J Neurol (2012) 259:1502–1508
DOI 10.1007/s00415-012-6497-3
TECHNIQUES IN CLINICAL SCIENCE
Nerve conduction and electromyography studies
N. M. Kane • A. Oware
Received: 21 February 2012 / Revised: 22 March 2012 / Accepted: 23 March 2012 / Published online: 22 May 2012
Ó Springer-Verlag 2012
Abstract Nerve conduction studies (NCS) and electro-
myography (EMG), often shortened to ‘EMGs’, are a
useful adjunct to clinical examination of the peripheral
nervous system and striated skeletal muscle. NCS provide
an efficient and rapid method of quantifying nerve con-
duction velocity (CV) and the amplitude of both sensory
nerve action potentials (SNAPs) and compound motor
action potentials (cMAPs). The CV reflects speed of
propagation of action potentials, by saltatory conduction,
along large myelinated axons in a peripheral nerve. The
amplitude of SNAPs is in part determined by the number of
axons in a sensory nerve, whilst amplitude of cMAPs
reflects integrated function of the motor axons, neuro-
muscular junction and striated muscle. Repetitive nerve
stimulation (RNS) can identify defects of neuromuscular
junction (NMJ) transmission, pre- or post-synaptic. Needle
EMG examination can detect myopathic changes in muscle
and signs of denervation. Combinations of these proce-
dures can establish if motor and/or sensory nerve cell
bodies or peripheral nerves are damaged (e.g. motor neu-
ronopathy, sensory ganglionopathy or neuropathy), and
also indicate if the primary target is the axon or the myelin
sheath (i.e. axonal or demyelinating neuropathies). The
distribution of nerve damage can be determined as either
generalised, multifocal (mononeuropathy multiplex) or
focal. The latter often due to compression at the common
entrapment sites (such as the carpal tunnel, Guyon’s canal,
cubital tunnel, radial groove, fibular head and tarsal tunnel,
to name but a few of the reported hundred or so ‘entrap-
ment neuropathies’).
N. M. Kane (&)
A. Oware
Grey Walter Department of Clinical Neurophysiology,
Frenchay Hospital, Bristol BS16 1LE, UK
e-mail: nick.kane@nbt.nhs.uk
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Keywords Nerve conduction studies
Electromyography

Sensory nerve action potential
Compound motor action
potential and repetitive nerve stimulation
Background
Introduction
Although individual elements of the EMG study may be
diagnostically specific in certain conditions (Table 1), the
wise neurophysiologist will select a range of tests based on
clinical assessment that not only confirm, or lend support
to, a specific diagnosis, but also rule out other alternative
diagnoses. For this reason, it is better for the referrer to
provide a diagnostic hypothesis, or differential, rather than
specify a particular test in an anatomical region.
Limitations
Although there is variation in the approach and grading of
abnormality by practitioners, who may be drawn from
neurology, rheumatology and rehabilitation medicine, there
are areas of broad consensus and some standardization.
Electromyography is generally safe, reasonably tolerated
by most patients and should not be unduly painful,
although they may be briefly uncomfortable. Some pre-
cautions may need to be taken in patients with implanted
cardiac defibrillators, and needle EMG in patients who are
anticoagulated or have bleeding diathesis [1]. Nerve con-
duction studies/EMGs have a questionable role in the
diagnosis of polyneuropathy of known cause (e.g., diabetes
mellitus, alcohol abuse, renal failure), isolated small fiber
neuropathy, children with pes cavus and normal neurology,
neuroimaging proven ‘discogenic’ radiculopathy and
J Neurol (2012) 259:1502–1508 1503

