude.
Error 4 — Insufficient stimulation
Produces a small response.
Error 5 — Stimulus artefact
Obscures the response.
Error 6 — Electrical noise
Reduces signal-to-noise ratio.
Error 7 — Wrong nerve identification
Produces an invalid study.
17.55 Sensory NCS Quality-Control Sequence
Before interpreting a low or absent SNAP:
Temperature
↓
Electrode placement
↓
Stimulator position
↓
Stimulus intensity
↓
Ground
↓
Filters
↓
Distance
↓
Noise
↓
Repeatability
↓
Interpretation
17.56 SNAP Versus CMAP
|
Feature |
SNAP |
CMAP |
|
Full name |
Sensory Nerve Action Potential |
Compound Muscle Action Potential |
|
Recorded from |
Sensory nerve |
Muscle |
|
Typical amplitude |
µV |
mV |
|
Stimulation |
Sensory nerve |
Motor nerve |
|
Neuromuscular junction involved |
No |
Yes |
|
Common use |
Sensory axon assessment |
Motor axon/motor pathway assessment |
17.57 Sensory NCS Signal Pathway
Stimulator
↓
Sensory axons
↓
Action potential propagation
↓
Recording electrodes
↓
Differential amplifier
↓
Filters
↓
ADC
↓
Digital waveform
↓
Latency + amplitude + duration
↓
Conduction velocity
↓
Clinical interpretation
17.58 Practical Protocol
A simplified sensory NCS protocol is:
Step 1
Identify the nerve.
Step 2
Position the patient comfortably.
Step 3
Warm the limb if required.
Step 4
Prepare the skin.
Step 5
Place recording electrodes.
Step 6
Place ground electrode.
Step 7
Place stimulating electrodes.
Step 8
Measure the distance.
Step 9
Apply a low stimulus.
Step 10
Increase stimulus intensity.
Step 11
Obtain a reproducible SNAP.
Step 12
Measure onset latency.
Step 13
Measure peak latency if required.
Step 14
Measure amplitude.
Step 15
Assess duration and morphology.
Step 16
Calculate conduction velocity when appropriate.
Step 17
Repeat or compare with another nerve when indicated.
17.59 Interpretation Framework
A useful sequence is:
Question 1
Is the response technically valid?
Question 2
Is the limb temperature appropriate?
Question 3
Is the SNAP present?
Question 4
Is the amplitude appropriate?
Question 5
Is latency appropriate?
Question 6
Is conduction velocity appropriate?
Question 7
Is there dispersion?
Question 8
Is the abnormality focal or generalized?
Question 9
Does the pattern fit the clinical anatomy?
17.60 Technical Versus Pathological Abnormality
An abnormal SNAP should not immediately be labelled:
"Peripheral neuropathy."
First determine whether the abnormality could result from:
Only after technical validation should pathology be considered.
17.61 Key Points
1. Sensory NCS records sensory nerve action potentials.
2. SNAPs are usually measured in microvolts.
3. SNAPs are generally much smaller than CMAPs.
4. Orthodromic conduction follows the physiological sensory direction.
5. Antidromic conduction travels in the opposite direction.
6. Antidromic techniques often produce larger responses.
7. Sensory amplitude is influenced by many technical and biological factors.
8. Temperature significantly affects sensory conduction.
9. Accurate distance measurement is essential.
10. Small SNAPs require excellent signal-to-noise conditions.
11. Stimulus artefact can obscure sensory responses.
12. Sensory studies are useful in focal entrapment neuropathies.
13. Distal SNAPs may remain preserved in many radiculopathies.
14. Reduced SNAPs may support lesions distal to the dorsal root ganglion.
15. Axonal sensory neuropathy commonly reduces SNAP amplitude.
16. Demyelinating disorders may produce marked slowing and dispersion.
17. Absent responses must be technically verified.
18. Comparative sensory studies can improve detection of focal abnormalities.
17.62 Review Questions
1. What is a SNAP?
2. Why is a SNAP usually measured in µV?
3. Define orthodromic conduction.
4. Define antidromic conduction.
5. Why can antidromic studies produce larger responses?
6. What is sensory onset latency?
7. What is sensory peak latency?
8. How is sensory conduction velocity calculated?
9. Why is temperature important?
10. What causes a low SNAP amplitude?
11. What causes an absent SNAP?
12. What is temporal dispersion?
13. What is the significance of the dorsal root ganglion?
14. Why can sensory responses remain preserved in radiculopathy?
15. How can comparative sensory studies help in carpal tunnel syndrome?
16. List five technical errors that can produce a falsely abnormal sensory study.
17.63 Practical Exercise
Case 1
A patient has:
Question: What technical factor should be corrected before interpreting the study?
