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Nerve conduction studies

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 clinical

Nerve conduction
William Huynh
Matthew C Kiernan studies
This article forms part of our ‘Tests and results’ series for 2011 which aims to provide information In addition to these diagnostic and monitoring
about common tests that general practitioners order regularly. It considers areas such as indications,
roles, clinical neurophysiology may provide
what to tell the patient, what the test can and cannot tell you, and interpretation of results.
information about prognosis and can guide
management.
Keywords: nerve conduction studies; electrodiagnosis; electromyography; peripheral Precautions
neuropathy; nerve disorders
Cardiac pacemakers or defibrillators are not an
absolute contraindication but discussion with the
patient’s cardiologist is advisable, particularly if
Nerve conduction studies (NCS) and needle the stimulation site is in close proximity to the
electromyography (EMG) are collectively chest wall. Studies have demonstrated the safety
termed ‘clinical neurophysiology’. They of routine NCS in patients with implanted cardiac
enable the clinician to detect signs that devices.1
cannot be confirmed by neurological As EMG involves insertion of fine needles,
examination alone and can guide diagnosis care is also required for patients prescribed
and treatment. anticoagulation therapy (eg. warfarin) to avoid the
development of haematoma.
Indications
Clinical neurophysiology aids diagnosis of disorders
Patient information and
preparation
of the peripheral nervous system (Table 1). Testing
helps to: Nerve conduction studies involve the stimulation
• localise the site or level of the lesion; of nerves with small electrical impulses over
determining if the pathology involves the several points (usually limbs) and measuring the
peripheral nerve, neuromuscular junction, resultant responses. Surface electrodes are used
plexus, nerve root or anterior horn cells to both deliver and detect the electrical impulses
• identify the pathophysiology, in particular (Figure 1). The test is safe and well tolerated
distinguishing axonal loss from demyelination with only minor discomfort and no long term side
• diagnose mononeuropathies (eg. common nerve effects. Most patients describe the effects as a
entrapments such as carpal tunnel syndrome, ‘tingling’ or ‘tapping’ sensation.
ulnar neuropathy at the elbow and peroneal Patients should avoid prior application of topical
palsy) creams as these may increase skin resistance
• diagnose more diffuse processes (eg. to the applied current, and therefore require
generalised peripheral neuropathy due to stronger levels of electrical stimulation. In cold
diabetes or inflammatory neuropathy such as environments, the limbs may need warming as cool
Guillain-Barré syndrome). peripheries (<32°C) slow the conduction velocity
Nerve conduction studies are also used to of nerves. No fasting is required and patients
monitor nerve function over time to determine can return to normal activities such as driving
disease progression, to assess the complications immediately afterwards. Patients may continue to
of treatment (eg. chemotherapy), as well as take all their regularly prescribed medications.
identifying the disease course (acute/subacute/ Nerve conduction studies are performed
chronic). by clinical neurophysiologists, usually in an

Reprinted from Australian Family Physician Vol. 40, No. 9, SEPTEMBER 2011 693
clinical Nerve conduction studies

Table 1. Common conditions referred to clinical neurophysiology

Level of lesion(s) Common disorder Common presenting symptoms
Peripheral nerve Carpal tunnel syndrome Sensory disturbance of hands and fingers with
entrapment syndromes nocturnal exacerbation
Ulnar neuropathy at elbow Sensory disturbance of digits four/five; weakness and
wasting of intrinsic hand muscles
Peroneal palsy at fibular neck Foot drop
Polyneuropathy • Metabolic (eg. diabetes) Length dependent sensory and/or motor impairment
• Toxic (eg. alcohol)
• Medications (eg. chemotherapy)
• Hereditary
Plexus Brachial plexus Unilateral shoulder pain with sensory disturbance and
(eg. brachial neuritis) weakness in upper limb
Nerve root Cervical radiculopathy Neck and upper limb pain; sensory disturbance and
weakness in arm/hand/fingers
Lumbosacral radiculopathy Lower back pain; sciatica type symptoms and weakness
in lower limb
Anterior horn cell Motor neuron disease (amyotrophic Progressive limb weakness; bulbar weakness; muscle
(‘neuronopathy’) lateral sclerosis) fasciculations
Neuromuscular junction Myasthenia gravis Fatiguable proximal weakness; diplopia; bulbar
weakness
Muscle Inflammatory myopathies (eg. Proximal muscle weakness and myalgia; elevated serum
polymyositis) creatine kinase

