1. Electrodiagnostic Studies (more than you ever cared to know)
Pete Vonderau, MD
Physical Medicine and Rehabilitation
THE REHAB DOCTORS

2. Objectives Review pertinent neuromusculoskeletal anatomy
Explain how nerve conduction studies and needle examinations are performed
Review common indications for NCS/EMG studies

3. Electrodiagnostic Studies
Two parts (often collectively referred to as “EMG”)
Nerve Conduction Studies = Nerve Stimulation
EMG (Electromyography) = Needle Exam
Why is it performed?
To evaluate nerve function (assess for nerve or muscle injury)
MRI only evaluates structure
Also for localization of injury, severity, prognosis, ruling out other disease
Commonly indicated for peripheral nerve injury
Performed by physiatrists and neurologists

4. Interpreting EMG/NCS studies requires a solid understanding of Neuromusculoskeletal Anatomy

5. Spine Anatomy Primary motor neuron is the anterior horn cell
Resides in the ventral gray matter of SC
Axons exit as motor roots, combine to form peripheral nerves, innervate muscle
Primary sensory neuron is DRG
Resides in intervertebral foramen
Accepts sensory input from body via pre-ganglionic fibers
Spinal nerves
Composed of ventral (motor) and dorsal (sensory) nerve roots
Divides into dorsal and ventral rami
Ventral rami combine to form plexuses

6. Nerve Anatomy
Each motor (AHC) or sensory neuron (DRG) has one axon (fiber through which impulses are sent)
Each axon surrounded by Schwann cell (makes myelin)
Motor axons and large sensory axons (proprioception) are myelinated (electrically insulated)
Small nerves lack insulation (pain, temperature, autonomic)
Axons are bundled into fascicles
Peripheral Nerve is composed of many fascicles

7. Nerve Physiology
All Cells (including axons of neurons) maintain an Equilibrium Potential
Na/K Pump, cell membrane permeability, and diffusion potentials work together, resulting in the inside of the cell having a negative potential compared to outside (-70mV)

8. Nerve Physiology: Conduction
Nerves transmit information via Action Potentials
Electrical stimulation of nerve causes inside to become more +
Threshold reached at which voltage-gated Na+ channels open briefly, charge inside ↑ rapidly (cell depolarizes)
Na+ flows down nerve to propagate the action potential along nerve (voltage change)
Then gates close and membrane potential increases again
This AP can be measured

9. Nerve Physiology: Saltatory Conduction
A Schwann cell surrounds each axon and can myelinate the axon
Myelin electrically insulates motor axons and larger sensory axons (not small sensory fibers)
Na+ channels are not continuous down nerve but are clustered at Nodes of Ranvier
Conduction jumps from node to node, which is much faster than unmyelinated nerves (10-20x)

10. Motor Nerves: Muscle Contraction
Signal sent from AHC in spinal cord, down axon
At the Neuromuscular Junction, Ach is released
Ach binds muscle membrane, opening Na+ channels, thus depolarizing muscle fiber membrane (voltage change)
Sarcoplasmic reticulum releases Ca++, which binds troponin to start muscle contraction via overlap of actin and myosin

11. Motor Unit Skeletal muscle composed of many fascicles Motor Unit
Fascicles contain thousands of muscle fibers (muscle cells)
Motor Unit
Defined as the motor neuron, its axon, and the muscle fibers it innervates
These fibers depolarize nearly simultaneously, creating a motor unit action potential (electric potential)
We can place a needle into the muscle and measure this electric potential

12. Sensory Nerves Activated by sensory input
Mechanoreceptors
Light touch, pressure, muscle stretch (proprioception)
Myelinated fibers
Nociceptors
Pain (unmyelinated)
Thermoreceptors
Temperature (unmyelinated)
Action potentials travel proximally to the DRG, then on to spinal cord

13. Nerve Conduction Studies

14. Nerve Stimulation
We can stimulate a nerve by sending negative charges around the nerve
Reduces the resting membrane potential and cause the action potential to start anywhere along the nerve
Motor or sensory nerves can be stimulated
Stimulating a motor nerve can result in muscle contraction
Stimulating a sensory nerve gives a buzzing sensation
We attempt to stimulate all of the axon fibers of the target nerve

15. Sensory Nerve Conduction Studies
We measure the electric potentials farther along the nerve with skin electrodes
The computer amplifies the potentials and records them on the computer screen
Recorded values
Distal latency (conduction time over distal limb to electrodes)
Amplitudes (functioning axons)
Conduction Velocity (dist/time)
Compare to normal values or other limb

16. Sensory Nerve Conduction Studies: Uses
Most sensitive for focal mononeuropathies (CTS)
Sensory nerves more prone to injury
The only test for pure sensory cutaneous nerve (cheiralgia paresthetica)
Sensory peripheral neuropathy
Localization: Separating pre-DRG from post-DRG injury
Sensory NCS will be normal if lesion proximal to DRG