Table 1 Specific diagnostic EMG tests for particular conditions etiological differential—see Table 3. However, while
Condition Diagnostic test Ancillary tests
EMGs may detect changes in nerve or muscle electro-
physiology prior to clinical signs, rarely do they identify
AHC disease Needle EMG NCS the causative agent. Etiology must be established by the
Radiculopathy Needle EMG NCS, F waves clinical history and/or ancillary serological investigations
Plexopathy NCS Needle EMG (i.e., EMGs are physiologically sensitive but not disease
Neuropathy specific). In addition, there are limitations to both their
Demyelinating NCS, F waves Needle EMG interpretation and application, particularly at the extremes
Axonal loss NCS Needle EMG of life because of maturation and the effects of aging on the
Entrapment neuropathy NCS Needle EMG peripheral nerves. After 30 years of age, the motor CV
Defect of NMJ slows by *1 m/s per decade and sensory CV slows by
MG RNS SF EMG *2 m/s per decade [8]. Other factors, both physical and
LEMS RNS SF EMG physiological, have to be factored in when interpreting
Myopathy Needle EMG NCS NCS. The most important of these is body temperature.
Ideally, the limb skin temperature should be 32–34 °C in
EMG electromyography, SF EMG single-fiber electromyography
the upper and[31 °C in the lower limb during the test. For
certain muscle disease (e.g., muscular dystrophies, genetic temperatures lower than this, a correction factor of
and metabolic myopathy), because these can all be confi- 1.5–2 m/s per degree Celsius temperature change can be
dently diagnosed by other means. In the authors’ experi- applied [12]. Other factors include gender, height, body
ence, EMG is not indicated in pain syndromes without mass index and the individual technique used. These
neurology, in particular complex regional pain type 1 and variables prevent the publication of universally accepted
‘fibromyalgia’, because they have reliable clinical diag- ‘normal values’. Ideally, these should be established in
nostic criteria, and NCS are usually painful for patients each department using its own equipment and chosen
with these conditions due to hyperalgesia or allodynia. techniques for various age cohorts. There is no interna-
tionally agreed principle on how normal values should be
Clinical role displayed (e.g., lower limits of normal, mean, and standard
deviations, percentiles, or z scores). It should be borne in
In the appropriate clinical context, internally consistent mind that there is some overlap between NCS values in the
combinations of EMG abnormalities can confirm neuro- normal and disease states. ‘Normal’ EMG studies do not
logical conditions that affect the anterior horn cell (AHC) therefore exclude neurological disease. There are pitfalls
(motor neuron), nerve roots (radiculopathy), dorsal root for even experienced operators, which can lead to overin-
ganglia, the plexus (brachial or lumbo-sacral plexopathy), terpretation of results. Conversely, in the course of an
peripheral nerves, NMJ (pre- or post synaptic) and mus- EMG it is not uncommon for a neurophysiologist to detect
cle—see Table 2. It can often be inferred that the primary lesions apparently asymptomatic to the patient, until a
pathophysiological process affecting peripheral nerves is probing history is taken. The requesting physician should
due to inflammation or axonotmesis, which may narrow the be able to understand the studies and be prepared to

Table 2 General scheme for electro-diagnosis of various neurological conditions

Condition SNAPs cMAPs EMG RNS

AHC disease N Ampl.; CV B N Denervation in [3 regions. IP ; Usually N or decrement

Radiculopathy N Ampl.; CV B N Denervation in root territory. IP ; Usually N
Plexopathy Ampl.; CV N Ampl.; CV B N Denervation in plexus territory Usually N
Neuropathy
Demyelinating Ampl.; CV ; Ampl.; CV ; Usually N but IP ; Usually N
Axonal loss Ampl.; CV N Ampl.; CV N Diffuse/distal denervation. IP ; Usually N
Entrapment neuropathy Ampl.; Focal CV ; Ampl.; Focal CV ; Denervation in nerve territory Usually N
Defect of NMJ
MG N Usually N Usually N Decrement
LEMS N Ampl.; CV N Usually N Decrement at 3 Hz RNS
Myopathy N Usually N Small polyphasic MUPs. IP dense Usually N or decrement
Ampl amplitude, CV B N conduction velocity is normal or slightly reduced. ; reduced, N normal, IP interference pattern

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Table 3 Combinations of EMG

Process SNAP Ampl. DML cMAP Conduction Temporal F-waves
changes that suggest a particular
block dispersion
pathophysiology
DML distal motor latency, Demyelination ; or – : N or ; ? ? :
N normal, ? present, – absent, ; Axonotmesis ; or – N ; – – N or slight :
reduced amplitude, : delayed

question them if they do not correlate with the clinical

findings. Electromyography have no role in the diagnosis
of conditions affecting the brain and spinal cord, even
though they may be abnormal on occasions.

