emg and ncs: a practical approach to

EMG AND NCS: A PRACTICAL
APPROACH TO ELECTRODIAGNOSTICS
Dr. Harp Sangha, Dr. Tania R. Bruno
Staff Physiatrists
Toronto Rehab—UHN
Lecturers, Department of Medicine
University of Toronto
February 1, 2013
Objectives
• At the end of this session, participants should:
– Be able to identify the basic nerve conduction
studies (NCS) and needle EMG tests used to assess
peripheral nervous system dysfunction
– Determine the types of clinical questions that can
be answered by way of NCS/EMG
Outline
• Introduction
– Overview of the principles of electrodiagnostic
testing
• Review of relevant anatomy and pathophysiology
• Nerve conduction studies and EMG simplified
through relevant cases typically seen in a
sports medicine clinic
Introduction
• Diagnostic imaging is to structure what
electrodiagnostic tests are to function
• Diagnostic imaging and electrodiagnostic
findings are complementary and one does not
replace the other
• By capitalizing on our understanding of
electrical signals throughout the body, we can
capture and record biological responses
previously hidden to our view
Anatomy/Physiology
Anatomy/Physiology
Anatomy/Physiology
Anatomy/Physiology
Anatomy/Physiology
Anatomy/Physiology
• What do we mean by the Peripheral Nervous
System (PNS)?
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–
–
–
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Motor neuron (anterior horn cells)
Sensory neuron (dorsal root ganglion)
Nerve root
Plexus (brachial, lumbar and lumbo-sacral)
Peripheral Nerve
Neuromuscular Junction
Muscle
NB PNS includes CN III-XII
Anatomy/Physiology
Nerve Damage and Repair
WALLERIAN DEGENERATION
• The time course is very
predictable:
– completes in 7 days
for motor nerves
– completes in 11 days
for sensory nerves
WALLERIAN DEGENERATION
Nerve Damage and Repair
“DYING BACK”
• Remember:
– Distal parts of the
neuron are vulnerable
due to their distance
from the cell body
(metabolic power
house for the entire
structure)
– This mechanism is
operant in many
polyneuropathies
AXONAL DEGENERATION
Nerve Damage and Repair
SEGMENTAL DEMYELINATION
• Demyelination:
– Leaves the underlying axon
intact
– Membrane function obviously
changes and the ability to
conduct electrical impulses
declines
– Myelin regeneration is
possible but never repairs as
well as the original
• Typically thinner and
shorter in terms of axonal
coverage
SEGMENTAL DEMYELINATION
NCS/EMG
• As an extension of the history and physical
exam, Electrodiagnosis (Nerve Conduction
Studies and Electromyography) can be
invaluable in identifying the type, severity and
location of nerve injury post-operatively
NCS/EMG
Electrodiagnostic testing
Two Main Components:
• Nerve conduction studies (NCS)
• Needle electromyography (EMG)
NCS
• Test both Motor and Sensory
Measure:
– Amplitude
– Velocity (distance
divided by time)
• Uses a gradually increased amount of electrical
stimulation in order to obtain an
motor/sensory response
Spinothalamic vs Proprioception
Pathways
SPINOTHALAMIC
PROPRIOCEPTION
• Pain & temperature
• Naked nerve endings
• A and C fibers (small,
slow)
• Proprioception
• Specialized receptor organelles
• A and A fibers (large, fast)
Electrodiagnostic studies:
Nerve Conduction Studies
NCS will only study large-myelinated nerve fibers, distal to
the DRG.
Hence, they are normal in myelopathy, radiculopathy and
small-fiber neuropathy, despite clinically evident sensory
loss.