outpatient rooms setting. Typically, NCS take

between 15 minutes and an hour, depending on
the number of sites requiring testing and the
complexity of the clinical presentation.
A Medicare rebate is available for the study
and varies depending on the complexity of the
study and the number of nerves examined.
Conduction = distance (elbow-wrist)
Principles of nerve conduction velocity latency (elbow) – latency (wrist)
studies
250 mm
Sensory, motor or mixed nerves can be studied. Eg. CV = = 55.6 m/s
7.5 ms –3 ms
Pairs of electrodes are used – one to initiate the
impulse and the other to record the response
Peak
Amplitude

further along the path of the nerve (distally 5 mV

within the innervated muscle for motor nerves 3 ms

Duration
or proximally along sensory nerves). For motor Wrist
Onset Figure 1. Motor conduction study of the
nerves, a depolarising square wave current is latency
median nerve with recording electrodes
applied to the peripheral nerve to produce a
over the abductor pollicis brevis muscle
compound muscle action potential (CMAP) due and resultant CMAP responses following
Elbow
to summation of the activated muscle fibres. stimulation of the nerve at the wrist and elbow
In sensory nerves, a propagated sensory nerve
action potential (SNAP) is created in a similar • latency (ms) – from stimulus to onset of conduction, and is reduced in demyelinating
manner. evoked response processes).
The parameters obtained and used for • duration of response (ms)
interpretation include (Figure 1): • conduction velocity (m/s) – calculated from the
Late responses
• amplitude – from baseline to peak (reflects the distance between stimulation and recording Late responses can be used to assess more
number of conducting fibres and is reduced in points, divided by latency (reflects integrity proximal segments of the peripheral nervous
axonal loss) of the myelin sheath important for impulse system, such as the plexus and nerve roots.

694 Reprinted from Australian Family Physician Vol. 40, No. 9, SEPTEMBER 2011
 Nerve conduction studies clinical

a proportion of motor neurons, resulting in a area/amplitude of at least 50% at a proximal

2 mV
delayed and smaller muscle response as the compared to a distal site of stimulation).
5 ms impulse travels back down the motor nerve. Conventional NCS may be unremarkable in the
Wrist
The H reflex, which is elicited by submaximal case of demyelinating diseases involving the more
stimuli, is the electrical equivalent of a tendon proximal segments (eg. Gillain-Barré syndrome),
jerk (or monosynaptic stretch reflex) and involves in which case, prolongation of the F wave and H
stimulation of a sensory axon to produce a reflex latencies may be the only abnormality.
delayed motor response. Amplitude is less
Electromyography
relevant for late responses – useful parameters
Elbow of F waves and H reflexes are their presence and Electromyography is typically undertaken in
minimal latencies. conjunction with NCS when more specific
Figure 2. Median nerve CMAP recorded information is required. Electromyography is
over abductor pollis brevis demonstrating Interpretation most commonly used to investigate weakness
temporal dispersion when stimulating at the
wrist (top) and elbow (bottom) When interpreting NCS data, initial considerations and helps distinguish myopathic from neurogenic
are: causes. Fine needles are inserted into muscle
• Is the compound potential normal in size and fibres and then the patient is asked to contract
These proximal segments are not accessible shape, or reduced? these muscles. Electromyography enables
by routine NCS techniques and is not possible • Is the conduction velocity normal? assessment of the morphology of single motor
to position the electrodes in close proximity to Table 2 outlines key differences between units (neuron, axon and innervated muscle fibres)
the spinal cord or its nearby structures. This is NCS results in axonal loss and demyelinating and the recruitment pattern of these units.
important as proximal segments may be the only processes. As a simple rule, axonal degeneration Changes in EMG morphology reflect changes in
site of pathology, for example, in radiculopathy leads to a loss of amplitude and demyelination the number and size of muscle fibres innervated
due to disc protrusion or in polyradiculopathy leads to prolonged conduction time. by single motor axons. Neurogenic lesions
from Guillain-Barré syndrome. Late responses typically demonstrate polyphasic large motor
Axonal loss
also provide information about longer nerve units with a reduced recruitment pattern, while
pathways so may detect some conduction The most common abnormality is reduction in myopathic motor units are small and polyphasic
abnormalities that would not be identified on compound amplitude reflecting fewer functioning with early recruitment. Electromyography
the shorter NCS range, particularly in diffuse axons. With myelin relatively intact, the also enables the pattern of abnormality to be
or multisegmental disease processes. The late remaining axons conduct normally with normal determined to assist in diagnosis and localisation
responses occur approximately 20–35 ms and latencies and conduction velocities. However, as of a lesion. The stage of the neurogenic lesion
45–60 ms after stimulation in the upper and axonal degeneration progresses, latencies can (acute, subacute or chronic) as well as its
lower limbs respectively, and include the F be mildly prolonged and conduction velocities recovery, may also be assessed.
waves (‘F’ for foot, the original recording site) slightly slowed because of loss of larger, fast Common indications that may necessitate
and H reflexes (named after Hoffman who first conducting fibres. EMG include: to diagnose myopathies, to
described the reflex). F waves result from the differentiate between radiculopathy and
Demyelination
backfiring of activated motor neurons when a peripheral nerve lesions, to localise the level of
supramaximal stimulus is applied at a point along Loss of myelin slows conduction which manifests peripheral nerve or root lesions, and to detect
the motor nerve. Essentially the impulse travels as significant reduction in conduction velocities widespread denervation that would be present
proximally up the motor axon from the site of and temporal dispersion (increase in the duration). in motor neuronopathies such as motor neuron
initiation to the spinal cord. Here it activates Conduction block can also occur (a reduction of disease.