Methods

Sensory studies

Nerves are stimulated percutaneously with square wave

electrical pulses using a variety of bipolar electrodes (rings
for digits and a two pronged probe or bar electrode else-
where, see Figs. 1, 2). The responses are recorded with Fig. 1 Ulnar (F5) ring stimulation orthodromic sensory nerve action
bipolar surface bar or disc electrodes over sensory nerves. potential recording setup (note green ground electrode and grey-
Adequate skin preparation is required to reduce resistance. colored skin temperature probe)
During electrical stimulation, the patient must be earthed
via a ground electrode placed between the stimulating and
recording electrodes. This helps to reduce stimulus artefact.
Sensory nerve action potentials are directly recorded from
the stimulated nerve, either ‘orthodromically’ (i.e., in the
same direction as physiological conduction) or ‘antidrom-
ically’ (i.e., propagation in the opposite direction to phys-
iological conduction). Orthodromic and antidromic
stimulation are both valid techniques with relative merits
such that the two are frequently used in an EMG study.
‘Averaging’ a number of individual responses is usually
necessary to record SNAPs, to improve ‘signal-to-noise
ratio’. The SNAPs waveforms are of bi- or triphasic mor-
phology (Fig. 3). The amplitude of which can be measured
from the negative peak to the subsequent positive trough
(peak to peak) or baseline to the negative peak (in Fig. 2 Radial antidromic sensory nerve action potential recording set
microvolts). up with stimulation probe
In clinical practice, due to their relative tolerability,
SNAPs are usually recorded first. The most commonly good overall assessment of the post-ganglionic sensory
studied nerves are the median, ulnar, radial, superficial nervous system in peripheral neuropathies. There are rec-
peroneal and sural. These include SNAPs involved in the ognizable patterns of SNAPs abnormalities in peripheral
commonest entrapment neuropathies of the arm (carpal neuropathies, for example ‘abnormal median and normal
tunnel syndrome and ulnar neuropathy at the elbow) and sural’ is common in acquired inflammatory demyelinating
leg (common peroneal neuropathy at the fibula head). An neuropathy [2], and in dorsal root ganglionopathies SNAP
abnormal SNAP places the lesion in the peripheral nervous abnormalities are widespread and non length dependent
system, or post-ganglionic. The SNAPs are generally [4]; in a length-dependent axonal neuropathy the sural and
unaffected by pre-ganglionic lesions such as AHC disease, superficial peroneal responses are usually affected first,
radiculopathy and myelopathy, along with disorders of the followed by the ulnar and then median, with relative
NMJ and muscle (and it should also be noted that they are sparing of the radial SNAP until the neuropathy is
normal in somatoform disorders). Furthermore, they give a advanced. In certain disorders the SNAPs may be absent