NCS
Waveform Parameters:
– Distal latency
– Amplitude
– Conduction Velocity
– Area
NCS
• Standard Nerve Conduction Studies:
– Upper and lower limb motor studies (median, ulnar,
radial and tibial and peroneal)
• Less commonly, musculocutaneous and axillary studies
– Upper and lower limb antidromic or orthodromic
sensory studies (median, ulnar, radial, sural and
superficial peroneal)
• Less commonly lateral and medial antebrachial , lateral
femoral cutaneous and saphenous
– Late responses: F waves and H-reflex
– Upper and lower limb mixed nerve studies
(transpalmar and medial/lateral plantar studies)
NCS
• Motor studies:
– The time for the electrical
signal to cross the
neuromuscular junction in
the form of
neurotransmitter release,
activate the muscle action
potentials and impulse to
travel to the surface
recording electrode is an
unknown
– Two point studies or more
are, therefore, essential
STANDARD STUDIES
SNAP
• Sensory studies:
– Distal latencies tend to be
much faster than in motor
studies
– They are highly susceptible to
distortion by shock artefact and
noise
NCS
NCS/EMG
EMG
EMG
• Insertion of a needle electrode in various
muscles
• Recording muscle activity at rest and during
activity (volitional activity)
EMG
Fibrillation
Fasciculations
Normal voluntary activity
Electromyography
• Insertional Activity: electrical signals
generated by mechanically deforming the
muscle fiber membrane; response varies
depending on whether there is or is not
proper nervous input to the muscle
membrane
• Spontaneous Activity: abnormal electrical
discharges generated depending on state of
nervous input and health of the muscle
Electromyography
• Motor Unit Action Potentials: waveforms of
summated action potentials from all fibers
innervated by the same alpha motor neuron
(stability, morphology, firing rate assessed)
• Recruitment: organized pattern of voluntary
muscle fiber firing generated in relation to the
contractile force output required
• Interference pattern: recording of all possible
motor unit action potentials at maximum effort
Example: Spontaneous Activity
Positive Sharp Waves
Fibrillation Potentials
EMG/NCS
• Indications:
– Entrapment neuropathy (carpal tunnel, ulnar neuropathy,
etc.)
– Radiculopathy
– Polyneuropathy
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Plexopathy
Myopathy/Myositis
ALS
Myasthenia gravis
– Any combination of the above
Focal Neuropathies
Carpal Tunnel Syndrome (CTS)
Motor study
mV
Sensory study
CTS
• Normal Motor = onset latency < 4.2ms, amp >5.0mV
• Normal Sensory = peak latency < 3.7ms, amp >20µV
• Conduction Velocities in upper extremities generally >50m/s
Radiculopathy
• EDx in Radiculopathy:
– Confirms diagnosis and suggests severity
– Determines: level, acute versus chronic process
– Serial studies can monitor improvement versus
deterioration
• Part of interventional (epidural) or surgical planning
– Very low yield in pure sensory c/o or pain
– Higher yield with weakness and reflex changes
Radiculopathies
• “Numbness” and
pain in the
appropriate
dermatomal
distribution.
• Often associated
with focal myotomal
weakness, focal
hyporeflexia and
back pain.
Radiculopathy– Electrodiagnostic
studies
Nerve conduction studies:
• generally normal (unless severe)
EMG:
• denervation changes (fibrillation potentials and
fasciculations) within muscles innervated by the
root involved and paraspinal muscles adjacent to
the root
• other muscles in the same extremity and any
other muscles are normal
Needle EMG in
Radiculopathy
• Acute/Subacute changes:
– Fibrillations, Positive sharp waves (i.e. spontaneous activity)
– Suggests active process more likely to require work-up and
more involved management
• Chronic
– Motor Unit Changes
– Normal  Polyphasic  large amplitude
– If no new denervation, after 4-6 months, unable to
determine how longstanding such changes are
• Acute (spontaneous activity) - weeks
• Chronic (Motor Unit Analysis) – months-years
Polyphasic
Large amplitude
What Level?
EMG shows:
-denervation changes
(fibrillation potentials and
PSWs) within muscles
innervated by the root involved
and paraspinal muscles
adjacent to the root
-other muscles in the same
extremity and any other
muscles are normal
Radiculopathy
• When not to refer:
– Low back/neck pain w/o radicular pattern –
patients should be treated medically and imaged
as appropriate...