Table 2. Nerve conduction parameters observed in axonal degeneration or demyelination

Axonal degeneration Demyelination

Sensory or motor amplitudes Small or absent Normal or slightly reduced
Distal latencies Normal Prolonged
Conduction velocities Normal or slightly reduced Significantly reduced
F wave latencies Normal or slightly prolonged Significantly prolonged or absent
H reflex latencies Normal or slightly prolonged Significantly prolonged or absent
Conduction block/temporal dispersion Not present Present

Reprinted from Australian Family Physician Vol. 40, No. 9, SEPTEMBER 2011 695
clinical Nerve conduction studies

Limitations, pitfalls and Sensory

interpretation issues Nerve/sites Rec. site Amp. Reference Velocity Reference
• NCS test large myelinated fibres (µV) range (m/s) range
corresponding to the sensory modalities of (mean±SD)
fine touch, vibration and proprioception. Small L sural
fibre neuropathies that present with pain may Calf Lateral malleolus 23 19±7 40.8 >40
therefore have normal sensory studies. Other R sural
diagnostic tests such as quantitative sensory Calf Lateral malleolus 24 19±7 41 >40
and autonomic testing may be required R radial (superficial)
• Anomalous innervation, such as Martin-Gruber Snuff box Forearm Absent 48±15 >50
anastomosis in the upper limb, may complicate
Sensory studies were normal in the lower limbs but absent in the upper limbs. This
nerve conduction studies and its interpretation ‘sural sparing’ pattern may typically be observed with acquired immune mediated
• Early in the course of disease (eg. Guillain- neuropathies.
Barré syndrome or carpal tunnel syndrome), Motor NCS
changes may be relatively subtle and therefore
Nerve/sites Latency Reference Ampl. Reference Velocity Reference
missed. A repeat study may be required at a (ms) range (mV) range (m/s) range
later time to confirm the diagnosis (mean±SD)
• Late responses provide some information L tibial malleolus – AH
about proximal segments of the peripheral Ankle 6.80 <6 max 3.6 11.6±4.3
nervous system, however, NCS may still Popliteal 19.15 2.9 30.4 >40
miss disorders that only affect nerve roots or fossa
plexus. EMG may be useful in this situation R median – APB
Wrist 8.05 <3.5 3.6 9.5±2.7
• Reference values for comparison are
Elbow 16.10 3.4 24.8 >50
derived from studies of neurologically
‘normal’ subjects frequently reported as Motor studies demonstrated prolongation in the distal latencies (red) and reduction in
95% confidence limits. For this reason, the the conduction velocities (blue), with only mild reduction in CMAP amplitudes. This
neurophysiologist may need to assess a is typical of a demyelinating process. The motor responses demonstrated temporal
number of parameters together with the dispersion in the morphology of the potential (Figure 2 compared to the normal
waveform in Figure 1). This is another hallmark of demyelination, where fibres conduct
relevant clinical information when interpreting
at different speeds due to myelin loss.
the results
F waves
• Nerve conduction varies across different age
Nerve Min. F latency Reference Persist (%)
groups. This is particularly important when
(ms) range
interpreting sural sensory responses in an
(mean±SD)
older age group (>65 years) or paediatric
L tibial – AH 81.85 52.3±4.3 100
patients where reference values are not well
R median – APB 67.05 29.1±2.3 20
defined
• As NCS results are highly context specific,
F waves in the upper and lower limbs were markedly prolonged in latency (green),
tests ordered with a clear indication and suggesting a demyelinating process affecting the more proximal segments of the
specific clinical question will yield more useful nerves. The reduced F wave persistence in the upper limbs (20%) suggested that only
information. some of the responses were getting through indicating the presence of conduction
block more proximally.
Case study Needle EMG demonstrated widespread acute and chronic neurogenic features in the
Jane, 45 years of age, presented with a 9 upper and lower limbs.
week history of progressive paraesthesia In total, the neurophysiological results were consistent with an acquired demyelinating
and weakness involving her fingers and feet polyradiculoneuropathy. Together with the clinical presentation and the duration
bilaterally. She was otherwise well with no of symptoms (>8 weeks), a diagnosis of chronic inflammatory demyelinating
comorbidities or antecedent illness. Jane polyradiculoneuropathy (CIDP) was reached. Lumbar puncture demonstrated elevated
had no relevant family history and was not cerebrospinal protein and normal white cell count (albumino-cytological dissociation)
prescribed any medications. Neurological again consistent with CIDP. Jane was treated with interval intravenous immunoglobulins
examination demonstrated moderate (IVIg) and made an excellent clinical and neurophysiological improvement.
weakness in the distal limbs bilaterally
Figure 3. Jane’s nerve conduction study results
associated with globally absent reflexes.