Case 2
A patient has:
Question: Why can the sural SNAP remain normal?
Case 3
A patient has:
Question: Does this pattern suggest a focal lesion or a more generalized sensory process?
17.64 Chapter Summary
Sensory NCS measures the electrical conduction of peripheral sensory axons.
The recorded signal is:
Sensory axon activation
↓
Action-potential propagation
↓
Extracellular electrical field
↓
SNAP
↓
Amplification
↓
Filtering
↓
Digital conversion
↓
Latency + amplitude + duration
↓
Interpretation
Because SNAPs are small, technical quality is particularly important.
The examiner must control:
Temperature + electrode position + stimulation + distance + grounding + noise + instrumentation
before assigning pathological significance to an abnormal sensory response.
The most important anatomical principle is the relationship between the sensory nerve and the dorsal root ganglion, because it helps explain why sensory NCS can be normal in some radiculopathies while abnormal in many peripheral neuropathies and plexopathies.
Absolutely. We will complete Book 1 continuously, keeping the same technical/clinical style and avoiding stopping after every chapter.
Below are the remaining chapters, following Chapter 21.
BOOK 1
NERVE CONDUCTION STUDIES (NCS) AND ELECTROMYOGRAPHY (EMG)
Technical Physics, Instrumentation, Physiology and Clinical Protocols
CHAPTER 22
SENSORY NERVE CONDUCTION STUDIES
22.1 Introduction
Sensory nerve conduction studies evaluate the electrical conduction of peripheral sensory nerves.
Unlike motor NCS, where the response is recorded from muscle as a CMAP, sensory NCS records directly from a sensory nerve as a:
Sensory Nerve Action Potential
SNAP
The basic pathway is:
Electrical stimulus
↓
Sensory axon depolarization
↓
Action potential propagation
↓
Recording electrode
↓
Amplifier
↓
Filtering
↓
Digital waveform
↓
Measurement
22.2 SNAP
The SNAP represents the summed extracellular electrical activity of multiple sensory axons.
It is usually much smaller than the CMAP.
Typical units are:
µV
rather than mV.
22.3 Antidromic and Orthodromic Studies
Antidromic
The stimulus travels opposite to the normal physiological sensory direction.
Orthodromic
The stimulus travels in the normal physiological direction.
Both approaches can be used depending on the nerve and laboratory protocol.
22.4 Sensory Latency
Sensory latency is the interval between:
Stimulus
and:
Onset of the sensory response.
Latency may be measured to:
The laboratory must use a consistent measurement method.
22.5 Sensory Conduction Velocity
For a sufficiently appropriate sensory study:
[
SCV=\frac{Distance}{Latency}
]
For example:
Distance = 140 mm
Latency = 3.0 ms
[
SCV=\frac{140}{3}=46.7,m/s
]
22.6 SNAP Amplitude
SNAP amplitude is strongly influenced by:
A low SNAP may indicate sensory axonal loss, but technical factors must always be excluded.
22.7 Sensory Nerve Action Potential Shape
Important features include:
22.8 Temperature
Cold limbs can produce:
Therefore temperature control is particularly important for sensory studies.
22.9 Sensory NCS in Polyneuropathy
A length-dependent peripheral neuropathy may produce:
Reduced or absent distal SNAPs
especially in the lower limbs.
The pattern can help distinguish:
22.10 Sensory NCS in Radiculopathy
A key principle is:
Sensory nerve cell bodies are located in the dorsal root ganglion.
Many root lesions occur proximal to the dorsal root ganglion.
Therefore SNAPs may remain relatively preserved in radiculopathy.
This makes sensory NCS particularly useful in distinguishing:
Radiculopathy
from:
Distal peripheral neuropathy.