Live Demonstration
Case I
• 45 year old female
• Nocturnal parathsesias to left hand 1 year ago
• Has progressed to bilateral symptoms constant to left, and intermittent to right
Case I
• What is the diagnosis?
• Is it purely demyelinating?
Case II
• 64 year old gentleman presents with footdrop
• Complaints of numbness over the dorsum of
the foot
• Examination
– Ankle DF, Everters, and Toe extensors 2/5, all
other muscles 5/5
– Sensory loss over dorsum of foot
Case II
• Provide a differential diagnosis
• What diagnosis does the EDx suggest?
When to refer for EMG/NCS
• Polyneuropathy:
– Consider risk factors (including DM and ETOH)
– Not an early test
– Serology should come first
Peripheral Nerve Disease (Neuropathy)
• Large-Fiber Neuropathy
– diabetes, ETOH, drug induced (taxol, cis-platinum),
Vit B12 deficiency, autoimmune, infection,
hereditary, idiopathic
• Small-Fiber Neuropathy (normal NCS*)
– diabetes, connective tissue diseases,
sarcoidosis, hypothyroidism, vitamin B12
deficiency, paraproteinemia, hiv, celiac
disease, paraneoplastic syndrome,
idiopathic
Small-Fiber Neuropathy–
Electrodiagnostic studies
COMPLETELY NORMAL
Large-Fiber Neuropathy
• History:
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–
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–
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Constant unsteadiness
Frequent falls
slow (months/years) progression
numbness, tingling, pain are less salient feature
first involves feet/legs then hands/arms
Large-Fiber Neuropathy
• Examination:
– Decreased proprioception (joint position) and
vibratory sense (tuning fork) in a “stocking and
glove” distribution
– Normal OR decreased temperature/pain sensation
in a “stocking and glove” distribution
– Reflexes are decreased (legs > arms)
– Gait is very unsteady (wide-based)
– Weakness in feet > hands is a late sign
Large-Fiber Neuropathy–
Electrodiagnostic studies
Nerve conduction studies:
• decreased amplitude or absent responses
• changes are greater in the lower extremities than
upper extremities
EMG:
• normal
• in longstanding disease it may show denervation
in distal muscles
Polyneuropathy EDx Studies
• Nerve conduction studies (NCS)
– the most important non-serologic test for the diagnosis of
neuropathy
• Electromyography (EMG)
– helps evaluate the effect on muscles
– rules out muscle disease
Myopathy – Electrodiagnostic studies
Nerve conduction studies usually normal (motor and
sensory nerves)
EMG Spontaneous activity at rest (fibrillations, PSW)
Small units when symptomatic muscles are activated
even with maximal effort
When else to refer for EMG/NCS
• ?ALS, ?MG, ?plexopathy:
– Much less common  Therefore, discussion of EDx
findings out of scope of this talk
– Serology/consultation/imaging/treatment should
occur in parallel with EMG/NCS
Why EMG/NCS by Physiatry?
• Often in primary care setting, presentation is
not clearly MSK or neurological
– Eg. ?True radiculopathy vs ?MSK entity with
referred symptoms
• Management
– Medications, F/U, physio, bracing,
injections/epidurals, surgical referrals,
investigations/Tx of MSK entities
EMG/NCS
• Extension of clinical diagnosis – NOT to make a
dx
• Grade severity (mild, moderate, severe) i.e.
define the need for medical or surgical
intervention
• Exclude other diagnosis
• Prognosis (myasthenia, ALS, GBS)
Conclusion
• Integrity of the motor and sensory nerves can be
ascertained directly from NCS
• Direct information regarding health of muscle and the
neuromuscular junction and indirect information
regarding state of muscular innervation is provided by
EMG
• Knowing the root level, plexus and terminal branch
innervation of each sampled muscle can help localize
the site of nerve lesion and provide information
regarding the acuity or chronicity of that lesion
Conclusion
• If appropriately timed (i.e. not too early postinjury), NCS and EMG can be an invaluable
tool
• Identification/confirmation of injury or
pathology; prognostication of recovery/degree
of likely residual deficits; localization of lesion
site can lead to appropriate treatment, be it
compensatory or restorative