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J Neurol (2012) 259:1502–1508
Fig. 3 Normal median (Digits 2 and 3), ulnar (Digit 5) and median
(Me) and ulnar (Ul) palm to wrist SNAPs. Dig. digit, DIST distance,
LAT onset latency, CV conduction velocity (m/s), AMP amplitude
(microvolts)
but the motor responses unaffected (e.g., sensory gangli-
onopathies, ataxia telangiectasia, Friedreich’s ataxia, abe-
talipoproteinemia, hereditary sensory and autonomic
neuropathies). It should be remembered that common
causes of sensory motor peripheral neuropathy may man-
ifest with only sensory changes in the early stages, because
of the selective vulnerability of the large sensory fibers
(e.g., diabetes mellitus, connective tissue disease and
vitamin B12 deficiency). Lesser-studied sensory nerves
include: the lateral antebrachial (musculo-) cutaneous
nerve (for upper trunk/lateral cord brachial plexus), the
medial antebrachial cutaneous nerve (affected in ‘neuro-
genic’ thoracic outlet syndrome and other lower trunk/
medial cord lesions), the lateral femoral cutaneous nerve of
the thigh (affected in ‘meralgia paresthetica’), and the tibial
(medial and lateral) plantar nerves (involved in ‘tarsal
tunnel syndrome’). Symmetry of the SNAPs from the right
and left sides should always be assessed whenever the
unusual sensory mononeuropathies or mononeuropathy
multiplex are suspected. In the latter, it should be borne in
mind that after a period of time-summated mononeuropa-
thies may electrophysiologically resemble a symmetric
length-dependent axonal neuropathy.
Motor studies
Compound motor action potentials are recorded over a
muscle belly, with the active recording electrode at the
motor point (motor end plate) and the reference electrode
over the tendon, using bar or self-adhesive disc electrodes.
The cMAP, sometimes called M wave, is measured from
the baseline to the negative peak (in millivolts). Electrical
stimulation is performed along a motor nerve at two or
more points. This enables CV to be calculated for different
segments of the nerve (e.g., for the ulnar nerve in the
forearm, across the elbow, in the arm above the elbow, see
1505
Fig. 4 a, b, c). The terminal or distal latency is measured in
milliseconds from the stimulus artefact to the onset of the
negative response, and CV (in m/s) calculated by distance
between two stimulation points divided by the proximal
latency minus the distal latency. How much electricity
should be delivered to a nerve varies in health and disease,
but the operator is attempting to achieve ‘supra-maximal’
stimulation, where the stimulus intensity is set at about
10–25 % greater than that required to achieve a maximum
amplitude motor response [6]. F waves are quite variable
low amplitude ‘late’ motor responses recorded after supra-
maximal stimulation of a motor nerve. They result from
backfiring of antidromically activated AHCs. In practice,
the most common measure is the minimum F wave latency
in a train of 10–20 responses. Their latency is influenced by
the height or limb length and age of the subject. They have
the advantage of studying a long section of motor nerve
including its proximal portion and the AHCs. F-wave fre-
quency and amplitude may be affected by CNS disorders
[7].
In clinical practice, the most commonly studied nerves
are the median, ulnar, peroneal and tibial nerves, although
other peripheral and cranial nerves along with nerve roots
can be assessed using similar techniques. Motor NCS have
the distinct advantage of studying several segments along
an individual nerve, which can help to localize a nerve
lesion, particularly in the case of focal motor conduction
abnormality due to entrapment neuropathy (Fig. 5). In
contrast to SNAPs, the cMAPs and F waves are frequently
affected by intra-spinal pathology, such as AHC disease,
myelopathy, and radiculopathy, and by diseases of the NMJ
and striated muscle. With loss of the largest motor neurons
there may be apparent ‘peripheral’ motor conduction
slowing, producing false distal localization. Similarly,
distal entrapment neuropathies may cause ‘proximal’
motor conduction slowing due to preferential dysfunction
(block) or dying back of the large diameter axons. Motor
NCS and F waves are especially helpful in not only con-
firming a diagnosis of peripheral neuropathy, but in clas-
sifying it into axonal, demyelinating and mixed forms, as
well as characterizing the pattern of demyelination or
dysmyelination, which may provide etiological clues (i.e.,
acquired inflammation or inherited dysmyelination). Motor
axonal loss typically causes decreased cMAP amplitude
with relative preservation of the motor CV, although as the
axons continue to ‘fall out’ the CV may drop proportion-
ally. It should be remembered that axonal loss can occur
with lesions affecting the AHC, anterior spinal root, plexus
or peripheral nerve, but the combination of attenuated
SNAPs will locate the pathology to the peripheral nervous
system. Motor nerve demyelination results in combinations
of prolonged distal latency, slowing of CV, conduction
block, temporal dispersion and delayed F waves.
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Fig. 4 a Ulnar motor nerve conduction study set up, stimulating at
wrist and recording the cMAP from abductor digiti minimi (ADM).
b Ulnar motor nerve conduction study set up, stimulating below