22.11 Entrapment Neuropathy
Sensory NCS is highly useful in focal entrapment neuropathies.
Examples:
Comparison studies can increase diagnostic sensitivity.
22.12 Side-to-Side Comparison
When appropriate:
Right nerve
versus:
Left nerve
may be compared.
This is useful when absolute reference ranges overlap.
22.13 Sensory NCS Quality Checklist
☐ Limb warm
☐ Correct nerve identified
☐ Accurate distance
☐ Appropriate electrode placement
☐ Adequate skin preparation
☐ Low noise
☐ Reproducible waveform
☐ Appropriate filters
☐ Correct latency measurement
☐ Correct amplitude measurement
CHAPTER 23
F-WAVES, H-REFLEX AND LATE RESPONSES
23.1 Introduction
Late responses provide additional information about motor nerve conduction beyond conventional distal and proximal stimulation.
The major late responses are:
23.2 F-Wave
The F-wave is generated after supramaximal distal motor nerve stimulation.
The stimulus travels:
Antidromically
toward the spinal cord.
A small proportion of motor neurons respond by backfiring.
The impulse then travels:
Orthodromically
back toward the muscle.
23.3 F-Wave Pathway
Distal stimulation
↓
Motor axon
↓
Spinal motor neuron
↓
Backfiring
↓
Motor axon
↓
Muscle
↓
F-wave
23.4 F-Wave Latency
F-wave latency reflects conduction through a long motor pathway.
It is influenced by:
23.5 F-Wave Persistence
Not every stimulus produces an F-wave.
Therefore multiple stimuli are commonly delivered.
Persistence refers to:
The proportion of stimuli producing identifiable F-waves.
23.6 F-Wave Chronodispersion
Different motor neurons may produce F-waves at different latencies.
The spread between the earliest and latest responses is:
Chronodispersion.
Increased dispersion can occur with conduction abnormalities.
23.7 H-Reflex
The H-reflex is an electrically evoked reflex response.
It is analogous to a simplified:
Monosynaptic spinal reflex.
The stimulus preferentially activates sensory afferents.
The signal travels:
Sensory nerve
↓
Spinal cord
↓
Motor neuron
↓
Motor nerve
↓
Muscle
23.8 H-Reflex Pathway
Ia sensory afferent
↓
Spinal cord
↓
α-motor neuron
↓
Motor axon
↓
Muscle
↓
H-reflex
23.9 Clinical Use
The H-reflex can be useful in selected conditions involving:
It is commonly recorded from the soleus using tibial nerve stimulation.
23.10 Limitations
H-reflex interpretation depends on:
It should not be interpreted in isolation.
CHAPTER 24
NERVE CONDUCTION IN COMMON PERIPHERAL NERVES
24.1 Introduction
A competent electrodiagnostic practitioner must understand the anatomy of major peripheral nerves.
The major nerves commonly examined include:
24.2 Median Nerve
Important clinical application:
Median neuropathy at the wrist.
Motor studies commonly record from:
Thenar muscles.
Sensory studies may assess:
24.3 Ulnar Nerve
Important clinical application:
Ulnar neuropathy at the elbow.
Motor stimulation may include:
Recording is commonly performed from an ulnar-innervated hand muscle.
24.4 Radial Nerve
Radial sensory studies can evaluate:
Superficial radial sensory conduction.
Motor studies may assess radial-innervated muscles depending on the clinical question.
24.5 Sural Nerve
The sural nerve is a sensory nerve.
It is particularly useful in evaluating:
Length-dependent peripheral neuropathy.
Absent or reduced sural responses may be an important abnormal finding.
24.6 Peroneal Nerve
Motor studies can assess:
Common peroneal nerve function.
Recording is often obtained from an anterior leg or foot muscle depending on protocol.
24.7 Tibial Nerve
The tibial nerve is evaluated by recording from an appropriate plantar-flexor muscle.
It is useful in:
24.8 Comparative Studies
Comparison between nerves can improve sensitivity.
Examples:
CHAPTER 25
ELECTRODIAGNOSTIC LOCALIZATION
25.1 Introduction
The ultimate purpose of NCS/EMG is not simply to produce numbers.
It is to determine:
Where is the lesion?