17. Normal Values (Sensory NCS)
Sensory Nerve
Distal Latency
Amplitude
Cond. Veloc.
Median Antidromic (II)
<3.6 msec
>15 μV
>56 m/s
Ulnar Antidromic (V)
<3.1 msec
>10 μV
>54 m/s
Median Palmar
<2.3 msec
>50 μV
Ulnar Palmar
>55 m/s
Diff ≤ 0.3
Dorsal Ulnar Cutaneous
<2.6 msec
>8 μV
Superficial Radial Antidromic
<2.9 msec
>20 μV
>49 m/s

19. Motor Nerve Conduction Studies
Stimulate over a motor nerve
Action Potential travels down motor nerve, depolarizes muscle, resulting in a muscle contraction
The electric potential (mV) from muscle contraction is recorded on the skin over the muscle belly
Attempt to activate all the axons of the nerve
Increase stimulation until amplitude no longer increases

20. Motor Nerve Conduction Studies: Measurements
Motor Distal Latency: reflects time for nerve conduction + NMJ transmission + Muscle conduction
Amplitude: reflects the summation of potentials from all functioning motor units
Amplitudes can be low due to injury to AHC, nerve root, peripheral nerve axon, demyelination, NMJ dysfunction, myopathies

21. Normal Values (Motor NCS)
Motor Nerve
Dist. Lat.
Amplitude
Cond Velocity
Median (APB)
< 4.5 msec
>4.0 mV
>48 m/s
Ulnar (ADM)
<3.6 msec
>6.0 mV
>51 m/s
Radial (EDC)
<3.1 msec
>67 m/s
Peroneal (EDB)
<6.6 msec
>2.0 mV
>41 m/s
Tibial (AH)
<6.1 msec
>40 m/s

23. F waves This is a way of assessing the proximal motor nerve
With distal stimulation, 1-2% of motor fibers will carry signal proximally to SC, then back down to muscle
We can measure the latency (response time)
Prolonged latency may be due to proximal nerve injury: radiculopathy, plexopathy, GBS
Not a very sensitive test

24. Pathophysiology: Axonal Injury
AKA Axonotmesis
“Defective wires”
Individual axons no longer function
Fewer axons remain within each nerve fascicle
For sensory nerves, there may be some impairment of sensation (numbness, tingling, absent reflexes)
For motor nerves, there may be weakness and ATROPHY
Atrophy due to muscle cells no longer being innervated

25. Pathophysiology: Axonal Injury
Causes
Nerve trauma or compresssion, metabolic disorders (DM), congenital disease, etc
Nerve Conduction Studies
Low amplitudes, both proximal and distal
Amplitude loss proportional to axon loss
Complete nerve trans-section results in no distal response
Relatively preserved DL and CV
Prognosis
Guarded
Intact axons can slowly sprout to denervated muscle fibers

26. Pathophysiology: Demyelinating Injury
AKA Neurapraxia
“Defective insulation”
Axons are intact, but the myelin sheath (insulation) is damaged
May result in numbness or tingling (sensory nerves), or weakness (motor nerves) but NO atrophy because the axon is still intact

27. Demyelinating Injury: NCS
Stimulating PROXIMAL to injury reveals slowed CV and prolonged DL
Low proximal amplitude if conduction block (complete conduction block possible=no proximal response)
Stimulating distal to the lesion will elicit a normal response
If you cannot stimulate proximal to the lesion, NCS will be normal (radic)
Causes: compression, ischemia, autoimmune, congenital disorders
Prognosis is good if nerve can be decompressed (remyelination often occurs over 4-6 weeks)

28. NCS Examples A: Normal B: Axonal Loss C: Uniform Demyelination
Low amplitude prox & distal, Normal DL
Poor prognosis
C: Uniform Demyelination
Prolonged DL, Slow CV, normal amplitude (seen in CMT)
D: Focal Demyelination with Conduction Block
Low amplitude with proximal stimulation, slow CV, temporal dispersion
Better prognosis than B

29. Needle Exam
This is done to analyze the electrical activity of voluntary muscle
A needle electrode is placed into the muscle
Extracellular potentials created by muscle depolarization are recorded, then amplified and converted to audible sound
Electrical activity is assessed at rest and while the muscle is contracted

30. Needle Exam: Spontaneous Activity
Muscle at rest (not contracting) is at electrochemical equilibrium
There are no action potentials, so the needle should record no activity (silence)
Axonal Injury (Denervation injury)
Due to injury to AHC, nerve root, peripheral nerve
Muscle fibers that lack innervation will fire spontaneously in an regular pattern called a fibrillation potential (abnormal)
Takes 3-4 weeks for these to develop, resolve if sprouting occurs
Demyelinating disorders will NOT cause fibrillation potentials

31. Needle Exam: Fibrillation Potentials

32. Needle Exam: Voluntary Activity
Ask patient to contract muscle
Needle records extracellular potentials from one motor unit (all fibers innervated by one axon), all firing in near synchrony near the needle tip
Amplified and displayed on monitor

33. Needle Exam: Voluntary Activity
Assess the following:
Number of units firing
Frequency
Duration of waveform
Configuration of waveform
Biphasic, Triphasic
Phases
Amplitude
Recruitment