elbow. c Ulnar motor nerve conduction study set up, stimulating
above elbow
Conduction block is the failure of action potentials to
propagate past a particular point, causing a drop in cMAP
amplitude from the distal to proximal stimulation sites (see
Fig. 5). Temporal dispersion is due to the relative desyn-
chronization of components of the cMAP due to different
rates of conduction in the motor axons. Traditionally, in
inherited demyelinating neuropathy (e.g., Charcot Marie
Tooth, CMT), the conduction slowing is relatively uniform
across different nerve segments and nerves, while in
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Fig. 5 Abnormal ulnar motor nerve conduction study from ADM,
showing conduction slowing (12.2 m/s) and partial conduction block
(35 %) at the elbow. ADM abductor digiti minimi, dLAT distal
latency, CV conduction velocity, AMP amplitude (in millivolts)
acquired demyelinating neuropathies (e.g., Guillain-Barré
syndrome and chronic inflammatory demyelinating poly-
neuropathy) it is nonuniform [10]. In the era of molecular
diagnosis, it has become apparent that this separation is not
entirely clear cut, and a number of inherited disorders may
have nonuniform or multifocal motor conduction slowing
(e.g., hereditary neuropathy with a liability to pressure
palsies, leukodystrophies, CMT-X with connexin 32
mutations) [11]. Mixed neuropathies with both axon loss
and demyelination can occur in diabetes mellitus, chronic
kidney and liver disease.
Repetitive nerve stimulation
Repetitive nerve stimulation is an extension of the motor
nerve conduction study. It involves stimulating the nerve
with a train of identical square wave pulses, typically 10 at
3 Hz, in an attempt to stress the natural reserve of the NMJ,
called the ‘‘safety factor’’. This is a screening test for
disorders of NMJ transmission, including myasthenia gra-
vis (MG), Lambert-Eaton myasthenic syndrome (LEMS),
botulism and congenital myasthenic syndromes (CMS),
which can usually be diagnosed by serology (i.e., acetyl-
choline receptor or muscle-specific kinase antibodies,
voltage gated calcium channel antibodies, and botulinum
toxin assay) and genetic tests for some CMS. Any of these
conditions can lead to a failure, or blocking, of muscle fiber
excitation at the NMJ, which manifests as a reproducible
initial progressive reduction by greater than 10 % of the
cMAP amplitude on RNS, called ‘‘decrement’’ (typically
measured on the 4th or 5th motor response—see Fig. 6). In
clinical practice, a combination of distal and proximal
muscles should be examined. The intrinsic hand muscles
are well tolerated, easy to immobilize but less sensitive.
Proximal and facial muscles (anconeus, trapezius, nasalis
and/or orbicularis oculi) are more sensitive, but less well
tolerated and prone to movement artefacts. High frequency
J Neurol (2012) 259:1502–1508
Fig. 6 Repetitive nerve stimulation study, at 3 Hz from ADM,
showing a significant decrement in a patient with LEMS
RNS ([20 Hz) can be used to demonstrate a cMAP
amplitude increase or facilitation, which may help distin-
guish pre-synaptic (e.g., LEMS, botulism and some CMS)
from post-synaptic disorders (MG), but it is painful. Brief
exercise of *10–20 s (maximum contraction) is usually
sufficient to increase the cMAP amplitude significantly in
LEMS (typically[100 %). The most sensitive neuro-
physiological test of NMJ transmission is single-fiber
electromyography (SF EMG). This can be time consuming
and technically challenging. In focal MG, when antibody
testing may be negative, SF EMG is frequently diagnostic
and can be adequately performed using a disposable small
facial concentric needle. In essence, two muscle fiber
potentials (a ‘pair’) belonging to the same motor unit are
recorded simultaneously and the interpotential interval
variation is measured in microseconds. This variability, or
‘‘jitter’’, is increased in defects of NMJ transmission as
well as disorders of the terminal nerve fiber and muscle. A
routine concentric needle EMG should therefore also be
performed to exclude nerve and muscle disorders.
Needle EMG studies
The electrical activity of striated muscle, motor unit
potentials (MUPs), can be recorded in different ways, but
in clinical studies the concentric needle EMG (CNE) is the
most commonly used. The concentric needle consists of a
wire (the active electrode) inside a cannula (the reference
electrode), exposing a recording surface at the tip, typically
of 0.07 mm2. The muscle is examined for ‘‘insertional
activity’’ (increased in denervation, inflammatory pro-
cesses and myotonic disorders, or decreased in fibrosis,
fatty infiltration and during episodes of periodic paralysis)
and at rest for ‘‘abnormal spontaneous activity’’ (fibrilla-
tion potentials, positive sharp waves, fasciculations, myo-
tonic discharges, neuromyotonic or complex repetitive
discharges). Individual motor unit morphology and their
recruitment to ‘‘interference pattern’’ (IP) are examined
during increasing voluntary activation [13]. Signs of
‘‘active’’ denervation, fibrillations potentials and positive
sharp waves, appear about 10–28 days after motor axon
degeneration depending on the distance of the muscle from
the site of injury [3] (Note ‘‘active’’ is in a sense a
1507
misnomer as these changes may persists for many years
after axon loss). Spontaneous activity can also be seen in