Possible levels include:
1. Root
2. Plexus
3. Peripheral nerve
4. Neuromuscular junction
5. Muscle
6. Motor neuron
25.2 Root Lesion
A radiculopathy affects:
Spinal nerve root.
Typical electrodiagnostic clues may include:
25.3 Plexopathy
A plexopathy affects:
Brachial or lumbosacral plexus.
Findings may involve:
Localization requires careful anatomical analysis.
25.4 Mononeuropathy
A mononeuropathy affects:
One peripheral nerve.
Findings should follow the anatomical distribution of that nerve.
25.5 Polyneuropathy
A polyneuropathy affects:
Multiple peripheral nerves.
A common pattern is:
Length dependence.
The longest nerves are often affected first.
25.6 Motor Neuron Disorder
Motor neuron disorders primarily involve:
Motor neurons and their axons.
NCS may show reduced CMAPs, while needle EMG may demonstrate widespread:
Clinical correlation is essential.
CHAPTER 26
NEEDLE EMG: QUANTITATIVE MUAP ANALYSIS AND RECRUITMENT
26.1 Introduction
Needle EMG provides information about:
26.2 MUAP Parameters
The principal parameters are:
Amplitude
Duration
Number of phases
Turns
Area
Recruitment
26.3 MUAP Amplitude
Large MUAPs may occur when:
Motor units become enlarged through collateral reinnervation.
Small MUAPs may occur when:
Individual motor units contain fewer muscle fibres.
26.4 MUAP Duration
Long duration may reflect:
Increased temporal dispersion
among fibres belonging to a motor unit.
Short duration is often associated with:
Myopathic motor units.
26.5 Polyphasia
Polyphasia means an increased number of phases.
It may occur during:
Reinnervation.
It can also occur in:
Myopathy.
Therefore it must be interpreted with other parameters.
26.6 Recruitment
Recruitment is the progressive activation of motor units with increasing force.
Weak contraction
Few motor units.
Moderate contraction
More motor units.
Strong contraction
Many motor units.
26.7 Interference Pattern
At maximal voluntary contraction, many motor units fire simultaneously.
The waveform becomes:
Dense and complex.
This is the:
Interference pattern.
26.8 Reduced Interference Pattern
Reduced recruitment produces:
Less dense interference.
The remaining units may fire at high frequency.
26.9 Early Recruitment
Myopathic muscle units may generate less force.
Therefore many motor units are recruited early.
This produces:
Early recruitment.
CHAPTER 27
NEUROGENIC AND MYOPATHIC EMG PATTERNS
27.1 Neurogenic Pattern
Typical findings include:
27.2 Chronic Neurogenic Process
A typical sequence is:
Axonal loss
↓
Denervation
↓
Collateral sprouting
↓
Reinnervation
↓
Large motor unit
↓
Large/long-duration MUAP
↓
Reduced recruitment
27.3 Myopathic Pattern
Typical findings may include:
27.4 Active Myopathy
Some inflammatory or necrotizing muscle disorders may produce:
27.5 Chronic Myopathy
Chronic myopathy may demonstrate:
27.6 Important Principle
There is no single EMG finding that independently establishes:
Neuropathy
or:
Myopathy.
Diagnosis requires:
Pattern + distribution + clinical context + NCS + EMG.
CHAPTER 28
ELECTRODIAGNOSTIC APPROACH TO COMMON DISORDERS
28.1 Carpal Tunnel Syndrome
Carpal tunnel syndrome is:
Median neuropathy at the wrist.
Important electrodiagnostic features may include:
28.2 Ulnar Neuropathy at the Elbow
Possible findings:
The study should use accurately measured distances.
28.3 Polyneuropathy
Possible findings:
The pattern determines whether the process appears predominantly:
Axonal
or:
Demyelinating.
28.4 Radiculopathy
Possible findings:
NCS may be relatively normal in some radiculopathies.
28.5 Peroneal Neuropathy
May produce:
28.6 Motor Neuron Disease
Potential findings include:
The diagnosis remains clinical and requires appropriate criteria.
CHAPTER 29
NEUROMUSCULAR JUNCTION AND REPETITIVE NERVE STIMULATION
29.1 Introduction
Routine NCS and EMG assess nerve and muscle function.