34. Needle: Abnormal Voluntary Activity
Axonal Injury (Denervation)
In the subacute period (4-6 weeks, get polyphasic motor unit potentials as other intact axons send new sprouts to denervated fibers, which must myelinate
Beyond 6 weeks, the amplitude increases and duration increases as remaining intact axons now command more fibers at one time

35. Radiculopathy This is injury to the spinal nerve root
Many causes, but most common is nerve impingement by herniated disc
Impingement can affect ventral (motor) or dorsal (sensory) nerve root, or both
Routine NCS of Lumbar Radic:
Peroneal and Tibial Motor NCS with F
Sural and Peroneal Sensory NCS
Needle: Tibialis Anterior, Medial Gastrocnemius, Peroneus Longus, Vastus Medialis, TFL, Gluteus Maximus, Paraspinal muscles

36. Radiculopathy Nerve Conduction Studies are often normal
Sensory studies are normal because the sensory nerve is proximal to the DRG
Motor are normal unless there is a severe axonal injury (because muscles are innervated by multiple roots)
So why do NCS? – to rule out plexus or peripheral nerve injury
Needle examination is the key
Axonal injury will demonstrate fibrillation potentials after 3-4 weeks
Later, polyphasic motor unit potentials are seen, followed by long duration/high amplitude motor units
Diagnosis requires abnormalities in at least 2 muscles innervated by same root but different nerves

37. Myotomes and Dermatomes
Iliopsoas
L 2 3 4
Rectus Femoris
Adductor Longus
Gracilis
Vastus Lateralis
Vastus Medialis
Tibialis Anterior
L 4 5
EHL
Peroneus Tertius
L 5 1
EDB
L 4 5 1
Peroneus Longus
Internal Hamstrings (SM/ST)
External Hamstring (BFLH)
External Hamstring (BFSH)
L 5
Gluteus Medius
TFL
Gluteus Maximus
L 5 1 2
Tibialis Posterior
FDL
Abductor Hallucis
S 1 2
Abductor Digiti Minimi Pedis
Gastrocnemius (Medial)
Gastrocnemius (Lateral)
Soleus
Reflexes
Patellar
L 3 4
Internal Hamstring
L 5
Achilles S1

38. Radiculopathy: Caveats
Pure sensory radiculopathy will result in a normal study
Pre-ganglionic fibers intact
Pure demyelinating radiculopathy will result in a normal study
What is the diagnostic sensitivity of EMG?
Estimated to be 60-70% based upon AANEM review of literature

39. Carpal Tunnel Syndrome
Injury to the median nerve within the carpal tunnel of the wrist, typically due to compression
Routine Study
Sensory NCS: Median and Ulnar antidromics, Palmar studies
Motor NCS: Median and Ulnar Motor with F waves
Needle Exam: Deltoid, Triceps, Pronator Teres, FDI, APB
Rule out
ALS, Cervical radiculopathy, brachial plexopathy, proximal median neuropathy, peripheral neuropathy

42. Carpal Tunnel Syndrome: Classification
Mild CTS
Prolonged sensory (or palmar) distal latency
Compare median and ulnar palmar DL
Reduced sensory (or palmar) amplitude
Moderate CTS
Prolonged motor distal latency
Severe CTS
Absent sensory response
Reduced motor amplitude
Needle evidence of fibrillation potentials or long duration/high amplitude motor unit potentials

43. Carpal Tunnel Syndrome
What is the diagnostic sensitivity of NCS?
Sensory antidromics: 65% sensitivity for CTS
Palmar studies: 74% sensitivity for CTS (Mayo)

44. Summary: What you need to know
EMG/NCS is useful to further evaluate complaints of numbness, tingling, weakness, and atrophy thought to be related to the peripheral nervous system
Indications
Peripheral nerve injury
Carpal Tunnel Syndrome, Ulnar neuropathy, Peroneal Neuropathy
Peripheral Neuropathy
Plexopathy (Brachial, Lumbosacral)
Radiculopathy
Motor Neuron Disease (ALS)
Myopathy
NMJ Junction Disorders (Academic Centers?)

45. What you need to know (Cont)
Wait 3-4 weeks after nerve injury before ordering an EMG test
Fibrillation potentials take time to develop
Anti-coagulation may limit needle examination
Nerve conduction studies are falsely reduced in obese, edematous limbs
EMG/NCS does not evaluate injury to the central nervous system (stroke, spinal cord injury, etc)
EMG/NCS cannot assess for small fiber peripheral neuropathies (unmyelinated nerves)
Demyelinating nerve injuries have a much better prognosis
Improvement over 4-6 weeks if decompressed
Axonal nerve injuries have a more guarded prognosis
1-2 years to see maximum improvement

46. My Perspective on EMG/NCS
A thorough history and comprehensive musculoskeletal exam will yield the diagnosis >90% of time
EMG is useful in the following situations
When the patient’s presentation is non-physiologic or their effort on exam is unreliable (EMG is objective)
When imaging findings do not match clinical findings

47. Thank You!