696 Reprinted from Australian Family Physician Vol. 40, No. 9, SEPTEMBER 2011
 Nerve conduction studies clinical

Sensory examination did not reveal definite Matthew C Kiernan MBBS, PhD, DSc, FRACP, is
abnormalities. Professor of Medicine and Consultant Neurologist,
Jane’s nerve conduction study results, along Neuroscience Research Australia and Prince of
with an accompanying explanation, are Wales Clinical School, University of New South
presented in Figure 3. Wales, Sydney, New South Wales.

Conflict of interest: none declared.

Key points
Reference
• Nerve conduction studies help determine at 1. Schoeck AP, Mellion ML, Gilchrist JM, Christian
FV. Safety of nerve conduction studies in patients
which level of the peripheral nervous system
with implanted cardiac devices. Muscle Nerve
the pathology is located, and are useful for the 2007;35:521–4.
diagnosis and monitoring of a number of focal
and diffuse conditions.
• Nerve conduction studies can help
distinguish axon loss (loss of amplitude) from
demyelinating conditions (slowed conduction).
• Nerve conduction studies are safe and well
tolerated but care is required in patients with
a pacemaker or implantable defibrillator.
• Late responses are an important indirect
assessment of the proximal segments
(nerve roots and plexus) and may be the only
abnormality in many pathologies.
• Interpretation of NCS is highly context
specific, hence clear clinical information will
yield more useful results.

Further reading
• Cheah BC, Kiernan MC. Neurophysiological
methodologies: diagnosis of peripheral nerve
disease and assessment of pharmacological
agents. Curr Opin Investig Drugs 2010;11:72–9
• Fuller G. How to get the most out of nerve
conduction studies and electromyography. J
Neurol Neurosurg Psychiatry 2005;76 (Suppl
2):ii41–6
• Katirji B. The clinical electromyography
examination. An overview. Neurol Clin
2002;20:291–303
• Kimura J. Facts, fallacies, and fancies of
nerve conduction studies: twenty-first annual
Edward H. Lambert Lecture. Muscle Nerve
1997;20:777–87
• Mallik A, Weir AI. Nerve conduction studies:
essentials and pitfalls in practice. J Neurol
Neurosurg Psychiatry 2005;76(Suppl 2):ii23–31
• MBS Online. Available at www.mbsonline.gov.
au/internet/mbsonline/publishing.nsf/Content/
print-on-demand.

Authors
William Huynh MBBS, BSc, FRACP, is Consultant
Neurologist, Clinical Neurophysiologist and
Associate Lecturer, Neuroscience Research
Australia and Prince of Wales Clinical School,
University of New South Wales, Sydney, New
South Wales. [email protected]

Reprinted from Australian Family Physician Vol. 40, No. 9, SEPTEMBER 2011 697

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