Repetitive nerve stimulation:
RNS
evaluates transmission across the:
Neuromuscular junction.
29.2 Basic Principle
A nerve is stimulated repeatedly.
The muscle response is measured after each stimulus.
The examiner assesses:
Change in CMAP amplitude or area.
29.3 Low-Frequency Stimulation
Low-frequency stimulation may demonstrate:
Decrement
in certain neuromuscular-junction disorders.
29.4 High-Frequency Stimulation
Higher-frequency stimulation can reveal:
Increment
in some presynaptic disorders.
29.5 Decrement
A progressive reduction in CMAP response after repetitive stimulation may indicate impaired:
Neuromuscular transmission.
29.6 Increment
An increase in CMAP amplitude following activation or high-frequency stimulation can occur when presynaptic neurotransmitter release is enhanced.
29.7 Technical Requirements
RNS is highly technique-dependent.
Important variables include:
CHAPTER 30
SAFETY, QUALITY ASSURANCE AND STANDARDIZATION
30.1 Introduction
High-quality electrodiagnostic medicine requires more than correct interpretation.
It requires:
Patient safety
Technical accuracy
Reproducibility
Documentation
Quality assurance
30.2 Patient Identification
Before testing:
☐ Confirm patient identity
☐ Confirm clinical indication
☐ Confirm requested nerves/muscles
☐ Explain procedure
☐ Obtain appropriate consent
30.3 Infection Prevention
Follow:
30.4 Equipment Maintenance
Equipment should undergo:
30.5 Temperature Standardization
Document limb temperature where relevant.
If temperature is inadequate:
Warm the limb
and:
Repeat the study.
30.6 Reference Values
Reference values should be:
30.7 Documentation
A complete report should document:
Patient information
Clinical indication
NCS results
EMG findings
Temperature where relevant
Technical limitations
Interpretation
Impression
CHAPTER 31
REPORTING NCS AND EMG
31.1 Introduction
A good electrodiagnostic report should be:
Accurate
Structured
Concise
Clinically meaningful.
31.2 NCS Table
A useful NCS table may contain:
|
Nerve |
Recording site |
Latency |
Amplitude |
Distance |
Velocity |
|
Median |
Thenar |
— |
— |
— |
— |
|
Ulnar |
Hypothenar |
— |
— |
— |
— |
|
Peroneal |
Foot |
— |
— |
— |
— |
|
Tibial |
Foot |
— |
— |
— |
— |
|
Sural |
Ankle |
— |
— |
— |
— |
31.3 Needle EMG Table
|
Muscle |
Insertion |
Fib/PSW |
Fasciculation |
MUAP |
Recruitment |
|
Muscle 1 |
Normal |
None |
None |
Normal |
Normal |
|
Muscle 2 |
Increased |
+ |
None |
Large |
Reduced |
|
Muscle 3 |
Normal |
None |
None |
Small |
Early |
31.4 Interpretation
The interpretation should answer:
Is the study normal?
If abnormal:
What physiological process is present?
Where is it localized?
Is it acute, chronic, or mixed?
What is the most likely electrodiagnostic diagnosis?
31.5 Example Impression
Abnormal study.
The findings are consistent with a predominantly length-dependent sensorimotor axonal polyneuropathy. There is no convincing electrodiagnostic evidence of a focal median neuropathy at the wrist or an active lumbosacral radiculopathy on the muscles sampled.
CHAPTER 32
TROUBLESHOOTING AND ARTEFACT RECOGNITION
32.1 Introduction
Artefact is one of the most important causes of incorrect electrodiagnostic interpretation.
The examiner must recognize:
Electrical artefact
Movement artefact
Stimulus artefact
Electrode artefact
Physiological contamination
32.2 Electrical Artefact
Typical appearance:
Regular repetitive interference.
Common causes:
32.3 Movement Artefact
Typical appearance:
Large baseline shifts.
Cause:
32.4 Stimulus Artefact
Usually occurs immediately after stimulation.
It may obscure:
Very early responses.
32.5 Poor Electrode Contact
May cause:
Solution:
Reposition and improve contact.
32.6 Needle Artefact
Needle movement can produce large electrical potentials.