myopathy. Abnormal spontaneous activity is not seen in
normal healthy muscle, with the exception of (benign)
fasciculations. The morphology of the MUP can be asses-
sed qualitatively by its appearance and sound, or quanti-
tatively by measuring its amplitude, duration, number of
phases (shape) and stability. In general terms ‘‘chronic
partial denervation’’, as a result of axonotmesis and sub-
sequent collateral reinnervation after axon loss, produces
enlarged, long duration, polyphasic (5 or more phases)
unstable MUPs recruiting to a reduced IP (when 20–40 %
of MUPs are lost) (see Fig. 7). Myopathies on the other
hand, typically produce small, short duration, polyphasic,
unstable MUPs which recruit briskly to a dense low voltage
IP. This dissociation is not always so clear in clinical
practice, for example ‘‘nascent’’ neurogenic potentials can
resemble myopathic potentials and in chronic myopathies,
some MUPs may appear enlarged. Furthermore, in some
conditions affecting nerve and muscle, so called ‘‘neur-
omyopathies’’, both neurogenic and myopathic MUPs can
coexist (e.g., inclusion body myositis, mitochondrial cyt-
opathies such as Kearns-Sayre syndrome, critical illness
neuromyopathy, alcohol, and drugs including colchicine,
chloroquine) [9]. Concentric needle electromyography
examination may be normal is some myopathies (e.g.,
genetic and metabolic). Most myopathies do not show
specific diagnostic EMG features but the distribution of
abnormalities in combination with clinical findings can
often distinguish different myopathies (e.g., facio-scapulo-
humeral dystrophy and inclusion body myositis).
In our practice, needle EMG studies are most useful in
confirming the diagnosis of AHC disease, and in predicting
prognosis of traumatic nerve injuries. The clinical neuro-
physiologist’s role in amyotrophic lateral sclerosis (ALS)
or motor neuron disease (MND) requires the demonstration
of EMG signs of lower motor neuron degeneration in two
Fig. 7 Cartoon of concentric needle examination in axon degener-
ation, effects of denervation and reinnervation. Red normal muscle
fiber (biphasic MUP), Green reinnervated muscle fiber (polyphasic
MUP), Grey denervated muscle fiber (spontaneous activity with
positive sharp waves and fibrillations) NB Not to scale
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Table 4 Outline EMG findings in traumatic nerve injury
Classification Patho-physiology
Neurapraxia Focal demyelination
Axonotmesis Some axons disrupted but epineurium intact
Neurotmesis All axons and epineurium disrupted
N normal, CB conduction block, IP interference pattern, Ampl.; decreased, SA spontaneous activity (e.g., fibrillations and positive sharp waves)
or more of the four regions (bulbar, cervical, thoracic and
lumbosacral spinal cord) in the form of active and chronic
partial denervation, combined with clinical upper motor
neuron signs to fulfill the El Escorial or Awaji criteria for
definite ALS/MND [5]. In the course of the study, it is
important to exclude other diagnoses, in particular multi-
focal motor neuropathy with conduction block, which is a
potentially treatable mimic of AHC disease. Following
traumatic nerve injury, caused by lacerations, fractures,
dislocations and crushing, EMG studies at *21 days can
be helpful in establishing the predominant pathophysiology
and prognosis (Table 4). There can be considerable overlap
in the pathophysiology, and timing of the study is crucial to
avoid underestimating the extent of axonal injury and
incorrect localization in the acute phase. Occasionally,
needle EMG in the first few days following traumatic nerve
injury may help to avoid unnecessary immediate surgical
nerve repair. In a muscle that appears to be completely
paralyzed, the presence of volitional motor units on EMG
proves that there are some fibers in continuity. Generally,
such lesions do not require immediate repair.
Conclusions
In summary, EMGs are a useful extension of the neuro-
logical examination and can efficiently and safely answer
specific questions in certain clinical scenarios, which
should be contextual and hypothesis driven. They can often
localize neurological lesions and give clues to pathophys-
iology, thereby etiology, which may guide further investi-
gation and/or management. We would argue that the
principal use in common clinical conditions such as carpal
tunnel syndrome is not only in lending support to the
clinical diagnosis, but in excluding other pathology such as
generalized neuropathy or cervical radiculopathy, and in
helping to predict the prognosis based on neurophysio-
logical severity. Similarly in motor neurone disease, the
role is not only confined to diagnosis, but in excluding
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J Neurol (2012) 259:1502–1508
SNAPs cMAPs CNE Prognosis
N N or CB N but IP ; Recovery, up to 3–6 months
Ampl.; Ampl.; SA and IP ; Variable, depending on degree
Absent Absent SA no MUPS Surgery. No spontaneous recovery
treatable conditions such as multifocal motor neuropathy
with conduction block. They are however rarely disease
specific, are operator dependent, restricted to the large
myelinated nerve fibers, and can be confounded by physi-
ological and non-physiological variables, leading to a lack
of International accepted normal values or diagnostic
criteria.
Conflicts of interest None.
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