The examiner should distinguish:
Movement-induced activity
from:
Persistent spontaneous activity.
CHAPTER 33
ADVANCED ELECTRODIAGNOSTIC PHYSICS
33.1 Bioelectric Field
A depolarizing nerve or muscle fibre creates a changing electrical field in surrounding tissue.
The electrode detects the voltage difference generated by this field.
33.2 Volume Conduction
Electrical signals spread through biological tissues.
This is called:
Volume conduction.
Therefore an electrode can detect activity:
Some distance away
from its exact source.
33.3 Distance and Amplitude
As the recording electrode moves farther from the active source:
Signal amplitude generally decreases.
This explains why electrode placement is critical.
33.4 Differential Recording
The recording system measures:
[
V_{active}-V_{reference}
]
This reduces common signals and emphasizes local differences.
33.5 Spatial Cancellation
If electrical activity reaches the active and reference electrodes similarly, the differential signal may become small.
This can cause:
Apparent low amplitude.
Therefore electrode geometry matters.
33.6 Temporal Summation
A compound response is created by summation of many individual fibre responses.
If the fibres activate simultaneously:
Large narrow waveform.
If activation becomes asynchronous:
Broader waveform.
This principle explains temporal dispersion.
33.7 Phase Cancellation
When individual fibre action potentials occur at different times, positive and negative components can partially cancel.
This can reduce:
Peak amplitude.
Thus amplitude reduction does not always equal axonal loss.
CHAPTER 34
INTEGRATED ELECTRODIAGNOSTIC PROTOCOL
34.1 Step 1 — Clinical Question
Determine:
What are we trying to diagnose?
Examples:
34.2 Step 2 — Neurological Examination
Assess:
34.3 Step 3 — Select NCS
Select:
Motor nerves
Sensory nerves
Late responses
according to the clinical question.
34.4 Step 4 — Technical Validation
Check:
34.5 Step 5 — Needle EMG
Select muscles based on:
Root
Peripheral nerve
Plexus
Muscle
distribution.
34.6 Step 6 — Analyze the Pattern
Determine:
Neurogenic?
Myopathic?
Demyelinating?
Axonal?
Focal?
Generalized?
34.7 Step 7 — Localize
Determine the most likely level:
Root
↓
Plexus
↓
Peripheral nerve
↓
Neuromuscular junction
↓
Muscle
↓
Motor neuron
34.8 Step 8 — Integrate
Combine:
History
Examination
NCS
EMG
=
Electrodiagnostic conclusion
CHAPTER 35
REFERENCE DATA, NORMAL VARIATION AND INTERPRETATION
35.1 Normal Does Not Mean Identical
Normal nerve conduction values vary with:
35.2 Age
With increasing age:
Age-specific reference values are therefore important.
35.3 Height
Taller individuals have longer peripheral nerves.
This can influence:
35.4 Temperature
Cold temperature can produce substantial changes.
Therefore a study performed on a cold limb may appear:
Abnormally slow.
35.5 Laboratory-Specific Norms
Each laboratory should establish or validate appropriate reference values.
Published reference ranges should not be transferred blindly between laboratories.
35.6 Borderline Values
A borderline abnormal value should be interpreted with:
CHAPTER 36
FINAL INTEGRATED REVIEW
36.1 The Complete Electrodiagnostic Concept
NCS and EMG combine:
Anatomy
Physiology
Physics
Electronics
Signal processing
Clinical medicine.
36.2 The Complete NCS Pathway
Stimulus
↓
Peripheral nerve
↓
Action potential
↓
Target
↓
Response
↓
Electrode
↓
Amplifier
↓
Filter
↓
ADC
↓
Measurement
↓
Interpretation
36.3 The Complete EMG Pathway
Motor neuron
↓
Axon
↓
Neuromuscular junction
↓
Muscle fibre
↓
Extracellular electrical field
↓
Needle electrode
↓
Amplifier
↓
Filter
↓
ADC
↓
MUAP
↓
Recruitment
↓
Localization
36.4 The Five Major Electrodiagnostic Questions
Every study should ultimately answer:
1. Is the study technically adequate?
2. Is there an abnormality?
3. Is the process axonal, demyelinating, myopathic or another physiological pattern?
4. Where is the lesion?
5. Does the electrodiagnostic pattern fit the clinical presentation?
36.5 MASTER ELECTRODIAGNOSTIC ALGORITHM
Patient with neurological symptoms
↓
Clinical history
↓
Neurological examination
↓
Define anatomical hypothesis
↓
Select NCS
↓
Sensory NCS
Motor NCS
Late responses
↓
Validate technical quality
↓
Select muscles for EMG
↓
Needle insertion
↓
Resting activity
↓
Spontaneous activity
↓
MUAP morphology
↓
Recruitment
↓
Distribution
↓
Localization
↓
Physiological classification
↓
Clinical correlation
↓
FINAL ELECTRODIAGNOSTIC IMPRESSION
36.6 Final Practical Checklist
Before signing an NCS/EMG report:
☐ Correct patient
☐ Correct clinical question
☐ Appropriate nerves tested
☐ Appropriate muscles tested
☐ Limb temperature considered
☐ Distances accurate
☐ Supramaximal stimulation achieved
☐ Electrodes correctly positioned
☐ Waveforms reproducible
☐ Artefact excluded
☐ NCS interpreted
☐ EMG interpreted
☐ Distribution considered
☐ Localization considered
☐ Acute/chronic features considered
☐ Technical limitations documented
☐ Clinical correlation performed
☐ Final impression clearly stated
36.7 FINAL SUMMARY OF BOOK
Nerve conduction studies and electromyography are complementary components of electrodiagnostic medicine.
NCS primarily evaluates:
Needle EMG evaluates:
Physics provides:
Anatomy provides:
Clinical medicine provides:
Interictal electroencephalography (EEG) is an essential tool for detecting nonepileptiform neurophysiological dysfunction. While neuroimaging provides structural detail, EEG reveals functional abnormalities — even when imaging is normal. Nonepileptiform EEG abnormalities often correlate with the degree of cerebral dysfunction and can track clinical improvement or deterioration over time.
EEG abnormalities may be focal or diffuse, reflecting localized or generalized disturbances. Although these abnormalities lack specificity for underlying etiology, they provide valuable diagnostic, monitoring, and prognostic information.
Nonepileptiform EEG abnormalities are grouped into: - Focal abnormalities - Diffuse abnormalities
Each category highlights distinct patterns of dysfunction involving white matter, gray matter, or both.
Focal EEG abnormalities represent localized cerebral dysfunction. These abnormalities may arise from: - Structural lesions (tumor, ischemia, hemorrhage, trauma, infection) - Postictal states - Transient physiological disturbances
· Persistence
· Poor reactivity to stimuli
· Morphological distortion
· Concomitant loss of faster frequencies
Alpha asymmetry indicates hemispheric dysfunction. - A persistent asymmetry >1 Hz in posterior dominant rhythm is abnormal. - Amplitude asymmetry >50% is significant.
Alpha asymmetry (slower over the right hemisphere) in a patient with an acute right fronto-parietal ischemic infarction.
Figure 10A – Alpha asymmetry with right hemisphere slowing.
Right hemisphere suppression in a patient with a right hemisphere intracerebral hemorrhage. Note the dramatic difference in amplitude at standard sensitivity settings of 7 uV/mm
Figure 10B – Right hemisphere suppression due to intracerebral hemorrhage.
Focal delta activity restricted to one or two electrodes suggests localized white matter dysfunction. - Heightened significance when faster frequencies are absent. - Persistent focal delta strongly correlates with structural lesions.
Diagram Placeholder: Figure 11A – Right temporal delta slowing in ganglioglioma.
Diagram Placeholder: Figure 11B – Intracranial EEG showing focal delta.
TIRDA consists of rhythmic bursts of delta activity localized to temporal lobes. - Strongly associated with temporal lobe epilepsy. - Often occurs alongside epileptiform discharges.
Diagram Placeholder: Figure 12 – Left temporal TIRDA.
This pattern is less predictive of structural pathology compared to continuous slowing. - Suggests mild or transient cerebral dysfunction.
Diagram Placeholder: Figure 13 – Polymorphic delta in left temporal–parietal region.
This pattern has high correlation with underlying structural lesions. - Seen in stroke, tumors, trauma, hemorrhage, and infection. - May resolve if pathology is transient (e.g., transient ischemic attack).
Diagram Placeholder: Figure 14A – Left hemispheric delta slowing in ischemic infarct.
Diagram Placeholder: Figure 14B – Reversible regional slowing in transient aphasia.
Delta frequencies 3.5 Hz with variable morphology. - Indicates supratentorial lesion affecting ipsilateral white matter. - Persistence increases likelihood of structural lesions. - May also appear transiently (TIA, migraine, postictal states, head injury).
Diagram Placeholder: Figure 15A – Right hemisphere polymorphic delta in infarct.
Diagram Placeholder: Figure 15B – Drug-induced slowing during Wada test.
Normal sleep spindles are synchronous by age 2. - Persistent unilateral reduction or slowing indicates thalamocortical dysfunction.
Clinical Example: Right thalamic glioma.
Diagram Placeholder: Figure 16 – Asymmetric sleep spindles.
This pattern may assist in diagnosing orthostatic tremor. - Frequency range: 14–24 Hz. - Maximal at Cz. - Correlates with EMG tremor activity.
Diagram Placeholder: Figure 17 – Midline fast rhythm in orthostatic tremor.
(Content will expand once diffuse abnormality section from slides is added.)
Diffuse abnormalities often indicate generalized encephalopathy and may reflect: - Metabolic disorders - Hypoxic injury - Drug toxicity - Systemic illness affecting cerebral function
Nonepileptiform abnormalities help clinicians: - Monitor progress of encephalopathy - Identify lateralization of dysfunction - Differentiate transient vs structural causes - Evaluate postictal states - Support diagnosis when neuroimaging is normal
Nonepileptiform EEG abnormalities offer critical insights into cerebral dysfunction, aiding diagnosis and management in both acute and chronic neurological conditions. Although nonspecific, their patterns provide valuable localization, prognostic, and monitoring information.
Diagrams referenced in this chapter correspond to the user’s PowerPoint file: Abnormal Nonepileptiform EEG fileciteturn0file0.
They can be inserted during book formatting at the specified placeholders above.
Neurophysiology is the scientific study of the functional properties of the nervous system, encompassing cellular, molecular, and systemic mechanisms that underpin neuronal signaling and information processing. It integrates principles of electrophysiology, biophysics, neurochemistry, and systems biology to explain how neural circuits generate behavior, control homeostasis, and respond to environmental stimuli.
At the cellular level, neurophysiology focuses on the electrochemical dynamics of neurons and glia, particularly ion channel function, membrane potentials, and synaptic transmission. Key processes include the generation and propagation of action potentials, excitatory and inhibitory postsynaptic potentials, and neurotransmitter release and receptor activation. These phenomena are crucial in determining neuronal excitability and network behavior.
At the systems level, neurophysiology explores sensory and motor integration, autonomic regulation, cortical processing, rhythmic activity (e.g., circadian rhythms, oscillations), and plasticity mechanisms such as long-term potentiation (LTP) and long-term depression (LTD), which form the basis of learning and memory.
Furthermore, the discipline is central to understanding the pathophysiology of neurological diseases. Aberrant neurophysiological processes underlie disorders such as epilepsy (hyperexcitability and hypersynchrony), Parkinson’s disease (dopaminergic system dysfunction and altered basal ganglia circuitry), and neuropathic pain (abnormal peripheral and central sensitization).
RESTING POTENTIAL
ACTION POTENTIAL
:watermark(/images/watermark_5000_10percent.png,0,0,0):watermark(/images/logo_url.png,-10,-10,0):format(jpeg)/images/overview_image/4380/IZEhSJ2GrTZVmXEU8IAkcA_P19_action_potential_membrane_CSR_en.jpg){kind=logo}
SYNAPTIC TRANSIMITION REFLEX ARC Motor and Sensory Homunculus EEG WAVES
Health Africa is a tight-knit community of scientific, medical, and life sciences experts that produce and share the latest information, in a readable, understandable way. Also join our social nework group Health Africa Conference for convenient communication.
For All Enquiries Contact Us
Register an account today and get great deals, offers and customised products only for you.
Specialist Consultant
Is there anything I can help you with?.
00:00Customer Support
Is there anything I can help you with?.
00:00